Volume 59, Supplement 1 January 2017

Indian Journal of Psychiatry • Volume 59 • Supplement 1 • January 2017 • Pages S***-S***

& IPS Clinical Practice Guidelines

Covered in
Science Citation for Psychiatrists in India
Reports (JCR)
(Revised Edition 2016)

Schizophrenia, Depression, Bipolar Disorder, Generalized Anxiety

Disorder & Panic Disorder, Obsessive Compulsive Disorder,
Sexual Dysfunctions, Sleep Disorders

Task Force on
Clinical Practice Guidelines
for Psychiatrists in India
National Workshop held at Jaipur 24 & 25 Oct. 2015
and on 6 & 7, Aug. 2016

Guest Editors:
Shiv Gautam
Ajit Avasthi
Sandeep Grover

Online at
www.indianjpsychiatry.org Published by: Indian Psychiatric Society
 Indian Journal of
Psychiatry OFFICIAL PUBLICATION OF THE INDIAN PSYCHIATRIC SOCIETY
Print ISSN 0019-5545
E-ISSN 1998-3794

Honorary Editor SK Tandon, Bhopal Joesph Calabrese, U.S.A.

T. S. Sathyanarayana Rao R Thara, Chennai Jonathan M. Meyer, U.S.A.
Professor, Vikram Kumar Yeragani, Bangalore Juan E. Mezzich, U.S.A.
Department of Psychiatry, J. S. S. University Vinod Sinha, Ranchi Julio Arboleda Florez, Canada
JSS Medical College and Hospital, Vivek C. Kirpekar, Nagpur K. W. M. (Bill) Fulford, U.K.
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Chittaranjan Andrade, Bengaluru Asim Kumar Mallick A. K. Kala Richard Balon, U.S.A.
9440422626 P. S. V. N. Sharma Arbinda Bramha Robert B. Pohl, U.S.A.
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Joseph P. Varghese Sudhir Kumar Sekhar Saxena, Geneva
Honorary Deputy Editors Kangan Pathak Vihang N. Vahia Sheila Hollins, U.K.
K. S. Shaji, Trissur Neelanjan paul Soumithra Ghosh Solomon Rataemane, South Africa
9495170655 Subhash Chander Bhatia, U.S.A.
drshajiks@gmail.com Indian Advisory Board
Subodh Dave, U.K.
A. B. Ghosh Narendra N. Wig Thomas Craig, U.K.
O. P. Singh, Kolkota Abraham Varghese Prasanna Raj
9434013231 Tony Elliott, U.K.
A. K. Agarwal P. Raghurami Reddy Vijoy K. Varma, U.S.A.
opsingh.nm@gmail.com A. K. Tandon R. Srinivasa Murthy Vikram Kumar Yeragani, U.S.A.
Honorary Assistant Editor Col. G. R. Golecha R. Sathianathan Vikram Patel, U.K.
G. G. Prabhu S. C. Malik
Abhinav Tandon, Allahabad
08400951567
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Ajay Singh, Mumbai Afzal Javed, U.K. A. Venkoba Rao 1968 to 1976
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Margoob Mustaq Ahmed, Srinagar Driss Moussaoui, Morocco Nimesh G. Desai 2005 to 2006
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Indian J Psychiatry 59 (Supplement 1), January 2017 i
 Indian Journal of
Psychiatry
OFFICIAL PUBLICATION OF THE INDIAN PSYCHIATRIC SOCIETY

IPS Executive Council Members International affairs

President Chairperson: E. Mohandas
G. Prasad Rao, Hyderabad Co-chairperson: Rajesh Nagpal
prasad40@gmail.com Convener: Venu G Jhanwar
Vice President: President elect Constitution
MSVK Raju, Pune Chairperson: R.R. Ghosh Roy
msvkraju@gmail.com Co-chairperson: V.K. Sinha
General Secretary Convener: Shanti Bala K
Gautam Saha, Kolkata Mental Hospitals
drgsaha@yahoo.co.in Chairperson: Nirmal Bera
Hon. Treasurer Co-chairperson: Ram Ghulam Razdan
Mukesh P Jagiwala, Surat Convener: Nishant Goyal
mukeshjagiwala@yahoo.co.in Membership
Hon. Editor Chairperson: Prabir Paul
T. S. S. Rao Mysore Co-chairperson: U.K. Sinha
tssrao19@yahoo.com Convener: Ajish Mangot
Immediate Past President Parliamentary
Vidhyadhar Watve, Pune Chairperson: Sunil Mittal
vidyadharw@gmail.com Co-chairperson: Rajesh Sagar
Immediate Past Secretary Convener: Krishna Kadam
N N Raju PG Psychiatry Education
drnnraju@gmail.com Chairperson: Sudhir Bhave
Executive Council Members (Direct) Co-chairperson: Nitin Gupta
Kishore Gujar, gujarkishor46@yahoo.co.in, Convener: Abir Mukherjee
Mrugesh Vaishnav, drmrugesh@rediffmail.com, Finance
Om Prakash Singh, opsingh.nm@gmail.com, Chairperson: R Ponnudurai
Arabind Brahma, Co-chairperson: Arun Marwale
drarabindabrahma04@yahoo.com Convener: C.R. Mohapatra
Kshirod Kumar Mishra, IPS Publication
drkkmishra2003@yahoo.co.uk, Chairperson: Vinay Kumar
Om Prakash, drjhirwalop@yahoo.co.in, Co-chairperson: Sandip H Shah
Sunil Goyal, dr_sgoyal@yahoo.co.in Convener: Amlan Kusum Jana
Website
Zonal Representative Chairperson: Mainak Mukherjee
Central Zone Co-chairperson: Abhijeet Faye
Shashi Rai, shashi5284@rediffmail.com Convener: Samrat Kar
Jai Prakash Narayan, jpny62@yahoo.co.in Education Research & Training Foundation
East Zone Chairperson: Ajit Avasthi
Hiranya Goswami, goswamihiranya57@gmail.com Co-chairperson: T Jagadisha
Sanjay Munda, drsanjaymunda@gmail.com Convener: Adarsh Tripathi
North Zone Social Security Scheme
B.S. Shekhawat, shekawatbharat1@gmail.com Chairperson: Sarvesh Chandra
Lalit Batra, dr_lalitbatra@yahoo.com Co-chairperson: Kaushik Gupte
South Zone Convener: V.G. Kulkarni
Abhay Matkar, drabhaymatkar@hotmail.com IPS Headquarters:
K. Uday Kumar, udayaspandana@gmail.com Chairperson: N K Bohra
West Zone Co-chairperson: Rajesh Rastogi
D M Dhavale, dmdhavale@gmail.com Convener: Brahmdeep Sindhu
Kaushik Gupte, guptekaushik@gmail.com
Speciality Sections
Assistant General Secretaries Military Psychiatry
Manaswi Gautam, Abdul Majid, Chairperson: R.C. Das
Neelanjana Paul, Vishal Indla Co-chairperson: Jyoti Prakash
Sub Committees Convener: Rajeev Saini
Awards Biological Psychiatry
Chairperson: I.R.S. Reddy Chairperson: A. Jagadish
Co-chairperson: Verghese Punnose Co-chairperson: Ganesan Venkatasubramanian
Convener: Venkata Ramana Cherukuri Convener: Vaibhav Dubey
CME Child and Adolescent Psychiatry
Chairperson: T.P. Sudhakar Chairperson: Debasish Konar
Co-chairperson: Sri Kumar Mukherjee Co-chairperson: Shanti Nambi
Convener: Aleem Siddique Convener: Anweshak Das
Ethics Community Psychiatry
Chairperson: Roy Abraham Kallilvayalil Chairperson: B.S. Chavan
Co-chairperson: Fiaz Ahmed Sattar Co-chairperson: V.D. Meel
Convener: Bhavesh Lakdawala Convener: Sanjay Gupta
Journal Geriatric Psychiatry
Chairperson: T S S Rao Chairperson: S.C. Tiwari
Co-chairperson: Malay Ghosal Co-chairperson: Alka Subramanyam
Convener: Abhinav Tandon Convener: Samir Kumar Praharaj
ii Indian J Psychiatry 59 (Supplement 1), January 2017
 Indian Journal of
Psychiatry OFFICIAL PUBLICATION OF THE INDIAN PSYCHIATRIC SOCIETY

Forensic Psychiatry Clinic Software Development

Chairperson: C.L. Narayanan Chairperson: Umesh Nagapurkar
Co-chairperson: Basudev Das Co-chairperson: Sanjay Phadke
Convener: Sanjay Garg Convener: Vipul Singh
Rehabilitation Psychiatry Public Education & Stigma Reduction
Chairperson: C.R.S. Ramasubramanian Chairperson: Avdesh Sharma
Co-chairperson: V.K. Radhakrishnan Co-chairperson: Rajeev Gupta
Convener: V.D. Aravind Convener: P. Himakar
Private Psychiatry Media and Mental Health
Chairperson: Param Kulhara Chairperson: Jayanta Das
Co-chairperson: Pramod Kumar Co-chairperson: G.S.P. Raju
Convener: Amrit Pattojoshi Convener: Ranjan Bhattacharyya
Substance Use Disorders Young Psychiatrists’ Forum
Chairperson: Pratima Murthy Chairperson: Jay Shastri
Co-chairperson: Debasish Basu Co-chairperson: Debjani Bandyopadyay
Convener: Atul Ambekar Convener: Anitha Ravirala
Law and Ethics Workshop & Training
Chairperson: G. Gopalakrishnan Chair Person: P.K. Dalal
Co-chairperson: Tushar Jagawat Co-chairperson: Rashmin M. Cholera
Convener: Manu Arora Convener: K. Narasimha Reddy
Sexual Disorders SAARC Affairs
Chairperson: Uday Chaudhury Chairperson: U.C. Garg
Co-chairperson: Partha Pratim Roy Co-chairperson: Kuruvilla Thomas
Convener: Parth Vaishnab Convenor: Anil Prabhakaran
Women and Mental Health Pharmacological Management
Chairperson: Smita Deshpande Chairperson: Chittaranjan Andrade
Co-chairperson: M. Gowri Devi Co-chairperson: R.C. Maniar
Conveners: Srikala Bharath, Geeta Desai Convener: Sarmila Sarkar
General Hospital Psychiatry: Non Pharmacological Management
Chairperson: Lalit Batra Chairperson: Philip John
Co-chairperson: Radhika Reddy Co-chairperson: I.R. Rajkumar
Convener: Shahul Ameen Convener: Sagar Lavania
Suicide Prevention Yoga and Meditation
Chair Person: Subhangi Parker Chairperson: B.N. Gangadhar
Co-chairperson: Lakshmi Vijay Kumar Co-chairperson: P. Kishen
Convener: Sujit Sarkhel Convener: G.V. Ramana Rao
Parinatal Psychiatry Spirituality and Mental Health
Chairperson: Prabha Chandra Chairperson: S. Vijaya Kumar
Co-chairperson: Sonia Parial Co-chairperson: MVR Sharma
Convener: Anita Gautam Convener: Lt. Col. Harihar
Task Forces Boundary Guidelines
Practice Guidelines Chairperson: Ajit Bhide
Chairperson: Shiv Gautham Co-chairperson: Sunita S. Kurpad
Co-chairperson: Ajit Avasthi Convener: P. Srilakshmi
Convener: Sandeep Grover PWD Act & Certificate Guidelines
Mental Health Care Bill Chairperson: Asim Kumar Mallick
Chairperson: Rakesh Kumar Chadda Co-chairperson: Thomas John
Co-chairperson: B.M. Suwalka Convener: K. Ramakrishnan
Convener: Mahesh Gowda NGOs/Patients Career Group
Mental Health Policy Chairperson: G. Swaminath
Chairperson: Savita Malhotra Co-chairperson: Amarnath Mallik
Co-chairperson: Chandrasekhar Kammammettu Convener: R.Vikram
Convener: Deepanjali Medhi School Education/Counseling
Liaison of Mental Health Chairperson: Kesri Chavda
Chairperson: Dinesh Narayan Co-chairperson: Khyati Mehtalia
Co-chairperson: Hardeep Singh Convener: Arti V. Mehta
Convener: Kaustav Chakraborty Conference Guideline
UG Education Chairperson: Rajeev Jain
Chairperson: Mohan Chandran Co-chairperson: Abhay Matkar
Co-chairperson: P.B. Behere Convener: T. Sudhir
Convener: Mamta Sood Tribunal IPS
Administrative Psychiatry A.K. Agarwal (Chairperson)
Chair Person: Tophan Pati A.B. Ghosh, James Anthony, S. Nambi,
Co-chairperson: Nilesh Shah P. Palanniappan
Convener: A.K. Handigol
Disaster Management IPS Election Commission
Chairperson: Margoob Mustaq Ahmed Chairperson: Vivek Kirpekar
Co-chairperson: Arnab Banerjee Returning Officer: K. Sudharshan
Convener: Harish Delanthabettu Election officer: Roop Kumar Siddana
Indian J Psychiatry 59 (Supplement 1), January 2017 iii
 Indian Journal of
Psychiatry OFFICIAL PUBLICATION OF THE INDIAN PSYCHIATRIC SOCIETY
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Indian J Psychiatry 59 (Supplement 1), January 2017
 Indian Journal of
Psychiatry OFFICIAL PUBLICATION OF THE INDIAN PSYCHIATRIC SOCIETY
Volume 59, Supplement 1, January 2017

CONTENTS

Clinical Practice Guidelines S1

Changing times, moving ahead!: G Prasad Rao, President S2

Commitment for Clinical Excellence: MSVK Raju S3

Meeting the needs!: Gautam Saha S4

EDITORIAL
Clinical Practice Guidelines: Principles for Clinical Practice: T.S. Sathyanarayana Rao, Abhinav Tandon S5

IPS Task Force on Clinical Practice Guidelines Workshop held on Oct, 24, 25, 2015 S7

IPS Task Force on Clinical Practice Guidelines Workshop held on Aug, 6 & 7, 2016 S8

Preamble of the Clinical Practice Guidelines: Shiv Gautham, Ajit Avasthi, Sandeep Grover S9

ORIGINAL ARTICLE
Indian Psychiatric Society Survey on Clinical Practice Guidelines: Sandeep Grover, Ajit Avasthi S10

CLINICAL PRACTICE GUIDELINES

Clinical Practice Guidelines for Management of Schizophrenia: Sandeep Grover, Subho Chakrabarti,
Parmanand Kulhara, Ajit Avasthi S19

Clinical Practice Guidelines for the management of Depression: Shiv Gautam, Akhilesh Jain,
Manaswi Gautam, Vihang N. Vahia, Sandeep Grover S34

Clinical Practice Guidelines for Management of Bipolar Disorder: Nilesh Shah, Sandeep Grover,
G. Prasad Rao S51

Clinical Practice Guidelines for the Management of Generalised Anxiety Disorder (Gad) and
Panic Disorder (Pd): Shiv Gautam, Akhilesh Jain, Manaswi Gautam, Vihang N. Vahia, Anita Gautam S67

Clinical practice guidelines for Obsessive-Compulsive Disorder: Y.C. Janardhan Reddy,

A. Shyam Sundar, Janardhanan C. Narayanaswamy, Suresh Bada Math S74

Clinical Practice Guidelines for Management of Sexual Dysfunction: Ajit Avasthi, Sandeep Grover,
T S Sathyanarayana Rao S91

Clinical Practice Guidelines for Sleep Disorders: Ravi Gupta, Sourav Das, Kishore Gujar, K K Mishra,
Navendu Gaur, Abdul Majid S116

Indian J Psychiatry 59 (Supplement 1), January 2017 v

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vi Indian J Psychiatry 59 (Supplement 1), January 2017

 TASK FORCE ON CLINICAL PRACTICE GUIDELINES

Clinical Practice Guidelines

We have great pleasure in placing in your hands the out
come of two workshops on Clinical Practice Guidelines
organised by Task force on Clinical Practice Guidelines
organised at Jaipur - First on Oct 24 & 25th 2015 on
Depression, Schizophrenia and BPAD under leadership of
Dr. V G Watve as President and Dr. N.N. Raju as Hon. Gen.
Secretary of Indian Psychiatric Society and Second on Aug.
6th and 7th 2016 on OCD, GAD & Panic Disorder, Sexual
Dysfunctions and Sleep Disorders under leadership of Dr. G.
Prasad Rao as President and Dr. Gautam Saha as hon. General
Secretary of Indian Psychiatric Society. In each workshops
39 experts from different parts of the country participated
and contributed their wisdom (List of Participants experts
given earlier).
suggested. The outcome is in your hands for ready use in
day to day clinical practice for reference.
On behalf of the Task Force we extend heartfelt thanks to
the executive council of two successive years for giving us
the opportunity to serve Indian Psychiatric Society.
We are grateful to Dr. T.S.S. Rao, editor IPS for Printing the
CPG Guidelines as supplement at a short notice.
Long Live IPS.
Jai Hind

As in earlier Guidelines the draft papers were revised after Dr. Shiv Gautam Dr. Ajit Avasthi Dr. Sandeep Grover
obtaining the consensus of house on each guideline and Chairman Co- Chairman Convenor
the draft papers were revised in the light of ammendments

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DOI:
How to cite this article: Clinical Practice Guidelines. Indian J
10.4103/0019-5545.196963
Psychiatry 2017;59:1.

© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow S1

 MESSAGE FROM THE PRESIDENT
Changing times, moving ahead!
Dear Colleagues,
Greetings from the President’s desk !
The publication of Clinical Practice Guidelines for
Psychiatrists’ in India, by the Indian Psychiatric Society
in 2004, were the first set of guidelines. These have
remained in use for over a decade by all members and
were of use in the practice and had also been used by the
members in defending their clinical decisions in the court
of law.
In last one decade there have been further advancements
in understanding various aspects of psychiatric disorders.
Hence, it was thought that time has come to acknowledge
the advances in Psychiatry to be translated into the practice
of Psychiatry in India. With this thinking, I must place on
record that during Hyderabad ANCIPS on January 11th,
2015, the Executive Council, under the leadership of Dr.
Vidhyadhar Watve decided to start the process of revision of
existing Clinical Practice Guidelines. As part of the revision,
first an online survey was conducted to understand how
the earlier versions of the guidelines were used and what
are the expectations of the membership from the revised
guidelines. Based on the findings of this survey, the lead
authors were advised to formulate guidelines, which
would be evidence based and at the same time more users
friendly.
Over the last 2 years, experts working in the various
areas of psychiatry, after a painstaking brainstorming,
had churned out the best way to practice. The Clinical
Practice Guidelines for schizophrenia, bipolar disorder
and depressive disorders, so summarized had been
presented at Bhopal ANCIPS 2016. The Clinical Practice
Guidelines for these disorders were also displayed in
the Indian Psychiatric Society website for the comments
from the membership during the month of September
2016‑ November 2016. Suggestions received were
considered and if required changes have been made in the
recommendations.
The Clinical Practice Guidelines for Obsessive Compulsive
Disorder, Generalized Anxiety Disorder, Sexual Dysfunction
S2 © 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow
and Sleep Disorders have also been formulated and these
will also be presented in ANCIPS 2017.
I congratulate Prof. Shiv Gautam, Prof. Ajit Avasthi and Dr.
Sandeep Grover, for their dedication, hardwork, diligence
and precision in making this possible. Additionally, I also
thank the members of various expert groups for their inputs
in improving the guidelines. I thank all of them on behalf of
Indian Psychiatric Society.
I have no doubt that the revised Clinical Practice Guidelines
would be useful and informative not only to clinicians but
also to all mental health professionals.
I thank all the members of my Executive Council for their
inputs and participation. During the coming years we
are going to work on and bring further Clinical Practice
Guidelines for few more disorders. I am sure these
guidelines would of immense help to all.
Dr. Gundugurti Prasad Rao
President, Indian Psychiatric Society
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DOI:
10.4103/0019-5545.196964
How to cite this article: Rao GP. Changing times, moving
ahead!. Indian J Psychiatry 2017;59:2.
 CLINICAL PRACTICE GUIDELINES

Commitment for Clinical Excellence

It is the fundamental duty of any professional body of Dr (Brig) M S V K Raju

doctors to put in place a framework of uniform clinical
practice that is based not only on scientifically obtained Veteran Armed Forces Medical Services
evidence available from all parts of the world but also
on evidence obtained from research carried out in home Vice President (President Elect), Indian Psychiatric Society
country. Since 2005 the Indian Psychiatric Society has been
providing systematically developed patient care strategies This is an open access article distributed under the terms of the Creative
to its members for effective clinical decision making and Commons Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non‑commercially, as long as the
delivery of care that is comparable to globally current
author is credited and the new creations are licensed under the identical terms.
standards.
For reprints contact: reprints@medknow.com

The present compilation of Clinical Practice Guidelines,

touching upon a broad gamut of conditions including Access this article online
Schizophrenia, Bipolar disorders, Depression, OCD, Quick Response Code
sleep disorders and sexual dysfunctions, will cater to a Website:
major chunk of clinical load that a psychiatrist generally www.indianjpsychiatry.org
encounters in practice. The guidelines will definitely spare
the harried psychiatrists from the time and effort spent in
DOI:
obtaining needed information from various sources.
10.4103/0019-5545.196965

The exertions of the team headed by Prof Shiv Gautam, Prof

Ajit Avasthi and Dr Sandeep Grover manifesting in the form
of clinical practice guidelines are ample testimony of their
How to cite this article: Raju M. Commitment for Clinical
tenacious commitment to excellence and therefore need to
Excellence. Indian J Psychiatry 2017;59:3.
be commended in full measure.

© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow S3

 MESSAGE FROM HON. GENERAL SECRETARY

Meeting the needs!

It is indeed a matter of great pleasure to let you all know
that Indian Psychiatric Society (IPS) is bringing out revised
“Clinical Practice Guidelines (CPGs)” for management of
various psychiatric disorders.
In earlier years, IPS has developed CPG for psychiatrists in
India and for management of various psychiatric disorders
and other issues important for practice of psychiatry in five
volumes from 2005 to 2009 under the expert guidance of
Prof. Shiv Gautam and Prof. Ajit Avasthi.
All the contributors earn our sincere gratitude for their
efforts on this publication.
I thank Prof. Shiv Gautam, Prof. Ajit Avasthi and
Dr. Sandeep Grover along with all the authors for
completing such arduous task. This has been possible due
to outstanding support from President Dr. G. Prasad Rao,
Vice President Dr. M. S. V. K. Raju and other EC Members.
Long live IPS !

This year, the CPGs Task Force of IPS led by Prof. Shiv Dr. Gautam Saha
Gautam as Chairperson, Prof. Ajit Avasthi as Co‑Chairperson
and Dr. Sandeep Grover as Convenor has developed the CPG Hon. General Secretary, Indian Psychiatric Society
to serve as an evidence‑based framework for practitioners’
in clinical decision‑making. I hope these guidelines become This is an open access article distributed under the terms of the Creative
among the most comprehensive, evidence‑based CPGs for Commons Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non‑commercially, as long as the
these disorders. It summarizes treatment recommendations author is credited and the new creations are licensed under the identical terms.
and describes elements of psychiatric management in
For reprints contact: reprints@medknow.com
the formulation and implementation of a treatment plan.
Besides the clinical issues, the guideline examines specific
socio‑cultural and feasibility issues which influence Access this article online
treatment plan, e.g., psychiatric factors, demographic and Quick Response Code
psychosocial variables, and co‑morbid general medical Website:
conditions. It provides a review and synthesis of available www.indianjpsychiatry.org
evidence regarding the efficacy of various treatments,
continuation treatment and maintenance treatment. DOI:
10.4103/0019-5545.196966
Indian Psychiatric Society is really happy to promote the
latest clinical developments in the field of disorders and I
believe that these CPGs will be of great use to all the mental
health professionals, especially to the clinicians, post
How to cite this article: Saha G. Meeting the needs!. Indian
graduate students and researchers. I wish that IPS will come
J Psychiatry 2017;59:4.
up with more CPGs on various psychiatric topics in future.

S4 © 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow

 EDITORIAL
Clinical Practice Guidelines: Principles for Clinical Practice
T.S. Sathyanarayana Rao1, Abhinav Tandon2
1
Professor, Department of Psychiatry, JSS Medical College and Hospital, JSS University, Mysore, 2Asst Editor, Indian Journal
of Psychiatry, Consultant Neuropsychiatrist, Dr AK Tandon Neuropsychiatric Centre, Allahabad, India
“Principles are guidelines for human conduct that are
proven to have enduring, permanent value.”--- Stephen
Covey
A revision of the clinical practice guidelines (CPGs) by Indian
Psychiatric Society(IPS) was long overdue, considering
the intensity and momentum of current research in
Neurosciences. This daunting task was taken up and
completed by an expert group of academicians, after an
initial online survey and later taking into consideration the
opinion of the members of IPS, through open suggestion
online. The online survey gave an insight into the usage of
the existing guidelines and the expectations from members;
prepublication copy of the revised guidelines were available
online for comments and suggestion from the members
which were then streamlined and incorporated.
Field and Lohr in 1990 have described Clinical practice
guidelines (CPGs) as: “systematically developed statements
to assist practitioners and patient decisions about
appropriate health care for specific circumstances”.1 The
Institute of Medicine defines clinical practice guidelines
as “…statements that include recommendations,
intended to optimize patient care, that are informed
by a systematic review of evidence and an assessment
of the benefits and harms of alternative care options”.2
CPGs act as a valuable source of information for health
care providers in maintaining treatment standards which
are up-to-date, evidence based and in accordance with
the latest advancements. Guidelines assist the clinicians
in the decision making process, help them in taking
difficult decisions in complicated cases and allows them
to follow a particular treatment course (vs another
available one) for the best desired outcome. Guidelines
help clinicians defend themselves in the Court of Law.
Guidelines describe clinical care based on best available
evidence, help maintain consistency in clinical practice,
focus on appropriate usage of resources, help in quality
control, guide in developing pathways of healthcare which
are cost effective and give insight for future research.3
Patients suffering from the same problem are likely to
receive different care depending on the place, clinician or
hospital. Guidelines can simplify this problem by making
it more likely that patients receive similar care regardless
of the hospital or doctor treating them.4 Patients are
increasingly becoming aware of treatment options through
© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow
print and electronic media where they come across lay
guidelines; doctors need to inform the patients regarding
available treatment alternatives, their potential harms
and benefits, where clinical guidelines work as the best
available educative tool. CPGs highlight gaps in known
literature where treatment recommendations are not
clear cut; hence it helps in identifying areas where future
research should be focused. Guidelines often act as one of
the reference points in audits of clinicians and hospitals
for rating them with best care practices.5 It is easier for
insurance companies to pay for standardized treatment
practices; public perception is likely to improve if a health
care facility adheres to CPGs and publicizes the same. It is
likely that economic advantages of following CPGs is one
of the main reasons for their popularity.6
The phrase “evidence- based medicine” refers to the use
of treatment that has been tested rigorously to the point
of its becoming “state of the art.”7 EBM has received both
support and criticism from academicians and clinicians.
Evidence based medicine (EBM) contributes to improved
quality of CPGs and hence better clinical care given to the
patients. Original research and systematic reviews provide
the best evidence and have the potential to provide the best
health care at the lowest cost.8 EBMs are best considered
as educative tools, which should be used by the clinician
for the appropriate group of patients and as check sheets
during the process of treatment.7 Evidence for a specific
treatment, needs to be combined with experience of the
clinician and patient’s preference for the best possible
outcome.
Though it has been found in rigorous evaluations that
clinical practice guidelines improve quality of health care,
whether they do so in daily practice is less clear.1This may
be partially because patients, clinicians and managers
define quality differently and the current evidence
about the effectiveness of a particular guideline may be
incomplete. The most important drawback of guidelines
is that they may not represent the most appropriate
treatment for the individual patient. The members of the
expert panel for guidelines development may be mislead
by the scientific evidence due to lack of well designed
studies; another reason for flawed guidelines may be due
to misinterpretation of scientific information.4 The expert
panel may be biased in favour of a particular treatment
S5
 Rao and Tandon: CPGs for Clinical Practice
due to flawed personal recollections when conflicting
data are available for different treatment options.9 Due
to inadequate time and resources detailed scrutiny of all
available evidence may not have been possible. Finally
suboptimal treatments may be recommended to control
the cost of treatment or balance the interests of doctors
and healthcare systems. CPGs may cross the boundary
between benefit and harm when clinicians seek for secular
(but often self-benefitting) management procedures.
Common recommendations often don’t take into account
the individual medical and psychiatric history of the patient
and care at the individual level may not be optimal.10
Flawed guidelines compromise quality of care and can
misguide the clinicians. Due to time limitations clinicians
often find usage of guidelines inconvenient. Algorithms
in clinical guidelines which convert patient care into a
binary system of yes/no are likely to do grave injustice
to the practice of medicine involving complex decision
making. A theoretical concern is that of clinicians getting
sued for not following guidelines.11 Flawed guidelines
can also compromise future research and burden health
care delivery systems. Hence the editorial team believes
that pragmatic use of guidelines which are tailored for
the individual, family and the community encompassing
nuances of reality and humane treatment are the best
options. We are confident these guidelines which are brain
child of the best possible expertise in the speciality will go
a long way in meeting the expectations of the therapists,
clients and the society.
The earlier guidelines were published by the CPG task force
but was made available at our IJP Website. The editorial
team is grateful for the responsibility bestowed on us to
publish to make it available as a supplement of IJP for the
easy documentation, dissemination and availability to all,
all the time. We are confident that it will serve the purpose
of IPS and all the stake holders.
Happy Reading! Long live IPS.
S6
REFERENCES
1. Field MJ, Lohr KN (Eds). Clinical Practice Guidelines: Directions for a New
Program, Institute of Medicine, Washington, DC: NationalAcademy Press, 1990.
2. Consensus report, Institute of Medicine. Clinical practice guidelines we
can trust. March 23, 2011. http://www.iom.edu/Reports/2011/Clinical-
Practice-Guidelines-We-Can-Trust.aspx
3. OPEN CLINICAL: Knowledge Management for medical care: Clinical
Practice Guidelines. Available at: http://www.openclinical.org/guidelines.html
4. Woolf SH, Grol R, Hutchinson A, Eccles M, Grimshaw J. Clinical
guidelines: Potential benefits, limitations, and harms of clinical guidelines.
BMJ. 1999 Feb 20; 318(7182): 527–530.
5. Agency for Health Care Policy and Research. Using clinical practice
guidelines to evaluate quality of care. 1. Issues. Rockville, MD: US
Department of Health and Human Services, Public Health Services; 1995.
(AHCPR publication No 95-0045.)
6. Shapiro DW, Lasker RD, Bindman AB, Lee PR. Containing costs while
improving quality of care: the role of profiling and practice guidelines. Annu
Rev Public Health. 1993;14:219–241.
7. Loewy EH.Ethics and Evidence-Based Medicine: Is There a Conflict?
MedGenMed. 2007; 9(3): 30.
8. Lewis SJ, Orland BI. The importance and impact of evidence-based
medicine. J Manag Care Pharm. 2004 Sep;10(5 Suppl A):S3-5.
9. Kane RL. Creating practice guidelines: the dangers of over-reliance on
expert judgment. J Law Med Ethics. 1995;23:62–64.
10. Woolf SH. Shared decision-making: the case for letting patients decide
which choice is best. J Fam Pract. 1997;45:205–208.
11. Hurwitz B, Eccles M. Legal, political and emotional considerations of
clinical practice guidelines. BMJ (in press).
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DOI:
10.4103/0019-5545.196967
How to cite this article: Rao TS, Tandon A. Clinical Practice
Guidelines: Principles for Clinical Practice. Indian J Psychiatry
2017;59:5-6.
Indian J Psychiatry 59 (Supplement 1), January 2017
 IPS TASK FORCE

IPS Task Force on Clinical Practice Guidelines Workshop held on

Oct, 24, 25, 2015

Chairman : Dr. Shiv Gautam

Co- Chairman : Dr. Ajit Avasthi
Convenor : Dr. Sandeep Grover
Ex. Officio Members : Dr. V.G. Watve, President IPS
: Dr. N.N Raju, General Secretary IPS

CIPS GUIDELINE COMMITTEE ON DEPRESSION :
Dr. Shiv Gautam (Jaipur), Dr. N.N. Raju (Vishakhapatnam),
Dr. S.C. Tiwari (Lucknow), Dr. Roop Sidhana (Shri Ganga
Nagar), Dr. I.D. Gupta (Jaipur), Dr. Manaswi Gautam
(Jaipur), Dr. Anita Gautam (Jaipur), Dr. Akhilesh Jain (Jaipur),
Dr. Tushar Jagawat (Jaipur), Dr. T.S.S. Rao (Mysore),
Dr. K.K Mishra (Vishakhapatnam), Dr. Gautam Saha (Kolkata),
Dr. Navendu Gaur (Ajmer)
IPS GUIDELINE COMMITTEE ON
SCHIZOPHRENIA :
Dr. Ajit Avasthi (Chandigarh), Dr. Sandeep Grover
(Chandigarh), Dr. Subho Chakrabarti (Chandigarh), Dr. Lalit
Batra (Jaipur), Dr. B.N. Gangadhar (Bangalore), Dr. P.K. Dalal
(Lucknow), Dr. Kishore Gujar (Pune), Dr. O.P Singh (Kolkata),
Dr. Bharat Singh (Kota), Dr. Abhay Matkar (Bangalore),
Dr. Devendra Vijayvargiya (Kota), Dr. R.K. Solanki (Jaipur),
Dr. Mrugesh Vaishnav (Ahmedabad), Dr. Vivek Kirpekar
(Nagpur), Dr. Vihang Vahia (Mumbai), Dr. D.K. Sharma
(Kota), Dr. Mahendra Jain (Ajmer), Dr. Asim Kumar Mallick
(Kolkata), Dr. C.L. Narayaan (Patna)
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DOI:

Dr. Adarsh Tripathi (Lucknow) 10.4103/0019-5545.196968

IPS GUIDELINE COMMITTEE ON BPAD :

Dr. Neelesh Shah (Mumbai), Dr. Anup Bharati (Mumbai),
Dr. Madhu Nijhawan (Jaipur), Dr. Vinay Kumar (Patna),
Dr. Vidhyadhar Watve (Pune), Dr. G. Prasad Rao (Hyderabad),
How to cite this article: IPS Task Force on Clinical Practice
Guidelines Workshop held on Oct, 24, 25, 2015. Indian J
Psychiatry 2017;59:7.

© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow S7

 IPS TASK FORCE

IPS Task Force on Clinical Practice Guidelines Workshop held on

Aug, 6 & 7, 2016

Chairman : Dr. Shiv Gautam

Co- Chairman : Dr. Ajit Avasthi
Convenor : Dr. Sandeep Grover
Ex. Officio Members : Dr. G. Prasad Rao, President IPS
:Dr. Gautam Saha, General Secretary IPS
IPS GUIDELINE COMMITTEE ON OCD :
Dr. Y.C.J. Reddy (Bangalore), Suresh Badamath
(Bangalore), Adarsh Tripathi (Lucknow), Om Prakash
Singh (Kolkata), Paramjeet Singh (Jaipur), Tushar Jagawat
(Jaipur), Aleem Siddiqui (Aligarh), K.K. Verma (Bikaner),
D.M. Mathur (Udaipur)
IPS GUIDELINE COMMITTEE ON GAD & PANIC
DISORDER :
IPS GUIDELINE COMMITTEE ON SLEEP
DISORDERS
Ravi Gupta (Dehradun), Lalit Batra (Jaipur), Gautam Saha
(Kolkata), R.K. Solanki (Jaipur), Amrit Pattojoshi (Orissa
Bhubaneswar), Kshirod Kumar Mishra (Nagpur) , Kishor Gujar
(Pune), Navendu Gaur (Ajmer), Abdul Majid (Shrinagar)
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Shiv Gautam (Jaipur), Nilesh Shah (Mumbai), S.C. Tiwari For reprints contact: reprints@medknow.com

(Lucknow), Vihang N. Vahia (Mumbai), I.D. Gupta (Jaipur),

Access this article online
Pratap Sharan (New Delhi), Devendra Vijay Vergiya (Kota),
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B.N. Gangadhar (Bangalore), Akhilesh Jain (Jaipur), Anita Website:
Gautam (Jaipur) www.indianjpsychiatry.org

IPS GUIDELINE COMMITTEE ON SEXUAL

DOI:
DYSFUNCTION :
10.4103/0019-5545.196969

Ajit Avasthi (Chandigarh), T.S.S. Rao (Mysore), Mrugesh

Vaishnav (Ahmedabad), Sanjay Jain (Jaipur), Sandeep
Grover (Chandigarh), G. Prasad Rao (Hyderabad), How to cite this article: IPS Task Force on Clinical Practice
Guidelines Workshop held on Aug, 6 & 7, 2016. Indian J
Neelanjana Paul (Kolkata), Mukesh P. Jagiwala (Surat),
Psychiatry 2017;59:8.
Roop Sidana (Shri Ganganagar), M.S. Bhatia (New Delhi)

S8 © 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow

 PREAMBLE OF THE CLINICAL PRACTICE
Preamble of the Clinical Practice Guidelines
Shiv Gautham, Ajit Avasthi, Sandeep Grover
From 2005 onwards, the Indian Psychiatric Society came up
with treatment guidelines for various psychiatric disorders
to meet the requirements of our patients in the context
of prevailing existing resources. There have been several
developments in the management of these disorders
since then. In view of the same, it was decided to update
the existing treatment guidelines for various psychiatric
disorders. These new set of guidelines attempt to update
the previous guidelines by emphasizing what is new in
the field. These guidelines should be read in conjunction
with the earlier version of the clinical practice guidelines as
developed and published by the Indian Psychiatric Society
in the year 2005 & 2006.
These guidelines are not particularly applicable to any
specific treatment setting and may need minor modifications
to suit the needs of patients in a specific setting. The
recommendations are primarily meant for adult patients.
The needs of children or the elderly may be different. Finally,
it is expected that recommendations made will have to be
tailored to suit the needs of individual patients. Although
these guidelines focus on management of various disorders,
yet the clinicians need to remember that management must
focus on the whole patient and not just the disorder. The
recommendations given as part of the revised guidelines
are based on the available evidence base, expert consensus
and the feedback obtained from the membership.
Several factors influence the treatment of various
psychiatric disorders. Common ingredients of management
plan are shown in Table-1. Particular consideration needs
to be given to clinical parameters like cross-sectional and
longitudinal course of symptoms, type of predominant
symptoms, presence or absence of medical comorbidity,
comorbid substance abuse/dependence, life stage of
patients and their special needs. Socio-cultural factors e.g.
© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow
beliefs about the illness and their treatments are particularly
important, as are the availability of treatment-resources.
The general goals of treatment should be to decrease the
frequency, severity and impact of episodes (exacerbations)
and maximize functioning between the episodes. Specific
goals will depend on the specific phases of illness.
Table 1: Common ingredients of a management plan
Comprehensive assessment of all factors that might impinge on treatment
Most patients will require comprehensive and continuous treatment for
long periods
Evolving a treatment plan, which should be regularly updated according to
changing needs of patients and caregivers
Holistic biopsychosocial approach to treatment
Forming a therapeutic alliance with the patient
Active collaboration with the family
Ensuring adherence to treatment
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DOI:
10.4103/0019-5545.196970
How to cite this article: Gautham S, Avasthi A, Grover
S. Preamble of the Clinical Practice Guidelines. Indian J
Psychiatry 2017;59:9.
S9
 ORIGINAL ARTICLE

Indian Psychiatric Society Survey on Clinical Practice Guidelines

Sandeep Grover, Ajit Avasthi
Department of Psychiatry, Post Graduate Institute of Medical Education and Research, Chandigarh, India

ABSTRACT

Aim: This survey aimed to assess the utility of the earlier published clinical practice guidelines (CPGs) by IPS and to
understand the expectations of members of Indian Psychiatric Society from the proposed revised CPGs. In addition, the
survey also evaluated the current level of practice of psychiatry in terms of availability of different investigation facilities,
prescription patterns in terms of use of polypharmacy, and competence in carrying out certain nonpharmacological
treatments.
Methodology: An online survey was received by 3475 psychiatrist, of whom 608 (17.5%) participants completed the
survey.
Results: Almost all (93.8%) of the psychiatrists agreed that there should be separate CPGs for Indian setting. In terms
of problems with the previous version of the CPGs, this survey shows that the previous version of guidelines was used
in making clinical decisions by only one‑third (31.25%) of the participating psychiatrists. The major limitations of the
previous version of CPGs which were pointed out included the lack of consideration of socio‑cultural issues (33.2%),
lack of recommendations for many clinical situations that are encountered in clinical practice (43.15) and poor
dissemination (35.2%). In terms of expectations, the membership expects the society to come up with guidelines, which
are shorter in length (82.2%), has significant proportion of information in the form of tables and flow diagrams (58.7%),
besides the evidence base must also take expert opinions into account (84.7%), must be circulated before adopting (88.7%),
must be disseminated by displaying the same on the website (72%), and also by sending the same by E‑mails (62%).
Further, the membership expects the IPS to design online continuing medical education program on CPGs (54.3%). The
survey also suggests that it is feasible on the part of more than two‑third of the psychiatrists to monitor the metabolic
parameters in routine clinical practice and carryout various nonpharmacological treatments. Majority of the psychiatrist
opined that polypharmacy is not used in more than 25% of patients with schizophrenia and depression and hence the use
of polypharmacy should be recommended judiciously.
Conclusion: This survey shows that the membership of the IPS is interested in having own guidelines for the management
of various psychiatric disorders in Indian setting. Further, the survey provides insights into why the previous versions of
the guidelines were not very popular and what IPS should do improve the acceptability of guidelines in future.

Key words: Clinical practice guidelines, guidelines, India, Indian Psychiatric Society

INTRODUCTION
Address for correspondence: Dr Sandeep Grover,
Department of Psychiatry, Postgraduate Institute of Medical Indian Psychiatric Society (IPS), started publishing clinical
Education and Research, Chandigarh ‑ 160 012, India. practice guidelines (CPGs) for the management of various
E‑mail: drsandeepg2002@yahoo.com
This is an open access article distributed under the terms of the Creative
Access this article online
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DOI:
How to cite this article: Grover S, Avasthi A. Indian
Psychiatric Society Survey on Clinical Practice Guidelines.
10.4103/0019-5545.196971
Indian J Psychiatry 2017;59:10-8.

S10 © 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow

 Grover and Avasthi: Survey on clinical practice guidelines
psychiatric disorders in the year 2005 and between the
year 2005 and 2009, published five volumes of treatment
practice guidelines, covering most of the psychiatric
disorders.[1‑5] A survey was conducted in the months of
October–November 2008, to evaluate the usefulness,
awareness, and implementation of IPS‑CPGs. The survey was
sent to 1100 psychiatrists, of whom 107 responded to the
survey. Among the responders, only half of the responders
were aware about the four published volumes of the
guidelines at that time, and only 12.7% of the responders had
read all the four volumes. About two‑thirds of the responders
had referred to these guidelines in their clinical practice,
either occasionally (46.1%), often (16.7%), or always (2%).
More than two‑thirds of the responders considered these
guidelines to be helpful in making day‑to‑day clinical decisions
in their practice, either occasionally (48%), often (19.6%),
or always (3.9%). In the open‑ended questions, many of
the responders discussed their dissatisfaction with these
guidelines and gave suggestions as to how these guidelines
could be improved. Some of the areas of dissatisfaction
were the lack of uniformity, lack of consideration of local/
cultural issues into account, not very useful, lengthy, not user
friendly, poor quality of printing and typological errors. Some
of the suggestions which emerged from this survey included,
rather than having guidelines on the basis of evidence base
only, guidelines may be drawn on the basis of consensus and
may be field tested. Further, the IPS should try to focus on
drawing guidelines only on few disorders, rather than having
guidelines for everything. In terms of circulation, participants
suggested that the guidelines should be sent to all the Indian
psychiatrists, and must be made available on the society’s
website or on the website of the journal.[6]
Besides criticism, many participants had expressed that
overall it was good initiative of IPS and the society should
continue to formulate guidelines and must update the
same regularly. In 2015, IPS, again formed the Task force to
formulate/update the CPGs for various disorders. Keeping
in view the findings of the previous survey, the Executive
Committee of the IPS and Task force on CPGs in its first
meeting decided to carry out a survey, which should assess
the scenario in practice and must take the realities into
consideration while formulating recommendations as part
of various treatment guidelines. Accordingly, the aims of this
survey were to assess the (1) utility of the earlier published
CPGs by IPS; (2) expectations from the new CPGs; (3) current
level of practice of psychiatry in terms of availability and
use of different investigation facilities; and (4) prescription
patterns in terms of use of polypharmacy and competence
in carrying out certain nonpharmacological treatments.
METHODOLOGY
This survey was conducted by using Survey Monkey platform.
Based on the E‑mail address database of various members of
the society and E‑mail addresses of the trainee psychiatrist
Indian J Psychiatry 59 (Supplement 1), January 2017
collected by the authors, the survey was sent to 4394 E‑mail
addresses. The survey was approved by the ethics committee
of the research and training foundation of the IPS. The cover
letter of the survey mentioned that the IPS has decided to
revise CPGs for the management of schizophrenia, bipolar
disorder, and depression, and the Executive Committee
of IPS was seeking inputs from its membership prior to
finalizing the CPGs. The participants were also informed
that a symposium on the CPGs will be held during the
ANCIPS‑2016. The participation in the survey was voluntary
and the participants had the option of “opt‑out” from the
survey. Completion of the survey implied informed consent.
The survey was sent twice a week for 6 consecutive weeks.
Those who responded to the survey or “opted out” were
not sent the reminders. Those who completed the survey
partially were also sent reminders in between to complete
the survey. The survey questionnaire included 41 questions
and required about 15–20 min to complete.
The data were analyzed by SPSS (SPSS for Windows, Version
14.0. Chicago, SPSS Inc.). Continuous variables were
analyzed in the form of mean, standard deviation, median,
and range. Categorical variables were analyzed as frequency
and percentages.
RESULTS
Of the 4394 E‑mail addresses, the invitation to participate
“bouched‑back” for 712 E‑mail addresses and for 207 E‑mail
addresses, people opted out to participate in the survey.
Out of the eligible, 3475 participants, 608 (17.5%) of the
participants completed the survey. The mean age of the
participants was 41 (standard deviation [SD] 11.78) years,
with a range of 26–79 years and a median of 38 years.
As is evident from Table 1, about 80% of the participants
were  ≤50  years with majority of the participants were in
the age range of 31–40 years. Four‑fifth of the participants
were males and about one‑fifth were females. More than
three‑fourth (77.5%) of the participants had done MD only
or had done MD along with an additional degree. The mean
total experience in psychiatry, including the training period
was 14.22 (SD ‑ 10.89) years, with a median of 10 years and
range of 1–53 years. Three‑fifth of the participants were in
the government jobs (either fulltime government job only
or government job with private practice) and two‑fifth were
in full‑time private practice only. In terms of place of work,
one‑fourth were in full‑time private practice, one‑fifth were
in the government medical colleges (without any private
practice). About one‑sixth were in central institutes [Table 1].
In terms of location, about three‑fourth of the psychiatrist
were practicing in the heart of the large city or in the
suburbs of a large city. One‑fifth were practicing in a town
and very few were practicing in villages. On an average, a
psychiatrist was seeing 30 (SD 26.2) patients a day with a
median of 25 patients a day and a range of 2–200. The mean
duration of time spent in consultation for a new patient was
S11

Table 1: Profile of participants (n=608)
Variable
Age (years)
Age categories (in years)
<30
31-40
41-50
51-60
61-70
>70
Gender‑male/female
Qualification (n=594)
MD only
MD along with one or more degrees
DPM
DPM + DNB
DNB only
MRCPsych/FRCPsych
DPM + MRCPsych/FRCPsych
Total experience in psychiatry (including
the number of years of training in
psychiatry)
Type of setting in which you are
working (n=572)
Full time government job with no
private practice
Full time private practice
Government job with private practice
Main place of work (n=590)
Central institute
Full time private practice
Government Medical College
Government medical college with
private practice
Private Medical College
Private Medical College with private
practice
Mental hospitals
Charitable hospital
Main place of work (n=595)
In the heart of a large city
In the suburb of a large city
Town
Village
Number of patients seen by you in the
outpatient clinic on a typical day (type
in just the number)
Average amount of time spent in
evaluating a new patient (in min‑enter
just the number)
Average amount of time spent in
evaluating a repeat visit patient (in
min‑enter just the number)
Are you part of the expert group for the
formulation of clinical practice guideline
by the Indian Psychiatric Society?
The additional degrees included DM/DPM/DNB/MRCPsych/FRCPsych/
FRANZPsych. DPM – Diploma in Psychological Medicine; DNB – Diplomate
of National Board
27.9 (SD ‑ 16.3; median 25) min and that for an old follow‑up
patient was 11.91 (SD ‑ 6.94; median 10) min. Only a small
proportion (7.4%) of the participants had been part of the
IPS CPG formulation groups in the past.
S12
Grover and Avasthi: Survey on clinical practice guidelines
Views about guidelines
Mean (SD)/frequency (%) A majority (81.6%) of the participants reported that
41 (11.78) (median: 38; they do follow some treatment guidelines for the
range 26-79) management of patients with severe mental disorders
such as schizophrenia, bipolar disorder, or depression.
107 (17.6) Among those who were using guidelines, in terms of most
266 (43.6)
commonly followed guidelines for the management of
111 (18.3)
67 (11) patients with severe mental disorders, about two‑fifth (41%)
45 (7.4) were following Maudsley Prescribing Guidelines and about
12 (2) one‑fourth (28.65%) were following American Psychiatric
479 (78.8)/129 (21.2) Association guidelines. About one‑seventh (14.3%) were
following National Institute of Clinical Excellence (NICE)
353 (58.1)
118 (19.4) guidelines and another one‑seventh (14.63%) were following
80 (13.2) IPS guidelines [Table 2]. Majority (82.24%) of those who
25 (4.1) were using various guidelines reported that they were able
11 (1.8) to use the guidelines only partially.
4 (0.7)
3 (0.6)
14.22 (10.89) (median: 10;
When enquired about having separate CPGs for Indian
range 1-53) setting majority (93.8%) of the participants answered in
affirmation. When asked about earlier IPS guidelines,
83.3% of the participants were aware about the same and
about half (52.1%) had used the IPS guidelines. Those who
238 (41.6)
used the same had most often used the same to update
224 (39.2) their knowledge (43.5%). About one‑third (31.25%) used
110 (19.2) the same for taking day to day clinical decisions and
one‑fourth (25.65%) used it for teaching and few (11%)
95 (16.1) had used the same for defending themselves in the court
151 (25.6)
125 (21.2)
of law. When asked to report about the problems with
62 (10.5) the earlier version of the guidelines, the most commonly
reported problem was that these do not address many
44 (7.5) clinical situations that are encountered (43.1%), followed
62 (10.5) by problems in dissemination (35.2%), do not address the
33 (5.6)
socio‑cultural issues encountered in practice (33.2%), and
18 (3.1) not evidence based (20.2%). Other details are shown in
Table 2.
370 (62.4)
88 (14.8) Expectations from the revised clinical practice guidelines
117 (19.2)
When asked about their expectations from the upcoming
18 (3.0)
31.6 (26.20) (median: 25; CPGs, most of the participants expected that the guidelines
range 2-200) should be at best of <5 pages (45.8%) or 5–10 pages (36.4%)
of Indian Journal of Psychiatry (IJP) [Table 3]. More than half
27.9 (16.3) (median: 25; of the participants expected the CPGs to be presented in
range 6-120)
the form of tables and flow diagram format. Majority of the
11.91 (6.94) (median: 10; participants expected that the guidelines must be based
1-60) on evidence base along with expert opinion (84.7%), must
be circulated before being adopted (88.7%) and having a
45 (7.4) symposium in ANCIPS would be beneficial (91.4%). When
asked about how to improve the use of CPGs, majority
of the participants expected that the guidelines must
be made available on the IPS website (72%) and this was
followed by the expectation of receiving the softcopy of
guidelines by E‑mail (62%) and presenting major parts of the
guidelines in the form of flow charts and tables (58.7%) and
by conducting online continuing medical education (CME)
programs on the CPGs (54.3%) and least proportion of the
participants (47.4%) considered sending parts of guidelines
Indian J Psychiatry 59 (Supplement 1), January 2017
 Grover and Avasthi: Survey on clinical practice guidelines

Table 2: Views about guidelines (n=608) Table 3: Expectations from the guideline (n=608)

Variable Frequency (%) Variable Frequency (%)
Do you generally follow any treatment guidelines 496 (81.6) What should be the length of the CPGs for each disorder,
published by any psychiatric association for management which you think could be easily referred to in day to day
of your patients with severe mental disorders like clinical practice (n=579)
schizophrenia, bipolar disorder or depression? <5 pages of IJP 265 (45.8)
Most commonly followed treatment guidelines (n=485) 6-10 pages of IJP 211 (36.4)
National institute of clinical excellence 70 (14.3) 10-20 pages of IJP 74 (12.8)
American psychiatric association 139 (28.65) 20-30 pages of IJP 18 (3.1)
Maudsley prescribing guidelines 199 (41.03) 30-40 pages of IJP 11 (1.9)
Indian psychiatric society guidelines 71 (14.63) Should CPGs for each disorder be presented in the form 320 (52.6)
Canadian network for mood and anxiety treatments 6 (1.23) of flow diagrams/tables only?‑yes
If you follow any treatment guidelines, do you find it Recommendations of CPGs be drawn on the basis
useful in your clinical practice (n=490) of (n=589)
Able to follow the guidelines completely 84 (17.1) Both evidence base and expert opinion 499 (84.7)
Able to follow the guidelines partially 403 (82.24) Evidence base only 67 (11.4)
Not able to follow the guidelines 3 (0.6) Expert opinion only 7 (1.2)
Do you think that there is a need to have separate 556 (93.8) Other 16 (2.7)
clinical practice guidelines for Indian setting Is there a need for circulation of the CPGs to membership 539 (88.7)
Are you aware that Indian psychiatric society 506 (83.2) of IPS for inputs before adopting the guidelines?‑yes
had published the clinical practice guidelines for Will symposium on CPGs at ANCIPS be beneficial to the 556 (91.4)
management of various psychiatric disorders in the members of IPS?‑yes
past (i.e., between the year 2005 and 2010)? What should be done to increase the use of IPS CPGs in
Did you ever use the previously published clinical 317 (52.1) clinical practice
practice guidelines by the Indian psychiatric society? Making the guidelines available on the IPS website 438 (72)
If you ever used clinical practice guidelines published by Sending the copy of guidelines by email 377 (62)
Indian psychiatric society, did you find it useful for Sending parts of guidelines in the form of small 288 (47.4)
In taking day‑today clinical decisions 190 (31.25) educational capsules through email on regular basis
Updating your knowledge 221 (43.5) Presenting major parts of the guidelines in the form of 357 (58.7)
Defending yourself in court of law 67 (11) flow charts and tables
Teaching your students 156 (25.65) Online CME programs on the clinical practice 330 (54.3)
What do you think are the problems with the clinical guidelines
practice guidelines published by Indian psychiatric Is there a need to make the practice of psychiatry as per
society the IPS CPGs binding on the membership (n=590)
Too short 21 (3.45) Cannot say 124 (21)
Too long 82 (13.5) Definitely 33 (5.6)
Do not address the socio‑cultural issues encountered 202 (33.2) May be 146 (24.7)
in practice Not at all 287 (48.6)
Do not address many clinical situations that are 262 (43.1) CPGs – Clinical practice guidelines; CME – Continuing medical education;
encountered IPS – Indian Psychiatric Society
Not evidence based 123 (20.2)
Too much emphasis on pharmacotherapy 88 (14.5) Only two‑fifth (42.6%) had access to serum valproate levels
Poorly disseminated 214 (35.2)
and urine drug screen (40.6%). However, very few had access
to positron‑emission tomography and serum clozapine
in the form of small educational capsules through E‑mail on levels [Table 4]. For at least two‑third of the psychiatrists,
regular basis would be of benefit. About half (48.6%) of the it was possible to measure height, weight, blood pressure,
participants considered that the society should not make fasting blood glucose levels, and the lipid profile. More than
it mandatory for its membership to follow the CPGs and half (55.3%) also reported that it was feasible to measure
very few (5.6%) considered that it should definitely be made waist circumference of their patients.
mandatory.
Investigations carried out routinely prior to starting of
Feasibility of investigations various psychotropic medications
In terms of feasibility of carrying out investigations, for In terms of current practice, in general, more investigations
majority of the participants (>75%), it was feasible to were being done prior to starting of antipsychotics
order and get reports of hemogram, fasting blood glucose and mood stabilizers, when compared to the use of
levels, serum electrolytes, liver function test, renal function antidepressants. Investigations done prior to starting
test, lipid profile, thyroid function test, ultrasound of of antipsychotics by more than half of the psychiatrists
abdomen and pelvis, electroencephalogram, computerized included hemogram, fasting blood glucose levels, and
tomography of brain, X‑ray chest, and electrocardiogram. lipid profile. Further more than half of the psychiatrists
More than two‑third of the participants also had access to also monitored the same while using antipsychotics
serum lithium levels and magnetic resonance imaging. More [Tables 5 and 6]. Investigations done by about half or
than half had access to Vitamin B12 and Vitamin D levels. more psychiatrists, prior to starting of mood stabilizers

Indian J Psychiatry 59 (Supplement 1), January 2017 S13

 Grover and Avasthi: Survey on clinical practice guidelines

included hemogram, fasting blood glucose levels, liver
function test, renal function test, and thyroid function test.
Of these, only liver function tests, renal function tests,
and thyroid function tests were being monitored while
using mood stabilizers. In general, fewer psychiatrists
carried out investigations prior to starting and while using
various antidepressants. The most commonly carried out
investigations included hemogram, fasting blood glucose
level, and thyroid function test.
In terms of option given for other investigations, few reported
evaluating serum drug levels (lithium and valproate) (5.9%)
and serum prolactin (3.8%), while monitoring patients on
various psychotropic medications.

Table 4: Feasibility of investigations (n=608) Majority of the psychiatrists were carrying out renal
Variable Frequency (%) function test (84.9%), thyroid function test (78%), and serum
What all investigations are feasible at the clinical setting electrolytes prior to starting of lithium. However, very few
in which you practice (tick on whichever are feasible) psychiatrists reported evaluating 24 h urine osmolality and
Hemogram 554 (91.1) 24 h proteins prior to starting of lithium. Very few (5.6%)
Fasting blood glucose levels 555 (91.3) of psychiatrist reported not carrying out any investigations
Serum electrolytes 528 (86.8)
Liver function test 553 (91.0)
prior to starting of lithium.
Renal function test 535 (88.0)
Lipid profile 519 (85.4) Prescription practices
Thyroid function test 529 (87.0) When asked about polypharmacy, 26.8–32.37% of the
Serum lithium levels 435 (71.5)
participants reported using combination of antipsychotic
Serum valproate levels 259 (42.6)
Serum clozapine levels 90 (14.8) continuously for more than 2 weeks to manage acute phase of
Urine drug screen 247 (40.6) illness of patients with schizophrenia, depression, or bipolar
Ultrasound of abdomen and pelvis 458 (75.3) disorder [Table 7]. Combinations of antidepressants were
EEG 459 (75.5) used by 23% of participants in the management of acute phase
CT of brain 484 (79.5)
X‑ray chest 482 (79.3)
depression. Combinations of two classical mood stabilizers
MRI of brain 407 (66.9) (i.e., lithium, valproate, lamotrigine, carbamazepine, etc.,)
PET 111 (18.3) were used by 18.63% only for the management of mania.
Electrocardiogram 485 (97.8) However, combination of mood stabilizer (i.e., lithium,
Vitamin B12 levels 365 (60.0) valproate, lamotrigine, carbamazepine, etc.,) and an
Folic acid levels 289 (47.5)
Vitamin D levels 322 (53.0) antipsychotic medication were used for the management of
Which of the following is feasible to measure in all acute phase of mania by 58.3% of the participants.
patients before starting psychotropics (tick as many as
applicable) About one‑fourth (24.12%) of the participants, reported using
Height 436 (71.7)
the combination of antipsychotics in the stabilization/stable
Weight 541 (89.0)
Waist circumference 336 (55.3) phase of schizophrenia. In terms of management of bipolar
Hip circumference 239 (39.3) disorder in the maintenance phase, combination of a classical
Waist‑hip ratio 250 (41.1) mood stabilizer and antipsychotic medication was used in
Blood pressure 552 (90.8) about 40.5% of patients and this was followed by the use
Fasting blood glucose levels 477 (78.5)
Lipid profile 394 (64.8)
of a combination of two classical mood stabilizers (21.04%)
PET – Positron emission tomography; MRI – Magnetic resonance imaging;
or combination of two classical mood stabilizers and an
CT – Computed tomography; EEG – Electroencephalogram antipsychotic medication (14.71%).

Table 5: Investigations carried out routinely prior to starting of various psychotropic medications
Antipsychotics (%) Antidepressants (%) Mood stabilizers (%)
Hemogram 383 (63) 302 (49.7) 352 (57.9)
Fasting blood glucose levels 453 (74.5) 252 (41.4) 304 (50.0)
Serum electrolytes 155 (25.5) 191 (31.4) 224 (36.8)
Liver function test 304 (50.0) 213 (35.0) 374 (61.5)
Renal function test 256 (42.1) 197 (32.4) 364 (59.9)
Lipid profile 327 (53.8) 120 (19.7) 200 (32.9)
Thyroid function test 168 (27.6) 295 (48.5) 318 (52.3)
Urine drug screen 36 (5.9) 25 (4.1) 32 (5.3)
EEG 35 (5.8) 20 (3.3) 46 (5.3)
Electrocardiogram 276 (45.4) 186 (30.6) 211 (34.7)
Vitamin B12 levels 36 (5.9) 93 (15.3) 40 (6.6)
Folic acid levels 12 (2) 46 (7.6) 25 (4.1)
Vitamin D levels 25 (4.1) 66 (10.9) 23 (3.8)
EEG – Electroencephalogram

S14 Indian J Psychiatry 59 (Supplement 1), January 2017

 Grover and Avasthi: Survey on clinical practice guidelines

Table 6: Investigations carried out while monitoring patients on various psychotropic medications
Antipsychotics (%) Antidepressants (%) Mood stabilizers (%)
Hemogram 318 (52.3) 199 (32.7) 267 (43.9)
Fasting blood glucose levels 476 (78.3) 209 (34.4) 256 (42.1)
Serum electrolytes 133 (21.9) 181 (29.8) 199 (32.7)
Liver function test 290 (47.7) 176 (28.9) 369 (60.7)
Renal function test 191 (31.4) 146 (24.0) 329 (64.1)
Lipid profile 387 (63.7) 125 (20.6) 212 (34.9)
Thyroid function test 125 (20.6) 235 (38.7) 320 (62.6)
Urine drug screen 22 (3.6) 18 (3.0) 25 (4.1)
EEG 25 (4.1) 14 (2.3) 24 (3.9)
Electrocardiogram 216 (35.5) 137 (22.5) 146 (24.0)
Vitamin B12 levels 18 (3.0) 50 (8.2) 29 (4.8)
Folic acid levels 8 (1.3) 23 (3.8) 19 (3.1)
Vitamin D levels 14 (2.3) 33 (5.4) 11 (1.8)
EEG – Electroencephalogram

Table 7: Polypharmacy prescription practices (n=608)

Variable Mean (SD)/frequency (%)
• In what proportion of patients with schizophrenia do you use a combination of 28.23 (30.02) (median 20; range 0-100)
antipsychotic continuously for >2 weeks to manage acute phase of illness
• In what proportion of patients with depression do you use a combination of 26.8 (32.01) (median 10; range 0-100)
antipsychotics continuously for >2 weeks to manage acute phase of illness
• In what proportion of patients with bipolar disorder do you use a combination 32.37 (31.64) (median 20; range 0-100)
of antipsychotics continuously for >2 weeks to manage acute phase of illness
• In what proportion of patients with schizophrenia do you use combination of 24.12 (21.84) (median 20; range 0-100)
antipsychotics during the stabilization/stable phase of illness
• In what proportion of your patients with depression do you use a combination 22.88 (24.99) (median 15; range 0-100)
of antidepressants to manage acute phase of management
• In what proportion of your patients with mania do you use a combination of 18.63 (20.48) (median 10; range 0-100)
2 classical mood stabilizers during the acute phase (i.e., lithium, valproate,
lamotrigine, carbamazepine etc.)
• In what proportion of your patients with mania do you use a combination of 58.34 (32.23) (median 70; range 0-100)
one or more classical mood stabilizers (i.e., lithium, valproate, lamotrigine,
carbamazepine etc.) and an antipsychotic medication during the acute phase
• In what proportion of your patients with bipolar disorder do you use a 21.04 (17.93) (median 20; range 0-100)
combination of 2 or more classical mood stabilizers (i.e., lithium, valproate,
lamotrigine, carbamazepine etc.) for maintenance treatment
• In what proportion of your patients with bipolar disorder do you use a 40.54 (26.33) (median 40; range 0-100)
combination of one classical mood stabilizers (i.e., lithium, valproate,
lamotrigine, carbamazepine etc.) and an antipsychotic for maintenance
treatment
• In what proportion of your patients with bipolar disorder do you use 2 classical 14.71 (16.34) (median 10; range 0-100)
mood stabilizers (i.e., lithium, valproate, lamotrigine, carbamazepine etc.) and
one or more antipsychotic for maintenance treatment
SD – Standard deviation

Competence in nonpharmacological interventions
Majority of the psychiatrist (>80%) considered their
competence to carry out psychoeducation, cognitive
behavior therapy, behavior therapy, family intervention,
and relaxation exercises as “average” or “above average”
or “excellent.” However, for psychoeducation, only 64.4%
considered their competence as “average” or “above
average”. In terms of carrying out cognitive remediation
therapy, only about half of the participants reported their
own competence as average or above average [Table 8].
DISCUSSION
and to understand the expectations of the membership with
regard to the revised CPGs. In addition, the Task force of IPS
on CPGs was also interested in understanding the feasibility
of making certain recommendations such as carrying out
investigations for the evaluation of metabolic syndrome
and various nonpharmacological treatments.
As there are no such surveys which have looked into these
aspects of practice of psychiatry, it would be difficult to
compare the findings of the present survey with existing
literature. Hence, we would discuss the findings of this
survey in the context of formulation of newer guidelines.

This survey intended to have basic information about the The present survey suggests that in Indian setting,
dissatisfaction and utility of previous version of CPGs of IPS majority of the psychiatrists follow one or other treatment

Indian J Psychiatry 59 (Supplement 1), January 2017 S15

 Grover and Avasthi: Survey on clinical practice guidelines
Table 8: Competence in nonpharmacological interventions (n=608)
How would you rate your competence in Above average (%)
delivering the following interventions (n)
Psychoeducation (536) 276 (51.5)
Cognitive behavior therapy (532) 140 (26.3)
Behavior therapy (531) 181 (34.1)
Cognitive remediation therapy (524) 89 (17)
Family intervention (535) 225 (42.0)
Relaxation exercises (532) 220 (41.3)
guidelines for the management of their patients with severe
mental disorders. This finding is very similar to the previous
survey in which only 8.8% of psychiatrists had reported not
following any specific treatment guidelines in managing
their patients.[6] In terms of preference, a large proportion
of psychiatrists was following treatment guidelines issued
by other associations, i.e., Maudsley Prescribing Guidelines,
American Psychiatric Association, and NICE and only a very
small proportion of psychiatrists based their day to day
clinical decisions based on IPS guidelines. This finding can
be interpreted as possible lack of satisfaction with the IPS
guidelines. This lower reliance on IPS guidelines also can
be due to the lack of awareness about these guidelines in
about one‑sixth of the participants.
In terms of applicability, majority of the participants
reported that they were able to use guidelines of different
associations only partially in their clinical practice. This
suggests that guidelines issued by various associations
probably are not in tune with the real life situations
faced by the psychiatrists and hence any new guidelines
must take these situations into account while making
recommendations.
When asked about the need for separate CPGs for Indian
setting, almost all (93.8%) of the participants expressed
the need to have separate treatment guidelines for Indian
setting. This finding clearly reflects that there is a need for
development of treatment guidelines by the IPS. Hence, it
can be said that decision of IPS to revise these guidelines is
in the right direction. In terms of using the previous version
of guidelines only 52.1% of psychiatrists reported ever
using the IPS guidelines. Only one‑third of the psychiatrists,
who used the IPS guidelines, reported that these were
useful in making day to day clinical decisions. In terms of
implementation of treatment guidelines, studies from other
parts of the world show that the barriers to implementation
to various treatment guidelines include organizational
resources, health care professional’s own characteristics,
and perception of guidelines and implementation
strategies.[7] Accordingly, it is important for the IPS to keep
these facts in mind to reduce the barriers in implementation
of treatment guidelines.
In terms of expectations, majority of the participants
expressed the need to have shorter documents, with lot of
S16
Average (%) Excellent (%) Poor (%)
69 (12.9) 187 (34.9) 4 (0.75)
256 (48.1) 42 (7.9) 94 (17.7)
251 (47.3) 48 (9.0) 53 (10.0)
216 (41.2) 12 (2.3) 207 (39.5)
192 (35.9) 78 (14.6) 40 (7.5)
188 (35.3) 91 (17.1) 33 (6.2)
information being provided in the form of flow diagrams
and tables and drawing the recommendations based
on the evidence base and expert opinion. In addition,
the membership expects that the society should make
these guidelines available to them electronically through
various resources. In addition, a significant proportion of
the members expect that having online CME program on
guidelines could be of help IPS must take these views into
account while circulating the revised guidelines.
In terms of problems with the existing guidelines, a
significant proportion of participants reported that
the guidelines do not take into consideration various
socio‑cultural issues encountered in practice, do not
address many clinical situations that are encountered,
are not evidence based and there is too much emphasis
on pharmacotherapy. In addition, about one‑third of
the participants also pointed out the issue of poor
dissemination of these guidelines. This again suggest that
revised version of guidelines must focus on these issues
and must be disseminated properly.
IPS Task force on formulation of treatment guidelines must
take these insights in terms of problems with earlier version
of the guidelines and expectations of the membership in
formulation of future CPGs. Some of the issues like making
the recommendations on the basis of current evidence base
can easily be done by carrying out proper review of the
existing literature and drawing recommendations based on
the same. The newer guidelines should provide adequate
information about the nonpharmacological treatments, so
that these can be easily incorporated into clinical practice
and emphasis on the use of only pharmacological measures
must be reduced. Problem of dissemination must be
addressed by publishing the guidelines as part of the IJP and
possibly making the guidelines available at the IJP website
and sending the guidelines to the membership by E‑mail. IPS
must look at developing online CME program for improving
the acceptability of CPGs. This can be done probably by
having CME program which can evaluate the knowledge
of the participant about the content of IPS guidelines.
This program can also possibly help in evaluating specific
dissatisfactions with the guidelines. In future, there is a
need to carry out a survey to understand the socio‑cultural
aspects and the clinical situations, which clinicians feel that
the guidelines do not address.
Indian J Psychiatry 59 (Supplement 1), January 2017
 Grover and Avasthi: Survey on clinical practice guidelines
Members of all the societies expect their leaders to fulfill
their demands and aspirations. In the survey, a very large
proportion of the psychiatrists expressed that having a
symposium in ANCIPS is going to help in formulation of
guidelines. The Task force on the formulation of treatment
guidelines organized a symposium on the revised CPGs in
ANCIPS 2016. The attendance in this symposium was far
less than expected. This possibly reflects the apathy of the
membership on this issue. Till the membership does not
take up their own responsibility sincerely, just blaming the
leadership and people involved in the task of formulation
would be unfair. Accordingly, the membership should take
up their own responsibility more sincerely and provide their
inputs on this endeavor so that a collective effort can result
in the formulation of CPGs which are practical and can be
used.
Over the last 1–2 decades, development of metabolic
syndrome with the use of psychotropics has become
an important issue. Various associations have issued
guidelines for monitoring of metabolic syndrome. This
survey clearly shows that it is feasible for majority of the
psychiatrists to carry out most of the routine investigations
in their clinical practice. Further, it was also feasible to
carryout anthropometric evaluation on part of majority of
psychiatrists. In terms of current practice too, it was evident
that a significant proportion of psychiatrists were already
carrying out baseline investigations and also were ordering
for investigations while using psychotropics in long run.
Accordingly, the recommendations of guidelines in terms
of carrying out baseline investigations and anthrometric
evaluation must take these into account. Accordingly,
the guidelines may recommend monitoring of metabolic
parameters for patients recommended antipsychotic and
mood stabilizers. If in future, these recommendations are
followed by the practicing psychiatrists in routine clinical
practice, this could possibly help in detecting metabolic
abnormalities at early stages and prevention of development
of chronic physical illnesses such as diabetes mellitus and
hypertension. This all can probably also help in reduction
in premature cardiovascular mortality. The findings of this
survey also shows that majority of the psychiatrists follow
the basic recommendations for prelithium investigations.
Accordingly, future guidelines must make recommendations
of this with ease.
There is a general perception that there is high rate of
polypharmacy in routine clinical practice. Some of the
psychiatrists argue about this issue and give this as an excuse
for not following treatment guidelines. Some claim that
most patients require polypharmacy and it is not possible
to manage patients with monotherapy during the acute and
maintenance phase. Keeping these views in mind, there is
always a pressure of recommending polypharmacy as part
of CPGs. However, findings of the current survey clearly
shows that in general, polypharmacy is not practiced for
Indian J Psychiatry 59 (Supplement 1), January 2017
significant proportion of patients with schizophrenia and
depressive disorders. However, a significant proportion of
patients with bipolar disorder receive polypharmacy during
the acute and maintenance phase treatment. Accordingly, it
can be said that guidelines should judiciously recommend
the use of polypharmacy.
In terms of nonpharmacological treatment, more than
half of the psychiatrists reported average or above
average competence in carrying out nonpharmacological
treatments such as psychoeducation, cognitive behavior
therapy, behavior therapies, family interventions, and
relaxation exercises. These findings suggest that future
guidelines must provide more information about the
role of these interventions in management of various
psychiatric disorders. Further, the findings also suggest that
a significant proportion of psychiatrists are not very well
versed with cognitive remediation therapy. Accordingly, as
capacity building measure, IPS must hold workshops and
symposiums on cognitive remediation therapy, so that
these can be practiced more often by its membership.
This survey has certain limitations. The survey did not
evaluate the specific level of dissatisfaction among the
psychiatrists with regard to the existing guidelines. Further
the survey did not evaluate the specific expectations of the
psychiatrists from the newer guidelines. This survey did
not endeavor to assess the barriers to the implementation
of treatment guidelines in clinical practice. Only about
one‑sixth of the membership participated in this survey.
Due to this, generalizability of this survey can be
questioned.
CONCLUSION
The present survey shows that the majority of the psychiatrists
are interested in having own CPGs and at present follow
one or other treatment guidelines for the management of
patients. In terms of problems with the previous version
of the CPGs, this survey shows that the previous version of
guidelines were used for making clinical decisions by a very
small proportion of psychiatrists only. The major limitations
of the previous versions which were pointed out included
the lack of consideration of socio‑cultural issues, lack of
recommendations for many clinical situations that are
encountered in clinical practice and poor dissemination. In
terms of expectations, the membership expects the society
to come up with guidelines, which are shorter in length, has
more information in the form of tables and flow diagrams,
should take expert opinions into account, must be circulated
before adopting, must be disseminated by displaying the
same on the website, and also by sending the same by
E‑mails. Further, the membership expects the organization
to design online CME program on CPGs. The survey also
suggests that it is feasible to monitor the metabolic
parameters in routine clinical practice and carryout various
S17
 Grover and Avasthi: Survey on clinical practice guidelines

nonpharmacological treatments. In addition, the survey Disorder and Panic Disorder. Vol. 1. Jaipur: Indian Psychiatric Society;
2005.
suggests that polypharmacy is not used much; hence its use 2. In: Gautam S, Avasthi A, editors. Indian Psychiatric Society. Clinical
should be recommended judiciously. Practice Guidelines for Management of Substance Abuse Disorders,
Sexual Dysfunctions and Sleep Disorders. Vol. 2. Jaipur: Indian Psychiatric
Society; 2006.
Financial support and sponsorship 3. In: Gautam S, Avasthi A, editors. Indian Psychiatric Society. Geriatric
Psychiatry Clinical Practice Guidelines. Vol. 3. Jaipur: Indian Psychiatric
Nil. Society; 2007.
4. In: Gautam S, Avasthi A, editors. Indian Psychiatric Society. Child and
Conflicts of interest Adolescent Psychiatry Clinical Practice Guidelines for Psychiatrists in
India. Vol. 4. Jaipur: Indian Psychiatric Society; 2008.
There are no conflicts of interest. 5. In: Gautam S, Avasthi A, editors. Indian Psychiatric Society. Forensic and
Legal Issues. Vol. 5. Jaipur: Indian Psychiatric Society; 2009.
6. Grover S, Avasthi A. Views about clinical practice guidelines of the Indian
REFERENCES Psychiatric Society: A survey of psychiatrists in India. Indian J Psychiatry
2009;51:127‑33.
1. In: Gautam S, Avasthi A, editors. Indian Psychiatric Society. Clinical Practice 7. Forsner T, Hansson J, Brommels M, Wistedt AA, Forsell Y. Implementing
Guidelines for Psychiatrists in India on Schizophrenia, Depression, Bipolar clinical guidelines in psychiatry: A qualitative study of perceived facilitators
Affective Disorders, Obsessive Compulsive Disorder, Generalized Anxiety and barriers. BMC Psychiatry 2010;10:8.

S18 Indian J Psychiatry 59 (Supplement 1), January 2017

 CLINICAL PRACTICE GUIDELINES
Clinical Practice Guidelines for Management of Schizophrenia
Sandeep Grover, Subho Chakrabarti, Parmanand Kulhara, Ajit Avasthi
Department of Psychiatry, PGIMER, Chandigarh
Participants of expert group on CPG for Schizophrenia
B.N. Gangadhar, P.K. Dalal, Lalit Batra, Kishore Gujar,
O.P Singh, Bharat Singh, Abhay Matkar, Devendra
Vijayvargiya, R.K. Solanki, Adarsh Tripathi
INTRODUCTION
Schizophrenia is a serious mental disorder with prevalence
rates of 2-3 per 1000 reported from India. The impact of
schizophrenia on patients, their families and the wider
society are no different from what has been observed in
the rest of the world. However, resource constraints,
poverty, lack of education and inadequate access to health
care facilities for patients make the problem of providing
care particularly daunting in India. In 2005, the Indian
Psychiatric Society came up with treatment guidelines for
schizophrenia tailored to meet the requirements of our
patients in the context of prevailing existing resources.
There have been several developments in the management
of schizophrenia since then. These new set of guidelines
attempt to update the previous guidelines by emphasizing
what is new in the field. These guidelines ought to be read
in conjunction with the earlier version of the treatment
guidelines on schizophrenia as developed and published by
the Indian Psychiatric Society in the year 2005.
SCOPE OF THIS DOCUMENT
The major emphasis of the current guidelines is on areas in
the management of schizophrenia, which have witnessed
significant developments since the publication of the
Address for correspondence:
Dr. Ajit Avasthi, Department of Psychiatry,
Postgraduate Institute of Medical Education and Research,
Chandigarh ‑ 160 012, India.
E-mail: drajitavasthi@yahoo.co.in
Access this article online
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Website:
www.indianjpsychiatry.org
DOI:
10.4103/0019-5545.196972
© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow
previous guidelines. These guidelines are not particularly
applicable to any specific treatment setting and may need
minor modifications to suit the needs of patients in a
specific setting. The recommendations are primarily meant
for adult patients. The needs of children or the elderly with
schizophrenia may be different. Finally, it is expected that
recommendations made will have to be tailored to suit the
needs of individual patients.
Assessment and evaluation (table-1)
A comprehensive assessment of the patient and his/her
caregivers needs to be carried out. The cornerstone of this
assessment is a detailed history and physical and mental state
examinations. Efforts should be made to obtain information
from all sources, especially the family. Wherever possible,
diagnosis of schizophrenia be preferably made according
to current diagnostic criteria, as such a diagnosis is more
reliable. A reliable diagnosis facilitates communication
among clinicians, and allows for better applicability
of evidence-based recommendations. Many clinical
conditions that may mimic schizophrenia include mood
disorders, substance-induced psychoses and psychoses
secondary to physical illnesses. These should be ruled out
as far as possible by history, examination and additional
investigations. In some instances a definitive diagnosis may
need time. Further, because of the enormous psychosocial
consequences a diagnosis of schizophrenia needs to be
made with great caution and sensitivity. In doubtful cases,
a medication-free observation period can be considered.
However, consideration of medication free period need to
be balanced against the risks of delaying treatment or the
potential for harm to self and others in acutely ill patients.
It is important to remember that diagnosis is not a one-time
affair, but a continuous process. Accordingly, based on the
subsequent information from patients and caregivers, and
on repeated clinical evaluations the diagnosis may need re-
evaluation.
This is an open access article distributed under the terms of the Creative
Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non-commercially, as long as the
author is credited and the new creations are licensed under the identical terms.
For reprints contact: reprints@medknow.com
How to cite this article: Grover S, Chakrabarti S, Kulhara
P, Avasthi A. Clinical Practice Guidelines for Management of
Schizophrenia. Indian J Psychiatry 2017;59:19-33.
S19
 Grover, et al.: CPG for Schizophrenia
The assessment should cover all other areas such as
symptom dimensions, symptom-severity, comorbid
psychiatric and medical conditions, particularly comorbid
substance abuse, the risk of harm to self or others, level of
functioning and the socio-cultural milieu of the patient. A
high index of suspicion along with thorough assessment can
help in detecting most patients with comorbid substance
abuse/dependence. Wherever, facilities are available, urine
or blood screens (with prior consent) can be used to confirm
the presence of comorbid substance abuse/dependence. A
thorough physical examination need to be done to rule out
presence of any physical illness and also to rule out psychoses
secondary to physical illnesses. This may be supplemented
by the judicious use of investigations. Wherever possible,
unstructured assessments need to be supplemented by
ratings on appropriate standardized rating scales. Other
options such as detailed cognitive testing can be done if
required and feasible. The use of neuroimaging may be
indicated in those with first-episode psychosis, neurological
signs, non-response to treatment and elderly patients.
Assessments of caregivers may focus on areas such as their
knowledge and understanding of the illness, their attitudes
and beliefs regarding treatment, the impact of the illness on
them and their personal and social resources.
It is important to remember that assessment is an ongoing
process. As the treatment progresses other areas such as response
to treatment, side effects, treatment adherence, the impact of
patient’s immediate environment, disability assessments, other
health-care needs, ease of access and relationship with the
treatment team may need to be assessed separately.
Formulating a treatment plan (figure 1)
Formulation of treatment plan involves deciding about
treatment setting, treatments to be used and areas to be
addressed. Patients, caregivers and staff involved in care
may be consulted while preparing the treatment plan.
Treatment plans be needs-based, practical, feasible and
flexible. These should be continuously re-evaluated and
modified as required.
Choice of treatment settings
The basic principle while choosing a treatment-setting
is to provide care in the least restrictive setting, which
nevertheless meets the needs of patients and caregivers. The
commonest treatment settings would be either outpatient
clinics or inpatient wards. In some instances resources for
long-term inpatient care, or community or residential care
may be available. The bulk of the patients would probably
receive treatment in outpatient settings. Given their severe
shortage, inpatient beds are likely to be scarce. Common
indications for inpatient care during acute episodes are
shown in table-2. Whenever possible patient admitted to
the inpatient setting should have accompanying family
caregivers. In case inpatient care facilities are not available,
S20
Table 1: Components of assessment and evaluation
Basic assessments
• Comprehensive assessment of both patients and caregivers
• Complete history with information from all possible sources
• Physical examination‑ record data such as blood pressure, weight and
wherever indicated body mass index and waist circumference
• Mental state examination
• Establish diagnosis according to current diagnostic criteria
• Differential diagnosis by ruling out secondary psychoses
• Areas to be evaluated: symptom‑severity, symptom‑dimensions (reality
distortion, disorganization, negative, depressive and cognitive
symptoms), comorbid physical, psychiatric and substance use
conditions, risk of harm to self and others, level of functioning and
socio‑cultural milieu of the patient
• Basic investigations: haemogram, blood sugars and lipid levels, liver
functions, renal functions, electrocardiogram (focus on QTc)
• Assessments of caregivers: knowledge and understanding of the illness,
attitudes and beliefs regarding treatment, impact of the illness on them,
personal and social resources
• Ongoing assessments: response to treatment, side effects, treatment
adherence, the impact of patient’s immediate environment, disability
assessments, other health‑care needs, ease of access and relationship
with the treatment team
Additional/Optional assessments
• Use of standardized rating scales to rate all aspects of the illness
• Psychological testing for cognitive functions
• Neuroimaging especially in those with first‑episode psychosis,
neurological signs, non‑response to treatment and elderly patients
Table 2: Some indications for inpatient care during
acute episodes
• Presence of suicidal behaviour which puts the life of the patient at risk
• Presence of severe agitation or violence which puts the life of others at risk
• Refusal to eat which puts the life of patient at risk
• Severe malnutrition
• Patient unable to care for self to the extent that she/he requires constant
supervision or support
• Catatonia
• Presence of general medical or comorbid psychiatric conditions which
make management unsafe and ineffective in the outpatient setting
than the patient and/or family need to be informed about
such a need and admission in nearest available inpatient
facility may be facilitated.
Options for management for schizophrenia
Treatment options for management of schizophrenia
can be broadly classified as antipsychotic medications,
electroconvulsive therapy (ECT), adjunctive medications
and psychosocial interventions (table-3).
Pharmacological treatment
Choice of antipsychotic medication
The essential choice is between using an antipsychotic
belonging to the class of typical antipsychotics (FGA- first-
generation antipsychotic) or from the atypical group (SGA-
second-generation antipsychotic). Since the publication of
the previous guideline there is somewhat greater clarity on
this matter. The bulk of the evidence including large-scale
real-world studies indicates that there is very little difference
Indian J Psychiatry 59 (Supplement 1), January 2017
 Grover, et al.: CPG for Schizophrenia

Patient with Psychotic features

Consider differential diagnoses like

• Organic Mental Conditions
• Acute and transient psychotic disorder
• Persistent Delusional disorder
• Schizoaffective disorder
• Severe depression with psychotic symptoms
• Mania with psychotic symptoms
• Drug induced psychosis

Establish the diagnosis of schizophrenia

Assessment
• Severity of illness
• Risk of harm to self and others
• Comorbid substance use/dependence
• Level of functioning
• Detailed Physical examination
• Record- blood pressure, weight and wherever indicated body mass index and waist
circumference
• Mental Status Examination
• Investigations- haemogram, liver function test, renal function test, fasting blood glucose
level, electrocardiogram (focus on QTc)
• Treatment history- response to previous medication trials, compliance, side effects, etc.
• Patient’s and caregivers beliefs about the cause of illness and beliefs about the treatment
• Assessment for social support, stigma, coping
• Assessment of caregiver burden, coping and distress

• Decide about treatment setting- consider inpatient care in case of suicidality, severe agitation
and violence, malnutrition, catatonia, patient unable to care for self to the extent that she/he
requires constant supervision or support, comorbid general medical conditions making
management difficult at the outpatient setting
• Liaison with other specialists depending on the need of the patient

Pharmacological Management Electroconvulsive therapy Non-Pharmacological

• Choose an antipsychotic based on past • Catatonia, affective Management
treatment response, past history of side symptoms, rapid control • Psychoeducation
effects, cost, comorbidity, Patient/family of symptoms, suicidality, • Psychosocial
preference, preferred route of past response to ECT, intervention
administration, availability, current metabolic augmentation etc.
profile, past history of compliance,
treatment resistance

Figure-1: Initial evaluation and management plan for schizophrenia

Table 3: Options for management for schizophrenia in terms of efficacy, adherence and other subjective aspects
Antipsychotic medications between the FGA and the SGA group, or between individual
First‑generation antipsychotic medications (Oral/parenteral/depot or long antipsychotics belonging to either group. The only exception
acting‑ preparations) to this trend is clozapine, which appears to be more
Second‑generation antipsychotic medications (Oral/parenteral/depot or long efficacious than any other antipsychotic in patients with
acting‑ preparations)
Somatic treatments
treatment resistance. It follows from this that the choice of
Electroconvulsive therapy (ECT) the antipsychotic will depend on factors other than efficacy.
Adjunctive medications Some of these factors are included in table-4.
Anticholinergics, antidepressants, benzodiazepines, hypnotic‑sedatives,
anticonvulsants, lithium carbonate Dose
Psychosocial interventions
Family intervention, cognitive behavioural therapy, social skills training,
The recommended dose of various oral antipsychotics
cognitive remediation, individual therapy, group therapy, vocational available in India is shown in table-5. In general patients
rehabilitation, early‑intervention programmes, case management, with first-episode psychosis respond to lower doses. The use
community mental‑health teams, crisis resolution teams of high or very high doses (mega doses) of antipsychotics,
Other measures if required, may be used with caution in exceptional
Lifestyle and dietary modifications
circumstances. It is noted that Indian patients require lower

Indian J Psychiatry 59 (Supplement 1), January 2017 S21

 Grover, et al.: CPG for Schizophrenia

doses of antipsychotic drugs compared to patients from the Table 4: Factors that influence selection of
West. Although this is suggested by clinical experience and antipsychotics
pharmacokinetic studies of Asian patients, there is little • Past treatment response
evidence for, or against this supposition from clinical trials. • Cost of treatment, affordability
• Psychiatric comorbidity
Route of administration • Medical comorbidity
• Side effects
Acutely agitated patients often require parenteral • Patient or family preference
administration of antipsychotics to rapidly control the • Preferred route of administration
behavioural disturbance. Liquid or mouth-dissolving • Concomitant medications
formulations are often helpful in non-compliant patients. • Non‑adherence
Depot preparations are generally not used in acutely • Treatment resistance
agitated patients except zuclopenthixol acetate, which has
a half-life of about 20 hours. In general, it is recommended Table 5: Recommended therapeutic dose ranges for
that one drug is to be used by one route in order to minimise various antipsychotics
drug interactions and simplify clinical observations.
Usual daily dose Maximum
(in mg/day) daily dose
Depot preparations (table-6) are often helpful in ensuring First Generation Antipsychotics (FGAs)
medication-compliance and may be used in situations Chlorpromazine 300‑800 800
where compliance is a problem. Depot injectables may Haloperidol 5‑20 20
also be used if patients/relatives indicate a preference for Penfluridol 20‑60 mg/week 250 mg/week
this kind of treatment. Test doses are administered at the Perphenazine 12‑64 64
Pimozide 4‑10 10
start of treatment. When used, depot preparations need to
Thioridazine 300‑800 800
be prescribed within the standard recommended dosage Trifluoperazine 15‑30 30
and interval range to achieve optimum effectiveness in Zuclopenthixol 10‑50 50
preventing relapse. Second Generation Antipsychotics (SGAs)
Amisulpride 50‑800 1200
Aripiprazole 10‑30 30
Adequate antipsychotic trial
Asenapine 10‑20 20
The minimum recommended duration of treatment to Blonanserin 2‑8 24
consider it to be an effective trial for all antipsychotics is use Clozapine 150‑600 900
of medication in the highest tolerable dose for 6-8 weeks, Iloperidone 12‑24 24
with the exception of clozapine, where the minimum period Olanzapine 10‑30 30
Paliperidone 3‑12 12
of treatment is at least 3-6 months.
Quetiapine 300‑800 800
Risperidone 2‑8 16
Response Ziprasidone 80‑200 200
Antipsychotics are known to produce a significant remission Zotepine 75‑300 300
of positive symptoms. This could thus be a reasonable goal
of treatment during the acute phase. Antipsychotics are less
effective in management of negative symptoms, therefore a
Table 6: Antipsychotic depot preparations available in
mild to moderate reduction in negative symptoms is often
India
acceptable. Response indicators for other aspects of the
Name of antipsychotic Usual 2‑4 weekly dose in mg
illness (e.g. cognitive symptoms) are not clear. Patients on
Zuclopenthixol decanoate 200
antipsychotics need to be monitored regularly to ascertain
Paliperidone palmitate 234 initially followed by 117 monthly
the level of response and the emergence of side effects. Fluphenazine decanoate 12.5‑50
Haloperidol decanoate 50
Non-response (Figure-2) Risperidone depot 25‑50
In case a patient fails to respond to an antipsychotic (RisperidalConsta)
medication, poor compliance or non-compliance need Olanzapine pamoate 210‑405
to be evaluated prior to switching the medication to
another antipsychotic. If a patient is found to have poor with good compliance, a change in antipsychotic may be
compliance or non-compliance to medications, all efforts considered. Clozapine need to be considered after failure of
are to be made to understand the causes responsible for sequential trials of 2 antipsychotics (at least one of which is
lack of compliance and appropriate steps need to be a SGA). Clozapine may also be considered earlier in patients
taken to handle the problem. However, if a patient fails to who are violent, at risk for suicide, not responding to their
respond to an adequate trial of an antipsychotic medication current medication and those experiencing intolerable side
(i.e., adequate dose for at least 6-8 weeks duration) taken effects with two different classes of antipsychotics.

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 Grover, et al.: CPG for Schizophrenia

Patient given an adequate Adequate Response

antipsychotic trial (adequate dose for • Continue with the same
atleast 6 weeks duration) dose of antipsychotic
medication and keep on
monitoring the side effects

Non-response to treatment

Evaluation
• Re-evaluate the diagnosis
• Medication compliance

True Non-response Pseudo Non-response due to poor compliance

• Change the antipsychotic • Evaluate the causes, address the same and
medication ensure compliance
• In case of poor compliance due to intolerable
side effects –consider change of antipsychotic
(oral/depot)

Failure of 2 adequate trials of Adequate Response

antipsychotic, one of which is SGA • Continue with the same dose of
• Consider clozapine antipsychotic medication and keep
on monitoring the side effects

Inadequate Response to clozapine

• Consider combining clozapine with ECT
or another antipsychotic medication
• More intensive psychosocial intervention

Figure 2: Evaluation of patient with non-response to antipsychotic medications

Combination of antipsychotics is not recommended. It is better to start these drugs when

There is limited evidence for the efficacy of combination
of antipsychotics. In the initial phase, a clinician may
be compelled to use a combination of antipsychotics to
manage agitation, but caution need to be exercised while
doing so. These should be used on SOS basis and for
shortest possible time. Combinations of antipsychotics for
prolonged periods may be avoided, except in patients not
responding to clozapine.
ADJUNCTIVE MEDICATIONS
Although antipsychotic agents are the mainstay of
treatment of schizophrenia, management may involve
use of adjunctive treatments like with antidepressants,
mood stabilizers or benzodiazepines. However, these can
be used with proper rationale and for shortest possible
duration. At every assessment a proper evaluation need
to be done for the continuation of the same. Lithium and
other mood stabilizers can be prescribed in agitated,
overactive patients or those with affective symptoms
responding poorly to their current drug. Benzodiazepines
can be useful in managing agitation and sleep disturbance.
Antidepressants may be of use in post-psychotic depression
and may be avoided when the patient has florid psychotic
symptoms. In general prophylactic use of anticholinergics
the patient actually develops extrapyramidal side effects.
Whenever anticholinergic agents are required, use may be
limited to lowest possible doses and for shortest possible
time.
ELECTROCONVULSIVE THERAPY (ECT)
As in many other developing countries ECT is used quite
frequently in schizophrenia in India. The evidence for
efficacy of ECT in the acute phase of schizophrenia is
somewhat controversial. There is evidence for augmentation
and acceleration of response. ECT is used in conjunction
with antipsychotics in the acute phase, but the extent of the
benefit of adding ECT to antipsychotics is unclear and the
positive effects seem to last only for the first few weeks of
treatment. However, there may be some merit in adding ECT
to the treatment regimen in patients who respond poorly to
antipsychotics. The more unequivocal indications for ECT
in combination with antipsychotics are included in table-7.
ECT is not useful in chronic schizophrenia and there is not
enough evidence to recommend its use in the longer term
except in exceptional circumstances. Finally, whenever ECT
is used adequate information and support for patients and
caregivers, informed consent, proper administration and
careful monitoring of response and side effects be done.

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 Grover, et al.: CPG for Schizophrenia
PSYCHOEDUCATION FOR PATIENTS AND OR
FAMILY (TABLE-8)
Psychoeducation may be considered both for the patient and
family members. The aim is to educate the patient and family
about the illness. Simple and brief explanations about the
nature of the patient’s illness, treatments, likely side effects,
likely length of treatment etc. can be offered. Relatives also
need to be given time to confront the painful fact of the illness,
and what it entails for the patient and the family as a whole.
It is important that professionals are careful and considerate,
but clear and thorough in their use of clinical language and
in the explanations they provide. No blame is to be attached
to the family. Treatment adherence will be another main
objective at this stage. Prior to every session, feedback of the
previous sessions may be taken and psychoeducation is to be
tailored to the needs of the patient and the caregivers.
PSYCHOSOCIAL INTERVENTIONS
Psychosocial interventions are acknowledged to be an
integral part of management of schizophrenia. Different
psychosocial interventions including family treatments,
cognitive behavioural therapy, social skills training, cognitive
remediation, individual supportive therapy, group therapy,
vocational rehabilitation, case management, use of community
Table 7: Possible indications of use of ECT in patients of
schizophrenia
• Catatonic symptoms
• Affective symptoms
• Need for rapid control of symptoms
• Presence of suicidal behaviour which puts the life of the patient at risk
• Presence of severe agitation or violence which puts the life of others at risk
• Refusal to eat which puts the life of patient at risk
• History of good response in the past
• Patients not responding to adequate trial of an antipsychotic medication
• Augmentation of partial response to antipsychotic medication
• Clozapine resistant schizophrenia
• Not able to tolerate antipsychotic medications
Table 8: Basic components of Psychoeducation
• Assessing the knowledge of the patient and caregivers about aetiology,
treatment and prognosis
• Introducing the diagnosis of schizophrenia into discussion
• Discussing about various symptom dimensions
• Providing information about aetiology
• Providing information about treatment in terms of available options, their
efficacy/effectiveness, side effects, duration of use
• Discussing about importance of medication and treatment compliance
• Providing information about possible course and long term outcome
• Discussing about problems of substance abuse, marriage and other issues
• Discussing about Communication patterns, problem solving, disability
benefits
• Discussing about relapse and how to identify the early signs of relapse
• Dealing with day today stress
• Improving insight into illness
• Handling expressed emotions and improving communication
• Enhancing adaptive coping to deal with persistent/residual symptoms
S24
mental-health teams and of crisis resolution teams have been
proven to be useful in the management of schizophrenia.
The usefulness and delivery of psychosocial treatments has
probably not attracted the research attention it deserves in the
Indian context. Nevertheless, there is ample Indian evidence
and experience with family treatments, rehabilitation and
other modalities such as community programmes, yoga and
cognitive remediation. Based on these data, psychosocial
interventions, from the simple to the complex, can be
recommended for patients with schizophrenia and their
families. An approach which prioritizes the needs of patients
and their families could be followed.
FAMILY INTERVENTIONS
There has been a long tradition in India of involving
families in the care of their members with mental illness.
There are several studies documenting the delivery of
family interventions. Several formats of predominantly
psychoeducational treatments such as informal or
unstructured programmes, structured treatments, group-
based interventions, and integrated psychosocial treatments
have been tried. From the number of controlled trials it
appears that a wide range of interventions and treatment-
delivery, from the simple to the complex, may be useful
in the Indian context. The basic emphasis need to be on
continued contact and medication adherence while offering
emotional and practical support. A needs-based approach,
in which interventions are tailored to the background
and needs of the families, is more likely to enhance their
acceptability and positively influence the readiness of
families to participate in such interventions.
ADVISE FOR LIFE STYLE AND DIETARY
MODIFICATIONS
All the patients are to be advised for a change in the life
style and diet to reduce the risk of metabolic side effects
and cardiovascular morbidity and mortality. These include
physical exercises, dietary modifications and abstinence
from smoking etc.
REHABILITATION
Similar to family treatments, rehabilitation programmes
need to be be culturally moulded and adapted to the
needs of patients and their families. However, unlike family
interventions, resources for more elaborate rehabilitation
strategies may not be available in every centre. Nevertheless,
relatively simple and inexpensive strategies can form a part
of the overall psychosocial intervention package.
INDIVIDUAL SUPPORTIVE THERAPY
A supportive empathic relationship between patients and
professionals, in which good listening promotes a lasting
Indian J Psychiatry 59 (Supplement 1), January 2017
 Grover, et al.: CPG for Schizophrenia
therapeutic alliance is an essential part of good practice.
Additional elements could include support and advice,
encouraging continued engagement, treatment-adherence
and healthy lifestyles. Efforts to minimize stress may also
be beneficial. Individual support along with medication is
the most commonly practiced treatment in schizophrenia.
Patients and families consistently rank individual support as
among the most highly valued services offered to patients
with schizophrenia.
OTHER PSYCHOSOCIAL INTERVENTIONS
Other interventions that hold promise are home-based
care, support groups for caregivers, community-based
interventions, cognitive training or remediation, and yoga.
More research on the efficacy of these strategies and their
wider implementation is needed.
Basic components of any psychosocial intervention are
depicted in table-9. For more specific recommendations
other sources may be consulted.
TREATMENT ADHERENCE
Adherence is defined as “the extent to which the
patients’ behaviour, in terms of regular clinic visit, taking
medications, following diets, executing lifestyle changes,
coincide with the clinical prescription”. Non-adherence
in this context thus denotes failure to enter a treatment
programme, premature termination of treatment, or
incomplete implementation of instructions, including
those that pertain to medication administration. Evidence
suggests that about half of the patients with schizophrenia
do not comply with the treatment recommendations,
about one-third miss their appointments with the
clinicians and 20-60% of patients drop out from treatment.
Common factors associated with poor medication non-
compliance are shown in table-10. Factors consistently
linked to non-adherence include poor insight, negative
attitude or subjective response to medication, comorbid
substance abuse, and poor therapeutic alliance. Clinicians
need to make efforts to reduce the rates of medication
compliance and treatment non-adherence. It is important
for the clinicians to understand that besides the
contextual or situation factors, patient related factors
and illness related factors, certain clinician related
factors are responsible for poor medication compliance
and higher dropout rates. Some of the common clinician
related factors which may be relevant in Indian context
include poor communication between the clinician and
the patient/caregiver, poor therapeutic alliance and non-
collaborative decision-making. Hence, clinicians need to
focus on better communication and improve therapeutic
alliance with patient and the family to improve overall
outcome. Whenever clinicians encounter poor medication
Indian J Psychiatry 59 (Supplement 1), January 2017
Table 9: Recommendations about psychosocial
interventions
• Assessment of psychosocial factors involving the patient and the family is
an integral part of psychosocial interventions.
• There is a wide range of interventions that have proved useful in Indian
settings
• Choice of the intervention will be shaped by the needs of patients and
their families as well as the resources available.
• Basic components of any intervention include: promoting a therapeutic
alliance with the patient and the family, encouraging ongoing
engagement, information about various aspects of the illness, focusing on
treatment‑adherence and healthy lifestyles, and offering emotional and
practical support.
Table 10: Factors associated with poor medication
compliance
Demographic risk factors
• Younger age, male gender, unemployment, lower socioeconomic status
Patient related factors
• Knowledge about illness and treatment, perceived need for
treatment (insight), motivation, beliefs about treatment risks and benefits,
past experiences/“transference”, past history of adherence, self‑stigma
Social risk factors
• Living independently, poor social support, poor financial support
Clinical risk factors
• Poorer premorbid functioning, earlier age of onset, prior history of
non‑adherence
Symptom‑related risk factors
• Lack of insight, paranoia, grandiose delusions, conceptual
disorganization, impaired cognition, substance abuse, comorbidities,
depression, refractoriness, spontaneous remissions
Treatment‑related risk factors
• Medication side effects, poor treatment alliance, complex dosing,
negative experience of medication, route of administration, length of
treatment, cost of treatment, number of medications
Service‑related risk factors
• High cost of medication, poor accessibility of treatment services
Family/caregivers‑related risk factors
• Lack of supervision, negative attitudes towards treatment, lack of
knowledge about medicines, nature of relationship with patient,
perceived need for treatment, beliefs about benefits and risks with
continued treatment, involvement in treatment, stigma, financial
constraints, support from other sources
Clinician/provider related factors
• Therapeutic alliance, frequency and nature of contact with clinicians,
expected duration of treatment, duration of past treatment, accessibility
to clinicians and services, reimbursement, psychoeducation and
psychosocial treatment, complexity of administration
or treatment compliance, all efforts need to be made
to understand the reasons behind the same. Proper
evaluation of non-adherence need to cover assessment
of familial, social, biological and pharmacological
perspectives. Patients/caregivers concerns need to be
addressed by proper psychoeducation and modification of
pharmacological treatment. Medication compliance can be
improved by using depot preparations and use of mouth
dissolving formulations under supervision. Evidence
also suggests beneficial effects of cognitive-behavioural
approaches and motivational interviewing.
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 Grover, et al.: CPG for Schizophrenia
PHASES OF ILLNESS/TREATMENT
Management of schizophrenia can be broadly divided into
three phases, i.e., acute phase, continuation treatment or
stabilization phase, maintenance or stable phase. Some
patients may present very early in a prodromal phase and
appropriate strategies for detection and management for
this phase might be required.
Prodromal stage
It is now well known that onset of frank psychosis is often
preceded by psychological and behavioral abnormalities
involving cognition, emotion, perception, communication,
motivation and sleep. These symptoms may precede the
psychosis by weeks to years. Various diagnostic systems
categorise the symptoms as: basic symptoms, attenuated
positive symptoms, brief limited intermittent psychotic
symptoms, features of schizotypal personality disorder,
genetic risk paired with functional deterioration, as well
as general symptoms that are not specific to psychosis.
Evidence also suggests that many patients with prodrome,
especially the high risk group have higher chance of
conversion to frank schizophrenia. Conversion rates have
been reported to range from 25-40%. Further, prodrome
itself may have negative impact on the social, emotional
and cognitive development. Therefore, now more and
more emphasis is laid on early detection and intervention.
Factors which have been shown to predict conversion to
psychosis include presence of genetic risk with recent
deterioration in functioning, higher degree of unusual
thought content, suspiciousness/paranoia, presence of
social impairment, longer duration of symptoms, high
levels of depression, reduced attention and history of
substance abuse. In terms of management of prodrome
it is suggested that treatment ought to be based on the
needs of the patient. There is some evidence to suggest
that use of antipsychotics in prodromal phase can delay the
conversion to psychosis and antidepressants may be useful
in symptomatic improvement in a sub-group of patients.
However, at present evidence for use of antipsychotics in
prodromal phase is not convincing to recommend its use in
all patients. There is also preliminary evidence to suggest
the beneficial effect of certain agents like omega-3 fatty
acids. In contrast, evidence suggest that psychological
interventions like cognitive behaviour therapy, cognitive
therapy, psychosocial stress management, etc can improve
functioning and symptomatology during the prodromal
phase, although the active components of these treatments
are not well known. Accordingly, whenever a patient
presents with symptoms suggestive of prodromal phase of
schizophrenia, initial management is done in the form of
psychosocial intervention. Use of pharmacotherapy need to
be weighed against the side effects of antipsychotics and
sensitization of dopamine receptors in brain, which can
possibly lead to supersensitivity psychosis or rapid-onset
psychosis following stoppage of antipsychotic medication.
S26
MANAGEMENT IN THE ACUTE PHASE OF
TREATMENT
Most patients in this stage are likely to exhibit florid
psychotic symptoms such as delusions or hallucinations,
disorganized thinking and behavioural disturbances. Their
functioning may be severely impaired and they can be at
risk of harming themselves or others. Additionally both the
patient and the family might have considerable difficulty in
coming to terms with the onset of acute symptoms. The
various aspects of management in the acute phase are
included in table-11.
MANAGEMENT IN THE CONTINUATION
TREATMENT PHASE
This phase begins once the acute symptoms reduce in
severity or remit and conventionally lasts for about 6-12
months. Different components of this phase are shown in
table-12. Consolidation of remission, continued reduction
in symptoms and prevention of early relapses are the usual
treatment objectives during this phase. Reduction of stress
on the patient and the family by continuing engagement
Table 11: Management in the acute phase
Comprehensive assessment (psychiatric/medical/psychosocial)
Deciding on goals of treatment
Patients
Eliminate/reduce symptoms of schizophrenia and improve the level of
functioning
Promote safety, reduce risk of harm, reduce stress
Caregivers
Minimise caregiver distress
Offer help to enable them to cope with the illness in their relative
Both
Develop a therapeutic alliance and provide opportunities for patients and
caregivers to actively engage in treatment
Offer basic information and support tailored to needs of patients and
caregivers
Choice of treatment setting
Antipsychotic treatment
Choice of drug
Dose
Route of administration
Duration of treatment
Determining response or non‑response
Combining antipsychotics
Use of adjunctive medications when indicated
Use of ECT when indicated
Psychosocial interventions‑ relatively basic and mainly for the purpose
of fulfilling the goals of treatment listed above
Planning for further treatment
Table 12: Management in the continuation treatment
phase
Determining goals
Further assessment
Antipsychotic treatment
Psychosocial interventions
Monitoring for response, side effects and treatment adherence
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 Grover, et al.: CPG for Schizophrenia
and support and enhancing their adaptation to life after
discharge from the hospital, are other important goals of
management. Management includes continuing medication
treatment, monitoring of response and side effects and
furthering psychosocial interventions. Medications need
to continue preferably at the same dose for the next 6-12
months. The continued goals of psychosocial treatment are
to maintain treatment engagement and adherence, offer
support for patients and their families and help prepare
the patient for life in the community. More elaborate
psychosocial interventions may be tried at this stage.
Finally, regular monitoring of response, side effects and
treatment-adherence needs to continue.
MANAGEMENT IN THE MAINTENANCE OR
STABLE PHASE
During this phase of illness, symptoms are stable and
usually less severe than in the acute stage. Negative
symptoms may predominate and deficits in social and
occupational functioning become more apparent.
Maintaining or improving level of functioning, prevention
of recurrences and promoting psychological/personal
recovery are the major aims of treatment during this
phase of management. Different components of this phase
are shown in table-13.
During this phase, follow-ups can be scheduled once every
2-3 months and more frequently in times of crises, or if
desired by the family. During this phase of management,
regular feedback need to be obtained from the family.
Any new issues that arise are discussed and some of the
previous issues may need reemphasis. Management in
the stable phase involves carrying forward the gains
achieved. The management plan should be relooked for
any need for change. It also involves determining the
goals, continuing further assessment, continuing with
antipsychotic medications and monitoring of side effects
and furthering the psychosocial interventions. In addition
the management need to focus on rehabilitation, enhancing
personal recovery.
Goals of treatment: The goals of treatment during this
phase are to maintain or improve functioning, improve
quality of life and facilitate personal recovery. Psychotic
exacerbations need to be effectively treated. Adverse effects
are to be noted and managed.
Table 13: Management in the maintenence phase
• Determining goals
• Re‑evaluating/modifying the treatment plan
• Assessments and monitoring
• Antipsychotic treatment
• Psychosocial interventions
• Monitoring for response, side effects and treatment adherence
• Early intervention for relapses
Indian J Psychiatry 59 (Supplement 1), January 2017
Re-evaluating/modifying the treatment plan: As time elapses
the nature of the illness, problems faced by the relatives,
needs of the patient and the family and previously determined
targets are all expected to change. Regular contact, awareness
and monitoring are needed to detect these changes. Ongoing
assessment is thus essential. It allows those modifications to be
made in the treatment plan, which are required to accommodate
any new problems or demands that may have arisen.
Assessments and monitoring: Monitoring is required for
assessing response and for side effects that may emerge. Further
assessments may be required during this period especially
if psychosocial treatments are being planned. Information
should be obtained from the patients, family members, and
other available sources. Frequency of contact will depend
on several factors such as clinical state, the distance of the
hospital from the patient’s home, social support available for
the patient, the type of treatment being administered etc.
Antipsychotic treatment
Dose: The dose of the antipsychotic needs to be
individualized. A balance has to be struck between the
need to reduce side effects and the need to prevent relapse.
Stable patients who do not have positive symptoms may
be candidates for reduction in doses. Doses need to be
reduced gradually at the rate of about 20% every 6 months
till a minimum effective dose is reached.
Reduction of dose/ withdrawal of antipsychotic medication
may be be undertaken gradually whilst regularly monitoring
signs and symptoms for evidence of potential relapse.
Following withdrawal from antipsychotic medication,
monitoring for signs and symptoms of potential relapse, need
to continue, for at least 2 years after the last acute episode.
Any re-emergence of symptoms is to be immediately treated.
Duration of treatment: Duration of treatment depends on
a number of factors and will need to be individualized. The
suggested guidelines are as follows:
• First-episode patients ought to receive 1-2 years of
maintenance treatment
• Patients with several episodes or exacerbations are to
receive maintenance treatment for 5 years or longer
after the last episode
• Patients with history of aggression or suicide attempts
should receive treatment for longer period or lifelong.
The usual indications for use of long term or lifelong
antipsychotic medications are shown in table-14.
Psychosocial interventions
The psychosocial interventions started in the previous
treatment phases is to be continued and the gains obtained
till now should be evaluated. Further, the clinicians should
evaluate as to whether any change is required in terms of
goals and strategies used.
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 Grover, et al.: CPG for Schizophrenia
Table 14: Indications for life long/long term use of
antipsychotic medications
History of multiple relapses while on treatment
History of relapses when the medications are tapered off
History of 2 episodes in last 5 years
History of suicidal attempts
Presence of residual psychotic symptoms
Family history of psychosis with poor outcome
Comorbid substance dependence
Rehabilitation
Facilities for vocational rehabilitation are scarce. However,
if the patient is already working efforts can be made to help
out in any problems at the work place, which could be due
to the effects of the illness. If the patient is unemployed,
their suitability for work needs to be assessed. If he is
ready for work, he is to be encouraged to seek appropriate
jobs. However, if the patient requires rehabilitation then
culture-specific characteristics for that rehabilitation
programme need to be adopted in order to be successful.
Early intervention for relapses
The management plan needs to be organised to respond as
quickly as possible to any relapses in the patient’s condition.
Patients and relatives need to be educated to recognise early
symptoms of a relapse. They need to be told about the need
for early intervention in impending cases of relapse. They need
to have easy access to treatment facilities such as emergency
services or inpatient settings, which will cater to the needs
of a patient on the verge of a relapse. Contact need to be
increased during this phase. Crisis intervention measures
such as brief admissions or frequent home visits need to be
adopted, whenever feasible. All these are important steps in
efficient detection and treatment of relapses.
SPECIAL SITUATIONS
Clinicians often encounter certain clinical situations which
either require special attention or can influence treatment
decisions. Management of these situations is summarised
in table-15.
SIDE EFFECTS AND THIER MANAGEMENT
Antipsychotics are associated with many side effects, which
require intervention. Some of the common side effects that
can be very distressing to the patients include extrapyramidal
side effects, cardiovascular side effects, sexual dysfunction
and metabolic side effects. The cardiovascular side effects
can be life threatening too. The common management
strategies for these side effects are shown in table-16.
Extrapyramidal side effects: Extrapyramidal side effects
(EPS) are often noted in patients receiving FGAs, especially
high potency antipsychotic medications. However, EPS is
S28
also seen with SGAs. The acute EPS include acute dystonia,
pseudo-parkinsonism and akathisia. Acute EPS is usually
seen during the first few days or weeks of starting treatment,
is dose dependent and subsides with stoppage of offending
agent. Chronic EPS is usually seen after prolonged use
(months to years) of antipsychotics and these include
tardive dyskinesia, tardive dystonia and tardive akathisia. It
is important to note that chronic EPS is not dependent on
the dose of antipsychotics and persists even after stopping
the offending agent. It is important to be aware of the risk
factors for development of these side effects (table-17).
In case a patient is experiencing Parkinsonism during the
initial phase of treatment, the first step of management
involves lowering the dose of the antipsychotic medication.
If reduction in dose is associated with unacceptable efficacy
than change of antipsychotic medication may be considered.
When change of antipsychotic medication is considered, a
medication with lower EPS potential need to be opted. In
patients who respond to an antipsychotic and continue to
experience Parkinsonism, a short course of anticholinergic
medications may be considered.
Acute dystonia is also seen during the initial phase
of treatment, i.e., after receiving first few doses of
antipsychotics. Acute dystonias respond dramatically
to administration of parenteral anticholinergic or
antihistaminergic medications. Recurrence of acute
dystonias can also be prevented by using a short course of
anticholinergic medications.
First step in management of acute akathisia involves
reduction in dose or changing the antipsychotic to a
medication with lower EPS potential. Some patients
may require the use of medications like beta-blockers
and benzodiazepines like clonazepam or lorazepam for
management of akathisia.
Neuroleptic Malignant Syndrome (NMS): It is an acute
psychiatric emergency, which has been reported to occur more
often with FGAs. However, data in the form of case reports
and case series also suggest association of almost all SGAs with
development of NMS. Various factors which increase the risk
of NMS are shown in table-18. Management involves stopping
the antipsychotic medication, supportive measures and use of
bromocriptine, amantadine or dantrolene. Use of lorazepam
may also be helpful and those patients with NMS, who donot
respond to these treatments, may benefit with ECT.
Sedation: Many antipsychotics are known to cause sedation
by virtue of their antihista-minergic, antiadrenergic, and
anti-dopaminergic action. The risk of sedation is high with
chlorpromazine, clozapine and quetiapine. Initial strategy
should be to wait and watch and if this is not beneficial, if
possible dose reduction must be considered.
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Table 15: Issues related to special situations

Special situation Strategies
First‑episode • Longer duration of untreated psychosis is powerful predictors of subsequent poor outcome
psychosis and early • Attempts need to be made to reduce the duration of untreated psychosis, to promote remission through effective
intervention pharmacological and psychosocial interventions, to maximize functioning, and to prevent relapse and other adverse
outcomes
• Early detection, comprehensive assessment, emphasis on continued engagement, and flexible treatment enable early
intervention services to meet these goals
• It is still not clear for how long patients with first‑episode psychosis are to continue maintenance antipsychotic medication
• A 1‑2 year period is usually recommended, though many patients may require longer periods, and some may require shorter
periods of treatment
Suicidality in • Suicide is more common during the initial period after discharge from the hospital
schizophrenia • Risk factors which have been specifically associated with suicide among patients with schizophrenia include younger age,
high socio‑economic status, high premorbid scholastic achievement and high intelligence quotient, high aspirations and
expectations, early age of onset, younger age at first hospitalization, a chronic and deteriorating course with multiple relapses
and higher level of insight into the illness
• Some of the treatment related issues which have been shown to be associated with suicide include inadequate treatment, poor
medication adherence, poor response to treatment and akathisia
• As it is not possible to predict suicidal behaviour, clinicians need to pay greater attention to presence of suicidal ideations,
which are predictors of suicidal attempt and suicide at every phase of treatment
• High risk management need to be followed during the initial phase of admission and every effort need to be made to retain
the patient in the inpatient set‑up
• Adequate treatment of psychotic symptoms with antipsychotic medication and of depression when present with appropriate
therapy can prevent suicide
• Clozapine has been shown to reduce the risk for suicidal behaviours. Accordingly, it may be preferred for patients who have
multiple suicide attempts or persistently report suicidal ideations.
• Psychoeducation of patient and family need to focus on discussing about warning signs of suicide. Patients
experiencing severe distress due to a feeling of loss, stigma etc., need to be provided psychological support and
monitored closely.
Violence and • All patients are to be evaluated for violence and dangerousness during every assessment, especially during the acute phase of
Aggression in illness
Schizophrenia • Whenever a patient is found to have serious threat for violence or exhibits violence, inpatient management is to be
considered
• Injectable antipsychotics like haloperidol or lorazepam can be used for management of violence and aggression
Comorbid Substance • Presence of substance use disorder is often associated with overall poor outcome of illness
use Disorders • Clinicians also need to pay attention to these disorders and the additional aims of the treatment are abstinence from the
substances or at least harm reduction
• Pharmacological agents shown to be effective for management of detoxification and pharmaco‑prophylaxis for different
substance use disorders may be considered if required
• Psychosocial interventions like relapse prevention counselling, cognitive behavioural interventions and motivation
enhancement treatment may be included in the treatment plan
• Patients are to be continuously monitored for relapse of substance use disorder
Depression • A rational approach to treating depression in schizophrenia first needs to consider and rule out organic conditions, negative
symptoms, antipsychotic associated side effects (dysphoria, akinesia and akathisia), schizoaffective depression, stress‑related
reactions, and an impending psychotic episode
• Controlled trials with SGAs have shown that they are superior to FGAs in their antidepressant efficacy.
• Clozapine may be particularly effective in patients at high risk for suicide
• Antidepressants are generally ineffective during the acute phase. They may even worsen the psychosis, and are best
avoided
• On the other hand, results of controlled trials have demonstrated the efficacy of adjunctive antidepressant therapy in
post‑psychotic depression
• Clinical experience suggests that ECT may be helpful
Catatonia • Whenever a patient with schizophrenia presents with catatonia, all possible differential diagnosis for catatonia is to be
considered. Appropriate investigations may be carried out and the underlying causes are to be managed
• Initial management may involve use of benzodiazepines, especially lorazepam, which leads to symptomatic relief in
significant proportion of cases
• In case the catatonia does not respond to benzodiazepines or relapse after stopping benzodiazepines, ECT is to be
considered
Negative symptoms • First step in management of predominant negative symptoms is to rule out secondary negative symptoms. However, if
negative symptoms persist, they are presumed to be primary negative symptoms of the deficit state
• No treatments have proven efficacy for management of primary negative symptoms, although some benefit has been reported
with clozapine and amisulpride
• Psychosocial interventions in the form of social skill training, token economy may be attempted

Contd...

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 Grover, et al.: CPG for Schizophrenia

Table 15: Contd...
Special situation Strategies
Obsessive • Obsessive compulsive disorder/Obsessive compulsive symptoms are common in patients with schizophrenia and these may
compulsive be part of the prodrome of schizophrenia, may be part of clinical manifestation of schizophrenia along with other symptoms,
symptoms in may be treatment emergent or may precede the onset of schizophrenia
schizophrenia • Treatment emergent obsessive compulsive symptoms are commonly reported with SGAs like clozapine, olanzapine and
risperidone
• There is little evidence in the form of randomized controlled trials for management of obsessive compulsive symptoms in
schizophrenia
• In general it is suggested that if the obsessive compulsive symptoms appear to be part and parcel of schizophrenia, initially
patients may be treated with antipsychotics only and the obsessive compulsive symptoms need to be monitored
• If the obsessive compulsive symptoms are considered to be treatment emergent then reduction in dose of antipsychotic,
change of antipsychotic or use of antiobsessional agents are to be considered
• Among the antiobsessional agents, there is some data for the efficacy of clomipramine and fluvoxamine
• Cognitive behaviour therapy in the form of exposure and response prevention has also been tried with beneficial effects
Comorbid Physical • Patients with schizophrenia have high rate of physical illnesses
illnesses • All patients need to receive thorough assessment for possible physical illnesses and depending on the feasibility may be
investigated as per the requirement
• Those with comorbid physical illnesses need to be continuously monitored during all the phases of treatment
• Comorbid physical illnesses and concomitant medications need to be taken into account while selecting the treatment setting
and antipsychotic medication per se
Treatment‑resistance • The first step in the management of treatment‑resistance is to establish that the disorder has failed to respond to adequate
schizophrenia (TRS) trials of antipsychotics in terms of dosage, duration and adherence
• Other causes of non‑response need to be considered such as, non‑compliance, adverse effects, comorbid conditions such as
substance misuse, before actually diagnosing treatment refractoriness
• Clozapine has been reported to be beneficial among patients with TRS
• The role of ECT in TRS has not been examined, although studies suggest that it could be useful
• Chosocial interventions such as cognitive therapy, family treatment, assertive outreach or crisis intervention are also
beneficial.
Clozapine – • There is some evidence to suggest that combining ECT with clozapine improves the outcome of patients who donot respond
resistance to clozapine alone
• Evidence for usefulness of combining clozapine with other antipsychotics, antidepressants, mood stabilizers is limited and
not convincing
Difficult to treat • Factors which make the patient difficult to treat include: inadequate response to antipsychotic, problems of adverse drug
schizophrenia effects, poor medication compliance, comorbidities, treatment failure and relapse on adequate drug dosages
• Issues related to medication compliance and adverse effects need to be addressed
• Antipsychotic need to be selected keeping the medical and psychiatric comorbidities in mind
• Patients with treatment resistance may be treated with clozapine.
• Patients having relapse of symptoms despite adequate dosages of 2 or more antipsychotics may also be treated with clozapine.
• Psychosocial factors influencing medication compliance need to be evaluated and addressed
Pregnancy • Many patients with schizophrenia have unplanned pregnancies and because of illness related variables, compared to those
without schizophrenia, women with schizophrenia more commonly have pregnancy outcomes in the form of low birth
weight, preterm birth, still birth and perinatal deaths
• Patients and caregivers need to be counselled about pregnancy and the risks and unplanned pregnancies may be avoided
• Most of the psychotropics belong to category ‘C’ or ‘D’, except for clozapine
• In general it is said that high potency antipsychotics have lower risk of foetal malformations
• Any decision to start antipsychotics, continue or discontinue antipsychotics need to take into account current level of
symptomatology, longitudinal course of symptoms, risk of relapse with stoppage of medication, effect of a particular
antipsychotic on foetal malformation and obstetrical complications
• All decisions about medications are to be taken after proper consultation with the patient, spouse and caregivers. A close
liaison with the obstetricians is helpful in monitoring patients during the pregnancy

Anticholinergic and antiadrenergic side effects: These
side effects manifest as dry mouth, blurred vision,
constipation, urinary retention, thermoregulatory effects,
impaired learning and memory and slowed cognition. Some
patient may develop confusion, delirium, somnolence and
hallucinations due to severe anticholinergic side effects.
Anticholinergic side effects are more commonly seen with
clozapine and chlorpromazine. It is reported that the
anticholinergic side effects are usually dose-dependent
and reduce with reduction in the dose of antipsychotic or
concomitantly used anticholinergic agent.
Cardiovascular side effects: Among the cardiac side effects, the
commonly encountered side effects include QTc prolongation,
orthostatic hypotension and tachycardia. QTc interval of
more than 500 milliseconds is associated with elevated risk
of ventricular arrhythmias, known as “torsades de pointes”,
which may lead to ventricular fibrillation and sudden cardiac
death. Among the older antipsychotics, thioridazine, pimozide
and high dose of intravenous haloperidol are reported to be
associated with increased risk of QTc prolongation. Among
the SGAs, ziprasidone is reported to have higher risk of
QTc prolongation; however, this has not been shown to be

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 Grover, et al.: CPG for Schizophrenia

Table 16: Management of Side Effects of Antipsychotics

Side effect First Step Other options
Antipsychotic induced Parkinsonism Reduce the dose Change the antipsychotic to an antipsychotic with lower EPS
potential
Acute dystonia Parenteral ‑ anticholinergic or antihistaminergic Short term use of anticholinergics to prevent recurrence
medications
Acute Akathisia Reduce the dose Change the antipsychotic to an antipsychotic with lower EPS
potential
Use‑ beta‑blockers, benzodiazepines
Tardive dyskinesia Stop the offending agent Clozapine in case there is worsening of psychosis
Vitamin‑E, benzodiazepines, anticholinergics
Tardive dystonia Stop the offending agent Clozapine in case there is worsening of psychosis
Neuroleptic malignant syndrome Stop the offending agent In treatment refractory NMS consider ECT
Supportive measures
Bromocriptine, amantadine, dantrolene
Lorazepam
QTc prolongation Reduce the dose Stop the offending agent
Change the antipsychotic to an antipsychotic with lower
potential for QTc prolongation
Orthostatic hypotension Reduce the dose Stop the offending agent
Change to an antipsychotic with lower antiadrenergic or no
antiadrenergic activity
Use of stockings, increasing the salt intake, fludrocortisone
Tachycardia due to anticholinergic Wait and watch for sometime in those without Peripherally acting beta‑blockers
action cardiac disease
Hyperprolactinemia and Sexual Reduce the dose Change to an antipsychotic with lower potential to cause
dysfunction hyper‑prolactinemia
Consider use of bromocriptine or amantidine if there is
hyperprolactinemia
Sexual dysfunction not associated with
hyperprolactinemia‑ Yohimbine, Cyproheptadine,
Imipramine (for retrograde ejaculation), Phospho‑diaesterase
inhibitors (for erectile dysfunction), antidepressants like
paroxetine, dapoxetine (for premature ejaculation)
Sedation Wait and watch – most patients develop tolerance In case of persistent sedation
Reduce the dose
Change to night time dose, if using the medication in divided
doses
Change to a less sedating agent
Anticholinergic and antiadrenergic Stop concommitant anticholinergic agent if used Change to an antipsychotic with lower anticholinergic properties
side effects Reduce the dose Constipation‑ high fibre diet, increase water intake, laxatives
In case of severe side effect like delirium
stoppage of offending agent may be required

associated with sudden cardiac deaths. In case, there is QTc anticholinergic activity, as seen with clozapine may be
prolongation, change of antipsychotic is to be considered. managed with low dose peripherally acting beta-blockers.

Hypotension associated with various antipsychotics is attributed
to antiadrenergic activity. It is commonly seen with clozapine,
risperidone, quetiapine. Among the FGAs, hypotension is often
seen with chlorpromazine. Hypotension can be prevented
by starting with lower doses and slow upward titration of
medication. When a patient develops hypotension with a
particular antipsychotic medication, the first step in management
is to reduce the dose of the offending agent. If this does not
help than switching to another agent with lower antiadrenergic
activity is to be considered. Additional management strategies
include use of stockings, increasing the salt intake and use of
fludrocortisone, which is a fluid retaining corticosteroid.
Tachycardia may be associated with hypotension or it may
result due to anticholinergic activity. Tachycardia due to
Hyperprolactinemia and Sexual dysfunction: All antipsychotics
are shown to be associated with sexual dysfunction, although
the rates vary with different antipsychotics. In general, rates
of sexual dysfunction are reported to be higher with FGAs and
risperidone. One of the common causes for sexual dysfunction
with FGAs and risperidone is increase in prolactin levels,
which leads to disruption of hypothalamo-pituitary-gonadal
axis. Females have been reported to be more sensitive to
hyperprolactinemia related sexual dysfunction. First step in
management of hyperprolactinemia and sexual dysfunction
is reduction in the dose of antipsychotic medication. If this
option is not acceptable, change in antipsychotic is to be
considered. If change of antipsychotic is not possible, than
management with bromocriptine or amantidine may be
considered to lower the prolactin levels.

Indian J Psychiatry 59 (Supplement 1), January 2017 S31

 Grover, et al.: CPG for Schizophrenia

Table 17: Risk factors for acute and tardive Monitoring for metabolic side effects: It is now well known
extrapyramidal side effects with antipsychotics that compared to subjects in the general population,
Acute Dystonia patients with schizophrenia have high rates of metabolic
Use of high potency FGAs syndrome. Higher prevalence of metabolic syndrome
Young age suggests that clinicians need to monitor the patients for
Male gender emergence of metabolic side effects and manage the same
High doses
Intramuscular administration of antipsychotic medications
to reduce the cardiovascular morbidity and mortality.
Acute Akathisia Antipsychotics have also been shown to increase the risk
Use of high potency FGAs of development of diabetes mellitus. Further evidence
Tardive dyskinesia suggests that there is some discriminatory effect of various
Older age
antipsychotic medications on metabolic profile. Clozapine
Female gender combined with postmenopausal status
Use of FGAs and olanzapine have been reported to be associated
Use of high doses of antipsychotic medications with highest risk for development of weight gain, lipid
Antipsychotic‑induced parkinsonism abnormalities and elevation in blood glucose levels (See
Concurrent general medical conditions like diabetes table-18).
Affective disorder (particularly major depressive disorder)
Tardive dystonia
Use of high potency FGAs Considering the metabolic side effects associated with
Neuroleptic Malignant syndrome antipsychotics, various guidelines have been proposed and
Young age there are certain variations in the proposed monitoring
Male gender frequency. In general it is suggested that patients need to
Use of high potency antipsychotic
be monitored for metabolic disturbances at baseline, at
Rapid increase in the dose of antipsychotic
Use of intramuscular preparation 4-6 weeks and 12 weeks after starting antipsychotic and
Acute agitation then after every 3 months or at least annually (table-19).
Preexisting neurological disability However, those who have personal and family history of
Comorbid physical illness obesity, diabetes mellitus, dyslipidemia, hypertension
Dehydration
and/or cardiovascular disease are to be monitored 3
monthly.
Table 18: Risk of Metabolic side effects associated with
various antipsychotic medications6 However, in Indian setting, due to poor follow-up rates and
Antipsychotic medications Risk of lipid and/or Risk of available resources, it may not be feasible to monitor all the
glucose metabolism weight gain parameters regularly. Efforts need to be made to monitor
abnormalities the weight and fasting blood glucose levels at every
FGAs treatment facility. Patients managed at training centres and
Chlorpromazine High (limited data) Substantial resourceful settings may consider complete monitoring of
Fluphenazine Low (limited data) Neutral/low metabolic parameters.
Haloperidol, Perphenazine Low Neutral/low
Thioridazine High (limited data) Intermediate
SGAs If a patient develops metabolic abnormalities, switching
Clozapine, Olanzapine High Substantial of antipsychotic may be considered. In general if a patient
Quetiapine Moderate Intermediate gains more than 7% of the baseline weight or develops
Risperidone, Iloperidone, Mild Intermediate hyperglycemia, hyperlipidemia, hypertension or any other
Paliperidone, Sertindole
Lurasidone Low (limited data) Intermediate
significant cardiovascular or metabolic side effect, then
Zotepine Not reported Intermediate a change in antipsychotic is to be considered. However,
Asenapine Low (limited data) Low while considering switching, clinicians need to take into
Amisulpride Mild Neutral/low consideration the entire course of the illness, comorbid
Ziprasidone, Aripiprazole Low Neutral/low
physical illnesses, side effect profile of medication which

Table 19: Monitoring for metabolic disturbance while receiving various antipsychotic medications
Baseline 6 weeks after starting 12 weeks after starting Atleast annually
antipsychotics antipsychotics thereafter
Medical History X
Weight/waist circumference/BMI X X X X
Blood Pressure X X X X
Fasting glucose levels X X X X
Fasting lipids X X X X
Lifestyle modification advise X X X X

S32 Indian J Psychiatry 59 (Supplement 1), January 2017

 Grover, et al.: CPG for Schizophrenia
caused metabolic side effects and the potential side effects
with proposed medication to be used after switching. If
switching of antipsychotic is not possible then medications
like metformin or topiramate may be considered, along
with more intensive dietary and life style modifications. A
close liaison need to be maintained with endocrinologist
and cardiologist to provide best quality care to patients.
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S33
 CLINICAL PRACTICE GUIDELINES
Clinical Practice Guidelines for the management of Depression
Shiv Gautam, Akhilesh Jain1, Manaswi Gautam2, Vihang N. Vahia3, Sandeep Grover4
Director Professor, Director, Gautam Hospital & Research Center, Consultant Psychiatrist Gautam Hospital and Research
Center, 1Specialist Psychiatry ESI Hospital, 2Gautam Hospital and Research Center and Gautam Institute of Behavioural
Sciences and Alternative Medicine, Jaipur, 3Consultant Psychiatrist, Gaur Medical Health Clinic, Ajmer, 4Additional
Professor, Department of Psychiatry, Post Graduate Institute of Medical Education and Research, Chandigarh, India
Participants of expert group on CPG for Depression
Gautam Saha, I.D Gupta, Navendu Gaur, Tushar Jagawat,
Anita Gautam, T. S Sathyanarayana Rao
INTRODUCTION
Depression is a common disorder, which often leads to
poor quality of life and impaired role functioning. It is
known to be a major contributor to the global burden
of diseases and according to World Health Organization
(WHO), depression is the fourth leading cause of disability
worldwide and it is projected that by 2020, it will be
the second most common leading cause of disability.
Depression is also associated with high rates of suicidal
behaviour and mortality. When depression occurs in the
context of medical morbidity, it is associated with increased
health care cost, longer duration of hospitalization, poor
cooperation in treatment, poor treatment compliance and
high rates of morbidity. Depression is also known to be
associated with difficulties in role transitions (e.g., low
education, high teen child-bearing, marital disruption,
unstable employment) and poor role functioning (e.g.,
low marital quality, low work performance, low earnings).
It is also reported to be a risk factor for the onset and
persistence of a wide range of secondary disorders.
Available data also suggests that between one-third
and one-half of patients also experience recurrence of
depressive episodes.
Address for correspondence:
Dr. Sandeep Grover, Additional Professor, Department of
Psychiatry, PGIMER, Chandigarh, India.
E-mail: drsandeepg2002@yahoo.com
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www.indianjpsychiatry.org
DOI:
10.4103/0019-5545.196973
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ASSESSMENT AND EVALUATION (table-1)
Management of depression involves comprehensive
assessment and proper establishment of diagnosis. The
assessment must be based on detailed history, physical
examination and mental state examinations.History must be
obtained from all sources, especially the family. The diagnosis
must be recorded as per the current diagnostic criteria.
Depression often presents with a combination of
symptoms of depressed mood, loss of interest or pleasure,
decreased energy and fatigue, reduced concentration
and attention, reduced self-esteem and self-confidence,
ideas of guilt and unworthiness, bleak and pessimistic
views of the future, ideas or acts of self-harm or suicide,
disturbed sleep and diminished appetite. Depending on
the severity of depression some of these symptoms may
be more marked and develop characteristic features that
are widely regarded as having special clinical significance.
These symptoms are known as somatic symptoms of
depression and include symptoms of loss of interest or
pleasure in activities that are normally enjoyable, lack of
emotional reactivity to normally pleasurable surroundings
and events, waking up in the morning 2 hours or more
before the usual time, depression worse in the morning,
objective evidence of definite psychomotor retardation
or agitation (remarked on or reported by other people),
marked loss of appetite, weight loss (often defined as 5%
or more of body weight in the past month) and marked
loss of libido. It is important to note that for the diagnosis
of depressive disorder these symptoms need to be present
for at least 2 weeks and need to be associated with
psychosocial dysfunction.
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For reprints contact: reprints@medknow.com
How to cite this article: Gautam S, Jain A, Gautam M,
Vahia VN, Grover S. Clinical Practice Guidelines for the
management of Depression. Indian J Psychiatry 2017;59:34-50.
© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow
 Gautam, et al.: CPGs for depression

Table 1: Components of assessment and evaluation
Basic assessments
• Complete history with information from all possible sources
• Physical examination‑ look for thyroid swelling, evidence for
malnutrition or any specific nutritional deficiency
• Record blood pressure, weight and wherever indicated body mass index
and waist circumference
• Mental state examination
• Establish diagnosis according to current diagnostic criteria
• Differential diagnosis by ruling out secondary depression
• Rule out bipolar disorder, premenstrual dysphoric disorder
• Assess the severity, specifier, subtype of depression
• Areas to be evaluated: symptom‑severity,
symptom‑dimensions (psychotic symptoms, catatonic symptoms,
melancholic symptoms, reverse vegetative symptoms and cognitive
symptoms), comorbid physical, psychiatric and substance use
conditions, risk of harm to self and others, level of functioning and
socio‑cultural milieu of the patient
• Basic investigations: haemogram, blood sugars and lipid levels, liver
functions, renal functions, thyroid function test (if indicated)
• Assessments of caregivers: knowledge and understanding of the illness,
attitudes and beliefs regarding treatment, impact of the illness on them,
personal and social resources
• Ongoing assessments: response to treatment, side effects, treatment
adherence, the impact of patient’s immediate environment, disability
assessments, other health‑care needs, ease of access and relationship
with the treatment team
Additional/Optional assessments
• Use of standardized rating scales to rate all aspects of the illness
• Neuroimaging especially in those with first‑episode of depression seen
in late or very late age; those have neurological signs, those having
treatment resistant depression
Table 2: Some of the physical illnesses commonly
associated with depression
• Epilepsy • Disease
• Post stroke • Depression in Malignancy
• Parkinson’s Disease • Hypothyroidism
• Multiple Sclerosis • Hyperthyroidism
• Degenerative Brain Disease • Hyperparathyroidism
• Alzheimer’s Disease • Cushing’s Syndrome
• Coronary Artery • Addison’s disease
• Diabetes mellitus
Some of the patients with depression may present with
predominant complaints of aches, pains and fatigue and
they may not report sadness of mood on their own. A careful
evaluation of these patients often reveals the underlying
features of depression. However, it is important to note that
many patients with depression will also have associated anxiety
symptoms. With increasing severity of depression patients may
report psychotic symptoms and may also present with catatonic
features. Thorough assessment also ought to focus on evaluation
for comorbid substance abuse/dependence. Careful history of
substance intake need to be taken to evaluate the relationship
of depression with substance intoxication, withdrawal and
abstinence. Whenever required appropriate tests like, urine or
blood screens (with prior consent) may be used to confirm the
existence of comorbid substance abuse/dependence.
Many physical illnesses are known to have high rates of
depression. In some situations the physical illnesses have
causative role in development of depression, whereas in other
situations the relationship/co-occurrence is due to common
etiology. Some of the physical illnesses commonly associated
with depression are listed in Table-2. When depression
occurs in relation to physical illness attempt may be made
to clearly delineate the symptoms of depression and physical
illness. Further, while making the diagnosis, it maybe clearly
mentioned as to which diagnostic approach [i.e., inclusive
approach (symptoms are counted whether or not they might be
attributable to physical illness), substitute approach (nonsomatic
symptoms are substituted with somatic symptoms), exclusive
approach (somatic symptoms are deleted from the diagnostic
criteria) or best estimate approach] was followed. Further,
while reviewing the treatment history of medical illnesses,
medication induced depression must be kept in mind, as
many medications are known to cause depression (Table-3).
It is always important to take the longitudinal life course
perspective into account to evaluate for previous episodes
and presence of symptoms of depression amounting to

Table 3: Medications known to cause depression

Cardiovascular drugs Azathioprine Ampicillin Penicillin G Benzodiazepines Efavirenz
ACE inhibitors Bleomycin Chloramphenicol procaine Chloral hydrate Enfuvirtide
Calcium channel Cisplatin Methylphenidate (Ritalin) Streptomycin Ethanol Saquinavir
blockers Cyclophosphamide Chloroquine Sulfonamides Other drugs Zidovudine
Clonidine Doxorubicin Clofazimine Tetracycline Choline Anticonvulsants
Digitalis Vinblastine Cycloserine Trimethoprim Cimetidine Ethosuximide
Guanethidine Vincristine Cyclosporine Hormones Disulfiram Phenobarbital
Hydralazine Antiparkinsonian Dapsone Adrenocorticotropin Lecithin Phenytoin
Methyldopa drugs Ethambutol Anabolic steroids Methysergide Primidone
Procainamide Amantadine Ethionamide Glucocorticoids Phenylephrine Tiagabine
Propranolol Bromocriptine Foscarnet Oral contraceptives Physostigmine Vigabatrin
Reserpine Levodopa Ganciclovir Antipsychotic drugs Ranitidine Anti‑inflammatory
Thiazide diuretics Stimulants Griseofulvin Fluphenazine Statins agents
Guanabenz Amphetamines Isoniazid Haloperidol Tamoxifen NSAIDS
Zolamide diuretics withdrawal) Metoclopramide Sedatives and Antiretroviral drugs
Chemotherapeutics Caffeine Metronidazole antianxiety Atazanavir
6‑Azauridine Cocaine (withdrawal) Nalidixic acid drugs
Asparaginase Anti‑infective agents Nitrofurantoin Barbiturates

Indian J Psychiatry 59 (Supplement 1), January 2017 S35

 Gautam, et al.: CPGs for depression

dysthymia. Evaluation of history also takes into consideration
the relationship of onset of depression with change in
season (seasonal affective disorder), peripartum period and
phase of menstrual cycle. Further, the longitudinal course
approach may also take into account response to previous
treatment and whether the patient achieved full remission,
partial remission and did not respond to treatment.
induced switch. Presence of psychotic features, marked
psychomotor retardation, reverse neurovegetative
symptoms (excessive sleep and appetite), irritability of
mood, anger, family history of bipolar disorder and early
age of onset need to alert the clinicians to evaluate for the
possibility of bipolar disorder, before concluding that they
are dealing with unipolar depression.

An important aspect of diagnosis of depression is to rule
out bipolar disorder. Many patients with bipolar disorder
present to the clinicians during the depressive phase of
illness and spontaneously do not report about previous
hypomanic or manic episodes. Careful history from the
patient and other sources (family members) often provide
important clues for the bipolar disorder. It is often useful to
use standardized scales like mood disorder questionnaire to
rule out bipolarity. Treating a patient of bipolar depression
as unipolar disorder can increase the risk of antidepressant
Area to be covered in assessment include symptom
dimensions, symptom-severity, comorbid psychiatric and
medical conditions, particularly comorbid substance abuse,
the risk of harm to self or others, level of functioning and
the socio-cultural milieu of the patient.
In case patient has received treatment in the past, it is
important to evaluate the information in the form of type of
antidepressant used, dose of medication used, compliance
with medication, reasons for poor compliance, reasons for

Patient with Depressive features

Consider differential diagnoses like

• Organic Depression, medication induced depression,
substance induced depression, premenstrual dysphoric
disorder
• Rule out bipolar disorder

Establish the diagnosis of Depression

Assessment
• Severity of illness
• Risk of harm to self and others- current suicidal ideations, suicidal attempts;
past history of non-suicidal self-harm behaviour, past history of suicidal attempts,
severity of attempt
• Comorbid substance use/dependence
• Personality factors
• Level of functioning- work dysfunction
• Detailed Physical examination- thyroid swelling, evidence for nutritional deficiency,
and physical illness which could contribute to depression
• Record- blood pressure, weight and wherever indicated body mass index and waist
circumference
• Mental Status Examination
• Investigations- haemogram, liver function test, renal function test, fasting blood glucose level,
thyroid function test (if required), Urine pregnancy test (if required)
• Treatment history- response to previous medication trials, compliance, side effects, etc.
• Patient’s and caregivers beliefs about the cause of illness and beliefs about the treatment
• Assessment for social support, stigma, coping
• Assessment of caregiver burden, coping and distress

• Decide about treatment setting- consider inpatient care in case of suicidality, malnutrition,
catatonia, comorbid general medical conditions making management difficult at the
outpatient setting
• Liaison with other specialists depending on the need of the patient

Pharmacological Management Electroconvulsive therapy Non-Pharmacological

• Choose an antidepressant based on past • Catatonia, suicidality, Management
treatment response, past history of side severe depression, past • Psychoeducation
effects, cost, comorbidity, patient/family response to ECT, • Psychotherapeutic
preference, availability augmentation etc. intervention

Figure 1: Initial evaluation and management plan for Depression

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 Gautam, et al.: CPGs for depression
discontinuation of medication, response to treatment, side
effects experienced etc. If the medications were changed,
then the reason for change is also to be evaluated.
Wherever possible, unstructured assessments need to be
supplemented by ratings on appropriate standardized
rating scales. Depending on the need, investigations
need to be carried out. The use of neuroimaging may be
indicated in those with first-episode of depression seen in
late or very late age; those have neurological signs, those
having treatment resistant depression.
Besides, patients, information about the illness need to be
obtained from the caregivers too and their knowledge and
understanding of the illness, their attitudes and beliefs
regarding treatment, the impact of the illness on them and
their personal and social resources need to be evaluated.
FORMULATING A TREATMENT PLAN (FIGURE-1)
Formulation of treatment plan involves deciding about
treatment setting, medications and psychological treatments
to be used. Patients and caregivers may be actively consulted
while preparing the treatment plan. A practical, feasible and
flexible treatment plan can be formulated to address the needs
of the patients and caregivers. Further the treatment plan can
be continuously re-evaluated and modified as required.
EVALUATE THE SAFETY OF PATIENT AND
OTHERS
A careful assessment of the patient’s risk for suicide should
be done. During history inquiry for the presence of suicidal
ideation and other associated factors like presence of
psychotic symptoms, severe anxiety, panic attacks and
alcohol or substance abuse which increases the risk of suicide
need to be evaluated. It has been found that severity of
depressive symptomatology is a strong predictor of suicidal
ideation over time in elderly patients. Evaluation also includes
history of past suicide attempts including the nature of those
attempts. Patients also need to be asked about suicide in their
family history. During the mental status examinations besides
enquiring about the suicidal ideations, it is also important to
enquire about the degree to which the patient intends to act
on the suicidal ideation and the extent to which the patient has
made plans or begun to prepare for suicide. The availability
of means for suicide be inquired about and a judgment may
be made concerning the lethality of those means. Patients
who are found to possess suicidal or homicidal ideation,
intention or plans require close monitoring. Measures such as
hospitalization may be considered for those at significant risk.
CHOICE OF TREATMENT SETTINGS
Majority of the cases of depression seen in the clinical
setting are of mild to moderate severity and can be managed
Indian J Psychiatry 59 (Supplement 1), January 2017
at the outpatient setting. However, some patients have
severe depression which may be further associated with
psychotic symptoms, catatonic symptoms, poor physical
health status, suicidal or homicidal behaviour etc. In such
cases, careful evaluation is to be done to decide about the
treatment setting and whenever necessary inpatient care
may be offered. In general, the rule of thumb is that the
patients may be treated in the setting that is most safe and
effective. Severely ill patients who lack adequate social
support outside of a hospital setting may be considered
for admission to a hospital whenever feasible. The optimal
treatment setting and the patient’s ability to benefit
from a different level of care may be re-evaluated on an
ongoing basis throughout the course of treatment. Some
of the common indications for inpatient care are shown
in Table-4.
Table 4: Some indications for inpatient care during
acute episodes
• Presence of suicidal behaviour which puts the life of the patient at risk
• Refusal to eat which puts the life of patient at risk
• Severe malnutrition
• Catatonia
• Presence of general medical or comorbid psychiatric conditions that make
outpatient treatment unsafe or ineffective
All inpatients should have accompanying family caregivers.
In case inpatient care facilities are not available, than the
patient and/or family need to be informed about such a
need and admission in nearest available inpatient facility
can be facilitated.
THERAPEUTIC ALLIANCE
Irrespective of the treatment modalities selected for
patients, it is important for the psychiatrist to establish a
therapeutic alliance with the patient. A strong treatment
alliance between patient and psychiatrist is crucial for poorly
motivated, pessimistic depressed patient who are sensitive
to side effect of medications. A positive therapeutic alliance
always generates hope for good outcome.
ENHANCED TREATMENT COMPLIANCE
The successful treatment of major depressive disorder
requires adequate compliance to treatment plan. Patients
with depressive disorder may be poorly motivated and
unduly pessimistic over their chances of recovery with
treatment. In addition, the side effect or requirements of
treatment may lead to non-adherence. Patients are to be
encouraged to articulate any concern regarding adherence
and clinicians need to emphasize the importance of
adherence for successful treatment. Simple measures
which can help in improving the compliance are given in
table-5.
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 Gautam, et al.: CPGs for depression

ADDRESS EARLY SIGNS OF RELAPSE
Many patients with depression experience relapse.
Accordingly, patients as well as their families if appropriate may
Table 5: Measures which can improve medication
compliance
• When and how often to take medicines
• Preferably give once a day dosing
• Prescribe minimum number of tablets
• Always ask the patient about kind of formulation (e.g. tablet, capsule etc)
which they would prefer to take
• Check the whole prescription to avoid duplication of medication
• Explain the patient that the beneficial effect will be seen only after
2‑4 weeks of intake of medications
• Explain the patient the need to take medication even after feeling better
• Explanation of side effects, If patients asks about the side effects‑ explain
the patient about the same
• Explain the patient as to what to do‑ if they encounter side effects
• Encourage the patient to report side effects
• The need to consult with psychiatrist before discontinuing medications
be educated about the risk of relapse. They can be educated
to identify early signs and symptoms of new episodes. Patients
can also be asked to seek adequate treatment as early in the
course of a new episode as possible to decrease the likelihood
of a full-blown relapse or complication.
TREATMENT OPTIONS FOR MANAGEMENT
FOR DEPRESSION
Treatment options for management of depression can be
broadly be divided into antidepressants, electroconvulsive
therapy (ECT) and psychosocial interventions. Other less
commonly used treatment or treatments used in patients
with treatment resistant depression include repetitive
transcranial magnetic stimulation (rTMS), light therapy,
transcranial direct stimulation, vagal nerve stimulation,
deep brain stimulation and sleep deprivation treatment.
In many cases benzodiazepines are used as adjunctive
treatment, especially during the initial phase of treatment.

Table 6: Antidepressants Armamentarium

Antidepressant Usual dose range (mg/day) Common side effects
Selective serotonin reuptake inhibitors (SSRI)
Fluoxetine 20‑80 Sexual dysfunction, GI distress, weight loss/gain,
Paroxetine 20‑60 anxiety, insomnia
Fluvoxamine 50‑300
Sertraline 50‑200
Citalopram 20‑40
Escitalopram 10‑20
Tricyclic tertiary amines (TCAs)
Amitriptyline 50‑200 Sexual dysfunction, anticholinergic effects, drowsiness,
Doxepin 75‑300 orthostasis, conduction abnormalities, mild GI distress,
Imipramine 75‑300 weight gain
Clomipramine 75‑300
Tricyclic Secondary Amines
Desipramine 100‑300
Nortriptyline 25‑150
Protriptyline 15‑20
Tetracyclic
Maprotiline 50‑75
Unicyclic
Bupropion 150‑450 Mild GI distress, high risk of seizure after 450 mg/day
Norepinephrine Serotonin reuptake
Inhibitors (NSRI)
Venlafaxine 75‑300 Mild anticholinergics effects, drowsiness, conduction
Duloxetine 20‑60 abnormalities, GI distress
Milnacipran 50‑200
Desvenlafaxine
Norepinephrine Serotonin Reuptake
Enhance (NSRE)
Tianeptine 25‑50 Nausea, constipation, abdominal pain, headache,
dizziness and changes in dreaming
Noradrenaline and Specific Serotonin
Antidepressants (NaSSA)
Mirtazapine 15‑45 Mild anticholinergic effects, drowsiness, orthostasis,
conduction abnormalities, GI distress, weight gain
Atypical antidepressants/Serotonin
Modulators
Trazadone 150‑300 Mild anticholinergic effects, drowsiness, orthostasis,
Nefazodone 100‑300 conduction abnormalities, GI distress, weight gain,
severe hepatotoxicity
Contd...
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 Gautam, et al.: CPGs for depression
Table 6: Contd...
Antidepressant Usual dose range (mg/day)
Reversible Selective Mono Amine Oxidase
Inhibitors (RIMA)
Moclobemide
Mono Amine Oxidase Inhibitors (MAOI)
Phenelzine
Isocarboxazid
Tranylcypromine
Serotonin partial agonist reuptake
inhibitor (SPARI)
Vilazodone
Table 7: Factors that determine the selection of
Antidepressant Drug
Patient specific
• Patients preference
• Previous history of response/tolerability to medication in the patient or
family member
• Past side effects with medication
• Other medication being taken – drug interactions
• Patient’s age – with increasing age the pharmacokinetic and
pharmacodynamic changes become more important
• Comorbid medical illness (e.g., glaucoma, cardiac conditions)
• Comorbid psychiatric disorder/symptoms
• Gender issues – sexual dysfunction
• Intellectual and psychological capacities
Drug specific
• Side effects
• Cost
• Dosing strategy
• Type of formulation ‑ Tablet, Cap, Syrup
• Safety in overdose (Relative Toxicity) ‑ fatal overdose is significantly
• Lower with SSRIs than with tricyclic antidepressants
Additionally in some cases, lithium and thyroid supplements
may be used as an augmenting agent when patient is not
responding to antidepressants.
Antidepressants
Large numbers of antidepressants (Table-6) are available for
management of depression and in general all the antidepressants
have been shown to have nearly equal efficacy in the management
of depression. Antidepressant medication may be used as
initial treatment modality for patients with mild, moderate,
or severe depressive episode. The selection of antidepressant
medications may be based on patient specific and drug specific
factors, as given in Table-7. In general, because of the side
effect and safety profile, selective serotonin reuptake inhibitors
(SSRIs) are considered to be the first line antidepressants. Other
preferred options include tricyclic antidepressants, mirtazapine,
bupropion, and venlafaxine. Usually the medication must be
started in the lower doses and the doses must be titrated,
depending on the response and the side effects experienced.
Dose and duration of antidepressants
Patients who have started taking an antidepressant
medication should be carefully monitored to assess the
Indian J Psychiatry 59 (Supplement 1), January 2017
Common side effects
45‑90 Orthostatic hypotension, drowsiness,
30‑60 insomnia, headaches
20‑60
20‑40 Diarrhea, nausea or vomiting, and insomnia
response to pharmacotherapy as well as the emergence of
side effects and safety. Factors to consider when determining
the frequency of monitoring include severity of illness,
patient’s co-operation with treatment, the availability of
social support and the presence of comorbid general medical
problems. Visits may be kept frequent enough to monitor
and address suicidality and to promote treatment adherence.
Improvement with pharmacotherapy can be observed after
4-6 weeks of treatment. If at least a moderate improvement is
not observed in this time period, reappraisal and adjustment
of the pharmacotherapy should be considered.
Psychotherapeutic interventions
A specific, effective psychotherapy may be considered
as an initial treatment modality for patients with mild to
moderate depressive disorder. Clinical features that may
suggest the use of a specific psychotherapy include the
presence of significant psychosocial stressors, intrapsychic
conflict and interpersonal difficulties. Patient’s preference
for psychotherapeutic approaches is an important
factor that may be considered in the decision to use
psychotherapy as the initial treatment modality. Pregnancy,
lactation, orthe wish to become pregnant may also be an
indication for psychotherapy as an initial treatment. Various
psychotherapeutic interventions which may be considered
based on feasibility, expertise available and affordability are
shown in Table-8.
Cognitive behavioral therapy (CBT) and interpersonal
therapy are the psychotherapeutic approaches that have the
best documented efficacy in the literature for management
of depression. When psychodynamic psychotherapy is used
as specific treatment, in addition to symptom relief it is
frequently with broader long term goals.
The psychiatrist should take into account multiple
factors when determining the frequency of sessions for
individual patients, including the specific type and goals
of psychotherapy, the frequency necessary to create and
maintain a therapeutic relationship, the frequency of visits
required to ensure treatment adherence, and the frequency
necessary to monitor and address suicidality. The frequency
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 Gautam, et al.: CPGs for depression

of outpatient visits during the acute phase generally varies
from once a week in routine cases to as often as several
times a week. Regardless of the type of psychotherapy
selected, the patient’s response to treatment should be
carefully monitored. For a given patient, time spent and
frequency of visit may be decided by the psychiatrist.
Psychoeducation to the patient and, when appropriate, to
the family
Education concerning depression and its treatments can
be provided to all patients. When appropriate, education
can also be provided to involved family members. Specific
educational elements may be helpful in some circumstances,
e.g. that depression is a real illness and that effective
treatments are both necessary and available may be crucial
for patients who attribute their illness to a moral defect
or witch craft. Education regarding available treatment
options will help patients make informed decisions,
anticipate side effects and adhere to treatments. Another
important aspect of providing education is informing the
patient and especially family about the lag period of onset
of action of antidepressants. Important components of
psychoeducation are given in Table-9.
Combination of pharmacotherapy and Psychotherapy
There is class of patients who may require the combination
of pharmacotherapy and psychotherapy. In general, the
same issues that influence the choice of medication or
psychotherapy when used alone should be considered
when choosing treatments for patients receiving combined
therapy.
PHASES OF ILLNESS/TREATMENT
Management of depression can be broadly divided into three
phases, i.e., acute phase, continuation phase and maintenance
phase. Maintenance phase of treatment is usually considered
when patient has recurrent depressive disorder.
ACUTE PHASE TREATMENT
The goal of acute phase treatment is to achieve remission,
as presence of residual symptoms increase the risk of
chronic depression, poor quality of life and also impairs
recovery from physical illness. Treatment generally results
in improvement in quality of life and better functional
capacity. The various components of acute phase treatment
are shown in Table-10 and the treatment algorithm is shown
in figure-2 and 3.
In acute phase psychiatrist may choose between
several initial treatment modalities, including
pharmacotherapy, psychotherapy, the combination of
medication and psychotherapy, or ECT. Selection of an
initial treatment modality is usually influenced by both
clinical (e.g. severity of symptoms) and other factors
(e.g. patient preference).
Antidepressant medication may be used as initial treatment
modality for patients with mild, moderate, or severe major
depressive disorder. Clinical features that may suggest that
medication are the preferred treatment modality includes
history of prior positive response to antidepressant
medication, severity of symptoms, significant sleep and
appetite disturbance, agitation, or anticipation of the need
for maintenance therapy. Patients with severe depression
with psychotic features will require use of combination of
antidepressant and antipsychotic medication and/or ECT.
The initial selection of an antidepressant medication is
largely be based on the anticipated side effects, the safety
or tolerability of these side effects for individual patients,
patient preference and comorbid physical illnesses.
Dose and duration of antidepressants: Once an
antidepressant medication has been selected, it can be
started initially at lower doses and careful monitoring to

Table 8: Psychotherapeutic interventions for Depression

Type of therapy
Cognitive Behaviour Therapy (CBT)
Interpersonal Therapy (IPT)
Supportive psychotherapy
Behavioral Therapy (BT)
Marital Therapy (MT)
Family Therapy
Brief Psychodynamic Psychotherapy (BPD)
• Identifying problems, Identifying cognitive distortions/errors, generating alternative thoughts,
problem solving, mastery and pleasure rating, activity scheduling, anxiety management
strategies‑ relaxation exercises
• Focuses on losses, role disputes and transitions, social isolation, deficits in social skills, and other
interpersonal factor that may impact on the development of depression
• Allowing the patient to ventilate, providing emotional support, guidance, increasing the patient’s
self‑esteem, accepting feelings at face value, enhancing hope, enhancing adaptive coping
• Activity scheduling, social skills training and problem solving
• Marital therapy conceptualizes depression as an interpersonal context such that both members of
the marital dyad are included in therapy. Treatment includes behavioral exchange, communication
training, problem solving, and resolution of conflict around issues such as financial, sex, affection,
parenting, and intimacy
• When interpersonal problems in the context of pathological family dynamics are responsible for
depression, than family therapy may be considered. It would involve all the family members and
include similar principles as for marital therapy
• The premise of brief psychodynamic psychotherapy is that depressive symptoms remit as patient
learns new methods to cope with inner conflicts. Several different approaches have been described

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 Gautam, et al.: CPGs for depression

Mild to moderate Depression

Evaluate for the type and severity of depression

Evaluate for past history of depression
Evaluate for past history of treatment and response
Evaluate for family history of depression
Evaluate for physical and psychiatric comorbidity
Evaluate for concomitant drugs which patient is receiving
Evaluate for the presence of psychosocial stressors

Patient’s preference
No past history of depression
Mild to moderate depression Patient’s preference
Presence of psychosocial stressors Past and family history of
Past history of good response good response
Receiving other medications and high Low risk of drug interactions
risk of drug interactions Moderate depression

Psychotherapy Pharmacotherapy Remission

Remission

No response Partial response No response

Optimize the treatment Change antidepressant

Change to • Increase the frequency of psychotherapy or
antidepressant • Increase the dose of antidepressants to Switch to psychotherapy
maximum tolerable dose

Change/Combination
• If receiving psychotherapy – add antidepressants
• If receiving antidepressants – add psychotherapy or change the antidepressant

Augmentation/Combination
• If receiving antidepressants – add second antidepressants/
augmenting agent taking into consideration the issue of tolerability
and side effects

Figure -2: Treatment algorithm of mild to moderate Depression

Table 9: Basic components of Psychoeducation be done to assess the response to pharmacotherapy as

• Assessing the knowledge of the patient and caregivers about aetiology,
treatment and prognosis
• Explain about the diagnosis and symptoms of depression
• Explain that depression is a medical disorder which is treatable
• Explain about the lag period of onset of action
• Provide information about aetiology
• Provide information about treatment in terms of available options, their
efficacy/effectiveness, side effects, duration of use
• Discuss about importance of medication and treatment compliance
• Provide information about possible course and long term outcome
• Discuss about problems of substance abuse, interpersonal conflict, stress etc
• Discuss about how to deal with day today stress
• Discuss about communication patterns, problem solving etc
• Enhancing adaptive coping to deal with persistent/residual symptoms
• Discuss about relapse and how to identify the early signs of relapse
• Encourage healthy life styles
Indian J Psychiatry 59 (Supplement 1), January 2017
well as the emergence of side effects, clinical conditions,
and safety. Factors to consider when determining the
frequency of monitoring include severity of illness, patient’s
cooperation and presence with treatment, and availability
of social support andpresence of comorbid general medical
problems. Visits may be frequent enough to monitor and
address suicidality and to promote treatment adherence.
Improvement with pharmacotherapy can be observed after
4-6 weeks of treatment. If at least a moderate improvement
is not observed in this time period, reappraisal and
adjustment of the pharmacotherapy maybe considered.
In the initial phase, depending on the symptom severity and
type of symptoms, such as presence of insomnia or anxiety,
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 Gautam, et al.: CPGs for depression

Severe Depression

Evaluate for past history of depression

Evaluate for past history of treatment and response
Evaluate for family history of depression
Evaluate for physical comorbidity
Evaluate for concomitant drugs which patient is receiving
Evaluate for the presence of psychosocial stressors
Evaluate the cognitive functions
Evaluate for suicidality, oral intake

Patient’s preference
Past history of good response Patient’s preference
Receiving other medications Past and family history of good response
and high risk of drug interactions Low risk of drug interactions
Suicidal
Poor oral intake
Catatonic symptoms

Pharmacotherapy

ECT+ Pharmacotherapy
(ECT for treatment of acute disturbance and
antidepressants for the continuation phase)
Partial response

No response

Optimize the treatment

• Increase the dose of antidepressants to
maximum tolerable dose

No further response

 Switch to an antidepressant from same or different

pharmacological class or dual acting agent
 Add ECT
 Add second antidepressants/ augmenting agent
taking into consideration the issue of tolerability
and side effects

Figure 3: Treatment algorithm of Severe Depression

Table 10: Management in the acute phase
• Comprehensive assessment (psychiatric/medical/psychosocial)
• Deciding on goals of treatment
Achieving remission
Ensure safety of patient and others
• Choice of treatment setting
• Choosing a treatment modality: antidepressant medication, psychotherapy,
combined treatment with antidepressant and psychotherapy
• Use of adjunctive medications when indicated
• Use of ECT when indicated
• Psychoeducation
benzodiazepines or other hypnotics may be used for short
duration.
Failure to response: If at least some improvement (>25%)
is not observed following 4 week of pharmacotherapy, a
reappraisal of the treatment regimen be conducted and
a change in antidepressant may be considered. When
patient shows 25-50% improvement during the initial 4
weeks of antidepressant trial, the dose must be optimized
to the maximum tolerable dose. If there is less than 50%
improvement with 6-8 weeks of maximum tolerable dose
and the medication compliance is good, a change in
antidepressant may be considered.
If after 4-8 weeks of treatment, if a moderate improvement is
not observed, then a thorough review and reappraisal of the
diagnosis, complicating conditions and issues, and treatment
plan may be conducted. Reappraisal of the treatment
regimen may also include evaluation of patient adherence and
pharmacokinetic/pharmacodynamic factors. Following this
review, the treatment plan can be revised by implementing one
of several therapeutic options, including maximizing the initial
medication treatment, switching to another antidepressant
medication, augmenting antidepressant medications with
other agents/psychotherapy/ECT. Maximizing the initial

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 Gautam, et al.: CPGs for depression

Continuation Phase treatment

Treated with Treated with Treated with combination Treated with combination
antidepressants psychotherapy of psychotherapy and of antidepressants and
during the acute during the acute antidepressants during the ECT/antipsychotics during
phase phase acute phase the acute phase

Continue antidepressants Continue psychotherapy at Continue with Continue with

at the same dose for 6- the same or decreased antidepressants at the antidepressants and
9month after achieving frequency for 6-9 months same dose and antipsychotic at the same
remission after achieving remission psychotherapy at the dose and for 6-9 months
same or decreased after achieving
frequency for 6-9 remission
months after achieving
remission

Monitor for relapse of symptoms

No past H/O depression Past H/O depression

Discontinue treatment depression treatment Maintenance Treatment

Figure 4: Treatment algorithm for continuation phase treatment of depression

Maintenance Phase treatment

(H/O of ≥ 3 episodes)

• Treated with antidepressants during the acute • Treated with • Treated with
and continuation phase psychotherapy during antidepressants and
• Treated with combination of antidepressants the acute and psychotherapy during
and ECT/ antipsychotics during the acute continuation phase the acute and
and continuation phase continuation phase

• Continue with same treatment preferably for life long

• Monitor symptoms and treatment tolerability

Figure 5: Treatment algorithm for maintenance phase of depression

treatment regimen is perhaps the most conservative strategy. SSRI to another SSRI) or to one from a different pharmacologic
While using the higher therapeutic doses, patients are to be class (e.g., from an SSRI to a tricyclic antidepressant). Some
closely monitored for an increase in the severity of side effects expert suggests that while switching, a drug with a different
or emergence of newer side effects. or broader mechanism of action may be chosen.

Switching to a different antidepressant medication is a Augmentation of antidepressant medications may be helpful,

common strategy for treatment-refractory patients, especially
those who have not shown at least partial response to the
initial medication regimen. There is no consensus about
switching and patients can be switched to an antidepressant
medication from the same pharmacologic class (e.g., from an
particularly for patients who have had a partial response
to initial antidepressant monotherapy. Options include
adding a second antidepressant medication from a different
pharmacologic class, or adding another adjunctive medication
such as lithium, psychostimulants, modafinil, thyroid hormone,

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 Gautam, et al.: CPGs for depression
an anticonvulsant etc. Adding, changing, or increasing the
intensity of psychotherapy may be considered for patients
who do not respond to medication treatment. Following any
change in treatment, close monitoring need to be done. If at
least a moderate level of improvement in depressive symptoms
is not seen after an additional 4–8 weeks of treatment, another
thorough review need to be done. This reappraisal may include
verifying the patient’s diagnosis and adherence; identifying and
addressing clinical factors that may be preventing improvement,
such as the presence of comorbid general medical conditions
or psychiatric conditions (e.g., alcohol or substance abuse);
and identifying and addressing psychosocial issues that may
be impeding recovery. If no new information is uncovered to
explain the patient’s lack of adequate response, depending on
the severity of depression, ECT maybe considered.
Choice of a specific psychotherapy: Out of the various
psychotherapeutic interventions used for management
of depression, there is robust level of evidence for use of
CBT. The major determinants of type of psychotherapy
are patient preference and the availability of clinicians
with appropriate training and expertise in specific
psychotherapeutic approaches. Other clinical factors which
will influence the type of psychotherapy include the severity
of the depression. Psychotherapy is usually recommended
for patients with depression who are experiencing stressful
life events, interpersonal conflicts, family conflicts, poor
social support and comorbid personality issues.
The optimal frequency of psychotherapy may be based on
specific type and goals of the psychotherapy, the frequency
necessary to create and maintain a therapeutic relationship,
the frequency of visits required to ensure treatment
adherence, and the frequency necessary to monitor and
address suicidality. Other factors which would also determine
the frequency of psychotherapy visits include the severity
of illness, the patient’s cooperation with treatment, the
availability of social supports, cost, geographic accessibility,
and presence of comorbid general medical problems.
Besides the use of specific psychotherapy, all patients and their
caregivers may receive psychoeducation about the illness.
Role of Yoga and Meditation in management of
depression: Studies related to role of traditional therapies
like meditation, Yoga and other techniques have been
mostly published in documents of various organizations
propagating that particular technique. Well-designed
scientific studies to authenticate these claims need to
be conducted; however, efficacy of these techniques as
supportive/adjuctive therapy is widely accepted.
TREATMENT IN CONTINUATION PHASE
The goal of continuation phase is to maintain the gains
achieved in the acute phase of treatment and prevent relapse
S44
of symptoms. The treatment algorithm to be followed is
shown in figure-4. Patients who have been treated with
antidepressants in the acute phase need to be maintained on
same dose of these agents for 16-24 weeks to prevent relapse
(total period of 6-9 month from initiation of treatment). There
are evidences to support the use of specific psychotherapy
in continuation phase to prevent relapse. The use of other
somatic modalities (e.g. ECT) may be useful in patients where
pharmacology and/or psychotherapy have failed to maintain
stability in continuation phase. The frequency of visit during
the continuation phase may be determined by patient’s clinical
condition as well as the specific treatment being provided. If
maintenance phase treatment is not indicated for patients who
remain stable following the continuation phase, patients may
be considered for discontinuation of treatment. If treatment
is discontinued, careful monitoring be done for relapse, and
treatment to be promptly reinstituted if relapse occurs.
TREATMENT IN MAINTENENCE PHASE
The goal of maintenance phase treatment is to prevent recurrence
of depressive episodes. On an average, 50-85% of patients with
a single episode of major depression have at least one more
episodes. Therefore, maintenance phase treatment may be
considered to prevent recurrence. The duration of treatment
may be decided keeping in view the previous treatment history
and number of depressive episodes the person has had in the
past. Mostly the treatment that was effective for acute and
continuation phase need to be used in the maintenance phase
(Figure-5). Same doses of antidepressants, to which the patient
had responded in previous phase is considered. The frequency
of visit for CBT and IPTcan be reduced during the maintenance
phase (once a month). There is no consensus regarding the
duration and when to give and when not to give maintenance
treatment. There is agreement to large extent that patients
who have history of three or more relapses or recurrences need
to be given long-term treatment.
DISCONTINUATION OF TREATMENT
The decision to discontinue maintenance treatment may
be based on the same factors considered in the decision to
initiate maintenance treatment, including the probability
of recurrence, the frequency and severity of past episodes,
the persistence of depressive symptoms after recovery, the
presence of comorbid disorders, and patient preferences.
When the decision is made to discontinue or terminate
psychotherapy in the maintenance phase, the manner in
which this is done may be individualized to the patient’s
needs. When the decision is made to discontinue maintenance
pharmacotherapy, it is best to taper the medication over
the course of at least several weeks to few months. Such
tapering may allow for the detection of emerging symptoms
or recurrences when patients are still partially treated and
therefore can be easily returned to full therapeutic intensity.
In addition, such tapering can help minimize the risks of
Indian J Psychiatry 59 (Supplement 1), January 2017

Special situation
Suicidal risk
Psychotic features
Atypical features
Alcohol and/or substance
abuse or dependence
Depression with features of
obsessive‑compulsive disorder
Depression with panic and/or
other anxiety disorders
Depression with cognitive
dysfunction (pseudo
dementia)
Dementia
Post Psychotic Depression
Indian J Psychiatry 59 (Supplement 1), January 2017
Gautam, et al.: CPGs for depression
Table 11: Management of depression Special situations
Strategies
• Risk of suicide is high in patients with depression.
• Suicide risk to be assessed initially and over the course of treatment.
• If the patient has suicidal ideation, intention, and/or a plan, close surveillance is necessary.
• Whenever possible, information about presence of suicidal ideation in patient be shared with family members and
they need to be instructed for various safety measures to be taken.
• The risk of suicide in some patients recovering from depression increases transiently as they develop the energy
and capacity to act on self‑destructive plans made earlier in the course of their illness. However, it is not possible
to predict with certainly whether a given patient will kill himself or herself.
• A careful selection of antidepressants and ECT is an important decision to be taken by psychiatrist after
considering all related factors.
• Wherever feasible, the prescribed drugs need not be in the possession or reach of patient having suicidal intention.
• Depression with psychotic features carries a higher risk of suicide than does major depression uncomplicated by
psychosis
• It also constitutes a risk factor for recurrent depression.
• Depression with psychotic features responds better to treatment with a combination of antidepressants and
antipsychotics than to treatment with either component alone.
• ECT is also highly effective in depression with psychotic features.
• Atypical depressive feature include severe anxiety, vegetative symptoms of reversed biological functions (i.e.,
increased rather than decreased sleep, appetite, and weight), marked mood reactivity, sensitivity to emotional
rejection, phobic symptoms, and a sense of severe fatigue that creates a sensation of “leaden paralysis” or extreme
heaviness of the arms or legs.
• Tricyclic antidepressants yield response rates of only 35%‑50%. Response rates with MAO inhibitors are in
the range of 55%‑75% in patients with atypical depression. If it is determined that the patient does not wish to,
cannot, or is unlikely to adhere to the dietary and drug precautions associated with MAO inhibitor treatment, the
use of an alternative antidepressant is indicated.
• The results of several studies suggest that SSRIs, MAOIs, and possibly bupropion maybe more effective
treatment for atypical depression.
• Because of the frequent comorbidity of depression and alcohol or other substance abuse, efforts need to be made
to obtain a detailed history of the patient’s substance use.
• If the patient is found to have a substance use disorder, a program to ensure abstinence may be regarded as a
principle priority in the treatment.
• It is also advisable, if other factors permit, to detoxify such a patient before initiating antidepressant therapy.
• Benzodiazepines and other sedative hypnotics carry the potential for abuse or dependence and these may be used
cautiously except as part of a detoxification regimen.
• Hepatic dysfunction and hepatic enzyme induction frequently complicate pharmacotherapy of patients with
alcoholism and other substance abuse; these conditions require careful monitoring of blood levels.
• Clomipramine and the SSRIs have been demonstrated to be efficacious in the management of
obsessive‑compulsive symptoms in addition to their antidepressants efficacy.
• Panic disorder complicates major depression in 15%‑30% of the cases.
• TCAs and SSRIs may initially worsen, rather than alleviating anxiety and panic symptoms; these medications
may therefore be introduced at a low dose and slowly increased when used to treat such patients.
• High potency benzodiazepine like alprazolam and clonazepam may sometimes be used with benefit either in
combination with antidepressants or as the sole pharmacological agent for anxiety, with or without panic, coupled
with milder forms of depression.
• Signs and symptoms of cognitive inefficiency routinely accompany major depression.
• Some patients have both depression and dementia, while others have depression that causes cognitive
impairment (i.e., pseudo‑dementia).
• Several clinical features help in differentiating pseudo‑dementia from true dementia. Pseudo‑demented patients
generally exert relatively less effort but report more incapacity than patients with true dementia. In more
advanced stage, patients with dementia typically fail to recognize their cognitive failure.
• It is important that patients with major depression with cognitive disturbance are not misdiagnosed and thereby
denied the antidepressant medication or ECT.
• Depression related cognitive dysfunction is a reversible condition that resolves with treatment of the underlying
depression.
• Individuals suffering from dementia need to be prescribed antidepressants which have least potential of
anticholinergic effect, e.g., bupropion, fluoxetine, sertraline, and, of the tricyclic agents, desipramine or
nortriptyline. Alternatively, some patients do well when given stimulants in small doses.
• Among SSRIs, paroxetine may be avoided.
• ECT is also effective in depression superimposed on dementia, and it may be used if medications are
contraindicated, not tolerated, or if immediate resolution of the major depressive disorder episode is medically
indicated (such as when it interferes with the patient’s acceptance of food).
• Adding an antidepressant agent to the patient’s antipsychotic regimen can help in managing post‑psychotic
depression effectively.
Contd...
S45

Special situation
Depression during pregnancy
or following Childbirth
Seasonal depression
Depression in elderly
Depression in Children
Post‑ Stroke Depression
Cardiac disease:
Hypertension
S46
Gautam, et al.: CPGs for depression
Table 11: Contd...
Strategies
• Women in childbearing age may be counseled about the risk of becoming pregnant while taking psychotropic
medications.
• Whenever possible, a pregnancy is to be planned in consultation with psychiatrist so that medication may be
discontinued before conception if feasible.
• The clinicians need to carefully weigh the risks and benefits of prescribing psychotropic agents to the pregnant
patient, taking into consideration the possibilities of physical (especially during the first trimester) and behavioral
teratogenesis.
• In patients whose safety and well‑being require antidepressants medications, antidepressants may be justifiably
used, after the first trimester, if possible.
• ECT may be used as an alternative treatment; the current literature supports the safety for mother and fetus, as
well as the effectiveness of ECT during pregnancy.
• Postpartum depression is to be treated according to the same principles delineated for other depressive condition.
• However, issue of breast feeding and appropriate precautions need to be explained to patient and caregivers.
• Some individuals suffer annual episode of depression whose onset is in the fall or early winter, usually at the
same time each year.
• The depressive episodes frequently have atypical features such as hypersomnia and overeating.
• The entire range of treatments for depression may also be used to treat seasonal affective disorder, either in
combination with or as an alternative to light therapy.
• Antidepressants are effective in treatment of depression in old age.
• The high rates of adverse effects associated with TCAs suggest that these agents must not be used as the first line
agents.
• The lower rate of adverse events in the newer antidepressants (SSRIs) makes them more acceptable. However,
nortriptyline has a role in severe depression in the elderly.
• ECT has demonstrated efficacy in treatment of old age depression with the benefit of rapid response in the
severely ill with and without psychotic symptoms.
• There are evidences that SSRIs are effective in child and adolescent depression and these are generally the first
choice of drug.
• The commonly used SSRIs include fluoxetine. Other newer antidepressants have not been adequately evaluated
in childhood and use of all these classes of drugs may be used with careful monitoring.
• Psychotherapeutic interventions like CBT and IPT have also been shown to be efficacious in children and
adolescents.
• Post Stroke Depression is a common problem seen in at least 30‑40% of survivors of intra‑cerebral hemorrhage.
• Antidepressant drugs may be beneficial in managing depressive symptoms and allow faster Post Stroke
rehabilitation.
• Treatment is complicated by medical co‑morbidity and by the potential for interaction with other co‑prescribed
drugs.
• Fluoxetine and nortriptyline are probably the most standard and seen to be effective.
• The presence of specific cardiac conditions complicates or contraindicates certain forms of antidepressant
medication therapy, notably use of TCAs.
• Cardiac history is to be carefully explored before the initiation of medication treatment. Although TCAs have
been used effectively to treat depression in patients with some forms of ischemic heart disease, particular care
need to be taken in using TCAs in patients with a history of ventricular arrhythmia, subclinical sinus node
dysfunction, conduction defects (including asymptomatic conduction defects), prolonged QT intervals, or a recent
history of myocardial infarction.
• SSRIs, bupropion, and ECT appear to be safer for patients with preexisting cardiac disease, although the latter
may require consultation with a specialist and treatment modification before use. However, there are also reports
which suggest that SSRIs can also lead to arrhythmia.
• MAOIs do not adversely affect cardiac conduction, rhythm, or contraction but may induce orthostatic
hypotension and also run the risk of interacting adversely with other medications that may be taken by such
patients. There is anecdotal evidence that trazodone may induce ventricular arrhythmias, but this agent may be
avoided in elderly because of orthostatic blood pressure decrements.
• Consultation with the patient’s cardiologist before and during antidepressant medication treatment may be advisable
and is especially advisable during any treatment for a patient who has recently had a myocardial infarction.
• Antihypertensive agents and TCAs may interact to either intensify or counteract the effect of the antihypertensive therapy.
• The action of antihypertensive agents that block alpha receptors (e.g., prazosin) may be intensified by
antidepressant medications that block these same receptors, notably the TCAs and trazodone. TCAs may
antagonize the therapeutic actions of guanethidine, clonidine, or α‑methyldopa.
• Antihypertensive, like diuretics which mainly act on kidney, may precipitate SIADH, when given along with
SSRIs.
• Concurrent antihypertensive treatment, especially with diuretics, increases the likelihood that TCAs, trazodone,
or MAOIs will induce symptomatic orthostatic hypotension.
• β Blockers, especially propranolol, may be a cause of depressive disorder in some patients.
• Dose‑dependent elevations in blood pressure with venlafaxine are usually mild, although more severe elevations
have been observed, making this agent less preferable in patients with hypertension.
Contd...
Indian J Psychiatry 59 (Supplement 1), January 2017
 Gautam, et al.: CPGs for depression

Table 11: Contd...
Special situation Strategies
Diabetes mellitus • SSRIs may reduce serum glucose by up to 30% and cause appetite suppression, resulting in weight loss.
• Fluoxetine may be avoided, owing to its increased potential for hypoglycaemia, particularly in patients with
non‑insulin dependent diabetes. If fluoxetine is prescribed, the patient should be advised of the need to monitor
serum glucose levels regularly.
• T CAs are more likely to impair diabetic control as they increase serum glucose levels by up to 150%,
increase appetite  (particularly carbohydrate craving) and reduce the metabolic rate. They are generally
considered safe unless the diabetes is very poorly controlled or is associated with significant cardiac or
renal disease.
• Antidepressants such as amitriptyline, imipramine, duloxetine and citalopram are also used to treat painful diabetic
neuropathy.
Asthma • Antidepressant medications except MAOI may be used for patients with asthma without fear of interaction. Other
antidepressant like SSRIs, TCAs, etc., may be used for patient with asthma without any apprehension about drug
interaction.
Glaucoma • Antidepressants that cause or exacerbate acute close angle glaucoma include medications with anticholinergics,
serotonergic or adrenergic properties.
• TCAs have the greatest anticholinergic properties,
• SSRIs and SNRIs by virtue of their action on serotonin receptor can also cause mydriasis and thereby can produce
papillary block.
• Antidepressants lacking anticholinergic and serotonergic activity (bupropion) may be preferred.
• Benzodiazepines (Diazepam) have mild anticholinergics properties.
Obstructive uropathy • Prostatism and other forms of bladder outlet obstruction are relative contraindications to the use of antidepressant
medication compounds with antimuscarinic effects.
• Benzodiazepines, trazodone, and MAOIs may also retard bladder emptying.
• The antidepressant medications with the least propensity to do this are SSRIs, bupropion, and desipramine.
Parkinson’s disease • Bupropion, exerts a beneficial effect on the symptoms of Parkinson’s disease in some patients but may also induce
psychotic symptoms, perhaps because of its agonistic action in the dopaminergic system.
• MAOIs (other than selegiline, also known as L‑deprenyl, a selective type B MAOI is recommended in the treatment
of Parkinson’s disease) may adversely interact with L‑dopa products.
• Selegiline loses its specificity for MAO‑B in doses greater than 10 mg/day and may induce serotonin syndrome
when given in higher doses in conjunction with serotonin‑enhancing antidepressant medications.
• There is no evidence favoring any particular antidepressant medication from the standpoint of therapeutic efficacy
in patients with Parkinson’s disease complicated by depressive disorder.
• The theoretical benefits of the antimuscarinic effects of some of the TCAs in the treatment of patients with depressive
disorder with Parkinson’s disease are offset by the memory impairment that may result.
• ECT exerts a transient beneficial effect on the symptoms of idiopathic Parkinson’s disease in many patients.
• Amoxapine, an antidepressant medication with dopamine‑receptor blocking properties, may be avoided for patients
who have Parkinson’s disease.
• Lithium may in some instances induce or exacerbate parkinsonian symptoms.
Malignancy • In treatment of depression in subjects with malignancy, SSRI are considered to be the first line drugs. The advantage
of SSRI is that they can act as effective adjunct analgesic drugs, especially in neuropathic pain. Disadvantages
of SSRI are drug‑drug interaction with drugs that are metabolized by CYP450/3A4  (e.g.  cyclophosphamide,
doxorubicin). Fluoxetine, may be used with caution especially is patients with hepatic insufficiency, since it has
a long half‑life.
• TCAs are also good adjunct analgesics. But the disadvantages with TCAs are anticholinergic side effects and
orthostatic hypotension. They can also worsen their side effects of drugs like opioids (e.g. constipation and dry
mouth) which are often needed for pain control.
• Psychostimulants, with their rapid onset of action have some advantages for depressed cancer patients in the sense
of promoting a sense of well‑being, decreasing fatigue, stimulating appetite, potentiating the analgesic effect of
opioids and decreasing opioid induced sedation.
• The goal of psychological treatment in depressed patients with cancer is to reduce emotional distress, improve
morale, coping ability, self‑esteem and sense of control.
Drug induced depression • If medication induced depression is suspected, the suspected drug should be discontinued if possible and replaced
with another agent less likely to induce depression.
• When this is not possible or when discontinuation does not result in remission of the depressive symptoms,
pharmacotherapy for the depression may be considered.

Contd...

Indian J Psychiatry 59 (Supplement 1), January 2017 S47

 Gautam, et al.: CPGs for depression

Table 11: Contd...
Special situation Strategies
Liver disease • Liver impairment affects basic elements of medication pharmacokinetics, from absorption to metabolism,
distribution to elimination, changing drug levels, duration of action, and efficacy.
• Most antidepressants are highly protein‑bound‑ except, venlafaxine, and methylphenidate.
• In liver failure, a reduction in albumin and alpha1‑acid‑glycoprotein production, along with altered protein‑binding,
leads to higher levels of free pharmacologically‑active drug. This is offset by a compensatory increase in the rate of
hepatic metabolism, and this is especially important for drugs with low intrinsic clearance.
• Most antidepressants are highly lipid‑soluble and require hepatic metabolism (biotransformation into more polar
compounds) to allow them to be cleared from the body in urine or bile.
• Antidepressants can also be divided into two major categories of clearance, determined by their enzyme affinity.
Flow‑limited drugs have high hepatic extraction, and their hepatic clearance is dependent on the rate of delivery of
the drug to the liver. TCAs undergo significant first pass metabolism of greater than 50% after oral administration.
• Drugs with low hepatic‑enzyme affinity (e.g., paroxetine) are metabolized more slowly, as enzyme saturation is the
rate limiting step. The severity of impairment rather than the underlying aetiology is the most important factor to
consider in prescribing for this group. Renal function may also be affected.
• As the risk of drug toxicity increases with disease severity, lower starting and total doses of medication are
recommended (starting dose ‑about one forth that of adults).
Renal disease • In this group of patients, TCAs are probably safer than SSRIs.
• The degree of renal impairment rather than the cause is most important.
• Renal impairment may be present without a raised creatinine level. TCAs metabolites are excreted by the kidneys,
hence accumulation may occur. Of the SSRIs, sertraline is not recommended by its manufacturers in renal failure.
• Fluoxetine, citalopram and paroxetine may be started at very low dose in patients with a glomerular filtration rate
of at least>10 ml/min.
• Lithium may only be prescribed if absolutely necessary, at low doses, on alternate days, with frequent checking of
serum levels.
Perioperative period • TCAs may preferably be stopped prior to surgery. SSRIs and MAOI can interact with pethidine, pentazocine, and
dextromethorphan, at the pharmacodynamics levels and lead to serotonin syndrome, therefore such drugs may be
avoided during the perioperative period. However, SSRIs may not be discontinued in order to prevent anesthetic
interactions, except when the SSRI is used in combination with aspirin or an Non-steroidal anti-inflammatory
drugs and when the SSRI is used in patients over 80 years of age. In these patients, the balance of risks of
withdrawal and bleeding is to be discussed with patients. Because abrupt discontinuation can cause serious
withdrawal symptoms, the drugs may be gradually discontinued over few days to 2 weeks before surgery.
• Lithium can contribute to hemodynamic instabilities, interfere with sodium and potassium metabolism, and the
renal excretion of lithium can be reduced in presence of renal complications. The physical risk of intoxication,
with its detrimental and fatal risks for the central nervous system, is unacceptable. Therefore, lithium
discontinuation is recommended. Lithium can be stopped at once because no withdrawal symptoms occur.
• When, postoperatively, the patient is hemodynamically stable, is able and allowed to drink, and is not on new,
potentially interfering drugs, the medication may be restarted gradually.

antidepressant medication discontinuation syndromes.
Discontinuation syndromes have been found to be more
frequent after discontinuation of medications with shorter
half-lives, and patients maintained on short-acting agents
may be given even longer, more gradual tapering. Paroxetine,
venlafaxine, TCAs, and MAOIs tend to have higher rates of
discontinuation symptoms while bupropion-SR, citalopram,
fluoxetine, mirtazapine, and sertraline have lower rates. The
symptoms of antidepressants discontinuation include
flu-like symptoms, insomnia, nausea, imbalance, sensory
disturbances (e.g., electrical sensations) and hyperarousal
(agitation). If the discontinuation syndrome is mild,
reassurance may be sufficient. If mild to moderate, short-
term symptomatic treatment (analgesics, antiemetics, or
anxiolytics) may be beneficial. If it is severe, antidepressant
are to be reinstated and tapered off more slowly.
After the discontinuation of active treatment, patients
should be reminded of the potential for a depressive
relapse. Patient may be again informed about the early
signs of depression, and a plan for seeking treatment in
the event of recurrence of symptoms may be formulated.
Patients may be monitored for next few months to identify
relapse. If a patient suffers a relapse upon discontinuation
of medication, treatments need to be promptly reinitiated.
In general, the previous treatment regimen to which the
patient responded in the acute and continuation phase are
to be considered.
MANAGEMENT OF TREATMENT RESISTANCE
DEPRESSION
Initial treatment with antidepressant medication fails to
achieve a satisfactory response in approximately 20%-30%
of patients with depressive disorder. In some cases the
apparent lack of treatment response is actually a result
of faulty diagnosis, inadequate treatment, or failure to
appreciate and remedy coexisting general medical and
psychiatric disorders or other complicating psychosocial
factors. Adequate treatment for at least 4-6 weeks is

S48 Indian J Psychiatry 59 (Supplement 1), January 2017

 Gautam, et al.: CPGs for depression

necessary before concluding that a patient is not responsive who has not responded to medication is carrying out
to a particular medication. First step in care of a patient a thorough review and reappraisal of the psychosocial
and biological information base, aimed at revarifying the
Depression diagnosis and identifying any neglected and possibly
No Response to treatment
contributing factors, including the general medical
problems, alcohol or substance abuse or dependence,
other psychiatric disorders, and general psychosocial issues
impeding recovery. Algorithm for arriving at the diagnosis
Reassess diagnosis Correct the diagnosis and of treatment resistant depression is given in figure-6.
treat accordingly

Some clinicians require two successive trials of medications

Has the patient received
adequate doses for
sufficient duration?
Is adherence to medication
proper?
Are Side effects interfering
with treatment?
Look for emerging organic
causes, rule out any other
comorbidities/stressors
Figure 6: Algorithm for arriving at the diagnosis of Treatment
Resistant Depression
of different categories for adequate duration before
considering treatment resistant depression (TRD).
Management of TRD involves addition of an adjunctive
agent, combining two antidepressants, addition of ECT
or other somatic treatments like rTMS.Algorithm for
management of TRD is given in figure-7.
Addition of an adjunct to an antidepressant: Lithium
is the drug primarily used as an adjunct; other agents
in use are thyroid hormone and stimulants. Opinion
differs as to the relative benefits of lithium and thyroid
Treatment Resistant supplementation. It is reported that lithium is useful in over
Depression
50% of antidepressant nonresponders and is usually well
tolerated. The interval before full response to adjunctive
lithium is said to be in the range of several daysto 3 weeks.

Treatment Resistant
Depression

Partial or no response

Augmentation with Combination Other e.g. Lamotrigine,

ECT/
Lithium/Thyroid / Antidepressants fluvoxamine,
rTMS
Buspirone (TCA + SSRI) or Mirtazapine+ Bupropion,
(Bupropion + SSRI) Olanzapine etc. (Provide
Rationale)

Continuation Phase

Maintenance Phase

Figure 7: Algorithm for management of Treatment Resistant Depression

Indian J Psychiatry 59 (Supplement 1), January 2017 S49
 Gautam, et al.: CPGs for depression
If effective and well tolerated, lithium may be continued
for the duration of treatment of the acute episode. Thyroid
hormone supplementation, even in euthyroid patients,
may also increase the effectiveness of antidepressant
treatment. The dose proposed for this purpose is 25 μg/
day of triidothyronine increased to 50 μg/day in a week.
Simultaneous use of multiple antidepressants: Depression is
a chronic disabling condition in case patient does not respond
to single drug regimen; clinicians may use combination/
polytherapy with close monitoring of side effects and drug
interaction profile. Combinations of antidepressant carry
a risk of adverse interaction and sometimes require dose
adjustments. Use of a SSRI in combination with TCA has
been reported to induce a particularly rapid antidepressant
response. However, fluoxetine added to TCAs causes an
increased blood level and delayed elimination of the TCA,
predisposing the patient to TCA drug toxicity unless the dose
of the TCA is reduced. Another strategy involves combined
use of a tricyclic antidepressant and a MAO inhibitor, a
combination that is sometimes effective in alleviating severe
medication-resistant depression, but the risk of serotonin
syndrome necessitates careful monitoring.
Electroconvulsive therapy: Response to ECT is generally
good and the response rates are like any form of
antidepressant treatment and it may be considered in
virtually all cases of moderate or severe major depression
who do not respond to pharmacologic intervention.
Approximately 50% of medication resistant patients exhibit
a satisfactory response to ECT. Lithium may be discontinued
before initiation of ECT, as it has been reported to prolong
postictal delirium and delay recovery from neuromuscular
blockade.
Repetitive Transcranial Magnetic Stimulation (rTMS)
Repetitive transcranial magnetic stimulation (rTMS; a type of
TMS that occurs in a rhythmic and repetitive form) has been
put forward as a new technique to treat this debilitating
illness. Current evidence suggests that rTMS applied to the
left dorsolateral prefrontal cortex (DLPFC) is a promising
treatment strategy for depression, but not all patients show
a positive outcome. Current clinical outcome studies report
rather modest superiority compared with placebo (sham).
To date, it remains unclear which TMS parameters, such as
S50
stimulation duration and intensity, can produce the most
benefits. Moreover, there is no consensus of the exact brain
localization for individual coil placement.
MANAGEMENT OF SPECIAL CONDITIONS
Clinicians often encounter certain clinical situations which either
require special attention or can influence treatment decisions.
Management of these situations is summarized in table-11.
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(Edgmont).2006; 3: 57–63.
Indian J Psychiatry 59 (Supplement 1), January 2017
 CLINICAL PRACTICE GUIDELINES

Clinical Practice Guidelines for Management of Bipolar Disorder

Nilesh Shah, Sandeep Grover1, G. Prasad Rao2
Department of Psychiatry, L. T. M. Medical College and General Hospital, Sion, Mumbai, 1Department of Psychiatry,
Post Graduate Institute of Medical Education and Research, Chandigarh, 2Schizophrenia and Psychopharmacology Division,
Asha Hospital., Banjara Hills, Hyderabad, India

shown to have subthreshold BPAD with a range of 0.1 to 2.4%

Participants of expert group on CPG for Bipolar Affective
with a mean of 1.4 (SD-0.8). There is no nationwide study to
Disorder
evaluate the prevalence rates of BPAD in India. In a country
like India, patients have limited resources, poor knowledge
Vidhyadhar Watve, Mrugesh Vaishnav, Vivek Kirpekar,
about the disorder and treatment; have inadequate access
D.K. Sharma, Mahendra Jain, Asim Kumar Mallick,
to the health care facilities, which makes treatment of
C.L. Narayan, Anup Bharti, Madhu Nijhawan.
BPAD a challenge. Indian Psychiatric Society (IPS) made first
attempt to formulate Clinical Practice Guidelines (CPGs) for
INTRODUCTION
management of BPAD in 2005. Since then, over the last one
decade there have been several developments, especially in
Bipolar disorder (BPAD) is a serious mental disorder
the form of emergence of new evidence for some of the
characterized by episodes of depression, hypomania/mania
pharmacological agents. Accordingly, these new guidelines
and mixed episodes, with interepisodic recovery. However,
attempt to update the previous guidelines published by
many patients with BPAD continue to exhibit residual
IPS. These guidelines should be read along with the earlier
symptoms in the interepisodic period. The illness usually
version of the CPGs, published by IPS in 2005.
starts in adolescence or early adulthood and has significant
negative impact on the life of the sufferer and their caregivers.
ASSESSMENT AND EVALUATION [TABLE-1]
Patients with BPAD encounter educational difficulties, job
related problems, interpersonal difficulties, psychosocial
Assessment of patients is an ongoing process and
dysfunction, disability, marital problems, multiple suicidal
comprehensive assessment of a patient involves the
attempts, completed suicide and medication side effects.
assessment of patients themselves and their caregivers.
Additionally patients with BPAD have high rates of physical
The role of taking a proper history from the patient and
and psychiatric comorbidity. The prevalence rates of BPAD
all the available resources cannot be over-emphasized. In
vary from country to country. A large multinational study
addition to the history taking, proper attention must be
suggests that lifetime prevalence of BPAD-I ranges from
paid to the mental status examination. Diagnosis of BPAD
0-1% with a mean of 0.6 (SD-0.4). The prevalence rate of
is to be made on the basis of current diagnostic criteria,
BPAD-II ranges from 0 to 1.1% with a mean of 0.4 (SD-0.3).
because a diagnosis based on diagnostic criteria can be
Additionally a significant proportion of patients have been
considered more reliable, facilitates communication among
various clinicians and paves the way for management on the
basis of evidence based recommendations. It is important
Address for correspondence:
Dr. Nilesh Shah, Department of Psychiatry, L. T. M. Medical to remember that especially during the initial part of the
College and General Hospital, Sion, Mumbai - 400 022, illness, the symptoms may be confusing and at times it
Maharastra, India. may be difficult to distinguish symptoms of mania from
E-mail: drnilshah@hotmail.com,
other psychiatric syndromes like schizophrenia, acute
Dr. Sandeep Grover, Additional Professor, Department of
Psychiatry, PGIMER, Chandigarh, India.
E-mail: drsandeepg2002@yahoo.com
This is an open access article distributed under the terms of the Creative
Access this article online Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows
Quick Response Code others to remix, tweak, and build upon the work non-commercially, as long as the
Website: author is credited and the new creations are licensed under the identical terms.

www.indianjpsychiatry.org For reprints contact: reprints@medknow.com

DOI:
How to cite this article: Shah N, Grover S, Rao GP. Clinical
Practice Guidelines for Management of Bipolar Disorder.
10.4103/0019-5545.196974
Indian J Psychiatry 2017;59:51-66.

© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow S51

 Shah, et al.: CPGs for bipolar disorders
Table 1: Components of assessment and evaluation
Basic assessments
• Comprehensive assessment of both patients and caregivers
• Complete history with information from all possible sources in terms of
type of first episode in lifetime, predominant polarity of illness, duration
and severity of episodes, inter‑episodic recovery, presence or absence of
suicidal behaviour, violence and agitation, seasonal variation in onset of
symptoms, presence of rapid cycling and ultra‑rapid cycling features
• History taking focusing on precipitating factors‑ psychosocial stressors,
disturbances in biological rhythms
• Physical examination‑ record data such as blood pressure, weight and
wherever indicated body mass index and waist circumference
• Mental state examination
• Establish diagnosis according to current diagnostic criteria
• Differential diagnosis by ruling out secondary affective disorder
• Proper assessment of the current polarity of the illness
• Evaluate the risk for suicidal behaviour‑ suicidal ideations, intent, plans;
access to means for suicide, possible lethality in case patient uses the
means, psychotic symptoms in the form of commanding hallucinations,
severe anxiety, comorbid substance use, past history of suicidal
attempts and non‑suicidal self‑harming, family history of self‑harm and
completed suicide
• Areas to be evaluated during the current episode: symptom‑severity,
symptom‑dimensions, comorbid physical and psychiatric including
substance use conditions, risk of harm to self and others, level of
functioning and socio‑cultural milieu of the patient
• Past treatment history: type of medications used, response to treatment,
duration of use of treatment, side effects experienced and reasons for
discontinuation
• Basic investigations: haemogram, blood sugar and lipid levels, liver
functions, renal functions, electrocardiogram
• Assessments of caregivers: knowledge about illness, knowledge about
treatment, their attitudes and beliefs regarding treatment, the impact of
the illness on them and their personal and social resources in the form of
burden, distress, stigma, personal and marital life
• Ongoing assessments: response to treatment, side effects, treatment
adherence, issues of marriage and pregnancy, disability, other health‑care
needs, ease of access to treatment team, therapeutic alliance, etc.
Additional/Optional assessments
• Use of standardized rating scales to rate various aspects of the illness
• Psychological testing for cognitive functions
• Neuroimaging especially in those with atypical features, neurological
signs, non‑response to treatment, later age of onset and elderly patients
and transient psychosis and other psychiatric disorders.
A possibility of substance induced disorder or disorder
secondary to organic causes is to be considered, when
the symptoms are atypical or there is evidence of the use
of substance or underlying organic causes. Occasionally
establishing the definite diagnosis of BPAD may require
time.
The assessment may cover history of number of previous
episodes, type of first episode in lifetime, predominant
polarity of illness, duration and severity of episodes,
inter-episodic recovery, presence or absence of suicidal
behaviour, violence and agitation, seasonal variation in
onset of symptoms, presence of rapid cycling and features of
ultra-rapid cycling. Assessment of current episode may also
focus on the issues of severity of symptoms, suicidality and
agitation. Understanding the role of various psychosocial
S52
stressors and biological rhythms in onset of illness,
precipitation of relapse and continuation of symptoms need
to be understood thoroughly.
A thorough assessment includes assessment of comorbid
psychiatric and medical conditions. It is important to
remember that many a times; comorbidity is not very evident
during the acute episode of illness. The comorbid conditions
become more evident when the patient has come out of the
acute episode of the illness. Evaluation of comorbid substance
abuse needs to consider the type and frequency of substance
abuse. If the patient does not provide adequate information
about the substance use pattern, but there is high index of
suspicion, urine or blood screens (with prior consent) can be
used to confirm the existence of comorbid substance use/
dependence, wherever such facilities are available. Functional
impairment in various domains of life including impact of the
illness on the family functioning and psychosocial impact of
the illness on the caregivers is not to be neglected. A thorough
physical examination need to be done to rule out presence of
any physical illness and also to rule out episodes secondary
to physical illnesses. This may be supplemented by the
judicious use of investigations. Depending on the feasibility,
unstructured clinical assessments need to be supplemented
by documentation of severity and extent of symptoms on
appropriate standardized rating scales. Patients with bipolar
disorders also have cognitive deficits. Accordingly, depending
on the need, detailed cognitive testing may be undertaken.
The use of neuroimaging may be indicated in those with
atypical features, neurological signs, non-response to
treatment and having first episode of illness at a later age
and elderly. Caregiver’s assessment may involve evaluation of
their knowledge about illness, knowledge about treatment,
their attitudes and beliefs regarding treatment, the impact of
the illness on them and their personal and social resources
in the form of burden, distress, stigma, personal and marital
life etc.
In case patient has received treatment in the past, then it is
important to record the type of medications used, response
to treatment, duration of use of treatment, side effects
experienced and reasons for discontinuation.
Importance of ongoing assessment cannot be
underestimated. With progress in treatment, new issues like
response to treatment, side effects, treatment adherence,
marriage, pregnancy, disability, other health-care needs,
ease of access to treatment team and therapeutic alliance
may need to be assessed from time to time.
FORMULATING A TREATMENT PLAN [FIGURE 1]
Formulation of treatment plan will involve decision making
about the treatment setting, treatments to be used and areas
to be addressed. Treatment plan need to be formulated in
Indian J Psychiatry 59 (Supplement 1), January 2017
 Shah, et al.: CPGs for bipolar disorders

Patient with Affective Symptoms

Consider differential diagnoses like

• Organic Mental Conditions
• Substance induced disorder
• Acute and transient psychotic disorder
• Other psychotic disorders

Establish the diagnosis of BPAD

Assessment
• Severity of Current episode
• Risk of harm to self and others
• Comorbid substance use/dependence
• Level of functioning
• Detailed Physical examination
• Record- blood pressure, weight and wherever indicated body mass index and waist
circumference
• Mental Status Examination
• Investigations- haemogram, liver function test, renal function test, fasting blood glucose
level, electrocardiogram
• Treatment history- response to previous medication trials, compliance, side effects, etc.
• Patient’s and caregivers beliefs about the cause of illness and beliefs about the treatment
• Assessment for social support, stigma, coping
• Assessment of caregiver burden, coping and distress

• Decide about treatment setting- consider inpatient care in case of suicidality, severe agitation
and violence, malnutrition, catatonia, patient unable to care for self to the extent that she/he
requires constant supervision or support, comorbid general medical conditions making
management difficult at the outpatient setting
• Liaison with other specialists depending on the need of the patient

Electroconvulsive therapy Non-Pharmacological

Pharmacological Management
• Catatonia, rapid control Management
• Choose an agent based on the current
of symptoms, suicidality, • Psychoeducation
polarity, presence or absence of psychotic
past response to ECT, • Psychosocial
symptoms in the current episode, past
augmentation etc. intervention
treatment response, past history of side
effects, cost, comorbidity, patient/family
preference, preferred route of
administration, availability of medications,
current metabolic profile, past history of
compliance, treatment resistance

Figure 1: Initial evaluation and management plan for schizophrenia

consultation with patients, caregivers and other members
involved in the treatment team. Treatment plans may be
guided by the needs and be practical, feasible and flexible.
Further, the treatment plan is be re-evaluated from time to
time and be modified as per the needs.
CHOICE OF TREATMENT SETTINGS
In general, most of the patients with BPAD are managed
on the outpatient setting. However, some patients may
require inpatient care. Whenever possible patient admitted
to the inpatient setting should have accompanying family
caregivers. In case inpatient care is required and such
facilities are not available, than the patient and/or family
need to be informed about the need for inpatient care and
patient may be referred to the nearest available inpatient
facility and admission may be facilitated.
OPTIONS FOR MANAGEMENT OF BIPOLAR
DISORDER
Treatment options for management of BPAD can be broadly
classified as mood stabilizers, antidepressants, antipsychotic
medications, electroconvulsive therapy (ECT), adjunctive
medications and psychosocial interventions [Table-2]. Use of
various treatment options is guided by the phase of illness
(mania/hypomania/depression/mixed) in which patient
presents to the clinician and past treatment history.
PHARMACOLOGICAL MANAGEMENT OF
BIPOLAR DISORDER
The mainstay of management of BPAD is mood stabilizers.
The available mood stabilizers include lithium, valproate,
lamotrigine, carbamazepine/oxcarbazepine and topiramate.

Indian J Psychiatry 59 (Supplement 1), January 2017 S53

 Shah, et al.: CPGs for bipolar disorders
Lithium
Lithium is the oldest mood stabilizer used in the management
of BPAD. It has been found to be efficacious in management
of acute episode of either polarity and has been found to
be efficacious in prevention or relapse of episodes of either
polarity. Additionally, it has been shown to have a role in
prevention of suicide in patients with BPAD.
Prior to starting lithium, history need to be reviewed for
the presence of physical illnesses like renal dysfunction,
thyroid dysfunction and cardiac conduction abnormalities.
Additionally information needs to be reviewed for
presence of dermatological diseases. In case of women,
last menstrual period is to be ascertained and if required
urine pregnancy test need to be done. Further, prior to
starting lithium, patients need to be educated about the
various side effects of lithium, use of salt-restricted diet and
avoidance of medications (diuretics, angiotensin-converting
enzyme inhibitors, non-steroidal anti-inflammatory drugs,
cyclooxygenase-2 inhibitors, etc.) which can increase
serum lithium levels. Patients also need to be informed to
avoid dehydration. Whenever lithium is started, it need to
be started in low doses, preferably in divided doses and
the dose need to be titrated upwards with monitoring
of serum lithium levels. As steady state levels of lithium
are achieved after about 5 days of starting lithium or dose
increment, the levels are be done after 5 days of start of
treatment or change in the dose. However, the levels may
be checked earlier if patient manifests features of toxicity.
The serum levels of lithium, which are usually required for
management of acute episode, are in the range of 0.6 to 1.0
Table 2: Options for management for Bipolar disorder
Mood Stabilisers
• Lithium
• Divalproex/valproate
• Carbamazepine/Oxcarbazepine
• Lamotrigine
• Topiramate
• Gabapentin
Antidepressants
• Tricyclics, Selective serotonin reuptake inhibitors, Serotonin and
nor‑epinephrine reuptake inhibitors, bupropion, mirtazapine, etc.
Antipsychotic medications
• First‑generation antipsychotic medications (Oral/parenteral/depot or
long acting‑ preparations)
• Second‑generation antipsychotic medications (Oral/parenteral/depot or
long acting‑ preparations)
Somatic treatments
• Electroconvulsive therapy (ECT), transcranial magnetic
stimulation (rTMS), transcranial direct current stimulation (tDCS)
Adjunctive medications
• Anticholinergics, antidepressants, benzodiazepines, hypnotic‑sedatives,
anticonvulsants, lithium carbonate
Psychosocial interventions
• Social rhythm therapy, cognitive behavioural therapy, family
intervention, cognitive remediation, individual therapy, group therapy,
social skills training, vocational rehabilitation
Other measures
• Lifestyle and dietary modifications
S54
meq/litre and for prophylaxis range from 0.6 to 0.8 meq/
litre; however, few studies suggest that serum levels as low
as 0.4 to 0.8 meq/litre may be sufficient for prophylaxis,
albeit are associated with higher risk of relapse. Once the
dose is stabilized, patient may be shifted to once a day
dose to reduce the side effects and improve the medication
compliance. Serum lithium levels may be monitored every
3-4 months. Renal function tests need to be monitored
once in every 2-3 months during the initial 6 months of
therapy and thyroid function tests need to be monitored
once or twice during the first 6 months of treatment.
Later, renal and thyroid function tests may be monitored
once in 6 months to 1 year in clinically stable patients
and more frequently if so indicated (see table-3). Lithium
is usually preferred in patients who have classical mania,
bipolar depression, predominant polarity of illness is that
of depression, episodic course of illness, manic-depressive-
euthymic course, non-rapid cycling course of illness, lack
of mixed episode, older age of onset for BPAD, presence
of family history of BPAD and presence of family history of
lithium response.
Divalproex/valproate
Divalproex and its formulations (sodium valproate
and valproic acid) have been found to be useful in the
management of BPAD. It has been found to be efficacious
Table 3: Investigations prior to starting of lithium and
while monitoring lithium therapy
Pre‑lithium evaluation
• Serum Urea, Creatinine
• Serum electrolytes
• Thyroid function test
• May evaluate serum osmolality
• May evaluate 24 hour urine volume, proteins, creatinine, osmolality
• May calculate the eGFR
• Haemogram
• Urine Pregnancy test (in case of women)
• Electrocardiogram
• Fasting blood sugar
• Lipid Profile
• Anthropometry‑ height, weight, waist circumference
Monitoring of lithium therapy
• During the initial phase of illness, serum lithium levels must be done
after 5 days of a stable dose.
• Sample for serum lithium levels must be taken 12‑14 hours after the last
dose of lithium
• If the medication is being given as BD or TID dose, the morning dose
need to be withheld prior to collection of blood sample for serum
lithium level
Monitoring of side effects: at every visit enquire about polyuria/
polydipsia, gastrointestinal side effects; Check for tremor, dysarthria,
ataxia
Monitoring of serum lithium levels: Once the dose of lithium has been
stabilized the serum levels must be done once in every 3‑4 months; more
frequent monitoring may be done in elderly and those receiving with
concurrent medications like diuretics, and in those with renal impairment
Investigations to be repeated 6‑12 monthly as indicated: 24 hour urine
volume, urinary proteins, serum urea and creatinine, Thyroid function
tests, eGFR, S. Calcium
Indian J Psychiatry 59 (Supplement 1), January 2017
 Shah, et al.: CPGs for bipolar disorders
in management of acute mania and mixed episodes. The
evidence for its efficacy in acute depression is not as robust
as that for lithium. It is also efficacious in prevention of
mania and depression, when used during the maintenance
phase. As with lithium, prior to starting valproate, clinicians
need to review the medical history for presence of any
hepatic, haematological and bleeding problems. Prior
to starting of valproate, patient is to be educated about
the side effects, especially about signs and symptoms of
hepatic and haematological dysfunction. They need to be
instructed to report to the clinicians at the earliest if these
signs and symptoms emerge. Prior to starting valproate, it
is important to investigate the patient for liver function test
and haemogram. In young women, last menstrual periods
need to be ascertained and if required urine pregnancy test
need to be done to rule out pregnancy. As valproate is
associated with weight gain and metabolic abnormalities, it
may be a good practice to evaluate the lipid profile, fasting
blood glucose levels and anthropometry (Table-4).
Usually valproate is started in low doses, i.e., 250 mg BD or
250 mg TID and titrated upwards with monitoring of side
effects and serum levels. However, some of the studies
have also evaluated rapid titration of valproate dose with
initial dose of 20-30 mg/day and have shown that it is well
tolerated. Maximum daily dose which is recommended is
60 mg/day but most patients do not require such high doses.
The usual therapeutic serum levels which are considered to
be efficacious vary from 50 to 100µg/ml. Once the dose
of valproate is stabilized, the dosing schedule need to be
changed to OD or BD dosing to reduce the side effects and
improve compliance. In case OD dosing is given, extended
release formulation may be used. However, it is important
to remember that the bioavailability of extended release
formulations is about 15% less than the immediate release
preparations and the dose is to be increased accordingly.
Serum valproate levels are to be done after 5 days of starting
or increase in the dose of valproate. The sample need to
be collected after 12 hours in case patient is receiving
immediate release formulation, however, if the patient is
receiving extended release formulation, the sample may be
collected after 21 to 24 hours (table-5). There is evidence
to suggest that patients with BPAD-II, dysphoric or mixed
mania, rapid cycling affective disorder, stable episode
frequency, later age of onset of illness, shorter duration of
illness, long and severe course of illness respond well to
valproate. Other indicators for good response to valproate
include presence of comorbid alcohol use disorder, mental
retardation, anxiety and panic attacks, post-traumatic stress
disorders, marked sleep disturbances, explosive dyscontrol
and aggression and comorbid migraine.
Lamotrigine
The role of lamotrigine in management of BPAD has been
well studied now and it has been shown to be efficacious
in management of bipolar depression and prevention of
Indian J Psychiatry 59 (Supplement 1), January 2017
Table 4: Investigations prior to starting of valproate and
while monitoring valproate therapy
Pre‑valproate evaluation
• Haemogram
• Liver Function Test
• Urine Pregnancy test (in case of women)
• Fasting blood sugar
• Lipid Profile
• Anthropometry
Monitoring of valproate therapy
Routine monitoring of haemogram and liver function test is not
recommended. May be done every 6‑12 monthly in patients receiving
long term valproate therapy
The therapeutic range for serum valproic acid level is 50‑100 µg/mL
Serum valproate levels during initial titration are to be done after 5 days
of a stable dose.
When to collect the sample: sample may be collected after 12 hours in
case patient is receiving immediate release formulation, however, if the
patient is taking extended release formulation, blood sample need to be
collected 21‑24 hours after the last dose to estimate the serum valproate
levels
Table 5: Investigations prior to starting of valproate and
while monitoring valproate therapy
Pre‑Carbamezapine evaluation
• Haemogram
• Liver Function Test
• Urine Pregnancy test (in case of women)
• Renal Function test
• Serum electrolytes (in case of elderly)
• Fasting blood sugar
• Lipid Profile
• Anthropometry
Monitoring of carbamazepine therapy
• Monitoring of haemogram including platelet counts and liver function
test need to be done every 2 weekly during the initial 2 months of
treatment
• After first 2 months: if no abnormalities are noted during the first
2 months, than the Haemogram and liver function tests may be done
every three monthly.
• The therapeutic range for serum carbamazepine level is 4‑12 µg/ml
• Serum carbamazepine levels during initial titration are to be done after
5 days of a stable dose.
When to collect the sample: sample may be collected after 12 hours of
the last dose
relapse of depression. However, the most dreaded side
effect of lamotrigine includes skin rash, including Stevens
- Johnson syndrome and toxic epidermal necrolysis.
The skin lesions can occur any time during the therapy,
but are more often reported during the initial phase of
treatment and when used along with valproate. Evidence
suggests that the risk of skin rash can be reduced by
slow upward titration of the dose. Accordingly, while
considering lamotrigine, patients need to be informed
about the possibility of rash and told to contact the
treating psychiatrist in case rash is seen. When the rash
is more widespread, diffuse and associated with systemic
symptoms like fever or sore throat, lamotrigine may be
stopped. When initiated, lamotrigine may be started at
the dose of 25 mg/day for initial 2 weeks, then it may be
S55
 Shah, et al.: CPGs for bipolar disorders
given at the dose of 50 mg/day during the 3rd and 4th week.
After that 50 mg/day can be increased per week depending
on the therapeutic response.
Carbamazepine
Carbamazepine has been shown to be efficacious in the
management of acute bipolar mania and prevention of
relapse. Prior to starting carbamazepine, clinician needs
to focus on the history of blood dyscrasias and hepatic
dysfunction. When carbamazepine is considered, patients
need to be informed about the signs and symptoms of
hepatic dysfunction, haematological dysfunction and skin
reactions and told to report to the psychiatrist if these
symptoms emerge. Baseline investigation prior to starting
of carbamazepine may include complete haemogram, liver
function tests and renal function test (Table-5). When used
in elderly serum electrolytes may also be done, in view of the
risk of hyponatremia. Usual starting dose of carbamazepine
is 200 mg/day given in divided doses and titrated upward
slowly. Once the dose of 800-1000 mg/day is reached the
increment of dose may be slower and the usual maintenance
dose is about 1000 mg/day, but it can vary from patient to
patient and may be 200 to 1600 mg/day. The carbamazepine
therapeutic drug levels have not been established in patients
with BPAD and the serum levels of 4-12 µg/ml, which is
recommended for seizure disorders is commonly used. As
with lithium and valproate the serum levels need to be done
after 5 days of initiation of treatment or increment of dose.
Other anticonvulsants
There is lack of data in the form of double blind randomized
controlled trials for Oxcarbazepine, but small open label
studies suggests that it may be of some benefit as monotherapy
or add-on therapy in patients with refractory mania. The data
from open label studies suggest the usefulness of add-on
therapy with topiramate in patients with bipolar depression.
Studies which have evaluated the role of gabapentin in
management of mania have yielded negative results.
Antipsychotics
Over the last decade or so, many large multicentric double
blind placebo controlled and active comparator randomised
controlled studies have evaluated the role of various atypical
antipsychotics like olanzapine, quetiapine, aripiprazole,
risperidone, paliperidone, amisulpiride, asenapine,
ziprasidone and haloperidol etc. in the management of
bipolar depression, bipolar mania and for maintenance
phase treatment. Data from these studies suggest that
antipsychotics like olanzapine, quetiapine, aripiprazole,
risperidone, paliperidone and ziprasidone are effective in
the management of acute mania. There is evidence for use
of quetiapine monotherapy, and olanzapine and fluoxetine
combination in the management of bipolar depression.
There is evidence for lurasidone in the management of acute
episode of bipolar depression. Olanzapine and quetiapine
monotherapy or as adjunctive medications to lithium or
S56
valproate have been shown to be efficacious in prevention
of relapse of both depression and mania. Antipsychotics
like long acting risperidone, ziprasidone have been shown
to be beneficial in prevention of mania as monotherapy or
as adjunctive medications to lithium or valproate.
Combination therapy
There is evidence to suggest that when lithium or valproate
is combined with antipsychotics in the management of acute
mania, the efficacy is higher and the onset of action is faster
than that reported for single agent. Accordingly, depending
on the severity of mania, combinations may be used.
Electroconvulsive Therapy (ECT)
There is evidence for use of ECT in the management of acute
mania, mixed episode and bipolar depression. Indications
for use of ECT are shown in Table-6.
Benzodiazepines
Studies have evaluated the efficacy of adds-on
benzodiazepines like clonazepam and lorazepam to lithium
and current level of evidence suggests that the antimanic
properties of these agents are difficult to distinguish from
the sedative properties of these agents. Accordingly, these
agents are considered to be adjunctive agents, which may
be useful in management of acute episode. Further, there is
evidence to suggest the beneficial role of lorazepam in the
management of agitation and catatonia.
Other agents
Many other medications like calcium channel blockers,
zonisamide, levetiracetam, acamprosate, omega-3 fatty
acids, allopurinol etc, have been evaluated in small sample
size trials as monotherapy or add on agents. However,
available the evidence is not sufficient to recommend these
medications as first line agents in management of bipolar
mania and depression.
Antidepressants
Conventionally antidepressants have been used in the
management of bipolar depression. However, over the last 2
decades or so, use of antidepressants in patients with bipolar
Table 6: Possible indications of use of ECT in patients of
schizophrenia
• Bipolar depression not responding to adequate pharmacotherapy
• Bipolar mania not responding to adequate pharmacotherapy
• Catatonic symptoms
• Need for rapid control of symptoms
• Presence of suicidal behaviour which puts the life of the patient at risk
• Presence of severe agitation or violence which puts the life of others at risk
• Refusal to eat which puts the life of patient at risk
• History of good response in the past
• Augmentation of partial response to pharmacotherapy
• Not able to tolerate pharmacotherapy
• Treatment resistant illness
• Episodes of severe depression or mania during pregnancy
Indian J Psychiatry 59 (Supplement 1), January 2017
 Shah, et al.: CPGs for bipolar disorders
depression has emerged as a controversial topic in view of
the risk of antidepressant-induced manic/hypomanic switch.
Evidence from metanalysis suggests that use of antidepressants
along with mood stabilizers is superior to use of combination
of a mood stabilizer and a placebo and is not associated with
increased risk of manic switch. Most of the studies which
have not found adds-on antidepressants to be beneficial
have involved paroxetine, hence, if one want to avoid use of
an antidepressant, paroxetine is to be avoided. Among the
various antidepressants, bupropion has been reported to be
associated with lowest risk of antidepressant induced switch.
However, it is important to remember that antidepressants
should not be used as monotherapy, and in those with rapid
cycling affective disorder and mixed episodes.
Adequate trial
The minimum recommended duration of treatment to
consider it to be an effective trial for an acute manic episode
is about 3-4 weeks. In case of bipolar depression, a 6 weeks
trial is considered as an adequate trial.
NON-PHARMACOLOGICAL MANAGEMENT OF
BIPOLAR DISORDER
Psychosocial management as an adjunct to pharmacotherapy
has been shown to be of significant benefit during
the management of acute phase of bipolar depression
and maintenance phase of illness. Among the various
psychosocial interventions, data supports the use of
psychoeducation (individual and group), interpersonal and
social rhythm therapy (IPSRT), cognitive behaviour therapy
and family focused intervention. These psychosocial
interventions have been shown to be associated with
reduced risk of relapses, better functioning and better
treatment adherence. The basic components of all these
programs involve informing the patients about their illness,
identifying the early signs of relapse, handling stress,
maintaining social rhythms, addressing the interpersonal
issues and expressed emotions, problem solving and
enhancing medication and treatment adherence.
Psychoeducation for patients and or family (Table 7)
Psychoeducation may be considered both for the patient
and family members (Table 7). The aim is to be to
educate the patient and family about the illness. They
may be provided simple explanations about the nature
of the illness, treatment options, possible side effects of
medications and likely length of treatment etc. Caregivers
may also be provided with an opportunity to vent out their
feelings and distress. Psychoeducation may also address
the important issue of treatment adherence and identifying
early signs of new episode. It is important to remember that
psychoeducation is not a onetime event and prior to every
session, feedback of the previous sessions may be taken
and psychoeducation need to be tailored to the needs of
the patient and the caregivers.
Indian J Psychiatry 59 (Supplement 1), January 2017
Table 7: Basic components of Psychoeducation
• Assessing the knowledge of the patient and caregivers about aetiology,
treatment and prognosis
• Introduction of diagnosis
• Discussing the symptoms of depression, mania, hypomania and mixed
episodes
• Providing information about aetiology
• Dealing with day today stress
• Providing information about the importance of stress management and
regular habits
• Providing information about available treatment options, their efficacy/
effectiveness, side effects, duration of use
• Discussing about importance of medication and treatment compliance
• Providing information about possible course and long term outcome
• Discussing about problems of substance abuse, marriage and other issues
• How to detect early signs of relapse
• Discussing about Communication patterns, problem solving, disability
benefits
• Discussing about relapse and how to identify the early signs of new
episodes
• Improving insight into illness
• Handling expressed emotions and improving communication
• Enhancing adaptive coping to deal with persistent/residual symptoms
• Advise for lifestyle and dietary modifications
Interpersonal and social rhythm therapy (IPSRT)
This therapy is based on the theory that circadian rhythms in
patients with BPAD are vulnerable to external factors and any
disruption of circadian rhythms can precipitate an episode.
Accordingly, it emphasizes on regularizing the social rhythms
or routine of the patient and improving the interpersonal
relationships of the patients so that they can derive more
satisfaction in their social roles. The basic aim is to teach the
patient as to how they can prevent the development of a new
episode (Table-8). Patients are informed that new episodes
can be precipitated by poor medication adherence, stressful
life events and disruption of social rhythms. Patients are
provided with skills as to how they can address interpersonal
problems and issues in the social roles. They are also advised
to maintain a regular daily routine and pay attention to the
day to day stresses which can influence their daily routine
and how they can minimize the impact of these day to day
stressors on their daily routine.
Cognitive Behaviour therapy
Cognitive behaviour therapy (CBT) has been shown to be
efficacious in the management of bipolar depression and
during the maintenance phase of treatment. The basic
goals of CBT is to educate the patient about the illness,
teaching them cognitive behavioural skills for coping with
their illness and psychosocial stressors and problems
arising out of the same, enhance medication and treatment
compliance, monitor the symptoms to prevent relapse.
Family focused interventions
Family forms an integral part of treatment in Indian setting.
They are involved in treatment decision making, supervision
of treatment and monitoring of treatment. However, family
members can also contribute to relapse due to constant
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criticism, poor supervision or over-involvement. High
expressed emotion leads to increased risk of relapse and
poor outcomes. Studies have shown that family focused
interventions can reduce the chances of relapse, improve
medication adherence and reduce the frequency of
depressive episodes. Family focused interventions help
the relatives and patients to integrate the experiences
associated with mood episodes, acknowledging the
vulnerability of having future episodes, accepting the
need to continue with medications, educating the family
about the difference in patients personality and BPAD,
recognising and coping with stress and establishing a
functional relationship (Table-9).
Advise for life style and dietary modifications
As it is well known that patients with BPAD are at increased
risk for cardiovascular mortality and develop metabolic
side effects due to use of psychotropic medications, all
the patients need to be advised about life style and dietary
measures to reduce the risk of metabolic side effects and
cardiovascular morbidity and mortality. These include
physical exercises, dietary modifications and abstinence
from smoking, alcohol and other substances etc.
Rehabilitation
Rehabilitation programmes may be culturally moulded and
adapted to the needs of patients and their families.
Treatment adherence
Mediation and treatment adherence is very important for
management of patients with BPAD. Available evidence
suggests that 20-60% of the patients with BPAD become
non-compliant with medication and drop out of treatment.
Hence, all efforts need to be made to enhance the medication
compliance and treatment adherence. Measures which can
help in improving the compliance are given in table-10.
MANAGEMENT OF DIFFERENT PHASES OF
BIPOLAR DISORDER
Management of BPAD will depend on the phase of illness
in which patient presents to the clinician, i.e., bipolar
depression, bipolar hypomania/mania, first episode
hypomania/mania, mixed episode or clinical remission. In
addition to the phase of illness, factors which may help
in deciding about the pharmacological agent include past
history (number of episodes, type of episodes), comorbidity
(comorbid psychiatric/physical disorders, substance
dependence disorder), past treatment history (response,
side effects) and clinical course (rapid cycling), associated
symptoms (presence of psychotic symptoms) etc. In general
based on the level of evidence, various pharmacological
treatments are categorised as first line agents, second
line agents and third line agents. Selection of an agent
on the basis of current polarity and past history can be of
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Table 8: Basic components of Interpersonal and social
rhythm therapy (IPSRT)
Goals
• Stabilize daily routines and sleep/wake cycles
• Understand the bi‑directional relationship between moods and
interpersonal events
• Minimize or remove the interpersonal problems related to grief, role
transitions, role disputes, interpersonal deficits
Administered in 4 steps
Step‑1
• Give rationale for IPSRT
• History taking with special focus on understanding the relationship of
episodes with interpersonal problems and social routine
• Assess the patient’s current and past interpersonal relationships
• Educating the patient about bipolar disorder
• Identify interpersonal problem areas to focus, for example grief, role
transition, role dispute
• Agree on a topic to discuss
• Initiating the Social Rhythm Metric (i.e., quantify daily rhythms of life)
Step‑2
• Help the patient to establish a regular daily routine and resolve
interpersonal problems
• Analyse the communication patterns, identify the problematic
communication patterns, suggesting alternative communication
methods, role play
• Maintaining social rhythms
Step‑3
• In the continuation or maintenance phase encourage the patient to use
the skills learned in the previous phases of IPSRT
Step‑4
• Termination
Table 9: Basic components of Family focused
interventions
• Assessment of family
• Psychoeducation about symptoms, early recognition, etiology, treatment,
adherence
• Communication skills training ‑ behavioral rehearsal of effective speaking
and listening strategies
• Accepting that patient is vulnerable for having future episodes
• Able to differentiate between patient’s personality and bipolar disorder
• Recognising and coping with stress
• Problem‑solving skills training
• Establishing and maintaining a functional relationship
Table 10: Measures which can improve medication
compliance
• Explain when and how often to take medicines
• Preferably give once a day dosing
• Prescribe minimum number of tablets and medications
• Always ask the patient about kind of formulation (e.g. tablet, capsule etc)
which they would prefer to take
• Check the whole prescription to avoid duplication of medication
• Explain the patient/family that the beneficial effect will be seen only after
days to weeks of intake of medications.
• Explain the patient the need to take medication even after feeling better
• Explanation of side effects- If patients ask about the side effects, explain
the patient about the same.
• Explain the patient as to what to do‑ if they encounter side effects
• Encourage the patient to report side effects
• The need to consult with psychiatrist before discontinuing medications on
their own
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benefit, as in most cases, same agent is continued in the
maintenance phase.
The basic principles of management in the acute phase
are shown in Table-11. Clinicians may focus on carrying
out a comprehensive assessment (psychiatric/medical/
psychosocial), decide about the treatment goals, ensure
safety of the patient and others, decide about the treatment
setting, decide about the choice of medication in liaison
with the patient and the family by taking into account
the clinical and treatment related factors and institute
psychosocial interventions at the earliest so as to provide
comprehensive management. If patient is using alcohol or
other illicit substance, all efforts are to be made to stop
the same. Similarly, if a patient is on antidepressants and
presents with hypomanic/manic or mixed symptoms, these
need to be stopped immediately. Some of the indicators of
inpatient care are shown in Table-12.
All treatment decisions need to be made in consultation
with the patient and or family members and need to be
documented. Whenever mood stabilizers are used, the
required investigations need to be done prior to starting
of mood stabilizers, patient’s serum levels of medications
are to be monitored and other investigations need to be
repeated from time to time as indicated for various mood
stabilizers.
The evidence for efficacy of various agents in management of
different phases of illness (mania, depression, maintenance
phase) vary and it is important to be aware of the same.
Table-13, provides an update on the available level of
evidence for different phases of illness.
MANAGEMENT OF HYPOMANIA/MANIA/
MIXED EPISODE
The goal of management in mania/mixed episode is to
control the aggression, agitation and disruptiveness of
patients at the earliest. Depending of the severity of
symptoms, inpatient care may be considered. If patient is
on antidepressants then this is to be stopped immediately.
In terms of pharmacological management, first line agent
for management of mania may involve use of lithium or
valproate, olanzapine, haloperidol, quetiapine, aripiprazole,
risperidone, paliperidone or ziprasidone as monotherapy.
Typical antipsychotics like haloperidol, trifluoperazine and
chlorpromazine have also been used in the Indian scenario.
These are very useful in the management of irritability,
aggression, impulsivity and psychotic features. However,
these are associated with high incidence of extrapyramidal
reactions. However, there is some evidence to suggest that
combining lithium or valproate with an antipsychotic may be
more effective than any of these agents when used alone.
Indian J Psychiatry 59 (Supplement 1), January 2017
Table 11: Management in the acute phase
•Comprehensive assessment (psychiatric (including alcohol and
substance)/medical/psychosocial)
• Discontinue antidepressants if indicated (patient exhibiting hypomanic/
manic/mixed symptoms)
• Deciding on goals of treatment
• Patients
- Eliminate/reduce symptoms of phase of illness in which patient presents
with and improve the level of functioning
- Promote safety, reduce risk of harm, and reduce stress
• Caregivers
- Minimise caregiver distress
- Offer help to enable them to cope with the illness in their relative
• Both
- Develop a therapeutic alliance and provide opportunities for patients and
- Caregivers to actively engage in treatment
- Offer basic information and support tailored to needs of patients and
caregivers
• Choice of treatment setting
• Choice of medication
- Type and severity of current episode
- Type of past episode (s)
- Predominant polarity
- Past treatment history‑ response, side effects, compliance
• Use of adjunctive medications when indicated
• Use of ECT when indicated
• Psychosocial interventions
• Planning for further treatment‑ Pharmacoprophylaxis
Table 12: Some indications for inpatient care during
acute episodes
Mania/mixed
• Presence of severe agitation or violence which puts the life of others at
risk
• Presence of general medical or comorbid psychiatric conditions that
make outpatient treatment unsafe or ineffective
• Patient not responding to a combination of first line agents
• Treatment‑refractory mania/mixed episode
Depression
• Presence of suicidal behaviour which puts the life of the patient at risk
• Presence of severe agitation or violence which puts the life of others at
risk
• Refusal to eat which puts the life of patient at risk
• Severe malnutrition
• Patient unable to care for self to the extent that she/he requires constant
supervision or support
• Catatonia
• Presence of general medical or comorbid psychiatric conditions that
make outpatient treatment unsafe or ineffective
• Patient not responding to a combination of medications
Among these agents, lithium is thought to have slower onset
of action. Accordingly, it can be said that if the mania is
less severe, monotherapy be considered. However, if mania
is severe and associated with significant disruption than
combination therapy need to be considered. Use of adjunctive
benzodiazepines for short duration may be required.
Patients who refuse medications and are unmanageable may
be given depot antipsychotics like risperidone, paliperidone,
olanzapine or a depot of typical antipsychotic medication.
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Table 13: Comparison of several monotherapy and combination Pharmacotherapies for bipolar disorders
Bipolar Mania Bipolar Depression Mixed episodes Prevention of Prevention of
relapse of depression relapse of mania
Monotherapy
Lithium (Li) √ √ √ √ √
Valproate (V) √ @ √ √ √
Lamotrigine (L) X √ NA √ X
Carbamazepine (C) @ ? X @ @
Oxcarbazepine (O) ? NA NA NA NA
Topiramate (T) X X NA X X
Gabapentin X NA NA X X
Olanzapine (OLZ) √ ? ? √ √
Quetiapine (Q) √ √ NA √ √
Asenapine (ASP) √ NA NA NA ?
Aripiprazole (ARP) √ X ? X √
Risperidone (R) √ NA √ NA @
Paliperidone √ NA ? NA @
Haloperidol @ NA NA NA
Ziprasidone √ X ? NA @
Chlorpromazine ? NA NA NA NA
Clozapine ? NA NA NA NA
Cariprazine NA ? NA NA NA
Lurasidone NA @ NA NA NA
Combination
Li + V √ √ √ √ √
Li + OLZ √ NA NA ? √
Li + R √ NA NA NA √
Li + L NA @ NA NA NA
Li + C NA ? NA NA NA
Li + SSRI NA √ NA NA NA
Li + Venlafaxine NA ? NA NA NA
(Li/V) + ARP ? X NA NA NA
(Li/V) + ASP ? NA NA NA NA
(Li/V) + (Q/ARP/Z) NA NA NA NA √
V + OLZ NA NA ? NA NA
V + SSRI NA √ NA NA NA
OLZ + SSRI NA √ NA √ NA
OLZ + C X NA NA NA NA
R+C X NA NA NA NA
L+Q NA ? NA NA NA
√ – Established efficacy; @ – Efficacy not Established clearly; X – Established that not useful; ? – Evidence limited to open label studies; NA – Evidence not available

If a patient comes with a ‘breakthrough’ hypomanic/manic
episode, then the first step in the management involves
optimization of the ongoing agent. The optimisation can be
done by monitoring the serum levels of agents like lithium
and valproate. If required, additional antipsychotics and
benzodiazepines may be used, depending upon severity of
the episode.
If the first-line agent used in optimal dose fails (lack of
significant clinical benefit after 2 weeks of use), another
first line agent need to be added to the ongoing treatment.
Alternative strategies may include changing lithium to
valproate or vice versa, changing to carbamazepine, adding
antipsychotic medication if not used earlier, changing
the antipsychotic if used earlier. ECT may be considered
if patient is very disruptive, not responding to a trial of
combination of medications, has history of good response
to ECT in the past, pregnancy and those experiencing mixed
episode. Psychosocial interventions like psychoeducation
of patient and family and family focused intervention be
started at the earliest. Psychosocial interventions like CBT
or IPSRT, focused specifically on the patient, should be
considered when patient is cooperative.
MANAGEMENT OF BIPOLAR DEPRESSION
The main goal of management is to achieve euthymia,
normal level of functioning and to avoid switching to
hypomanic/manic episode. Among the various mood
stabilizers, there is ample evidence to suggest that lithium
and lamotrigine may be used as the first line medications in
the management of bipolar depression.
If the patient presents with a breakthrough episode, the
initial strategy is to check the medication compliance and
ensure adequate compliance. If compliance is not an issue,
initial strategy is to optimise the mood stabilizer which the
patient is already getting.

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 Shah, et al.: CPGs for bipolar disorders
If the patient is not on any mood stabilizer, than lithium or
lamotrigine may be considered. Among the antipsychotics,
data suggests that quetiapine monotherapy may also be
beneficial. There is evidence for use of olanzapine and
fluoxetine combination too. If the patient does not respond
to monotherapy with mood stabiliser or antipsychotics,
combination of these agents with antidepressants may
be considered. Use of antidepressants without the use of
concurrent mood stabilizer or an atypical antipsychotic is
to be avoided. Benzodiazepines may be used as per the
need. Psychosocial intervention in the form of CBT may also
be considered when the depression is of mild to moderate
severity. ECT may be considered, if depression is severe,
in presence of suicidality, risk of harm to others, catatonic
symptoms, psychotic symptoms, patient is pregnant, when
use of various psychotropics is limited due to concurrent
medical illnesses. There is preliminary evidence to suggest
the beneficial effect of transcranial magnetic stimulation
and direct cranial stimulation.
RAPID CYCLING AFFECTIVE DISORDER
Rapid cycling affective disorder (RCAD) is
characterised by having 4 or more episodes
(depression/mania/hypomania/mixed) in a single year.
These episodes should be separated from each other by
partial or full remission for at least 2 months or a switch
to an episode of opposite polarity. Many risk factors
(Table-14) have been identified for development of
RCAD. Accordingly, the first step in the management of
RCAD is to evaluate the patients for underlying medical
conditions which may be contributing to the RCAD. Among
medications, use of antidepressants has been shown to
increase cycling.
In terms of psychotropics, there is evidence to suggest that
lithium or valproate may be used as the first line agents.
Other mood stabilizers which can be considered include
lamotrigine. If patient does not respond to monotherapy,
then combination of mood stabilizers or a combination
of mood stabilizer and antipsychotic medication may be
considered.
MAINTENANCE TREATMENT FOR BIPOLAR
DISORDER
The primary goal of maintenance treatment is to prevent the
recurrence of episode of either polarity, reduce/eliminate
the residual symptoms and improve the overall functioning
of the patient. In terms of pharmaco-therapeutic agents, best
evidence for maintenance treatment is available for lithium
and valproate. In recent years evidence has also emerged for
use of olanzapine and quetiapine in prevention of recurrence
of both depressive and manic episodes. However, these may
be avoided because of associated higher risk of metabolic
Indian J Psychiatry 59 (Supplement 1), January 2017
Table 14: Risk factors for Rapid Cycling Affective
Disorder
Risk factors for RCAD
• Hypothyroidism
• Long term aggressive use of antidepressants
• Comorbid substance use
• Minor tranquilizer/stimulant or caffeine abuse
• Cyclothymic and hyperthymic temperament
• Female gender
• Menopause
• Temporal lobe dysrhythmias
• Several episodes/stressors as an effect of kindling
• Onset of illness as depression
• Frequent and more depressive episodes
• ? COMT/BDNF gene abnormality
• ? Biological rhythm disturbances like wakefulness, light exposure
side effects. Long acting risperidone has been shown to
be beneficial in prevention of recurrence. Lamotrigine has
been shown to be efficacious in prevention of depressive
episodes, but not for prevention of manic episodes.
Olanzapine, aripiprazole, ziprasidone and asenapine has
been shown to be of benefit in prevention of recurrence
of manic episodes, but not for depressive episodes.
Carbamazepine has also been shown to be effective in
prevention of recurrence; however, it is less preferred
compared to lithium and valproate because of its side effect
profile and drug interactions. Studies have also evaluated
the efficacy of lithium and valproate in combination with
various antipsychotics. Besides use of pharmacotherapy,
there is evidence to suggest the beneficial role of adjunctive
psychosocial intervention in the management of BPAD.
Maintenance ECT may also be considered in patients who
have responded to ECT during their acute episodes.
The general principle of management during the
maintenance phase of treatment is to continue the
medication started during the acute phase of illness.
Accordingly, while selecting the agent during the acute
episode, clinicians may take into consideration the patient’s
preference, clinical factors which may influence the long
term outcome, recurrence of episodes and side effects.
If the patients have more manic episodes then one may
prefer lithium, valproate or carbamazepine while for more
depressive episodes one may consider Lithium, lamotrigine
or quetiapine. In severe cases, combination of lithium and
valproate may be considered.
It is important to note that patients with mood disorders are
more vulnerable to extrapyramidal side effects like tardive
dyskinesia with long term use of antipsychotics, especially
typical antipsychotics. Patients who have been treated with
a combination of lithium and antipsychotic or valproate and
antipsychotic medication, the need for continued use of
antipsychotic need to be reassessed on the basis of longitudinal
course. Similarly, stoppage of antidepressants needs to be
considered once bipolar depression remits. Combination
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Bipolar Hypomania/Mania/Mixed Episode

Currently on treatment (Breakthrough Currently not on treatment

episode/switch in presence of First line therapy:
antidepressants) • Monotherapy: Lithium, valproate, antipsychotics
• Stop antidepressant- if patient • Combination: Lithium+ antipsychotic/
is getting the same valproate+antipsychotic
• Optimize the dose of the mood • Use Benzodiazepines as per the need
stabilizer which the patient is on • Use of depot antipsychotic may be considered
• If the symptoms do not respond if patient is not willing to take oral medications
to optimisation of the dose or are • ECT: may be considered with monotherapy or
severe, consider adding an combination therapy as per the indication
antipsychotic medication
• Benzodiazepines may be used
depending upon the need
Failure of adequate trial of
first line treatment

Second line therapy:

Failure of adequate trial of
first line treatment
Monotherapy: Change lithium to lamotrigine or vice
versa
Combination:
• Add antipsychotic if not used
• Change from Lithium+ antipsychotic to
valproate+antipsychotic medication
• Change from Valproate+antipsychotic to
lithium+antipsychotic medication
• Continue lithium/valproate and change the
antipsychotic medication
• Consider changing lithium/valproate to carbamazepine
• Use Benzodiazepines as per the need
• Use ECT if not considered earlier
• Consider clozapine if mania is treatment refractory
• Consider other agents

Figure 2: Management of Hypomania/ Mania/Mixed Episode

therapy during the maintenance phase is to be considered
only for those who have not responded to the optimal dose of
monotherapy during the maintenance phase of illness.
SPECIAL SITUATIONS
Clinicians often encounter certain clinical situations which
either require special attention or can influence treatment
decisions. Management of these situations is summarised
in table-15.
SIDE EFFECTS AND THEIR MANAGEMENT
Various classes of psychotropic medications used for the
management of BPAD are associated with many side effects,
which require intervention. The side effects associated
with antipsychotics are discussed in the clinical practice
guidelines for schizophrenia. The recommendations made for
monitoring of metabolic side effects associated with various
atypical antipsychotics may also be followed in patients with
BPAD, if long term antipsychotic medications are considered.
Use of lithium is associated with multiple side effects. These
side effects can be classified on the basis of occurrence (i.e.,
those occurring during the early or late phase of treatment)
and frequency (Common, uncommon, rare and very rare)
(Table-16). Most of these side effects can be managed with
reduction in dose of medication or shifting to a sustained
release preparation as the first line strategy.
The common management strategies for the side effects
associated with lithium, valproate and carbamazepine are
shown in Table-17.

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Bipolar Depression

Already on treatment Not on treatment

Valproate, Lithium First line therapy:

Olanzapine, Lamotrigine • Monotherapy/combination: Lithium, lamotrigine,
Risperidone, Antipsychotics quetiapine, olanzapine-fluoxetine combination,
other valproate+lithium, valproate+ antidepressant
atypicals • Combination: mood stabiliser/antipsychotics+
antidepressant
• Psychosocial intervention: if depression is
mild to moderate
• ECT: may be considered with monotherapy or
combination therapy as per the indication
Optimise the Optimise the
dose dose

• Add antidepressant – bupropion, SSRI

• Add or change to lithium, lamotrigine or quetiapine
• Consider changing from one agent (lithium/lamotrigine/quetiapine) to other
• Consider Valproate along with lithium or antidepressant
• Consider combinations
• Consider psychosocial intervention if the depression is mild to moderate
• Consider ECT as per the indication
• Consider rTMS, tDCS

Figure 3: Management of Bipolar Depression

Table 15: Issues related to special situations

Special Strategies
situation
Suicidality • Risk of suicide is high in patients with BPAD.
• Suicidal behaviour is seen during the depressive episode, mixed episode and also in manic episode. Suicide have also been reported
during the euthymic phase
• Clinicians need to carefully evaluate the patients for suicidal ideations, plans, suicidal attempts at every follow‑up.
• High risk management be instituted and inpatient management may be considered if the patient is at high risk.
• Psychoeducation of patient and family need to focus on discussing about warning signs of suicide. Patients experiencing severe distress
due to a feeling of loss, stigma etc., are to be provided psychological support and monitored closely.
• Use of lithium has been shown to lower the risk of suicide.
• ECT is an important therapeutic option in patients at high risk of suicide during an acute episode.
Catatonia • Catatonic features may be seen in both depressive and manic phase of illness.
• Whenever a patient with BPAD presents with catatonia, all possible differential diagnosis for catatonia need to be considered.
• Investigate to rule out organic cause (s).
• Initial management may involve use of benzodiazepines, especially lorazepam, which leads to symptomatic relief in significant proportion of cases.
• In case the catatonia does not respond to benzodiazepines or relapse after stopping benzodiazepines, ECT is to be considered.
Psychotic • Psychotic symptoms are seen in a significant proportion of patients with BPAD.
features • When present, use of antipsychotics is warranted.
Violence and • All patients, especially those in mania need to be evaluated for violence and dangerousness during every assessment, especially during
Aggression the acute phase of illness.
• Whenever a patient is found to have serious threat for violence or exhibits violence, inpatient management may be considered.
• Injectable antipsychotics like haloperidol or lorazepam can be used for management of violence and aggression.
Comorbid • Substance use can precipitate an episode, increase the frequency of episode, may be associated with RCAD, higher risk for suicide, poor
Alcohol and response to treatment, longer time to achieve remission, can influence the choice of medication, lead to higher vulnerability for side effects.
Substance • Both BPAD and substance use disorders need to be treated concurrently.
use Disorders • Efforts need to be made to keep the patient abstinent from alcohol and other substance(s), both during the acute episodes and during the
maintenance phase of illness.
Comorbid • Patients of BPAD have high rate of comorbid anxiety disorders, ADHD etc.
Psychiatric • Comorbid disorders, may not be evident during the acute episodes. Accordingly, patients need to be evaluated during the maintenance
disorders phase for any kind of comorbid psychiatric disorders.
• Management of comorbid disorders need to be done along with concurrent management of BPAD.
Comorbid • Patients with bipolar disorder have high rate of physical comorbidities.
Physical • All patients need to receive thorough assessment for possible physical illnesses and depending on the feasibility may be investigated as
illnesses per the requirement.
• Those with comorbid physical illnesses are to be continuously monitored during all the phases of treatment.
• Comorbid physical illnesses and concomitant medications also need to be taken into account while selecting the treatment setting and
antipsychotic medication per se.
Contd...
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Table 15: Contd...
Special Strategies
situation
Perioperative • When used during the perioperative period, lithium can contribute to hemodynamic instabilities, interfere with sodium and potassium
period metabolism, and the renal excretion of lithium can be reduced in presence of renal complications. Therefore it is recommended that
lithium need to be discontinued prior to surgery.
• Postoperatively, when the patient is hemodynamically stable, is able and allowed to drink, and is not on potentially interfering drugs, the
medication may be restarted gradually.
Pregnancy • Mood stabilizers, including lithium are considered to be teratogenic and associated with higher rate of congenital malformations.
• Pregnancy is to be planned.
• Whenever feasible, exposure to lithium, valproate, carbamazepine, lamotrigine need to be avoided during pregnancy. Hence, attempt
need to be made to discontinue these medications.
• If patient is not able to tolerate the discontinuation of medication, than the pros and cons of continuation of the medications during the
first trimester need to be discussed and documented.
• If required, lithium may be used during second and third trimester of pregnancy; Use the minimal optimal dose.
• If required, antipsychotics, especially high potency typical antipsychotics may be considered.
• Use folic acid during pregnancy.
• If patient is receiving mood stabilizer during the pregnancy – monitor alpha feto‑protein levels at 20 weeks.
Post‑partum • There is high risk of relapse during the post‑partum period.
& Breast • The new‑born be evaluated thoroughly, if the mother was on psychotropics during pregnancy for malformations, drug overdose and withdrawal.
feeding • Lithium need to be used with caution during the postpartum.
• When valproate is used during the post‑partum, liver function tests and haemogram of the neonate need to be monitored adequately.
Elderly • Have high rates of comorbid medical illnesses and substance use disorders.
• More sensitive to side effects of medications, at risk for fall and fracture of hip.
• May develop cognitive deficits with use of lithium or benzodiazepines.
• Start low and go slow.
Children & • Have high rates of comorbidity in the form of Attention‑hyperkinetic disorder (ADHD), conduct disorder, substance use disorders.
Adolescents • At times it may be difficult to distinguish between symptoms of mania and ADHD.
• Take longer time to stabilize.
• Data on use of lithium before 12 years of age is not available and use of lithium prior to this age is not recommended.
• Start at lower doses and titrate slowly.

MANAGEMENT OF TOXICITY Table 16: Side effects of lithium

Early onset side effects Common side effects
Among the lithium, valproate and carbamazepine, valproate Weight gain Short term dose related
has a wide therapeutic window. Lithium and carbamazepine Tremor Nausea, diarrhea, epigastric pain
toxicity may be fatal and are medical emergencies. The Anorexia, Nausea, Diarrhea Tremor
Aggravation of cutaneous Thirst, polyuria
therapeutic range for serum lithium levels varies from conditions Metallic taste
0.4 to 1.2 meq/litre. Toxic effects of lithium are usually Mild thirst Long term side effects
seen when the serum levels of lithium rise above 1.5meq/ Polyuria Weight gain
litre. When the levels exceed 2meq/litre, life threatening Late onset side effects Hypothyroidism in women
Nephrogenic diabetes insipidus Reduction in eGFR
side effects may emerge. Various signs and symptoms Hypothyroidism Tubular dysfunction
of toxicity with lithium, valproate and carbamazepine Thyroiditis Uncommon side effects
are shown in Table-18.Management of lithium toxicity Hyperthyroidism Fluid retention (oedema)
is an acute emergency and involves stoppage of lithium, Cognitive dulling Hypothyroidism
Rare side effects
maintaining the airways, maintaining an intravenous line
Acne
and use of haemodialysis if serum lithium levels are more Psoriasis
than 2.5 mEq/Litre. However, in patients with end stage Hair loss
renal disease, haemodialysis may be considered in levels Fatigue
below 2.5mEq/litre as well. Arrhythmia
Cognitive deficit
Seizures
Management of valproate toxicity also involve use of Sexual side effects
haemodialysis. However, there are no clear guidelines for Very Rare side effects
the same. Management of carbamazepine intoxication ↑WBC count
↑serum Ca++, Mg++
involves gastric lavage, hemoperfusion and use of supportive ↑ parathyroid hormone
measures. ↑blood sugar
Benign intracranial hypertension
Financial support and sponsorship Parkinsonism disease’s like
symptoms
Nil.

S64 Indian J Psychiatry 59 (Supplement 1), January 2017

 Shah, et al.: CPGs for bipolar disorders

Table 17: Management of side effects of mood stabilizers

Side effects Management
Lithium
Dose‑related side effects: polyuria, polydipsia, weight gain, Reduce the dose and/or shift to once a daily dose of medications, if the side effects
cognitive problems (e.g., dulling, impaired memory, poor still persist than use other medications:
concentration, confusion, mental slowness), tremor, sedation Tremors: beta‑blockers
or lethargy, impaired coordination, gastrointestinal distress Polyuria, polydipsia, edema: diuretics
(e.g., nausea, vomiting, dyspepsia, diarrhoea), hair loss, benign Acne: Topical antibiotics, retinoic acid
leukocytosis, acne, and edema Gastrointestinal side effects: give lithium after meals, change to lithium citrate
Electrocardiogram (ECG) Changes Cardiac Side effects: Reduce the dose, if the abnormalities persist, may have to stop
lithium in consultation with the cardiologist depending on the severity of the cardiac
conduction abnormalities
Renal Side effects: Impaired concentrating capacity, interstitial Renal side effects: Diuretics for impaired concentrating capacity‑ thiazides, amiloride
fibrosis, tubular atrophy
Hypothyroidism Hypothyroidism: Not an indication for stopping lithium, add levothyroxine
Dermatological: Reduce the dose, appropriate dermatological treatment, if does not
respond then may consider stopping lithium
Psoriasis Inositol supplementation, TNF α inhibitors (Etanercept), Conventional treatment of
Psoriasis (Topical corticosteroids, Keratolytics, Vitamin D analogues, Oral retinoids,
Psoralen, Ultraviolet A (PUVA) therapy , Methotrexate)
May have to consider stopping lithium in treatment resistant cases of psoriasis
Valproate
Dose‑related side effects: Gastrointestinal distress (nausea, Resolve with reduction in dose, if persist, then
vomiting, diarrhoea etc), tremor, sedation, benign hepatic GI disturbances: change of preparation from Valproic acid to Divalproex,
transaminase elevations Proton‑pump blockers, Histaminic blockers
Tremors: beta‑blockers
Hepatotoxicity Discontinuation of valproate
Leukopenia, Thrombocytopenia Discontinuation of valproate
Hair loss, increased appetite, weight gain Dietary restriction for increased appetite and weight gain
Polycystic ovarian disease May have to discontinue valproate if other options are available, metformin
Hepatic failure, haemorrhagic pancreatitis, and Discontinuation of valproate
agranulocytosis
Carbamazepine
Ophthalmological: diplopia, blurred vision Reduce the dose
Gastrointestinal: nausea Reduce the dose
Neurological: ataxia Reduce the dose
Dermatological: skin rashes Reduce/Stop Carbamazepine
Haematological: leukopenia, thrombocytopenia Mild leukopenia may resolve on its own, in case of severe leukopenia, stop the
medication
Electrolyte imbalance: Hyponatremia May require discontinuation of carbamazepine
Endocrine: hypothyroidism May require addition of levothyroxine
Serious side effects: agranulocytosis, aplastic anemia, Stop Carbamazepine, manage the medical condition
thrombocytopenia, hepatic failure,
Stevens‑Johnson syndrome, pancreatitis

Table 18: Signs and symptoms of Toxicity of lithium, Table 18: Contd...

valproate and Carbamazepine Carbamazepine
Lithium levels 1.5‑2‑5 meq/litre Dizziness, Ataxia, Sedation, Nystagmus, Ophthalmoplegia, Cerebellar
Neurological: Fine tremors, Apathy, Fatigue, Muscle weakness, and extrapyramidal signs, Impaired consciousness, Seizures, Respiratory
Hyperreflexia, Incontinence, Gait disturbances depression, Stupor, Coma, Tachycardia, Arrhythmia, Cardiac conduction
Gastrointestinal: nausea, vomiting, diarrhoea disturbances, Hypotension
Cardiovascular changes: Bradycardia, T‑wave changes, sinoatrial block, AV
block
Lithium levels >2.5 meq/litre Conflicts of interest
Neurological: course tremors, slurring of speech, dysarthria, ataxia, There are no conflicts of interest.
hypertonia, spasticity, rigidity, myoclonus, seizures, stupor, coma,
permanent neurological deficits
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Indian J Psychiatry 59 (Supplement 1), January 2017
 CLINICAL PRACTICE GUIDELINES

Clinical Practice Guidelines for the Management of Generalised Anxiety

Disorder (GAD) and Panic Disorder (PD)
Shiv Gautam, Akhilesh Jain, Manaswi Gautam, Vihang N. Vahia, Anita Gautam

Participants of expert group on CPG for Generalised
Anxiety Disorder (GAD) and Panic Disorder
S.C Tiwari, Nilesh Shah, I.D. Gupta, B.N. Gangadhar,
Devendra Vijay Vergiya, Pratap Sharan
INTRODUCTION
Short description of anxiety disorders
Generalized Anxiety Disorder (GAD)
Definition: One of the anxiety disorders, where the primary
symptoms of anxiety are present at most days for at least
several weeks at a time, and usually for several months. The
symptoms should usually involve elements of:
(a) Apprehension (worries about future misfortunes,
feeling “ on edge”, etc)
(b) Motor tension (restlessness, inability to relax, trembling)
(c) Autonomic over activity (light-headedness, sweating,
tachycardia, tachypnea, dry mouth etc)
The transient appearance of depressive symptoms, does
not rule out the diagnosis of GAD as main diagnosis. The
sufferer must not meet the full criteria for depressive
episode, phobic disorder, panic disorder or OCD.
Patients with generalised anxiety disorder have high anxiety
and are worried about intrapsychic conflicts or external
environmental events. They have multiple somatic symptoms
of anxiety, restlessness, difficulty in concentration, irritability,
fatigue, muscular tensions and difficulty in sleeping
particularly early insomnia. They have vague apprehension
about future events and fear of unknown. Common features
observed in anxiety disorders include:
Address for correspondence:
Dr. Shiv Gautam, Director Professor, Gautam Institute of
Behavioral Sciences and Alternative Medicine, Jaipur.
E-mail: dr_shivgautam@yahoo.com
Access this article online
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Website:
www.indianjpsychiatry.org
Panic Disorder- Episodes of intense fear or discomfort
accompanied by severe autonomic activity, palpitations,
sweating, dyspnoea, chocking sensation or other somatic
symptoms like chest pain, trembling, nausea, discomfort
or fluttering sensation in abdomen and impending fear of
death. Patient perceives it as a serious medical condition
and invariably reaches to a medical emergency setup where
after thorough physical evaluation he is declared normal.
Phobias-  Many patients with GAD suffer from irrational,
unrealistic fears and acute autonomic reactions to certain
specific situations or extreme fear to certan inanimate objects.
They include agarophobia (fear of open spaces) fear of crowds,
being out side home alone or traveling in a bus train or car.
Some may have fear in closed spaces (claustrophobia) fear of
heights (acrophobia) fear of opposite sex (hetero-phobia) fear
of sight of blood (erythrophobia) or fear of facing certain social
situations (social anxiety disorder) the common feature among
all phobias being intense fear, increased autonomic activity and
avoidance behavior (avoiding the fearful object or situation).
Obsessive compulsive disorder- (OCD) has been seperately
dealt with in details in these guidelines however the
patients suffering from OCD have recurrent repetitive
unwanted intrinsic thoughts (obsessions) or actions
(compulsions) or both which lead to extreme distress, loss
of time and impairment of functioning of the individual. The
obsessious include douts, ideas of contamination, sexual
thoughts or religious preoccupations or negative thoughts
towards gods/goddess, the compulsions include activities
like counting, checking, repeating, washing hoarding
and touching objects, some have to and fro movements
of body parts. Patient is aware of the irrationality of
thoughts/actions but cannot control them, which produces
intense anxiety and autonomic arousal with feelings of
helplessness and guilt.
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How to cite this article: Gautam S, Jain A, Gautam M,

DOI:
Vahia VN, Gautam A. Clinical Practice Guidelines for the
Management of Generalised Anxiety Disorder (GAD) and
10.4103/0019-5545.196975
Panic Disorder (PD). Indian J Psychiatry 2017;59:67-73.

© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow S67

 Gautam, et al.: CPG for GAD & Panic Disorder

Post-traumatic stress disorder (PTSD) - Usually it occurs after COMMON INGREDIENTS OF MANAGEMENT

a terrifying event that involving physical or psychological PLAN (FLOW CHART-1 AND 2)
traumatic event. It may also occure because of witnessing
or experiencing a serious harm to other significant persons The aim of management is to provide relief in psychological
in life. Patients have terrifying recollections of the event, or and somatic symptoms and minimize the impairment. This
nightmares. Some patients have an experience of living the can be addressed in following ways.
event in an illusionary or imaginary situation with hallucinations,
or flashback episodes. The patients suffer from intense 1. Pharmacotherapy
psychological or physical distress. Many patients develop loss The drug treatment of GAD is some times required as long
of interest, estrangement from others, sleep disturbances, as 6-12 month treatment, some evidence indicate that
irritability, diffi culty concentrating, hypervigilance, and treatment should be long term.
exaggerated startle response. This phenomenon may persist
for one month or more before it is diagnosed. 2. Psychotherapy
i. Cognitive behaviour therapy
Natural history and course ii. Behavioural techniques
The age of onset is difficult to specify, as most of the patients iii. Supportive Psychotherapy
have been anxious for long but report late. Nearly 1/3rd of iv. Insight oriented Psychotherapy
the patients who have GAD seek psychiatric treatment.
Many go to GPs, physicians, cardiologist, chest specialist Goals
for the somatic component of the disorder. Because of the • Psycho-education Direct explanation of the symptoms
high incidence of co-morbid mental disorders, the course and disorder to the patient and the family.
and prognosis is difficult to predict.The occurrence of • Monitoring of anxiety
several negative life events greatly increases the likelihood • Cognitive restructuring: Corrects the hypothesized
that the disorder will develop. In all, a chronic condition cognitive distortions and helps to identify and counter
may be life long. fear of bodily sensations.

Patient Presenting with Anxiety

GAD
Diagnosis by ICD 10 Criteria

Psychopharmacology Psychosocial Intervention Psychopharmacology

combined with Psychotherapy

Benzodiazepines

Clonazepam Cognitive – behaviour therapy Long-term outcome is better when

Chlordiazepoxida
Diazepam
Alprazolam
Iniate from minimum adequate
Dose/ prescribed for a limited
Period (6-8 weeks)
Use with caution for dependence
Relaxation therapy they are used in combination.
Yoga & Meditation
Supportive Psychotherapy
Insight therapy
Family therapy
Psycho education

SSRIs Paroxetine; Sertraline; Fluoxetine Appendix– Flowchart - 1

Venlafaxine GAD
SNRI
Mirtazapine
NaSSA
Other Buspirone

TCA Tricyclic & Tetra cyclic

Beta Blockers Propranolol

Flowchart 1: Management of Generalized Anxiety Disorder

S68 Indian J Psychiatry 59 (Supplement 1), January 2017

 Gautam, et al.: CPG for GAD & Panic Disorder

PANIC DISORDER
Diagnosed by ICD 10

Acute Attack Long Term Care

Psychopharmacological Psychotherapy Psychopharmacological Psychotherapy

Treatment Treatment

i. SSRI- i. CBT i. BZDs CBT

Fluoxetine ii. Psychodynamic ii. SSRIs Psychodynamic
Paroxitine Psychotherapy iii. TCAs Psychotherapy
Sertraline iii. Group therapy iv. Venlafaxine Group therapy
Fluvoxamine v. NaSSA
Citalopram vi. Beta Blockers
ii. BZDS (Propanlol)
Alprazolam Ravi Kiran Mathur
Clonazepam
Diazepam

iii. SNRI
Venlafaxine

iv. NaSSA

v. Beta Blockers : Propanlol

Useful when combined
With BZDs

vi. TCAs
Imipramine
Clomipramine

Flowchart 2: Management of Panic Disorder

Efficacy It includes history of present illness, current symptoms;

Cognitive Behavioural Therapy has proven efficy other
psychotherapies do help in ameliorating symptoms of
anxiety. It addresses cognitive distortions and somatic
symptoms. More effective with chronically anxious
patients, may need 8-10 sessions. It has been shown that
yogic techniques produced greater motivation to practice
than progressive relaxation Meditation was found to be as
effective as pharmacotherapy in controlling symptoms of
anxiety. The overall efficacy claims are backed by very few
Indian studies, but are useful. It requires considerable time
and discipline from the patients.
Adverse effects
These are relatively benign. Some patients may develop
dependence on the therapist and that needs cautious
vigil.
3. Combined pharmacological and psychotherapeutic
intervention
Long-term outcome is better when they are used in
combination.
ASSESSMENT AND EVALUATION
1. Performing a diagnostic evaluation
Psychiatric evaluation and physical examination
necessary.
past psychiatric history, general medical history and history
of substance use, personal history (eg. psychological
development, life events and response to those events),
social, occupational and family history; review of the
patient’s medications; physical and mental status
examination and adequate diagnostic tool and criteria.
Diagnose GAD according to ICD-10 (W.H.0,1992).
Anxiety should not be due to the other Axis I disorder
(eg. mood disorder, psychotic disorder, social phobia, OCD,
somatization disorder, hypochondriasis, PTSD) or a general
medical condition (eg. hyperthyroidism) or substance use
disorder (intoxication or withdrawal), (see appendix-1 for
flow chart).
2. Evaluating particular symptoms
Patients experience excessive anxiety but many of them
experience panic attacks, which may worsen the clinical
picture. The prolonged illness may cause depressive symptoms
with emergence of suicidality and substance abuse.
3. Evaluating severity of functional impairment
Many may continue to function in their social and
occupational lives with some impairment, others may
become severely incapacitated and give up their jobs and
is social duties. The impairment in different areas can be
assessed self-administered visual analog scale.

Indian J Psychiatry 59 (Supplement 1), January 2017 S69

 Gautam, et al.: CPG for GAD & Panic Disorder
FORMULATING TREATMENTS AND CHOICE OF
TREATMENT SETTINGS
The aim of management is to provide relief in psychological
and somatic symptoms and minimize the impairment. This
can be addressed in following way.
1. Establishing and maintaining atherapeutic alliance
The treatment of GAD may be long lasting hence the
alliance is crucial. Understanding the life events, the extent
and severity of symptoms requires confiding and lasting
therapeutic relationship.
Attention to the patient’s worries and fears are essential for
long term gains
2. Monitoringthe patient’s psychiatric status
The symptomatic improvement in psychological and
autonomic symptoms leads to greater confidence in the
treating doctor. The anxiety goes slowly with treatment
and bursts of severe symptoms during the treatment need
constant monitoring.
3. Pharmacotherapy
The drug treatment of GAD is some times is seen as
a 6-12 month treatment, some evidence indicate that
treatment should be long term.
a). Goals
Reduce psychological and autonomic symptoms and other
co morbid conditions. Improve occupational and social
functioning.
b). Efficacy
Little Indian data to address the issue; mainly western data
available.
c). Adverse effects
Different for different class of drugs.
Selective serotonin reuptake inhibitors (SSRIs), serotonin-
norepinephrine reuptake inhibitors (SNRIs), and pregabalin
are recommended as first line drugs due to their favorable
risk-benefit ratio, with some differentiation regarding
the various anxiety disorders. The common category of
pharmacological agents used in management of generialised
anxiety disorders include SSRIs,SNRIs, Pregabalin, TCAs,
Benzodiazepines, Antihistamines, Atypical antipsychotics,
and Antioxidants. Role of vitamin A, C and E has been
evaluated and recommended in adequate doses for patients
suffering from GAD.
Dosing
Majority of patients respond to the low dose of
antidepressants (with the exception of OCD). In the elderly,
S70
treatment should be started with half the recommended
dose or less in order to minimize initial adverse drug events.
The antidepressant dose should be increased to the highest
recommended therapeutic level if the initial treatment with
a low or medium dose fails.
For patients who do not improve with standard treatments,
a number of alternative options should be tried including
augmentation with small dose of antipsychotics or adding
another anxiolytic agent or addition of non-pharmacological
therapy like cognitive behavioral therapy (CBT) or Yoga,
Meditation and increased physical activity as described
below.
4. Non-pharmacological treatment
Non pharmacological treatment found useful in treatment
of anxiety disorders include supportive therapy, Exposure
therapy (e.g. gradual exposure in vivo, “flooding”) and response
prevention. Psychoeducational advice, and suggesions to not
to avoid feared situations are helpful in management.
Cognitive Behavioural Therapy: Adequate strength of
evidence is available for Individual CBT, Group CBT and Self-
directed CBT. Choosing between medications and CBT is
determined by a number of factors, particularly the patient’s
preference, treatment options at hand, adverse drug
effects, onset of efficacy, comorbidity (e.g. with depression),
financial considerations, time availability, accessibility of
psychiatric and psychological treatment resources, and
experience of the clinician.
Steps of CBT shall include:
1. Psychoeducation
2. Self-monitoring
3. Systemic exposure to panic inducing cues
4. Countering anxious beliefs
5. Exposure to fear cues
6. Modify [mal-adaptive behaviors
7. Relapse prevention
8. Dealing with transference issues
9. Resolving interpersonal and other emotional issues.
Initial expectations and anticipation favoring CBT
• Accept that the worrying is out of control
• Perhaps, worrying offers some protective value.
• CBT will facilitate future adversities, despite the worrying.
During the course of the treatment, revised
understanding:
• The reasons for worrying and fears cannot be controlled
• Subjectively learn to control response to the fears and
worries
• Learn to obviate the behaviour of worrying
• Worrying does not have a protective value
• Actually, worrying reinforces negative thinking
Indian J Psychiatry 59 (Supplement 1), January 2017
 Gautam, et al.: CPG for GAD & Panic Disorder
Excesive worrying increases likely hood or more
anxieties in the future
CBT does not alter the method of managing source of
the worries
CBT helps to be better equipped to handle the future
stress.
Indian modules of psychotherapy
Several therapists have talked about Search of Indian
module of psychotherapy and it is a felt need to have such a
module, which is socially and culturally relevant.
Ancient Indian thought has provided very rich knowledge
regarding mind and its functioning. From the Vedic period
issues relating to mind, consciousness, understanding of
human life, its existence and the concept of Atman have
been widely studied and several explanations to improve
the quality of human life are available in Vedic and Post
Vedic literature. The Bhagvad Gita contains in condensed
form all the philosophical and psycholoical wisdom of the
Upanishads. Bhagwad Gita describes all aspects of yoga,
psychology and is unique among the psychlogical and
philosophical teachings for a student of psychotherapy,
various aspects of psychotherapeutic techniques are
described in it.
In this excellent module of Psychotherapy through
18 chapters way of self knowledge, the Yoga of action
(karma) knowledge of renunciation and action, the path of
meditation, knowledge of the absolute and eternal, yogic
vision, yoga of devotion, profound knowledge of three
Gunas and the wisdom of renunciation and liberation
have been described at length, which leads to personality
transformation of Arjuna. In the modern psychotherapy,
cognitive restructuring is the goal of psychotherapy, which
has been accomplished a great deal through Bhagwad Gita.
Prekshadhayan
A Jain Meditational technique propounded by Acharya
Mahapragya, which includes relaxation, meditation,
yoga, asanas and pranayam, a comprehensive capsule of
behavioural management has been tried in management of
GAD. On mental level, it proves to be an applied method
to train the mind to concentrate. It offers a way to treat
serious anxiety disorders with or without drugs. Large trials
of this technique are still awaited. At present, few scientific
studies are available.
5. Providing Education To The Patient And Family
This seemingly unimportant aspect is most relevant to
Indian settings where awareness of psychiatric illness and its
realization and need for treatment with compliance is little.
Many feel dejected, angry, isolated and may have suicidal
ideas. Family and the patient need to be told that this is like
any other illness that needs treatment and success depends
on compliance.
Indian J Psychiatry 59 (Supplement 1), January 2017
6. Addressing early signs of relapse
The education that the illness is a chronic relapsing
illness is essential and emergence of anxiety with or
without treatment should be promptly treated. Sudden
discontinuation may lead to emergence of withdrawal
symptoms thus early recognition by the patient and the
family helps in prompt treatment.
MANAGEMENT AS PER THE DIFFERENT STAGES
OF THE ILLNESS
The treatment recommendations for the different anxiety
disorders are summarized in Table I. Some antianxiety drugs
are effective in all anxiety disorders, whereas some drugs
have only been studied in specific anxiety disorders and thus
should be reserved for use in these particular disorders.
Panic disorder and agoraphobia. In acute panic attacks, mouth
desolving short-acting benzodiazepines and reassurance
to the patient may be sufficient. SSRIs SNRIs are first-line
treatments for longterm management. Patients should be
treated for atleast six to eight months or longer to prevent
relapses.
A combination of CBT and anxiolytic medication has been
shown to have the best treatment outcomes.
In GAD and Social anxiety disorder (SAD): Choice of Drugs for
Management are SSRIs, SNRIs and pregabalin. Buspirone and
hydroxyzine are second line treatment. Benzodiazepines
should only be used for long-term treatment when other
drugs or CBT have not shown results.
Specific phobia: Specific phobia should be treated with
behaviour therapy including systematic desensatisation.
SSRIs or short acting benzodiazepines should be tried in
cases not responding to behaviour therapy.
OCD: Choice of treatments is the SSRIs and the TCA
clomipramine. Cognitive behaviour therapy (CBT) and
exposure and response prevention are other proven
techniques of management.
PTSD: Choice of treatments includes the SSRIs and
venlafaxine. Therapeutic conversation, psychoeducation
and regrief therapy are non-pharmacological treatment
techniques advocated.
TREATMENT UNDER SPECIAL CONDITIONS
(FLOW CHART-3)
Pregnancy.The use of SSRIs and TCAs in pregnancy does not
have increased risk for malformations. It is recommended to
avoid paroxetine alprazolam use among pregnant women
or women planning to become pregnant.
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 Gautam, et al.: CPG for GAD & Panic Disorder
Anxiety Disorder
Child and Adolescent Geriatric
Population Population
Scant Literature in West Lower initial dose
and India Lower target dose
SSRIs Gradual escalation
BZDs
Flowchart 3: Management of Anxiety Disorders in Special Population
Breast-feeding. SSRIs and TCAs are excreted into breast milk,
they do not cause any harm to the new born because the
concentration in breast milk is very small however infants of
mothers on benzodiazepines, should be observed for signs
of sedation, lethargy, poor suckling, and weight loss, and if
high doses have to be used and long-term administration is
required, breast feeding should probably be discontinued.
Treating children and adolescents. Choice of treatment
should be SSRIs concerns about increased risk of suicidal
ideation and behavior have ben reported therefore careful
monitoring is advisable, presence of comorbid depression
should be looked fore.
Treating the elderly. Elderly have increased sensitivity for
anticholinergic properties, an increased risk for orthostatic
hypotension, and ECG changes during treatment with TCAs,
and possible paradoxical reactions to benzodiazepines,
which include depression, with or without suicidal
tendencies, phobias, aggressiveness, or violent behavior.
Thus, treatment with TCAs or benzodiazepines is less
favorable, while SSRIs appear to be safe.
Treatment of patients with severe Physical disease. Patients
with cardiovascular, cerebrovascular and endocrine disease,
irritable bowel syndrome, malignency, stroke, chronic
obstructive pulmonary disease (COPD) hyperthyroidism
may have associated anxiety reactions with their somatic
disease state. Such anxiety disorders may compound the
management and the prognosis of these primary conditions.
Advocated pharmacological agents in such conditions
include SSRIs and Venlafaxine.
WHEN TO STOP TREATMENT
Decesion to stop treatment will depend on clinical
response of the patients. Usualy the treatment is stopped
in a tapering manner after atleast 6 months stability of
clinical improvement and asymptomatic status of the
patient. Before stopping the treatment, the nature of illness
S72
Suicidal Patient Substance use
disorder
Adequate dose Treatment of substance
Inform patient’s family use disorder essential
possibilities of recurrence, response to triggers and his/
her ability to cope with the situation should be discussed
at length. Patient’s personal view should be included in
decesion making of stopping the treatment. Patient should
be encouraged to adapt alternative methods of anxiety
reduction like yoga, pranayam, relaxation techniques
including progressive muscular relaxation (PMR)/Shavasan
etc. which can be mastered by him before weaning off the
smallest dose of antianxiety medication. Mindfulness-Based
Cognitive Behavior Therapy (MBCBT) for reducing cognitive
and somatic anxiety and modifying dysfunctional cognitions
in patients with anxiety disorders has been tried where in
different versions of mindfulness meditation, cognitive
restructuring, and strategies to handle worry, such as,
worry postponement, worry exposure, and problem solving
have been employed. However, these studies are on small
number of patients and need carefull review for further
application.
MANAGEMENT OF SIDE EFFECTS OF
MEDICATION
Diffrent side effects will emerge with different category of
antianxiety medication. They should be carefully observed
and addressed to. Side effects of medication can be drug
related or dose related. If it is drug, related, alternative class
of drug should be tried for adequate length of time. If it is
dose related then the dose of the drug has to be reduced.
Things to remember for GAD:
1. Anticholinergic and cardiovascular side effects to be
kept in mind when using tricyclic and Tetra cyclic for
side effects. Precaution in suicidal patients.
2. Long-term treatment may be required.
3. Psychopharmacological therapy combined with
psychotherapy works better.
SUGGESTED READING
1. Guidelines for the pharmacological treatment of anxiety disorders,
obsessive – compulsive disorder and posttraumatic stress disorder in
Indian J Psychiatry 59 (Supplement 1), January 2017
 Gautam, et al.: CPG for GAD & Panic Disorder
primary care review article international Journal of Psychiatry in Clinical
Practice, 2012; 16: 77–84.
2. Generalised anxiety disorder in adults – diagnosis and management www.
bpac.org.nz keyword: anxiety.
3. Spirituality and mental health edited by Dr. Avdhesh Sharma, Published by
Indian J Psychiatry. 2008 Oct-Dec; 50(4): 233–237.
4. Indian Culture and Psychiatry, Shiv Gautam, Nikhil Jain, Published
by Indian Journal of Psychiatry year 2010 Volume 52 Issue 7
(P. 309-3013).
5. Prekshadhyan, Manaswi Gautam, published in spirituality and mental
health by Indian psychiatric society task force editor Avdesh Sharma
(2008-2009): 163-176.
6. Mental Health in Ancient india and its relevence to modern psychiatry.
Shiv Gautam Presidential Address, Indian Journal of Psychiatry (1999)
41 (1) 5-18 and “spirituality and mental health, task force (2008-2009):
25-52.
7. ORIGINAL ARTICLE: Role of antioxidants in generalised anxiety disorder
and depression Medhavi Gautam, Mukta Agrawal, Manaswi Gautam,
Praveen Sharma, Anita Sharma Gautam, Shiv Gautam Indian Journal of
Psychiatry, Year 2012, Volume 54, Issue 3 [p. 244-247].
8. Rickels, K., Schweizer.E. (1990) The clinical course and long term
Indian J Psychiatry 59 (Supplement 1), January 2017
management of generalized anxiety disorder. J. Clin. Psychopharmacology,
10, 101S.
9. Caulpepper.L. (2003) Evidence for using Atypical Antipsychotic in mood
and anxiety disorders. Primary Care Companion, Journal of Clinical
Psychiatry,5, Supl(3) page 27-32.
10. Chandrashekhar,C.R. and Reddy,M.V.(1998). Prevalence of mental and
behavioural disorders in India: A meta-analysis,UP, 40(2):149-157.
11. Levitt.J.T., Hoffman,E.C., Grisham, J.R., Barlow.D.H. (2001) Empirically
supported treatments for panic disorder. Psychiatr. Ann.,31,(8): 478.
12. Ontario guidelines for Management of Anxiety disorder.Primary
care(2000). 1st Edn. Pollock.M.H., Mathews.J., Scotter (1998) Gabapentin
as it for Anxiety disorder.American Journal of Psychiatry, 155,992.
13. Sahasi.G., Chawala.H.M., Dhar.N.K., Katiyar.M. (1991) Comparative
study of progressive relaxation and yogic techniques of relaxation in
management of anxiety Neurosis, UP 33 (1);27-32.
14. World Health Organization (1992) The ICD-10 Classification of Mental and
Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines.
World Health Organization, Geneva.
15. Vahia.V.N., Shetty.H.K., Motiwala, S., Thakkar.G., Fernandes.L,
Sharma, C.J. (1993) Effect of Meditation in Generalised Anxiety
Disorder,35 (2);87-92.
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 CLINICAL PRACTICE GUIDELINES
Clinical practice guidelines for Obsessive-Compulsive Disorder
Y.C. Janardhan Reddy, A. Shyam Sundar, Janardhanan C. Narayanaswamy, Suresh Bada Math
Department of Psychiatry, OCD Clinic, National Institute of Mental Health & Neurosciences (NIMHANS), Bangalore,
Karnataka, India
Participants of expert group on CPG for Obsessive
Compulsive Disorder
Adarsh Tripathi, Om Prakash Singh, Paramjeet Singh,
Tushar Jagawat, M, Aleem Siddiqui, K.K. Verma,
D.M. Mathur
INTRODUCTION
Obsessive-compulsive disorder (OCD) is a common
psychiatric illness with lifetime prevalence of 1-3% [1]. It is the
fourth-most common psychiatric illness and a leading cause
of disability. OCD is associated with significant impairment
in functioning, quality of life and disability. If untreated, OCD
is a chronic illness with a waxing and waning of symptoms.
A recent meta-analysis of long-term naturalistic prospective
studies demonstrated that nearly a half of patients experience
remission with much higher rates of remission in Indian
patients compared to those in the west [2]. Early diagnosis
and appropriate treatment may improve outcomes. Despite
OCD being a common mental illness, most seek treatment
after several years of suffering. Those who suffer from
OCD tend to be secretive about their symptoms and suffer
from shame and embarrassment. Less than a third of OCD
sufferers receive appropriate pharmacotherapy and even less
receive evidence-based psychotherapy.
Symptoms
The hallmarks of OCD are presence of obsessions and
compulsions. Obsessions are repetitive, unwanted,
Address for correspondence:
Y. C. Janardhan Reddy,
Professor of Psychiatry, NIMHANS, Bangalore 560029,
Karnataka, India.
E-mail: ycjreddy@gmail.com
Access this article online
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Website:
www.indianjpsychiatry.org
DOI:
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intrusive thoughts, images or urges that are mostly ego-
dystonic and cause severe distress or anxiety. Compulsions
(or rituals) are repetitive behaviours or mental acts that
are performed in response to an obsession to reduce
anxiety/distress or prevent a dreaded consequence.
Obsessions and compulsions are time consuming,
distressing and are often resisted unsuccessfully. Clinical
manifestations of OCD are remarkably similar across
cultures and geographic locations. Common obsessions and
compulsions and symptom dimensions identified through
factor-analytical studies are shown in Table 1.
Diagnosis
Many people experience intrusive thoughts and exhibit
repetitive behaviours. A diagnosis of OCD is made only if
symptoms are time consuming (e.g., more than an hour
per day), distressing or cause significant interference in
functioning. This is reflected in DSM-5 diagnosis of OCD
and in the upcoming ICD-11 [3]. The ICD-11 criteria for OCD
are likely to be very similar to the DSM-5 criteria [3, 4]. The
ICD-11 may include an insight specifier along the same lines
as DSM-5. There are sweeping changes to the description
of OCD in the proposed ICD-11. Duration criteria and
subtyping of OCD may be removed in the revision for lack
of evidence and clinical relevance. In ICD-10, a diagnosis of
OCD was discouraged in the presence of schizophrenia, tic
disorder or depression. This criterion too may be removed
paving the way to make a diagnosis of OCD even in the
presence of these comorbid disorders.
Another major change to the diagnosis of OCD is creation
of OCD and related disorders in DSM-5 (and in the ICD-
11) and exit from the group of anxiety disorders. Many
disorders are included in this group: body dysmorphic
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How to cite this article: Janardhan Reddy YC, Sundar AS,
Narayanaswamy JC, Math SB. Clinical practice guidelines
for Obsessive-Compulsive Disorder. Indian J Psychiatry
2017;59:74-90.
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 Reddy, et al.: CPGs for OCD
Table 1: Common symptoms of OCD
Obsessions
Contamination related obsessions
• Concern/disgust with bodily secretions and waste such as stools and urine
• Fear of dirt or germs/infections, concern with sticky substances
• Fear of getting ill because of contaminants (e.g., AIDS)
Sexual obsessions
• Unwanted, forbidden sexual thoughts, images or urges about strangers,
family friends, etc
• Sexual thoughts of molesting children, thoughts of sexual identity (am
I a gay?)
Harm/aggression related obsessions
• Fear might harm self or others (fear of jumping off the building, fear
of harming babies, stabbing a friend, running over pedestrians while
driving etc)
• Violent/horrific images (murders, mutilated bodies, accidents)
• Fear of uttering obscenities
Religious/blasphemy
• Sacrilege and blasphemy (blasphemous thoughts, fear of uttering insults
to God)
• Excessive concern about right/wrong, morality
Pathological doubts about daily activities (doubts of having not locked
doors, turned off gas knobs)
Need for symmetry and exactness
• Concern about things being not properly aligned, symmetrical, perfect
or exact
• With magical thinking (child may have an accident if things are not
properly arranged in kitchen)
Miscellaneous
• Need to know/remember (number plates, advertisements etc.)
• Intrusive non‑violent images, thoughts
• Superstitious fears (passing a cat, cemetery)
• Lucky/unlucky numbers, colors
Compulsions
Washing/Cleaning (excessive or ritualized hand washing, showering,
bathing, brushing/excessive cleaning of household items, floors, kitchen
vessels etc) in response to contamination obsessions
Checking
• In response to pathological doubts (appliances, locks, stove, doors)
• To prevent harm to self or others (check to make sure that you have not
caused accident, examining for injuries etc.)
Repeating
• Re‑reading or rewriting because you didn’t understand or write properly
• Repeating routine activities (going in and out of doorway, sit and stand
up repeatedly, repeating till you feel just right)
Counting (money, floor tiles)
Ordering and arranging (often till you feel just right)
Miscellaneous
• Mental rituals (praying, replacing bad thought with good thought)
• Superstitious behaviours
• Need to tell/ask/confess
Symptom dimensions[41]
• Contamination fears and cleaning/washing
• Forbidden thoughts (aggression, sexual, religious, and somatic
obsessions and checking compulsions)
• Symmetry (symmetry obsessions and repeating, ordering, and counting
compulsions)
• Hoarding (hoarding obsessions and compulsions)
disorder (BDD), trichotillomania (TTM), skin picking
disorder, hoarding disorder, substance/medication-
Induced obsessive-compulsive and related disorder
and obsessive-compulsive and related disorder due to
another medical condition. In the upcoming ICD-11, few
Indian J Psychiatry 59 (Supplement 1), January 2017
other conditions find a place in this group that include
tic disorders, hypochondriasis and olfactory reference
syndrome. All these disorders are grouped together based
on shared clinical features (e.g., repetitive behaviours),
comorbidity patterns, familiality, neuropsychological
deficits, treatment response and importantly shared brain
circuitry abnormalities. Hoarding disorder which may not
share many features with OCD is grouped along with OCD
because of historical association with OCD and obsessive-
compulsive personality disorder.
Comorbidity
OCD is often comorbid with other psychiatric disorders. It
is important to assess all patients with OCD for associated
psychiatric comorbidity since they may have an effect on
treatment outcome if left untreated. Depression and anxiety
disorders are present in over a half of patients seeking
treatment for OCD. Common comorbid disorders are
listed in Table 2. Those with early onset OCD, in particular
those with onset in childhood have high rates of attention
deficit hyperactivity disorder (ADHD), oppositional defiant
disorder (ODD) and tic disorders.
Bipolar disorder, in particular type 2, is reported to
be not uncommon in OCD [5]. Similarly, OCD is not
uncommon in those with primary diagnosis of bipolar
disorder [6, 7]. OCD when comorbid with bipolar disorder
tends to run an episodic course [8] with worsening of
symptoms in depressive phases and improvement in
hypomania/ mania phases. It is important to recognise OCD-
bipolar comorbidity because of treatment implications. The
specific serotonin-reuptake inhibitors (SSRIs) traditionally
used to treat OCD may induce switch to mania or rapid
cycling course.
Obsessive-compulsive symptoms and OCD are not
uncommon in schizophrenia. Nearly a third of schizophrenia
patients report OC symptoms or OCD. Presence of OCD
may have a negative effect on the long-term course of
schizophrenia. Therefore treatment of OCD with SSRIs
and cognitive-behavior therapy (CBT)/behavior therapy (BT)
may have to be considered although there is not much of
systematic evidence supporting their efficacy in treatment
of OCD in schizophrenia.
COMMON INGREDIENTS OF MANAGEMENT
PLAN
Common ingredients of managing OCD include the
following:
1. Detailed assessment of symptoms and comorbid patterns
including suicidal behaviours either by unstructured
clinical interview alone or supplementation with
structured assessments.
2. Decision on setting for treatment (outpatient vs. inpatient
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 Reddy, et al.: CPGs for OCD
Table 2: Comorbid disorders in OCD
Mood disorders
• Major depression
• Dysthymia
• Bipolar disorder
Anxiety disorders
• Panic disorder
• Generalized anxiety disorder
• Social Phobia
OCD related disorders
• Body dysmorphic disorder
• Hypochondriasis
• Trichotillomania
• Skin picking disorder
• Tic disorders
Attention deficit hyperactivity disorder
Oppositional defiant disorder
Personality disorders
• Obsessive‑compulsive personality disorder
• Anxious‑avoidant personality disorder
• Borderline personality disorder
• Schizotypal personality
Differential diagnoses to consider
• Depression (depressive ruminations are usually ego‑syntonic, reflective
of depressive cognitions such as self‑criticism, failure, regret, guilt,
pessimism without any compulsions)
• Generalized anxiety disorder (anxious ruminations are about real‑life
concerns and not associated with compulsions)
• Body dysmorphic disorder (concerns limited to physical appearance)
• Trichotillomania (limited to hair pulling)
• Skin picking disorder (confined to excessive skin picking)
• Hoarding disorder (difficulty in discarding or parting with possessions,
accumulation of possessions; not secondary to obsessions)
• Eating disorders (confined to weight and food)
• Tics (often preceded by premonitory sensations and not aimed at
neutralizing obsessions)
• Psychotic disorders (Even poor insight/delusional OCD is associated
with typical obsessional content and compulsions whereas delusions
have persecutory, grandiose themes with other symptoms such as
hallucinations or formal thought disorder)
• Obsessive‑compulsive personality disorder (enduring and pervasive
pattern of excessive preoccupation with perfectionism, orderliness
and rigid control; rigidity, stubbornness, scrupulosity and over
conscientiousness. Typically ego‑syntonic. No obsessions and
compulsions)
care depending upon the severity, treatment resistance
etc.)
3. Detailed psychoeducation of the patient and family
member (s) about OCD, its course and treatment
options including duration of treatment.
4. Choice of treatment: drugs vs. CBT vs. combination
5. In the Indian context, SSRIs are first-line treatments
preferred over CBT because of feasibility, affordability
and limited number of trained therapists. CBT may be
considered if SSRIs alone are not beneficial.
6. Discussion on side-effects of drugs; in women risks vs.
benefits of drugs during pregnancy and in the post-
partum period
7. Follow-up plan after initiating treatment
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ASSESSMENT AND EVALUATION
In routine clinical practice, use of structured /
semistructured interviews and rating scales may not be
necessary. They are optional. However, they may be used
when the clinician needs supplementary information. A list
of useful instruments in the assessment of OCD is provided
in Table 3.
The Yale-Brown Obsessive-Compulsive Scale (YBOCS) is the
most widely used severity rating scale for OCD in both adults [9]
and children [10] and is considered a gold standard instrument
to measure severity of OCD. It is a 10-item observer-rating scale,
also available as self-rated instrument. It measures the overall
severity of obsessive-compulsive symptoms for the preceding
week. The YBOCS is a global measure of symptoms and does
not provide severity of individual symptom dimensions. A
total score of ≥ 16 is considered to be indicative of clinically
significant OCD. The YBOCS severity scale also has an
associated symptom check list of 15 categories of obsessions
and compulsions including miscellaneous symptoms. The
checklist elicits both current (1 month) and past symptoms.
On the YBOCS item-11 insight scale, the insight is graded
as follows: 0 = excellent (fully rational thinking), 1= good
insight (readily acknowledges absurdity or excessiveness
but has some lingering doubts), 2 = fair insight (reluctantly
admits absurdity, but waivers; has some unrealistic fear but
no fixed conviction), 3 = poor insight (overvalued ideas;
maintains they are not unreasonable or excessive, but
acknowledges validity of contrary evidence), and 4 = lack
of insight (delusional). A higher score on the Y–BOCS item-
11 indicates poorer insight.
FORMULATING A TREATMENT PLAN
Formulating a treatment begins with correct diagnosis of OCD
as per the DSM or ICD classificatory systems. When feasible
a structured clinical interview is recommended to obtain a
comprehensive account of patient’s problems. Once a diagnosis
is established, a detailed assessment of symptom profile is
mandatory. Family members often accommodate patient’s rituals
and contribute to poor outcome. In most severely ill patients, an
elaborate family assessment may be needed. Once assessment is
complete, short-term and long-term goals of treatment have to be
established. Enhancing treatment adherence is a vital aspect of
formulating a treatment plan. It is important to educate patients
about lag in the onset of action of drugs and that improvement
may occur over several months of continuous treatment. Brief
education about basic principles of psychotherapy should
be explained if psychotherapy is being planned. Essentials of
formulating a treatment plan are summarized in Table 4. All
patients and their immediate family members should be provided
psychoeducation about OCD (Table 5).
Indian J Psychiatry 59 (Supplement 1), January 2017
 Reddy, et al.: CPGs for OCD
Table 3: Commonly used instruments to assess
OCD (optional)
Diagnostics interview schedules
• The Mini International Neuropsychiatric Interview (MINI)[42]
• Structured Clinical Interview for DSM‑5 (SCID‑5)[43]
Severity rating scales
• Yale‑Brown Obsessive‑Compulsive Scale (YBOCS): symptom checklist
and severity rating scale (adult and child versions)[9,10]
• Dimensional YBOCS (DYBOCS)[44]
Scales to assess insight in OCD
• Yale‑Brown Obsessive‑Compulsive Scale (YBOCS), Item 11[9]
• Brown‑Assessment of Beliefs Scale (BABS)[45]
• Overvalued Ideas scale (OVIS)[46]
Obsessive‑beliefs questionnaire (OBQ) to measure beliefs underlying
obsessions [47]
The Family Accommodation Scale (FAS) assesses the degree to which
family members of those with OCD accommodate patient’s compulsions/
rituals[48]
CHOICE OF TREATMENT SETTINGS
In the Indian scenario, treatment is either on an outpatient or an
inpatient basis. Outpatient treatment is usually sufficient for most
OCD patients who are mild to moderately ill and for those who
are likely to be adherent to treatment. Patients may be followed-
up at periodic intervals, initially once in a month or two and
subsequently at longer intervals depending upon the response to
treatment and tolerability and side-effects. Hospital treatment may
be considered for those who are at high suicide risk, dangerous
to self or others, and intolerant to side-effects. Many severely
ill and treatment-resistant patients may require prolonged (2-3
months) hospitalization for intensive treatment with CBT and for
rationalization of pharmacotherapy. Inpatient care may also be
required for severe depression, mania or psychosis that may be
comorbid with OCD. Admission in rehabilitation services may be
necessary for some patients who may not have benefited from
standard treatments including inpatient care.
PHARMACOLOGICAL TREATMENT
The clinical practice guideline is framed based on a
review of relevant scientific literature. As a first step, we
framed relevant questions which arise in the minds of the
practitioner while treating a patient suffering from OCD.
A literature search was conducted in PubMed to answer
these questions. We also reviewed the existing guidelines
on treatment of OCD [11-14]. After a thorough literature
review, the treatment strategies were rated based on the
Strength of Recommendation Taxonomy (SORT) [15].
Consistent evidence from multiple randomized controlled
trials (RCT) constitutes the highest level of evidence for a
recommendation. However, the external validity of RCTs has
been questioned due to the rigid protocols in undertaking the
studies. A practitioner may make a clinical decision based on
the available evidence considering other relevant factors that
influence the decision making process. A non-exhaustive list
of these factors might include psychiatric and other medical
Indian J Psychiatry 59 (Supplement 1), January 2017
Table 4: Essentials of formulating a treatment plan
Establishing a diagnosis if OCD
Diagnosis of comorbid disorders (optional structured clinical interview)
Detailed evaluation for a range of OCD symptoms (clinical interview/
YBOCS or similar check list)
Detailed symptom evaluation
• Identify principal symptoms that are the target of treatment (especially
useful to identify principal symptoms if CBT is planned)
• Identify proxy compulsions, avoidance and safety behaviours
• Determine level of insight
• Assess family accommodation of patient’s rituals
Short‑term goals
• To achieve clinical response and if possible remission
• Remission of depression, if comorbid
• Help deal with suicidal thoughts, behaviour if any
• To determine tolerability to medicines
• Identify and manage side‑effects
Long‑term goals
• Achieve recovery
• Restore psychosocial functioning and enhance quality of life
• Long‑term treatment to prevent relapses
Enhancing treatment adherence
• Psychoeducation to the patient and family members
• Provide education materials to patient and family members
• Deal with unrealistic expectations of quick recovery; educate
patients and family about lag in the onset of action of drugs and that
improvement may occur over several months
• Sensitise patient about potential side‑effects and help to deal with them
• Use medicines that are effective, easily available and affordable
• Treat comrbid disorders and personality disorders if any; if left
untreated may contribute to poor treatment adherence
Enhancing adherence to psychotherapy (CBT)
• Detailed education about principles behind exposure and response
prevention
• Reassure that exposure and response prevention will be graded and
tasks will be determined based on collaborative approach
• Emphasize the role of motivation, home‑work compliance and need to
tolerate some anxiety
• Reduce unrealistic expectations of quick recovery
comorbidities, previous treatment trials, affordability, accessibility,
hypersensitivity, side-effect profile, patients’ values etc.
RELEVANT CLINICAL ISSUES
1. First-line pharmacological treatment for OCD
Meta-analyses of RCTs show that selective-serotonin
reuptake inhibitors (SSRIs) are significantly more effective
than placebo in the treatment of OCD [16]. SSRIs are
associated with many adverse effects but are usually well
tolerated. The only other medication which has shown to be
consistently effective in OCD is the serotoninergic tricyclic
antidepressant clomipramine. Clomipramine has been found
to be significantly more effective than placebo in multiple
RCTs and meta-analysis of RCTs [16]. Network meta-analysis
comparing the efficacy of clomipramine vs. SSRIs failed to find
any efficacy advantage over SSRIs [16]. Most head-to-head
comparison trials have not found any significant difference
between the efficacy of clomipramine and SSRIs [17].
Further, meta-analyses and individual RCTs have found that
the tolerability of clomipramine is worse than that of SSRIs
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Table 5: Components of psychoeducation Table 6: Medications recommended as monotherapy in

• Obsessions and compulsions are symptoms of OCD and that they are OCD
similar in most people who suffer from OCD; OCD is a brain disorder Drug Suggested dosage Strength of recommendation*
• Obsessions are not a reflection of one’s character or unresolved mental
Escitalopram 20‑30 mg A
conflicts
Fluoxetine 60‑80 mg A
• Explain the link between the components-Obsessions, compulsions and
Fluvoxamine 200‑300 mg A
distress
Paroxetine 40‑60 mg A
• Clarify myths and misconceptions about the illness
Sertraline 150‑200 mg A
• Explain the biological and psychological basis of OCD : OCD is a
Citalopram 40‑60 mg A
problem of aberrant functioning of certain brain circuits involved in
Clomipramine 150‑225 mg A
disregarding unwanted thoughts, dysfunction of certain neurotransmitter
Venlafaxine 225‑300 mg B
systems such as serotonin and glutamate, faulty interpretation
and excessive importance given to certain intrusions resulting in *Based on modified Strength of Recommendation Taxonomy (SORT)[15]
A – Consistent, good‑quality patient‑oriented evidence i.e., Meta‑analysis of
manifestation of obsessions Randomized controlled trials (RCT) with consistent findings or high quality
• Discuss the course and outcome of OCD-regarding the waxing and individual RCT
waning course with optimism that outcome is good in a majority of the B – Inconsistent or limited‑quality patient‑oriented evidence i.e., systematic
people if adequately treated review/meta‑analysis of lower quality clinical trials or studies with inconsistent
• Provide information regarding the available treatment strategies : findings/lower quality clinical trial/cohort study/case‑control study
C – Consensus based clinical guidelines extrapolations from bench research,
pharmacotherapy and cognitive behavior therapy
disease‑oriented evidence, usual practice, opinion, case‑series
• Sensitize with the idea that treatment is a continued process and often
long‑term
• Educate that medications take time to work, sometimes as long as few Table 7: Predictors of response to SSRIs
months before appreciable improvement is seen
Clinical predictors of poor response
• Psychological treatment too needs sustained efforts and sometimes
Early age of onset
booster sessions
Longer duration of illness
• Prevention of relapse addressed within the general context of OCD as a
Poor insight
chronic disorder
Presence of hoarding, sexual/religious obsessions, cleaning/washing,
• Educate the family regarding the need to reduce expressed emotions
repeating/counting compulsions
such as criticality, accommodative behaviors and proxy compulsions;
Comorbidities in the form of tics and depressive disorder
thus being supportive in the treatment process
Comorbid schizotypal, borderline and anxious avoidant personality
disorders
Neuroimaging predictors
[13, 17]. The anticholinergic, cardiac and neurological side
Lower baseline orbitofrontal cortex (OFC) and anterior cingulate
effects of clomipramine may be problematic in this regard. cortex (ACC) metabolism and greater pretreatment caudate metabolism
predicted better response (PET studies)
CONSIDERING THE CONSISTENT EFFICACY Reduction in thalamic volume and increase in OFC volume is associated
AND BETTER TOLERABILITY, GUIDELINES with SSRI response (structural MRI)
Increased dorso-lateral prefrontal cortex (DLPFC) activation with
RECOMMEND SSRIs AS FIRST LINE
Stroop task and decreased activation of frontal regions with symptom
TREATMENT FOR OCD (TABLE 6). provocation task predicted good response
Genetic predictors
Choice of SSRI Specific polymorphisms in the promoter region of serotonin transporter (5
Meta-analyses comparing the different SSRIs [16] and direct HTTLPR) associated with treatment response
CYP2D6 polymorphisms associated with SSRI response
head-to-head comparisons [17,18] have not shown superiority
Ref:[49]
of any one SSRI over the other. SSRIs differ to some extent
in their propensity to cause certain adverse effects and drug
interactions. However, there is no unequivocal evidence to higher dose of SSRI than that used in depression (Table 5). A
suggest that these differences may be clinically meaningful. meta-analysis of fixed-dose comparison studies have found a
Recently, concerns have been raised regarding cardiac greater efficacy with higher doses of SSRI (60-80 mg fluoxetine
adverse effects with high dose of citalopram, which is equivalent) compared to medium (40-50 mg fluoxetine
commonly used in OCD. Hence, high-dose citalopram may be equivalent) and low doses (20-30 mg fluoxetine equivalent)
used with caution in those with risk for arrhythmias. [19]. However, all three dose ranges were significantly more
effective than placebo. The increased efficacy comes at the
THE PRACTITIONER IS RECOMMENDED TO cost of poor tolerability as evidenced by increased dropouts
CHOOSE AN SSRI FOR AN INDIVIDUAL PATIENT due to adverse effects [19]. A review of individual fixed-dose
BASED ON FACTORS SUCH AS PREVIOUS comparison studies found that the dose-response relationship
RESPONSE, COMORBIDITY, TOLERABILITY, is more evident for escitalopram, fluoxetine and paroxetine,
ACCEPTABILITY, ADVERSE EFFECTS, COST AND while it is less clear-cut for citalopram and sertraline [17].
DRUG INTERACTIONS. Clomipramine has not been tested in such fixed dose
comparison studies. However, most studies have employed a
Dose of SSRI flexible dosing at 150-250 mg [17]. It should be remembered
It is generally recommended that OCD be treated with a that there is likely to be inter-individual differences in

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 Reddy, et al.: CPGs for OCD

SSRI© CBT/BT
First line +SSRI**
CBT/BT #
treatments*
response

Response after No
15-20 sessions SSRI: If recovered or minimal
symptoms continue for 1-2
Yes years & then gradual taper
over several months.
Inadequate Indefinite treatment:
Continue till remission response Persistent symptoms,
with periodic booster previous history of relapses,
sessions for severe illness
4-6 months CBT: booster sessions for
4-6 months

Partial response No response

Options
Options • 2nd SSRI / CBT( if not
• CBT/BT (if not offered) Inadequate offered)
• Aripiprazole/risperidone response • Clomipramine / CBT (if
• Memantine not offered)
• Lamotrigine • Other untried SSRIs
• 5HT-3 antagonists • Venlafaxine

Inadequate
response

Other experimental treatments

• Ultra-high dose SSRI
• Augmentation with
clomipramine
• Ketamine
• rTMS€ /tDCS$
• Riluzole/N-acetyl cysteine

Ablative neurosurgery/ Deep

brain stimulation

Figure 1: Treatment algorithm for treating a patient with OCD. *First line treatment chosen based on feasibility and severity
of illness, #CBT/BT- Cognitive behavior therapy/Behavior therapy, @SSRI – Selective serotonin reuptake inhibitor, %rTMS-
repetitive transcranial magnetic stimulation, $ - tDCS- transcranial direct current stimulation. ** Preferred for severe OCD

pharmacokinetic profile of drugs due to intrinsic variations in
drug metabolism and drug interactions.
GUIDELINES RECOMMEND TREATMENT OF
OCD WITH HIGHER DOSE OF SSRIs. HOWEVER,
IF AN INDIVIDUAL PATIENT IS NOT ABLE TO
TOLERATE HIGHER DOSE, LOW TO MEDIUM
DOSE TREATMENT CAN BE CONSIDERED.
Duration of trial and dose titration
A recent meta-analysis of 17 RCTs found that SSRIs
separate from placebo as early as 2 weeks and that
majority of improvement occurs early on in the course
of treatment [20]. However, improvements seen early
in the course of treatment may not be always clinically
meaningful. In many patients, clinically meaningful
improvements may be seen only after weeks or months
of treatment. It is recommended that an adequate trial of
a SSRI (or clomipramine) should be at least for 12 weeks
to account for the lag in the onset of action. The APA
guidelines recommend upward titration to the maximum
FDA-approved doses by 4-6 weeks and continuation in that
dose for another 6-8 weeks or so to determine efficacy
[11]. Certain clinical and biological predictors of treatment

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 Reddy, et al.: CPGs for OCD

Non-response to 2 adequate trials with SSRIs Given the absence of evidence from placebo-controlled
trials, venlafaxine is not the first-line treatment for OCD.
Hence, the guidelines consider venlafaxine as a second-line
Add CBT/ BT Clomipramine if CBT / BT are not feasible monotherapy agent in the treatment of OCD.
No response
No response Mirtazapine has been studied as a monotherapy in two
Clomipramine BT / CBT
small open-label trials with inconsistent findings. Therefore,
mirtazapine cannot be recommended as monotherapy in
No response
No response treatment of OCD.
Switch to third SSRI Switch to third SSRI
3. Treatment strategy for non-responders to first-line
No response treatment
Definitions of treatment outcome [21] are given in
Add Risperidone or Table 8. Estimates suggest that around 40-70% patients
Aripiprazole to SSRI
show an adequate response to a trial of SSRI with a
No response
remission rate of 10-40% [16]. Clinicians often face the
subsequent challenge of partial and non-response to SSRIs.
Add 5-HT 3 antagonists / memantine / lamotrigine to SSRI
Continuing improvement has been noticed with prolonged
No response trial of SSRIs as discussed above. Hence, the initial trial
may be continued further if there is evidence of ongoing
Try untried SSRI or venlafaxine
improvement. A general treatment algorithm for OCD and
No response for non-responders to SSRIs is shown in Figures1 and 2
Inpatient intensive treatment with CBT / BT + SSRI for severe OCD
respectively.
Try outpatient CBT / BT for second time in mild-moderate OCD

a. Switching to another medication

No response
Switching to another first-line medication has been found
Ultra-high dose SSRIs, addition of clomipramine, rTMS , to be effective; experts provide a rough estimate of 40-
Mirtazapine, N-acetyle cysteine, Ketamine
50% response rate for the second SSRI and decreasing
No response response rates with further trials. Switching to a second
SSRI is suggested for non-responders to a first SSRI. In
DBS, ablative surgery for severe, chronic, treatment refractory OCD
partial responders, changing medication may entail
Figure 2: Strategies for non-responders to SSRIs. SSRI- loss of the response to the earlier medication. Hence,
Selective serotonin reuptake inhibitors, CBT/BT-Cognitive switching is recommended in partial responders only if
behavior therapy/behavior therapy, rTMS- repetitive there are severe persisting symptoms or upon failure of
transcranial magnetic stimulation other augmenting strategies such as CBT and atypical
antipsychotics.
response to SSRIs have been identified but they are not
robust predictors (Table 7). b. Switching / Augmenting with CBT/BT
It is uncertain whether initiating a combination of BT/CBT
GUIDELINES RECOMMEND CONTINUING simultaneously with SSRI is advantageous compared to
MAXIMALLY TOLERATED EFFECTIVE DOSE OF either treatment alone. However, CBT/BT has been proven
A SSRI FOR AT LEAST 12 WEEKS FOR JUDGING to be effective as an augmenter in partial/non-responders
ITS EFFICACY. GUIDELINES ALSO RECOMMEND to SSRIs [18, 22, 23]. Where feasible, CBT/BT is a potential
DOSE ESCALATION TO EFFECTIVE DOSE first-line augmenting option for partial/non-responders to
RANGES WITHIN 4-6 WEEKS AND CONTINUATION SSRI treatment.
IN THE SAME DOSE FOR ANOTHER 6-8 WEEKS.
c. Augmenting with another medication (Table 9)
2. Other medications that can be tried as monotherapy in The following medications have been commonly tried as
OCD augmenters to SSRIs. Atypical antipsychotics, risperidone
Venlafaxine, a serotonin-norepinephrine reuptake inhibitor and aripiprazole have the best evidence.
with preferential serotonergic action, has been studied
in comparison to paroxetine in a double blinded study i Antipsychotics
and clomipramine in a single blinded study. The studies Antipsychotics are the most widely studied augmenting
found no difference in the efficacy between venlafaxine agents of SSRIs [23]. The literature on antipsychotic
and the comparator agents in acute control of OCD. augmentation is fraught with methodological limitations

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Table 8: Definitions of treatment outcome in OCD

Consensus definitions and operationalization of treatment response, partial response, remission, recovery, and relapse for Obsessive‑Compulsive
Disorder (OCD)
Conceptual Definition
TREATMENT RESPONSE A clinically meaningful reduction in symptoms (time,
PARTIAL RESPONSE distress, and interference associated with obsessions,
compulsions, and avoidance) relative to baseline
severity in an individual who meets diagnostic criteria
for OCD
REMISSION The patient no longer meets syndromal criteria for the
disorder and has no more than minimal symptoms.
Residual obsessions, compulsions, and avoidance
may be present but are not time consuming and do not
interfere with the person’s everyday life
RECOVERY The patient no longer meets syndromal criteria for
the disorder and has had no more than minimal
symptoms. Residual obsessions, compulsions, and
avoidance may be present and slightly fluctuate in
severity over time but, overall, they are not time
consuming and do not interfere with the person’s
everyday life and therefore require no further
treatment. The clinician may begin to consider
discontinuation of treatment or, if the treatment
continues, the aim is to prevent relapse
RELAPSE After response or remission or recovery was achieved,
the patient experiences a return of symptoms.
For patients who were in remission or recovered,
obsessions, compulsions, and avoidance are again
sufficiently time consuming, distressing, and
impairing for the individual to meet diagnostic criteria
for OCD
Abbreviations: CGI‑I – Clinical Global Impression Improvement; CGI‑S – Clinical Global Impression Severity; (C) Y‑BOCS – (Children’s) Yale‑Brown Obsessive
Compulsive Scale; OCD – Obsessive-Compulsive Disorder. Ref: [21]. This table is reprinted with permission from the lead author of the Delphi survey. The table is
not part of the publication
Operationalization
A ≥35% reduction in (C) Y‑BOCS scores plus CGI‑I rating of
1 (‘very much improved’) or 2 (‘much improved’), lasting for
at least one week
A ≥25% but <35% reduction in (C) Y‑BOCS scores plus CGI‑I
rating of at least 3 (‘minimally improved’), lasting for at least
one week
If a structured diagnostic interview is feasible, the person no
longer meets diagnostic criteria for OCD for at least one week
If a structured diagnostic interview is not feasible, a score of
≤12 on the (C) Y‑BOCS plus CGI‑S rating of 1 (‘normal, not
at all ill’) or 2 (‘borderline mentally ill’), lasting for at least
one week
If a structured diagnostic interview is feasible, the person no
longer meets diagnostic criteria for OCD for at least one year
If a structured diagnostic interview is not feasible, a score of
≤12 on the (C) Y‑BOCS plus CGI‑S rating of 1 (‘normal, not
at all ill’) or 2 (‘borderline mentally ill’), lasting for at least
one year
For responders who did not necessarily remit/recover: The
person no longer meets the definition of ≥35% reduction
on (C) Y‑BOCS scores (relative to pre‑treatment) plus CGI‑I
rating of 6 (‘much worse’) or higher for at least one month
For remitters/recovered: OCD criteria are met again,
according to a structured interview (if feasible). Alternatively,
the person no longer meets the definition of remission/
recovery (i.e., the person again scores 13 or above on the (C)
Y‑BOCS) plus CGI‑I rating of 6 (‘much worse’) or higher
for at least one month or needs to be withdrawn prematurely
from the trial before one month has elapsed due to a severe
worsening of OCD symptoms. Discontinuation of the trial due
to reasons other than a worsening in OCD symptoms (e.g.,
suicide risk) is not considered a relapse

including small sample sizes, varying doses and duration of
treatment with both antipsychotics and concomitant SSRIs,
varying degree of treatment resistance etc. Two recent
meta-analyses of 14 RCTs on antipsychotic augmentation
found that antipsychotic as a group was significantly more
effective than placebo in decreasing YBOCS scores [24, 25].
About a third of patients responded to antipsychotic
augmentation. Aripiprazole and risperidone are consistently
found to be effective as augmenting agents. The evidence
for haloperidol should be interpreted with caution as it
was based on a single study. A fairly large RCT comparing
CBT, risperidone and pill placebo augmentation of SSRI
found that risperidone did not separate from placebo in
augmenting efficacy [26]. This study has raised questions
on the efficacy of risperidone as an augmenter. Quetiapine
and olanzapine have not been consistently found to be
effective, while other antipsychotics have not been studied
adequately. Meta-analyses do not throw any light on
adequate dose and duration of antipsychotic treatment
[24]. Antipsychotics should be used in low doses (e.g., 1-3 mg
of risperidone, 5-10 mg aripiprazole) for a period of at least
8 weeks for an adequate trial. Use of antipsychotics in the
long-run should be considered after weighing the benefits
and risks of long-term use.
BASED ON THE AVAILABLE EVIDENCE,
ARIPIPRAZOLE AND RISPERIDONE MAY
BE CONSIDERED THE FIRST CHOICE FOR
PHARMACOLOGICAL AUGMENTATION
ii. Glutamatergic agents
There is a strong theoretical rationale supporting the use
of glutamatergic drugs in OCD. The following glutamatergic
agents have been studied in OCD [23]:

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Table 9: Pharmacological augmenting agents in OCD iv. Other augmenting agents

Drug Suggested dosage $ Strength of recommendation* Buspirone, lithium and clonazepam have not been found
Aripiprazole 5‑10 mg A effective and hence are not recommended as augmenting
Risperidone 1‑3 mg A agents. The safety and efficacy of psychostimulants and
Haloperidol 2.5‑10 mg B opioid drugs have to be systematically studied before they
Memantine 10‑20 mg B are recommended for routine clinical use. Intravenous
Lamotrigine 100mg B
ketamine has been found to have acute anti-obsessive
Ondansetron 2‑4 mg twice a day B
Granisetron 1 mg twice a day B effects in a “proof-of-concept” study, which needs
$ ‑ Rough estimate based on available evidence replication and long term evaluation before the strategy can
*Based on modified Strength of Recommendation Taxonomy (SORT)[15] be recommended for routine clinical use.
A – Consistent, good‑quality patient‑oriented evidence i.e., Meta‑analysis of
Randomized controlled trials (RCT) with consistent findings or high quality
individual RCT B – Inconsistent or limited‑quality patient‑oriented evidence d. Other experimental strategies
i.e., systematic review/meta‑analysis of lower quality clinical trials or studies While there appears to be some short-term benefits for
with inconsistent findings/lower quality clinical trial/cohort study/case‑control
study C – Consensus based clinical guidelines extrapolations from bench intravenous clomipramine in treatment resistant patients,
research, disease‑oriented evidence, usual practice, opinion, case‑series the long term benefits are uncertain. This formulation is
not available in India and is not recommended at present
a. Memantine: found effective in 2 double blinded and for clinical use. There are a few uncontrolled trials
one single blinded RCT. demonstrating the utility of higher than recommended
b. Lamotrigine: found effective in 2 double blinded RCTs doses of SSRIs (up to 400 mg of sertraline, 40-50 mg of
c. Topiramate: effective in 2 small double-blind RCTs, but escitalopram) in resistant patients. This strategy should be
poorly tolerated considered experimental and may be used only in resistant
d. Riluzole: inconsistent results in two RCTs patients after exhausting other regular safer options.
e. N-acetylcysteine: conflicting results from three RCTs,
has to be studied further. ROLE OF OTHER NON-SOMATIC TREATMENTS

BASED ON THE EVIDENCE AND ITS RELATIVELY Around 20% of patients do not respond to available
BETTER TOLERABILITY, MEMANTINE IS pharmacological and psychological treatments.
PREFERRED OVER LAMOTRIGINE AS THE Neuromodulatory and neurosurgical treatments targeting
FIRST CHOICE GLUTAMATERGIC AUGMENTING the cortico-striato- thalamo-cortical (CSTC) circuits have
AGENT. been tried in resistant patients.

iii. Serotonergic agents NON-INVASIVE BRAIN STIMULATION

5HT-3 antagonists including ondansetron and granisetron
are reported to be effective and well tolerated in small RCTs
[27]. However, due to the methodological limitations of the
individual studies, 5HT-3 antagonists are recommended as
second line augmenting agents along with glutamatergic
agents.
Preliminary evidence suggests that clomipramine can
be an effective augmenting agent. Clomipramine and
SSRI combination should be used cautiously, especially
with fluoxetine and fluvoxamine, as they may increase
clomipramine related adverse effects (including serious
events like seizures, cardiac effects, serotonin syndrome)
due to pharmacokinetic interactions. Clomipramine
augmentation of SSRI may be tried but adequate precautions
need to be taken keeping in mind the potential adverse
effects of the combination.
Mirtazapine augmentation has been found to hasten the
response with no significant long term benefits [23] and
hence may be considered as an augmenting agent in partial
responders and non-responders.
TECHNIQUES
1. Electroconvulsive therapy(ECT)
ECT has not been systematically evaluated for the treatment
of OCD. Available evidence, in the form of case reports and
case series, do not provide evidence for the efficacy of ECT
[28]. Hence, ECT is not recommended as a treatment for
OCD and may be considered for the treatment of comorbid
conditions like severe mood and psychotic disorders, if
indicated.
2. Repetitive transcranial magnetic stimulation (rTMS)
rTMS entails the possibility of non-invasive and focal
stimulation of superficial cortical regions, thereby
increasing or decreasing their excitability based on the
frequency of stimulation. The regions implicated in OCD
are usually not accessible with available technology of
rTMS. Hence rTMS has been tried in superficial cortical
regions which have connections with other deeper
structures implicated in OCD. Controlled trials of low
frequency or high frequency rTMS over either dorsolateral
prefrontal cortex (DLPFC) have yielded conflicting results

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 Reddy, et al.: CPGs for OCD
but low frequency rTMS over supplementary motor area
(SMA) and orbitofrontal cortex (OFC) appear promising
[29]. However, the evidence has not been very consistent.
Overall, the findings have to be replicated in larger
samples with long term follow-up. There is no convincing
evidence that beneficial effects persist for longer than
the trial period. The guideline recommends rTMS as an
intervention for further research and not for routine
clinical use.
3. Transcranial direct current stimulation (tDCS)
tDCS is another focal and superficial cortical modulatory
intervention, which either increases or decreases the
excitability of the underlying cortex depending on the
polarity of the stimulating electrode. There are only a few
case reports and an open-label trial on tDCS in OCD. It
has to be evaluated more systematically before it can be
recommended for clinical use in OCD.
NEUROSURGICAL PROCEDURES
1. Ablative neurosurgery
Ablative neurosurgical procedures involve producing lesions
in specific regions of the CSTC circuit, which is hypothesized
to be dysfunctional in OCD. Reliable lesions can be produced
with the help of “invasive” stereotactic surgery or “non-
invasively” with the help of image guided gamma radiation.
Anterior cingulotomy and a refined version of capsulotomy
known as ‘gamma ventral capsulotomy’ are practiced
in treatment refractory OCD in a few centers. Due to the
irreversible nature, these procedures are generally employed
in treatment refractory patients (Table 10). Evidence primarily
in the form of uncontrolled studies suggests that around 40-
Table 10: Selection criteria for surgery
1. Severe (YBOCS >28) and chronic unremitting OCD
2. The disorder is causing substantial distress and impairment in
functioning (GAF ≤45)
3. The following treatment options tried systematically without appreciable
effect on the symptoms
• Adequate trial with at least 2 of the SSRI antidepressants for at least 3
months each
• Treatment with clomipramine at optimum dosage for at least 3 months
unless poorly tolerated
• Augmentation with at least 2 agents, one of them being an atypical
antipsychotic: atypical antipsychotic (ripseridone, aripiprazole),
clomipramine, memantine, ondansetron/granisetron
• At least one adequate trial of cognitive behavior therapy (at least 20
sessions of exposure and response prevention) or demonstrated inability
to tolerate the anxiety due to therapy
• Previous treatment trials have not been abandoned prematurely due to
solely mild side effects
4. Patient gives informed consent
5. Willing to participate in the pre‑operative evaluation and post‑operative
periodic follow‑up
Relative contraindications:
1. Comorbid intellectual disability, psychosis, bipolar disorder and severe
personality disorders
2. Clinically significant and unstable neurologic illnesses
Indian J Psychiatry 59 (Supplement 1), January 2017
60% of patients improve over 6-24 months following surgery.
There is some suggestion that capsulotomy may be more
effective procedure in OCD [30] and that its efficacy may be
similar to that of deep brain stimulation (DBS)[31]. Surgery
may be associated with short-term and persistent adverse
effects including personality changes, seizures and cognitive
adverse effects although rates are not high.
2. Deep brain stimulation
Deep brain stimulation (DBS) is a potentially reversible
procedure involving high frequency stimulation of
implanted electrodes in the brain. Although the mechanism
of action is poorly understood, it is hypothesized to modify
dysfunctional circuits. DBS for OCD has been evaluated
in sham controlled studies targeting nucleus accumbens,
ventral capsule/ventral striatum, anterior limb of internal
capsule, ventral caudate and subthlamic nucleus. A recent
meta-analysis found a responder rate of 60% with a mean
YBOCS reduction of around 45% [32]. DBS is an invasive
procedure and is associated with short term and long term
adverse effects. Further, the battery needs to be replaced
periodically which may be quite expensive. DBS can be
recommended in carefully selected refractory OCD patients
(Table 10) after discussion regarding the pros and cons of
the procedure.
The neurosurgical procedures are not curative in nature
and the procedures are only one aspect of a comprehensive
treatment program which should continue following
surgery.
Surgical procedures may be considered only in selective
patients after careful evaluation of patients for treatment
refractoriness, severity of illness and comorbidities.
Patients should be explained about the realistic possibility
of benefits and risks. They should be evaluated by an
independent team consisting of a psychiatrist, a neurologist
and a neurosurgeon for suitability for surgery. The treatment
should be conducted under close collaboration of a team
of psychiatrist, neurosurgeon, radiotherapist, imaging
specialist and psychologist with close monitoring of adverse
effects. Suggested criteria for suitability to undergo surgery
are shown in Table 10.
PSYCHOLOGICAL TREATMENTS FOR OCD
(TABLE 11)
A. Cognitive Behavioral Therapy (CBT) / Exposure
and Response Prevention (ERP)
Consistently, CBT/ERP has been shown to be efficacious in
the treatment of OCD [33]. All treatment guidelines have
suggested the use of CBT as a first-line treatment option.
CBT for OCD includes ERP.
CBT/ERP is a first-line treatment option for OCD. ERP is
the most important component of CBT along with belief
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 Reddy, et al.: CPGs for OCD
Table 11: Psychotherapy in OCD
Psychotherapy Strength of
recommendation
Cognitive behaviour therapy (including exposure A Where resources are available, 15-20 hours of therapist
and response prevention)
Behaviour therapy (exposure and response A and computerized CBT is very preliminary and it may be
prevention)
Mindfulness based cognitive behaviour therapy C
Acceptance and commitment therapy C
Stress management and relaxation training C
Thought stopping C B. Other Psychological therapies
Dynamic psychotherapy C 1. Acceptance and Commitment Therapy
*Based on modified Strength of Recommendation Taxonomy (SORT)[15]
modification. When facilities are available, CBT/ERP
monotherapy may be recommended in mild to moderately
ill patients. In severely ill patients a combination of CBT and
SSRI is recommended.
CBT as an augmentation strategy
It is uncertain whether initiating a combination of CBT/ERP
and SSRI is advantageous compared to either treatment
alone. However, CBT/BT is found to be effective in
augmenting SSRIs in partial/non-responders to SSRIs [34].
A recent study found CBT to be superior to risperidone and
placebo in augmenting SSRIs in OCD [35]. Patients in the CBT
group had significantly greater reductions in OCD symptom
severity compared with participants taking risperidone or
placebo. Risperidone was not superior to placebo on any
outcome measures.
When facilities for CBT are available, CBT / BT is
recommended as the first line augmenting strategy in
partial/non-responders to SSRI treatment.
Mode of CBT/ERP delivery and adaptations
Although various models are available for CBT in OCD,
the major components are psychoeducation, development
of symptom hierarchy, cognitive restructuring and ERP
(Table 12). The method of conducting ERP has been found
to be important with ‘therapist–assisted’ ERP producing
a greater change in symptom severity. Therapist-guided
exposure is better than self-guided exposure. The numbers
of CBT sessions have varied between 12 and 20 sessions
across various studies. It has ranged from intensive daily 2
hour sessions for 5 days a week for 3 weeks to less intensive
twice weekly sessions in other studies.
Even though group CBT has been compared with individual
CBT, the results have been mixed. While a couple of
studies have reported comparable efficacy for group and
individual forms of CBT, some other studies demonstrated
the superiority of individual mode of CBT compared to
the group CBT. Another adaptation of CBT which has
been examined in the recent years is the internet based
CBT (ICBT) and computerized CBT. They are found to be
S84
effective compared to supportive therapy / relaxation
methods [36, 37].
assisted CBT / BT may be considered. The evidence for ICBT
recommended in certain circumstances where regular face-
to-face CBT is not feasible.
This therapy aims to improve psychological flexibility
through the practice of acceptance and mindfulness in
addition to commitment and behavior modification exercises.
Preliminary evidence suggests its benefits but it needs to be
tested and compared with CBT in larger samples.
2. Stress management and relaxation training
These have been conventionally used in many studies
as control arm in studies CBT. Stress management and
relaxation training may have non-specific effects but there is
no evidence suggesting their efficacy in treatment of OCD.
3. Mindfulness based cognitive therapy
Mindfulness based therapy is thought to be useful in
OCD. Preliminary data suggests its utility in treating OCD.
Protocols for RCT are published but there is no published
evidence in the literature in clinical population.
4. Family inclusive treatments
Family-inclusive treatment (FIT) approaches aim to include
the family members in the treatment so as to improve
the family functioning, facilitate behavioral therapy etc.
Studies targeting family accommodation of obsessive-
compulsive symptoms report greater improvements in
patient functioning. Family members may be encouraged to
participate in CBT since family accommodation of symptoms
is associated with poorer treatment outcomes.
5. Others
The other forms of psychological therapies with isolated
studies include adjunct motivational interviewing to ERP
and Eye Movement Desensitization and Reprocessing
(EMDR). There is one study examining the role of brief
dynamic therapy in OCD with negative result. In addition,
the potential benefits of adding D-cycloserine prior to ERP
sessions has been examined in few studies.
MANAGEMENT AS PER THE DIFFERENT PHASES
OF ILLNESS
Acute phase
This includes decision on choice of treatment modality
(SSRI vs. CBT), implementation of treatment, monitoring for
the response and side-effects, and planning for sequential
Indian J Psychiatry 59 (Supplement 1), January 2017
 Reddy, et al.: CPGs for OCD

Table 12: Components of CBT for OCD

Step
Assessment
Psychoeducation
Formulate the therapy
Handling the thoughts
Challenging the dysfunctional
beliefs
Behavioral Experiments-Exposure
and Response prevention
Relapse prevention
Components
• Assess nature and severity of OCD symptoms (YBOCS symptom checklist and severity rating)
• Examine insight in to the OCD symptoms
• Assessment of safety behaviors and avoidance strategies employed by the patient
• Look for current comorbid conditions such as depression that may interfere with CBT
• Assess the motivation levels and personality attributes of the patient
• Family’s involvement (accommodating the symptoms, proxy compulsions, expressed emotions) needs to be
explored
• Educate regarding the nature of obsessions and compulsions
• Explain the cycle of propagation of obsessions through performing compulsions and by avoiding the stimuli
• Discuss in detail the rationale behind CBT (concepts of habituation, fear extinction and the role of
dysfunctional beliefs)
• Educate the family members about principles in CBT
• Formulation needs to be personalized
• Identify the specific cognitive distortions (maladaptive thinking patterns) such as exaggerated threat
perception, inflated responsibility, perfectionism, need to control thoughts etc.
• Develop a collaborative understanding of the formulation with the patient (e.g., the goal is to eliminate fear of
• HIV infection and not reduce/prevent the chances of contracting HIV)
• Explain the “neutral spectatorship” principle towards obsessions (don’t interpret them, observe )
• Demonstrate how offering active resistance to obsessions is counterproductive and increases their salience
• Foster the practice of gathering evidence for the thoughts (how likely would it happen/what is the worst
consequence/less threatening alternative explanations etc.)
• Socratic questioning initiated
• Examining the faulty appraisals with examples
• Preparing for behavioral experiments (exposure and response prevention)
• ERP forms the core of CBT. Exposure to anxiety provoking situations in a graded manner with negotiations
and contracts at every step
• Rationale of ERP with examples-explain the habituation and extinction principle with the aim of anxiety
reduction as well as disconfirmation of the fears
• Make a list of anxiety provoking situations/triggers in a hierarchical manner using subjective units of
distress (0 to 10 subjective rating by the patient)
• Expose the patient starting from the lowest anxiety provoking situation and gradually escalate the level. Each
session lasting for 1‑1 ½ hours , till the patient experiences reduction in distress/anxiety
• Homework assignments, consistent performance of ERP tasks insisted upon
• Explain that treatment is a continuous process
• Periodic booster sessions to review the situation and to troubleshoot emerging issues
• Anticipation of future concerns such as change in the form of symptoms, relapse under stress, emergence of
subtle avoidance behaviors etc
• Encourage regular work and other normal behaviors

treatment trials if initial treatments failed to produce MANAGEMENT OF COMORBID CONDITIONS

satisfactory improvement.
Maintenance treatment (How long the treatment should
be continued?)
There is evidence for ongoing improvement with continued
use of SSRIs and clomipramine in long term continuation
studies for a period of up to 1 year[18]. Guidelines
recommend continuation of SSRIs / clomipramine for at
least 1-2 years after achieving remission. Clinical experience
dictates that discontinuation of medication beyond that
period may be associated with increased chance of relapse.
Hence discontinuation of medications should be carefully
considered based on individual patient factors including
severity and duration of illness, past history of relapse on
discontinuation, residual symptoms, comorbidities etc.
Most patients may require continued pharmacotherapy to
prevent relapses. Medications are generally recommended
to be continued at the same dose that resulted in
improvement, unless the dosage is not tolerated.
Depression and Anxiety disorders
Most common co-occurring illness is major depression. The
Pharmacological treatment strategy does not change much,
however in severe depression CBT/ERP for OCD needs to
kept on hold until the patient recovers from depression.
Severe depression with prominent suicidal ideas needs
to be evaluated thoroughly and ECT may be considered if
indicated. Comorbid dysthymia is common and may require
individual therapy.
Comorbid anxiety disorder needs to be treated aggressively
since untreated anxiety disorder may contribute to poor
treatment outcome. Comorbid anxiety disorders may
require CBT in addition to SSRIs.
Tic disorders
Tic disorders show best response to antipsychotics
(haloperidol, pimozide, risperidone and aripirazole).

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 Reddy, et al.: CPGs for OCD
Although antipsychotics may be more effective, adrenegic α2
agonists (clonidine and guanafacine) may be tried first to treat
tics in view of adverse effects associated with antipsychotics.
Habit-reversal therapy (HRT) is a potential first-line treatment
option instead of or in combination with pharmacotherapy.
OCD patients with tic disorders may require a combination
of an SSRI and an antipsychotic. There is evidence that OCD
comorbid with tic disorders may not respond satisfactorily
to SSRI alone.
Bipolar Disorder
Comorbid bipolar disorder calls for a different treatment
strategy because SSRIs are well known to cause/exacerbate
hypomania or mania. Mood stabilization should be the
primary goal in treating OCD-bipolar patients [38]. In
many patients with comorbid bipolar disorder, OCD often
manifests / increases in severity in depressive episodes but
improves in mania / hypomania episodes. In such patients,
treatment with mood stabilizer alone may be considered.
If OCD persists outside of the mood episodes, CBT may be
preferred over SSRIs. However, if patient requires an SSRI,
it has to be prescribed under the cover of mood stabilizers
or an atypical antipsychotic.
Psychosis
OC symptoms and OCD are not uncommon in those with
schizophrenia; up to 25% of the schizophrenia patients
report clinically significant OCD symptoms. SSRIs may be
used in treating OCD comorbid with schizophrenia, but there
is limited published evidence. Some atypical antispychotics
such as clozapine, risperidone and olanzapine may induce
or even worsen OCD symptoms. In case of drug-induced OC
symptoms, if feasible, one may consider reducing dose or
changing to another antipsychotic.
Personality disorders
20% of the participants suffer from at least one comorbid
personality disorder (PD). The most common are obsessive-
compulsive, narcissistic and anxious avoidant personality
disorders. Presence of PD can complicate the course and
outcome. OCD patients with different comorbid PDs differ
in their therapeutic response to treatment. Borderline,
obsessive-compulsive and schizotypal personality disorders
can contribute to poor outcome. There are no systematic
studies comparing the effects of treatment in OCD coexisting
with PD. Generally it is agreed upon that a combination of
medications, CBT-ERP and individual therapy are advocated.
OCD during pregnancy and lactation
Medication should be guided primarily by its safety data,
severity of the illness, and benefit vs. risk to the developing
fetus. For newly diagnosed OCD during pregnancy and in
the post-partum period, CBT/ERP is the preferred option
[39]. Pre-pregnancy counseling for all women should
include planning pregnancy, folate supplementation,
S86
discussion with patient and spouse regarding options,
and active liaison with obstetricians, ultrasonologists and
pediatricians.
Following is the summary of SSRIs in pregnancy and lactation:
1. If the patient is symptom-free for a long period, an
attempt may be made to withdraw the SSRI gradually.
However, a risk of relapse following discontinuation
should be discussed.
2. Benefits vs. risks of continuing SSRIs during pregnancy
should be discussed keeping in mind the fact that OCD
can relapse following discontinuation.
3. SSRIs as a group do not appear to be major teratogens.
4. SSRIs, paroxetine in particular have been associated with
increased risk for cardiac malformations (septal defects)
(1.5-2%), as compared to the general population (1%)
but the evidence is inconsistent. Paroxetine may be
avoided; it is less safe than the other SSRIs.
5. Some studies have reported an association between SSRI
use in first trimester and anencephaly, craniosynostosis,
and omphalocele. However, it must be emphasized that
the risks are rare and absolute risks are small.
6. When taken in late pregnancy, SSRIs may increase the
risk of persistent pulmonary hypertension by more
than twofold in the newborn (absolute risk, 3 infants
per 1000 exposed vs. 1.2 infants per 1000 unexposed).
7. SSRIs have also been associated with decreased
gestational age, low birth weight and spontaneous
abortion
8. Following birth, serotonergic toxicity and antidepressant
discontinuation symptoms may manifest, therefore it is
important to liaise with pediatricians.
9. Sertraline, fluvoxamine and paroxetine are present in
very low concentrations in plasma of breast-fed infants
(<3% of maternal dose). It is surmised that they are
relatively safe during breast feeding. With fluoxetine
and citalopram, infants can receive up to 15% of the
maternal dose.
OCD in child and adolescent population
SSRIs and clomipramine are efficacious in treating OCD and
are superior to placebo with modest effect size [40]. CBT
has superior efficacy compared to SSRIs in children [40]. A
combination of CBT and SSRI seems to have no additional
advantage over CBT alone indicating that SRI treatment
adds little to concomitant CBT. However, combined
treatment is better than SSRI alone. In partial responders to
SSRIs, adding CBT is superior and efficacious as compared
to continuing a SSRI. In view of superior efficacy of CBT,
many guidelines advocate CBT as the first line treatment
in children. In children, where facilities are available, CBT
may be preferred over SSRIs as the first-line treatment. In
children with severe OCD, a combination of CBT and SSRI
is recommended over SSRI alone. SRIs are the alternative
first-line treatment for OCD in children in situations where
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 Reddy, et al.: CPGs for OCD

Table 13: Side‑effects of SSRIs

Somnolence Comment Management
Drowsiness, All SSRIs can cause somnolence Drowsiness: Prescribe bulk of dose at bedtime
insomnia Insomnia more common with fluoxetine Insomnia: Fluoxetine may be prescribed in the morning.
Benzodiazepines, Trazadone or zolpidem may be used for
insomnia
Hypotension Not a usual side‑effect
Conduction SSRIs have no effect on QTc and are not associated with SSRIs are generally safe in patients with cardiovascular
disturbances arrhythmias and conduction disturbances diseases including the post myocardial infarction period
Exception: Citalopram (? escitalopram) is associated with dose Sertraline appears to be the safest. Citalopram and escitalopram
related increase in QTc and Tosades de pointes in overdose should be used with caution in those at risk for arrhythmia
Anticholinergic Not prominent with SSRIs except with paroxetine Most get over the side‑effects. If they are troublesome, reduce
the dose or change the SSRI
Gastrointestinal Nausea, vomiting, diarrhea, dyspepsia and anorexia are common. Common GI side‑effects usually settle down with continued
Nausea more common with Fluvoxamine. Paroxetine can cause use. If they persist, reduce dose or change the SSRI. Proton
constipation pump inhibitors may be useful
SSRIs may increase the risk of gastrointestinal bleeding Use SSRIs with caution when co‑administered with aspirin,
NSAIDs or oral anticoagulants
Neurological Headache (and worsening of migraine), tremors and rarely Fine tremors, akathisia may respond to propranolol.
akathisia, extrapyramidal symptoms, seizures and dyskinesias Extrapyramidal symptoms respond to trihexiphenidyl.
Headache responds to acetaminophen prn
Activation/ Usually seen with fluoxetine Increase the dose gradually; benzodiazepines may help
agitation
Switch to mania/ Risk of switch to mania/hypomania is known in those with bipolar Always use under the cover of mood stabilizers or atypical
hypomania disorder antipsychotics
Sexual All SSRIs are associated with sexual dysfunction; prevalence may Identify if other causes such as depression and medical causes
dysfunction be as high as 60% are contributing to sexual dysfunction
All phases of sexual response are affected including decreased If possible, reduce dose or employ drug holidays but this
libido, erectile dysfunction, decreased vaginal lubrication, delayed approach has the risk of relapse
orgasm, and ejaculatory delay. Erectile dysfunction and ejaculatory Change to other SSRI may be considered
delay are worse with paroxetine compared to other SSRIs Siddenafil or tadalafil, cyproheptadine, and bupropion may
improve sexual dysfunction
Hyponatremia SSRIs are associated with hyponatremia because of syndrome of Hyponatremia is common in elderly. Monitoring is essential.
inappropriate secretion of antidiuretic hormone (SIADH). Risk Referral to specialists if serum level is <125 mmol/L
factors include old age, female gender, co‑administration of drugs
known to cause hyponatremia (diuretics, NSAIDs, ACE inhibitors
etc), reduced glomerular filtration rate, and medical comorbidity
Serotonin Nausea, vomiting, diarrhea, tremor, sweating, disorientation, Stop the offending drugs immediately. Symptomatic
syndrome restlessness, agitation, headache, increased heart rate, changes in management: benzodiazepines to treat agitation and/
blood pressure & temperature, twitching, tremors, myoclonic jerks, or seizures, intravenous fluids to maintain hydration,
hyperreflexia, high fever, seizures, arrthymias, agitation, confusion, anti‑emetic and anti‑pyretic medications. In severe cases,
delirium and even coma cyproheptadine (8‑12mg/day) is given orally
Can occur with very high doses of SSRIs or a combination of
SSRIs in high doses
Weight gain Known with all SSRIs although there may be initial weight loss. If weight gain is significant, an attempt may be made to shift to
Paroxetine is associated with weight gain more than other SSRIs another SSRI
Lifestyle modification may be discussed
Drugs such as topiramate may be tried
Suicidal SSRIs are associated with increased suicidal ideation and attempts Children on SSRIs should be monitored closely for emergence
behavior in children of suicidal thoughts
Discontinuation Abrupt discontinuation may cause discontinuation syndrome, Withdraw gradually. Taper SSRI by no more than 25% per
syndrome particularly with short‑acting drugs (dizziness, nausea, vomiting, week
diarrhea, headache, fever, sweating, chills, insomnia, paresthesias,
electric‑shock‑like sensations, anxiety, agitation, irritability,
disorientation). Reported mostly with paroxetine. Typically occur
within a week of discontinuation
Drug Fluoxetine, paroxetine and fluvoxamine inhibit cytochrome P‑450. Caution should be exercised in combining ceratin SSRIs
interactions Inhibit the metabolism and elevate levels of drugs metabolizedd by with drugs that are essentially metabolized by cytochrome
this system P‑450 system. SSRIs can elevate clomipramine level resulting
in more side effects, particularly seizures and serotonin
syndrome; this combination should be used judiciously and
patients have to be monitored closely

CBT is either not available or the child cannot comply with SSRIs in medically ill
CBT. SSRIs are generally safe in patients with cardiovascular

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 Reddy, et al.: CPGs for OCD
Table 14: Summary of treatment recommendations
• Establish a diagnosis of OCD. Assess for comorbid conditions such as
depression and anxiety disorders and certain personality disorders. It is
important to treat comorbid conditions since untreated comorbidity may
contribute to poor outcome
• Where feasible, employ instruments such as the YBOCS to assess
symptoms and their severity
• Psychoeducation of the patient and family about OCD, its course and
treatment options is essential
• SSRIs and CBT are the first‑line evidence based treatment options for
OCD. In the Indian context, SSRIs are often the preferred first‑line
treatment options
• All SSRIs are equally effective but they differ in their side‑effect profile.
Choice of an SSRI for an individual patient is based on factors such as
previous response, tolerability, acceptability, adverse effects, cost and
drug interactions
• Most patients require higher than the usual antidepressant dose of an SSRI
• There is no convincing evidence that clomipramine is superior to SSRIs.
Since clomipramine has many side‑effects, it is not recommended as the
first‑line treatment option. It may be considered if patient fails to respond
to 2 or more SSRIs
• An adequate trial of an SSRI (or clomipramine) should be for at
least 12 weeks in optimum doses. Premature discontinuation is not
recommended since most patients show improvement gradually over
several weeks
• SSRI has to be continued at least for 1‑2 years after remission However,
most patients may require indefinite continued treatment with a SSRI to
prevent relapses particularly those with severe and chronic illness, past
history of relapse on discontinuation and clinically significant residual
symptoms. SSRIs are generally recommended to be continued at the same
dose that resulted in improvement, unless the dose is not tolerated
• CBT alone may be recommended in mild to moderately ill patients if
facilities for CBT exist. However, most severely ill patients benefit from a
combination of an SSRI and CBT
• In partial responders and non‑responders to SSRIs, addition of CBT
is recommended as the first option. If CBT is not feasible, an atypical
antipsychotic in low dose (risperidone and aripiprazole) may be added as
an augmenting agent
• Inpatient treatment is recommended for severely ill, treatment
resistant patients and for comorbid conditions such as severe
depression
• ECT has no proven value in the treatment of OCD. There is inconsistent
evidence regarding the efficacy of rTMS; hence it is not recommended for
routine use
• DBS and ablative surgery may be considered in chronic, severely ill
treatment refractory OCD patients
problems. Citalopram (? Escitalopram) is associated with
arrhythmias but the risk is low and may not be clinically
significant, but may be used with caution or avoided in
those at risk for arrhythmias. SSRIs are widely used to
treat depression in diabetes. They may improve diabetic
parameters: improvement in HbA1c levels, reduced insulin
requirement, enhanced insulin sensitivity and improved
glycemic control. SSRIs are not hepatotoxic, but they
need to be used in lower doses and with caution in the
presence of significant hepatic impairment since all SSRIs
are biotransformed in liver. All SSRIs are metabolized by
the Cytochrome P450 system and fluoxetine, fluvoxamine,
and paroxetine also significantly inhibit P450 enzymes.
Therefore, these agents may potentially interfere with wide
variety of other medications. Interactions with other drugs
S88
need to be considered, particularly in elderly who are likely
to be on many medications for other medical conditions.
Citalopram / escitalopram and sertraline do not substantially
inhibit P450 enzymes and therefore are associated with less
drug interactions. All SSRIs are renally excreted. Depression
is common in those with chronic kidney disease (CKD)
and end stage renal disease (ESRD). If indicated SSRIs are
the preferred antidepressants. SSRIs such as paroxetine,
citalopram and escitalopram may have to be administered
in lower doses in CKD and ESRD in the background of
compromised renal functions. Since many patients with
CKD and ESRD also suffer from cardiovascular disorders,
citalopram (and perhaps escitalopram) may be used with
caution since high doses of citalopram is associated with
QTc prolongation and torsades de pointes.
Side Effects of SSRIs
The dosage of anti-obsessive drugs is usually higher than
the usual anti-depressant dose; hence it is important for
the clinician to discuss regarding the common side-effects.
This issue is important because patients need to be on
medications for a long duration. Sometimes an adjustment
in dose or a switch in the time of the day the dose is taken is
all that is needed. Rarely, stopping a particular medication
and switching to another medication may be required. Side-
effects of SSRIs and possible remedies are given in Table 13.
Summary
Recommendations are summarized in Table 14. The SSRIs
and CBT are the first-line treatment options for OCD. CBT
alone may be tried in mild to moderately ill patients if
facilities for CBT are available. In severe OCD, a combination
of SSRI and CBT is recommended. In the Indian context,
SSRIs are the preferred first-line treatment for OCD because
of limited resources for delivering CBT. SSRIs are effective,
well tolerated and safe. For partial responders and non-
responders to SRIs, CBT is an effective augmenting agent
followed by atypical antipsychotics. Although an attempt
may be made to taper and stop SSRI after 1-2 years of
sustained remission, most patients may require indefinite
continued treatment with a SSRI. DBS and ablative
surgery may be considered in chronic, severe OCD if other
established treatment options have failed to produce any
clinically significant improvement.
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Indian J Psychiatry 59 (Supplement 1), January 2017
 CLINICAL PRACTICE GUIDELINES
Clinical Practice Guidelines for Management of Sexual Dysfunction
Ajit Avasthi, Sandeep Grover, T S Sathyanarayana Rao1
Department of Psychiatry, PGIMER, Chandigarh, 1Department of Psychiatry, JSS Medical College Hospital, JSS University,
Mysore
Participants of the Expert group on CPG for
management of sexual dysfunction
Murgesh Vaishnav, G Prasad Rao, Neelanjana Paul,
Mukesh P Jagiwala, Roop Sidana, M S Bhatia
INTRODUCTION
Sexual functioning is a complex bio-psycho-social process,
coordinated by the neurological, vascular and endocrine
systems. In addition to the biological factors, the psychosocial
factors like societal and religious beliefs, health status,
personal experience, ethnicity and socio-demographic
conditions, and psychological status of the person/couple
play an important role in adequate sexual functioning of a
person. In addition, sexual activity incorporates interpersonal
relationships, each partner bringing unique attitudes, needs
and responses into the coupling. A breakdown in any of
these areas may lead to sexual dysfunction.
Prevalence of sexual dysfunction in general population is
very high. It is suggested that about 43% of women and 31%
of men have one or other kind of sexual dysfunction. Among
men, premature ejaculation is the most common male
sexual dysfunction. There is lack of consensus with regards
to the most common sexual dysfunction in women with
some studies reporting hypoactive sexual desire disorder
to be the most common entity, followed by orgasmic
and arousal disorders; whereas other studies suggest
that difficulty achieving orgasm and vaginal dryness to be
the most common type of sexual dysfunction in women.
Problems of sexual dysfunction may be lifelong or acquired,
general or situational.
Address for correspondence:
Dr. Ajit Avasthi, Department of Psychiatry, Postgraduate
Institute of Medical Education and Research,
Chandigarh ‑ 160 012, India.
E-mail: drajitavasthi@yahoo.co.in
Access this article online
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Website:
www.indianjpsychiatry.org
DOI:
10.4103/0019-5545.196977
© 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow
Although sexual problems are highly prevalent, these
are frequently under-recognized and under-diagnosed in
clinical practice. It is also noted that clinicians also have
lack of understanding about the approach for identification
and evaluation of sexual problem. It is often recommended
that the treating psychiatrists and collaborating specialists
need to possess broad knowledge and appropriate attitude
towards human sexuality.
The essential concepts underlying the management of sexual
problems are adoption of a patient-centered framework
for evaluation and treatment. Principles of evidence-based
medicine may be followed in both men and women in
diagnostic and treatment planning and adoption of common
management approaches for sexual dysfunction. The
purpose of these guidelines is to present a framework for the
evaluation, treatment, and follow-up of the patient/couple,
who presents with sexual dysfunction. We hope that these
guidelines would help in facilitating proper management of
patients presenting with various types of sexual dysfunction.
These guidelines are to be read along with the earlier version
of Indian Psychiatric Society Guidelines.
CLASSIFICATION OF SEXUAL DISORDERS
Compared to DSM-IVTR, DSM-5 has fewer categories
for describing sexual dysfunction and has provided
gender-specific sexual dysfunctions (Table-1). Other
major change in DSM-5 includes the duration criteria.
According to DSM-5 the minimum duration for making
the diagnosis of sexual dysfunction is 6 months (except
substance-/medication-induced sexual dysfunction) for
almost all the disorders and also specifies the frequency
of dysfunction to be 75-100%. DSM-5 has also done away
with the categories of sexual aversion disorder and sexual
dysfunction due to a general medical condition. The category
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How to cite this article: Avasthi A, Grover S, Sathyanarayana
Rao TS. Clinical Practice Guidelines for Management of Sexual
Dysfunction. Indian J Psychiatry 2017;59:91-115.
S91
 Avasthi, et al.: Sexual dysfunction

Table 1: Comparison of diagnostic categories of ICD‑10 & DSM‑5 of sexual disorders

Disorders according to ICD‑10 DSM‑5
sexual cycle
Sexual desire disorders Lack or loss of sexual desire Male hypoactive sexual desire disorder
Sexual aversion Female sexual interest/arousal disorder
Excessive sexual drive
Sexual arousal Failure of genital response Male
disorders Erectile disorder
Orgasm disorders Orgasmic dysfunction Male
Lack of sexual enjoyment Premature (early) ejaculation
Premature ejaculation Delayed ejaculation
Female
Orgasmic disorder
Sexual pain disorders Nonorganic dyspareunia Female
Nonorganic Vaginismus Genito‑pelvic pain/penetration disorder
Substance/Medication induced sexual dysfunction
Other sexual disorders
Paraphilias Paraphilic disorders
Gender identity disorders Gender Dysphoria
Gender Dysphoria in children
Gender Dysphoria in adolescent and adults
Other specified Gender Dysphoria
Unspecified Gender dysphoria
Other sexual dysfunction, not caused by
organic disorder or disease
Unspecified sexual dysfunction, not
caused by organic disorder or disease

of substance induced sexual dysfunction is now labelled as Table 2: Subtypes of sexual dysfunctions according to
Substance/Medication induced sexual dysfunction. The Not DSM‑5
Otherwise Specified (NOS) category has also been removed. Subtypes
The substance or medication-induced sexual dysfunction has Onset Lifelong: present since the Acquired: develops after a period
been retained as such. Various types of sexual dysfunctions onset of sexual functioning of normal functioning
are categorized on the basis of onset and context (Table-2). Context Generalized : not limited to Situational: limited to certain types
certain types of stimulation, of stimulation, situation or partner
situation or partner
ICD-10 describes sexual disorders under the headings
of: Sexual dysfunction, not caused by organic disorder
or diseases (F52) under the broad heading of Behavioral sideward curvature of penis and watery semen. Thus, there
syndromes associated with physiological disturbances are exaggerated apprehensions in males centered on sexual
and physical disorders, Gender Identity disorders (F64), performance on “First wedding night (Suhaag raat)”. Some
Disorder of sexual preferences (F65), Psychological and of the studies have also shown that many females who have
behavioral disorders associated with sexual development leucorrhoea, for which no infective or pathological cause
and orientation (F66), under the broad heading of Disorders could be found have psychasthenic syndrome or female Dhat
of adult personality and behavior. syndrome, similar to Dhat syndrome in males.

Other sexual disorders/dysfunctions in Indian context
Although both the nosological systems have classified sexual
disorders, but they don’t include certain sexual disorders
commonly seen by Indian clinicians. Indian researchers have
consistently alluded to the existence of certain unique socio-
culturally determined sexual clinical conditions such as, Dhat
syndrome and Apprehension about potency. Dhat syndrome has
been coded in ICD-10 under other neurotic disorders (F48.8),
but the diagnosis of apprehension about potency doesn’t find
mention. The clinical entity of apprehension about potency
is related to the commonly held belief in most of the Indian
sub-cultures that masturbation and night emissions before
marriage result in loss of potency in marital conjugal relations.
Masturbation is considered to be responsible for shrinkage or
Sexuality is understood as a broader concept which goes
beyond sexual dysfunctions. These guidelines are applicable for
management of sexual dysfunctions and some of the disorders,
like Dhat syndrome which are seen in the Indian context and
are associated with high rates of comorbid sexual dysfunctions.
ASSESSMENT OF PATIENTS WITH SEXUAL
DYSFUNCTIONS
Evaluation of any patient with sexual dysfunction requires
thorough understanding about the type of sexual
dysfunction, factors associated with or contributing to
sexual dysfunction and factors maintaining the sexual
dysfunction. Accordingly, proper evaluation includes

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 Avasthi, et al.: Sexual dysfunction

detailed history taking (sexual, medical and psychosocial),
focused physical examination, laboratory tests (routine
and specific) and consultation with appropriate specialists.
Careful attention always be paid to the presence of
significance comorbidities or underlying etiologies (e.g.,
cardiovascular disease, diabetes, depression).
Important aspects of evaluation of patients with sexual
dysfunctions
Discussing sex-related issues can be embarrassing both for
the clinician and the patient. Patients often carry the feeling
of failure or that they are abnormal. Clinicians should
anticipate the embarrassment of patient and acknowledge
that it could be difficult talking about such issues. For
example, the clinician may say, “Most people find it difficult
to talk about these things and may feel a bit embarrassed. I’d
just like to reassure you that everything you say is confidential
and that I’d like to help you if I can. The first step is to find out
exactly what’s going on so that we can figure out how to make
things right again. Please feel free to be open with me and to ask
questions whenever you have any doubt.” Some of the other
important issues for evaluation are given in Table-3.
The basic principles of sexual history taking are given in
table-4. The patient needs to be asked to describe their
problem in terms of time and manner of onset, its course
over the period, its current status, and associated medical
or psychological problems. While taking history, attention
must be given to features which can help in distinguishing
predominantly psychogenic from predominantly organic
sexual dysfunctions (Table-5). But, it is important to note
that, in many cases, organic and psychogenic factors may
coexist, particularly in individuals or couples with long-
standing or chronic sexual dysfunction. In such cases,
clinicians need to assess the independent and interactive
role of both organic and psychogenic factors.
An important aspect of sexual history taking in females is
to remember that women play different roles at different
times in their life. Many women have several roles-the
professional or worker, housewife, mother, daughter,
friend, and lover. It is often seen that the over the years
as the demands of other roles increase, lover role fades
away. Paying attention to these issues can be very useful,
and this information can be collected by using a process
called the “timetable of life.” Both partners can be asked
to fill in a timetable representing a typical week from their
initial interaction to the time of presentation. Various
aspects which can be covered during the assessment of a
week during a typical time frame may include, family time
(that is, with children and partners), work time (both at
work and work in the house), extended family time (with
parents and relations), social time, personal time, and
relationship time (time spent together as a couple). The
relationship time must also include information about the
sexual activity. A timetable almost always brings forward
various elements missing in the relationship and personal
time. Repeating the “timetable” for different times in life
and comparing it during courtship, when sexual desire
was probably good, with the timetable for a time when
sexual desire was low is useful and can show how priorities
change and how this influences desire for sexual activity.
Looking at what happens in a sexual situation often gives
much information about the defenses used when a patient
engages in sexual activity. Clinician may also note what
turns a patient on and off, how engorged he/she becomes
in the sexual experience, and whether loss of desire occurs
every time or it is situational. Other important aspects
which can enhance the understanding about the problem
include sexual fantasy, masturbation, genital functioning,
and contraception.
Psychosocial history: Psychological factors associated with
sexual dysfunction can be divided into three categories:

Table 3: Important aspects in evaluation of sexual dysfunctions

• Conduct the evaluation in a comfortable surroundings and ensure privacy
• Be empathic, non‑judgmental, and understanding
• Preferably use the language in which patient is comfortable
• Use neutral terms (as opposed to vulgar terms) and proper medical terms as long as these are in common usage (e.g., use `penis’ and `vagina’, but perhaps
`lips’ rather than `labia’)
• Use anatomical drawings to understand patients knowledge and explain sexual issues to the patient
• Reassure the patient that sexual dysfunction or adjustment problems are common and treatable. For example, “It is common for some people to .”
• Explain things in simple, clear and specific terms. Some patients may not be able to understand the language which is commonly used by clinicians and
may feel embarrassed to admit this. Hence, whenever new terms are used, provide alternatives or explanations. Check with the patients that they understand
the terms used.
• Start with general, non‑threatening questions first (e.g., “Do you have a regular partner?”) then ask more specific and potentially embarrassing
questions (e.g., “Do you also experience this problem when you masturbate, that is, when you touch or stimulate yourself?”).
• Assumptions must be avioded (e.g., sexual orientation, number of partners, sexual practices)
• If a couple has presented together, gather the information for a sexual history from each individual separately (i.e., not in each other’s presence).
• Conduct the evaluation in presence of a female attendant/relative while examining patients of opposite gender.
• Make sure that the `problem’ does not just reflect a lack of knowledge or unrealistic expectations on the part of the presenting individual or their partner.
• Understand the cultural and religious factors which influence sexual issues
• Although sexual dysfunction may occur in isolation, but in many cases there may be co‑existing problems contributing to the dysfunction (e.g., relationship
difficulties, psychiatric or physical illness) ‑ prioritize the treatment goals in such situations
• Assess psychological sophistication and motivation of the patient/couple

Indian J Psychiatry 59 (Supplement 1), January 2017 S93


Components
Basic goals of history taking
Basic questions in assessment
of sexual functioning for a
male
Past Treatment history
S94
Avasthi, et al.: Sexual dysfunction
Table 4: History taking for sexual disorders
Basic ingredients
• To understand the type of dysfunction and its cause
• To differentiate between potential organic and psychogenic causes in the etiology of a patient’s sexual problem
• To evaluate the potential role of underlying or comorbid medical conditions
• To assess the use of concomitant medications
LIBIDO/INTEREST
• Do you look forward to sex?
• Do you enjoy sexual activity?
• Do you fantasize about sex?
• Do you have sexual dreams?
• How easily are you sexually aroused (turned on)?
• How strong is your sex drive?
AROUSAL/PERFORMANCE
• When was the last time you had a satisfactory erection?
• How did you your problem start ‑ gradual or sudden?
• When did you have last normal erection?
• Do you experience morning or night time erections?
• Are you able to initiate an erection with sexual stimulation?
• Are you able to maintain an erection with sexual stimulation?
• Does your erectile dysfunction is related a specific partner or situation?
• Do you lose erection before penetration, or before climax?
• Do you have to concentrate to maintain an erection?
• Is there a significant bend in your penis?
• Do you experience pain while having erection?
• Do you have difficulty in certain sexual positions?
• Do you feel subjectively excited when you attempt intercourse?
• Does your vagina become sufficiently moist? (for females)
EJACULATION/ORGASM/SATISFACTION (males)
• Do you ejaculate when you have sex?
• Do you ejaculate when you masturbate?
• Do you ejaculate before you want to?
• How often you ejaculate before you want to?
• How often do you ejaculate before your partner wants you to?
• How does your partner react if you ejaculate before your partner wants you to?
• Do you take too long to ejaculate?
• Do you feel like nothing comes out?
• Do you experience pain with ejaculation?
• Do you see blood in your ejaculate?
• Do you have difficulty in reaching to orgasm?
• Is your orgasm satisfying?
• What percentages of sexual attempts are satisfactory to your partner?
ORGASM/SATISFACTION (females)
• Are orgasms absent and/or very delayed and/or markedly reduced in intensity?
• Is there adequate and acceptable stimulation with partner and/or with masturbation?
• Is the degree of trust and safety, you feel you need, present?
• Is there fear of letting go of control?
• What do you fear may happen that could be negative?
DYSPAREUNIA/VAGINISMUS (females)
• Where does it hurt?
• How would you describe the pain?
• When does the pain occur (with penile contact, once the penis is partially in, with full entry, after some
thrusting, after deep thrusting, with the partner’s ejaculation, after withdrawal, with subsequent micturation?)
• Does your body become tense when your partner is attempting, or you are attempting to insert his penis?
• What are your thoughts and feelings at this time?
• How long does the pain last?
• Does touching cause pain?
• Does it hurt when you wear tight clothes?
• Do other forms of penetration hurt (tampons, fingers)?
• Do you recognize the feeling of pelvic floor muscle tension during sexual contact?
• Do you recognize the feeling of pelvic floor muscle tension in other (non‑sexual) situations?
• Do you feel subjectively excited when you attempt intercourse?
• Does your vagina become sufficiently moist?
• Do you recognize the feeling of drying‑up?
Past treatment history for the presenting sexual problem‑local practitioners, Ayurvedic, Homeopathic, over the
counter medications, etc.
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 Avasthi, et al.: Sexual dysfunction

predisposing factors, precipitating factors, and maintaining Table 5: Differentiating features between psychogenic
factors (See table-6), which can co-exist with each other. and organic sexual dysfunction
The areas to be explored in psychosocial history are enlisted Characteristics Predominantly Organic Predominantly
in table-7. It is to be remembered that the existence of Psychogenic
an organic disease does not rule out the possibility of a Age Older Younger
coexisting psychogenic factor. Conversely, the presence Onset Gradual (except trauma or surgery) Acute
of psychogenic conditions, such as anxiety, anger, guilt, or Circumstances Global Situational
Symptom Course Consistent or progressive Intermittent
marital discord, need not be considered as evidence for a
Desire Normal to start with Decreased
sole primary causation. Organic risks Present Absent, variable
Partner problem Usually Secondary Usually at the onset
The current psychological state need to be assessed with Anxiety and fear Usually Secondary Usually Primary
special focus on symptoms of anxiety or depression, low
self-esteem and coping skills, previous and current partner
Table 6: Psychological factors associated with sexual
relationships, history of sexual trauma/abuse, occupational
dysfunctions
and social stresses, socioeconomic status, and educational
Factors
level. Sexual dysfunction may affect the patient’s self-esteem
and coping ability, as well as his or her social relationships Predisposing • Restrictive upbringing
factors • Disturbed family relationships
and occupational performance. These aspects need to be • Traumatic early sexual experience
assessed in each case. Clinicians need not assume that • Inadequate sexual information
every patient is involved in a monogamous, heterosexual • Insecurity in the psychosexual role
relationship. • Distraction
Precipitating • Unreasonable expectations
factors • Random failure
Considering the fact that sexual problems arise in the • Discord in the relationship
interpersonal context, the clinician need to carefully assess • Dysfunction in the partner
past and present partner relationships. Another important • Infidelity
aspect of psychosexual history is inquiring specifically about • Reaction to organic disease
the quality of the relationship between the couple with respect • Pregnancy/Childbirth
• Poor emotional intimacy
to nonsexual factors, i.e., how to they get along on most issues, • Expectation of negative outcome
communication patterns, gender equality/inequality, level • Depression or anxiety
of commitment, dealing with stress, etc. While interviewing Maintaining • Performance anxiety
the couple together it is important to note the dynamics factors • Guilt
between the partners. Relationship problems may be due to • Poor communication
• Loss of attraction between partners
intrinsic differences between the two, and expectations about • Impaired self‑image
sexual fulfillment may also vary. Many a times, lack of proper • Restricted foreplay
communication between the couple, which may be due to • Poor emotional intimacy
embarrassment, may be mistaken as lack of caring. • Depression or anxiety
• Expectation of negative outcome
• Fear of intimacy
Another important aspect of psychosocial evaluation is the • Sexual myths and misconceptions
identification of patient/couple needs, expectations from • Poor communication
each other, priorities and treatment preferences. These may
be significantly influenced by cultural, social, ethnic and
religious perspectives. Patient education about the problem evaluated. While evaluating women careful medical history
is also important in enhancing therapeutic relationship, is to be obtained about any health problem that might
communication between patient and physician and ensuring affect sexual anatomy, the vascular system, the neurological
patient compliance. Partner involvement is important. On the system, and the endocrine system. Indirect causes i.e.,
first visit, it is not always possible to involve the partner but factors that cause chronic pain, fatigue, and malaise may
efforts need to be made to involve the patient’s partner early also contribute to dyspareunia.
in the treatment process at the earliest. If the psychosocial
assessment reveals the presence of significant psychological Substance use History: Excessive use of alcohol or use of
distress or conflict between the couple, further evaluation other recreational drugs may cause sexual dysfunction,
and management may be carried out either prior to, or along either by a direct effect on the penile neurovascular system
with treatment of sexual dysfunction. or by causing increased secretion of prolactin, reduction in
production of testosterone, or both.
Medical history: Historical events related to the presence of
chronic disease, use of pharmacological agents, endocrine Treatment/Medication History: Clinicians should also enquire
disorders, prior surgeries and trauma is to be carefully about the medication intake, including prescription drugs,

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 Avasthi, et al.: Sexual dysfunction
Table 7: Psychosocial assessment of sexual dysfunctions
Variables Areas covered
Background • Marital history, Children, Educational level, Social
variables class, Occupation, Religious beliefs, family system
and relationships
Life style factors • Alcohol, Smoking, Opioids
Psychiatric history • Depression, Anxiety disorder
Sexual History
• Childhood and adolescent sexual learning and
activities
• Masturbation history, nocturnal emissions, Dhat,
Interpersonal sexual activity
• Breadth and flexibility of sexual script with all
partners
• “Time table of different phases of life”
Current sexual • Current masturbatory and interpersonal sexual
functioning activities
• Nature of the problem, onset, course, frequency
• Spontaneous sexual experiences (morning erections)
Relationship with • Harmony, Communication, Partner’s health
partner
Life stresses • Recent life stress, Current life stress, Losses
Expectations • Need, Expectations, Priorities, Treatment
from treatment preferences
over the counter medications and culturally sanctioned
aphrodisiacs. Medications commonly associated with sexual
dysfunction include diuretics (thiazides, spironolactone),
sympatholytics agents (Central agents like methyldopa ,
clonidine and peripheral agents like reserpine), alpha blockers,
beta blockers (particularly nonselective agents), angiotensin-
converting enzyme inhibitors, calcium channel blockers,
antipsychotics, antidepressants, benzodiazepines, buspirone,
lithium, disulfiram, digoxin, histamine H2-receptor blockers,
ketoconazole, niacin, phenobarbital, phenytoin, allopurinol,
gemfibrozil, clofiberate, phenobarbital, phenytoin, danazol,
GnRH agonists, oral contraceptives etc.
Physical Examination
Every effort be made to ensure the privacy, confidentiality
and personal comfort of the patient while conducting the
physical examination. Careful physical examination not only
corroborates the medical history but at times also reveals
unsuspected physical findings (e.g., decreased peripheral
pulses, vaginal atrophy, atrophic testes, penile plaque).
In addition, to the general and systemic evaluations, detailed
assessment of gonadal function, vascular competence,
neurological integrity, and genital organ normalcy is to
be performed on every patient. Patients suspected of
hypogonadism need to be assessed for evidence of muscle
development, size and structure of the penis, normal urethral
opening, hypospadias, size and consistency of the testes
and the prostate. Alcohol swabs can be used to test penile
temperature sensation. Bulbo-cavernosus reflex can be
elicited by squeezing the glans penis and assessing the evoked
contractions of external anal sphincter or bulbo-cavernosus
muscles. This reflex response is clinically detectable in 70% of
normal males. The penis also needs to be examined for evidence
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of any masses or plaque formation, angulation, unprovoked
persistent erection, or tight unretractable foreskin.
Similarly in females genital examination is often highly
informative, especially in cases of dyspareunia, vaginismus,
with a history of pelvic trauma and with any disease
potentially affecting genital health. If there are indications
from history, the opportunity for pap smear/sexually
transmitted disease investigation is to be taken.
Recommended Laboratory Testing
Recommended laboratory tests for men and women with
sexual problems typically include blood glucose levels,
cholesterol, lipids, hormonal profile and X-ray spine for spina
bifida. Additional laboratory tests (e.g., thyroid function)
may be performed at the discretion of the clinician, based
on the medical history and clinician’s judgment. When an
infective etiology for dyspareunia remains a possibility-
vaginal, cervical and vulval discharge microscopy/cultures
need to be performed.
Assessment of Knowledge and Attitude towards sex
Few patients may not actually have sexual dysfunction,
but may perceive the same, because of poor knowledge
and negativistic attitude towards sex. Further, in some
patients the sexual problems may be attributed to the
beliefs and cultural practices. Some of the scales like
Sexual Knowledge and Attitude Questionnaire and Dhat
syndrome Questionnaire, which have been validated in the
Indian context, may be used for structured assessment and
documentation. These scales can also help in determining
the area to be focused in sex education and psychoeducation.
Specialist Consultation and Referral
Patients with history of medical problems be referred to
appropriate specialty to evaluate the severity and state of
disease control (See table-8). Sometimes there may not be
a need for referral, but if patient requests for the same, it is
to be done. Further diagnostic evaluation also needs to be
conducted in case of lifelong or primary sexual dysfunction,
in the presence of specific anatomic or endocrine factors
and failure of initial therapy. Patients with hyposexual
desire and absent or retarded emission or anorgasmia may
need to be evaluated for the presence of diseases involving
the nervous system. Patients with prolonged or painful
erection need to be evaluated for the possibility of primary
penile disease, hematological disorder, or other systemic
diseases associated with penile complication.
By the end of assessment the clinician should be able to
answer the following questions for themselves to plan
management:
1. Does patient/couple actually have sexual dysfunction?
2. Whether the dysfunction is primarily psychogenic or
primarily organic?
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 Avasthi, et al.: Sexual dysfunction
3. If the dysfunction has organic etiology, then is there a
psychological overlay too?
4. If there are more than one dysfunction, then which is
the primary?
5. Does patient has any comorbid psychiatric disorder?
6. If subject has a psychiatric disorder, then is the sexual
dysfunction secondary to it?
7. If subject has a psychiatric disorder, then how severe it
is?
8. Is there a marital discord between the couple, which
needs to be addressed?
9. What is the motivation of the patient/couple to seek
treatment?
10. What is the level of psychological sophistication?
MANAGEMENT OF SEXUAL DYSFUNCTION
Principles of management
Management of sexual dysfunction involves patient centered
approach and clinicians are expected to consciously adopt
the patient’s perspective and respect the ideas, feelings,
expectations and values of their patients. Some of the basic
principles of patient centered approach are given in Table-9.
Formulation: After complete assessment, the first step in
the management is to provide the patient/couple a brief
and simple account of the nature of their problems and
possible contributory factors. The aims of the formulation
are threefold. First, it helps the couple to understand their
difficulties. This can be a source of encouragement, especially
if the therapist also explains how common such problems are.
Second, the therapist point out the likely contributory factors,
particularly the maintaining factors which will be the focus
of therapy, and thus establish a rationale for the treatment
approach. Finally, providing a formulation also helps to check
that the information obtained during the assessment has
been correctly interpreted. So the couples need to be always
asked to give a feedback of the formulation.
Balancing the partners: It is important for the therapist to
understand the contribution of individual partner to the
problem and need to strike a balance between individual
partners. The therapist must emphasize the need of
collaboration between the partners for the success of the
therapy. The therapist needs to emphasize positive aspects
of the couple’s relationship.
Treatment options: Treatments for various sexual
dysfunctions can be broadly classified into general
and specific measures. The general measures include
sex education and relaxation exercises. The specific
measures can be either pharmacological measures, non-
pharmacological measures or a combination of both.
Among the non-pharmacological measures, many types of
psychotherapies like psychodynamic, interpersonal, rational
Indian J Psychiatry 59 (Supplement 1), January 2017
emotive therapy, Master Johnson’s behavioural therapy or
its modifications, systematic desensitization, ban on sexual
intercourse and skill training in communication of sexual
preferences etc have been used. Unfortunately there are no
well designed studies which have evaluated the effectiveness
of these psychotherapies. Most of the studies done have
used convenience sampling, don’t describe their sample
adequately, have not used standard definitions for various
disorders and are silent about the therapist variables. Hence
the results cannot be generalized. Among all the techniques,
which have been used, cognitive behavioural measures of
Master Johnson or its modifications are the most popular
and have been found to be most useful.
Selection of treatment: The final selection of treatment is to
be according to patient/couple’s choice. The therapist needs
to inform the patient/couple about the available modalities
and help them to make a reasoned choice. Agreed treatment
goals need to be established at the start of treatment.
Figure-1 and 2 shows the general outline for management
of cases of sexual dysfunction presenting with or without
psychiatric comorbidity. Initial evaluation involves detailed
psychosexual history and getting the basic investigations.
Besides taking a proper history ,screening questionnaires
can be used to assess the sexual knowledge and attitude.
The initial evaluation will help in ascertaining the type(s) of
sexual dysfunction. The next step involves establishing the
probable etiological basis of the dysfunction, i.e., whether
the dysfunction is organic in origin, psychological in origin
or has components of both. If the dysfunction is organic in
origin the patient is to be referred to the concerned specialists
and need to be investigated and treated accordingly. It is
often seen that some patients may have sexual dysfunction
of organic origin, but would also have psychological factors
contributing to its maintenance. Such patients are the most
difficult to treat and require very good liaison between
the psychiatrist and the physicians. In patients who have
psychogenic sexual dysfunction, the next step involves
evaluation for sexual knowledge, relationship issues,
presence of comorbid psychiatric disorder, motivation and
psychological sophistication of the patient for treatment.
Assessing the sexual knowledge and relationship issues
are important aspect of treatment of sexual dysfunction as
many a time the patient/couple may not have any sexual
dysfunction per se but the reported complaints may be
arising due to faulty beliefs or relationship issues. If any of
these two factors are found to be contributing to the sexual
dysfunction, these need to be focused and once they have
been adequately addressed, the sexual dysfunction is to be
reassessed and if present needs to be treated adequately.
If comorbid psychiatric disorder is present, the next step
involves ascertaining – is it primary or secondary (primary-
psychiatric disorder causing sexual dysfunction; secondary –
psychiatric disorder is secondary to sexual dysfunction). The
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Table 8: Medical history, physical examination and investigations for sexual dysfunctions
Components Basic ingredients
Medical History • Cancer (bladder, prostate, uterus, cervix, rectum or other)
• Chronic fatigue or weakness
• Diabetes mellitus
• Heart disease (heart attack, chest pain with exercise or sex)
• Hormone problems (testosterone, thyroid, steroids)
• Hyperlipidemia (elevated cholesterol or triglycerides)
• Hypertension
• Joint pains (severe or chronic problems moving or changing positions)
• Kidney disease
• Neurological problems (Parkinson’s Disease, multiple sclerosis, spinal injury)
• Prostate problems
• Radiation therapy to bladder, prostate, uterus or rectum
• Sexually transmitted diseases
• Sleep apnea (severe snoring, daytime sleepiness)
• Trauma or injury to: penis, pelvis, perineum, testes, uterus or rectum
• Unexplained weight loss
• Urinary problems (urgency, frequency, hesitancy, weak stream, infection)
• Vascular disease (stroke, mini‑stroke, blockage of arteries, aneurysms)
Treatment history • Current medications for physical illnesses
Psychiatric history • Diagnosis, severity of current symptoms, treatment
Physical examination • Complete physical examination
• General physical examination to look for evidence of cardiovascular, neurological diseases
• Complete genital exam
• Secondary sexual characteristics (e.g., gynecomastia)
• Body hair, fat distribution
• Blood pressure, heart rate, peripheral pulses, edema
• Vibratory sensation
• Lower extremity strength and coordination
Investigations • Heamogram
• Renal function test, Liver function test
• Fasting blood sugar
• Hormonal studies‑ FSH, LH, Prolactin, testosterone
• X‑ray spine for spina bifida
• Lipid Profile
• Penile Doppler
Special investigations • Nocturnal penile tumescence and rigidity testing
• Penile tumescence monitoring (Nocturnal penile tumescence (NPT) monitoring evaluates the presence or absence of the
involuntary unconscious erections, which normally occur during the REM stages of sleep, during 1-3 nights. Normal
nocturnal tumescence has been defined as a total night erection time greater than 90 min and an increase in penis
circumference in excess of 2 cm. A change in circumference of 16 mm or 80% of a full erection is thought to reflect a
sufficient degree of penile rigidity for vaginal intromission)
• Estimation of structural abnormalities of penis (penile biopsy, penile imaging, electrical activity of corpus cavernosum
• Penile angiography, radionuclear scintigraphy and measurement of cavernous oxygen tension
• Neurological investigations [biothesiometry (assesses vibration perception threshold), dorsal nerve conduction velocity,
bulbocavernosus reflex (sacral reflex arc) latency, Pudendal nerve somatosensory (genitocerebral)‑evoked potential and
Perineal electromyography.
Assessment of Knowledge • Sexual Knowledge and Attitude Questionnaire
and Attitude towards sex • Dhat syndrome Questionnaire‑ available in 10 Indian languages which can be completed by the patients themselves
Relationship issues • General relationship between the couple, marital discord etc
Indications for • Patient request
referral to urologist/ • Primary ED (poorly sustained erections, lifelong)
Gynecologist/ • Anatomic penile deformities ‑ Peyronie’s Disease, hypospadias, chordee, Phimosis, Short penis, buried penis
Endocrinologist • Pelvic/perineal trauma
• Endocrinopathy
• Complex vascular problems
• Complex neurologic problems
• Vaginismus/Dyspareunia

patient who have primary comorbid psychiatric dysfunction treatment of sexual dysfunctions. While treating these
or those who have prominent psychiatric symptoms (may disorders adequate care needs to be taken in selecting
be secondary in origin), the psychiatric disorders is to the pharmacological agent, so that the dysfunction is not
be treated first and adequately before focusing on the worsened. In some cases the side effects of the drugs can in

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Patient presenting with sexual dysfunction

• Detailed psychosexual history

• Use questionnaires to assess the sexual knowledge & attitude
• Get the basic investigations done

Ascertain that the sexual dysfunction is not due to poor

sexual knowledge or poor relationship between the couple

Treat marital discord Ascertain that the sexual dysfunction is Sex Education
prior to treatment of not due to poor sexual knowledge or & reassess for
sexual dysfunction poor relationship between the couple the diagnosis

• Ascertain the type of sexual dysfunction

• Try to ascertain whether it is due to organic or psychological causes

Etiology- psychological in nature

Assess for comorbid psychiatric disorders

Etiology organic in Comorbid psychiatric Comorbid psychiatric

nature disorders present disorders absent

Refer to concerned specialist Follow figure-3 Assess motivation and

(Endocrinologist, Urologist, psychological sophistication
and Gynecologist)

Motivation low/ inadequate

psychological sophistication Motivation high/ adequate
psychological sophistication

Start with Pharmacotherapy; Manage with combination of non-

motivate the patient for non- pharmacological &
pharmacological management pharmacological measures

Figure 1: Treatment Algorithm for Evaluation & Management of a case of Sexual dysfunction

Table 9: Principles of treatment is to be treated first. An important aspect of treatment

• Inform the patient about all the available choices and guide them make a
choice
• Provide information to the patient in an unbiased manner about different
treatment options, their pros and cons
• Select the treatment as per the patient’s choice
• Provide adequate information about the treatment selected, including
advice on what to do and whom to contact in case of side effects,
problems and complications
• Do not deny treatment in case patient does not have a partner or is not
able to bring the partner
• Document the mutually agreed treatment goals
fact help in decreasing/ameliorating the sexual dysfunction,
for example, for a case of depression with premature
ejaculation selective serotonin reuptake inhibitors like
paroxetine may be beneficial. If the psychiatric disorder is
secondary and not prominent then the sexual dysfunction
involves understanding the motivation and psychological
sophistication. If the motivation for treatment is low or
if patient has poor psychological sophistication, then the
primary mode of treatment is pharmacotherapy. Patients
who are highly motivated and/or have good psychological
sophistication are to be treated with combination of non-
pharmacological and pharmacological therapies.
General Non-pharmacological measures: Education about
sexuality
The first step in the treatment of any sexual dysfunction
is sex education/psychoeducation. The sex education needs
to aim at normalization of the individual’s experiences
and reduce anxiety about sex by providing accurate
information. The various components of sex education are
shown in Table-10. Although all the areas are to be covered,

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 Avasthi, et al.: Sexual dysfunction

Patients presenting with sexual dysfunction & comorbid

psychiatric disorder

• Assess whether comorbidity is primary (psychiatric disorder causing sexual

dysfunction) or secondary (Psychiatric disorder is secondary to sexual
dysfunction)
• Assess the Severity of the comorbid disorder

Secondary
Primary or Secondary But
Prominent But Not prominent
Prominent

Treat sexual
dysfunction first

Intensive therapy based on

comorbid diagnosis

Assess motivation and

psychological sophistication

Select Pharmacotherapy taking into

consideration- severity of the disorder & type
of sexual dysfunction e.g. for a case of
Depression with PME give SSRIs or TCA;
Depression with ED give Trazodone

Motivation low/ inadequate Motivation high/ adequate

psychological sophistication psychological sophistication

Start with Pharmacotherapy;

Manage with non-
motivate the patient for non-
pharmacological measure ±
pharmacological management
Pharmacotherapy

Figure 2: Assessment and Management Algorithm for a case of sexual dysfunction with psychiatric comorbidity

special emphasis needs to be given to those areas, which
are directly related to the patient’s problem. Where ever
possible figures and diagrams are to be used for reference
and illustrations. In some cases the reading material can
also be provided to the couple/patient. Sex education and
teaching relaxation is to be carried out over about four
sessions.
General Non-pharmacological measures: Relaxation
exercises
Relaxation therapy should be taught to patient using
Jacobson’s Progressive Muscular Relaxation Technique or
Benson Henry Relaxation Technique. This can be combined
with the biofeedback machine so as to facilitate objective
evidence and mastering of anxiety by the patient.

Understand and clarify sexual myths: For some individuals,
inappropriate sexual beliefs or myths can cause problems
within a relationship. Individuals acquire expectations
about what sex should be like and how they or their partner
should behave. One of the components of sex-education is
to help the individual and his or her partner alter any sexual
beliefs that interfere with the individual’s enjoyment of sex.
Some of these apply equally to both men and women, while
others will be more relevant to one gender than the other.
Some of the common myths are given in Table-11.
Specific Non-pharmacological management of Sexual
Dysfunction
The specific non-pharmacological measures will vary according
to the type of sexual dysfunction. However, one of the
important components, of the specific measures includes home
work assignment for the couple. It is important to remember
that many of these measures are carried out simultaneously.
Homework assignment for the couple: The homework
assignment provides a structured approach, which allows

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Table 10: Aims and Components of education about sexuality

Aims of Sex Education
• Normalize the individual’s experiences (i.e., help the individual realize that there are many others who have the same needs, problems, and experiences)
• Reduce anxiety about sex by providing accurate information about arousal and normal sexual response, clarify sexual myths and dispel unrealistic
expectations
Components of Sex Education
• Discuss about anatomy of the sex organs
• Discuss about menstrual cycle, pregnancy, puberty, masturbation, formation of semen, nightfalls, types of sex, stages of sexual intercourse, normal male
and female sexual response cycle
• Educate the patient/couple about the wide variation in the extent and frequency of feelings of sexual desire from one individual to the next
• Educate patient/couple about the importance of the timing of sex. The time of day that suits one partner may not suit the other. Help the couple plan their
time so that they have regular blocks of time alone in which they can relax, enjoy each other’s company, and engage in sexual play if desired
• Educate the couple as to how to communicate with each other to express the desire for sex
• Educate partners about how to refuse sex diplomatically
• Educate patient/couple that sex will sometimes be refused and that the refusal is not necessarily an insult or a personal rebuff
• If culturally appropriate, encourage partners to accept the use of masturbation or manual stimulation if sexual advances are refused
• Remind couples that masturbation does not represent a lack of love or desire for one’s partner
• Assist shy or reluctant partners with learning to initiate sex more frequently
• Educate patient/couple about the fact that sexual desire levels fluctuate over the life span
• Encourage patient/couple to communicate their needs for desire and sexual arousal
• Encourage patient/couple to show each other what sort of stimulation is required for orgasm to occur (e.g., manual or oral stimulation)
• Educate males that some females may be able to have multiple orgasms (especially if a vibrator is used) and hence may sometimes find it pleasurable if
genital stimulation is continued after the initial orgasm
• Encourage patient/couple to talk about what kinds of caresses they do and do not like immediately before, during, or after orgasm (e.g., genital
stimulation after orgasm may be unpleasant)

Table 11: Common Myths about Sex this stage is to help the partners develop a sense of trust
• The man should be the sexual leader and closeness, to become more aware of what each one likes
• Masturbation is wrong and to encourage communication. Details of the procedural
• A woman should not initiate sex aspect of non-genital sensate focus session are given in
• Men should not express their emotions
Table-13. It is to be explained to the couple that they need
• A woman should always have sex when her partner makes sexual
approaches to “refrain from sexual intercourse and touching of each
• All physical contact must lead to sex other’s genitalia and the women’s breast” to ensure that they
• Good sex leads to a wild orgasm are not continually confronted by those aspects of sexuality
• A man feels like having sex at any time
that is most likely to cause anxiety, and to enable them to
• Sex equals intercourse
• Sex happens automatically concentrate on rebuilding their physical relationship by first
• A `respectable’ woman should not enjoy sex too much and should learning to enjoy general physical contact. Initial reactions
certainly never masturbate to these sessions vary according to the nature of the couple’s
• All other couples have sex several times a week; have orgasm every time problem. Some couple’s may find this enjoyable and others
they have sex & orgasm simultaneously
• There must be something wrong with the relationship if sex is not good
may react negatively. In some cases it will be appropriate for
• Cultural beliefs about formation of Semen and genital secretions the therapist to just acknowledge the problem and reassure
• Role of ‘Physical strength’ or ‘Muscle power’ in sexual performance and encourage the couple. In some cases therapist have to
• Size of the penis explain that this is understandable and expected, but that in
• Circumcision and sexual performance
• Bending of Penis
order to overcome a sexual problem like theirs it is necessary
• Vasectomy/tubectomy decreases sexual potency to approach it in a systemic fashion and with due course of
• Drugs enhance sexual potency in normal persons time they will begin to get pleasure out of their sessions and
• Porn increases sexual drive these would come as spontaneous behaviour.

the couple to rebuild their sexual relationship gradually. The
stages of this programme are labeled using the terminology
introduced by Master and Johnson (1970) is: non-genital
sensate focus, genital sensate focus and vaginal containment.
There are some basic principles of giving and carrying out
the homework assignments as shown in table-12.
Non-genital sensate focus: This assignment is particularly
helpful for a couple to establish physical intimacy in
a comfortable and relaxed fashion, and allows open
communication about feelings and desires. The basis aim of
Indian J Psychiatry 59 (Supplement 1), January 2017
Some couples will have more serious difficulties in the form
of negative responses to homework assignments, persistent
breaking of the ban on sexual intercourse, or cessation of
homework assignments. In such cases the focus of therapy
might have to be changed temporarily and sessions may
be required to help the partners express their feelings and
anxieties. In occasional cases no progress can be made in
developing understanding of why couple is encountering
difficulties. In such cases it is worth seeing the partners
separately to find out whether important information is
being withheld by one of them.
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Genital sensate focus: The couples, who go through the
non-genital sensate focus sessions successfully, need to
be told to move to the genital sensate focus sessions.
The aim and procedural aspect of genital sensate focus
are given in Table-14. As with the non-genital sensate
focus, some couples immediately find these sessions
pleasurable while others would react adversely. This
stage is particularly likely to generate anxiety, especially
about sexual arousal or intimacy, so it is very important
that the therapist specifically encourages partners to
focus on pleasurable sensations. Some of the techniques
for dealing with specific dysfunctions also need to be
introduced at this stage.
Table 12: Principles of giving and carrying out the
homework assignments
Components and goals of Homework Assignments:
• Aid in identification of specific factors (cognitions, attitudes), which
may be maintaining the sexual dysfunction
• The homework assignments also provides the couple the specific
techniques to deal with particular problems
Important Procedural Aspects of Homework Assignments
• The instruction need to be detailed and precise
• The therapist need to always check that the couple have fully registered
and understood the instructions before the treatment session ends
• When giving instructions the therapist needs to ask the couple how
they feel about the instructions and do they anticipate any difficulty. If
problems are anticipated, the therapist need to endeavor to resolve their
fears before they attempt the assignment
• A couple need not be asked to move to next stage of the programme
until they have mastered the current assignments
• A couple should never be left with the option of moving from one stage
to the next between treatment sessions depending on how they progress,
because uncertainty can be detrimental
• The couple need to be informed that the therapist will be asking for the
detail feedback on the progress at the next treatment session
Vaginal Containment: This stage is an intermediate one
in the introduction of sexual intercourse to the therapy
programme. It is relatively minor stage for couples whose
difficulties have by now largely resolved. For others it is
extremely important, especially when vaginal penetration
is the key step (e.g. ED, PME, and vaginismus). The couple
is instructed that when they both are feeling relaxed and
sexually aroused the women can introduce her partner’s
penis into her vagina and the partner to then lie still,
concentrating on any pleasant genital sensations. The best
position to attempt vaginal containment is female superior
position or a side to side position. The couple be asked to
maintain containment as long as they wish, and then they
can return to genital and non-genital pleasuring. The couple
can repeat the containment up to three times in any one
session. Once this stage is well established the couple to
introduce movement during containment, with preferably
women starting the movements first. With this the general
programme of sex therapy is completed and now the
treatment need to include superimposition of treatment for
specific sexual dysfunctions.
It is important to remember that during the whole therapy
feedback be taken after every session and any doubts/
misconceptions be clarified.
Home work assignments for single male
Management of sexual dysfunctions in single males also
involves same principles. The subject be provided with sex
education and thought relaxation exercises. The principles
of home work assignments for single male with erectile
dysfunction and premature ejaculation are given in Table-15
and Table-16. At the end the patient be counseled and
reassured that he can now indulge in heterosexual experience

Table 13: Non‑Genital Sensate Focus

Aims of non‑genital sensate focus
• To help the partners develop a sense of trust and closeness, to become more aware of what each one likes and to encourage communication
Frequency of homework sessions per week
• Do not impose a too rigid schedule, but make it clear to the couple that they should at least practice 3 sessions of homework per week
Procedural Aspect of non‑genital sensate focus
• One partner inviting the other partner for a home‑work session by giving explicit invitation
• Other partner should accept the invitation if he or she is feeling either positive or neutral about it. If the feeling is negative, it is important that the partner
conveys the same with explanation about such feeling
• Invitation by the partner who did not initiate at the first instance
Caressing session: don’ts
• Refrain from sexual intercourse
• Refrain from touching of each other’s genitalias and the women’s breast
Caressing session: do’s
• Can occur wherever the couple wishes, as long as they feel comfortable (but need to avoid becoming bored), warm and there is no risk of them being
disturbed
• Need to do in a way that gives pleasure to both of them
• During the early sessions this exercise need to be like a massage
• Need to begin with one partner exploring and caressing the other partner’s body all over, except for ‘no‑go’ areas
• The partners need to swap round when they wish to, so that the passive partner now takes over caressing
• During the caressing the passive partner need to focus on the sensations elicited by the caressing and need to provide feedback on what he/she likes and
dislikes and how things could be improved
• If any of the partner becomes sexually aroused during this stage, they need to enjoy this but need not go beyond the agreed limits of caressing
• There is no restriction to self‑masturbation if any partner wishes to, for relieving the sexual tension, but not to be done in presence of the partner

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 Avasthi, et al.: Sexual dysfunction
without difficulty. However, he be cautioned that it should be
done after few days, not in a hurry, and to be carried out in
familiar surroundings without guilt or fear and anxiety.
ERECTILE DYSFUNCTION
An important aspect of assessment of erectile dysfunction
is to distinguish between psychogenic and organic erectile
dysfunction (See table-17). Non-pharmacological measures
are to be used in patients with psychogenic or mixed
erectile dysfunction along with pharmacological agents.
Specific Non Pharmacological treatment for erectile
dysfunction
Men with psychogenic erectile dysfunction will usually
start experiencing erections during either non-genital or
Table 14: Genital Sensate Focus
Aims of genital sensate focus
• To make the couples caressing more sexual and arousing and also to
encourage them to continue discussing their feelings and desires
Procedural Aspect of genital sensate focus
• Continue with pattern of alternate inviting and taking turns at caressing,
but to extend this to include both partner’s genitalia and women’s breast
• Emphasize the need for this stage to be added to the previous one, and
not to replace it
• Taking turns of being active and passive need to continue
Caressing session: do’s
• Caressing need to be initially gentle and exploratory, without sexual
arousal being the objective; if any of the partners becomes sexually
aroused during this stage, they need to enjoy this
• Guiding the partners hand can again be a useful means of helping the
partner learn what is enjoyable
• Lotions can also be used if the couple wishes
• If either partner wish to experience orgasm they may feel free to do so,
but this is not to be the goal of the session
Table 15: Home work assignments for Single Male with
Erectile Dysfunction
Home work Assignment
• Read erotic material, or see erotic material in books/movies and to note
the sense of sexual pleasure out of the same and to focus on it
• In subsequent sessions patient is asked to be alone and imagine about
the content of erotic material
• In subsequent sessions, patient also need to be asked to visualize, as far
as possible, of being involved in the same erotic/sexual activity
• If patient perceives erection, he shouldn’t get anxious or excited about
the same and need to continue to concentrate on the erotic stimuli and
related pleasure
• In later sessions patient is advised to combine reading of and seeing
erotic material with his fantasy and to focus on himself in foreplay and
later, intercourse
• In subsequent sessions, reading, seeing and fantasizing is to be
combined with fondling of penis and additional masturbatory hand
movements on the penis by using non‑dominant hand
• Terminate masturbation before the desire for ejaculation
• At the end of the therapy the patient is instructed to fantasize about
himself indulging in sexual intercourse with the process of ejaculation
and orgasm
Don’ts to be followed during the initial sessions
• Not to look for the erection
• Not to note the extent of erection, if any
Indian J Psychiatry 59 (Supplement 1), January 2017
genital sensate focus. If the therapist suggests that during
the initial phase the man tries not to have an erection this
can have the opposite effect. Men with erectile dysfunction
often have difficulty attending to erotic stimuli, especially
when an erection develops, tending instead to think about
the quality of their erection or whether they will be able to
maintain it. The therapist need to specifically encourage the
man to focus his attention on the pleasurable sensations he
experiences during the partner’s genital caressing (the use
of a lotion can often heighten these sensations), areas of his
partner’s body that he finds arousing, and the pleasure of
witnessing his partner’s sexual arousal.
Pharmacological treatment for erectile dysfunction
Besides the psychological measures, other therapeutic
options for erectile dysfunction includes medications,
constriction ring, vacuum constriction devices, intra-
cavernosal injections, intra-uretheral medication devices,
penile prosthesis and reconstructive surgery (Table-18).
Oral erectogenic agents
Oral therapy with vasoactive agents has emerged as the
first line treatment and has transformed the management
of erectile dysfunction.
Phospho-diaesterase inhibitors (PDE-5 inhibitors), i.e.,
sildenafil, tadalafil, vardenafil have proven efficacy and
safety in men with erectile dysfunction and are considered
as first line pharmacotherapy for management of erectile
dysfunction. The profile of these drugs is shown in
table-19. Among the available PDE-5 inhibitors, sildenafil
and vardenafil have short half-life, whereas tadalafil have
relatively longer half-life. Available data also suggests the
safety of some of these PDE-5 inhibitors in patients with
erectile dysfunction associated with diabetes mellitus,
spinal cord injury, chronic renal failure, Parkinson’s disease,
antidepressant use and following radical prostatectomy. It
is important to remember that action of PDE-5 inhibitors
is dependent on androgens. Hence, in patients with
hypogonadism management with PDE-5 inhibitors may not
be effective and use of androgens may be an effective choice.
Adverse effects of PDE-5 inhibitors are generally mild and
dropout rates due to side effects are similar to placebo.
PDE-5 inhibitors are metabolized by the cytochrome P450
3A4 and as a result may affect metabolism of protease
inhibitors and antifungal medications. In general PDE-5
inhibitors have been shown to be safe and have not been
associated with increased risk of myocardial infarction.
However, it is important to remember that use of PDE-5
inhibitors is contraindicated in those receiving nitrate. Use
of PDE-5 inhibitors along with antihypertensive medication
like ACE inhibitors, angiotensin-receptor blockers, calcium
channel blockers and diuretics can result in small additive
decreases in blood pressure. Use of PDE-5 inhibitors along
with alpha blockers can result in orthostatic hypotension.
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There are no comparative trials to suggest superiority of
one PDE-5 inhibitor over the other. However, preliminary
data from some of the cross-over trials suggest that some
patients may respond better to one PDE-5 inhibitor than
to another. Accordingly, it can be said that a patient who
does not respond to one agent, may be shifted to another
PDE-5 inhibitor. Some preliminary data also suggest that a
proportion of patients who fail to respond to intermittent
dosing, may respond to daily dosing.
The selection of medication is to be done on the basis
of frequency of intercourse. Although very robust data is
not available, but daily use of tadalafil is associated with
improved endothelial function with a sustained effect after
its discontinuation, whereas such effects are not seen with
use of on-demand tadalafil.
Table 16: Home work assignments for Single Male with
Premature Ejaculation
Don’ts to be followed during the initial sessions
• Abstain from heterosexual intercourse and not to experiment during
these sessions
Home work Assignment/Procedural aspects
• Read erotic material, or see erotic material in books/movies, to visualize
it and note the sense of derived sexual pleasure with subsequent erection
of penis
• Imagine himself in the same situation
• In subsequent sessions, combine reading/seeing with gentle touching
of the penis or the testicles/groin region to enhance pleasure, but he
shouldn’t stroke the penis or indulge in masturbation
• Once, the previous step is mastered, patient is asked to combine the
imagery with fondling of penis so as to build up sexual pleasure and can
even indulge in masturbation
• While masturbation, when patient has the feeling of imminent
ejaculation, he is to be instructed to immediately stop masturbation and
practice squeeze technique
• At the end of the therapy the patient is instructed to fantasize about
himself indulging in sexual intercourse with the process of ejaculation
A subject who does not respond to 6-8 doses of a PDE-5
inhibitor with sexual stimulation at maximum dose is
considered as non-responder to a PDE-5 inhibitor. However,
it is to be remembered that most often patients fail to
respond due to incorrect use of PDE-5 inhibitors and these
include failure to use adequate sexual stimulation, adequate
dose and failure to wait for the adequate duration for the
action of the medication to start. It is to be remembered
that even though all the 3 PDE-5 inhibitors have onset of
action within 30 minutes of oral ingestion, in most patients a
lag of 60 minutes is required for sildenafil and verdenafil and
2 hours for tadalafil. Based on the half-life of the medication,
the normal window of efficacy of sildenafil and verdenafil is
6-8 hours after ingestion, whereas the window of efficacy
for tadalafil is about 36 hours. Patient prescribed PDE-5
inhibitors are to be adequately psychoeducated with respect
to dose of medication, timing of medication, relationship
of dosing with fatty meal, need for sexual stimulation and
window during which desired effect will be perceived.
Other oral erectogenic agents
Trazodone: One of the earliest drugs used in erectile
dysfunction was trazodone. Trazodone and its active
metabolite have antagonistic effect on 5HT2C receptors and
may also have adrenoceptor antagonistic action. Available
data suggest that trazodone is more efficacious than
placebo in mixed and psychogenic erectile dysfunction.
Yohimbine: It is a α2-adrenergic blocker. Before introduction
of sildenafil, yohimbine was the most widely used oral
medication for management of erectile dysfunction. Available
evidence suggests that it is more efficacious than placebo.
Apomorphine: Apomorphine is a dopamine agonist (D1 & D2
receptors) and its sublingual form (Apo-SL) is a new central
initiator of erection and has been found to be effective in
various types of erectile dysfunction.. Recent studies show

Table 17: Differentiating features between psychogenic and organic erectile dysfunction

Parameters Psychogenic Organic
Onset of disorder Situational with defined onset (onset Insidious
associated with specific emotional event)
Precipitating event Psychogenic condition Debilitating disease, vascular insufficiency or CNS
abnormality, penile trauma or interfering drugs
Erectile function before intromission May be present Usually absent except in patients with pelvic steal phenomenon
Erectile function after intromission Variable with different partners Usually absent
Erectile response to other sexual stimuli Usually present Usually absent
Nocturnal or morning erections Initially present and full, lost in longstanding Absent or reduced in frequency and intensity
dysfunction
Course of disorder Episodic or transient loss of erection Persistent and progressive erectile
Dysfunction
Associated ejaculatory disorder Premature ejaculation and intermittent loss of Retrograde or absent ejaculation
ejaculation
Nocturnal penile tumescence > 90‑180 min/night <60 min/night
Total time 0.2 cm 2 cm
Circumferential change >0.70 <0.60
Penile‑brachial index (PBI) <35 sec >40 sec
Bulbocavernosus reflex latency

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Table 18: Treatment options for erectile dysfunction
Oral Agents
• Sildenafil
• Tadalafil
• Vardenafil
• Trazodone
• Yohimbine
• Apomorphine
• Phentolamine
• L‑arginine
• Androgens (Testosterone)
Vasoactive Intracavernosal Injections (ICI)
• Phenotolamine mesylate
• Papavarine
• Vasoactive intestinal peptide (VIP)
• Forskolin
• Alprostadil
Intraurethral therapy
• Alprostadil
Transdermal therapy
• Testosterone
• Nitroglycerine
• Minoxidol
Vacuum constriction devices (VCD)
Penile Prosthesis
Reconstructive surgeries
that sublingual apomorphine has a safe cardiovascular
profile and thus making it a new treatment option for
patients with concomitant disease including cardiovascular
disease and diabetes mellitus.
Phentolamine: Oral phentolamine mesylate, is a competitive
inhibitor of α- adrenergic receptor. It also has the advantage
of lack of interaction with nitrates and hence has been
suggested as an alternative to treatment of erectile
dysfunction in patients with cardiac illness.
L-arginine: L-arginine is the precursor of Nitric Oxide (NO)
and has been shown to improve erections in 40% of patients.
Androgens
Androgens are useful for erectile dysfunction in men with
severe hypogonadism and may be useful as adjunctive therapy
when other treatments are unsuccessful by themselves. Libido
and an overall sense of well-being are likely to improve when
serum testosterone levels are restored to the reference range.
Some evidence suggests that combination of testosterone and
PDE-5 inhibitors yields better results. Usually testosterone
is used parenterally, either once a week or once in 2
weeks. Other methods of administration like skin patches,
testosterone gel is also available, but this is to be used daily
and is costly. Testosterone implants are also available, which
can last for 3-6 months. However, it is to be remembered that
use of exogenous androgens suppresses natural androgen
production. Elevated serum androgen has the potential to
stimulate growth of prostate gland and increase the risk of
cancer. Use of exogenous testosterone is also known to be
associated with erythrocytosis, elevated serum transaminase
Indian J Psychiatry 59 (Supplement 1), January 2017
levels, exacerbation of untreated sleep apnea, benign prostatic
hyperplasia, and an increased risk of adenocarcinoma of the
prostate. Accordingly, periodic examination of prostate,
estimation of prostate-specific antigen (PSA) and heamogram
are recommended in all patients receiving supplemental
androgens. Obtaining a testosterone level during therapy is
necessary for optimizing the dosage.
Vasoactive Intracavernosal Injections (ICI)
Since early1980s, till advent of sildenafil, intracavernous
injections were the mainstays of the treatment of erectile
dysfunction. The agents which have been used for
intracavernous injections include phentolamine mesylate,
papavarine, vasoactive intestinal peptide (VIP), forskolin
and alprostadil.
Phentolamine mesylate, an a - adrenoceptor antagonist
acts via increasing cAMP and decreasing intracellular Ca2+
and also possibly via nitric oxide synthase (NOS) activation.
Clinical efficacy and safety of intracavernosal mesylate has
been well documented.
Papavarine is a non-selective inhibitor of phosphodiesterase
(PDE) and acts by increasing cAMP thus decreasing
intracellular smooth muscle. It is used in papavarine (20-
80 mg) induced penile erection (PIPE) test to distinguish
between psychogenic and organic ED. However, it has
limited efficacy so it is used with other agents such as
phentolamine and with phentolamine and prostaglandin E1.
VIP and Forskolin which increase cAMP, have been found
to be efficacious in moderate to severe erectile dysfunction
resistant to monotherapy and polypharmacotherapy. No
pain at site of injection has been reported with VIP, which
is an advantage to patients.
Alprostadil, a synthetic prostaglandin E1 is an adenylate
cyclase activator and is now the drug of choice of intra-
cavernosal pharmacotherapy. Intracavernous alprostadil in
the dose of 5-40 μg is most efficacious as monotherapy. It
leads to erection in 5-15 minutes and the duration of ejection
depends on the dose of the medication used. It is reported
have an efficacy of more than 70% and has also been found to
be effective in patients with erectile dysfunction associated
with diabetes mellitus and cardiovascular disease. Patient
and partners also report high satisfaction rates. However,
in long run use of intra-cavernosal alprostadil is associated
with high dropout rates (41-68%), with most dropouts’
occuring during initial 3 months of therapy.
When used it is to be initially be given in the clinicians
office at the lowest dose and gradually the dose need to be
titrated to an adequate erectile response while monitoring
for syncope. Intracavernosal alprostadil is considered to be
more effective and better tolerated over the intraurethral
form. Due to this Intracavernosal alprostadil is preferred
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Table 19: Comparison of various PDE‑5 inhibitors

Sildenafil Vardenafil Tadalafil
Time to maximum plasma 30-120 (median 60) 30-120 (median 60) 30–360 (median 120)
concentration (T max) in minutes
Half‑life in hours 2.6 to 3.7 3.9 17.5
Plasma protein binding 96% 94% 94%
Bioavailability 41% 15% Not known
Onset of action in minutes 15‑60 25 16‑45
Duration of action1 4 4 36
Absorption Fatty meals cause a mean delay in Cmax of Fatty meals cause a Not affected by food
60 minutes reduction in CMAX
Available doses in mg 25, 50, 100 2.5, 5, 10,20 2.5, 5, 10,20
Recommended starting does in 50 10 10
mg/day
Maximum Dose in mg/day 100 20 20
Dose adjustments required • Patients >65 years old • Patients >65 years old • Patients >65 years old
• Hepatic impairment • Hepatic impairment • Hepatic impairment
• Renal impairment • Renal impairment • Renal impairment
• Concomitant use of potent cytochrome P450 3A4 •C oncomitant use of • Concomitant use of
inhibitors, such as ketoconazole, itraconazole, potent cytochrome potent cytochrome
erythromycin, clarithromycin, HIV protease P450 3A4 inhibitors, P450 3A4 inhibitors,
inhibitors (ritonavir and saquinavir) such as ketoconazole, such as ketoconazole,
• Concomitant use of rifampicin, phenobarbital, itraconazole, erythromycin, itraconazole, erythromycin,
phenytoin and carbamazepine, may induce CYP3A4 clarithromycin, HIV clarithromycin, HIV protease
and enhance the breakdown Concomitant use of protease inhibitors (ritonavir inhibitors (ritonavir and
cimetidine and saquinavir) saquinavir)
• Concomitant use of • Concomitant use of rifampicin,
rifampicin, phenobarbital, phenobarbital, phenytoin and
phenytoin and carbamazepine, may induce
carbamazepine, may induce CYP3A4 and enhance the
CYP3A4 and enhance the breakdown
breakdown
Contraindication Patients receiving organic nitrates either regularly or • Patients receiving organic • Any patient using organic
intermittently nitrates either regularly or nitrates either regularly or
Hypersensitivity to any component of the tablet intermittently intermittently
• Hypersensitivity to any • Hyper‑sensitivity to any
component of the tablet component of the tablet
Side effects Headache Headache Headache
Flushing Flushing Dyspepsia
Dyspepsia Rhinitis Back pain
Nasal congestion Dyspepsia Myalgia
Alteration in colour vision Sinusitis Nasal congestion
Recommended time between 1 hour 1 hour 1 to 12 hours
medication intake and intercourse

over intraurethral alprostadil. Common side effects of
intra-cavernosal alprostadil are penile pain, edema and
hematoma, palpable nodules or plaques, and priapism.
Patients are to be clearly informed about the chances of
occurrence of priapism and what do in such situation. The
patient is to be counseled that if the erections persists for
more than 4 hours, they need to seek emergency medical
help. Management of priapism in such situations involves
aspiration of blood from corpus cavernosum under local
anaesthesia. If this fails than intra-cavernosal phenylephrine
injection is to be given with proper monitoring for severe
hypertension, tachycardia and any arrhythmia.
Due to its synergistic action, it is often used with
phentolamine and papavarine. Some studies have
demonstrated that patients of erectile dysfunction preferred
combination [Phentolamine (0.25-1.5 mg) + Papavarine
(8-16 mg) + Prostaglandin E1 (10-20 μg)] to sildenafil,
regardless of the etiology.
A meta-analysis of 25,000 patients showed that the
advantage of mixing above agents is that lower doses of
drugs are required thus leading onto synergistic effects with
lesser side effect. Prominent side effects are pain, priapism,
corporal fibrosis and scar tissue formation. Also, being an
invasive procedure, many patients find it inconvenient to
inject repeatedly. Procedural complicacy, bleeding and
injury to urethra caused higher attrition rates at 1 year
follow-up of patients being treated with intracavernous
vasoactive drugs.
Intraurethral therapy
Medicated urethral system for erection (MUSE), which
contains 500-1000 mg of alprostadil, has shown success

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 Avasthi, et al.: Sexual dysfunction
rates varying from 43-69% in efficacy studies. It has
advantages that it can be self-administered and has little
systemic and local side effects.
Topical therapy (Transdermal delivery)
This option minimizes both systemic exposure and tissue
traumatization and involves administration of vasoactive
substances across skin of the penis. This has added benefit
from the patient’s perspective in being a less invasive
option. Pilot studies using Soft Enhanced Percutaneous
Absorption (SEPA) technology, give ground for optimism.
Preliminary evidence suggests that prostaglandin-E1+
SEPA are effective in 80-90% of patients. Nevertheless, this
option requires more intensive research before approval by
regulatory authorities.
Testosterone therapy for ED is indicated only in confirmed
cases of endocrinopathies and is to be reserved for
patients with documented hypogonadism. Transdermal
administration has been developed recently. Gel containing
2.5-5.0 mg of testosterone-applied daily to the abdomen,
back, thighs or upper arms have shown to produce normal
plasma testosterone levels. Patients using testosterone
skin patches have reported improvements in libido, sexual
function, energy and mood. Adverse skin reaction (9% of cases)
can be treated with topical hydrocortisone or antihistamine
cream. Serum prostate specific antigen (PSA) levels is to be
measured before testosterone therapy is started.
Nitroglycerine, a nitric oxide donor and minoxidil ointments
have met with only minimal success. Although still under
investigation, but these agents could acts as another tool in
the armamentarium for treating erectile dysfunction.
Vacuum constriction devices (VCD)
Vacuum devices work by exerting a negative pressure on
the penis, which results in an increase in corporeal blood
flow and erection. A constriction ring placed around the
base of the penis prolongs the erection by decreasing
corporeal drainage. The erection obtained with a vacuum
device is different from that obtained normally as there
is no relaxation of the trabecular smooth muscle. Instead
blood is trapped in the intra and extracorporeal regions
of the penis. The time taken to achieve an erection varies,
but is generally around 2-2.5 mins. The band need not be
left in the place for more than 20 mins. Majority of the
vacuum devices currently marketed use either a battery or
a hand pump to generate vacuum. Overall success rate with
VCD has been reported to be around 90%, with more than
80% of patients continuing with the device. Another study
quoted that 53% patients reported satisfaction with only
23% continuing with the device. Drawbacks of VCDs include
pain, petechiae, obstruction of ejaculation, penile pivoting,
numbness and slight bluish colouration due to cyanosis.
Almost all patients of ED can use VCDs. The vacuum devices
are contraindicated in patients with severe Peyronie’s
Indian J Psychiatry 59 (Supplement 1), January 2017
curvature, sickle cell anaemia or blood dyscrasias and those
on anticoagulants.
Penile Prosthesis
Since their introduction about 3 decades ago, penile
implants are still a widely chosen treatment option, mostly
after failure of all forms of therapy for erectile dysfunction.
There are various forms of penile prosthesis, i.e., semi-rigid
rod prosthesis consists of two rod like cylinders that are
implanted into corpora cavernosum, mechanical rods (Dura
II), malleable rods and inflatable penile prosthesis (Unitary,
two-piece, and three-piece devices). Usually 3 piece
inflatable penile prosthesis is preferred as it leads to more
natural erections. Postoperative complications of penile
implants include infection and mechanical malfunction.
Peri-prosthetic infection requires immediate antibiotic
therapy and removal of prosthesis.
Reconstructive surgery
Surgery for venous leakage involves penile venous ligation
or embolization. Venous ligation restores spontaneous
erections in only 50% of patients. Arterial revascularization
is an experimental procedure used for treatment of
vasculogenic ED. Upto 65% of patients report return of erectile
function following arterial revascularization, but careful
patient selection is necessary. Generally, good results are
obtained only in young men with pure arteriogenic erectile
dysfunction. A number of complications associated with
arterial revascularization including arterial haemorrhage,
glans-penis hyperemia, anastomotic occlusion, diminished
penile sensation and fibrosis.
Steps in the Management of Erectile Dysfunction
First step is to confirm the diagnosis of erectile dysfunction
as per the prevailing nosological system. The consensus is
that inability to attain and maintain an erection sufficient
to permit satisfactory sexual performance, lasting for more
than 6 months, is considered to be an indicator of presence
of erectile dysfunction. The general principles of evaluation
of erectile dysfunction are shown in Table-20. The most
important issue in management is evaluation for the organic
factors, look for comorbid psychiatric conditions, comorbid
sexual dysfunction and marital disharmony. However, it is
to be remembered that although the cause may be organic,
psychological causes can worsen the ED, so treating with
behavioural measures in such cases is also an important
step in the management. Once the evaluation is complete
the patient/couple is to be explained about the potential
beneficial and adverse effects of available treatment and
guide them to make an informed choice. The selection of
treatment strategy for erectile dysfunction is outlined in
figure-3. If patient has Dhat syndrome along with erectile
dysfunction, it is to be addressed first. Psychiatric disorders
and marital harmony is to be addressed prior to treatment
of erectile dysfunction and a similar protocol need to be
followed.
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Initial treatment involves providing sex education,
clarifying the myths, teaching relaxation exercises,
and sensate focus training. After assessing coexistent
problems, while providing formulation and sex education,
education about factors that create a normal sexual
response and erectile dysfunction can help patients
and their partners cope with sexual difficulties. It is
also important to change/remove/reduce the associated
modifiable or reversible factors, including lifestyle or
drug-related factors. Changes in lifestyle like smoking
cessation, control of diabetes/ cholesterol, weight loss and
reduction in stress are of prime importance. The success
of psychosexual therapy is guided by the motivation of
the patient, as this require him to work with the therapist
to understand what prevents him from experiencing
normal sexual arousal.
Follow-up plan is to be tailor made for the individual and
there is no single follow-up regime. However, regular
follow-up at 4 weeks for 6 months is usually recommended.
In terms of pharmacological treatments (see Table-21),
PDE-5 inhibitors are considered to be the first line therapy
in treatment of erectile dysfunction. The PDE-5 inhibitors
available in India include sildenafil, vardenafil and tadalafil.
Apomorphine sublingual has the advantage of quick onset
Table 20: General principles of evaluation of erectile
dysfunction
• Establish diagnosis based on the history, physical examination and
investigations as per requirement
• Establish the cause of erectile dysfunction (psychogenic, organic, mixed)
based on the history, physical examination and investigations as per
requirement
• Use validated questionnaires like International Index of Erectile
Function (IIEF) for grading the severity so as to monitor the response to
specific treatment
• Evaluate for presence of comorbid psychiatric disorders and establish the
relationship with erectile dysfunction (i.e., what is primary psychiatric
disorder or erectile dysfunction)
• Evaluate the severity of underlying organic cause and treat the primary
illness first

Treat Dhat Identification of Erectile Dysfunction Liaison with

syndrome & • Sexual, Medical, Psychosocial history specialist for
Marital Discord • Assessment of relationship with partner organicity
prior to (both sexual & non-sexual)
management of • Physical Examination
ED • Evaluate for Psychiatric comorbidity
• Evaluate for other sexual dysfunctions

Psychiatric comorbidity
present/ severe
Functional
erectile
dysfunction
Treat appropriately
and then focus on ED

First line therapy

• Sex Education, Relaxation, Sex therapy, Life style modification
• Oral erectogenic agents (PDE5 inhibitors)

• Evaluate for the reasons for lack of response- improper use of PDE-5
inhibitors, poor compliance with medication, missed physical comorbidities,
missed hypogonadism

Retrial with PDE-5 inhibitors

• Proper education about how to use PDE-5 inhibitors Erectile
• Change from intermittent use to daily use Dysfunction
• Combine with testosterone in case of presence of hypogonadism resolved

Second Line therapy:

• Change Oral Erectogenic Agent Reevaluate for
• Intracavernosal self injection Organic cause
• Intraurethral alprostadil
• Combine PDE-5 inhibitors with
second line agents

Figure-3: Treatment algorithm for management of patients with ED

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 Avasthi, et al.: Sexual dysfunction
of action. It is well tolerated and there is no interactive
action with other medications, food and alcohol. This can
be prescribed by physicians to patients with psychogenic
and a mild organic impotence. It is also used when PDE-5
inhibitors are contraindicated. VCDs are better accepted by
older patients especially who have a stable partner. Penile
pain, numbness and delayed ejaculation are some of the
side effects that treating psychiatrist need to be aware of.
Psychosexual therapy is also the first line treatment and it
is used in patients with significant psychological problems,
though psychological component may be present in all
cases of erectile dysfunction. It is used either alone or in
combination with other first line therapies. The motivation
of the patient is of utmost importance for any psychosexual
therapy. The major advantages are that it is non-invasive,
involves the partner, and leads to sustainable improvement
in sexual function and satisfaction. However, it takes time,
is associated with high dropout rates and is associated with
variable results.
If the first line therapies fail or are contraindicated than the
second line treatment includes use of intracavernosal and
intraurethral injections. Patient’s comfort and education is
very important while using intracavernosal and intraurethral
injections. Use of an automatic special pen that avoids
the needle view can avoid fear of penile puncture. It is
helpful in most cases of erectile dysfunction; however, it
is contraindicated in patients with hypersensitivity to drug
employed and priapism. Erection appears within 5-15 mins.
The psychiatrist is to be aware of the side effects like
priapism, penile pain and fibrosis. In cases where the penile
erection lasts more than 4 mins aspiration of blood by a
19 gauge needle has been suggested. If it still does not
resolve then 200mg of Phenylepherine intracavernosal
injections every 5 mins is recommended. Intraurethral PGE1
as semisolid pellets is a less invasive procedure but success
rates are lower. In case both first and second line therapies
fail, use of inflatable penile prosthesis can be considered.
Premature Ejaculation (PME)
Specific Non Pharmacological for specific sexual dysfunctions
It is considered that behavioural management is to be
the first line of therapy where ever possible. The specific
behavioural techniques for PME involves stop- start or
squeeze techniques, which are usually introduced during
genital sensate focus.
Table 21: Management of Erectile dysfunction
First line therapy: Phospho‑diesterase‑5‑inhibitors, apomorphine, vacuum
constriction devices and psychosexual therapy
Second ‑ line therapy ‑ intracavernosal and intraurethral injections:
prostaglandin E1, phentolamine, vasoactive intestinal peptide and
papavarine.
Third line therapy: penile prosthesis. The inflatable type is cosmetically
better but prosthesis infection is most problematic complication.
Indian J Psychiatry 59 (Supplement 1), January 2017
The stop-start technique developed by Masters and Johnson
is highly effective for the treatment of premature ejaculation
with success rates of as high as 90%. The technique aims
to increase the frequency of sexual contact and sensory
threshold of the penis. It is best carried out in the context
of sensate focus exercises because some males ejaculate
so early that direct stimulation of the penis of any kind
can trigger ejaculation straight away. Starting with non-
genital caresses allows the male more time to identify the
sensations that occur immediately prior to ejaculation. The
stop-start technique consists of the man lying on his back and
focusing his attention fully on the sensation provided by
the partner’s stimulation of his penis. When he feels himself
becoming highly aroused he is to indicate this to her in pre-
arranged manner at which point she need to stop caressing
and allow his arousal to subside. After a short delay this
procedure is repeated twice more, following which the
woman stimulates her partner to ejaculation. At first the
man may find himself ejaculating too early, but usually
gradually develops control. Later a lotion can be applied to
the man’s penis during this procedure, which will increase
his arousal and make genital stimulation more like vaginal
containment.
The squeeze technique is an elaboration of the stop-start
technique, and probably only needs to be used if the latter
proves ineffective. The couple proceeds as with the stop-
start procedure. When the man indicates he is becoming
highly aroused his partner should apply a firm squeeze
to his penis for about 15-20 seconds. During applying the
pressure, the forefinger and middle finger are placed over
the base of the glans and shaft of the penis, on the upper
surface of the penis, with the thumb placed at the base of
the undersurface of the glans. This inhibits the ejaculatory
reflex. As with the stop-start technique this is repeated
three times in a session and on the fourth occasion the man
may ejaculate.
Both procedures appear to help a man develop more control
over ejaculation, perhaps because he gradually acquires the
cognitive techniques associated with ejaculatory control,
or perhaps because he gradually becomes accustomed
to experiencing sexual arousal without getting anxious
(Hawton, 1989). Stop-Start technique and Squeeze technique
have been documented to have anywhere between 60-95%
success rates.
Pharmacological management of Premature Ejaculation
(PME)
Pharmacological treatment of premature ejaculation includes
use of topical anesthetic agent, tricyclic antidepressants and
selective serotonin reuptake inhibitors (SSRIs) (Table-22).
There is preliminary data for use of sildenafil and some of
the Chinese herbs. However, it is important to note that
none of these agents have been approved.
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Over the last few years, dapoxetine, another non-selective
SSRI, has been marketed specifically for management of PME.
Dapoxetine has been found to be efficacious in both lifelong
and acquired PME. Dapoxetine is associated with side effects
like nausea, diarrhoea, headache and dizziness. Combining
dapoxetine with PDE-5 inhibitors is associated with increased
risk of syncope. It is generally recommended that patient’s
blood pressure is to be evaluated prior to starting of dapoxetine.
Among the SSRIs, paroxetine has been found to be useful.
However, data also exist for the beneficial effect of sertraline.
Studies which have compared various SSRIs suggest that
paroxetine is superior to fluoxetine, clomipramine and
sertraline. Data also suggest that sertraline is better than
fluoxetine; however, the efficacy of clomipramine is not
significantly different from fluoxetine and sertraline.
Chinese herbs like S-S cream, which are used as topical agents,
have claimed good efficacy and favorable side effect profile.
PDE-5 inhibitors have also been evaluated for management
of PME. Some of the available data suggests that using
combination of SSRIs and PDE-5 inhibitors leads to better
outcome than use of SSRIs alone.
SSRIs can be used on continuous basis or on situation basis,
i.e. pre-intercourse. It is unclear as which of the two is
more effective. There is no clear consensus as to whether
SSRIs will effect an eventual cure of PME allowing for
discontinuation of the medication, or whether SSRIs will be
required for life. The general consensus is that PME usually
returns upon discontinuation of therapy.
Steps in management of Premature Ejaculation (PME)
Firstly, the diagnosis of premature ejaculation be made as
per the prevalent nosological system. The working diagnosis
of PME is made if ejaculation occurs sooner than desired
either before or soon after penetration causing distress to
either or both partner for more than 3 months. The general
principles of management are shown in Table-23.
The general guideline for selection of mode of treatment
is given in figure-4. The first step for treatment involves
evaluation for presence of comorbid sexual dysfunctions,
comorbid psychiatric disorders and marital discord. If
patient has erectile dysfunction or Dhat syndrome along
with PME, these is to be addressed first. If patient has a
psychiatric disorder it needs to be carefully evaluated – is it
primary or secondary to sexual dysfunction, and how severe
it is. If the psychiatric comorbidity is primary and/or severe,
it is to be addressed first. Sometimes the PME is secondary
to the poor interpersonal relationship between the couple,
so it needs to be addressed prior to treatment of PME.
Initial treatment involves providing sex education, clarifying
the myths, relaxation and correction of situational factors (if
S110
Table 22: Treatment options for premature ejaculation
Antidepressants Recommended dose
Non selective 25‑50 mg/day or 25 mg 4‑24 hours prior to intercourse
Serotonin
reuptake inhibitor
‑ Clomipramine
SSRI ‑ Fluoxetine 5‑20 mg/d ay
SSRI ‑ Paroxetine 10‑40 mg/day or 20 mg, 3‑4 hours prior to intercourse
SSRI ‑ Sertraline 25 to 200 mg or 50 mg 4‑8 hrs prior to intercourse
SSRI ‑Dapoxetine 30 mg and 60 mg, on demand use, 1‑2 hours before
intercourse
Tramadol 62 mg of tramadol oral dispersible tablets, and 89 mg
of tramadol oral dispersible tablets, used on demand
Topical therapies Dose
Lidocaine/ Lidocaine 2.5‑5%, 20‑30 mins. prior to intercourse
prilocaine cream
Table 23: General principles of evaluation of premature
ejaculation
• Establish diagnosis based on the history given by patient and the partner
• Proper physical examination of genitalia and secondary sexual characters
is necessary
• Evaluate the general relationship issues and marital discord between the
couple
• Look for comorbid sexual dysfunction, psychiatric morbidity and physical
illnesses
• Evaluate relationship with comorbid psychiatric disorders (i.e., what is
primary ‑ psychiatric disorder or premature ejaculation)
• Evaluate the severity of underlying organic cause and treat the primary
illness first
present) contributing/causing the dysfunction and following
the sensate focus training. It is considered that behavioural
management is the first line of therapy wherever possible.
But some authors suggest that men with lifelong premature
ejaculation need to be managed with a combination of
pharmacotherapy and behavioural management, while
those with acquired or situational PME can be treated with
pharmacotherapy and/or behavioral therapy according
to patient/partner preference. The specific behavioural
techniques for PME involves stop- start or squeeze techniques,
which are usually introduced during genital sensate focus. The
pharmacotherapy involves use of Dapoxetine, SSRIs, TCAs,
Buspirone and topical agents. If either of the therapeutic
measure fails then a combination of both may be tried.
Combination of SSRIs and PDE-5 inhibitors has also been
reported to lead to better outcome than use of SSRIs alone.
Selection of specific treatment modality is to be made based on
physician judgment and patient’s informed choice. The primary
outcome measure is to be the patient’s and partner satisfaction.
Risk and benefits of all treatment options are to be discussed
with patient prior to any intervention.
Dhat syndrome
The first step in the management of Dhat syndrome
involves evaluation for comorbid sexual dysfunctions,
Indian J Psychiatry 59 (Supplement 1), January 2017
 Avasthi, et al.: Sexual dysfunction

psychiatric disorders and presence of possible urinary
tract infection (UTI) and sexually transmitted diseases
(STD). Where ever there is a suspicion, local examination,
appropriate investigations for infective pathology and
phosphaturia need to be done and adequate treatment
is to be provided. Even after appropriate treatment, if
the symptoms persist then the subject is to be provided
adequate sexual knowledge.
Diagnosis is based
on sexual history
Evaluate for other sexual
dysfunctions
• ED
• Dhat syndrome
Whenever patient has comorbid Dhat syndrome along with
PME or ED, Dhat syndrome is to be treated first. If the
psychiatric comorbidity is primary and/or severe, it need to
be addressed first (See figure-5).
The most important aspect of treatment of Dhat syndrome is
providing adequate sex knowledge and clarifying sexual myths.
Sex education mainly focuses on anatomy and physiology
of sexual organs and their functioning with reference to
masturbation, semen formation, nocturnal emissions and
their functioning with genitourinary system independent of
gastro-intestinal tract etc. If there is the presence of associated
anxiety or depressive symptoms that impede the process of
Treat ED, Dhat therapy, anxiolytics or/and antidepressants can be added for
syndrome first
the least possible time and in the least possible doses.

Impaired sexual interest in men or women:

• Look for the presence of couple Treat marital
Treat psychiatric
morbidity if disharmony, depression, disharmony before Besides the general measures, no particular procedures are
prominent and anxiety, situational factors behavioural
management
used in the treatment of this problem. The main emphasis
severe
is on setting the right circumstances for sexual activity,
reducing anxiety, establishing satisfactory fore play, focusing
Discuss treatment options with patient and partner
attention on erotic stimuli and cognitions and resolving
Discuss the efficacy of each treatment options the general issues of relationship between the couple. It is
generally agreed that desire disorders have a substantially
PHARMACOLOGICAL poorer response to psychotherapy (<50%) than other forms
Topical anesthetic
Oral medications
NON-PHARMACOLOGICAL
Reassurance, Sexual education
of sexual dysfunction (≥ 70%). In addition, therapy tends
Antidepressants –Dapoxetine, SSRIs, TCA Relaxation to be more difficult and the conventional sex therapy
Buspirone, combination of SSRIs+PDE-5 Sensate focus
inhibitors Stop and start technique techniques (e.g., sensate focus) are generally inadequate.
Oral medications +Topical anaesthetic Squeeze technique
Hence, a more flexible and person centric approach to
treatment is required. Many authors have tried approaches
like cognitive-behavioral therapy, systems approach, script
Combination of Pharmacological & Non-Pharmacological treatment
modification, clinical hypnosis, guided fantasy exercises,
Figure 4: Guidelines for Premature ejaculation and sexual assertiveness training. Cognitive-behavioral

Dhat Syndrome

Treat with
appropriate
Pharmacotherapy,
Evaluate for comorbid sexual somatic treatment
Investigate & dysfunction and psychotherapy
Treat appropriately Evaluate for comorbid
in liaison with Psychiatric disorders
specialist Evaluate for possible UTI and
STD

Treat Dhat syndrome before ED / PME

Assess for sex knowledge & clarify the misconceptions
and myths
Provide knowledge about semen formation & nocturnal
emissions
Relaxation technique

Treat other sexual dysfunctions if present

Figure 5: Treatment Algorithm of Dhat syndrome

Indian J Psychiatry 59 (Supplement 1), January 2017 S111

 Avasthi, et al.: Sexual dysfunction

therapy emphasizes the role of thoughts and beliefs in
perpetuating the maladaptive behavior and is useful
when beliefs held by the patient or couple about norms
or responses is contributing to the sexual problem. The
“systems” approach, targets dynamics between the couple
and allows assessing the extent to which sexual dysfunction
is used by the couple to maintain a “sexual equilibrium”
within the relationship (i.e., the way sexual dysfunction is
used to regulate intimacy or to allow the share of blame
between partners for the failure of the relationship).
Steps in the management of impaired sexual interest in
men or women:
The most important issue in management is evaluation for
the organic factors, evaluation for presence of comorbid
psychiatric conditions, comorbid sexual dysfunction
and marital disharmony. But it is to be remembered that
although the cause may be organic, psychological causes
can decrease the sexual interest, these also need to be
focused adequately. Many couples have marital disharmony
associated with decrease sexual interest and treating the
same would be the only thing which is required.
Besides the general measures, no particular procedures
are used in the treatment of this problem. The main
emphasis is on setting the right circumstances for sexual
activity, reducing anxiety, establishing satisfactory fore
play, focusing attention on erotic stimuli and cognitions
and resolving the general issues of relationship between
the couple. More flexible and individualistic approach to
treatment is required. The general outline of management
is shown in figure-6.
Female sexual Dysfunction
Formulation of a treatment plan
Firstly female sexual disorders need to be diagnosed as per
the current definitions. Initial treatment planning requires a
thorough assessment of the patient, with the goals of support,
normalization, permission giving, sex education, stress
reduction, symptom alleviation, improve communication skills
(sexual & others) and attitude change. The thorough assessment
includes a comprehensive medical and psychological history of
the patient and her partner. Like in male sexual dysfunction,
psychiatrist treating female sexual dysfunction is to be aware
of the etiology including genitourinary, endocrinological,
vascular and neurological systems. The general principles of
assessment of female patients with sexual dysfunction are
given in Table-24. A multidisciplinary approach is of paramount
importance in female sexual dysfunction.
Vaginismus
It is important to remember that many women who present
with vaginismus have negative attitude towards sex and
quite a few are victim of sexual assault. Some may also
have the belief that premarital sex is wrong or sinful. This
belief may be so ingrained that, even when intercourse is
sanctioned by marriage, it may be difficult to relax physically
or mentally during sexual intercourse. Some times the cause
of vaginismus may be a fear that is instilled by friends or
family by suggesting that the first experience of intercourse
is likely to be painful or bloody. Another important cause of
vaginismus is fear of pregnancy.
The sex education needs to focus on clarifying normal
sexuality and reducing negative attitude for sex. Besides

Hypoactive sexual desire

Investigate & Treat Treat with

appropriately in appropriate
liaison with specialist Pharmacotherapy,
Evaluate for comorbid somatic treatment and
Psychiatric disorders psychotherapy
Evaluate for Marital problems
Look for organic causes
Treat general
marital issues prior
to sex therapy

Psychological management
• General behavioural management- relaxation, sex
education, clarification of myths, sensate focus
• Individual therapy
Pharmacological
• Apormorphine (Sublingual) , Bupropion
• Hormonal Treatment - estrogen, testosterone
• Sildenafil

Treat other sexual dysfunctions if present

Figure 6: Treatment Algorithm of Hypoactive sexual desire

S112 Indian J Psychiatry 59 (Supplement 1), January 2017

 Avasthi, et al.: Sexual dysfunction
Table 24: General principles of evaluation of female
sexual dysfunction
• Assessment of predisposing, precipitating and maintaining factors
• Evaluation of sexual relationship with partner
• Comprehensive medical and psychosexual history
• Assessment for sexual abuse, recurrent depression, substance abuse,
self‑harm and promiscuity
• Focused pelvic examination for pelvic trauma and PAP smear need to be
done in all cases of sexual dysfunction.
the use of general relaxation exercises, the relaxation
procedure also needs to focus on teaching the women to
relax muscles around the inner thigh and pelvic area.
The specific management involves the following stages:
1. Helping the woman develop more positive attitudes
towards her genitals. After fully describing the female
sexual anatomy, the therapist need to encourage
the woman to examine herself with a hand mirror
on several occasions. Extremely negative attitudes
(especially concerning the appearance of the genitals,
or the desirability of examining them) may become
apparent during this stage, possibly leading to failure
to carry out the homework. Some women find it easier
to examine themselves in the presence of the partners;
others may only get started if the therapist helps them
do this first in the clinic. If this is necessary a medically
qualified female therapist is to be involved.
2. Pelvic muscle exercises. These are intended to help the
woman gain some control over the muscles surrounding
the entrance to the vagina. If she is unsure whether or
not she can contract her vaginal muscles she may be
asked to try to stop the flow of urine when she next
goes to the toilet. The woman can later check that she
is using the correct muscles by placing her finger at the
entrance to her vagina where she need to be able to feel
the muscle contractions. Subsequently she is advised to
practice firmly contracting these muscles for an agreed
number of times (e.g. 10) several times a day.
3. Vaginal penetration. Once the woman has become
comfortable with her external genital anatomy she is
advised to explore the inside of her vagina with her
fingers. This is partly to encourage familiarity and partly
to initiate vaginal penetration. Negative attitudes may
also become apparent at this stage (e.g. concerning the
texture of the vagina, its cleanliness, fear of causing
damage, and whether it is ‘right’ to do this sort of
thing). The rationale for any of these objections is
to be explored. At a later stage the woman might try
using two fingers and moving them around. Once she is
comfortable inserting a finger herself, her partner need
to begin to do this under her guidance during their
homework sessions. A lotion (e.g. K-Y or baby lotion)
can make this easier. Graded vaginal dilators can be
used. However, clinical experience has shown that the
use of fingers is just as effective.
Indian J Psychiatry 59 (Supplement 1), January 2017
4. Vaginal containment. When vaginal containment is
attempted the pelvic muscle exercises and the lotion
are used to assist in relaxing the vaginal muscles and
making penetration easier. This is often a difficult
stage and the therapist therefore needs to encourage
the woman to gain confidence from all the progress
made so far. Persisting concerns about possible pain
may need to be explored, including how the woman
might ensure that she retains control during this stage.
5. Movements during containment: Once containment
is well established the couple is asked to introduce
movement during containment, with preferably women
starting the movements first. With this the general
programme of sex therapy is completed and now
the treatment needs to include superimposition of
treatment for specific sexual dysfunctions.
Steps in the management of vaginismus: Treatment is to
be individualized for each woman and/or partner, whenever
possible with their input. Psychological issues as well as
interpersonal issues need to be addressed first. The sex
education needs to focus on clarifying normal sexuality
and reducing negative attitude for sex. Besides the use of
general relaxation exercises, the relaxation procedure needs
to focus on teaching the women to relax muscles around
the inner thigh and pelvic area. The specific behavioural
management is to be followed.
Dyspareunia
Besides the general measures and sensate focus, treatment
of dyspareunia involves sex education. The sex education
need to focus on the importance of adequate arousal and
the couple may also be helped by specific suggestions for
modifying their usual intercourse positions. Couple may be
helped by avoiding positions that lead to deep penetration
(such as vaginal entry from the rear) and by adopting
positions in which the woman is in control of the depth
of penetration (woman on top) or in which penetration is
not too deep (side by side or `spoons’ position). Another
important aspect of treatment of dyspareunia due to
psychological causes is helping the woman become aroused
by teaching the sensate focus programme.
In woman with repeated pain experience on intercourse,
it is likely that they will tense up on future occasions in
anticipation of further pain. Such tension may actually
increase pain as the muscles may be more resistant to
penetration. Due to this, relaxation exercises prior to or
during intercourse may be helpful. Progressive muscle
relaxation prior to sexual activity may allow the women
to reduce the body tension, while more specific relaxation
exercises just prior to intercourse may help to relax the
muscles around the pelvic region and may enhance arousal.
As a woman acquires a number of coping techniques for
minimising the likelihood of pain, positive self-talk may be
helpful. Such self-talk can involve the woman reminding
S113
 Avasthi, et al.: Sexual dysfunction

herself that she is in control of the situation and she will be
the one to determine when penetration is to occur and how
deep penetration will be.
Steps in the management of Dyspareunia: As with most
of the other sexual dysfunctions, the first step is to rule
out other causes/factors that can cause pain. Also the
assessment needs to rule out vaginismus and dryness of
vagina. Treatment of dyspareunia includes sex education
and teaching sensate focus (Figure-7). In particular, it
may be helpful for the couple to avoid deep penetration
positions (such as vaginal entry from the rear) and to assume
positions in which the woman is in control of the depth of
penetration (woman on top) or in which penetration is not
too deep (side by side or `spoons’ position).
is generalized or partner specific needs to be explored.
Although empirically validated non-pharmacological
treatments are not available yet, individual/couples
therapy and medical/ psychological treatment have been
tried in desire disorders in females. In recent times, a
pharmacological agent, flibanserin has been approved for
the management of hypoactive sexual desire disorder in
premenopausal women. The recommended dose0 is 100
mg per day at bed time. Data from metanalysis shows
that compared to placebo, flibanserin is associated with
higher satisfying sexual events per month. Its use is
associated with side effects like dizziness, somnolence,
nausea, and fatigue. If a patient does not show
improvement, the drug needs to be discontinued after
8 weeks.

Arousal disorder Aversion disorders

It is very important to rule out comorbid desire disorders
before treating arousal disorders. If there is comorbid desire
disorder then it needs to be treated first before arousal
disorders are treated. There is no empirically validated
treatment available for arousal disorders due to the fact that
this is a less researched area. Approach usually depends on
the etiology of the arousal disorders. Sensate focusing, CBT,
systematic desensitization, individual and couples therapy,
directed masturbation and communication skills have been
tried in arousal disorders with moderate results.
Sexual abuse or rape, trauma, relationship problem, marital
problem can lead to sexual aversion disorder. Therefore,
all clinicians treating sexual aversion disorders need to
be aware of these causes. In Aversion disorders also no
empirically validated treatment is available however the
clinicians usually employ couple / individual therapy.
Termination of treatment
The termination of the treatment must be planned carefully.
The various strategies and component of termination are:

Desire disorders Prepare for termination from the start of treatment: The
Assessment regarding whether primary or secondary patient/couple should be told about the likely duration of
needs to be settled. Also, whether the desire disorder therapy at the beginning of the treatment. Setting the time

Dyspareunia
• Note: Dyspareunia should only be diagnosed if there is no
other sexual dysfunction such as vaginal dryness or
vaginismus that is causing the pain.

Investigate & • Evaluate for comorbid

treat sexual dysfunction
appropriately in • Evaluate for comorbid
liaison with Psychiatric disorders
Treat with
specialist • Evaluate for possible
appropriate
local pathology - UTI,
Pharmacotherapy,
STD, episiotomy scar,
somatic
endometriosis, ovarian
treatment and
cyst etc.
psychotherapy

Sex education
Provide information about suitable intercourse
positions
Progressive muscle relaxation prior to sexual activity
Positive self-talk
Sensate focus

Figure 7: Treatment Algorithm of Dyspareunia

S114 Indian J Psychiatry 59 (Supplement 1), January 2017

 Avasthi, et al.: Sexual dysfunction
frame will encourage the patient/couple to work on the
homework assignments.
Towards the end of treatment extend the intervals between
sessions: The intervals between the last two to three sessions
need to be extended to two to three weeks.
Prepare for relapse: The therapist need to prepare the couple
for relapse. About three-fourth of men will experience
recurrence of their problem following treatment. Hence,
treatment also needs to assist men to cope well with
relapse. Most recurrences occur in a temporal pattern (i.e.,
will occur more at certain times than at others) and usually
improve naturally or with self-initiated restart of treatment
techniques. The understanding that relapses are normal
expected helps to reduce the anxiety and sense of failure
that may otherwise prolong erectile difficulties.
Follow-up assessments: Follow-up assignments help the
therapist to evaluate the short-term effectiveness of
treatment.
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 CLINICAL PRACTICE GUIDELINES

Clinical Practice Guidelines for Sleep Disorders

Ravi Gupta, Sourav Das1, Kishore Gujar2, K K Mishra3, Navendu Gaur4, Abdul Majid5
Dept. of Psychiatry and Sleep Medicine, Himalayan Institute of Medical Sciences, Doiwala, Dehradun, 1Consultant
Psychiatrist and Sleep Specialist, Medica Superspeciality Hospital, Kolkata; Somnos Sleep Clinic, Kolkata. 2Dy. Medical
Superintendent, YCM Hospital, PCMC, Pimpri, 3HOD, Dept. of Psychiatry, JNMC, Wardha, 4Director, Gaur Mental-Health
Clinic, Ajmer-305001, 5Department of Psychiatry, SKIMS Medical College, Srinagar

Participants of expert group on CPG for Sleep Disorders
Ravi Gupta, Kishore Gujar, K K Mishra, Navendu Gaur,
Abdul Majid, Gautam Saha, Amrit Pattojoshi, RK Solanki
INTRODUCTION
Sleep disorders are common, still we have limited data
regarding the prevalence and management of sleep
disorders from India. Although the systematic research
is limited from our country, still case reports from Indian
population suggest that we see all kinds of sleep disorders.
Prevalence of various sleep disorders is shown in Table 1.
Among all, we have population data for two disorders from
Indian adult population- one is Obstructive Sleep Apnea
(OSA) and second is Restless Legs Syndrome (RLS). Sleep
problems have been investigated among Indian children
more frequently through variety of approaches, most
common through the questionnaire based screening in
school-based cohorts.
Knowledge of sleep disorders is essential for psychiatrists
for two reasons.First, some of the sleep disorders are
common in Psychiatric patients. They may be related directly
to the pathophysiology of psychiatric illness, or may be the
consequence of the treatment modalities offered. Insomnia
Address for correspondence:
Dr. Ravi Gupta,
Department of Psychiatry and Sleep Medicine, Himalayan
Institute of Medical Sciences, Doiwala, Dehradun.
E-mail: sleepdoc.ravi@gmail.com
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is a common complaint with a number of Psychiatric
disorders e.g., depression, anxiety, and withdrawal from the
substances that depress cerebral functioning. In addition,
we now have evidence that link the depression, bipolar
disorder and schizophrenia with the disordered circadian
rhythms and many of these patients show delayed sleep
wake phase cycle.Similarly, antidepressants are known
to induce a number of sleep disorders including NREM
parasomnias (sleep talking, sleep walking) as well as REM
parasomnias (REM sleep behavior disorder) and restless
legs syndrome.Antipsychotics may cause weight gain and
thus they may lead to obstructive sleep apnea in a number
of patients.Similarly, opioid users suffer from central sleep
apnea and during withdrawal many of them develop RLS.
Both these conditions may worsen the quality of the sleep.
Secondly, daytime manifestations of a number of sleep
disorders e.g., insomnia, hypersomnia, restless legs
syndrome, sleep apnea mimic that of Psychiatric disorders
e.g., depression, fibromyalgia, chronic fatigue syndrome
and somatoform disorders.
Considering the recent evidences and changes in the
management of sleep disorders,, Indian Psychiatric Society
has decided to update the existing guidelines. However,
few points must be kept in mind while you consider these
guidelines for your practice:
1. These are consensus statements
2. Original research in this area from India is limited. Most
of the literature reviewed has been generated from the
studies involving Caucasian and European population.
They are culturally, phenotypically and genetically
different from Indian population. All three factors-
This is an open access article distributed under the terms of the Creative
Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non-commercially, as long as the
author is credited and the new creations are licensed under the identical terms.

www.indianjpsychiatry.org For reprints contact: reprints@medknow.com

DOI:
How to cite this article: Gupta R, Das S, Gujar K, Mishra
KK, Gaur N, Majid A. Clinical Practice Guidelines for Sleep
10.4103/0019-5545.196978
Disorders. Indian J Psychiatry 2017;59:116-38.

S116 © 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow

 Gupta, et al.: CPGs for sleep disorders

culture, phenotype and genotype influence the sleep Table 1: Prevalence of various sleep disorders in general
patterns, pathophysiology of sleep disorders and their population
management- both pharmacological as well as non- Disorder Prevalence
pharmacological. Insomnia 10‑15%
Hypersomnia Not known
With this background, we will discuss the guidelines Obstructive Sleep Apnea# 14%
regarding management of individual sleep disorders. Restless legs syndrome# 2%
Delayed Sleep wake phase disorder 10%
Advanced Sleep Wake phase disorder 1%
INSOMNIA Shift worker disorder 2%
# Data from Indian population
ICD-10 defines insomnia as a condition where there is a
problem in initiating the sleep, staying asleep or waking up Table 2: Sleep Disorders that may mimic insomnia
early in the morning at least for 3 nights/week for at least Sleep related breathing disorders
1 month. It should be associated with significant distress • Obstructive sleep apnea
and persistent preoccupation with the deficiency of sleep. • Central sleep apnea
Central disorders of hypersomnolence
Narcolepsy
DSM-5 defines insomnia as a condition where a problem has Sleep related movement disorders
been reported in initiating , maintaining the sleep or there • Restless Legs Syndrome
is an early morning awakening. This problem should occur • Nocturnal Myoclonus (sleep starts)
despite adequate opportunities to fall asleep and must • Sleep Related leg cramps
• Sleep related bruxism
occur at least 3 nights a week. It should be associated with
• Sleep related rhythmic movement disorder
significant distress in the personal, social or occupational Parasomnias
life. If it persists for at least 1 month but less than 3 months, • Sleep‑walking
it is considered as episodic; if it persists for at least 3 months, • Sleep terrors
it is considered as persistent insomnia. • Nightmare disorder
Circadian Rhythm Sleep Disorders
• Advanced Sleep Wake Phase disorder
Our understanding regarding insomnia has changed over • Delayed Sleep Wake phase disorder
the years. Earlier we used to differentiate between primary • Shift worker disorder
and secondary insomnia, however, the recent research • Irregular Sleep wake rhythm disorder
Others:
has challenged this belief. Current literature suggests
• Sleep related asystole
that insomnia cannot be considered merely as a symptom • Sleep related epilepsy
of psychiatric disorders. It is rather co-morbid with the • Sleep related laryngospasm
psychiatric and other medical conditions, and if not treated
early, through the process of kindling it becomes chronic Through a careful history and clinical examination, these
which has multiple health and economic implications. conditions can be ruled out (Table 2).

For this reason, in the third edition of International
Classification of Sleep Disorder (ICSD-3), which appeared in
2014, insomnia has been divided into two categories: short
term insomnia disorder and chronic insomnia disorder. In
addition, subtyping of the primary insomnia into adjustment,
psychophysiological, paradoxical and idiopathic that
prevailed till ICSD-2 has been omitted. This has happened
for multiple reasons.First, all the insomnia sufferers have in
common one issue i.e., hyperarousal and second, change in
the sleep related behavior and compensatory mechanisms
were found similar across different insomnia subtypes.
Hence, all the modalities that are used for the treatment of
insomnia are directed towards reducing the hyperarousal.
Assessment and evaluation
Management of the insomnia case starts with the history
taking and general physical examination. It is of paramount
importance as a number of sleep disorders may mimic
insomnia. Hence, having knowledge regarding these mimics
will help the clinician to reach to an accurate diagnosis.
Indian J Psychiatry 59 (Supplement 1), January 2017
While taking the history of a patient with insomnia, special
focus should be provided to the initiation of symptoms,
its course and progression. Information from the
bed-partner/ room-partner who had seen the patient while
asleep should be sought and incorporated.(Table 3).
He should be asked for the daytime symptoms of insomnia,
as in their absence, insomnia can’t be diagnosed. Frequency
of symptoms must be asked along with the duration and
frequency of symptoms per week. It must be ensured
that the patient has adequate opportunities to fall asleep.
Excessive daytime sleepiness must be ruled out. Clues
regarding the predisposing, precipitating and perpetuating
factors of insomnia should be assessed in detail.
It is essential to ask for the sleep pattern while the patient was
asymptomatic and compare it with the sleep schedule during
symptomatic period. Sleep related behavior and rituals must
be asked before and after the symptoms onset as they may
provide a good idea about the possible interventions.
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 Gupta, et al.: CPGs for sleep disorders

Table 3: Information regarding a typical night
Information regarding
Sleep Schedule
Nocturnal Awakenings, if any
Pre‑bedtime behavior
Compensatory strategies
Addictive substances
Drugs
Environment of the bedroom
Time spent in bed in awake state
in a whole day
Description
• Time to bed
• Time to fall asleep
• Wake time
• Time taken to get up from bed
• Quality of nocturnal sleep
• Daytime Napping
• Timing
• Duration
• Quality of sleep during naps
• Number of naps
• Regularity of this schedule
• Number of awakenings
• Reasons for awakenings
• Time taken to fall asleep again
• What does he do since evening
• Mental state before going to bed
• Behavior and thoughts during
nocturnal awakenings
• Nature of substance consumed
• Usual timing
• Usual effect: Stimulant/
Somnolent
• Frequency of consumption
• Withdrawal/Intoxication
interfering with sleep
• If person is taking any drug,
then effect of drug on sleep
• Look for possible factors that
can interfere with sleep
Table 4: Other medical disorders that may induce sleep
disturbance
Cardiovascular
• Arrthythmias
• Congestive heart failure
• Myocardial infarction
• Varicose veins
Pulmonary
• Chronic obstructive pulmonary disease
• Interstitial lung disorder
• Scoliosis
GIT
• Peptic ulcer disease
• GERD
• Chronic constipation
CNS
• Intracranial space occupying lesions
• Dementia
• Seizures
• Stroke
• Parkinson’s disease
Neuromuscular disorder
Genitourinary
• Chronic kidney disease
• Benign Prostatic hypertrophy
Musculoskeletal:
• Rhumatoid arthritis
• Connective tissue diseases
Severity of insomnia may be assessed using a brief
questionnaire- Insomnia severity index, available in English
as well as Hindi.

This should be followed by a thorough general physical

Many of the patients with insomnia start worrying while
they are not able to fall asleep in the bed. Dysfunctional
thoughts before the bedtime or while in bed lead to
hyperarousal and they may be assessed using Dysfunctional
Beliefs and Attitudes about Sleep, which is available in
English as well as Hindi Language.
examination and if any system appears dysfunctional, that
should be examined in detail.
Sleep diary provides a good opportunity to assess the sleep-
pattern and helps in differentiating insomnia from circadian
rhythm sleep disorders. (Figure 2).

Many of the medical conditions may induce symptoms that
may mimic insomnia. Hence, the disorders provided in
Table 4 must be ruled out.
Algorithm for the diagnosis of insomnia is depicted in Fig 1.
Effect of the insomnia on the daytime functioning must
be assessed. Special care should be taken to differentiate
between fatigue and sleepiness. Mood during the day must
be assessed. Depression and other psychiatric disorders
that may mimic daytime symptoms of insomnia may be
differentiated by asking “how do you feel during the day
which is followed by a good night sleep?”. If the patient
reports a remarkable improvement, diagnosis of psychiatric
disorder shall be deferred till the insomnia resolves.
If the patient is undergoing any treatment for other medical
disorders (pharmacological as well as non-pharmacological),
its’ effect on the sleep should be examined.
At times, objective data is necessary to reach to a diagnosis
and in those cases actigraphy may be performed. In cases of
chronic insomnia that is not responding to treatment, video-
synchronized 24-channel polysomnography is desirable.
Formulating a treatment plan
Treatment of insomnia is individualized and tailor-made.
For the short term insomnia, pharmacotherapy is indicated,
while for the chronic insomnia, cognitive behavior therapy
for insomnia (CBT-I) is preferred.
Various hypnotic agents are described below. Importance
of behavioral intervention should not be underestimated
and it is better that they should be started even in cases
with short term insomnia. For example, a person might
be having genetic predisposition to insomnia and a recent
stress might have precipitated the insomnia, which could
be perpetuated by the dysfunctional beliefs about sleep or
maladalptive strategies to control it. Common maladaptive

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 Gupta, et al.: CPGs for sleep disorders

Paent presenng with complaints suggesve of insomnia

No
Adequate opportunies for sleep No Insomnia
Yes
No
Dayme Symptoms of Insomnia No Insomnia
Yes

Difficulty Iniang Sleep Early morning awakening

Difficulty maintaining Sleep
> 30 min for > 3 Nights/wk > 30 min for > 3 Nights/wk
> 30 min for > 3 Nights/wk

No Total Sleep Time normal

Symptoms of RLS Total Sleep Time Total Sleep
Abnormal acvity at night Snoring present if le to sleep
normal if le to sleep me
Yes Yes decreased
Yes
Yes Screen for NO

OSA
RLS Delayed Sleep Wake Phase Disorder
Seizures
Advanced sleep
Parasomnia wake phase
disorder
High Risk

Nocturnal EEG
REMBD Level 1
NREM
Polysomnography
Normal

NREM
No
Parasomnia
OSA or
Normal
RBD
Confirmed

Terminal Insomnia
Inial Insomnia Middle Insomnia

Duraon

<3 >3
months months

Short term Chronic

Insomnia Insomnia

Figure 1: Algorithm for the diagnosis of Insomnia

strategies that we see include, but not limited to- spending Goals of the therapy
excessive time in bed, start smoking or start drinking 1. Improve the sleep onset latency, total sleep time and
caffeine while awake, spending time on screen while awake reduce awakenings, thus improving sleep efficiency
or spending majority of the time during the day in bed. 2. Improving quality of sleep
3. Ameliorate or significantly reduce the daytime
Wherever indicated, opinion from a relevant specialist symptoms of insomnia
may be sought. If there is evidence of sleep disorders 4. Sustain the effect of treatment and reduce the chances
that mimic insomnia, management should be directed to of the relapse
those disorders, rather than the insomnia. In some cases,
insomnia is co-morbid with these sleep disorders, and in Choice of treatment settings
these cases, both should be treated. Treatment of insomnia is usually offered on an outpatient

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 Gupta, et al.: CPGs for sleep disorders

Figure 2: Sleep diary depicting long sleep onset latency with normal total sleep time when the patient is following natural pattern
of sleep. However, the patient gets the sleep late in the night and wakes up late in the morning. This data suggests delayed
sleep wake phase disorder

basis. Hospitalization may rather worsen the condition by
enhancing hyperarousal. However, in some patients it may
improve sleep by removing environmental factors and may
provide a clue to the underlying pathophysiology.
Pharmacological treatment
Pharmacological treatment for the insomnia is limited to short-
term insomnia and they are not routinely recommended for
the management of chronic insomnia. A wide variety of drugs
is available that may induce sleep e.g., benzodiazepines,
Benzodiazepine receptor agonists, sedating antidepressants,
second generation antipsychotics, antihistaminics, melatonin
and its agonists and orexin receptor antagonists. Table 5 shows
the factors that influence the choice of a particular drug.
Benzodiazepinesand benzodiazepine receptor agonists
(BzRA) are usually divided into short, intermediate and
long acting and one of them may be chosen based upon
the case. In general, short acting are preferred when the
patient is having difficulty in sleep initiation, intermediate
acting when the patient has difficulty in maintaining the
sleep and long acting when the patients complain of early
morning awakening. However, intermediate and long acting
agents may have residual daytime effects and may produce
the somnolence during the day (Table 6).
Melatonin and its agonists include the melatonin itself
and the molecules that act on MT1 and MT2 receptors.
Melationin is available as 3 mg tablet formulation.
This may be used to induce sleep, however, data do not
support its efficacy as a hypnotic agent. It is rather used
as a chronobiotic. Melatonin receptor agonists- ramelteon
(8-24 mg/day) and agomelatine (25-50 mg/day) are available
in India. Remelteon is a short-acting-drug with half-life of
around 3-4 hours. It shows an improvement in the time to fall
asleep with minimal adverse effects.Agomelatine is another
molecule that in addition to having an agonist action on
melatonin receptors, also has antagonist action on 5-HT2C
receptors. It has been found effective in improving both
sleep and mood in clinical trials, and because of it’s short
half life (1-2 h) is free from daytime somnolence.
Orexin-receptors antagonists have recently been discovered
for the management of insomnia. Controlled trial data is
available for one of the molecule i.e., Survorexant. It has
been found to improve total sleep time with variable findings

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 Gupta, et al.: CPGs for sleep disorders

on the nocturnal arousals and time spent awake after sleep
onset. Usual prescribing dose varies between 10-40 mg/day.
Common adverse effects include nausea abnormal dreams.
Sedating antidepressants e.g., tricyclics, trazodone and
mirtazapine may be used if there is comorbid psychiatric
disorder that warrants their use. In addition, they may also
be preferred when adverse effects of the benzodiazepines
and BzRAs are not tolerable. However, there are insufficient
evidences for their efficacy in insomnia.
Antihistaminicdrugs are available as over-the-counter drugs,
and they are commonly used for self medication.However,
data regarding their efficacy in insomnia is limited. However,
a tricyclic drug Doxeipin has been approved for the treatment
of insomnia in low doses (10 mg). At this dose, it primarily
acts on the H1receptors and work as an antihistaminic.
Antipsychotics are used off-label for the treatment of
insomnia, particularly chlorpromazine, clozapine, olanzapine
and qutiapine. However, we do not have data regarding their
efficacy as hypnotic agents. In addition, while prescribing
them, it is essential to consider potential adverse effects
e.g., metabolic syndrome and extrapyramidal symptoms.
Long term pharmacotherapy
Although the pharmacotherapy is not routinely
recommended for the long term treatment in view of
availablibility of non-pharmacological therapies, still, data
Table 5: How to choose a drug from the available
molecules?
Age of the patient and risks associated with sedation
Comorbid psychiatric and other medical disorders
Pharmacokinetic properties of the molecule in question
Drug interactions with other medication that the patient is taking
Adverse effects of the drug in question: short term as well as long term
Availability of the molecule
Cost of the drug
Allergy to the molecule in question
is available for treatement with Z drugs for as long as 6
months without any major adverse effects. Considering the
limited availability of trained CBT-I therapist, consensus
was reached that in certain circunstances where CBT-I
is not possible for any reason, pharmacothepray may be
institutedfor long term.
Non-Pharmaclogical therapies
Cognitive behaviour therapy for Insomnia (CBT-I) is
the mainstay of therapy for chronic insomnia. It is a
multicomponent therapy that includes education regarding
sleep physiology, sleep hygiene, addressing dysfunctional
beliefs, stimulus control therapy, sleep restriction and
relaxation training.Each of these components may be used
as a primary focus in a given patient which makes this
therapy highly individualized. In general, goal of the therapy
is to reduce the hyperarousal, hence, educating the patient,
cognitive restructuring (to address dysfunctional belief) and
relaxation are necessary in almost all patients. CBT-I has been
found effective for long term management of insomnia in
the randomized controlled trials comparing it with hypnotic
agents. It has been repeatedly shown that though, it takes
some time to show its effects, once they appear, they are
longer lasting as compared to pharmacotherapy and also
reduce the chances of relapse.One of the major advantages of
the CBT-I is the fact that it has also been found useful in cases
of insomnia co-occurring in context of medical disorders.
Since the CBT-I is time consuming and requires the expertise,
it has been tried to be delivered through internet, computer
and in groups.Though the computerized CBT-I has been
found superior to the placebo and pharmacotherapy, still it’s
efficacy has been found low when compared to the face to
face CBT-I. Administration of CBT-I in a group has also been
tried, with the results similar to the computerized CBT-I.
Results of sleep education and sleep hygiene alone have
been found to have limited value unless they are associated
with some other component of the CBT-I.

Table 6: Benzodiazepines and Benzodiazepine Receptor Agonists

Molecule Half Life (hr) Dose (mg/d) Formulations Common Adverse effects
Benzodiazepines
Oxazepam 3‑20 10‑30 mg Tablet Memory lapses, daytime sleepiness,
ataxia, fall, automatism, slurred speech
Trialzolam 1.5‑5.5 0.5‑1 mg Tablet
Lorazepam 10‑20 1‑4 mg Tablet/Injection
Alprazolam 6‑20 0.25‑1 mg Tablet/Sustained released
Diazepam 20‑50 5‑20 mg Tablet/Injection
Clonazepam 18‑40 0.5‑2 mg Tablet/Mouth dissolving
Nitrazepam 30‑40 5‑10 mg Tablet
Benzodiazepine
Receptor Agonists
Zaleplon 1 5‑10 Tablet Memory lapses, hallucinations,
Eszopiclone 5 1‑2 Tablet paradoxical excitement
Zolpidem 2‑4 5‑10 Tablet/Extended release/Sublingual low
dose/Sublingual high dose/Oral spray

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 Gupta, et al.: CPGs for sleep disorders
Exercise, especially the aerobic exercise along with the
sleep hygeine has been found to be beneficial for the
sleep and daytime activity. It has been found to reduce the
time taken to fall asleep and improve the sleep efficiency
in randomized control trials.Thus, patients should not be
advised not to engage into any exercise before bed-time, as
conventionally thought. Rather they should be allowed to
analyse their sleep reactivity towards the exercise and if is
found to interfere with sleep, then they should be advised
not to get engaged into it before bedtime.
One of the focus of the therapy is to reduce the total time
spent in bed in an effort to fall asleep by sleep restriction.
Evidence is less robust regarding the utility of the sleep
restriction therapy.However, a recent review suggested
that sleep restriction therapy is one of the most effective
components of the CBT-I.This must not be used in cases
of bipolar disorders and epilepsy as it may worsen the
comorbid medical condition.
In Indian context, since patients have been found focussing
on the daytime worries, rather than on the sleep, problem
solving technique may be added.Recently, mindfulness
based relaxation therapy has been found to improve the
sleep.Mindfulness based stress relaxation (MBSR) has
been found equally efficacious to the face to face CBT-I,
pharmacotherapy and better than sleep hygiene alone.This
has been found more efficacious when it has been included
as a component of CBT-I.
Management as per the different phases of illness
On of the major issues with the patients with chronic
insomnia is that they desperately want to sleep soon after
the initiation of treatment. However, CBT-I takes longer time
to improve the situation because it is delivered in sessions.
And each session has a focus which is guided by prevailing
sleep problems since last session. During CBT-I patient is
expected to maintain a sleep diary and change his cognition
and behavior. Many of the patients are not able to do that. In
those cases, the treatment is started with pharmacotherapy
along with the CBT-I. Gradually, the pharmacotherpay is
tapered and patient remains only on the CBT-I. Thus, patient
benefits from the immediate response of hypnotics that
reduces the burden and hyperarousal in addition to long
term benefits of CBT-I. Though many sleep specialists are
practicing it, still it has not been thoroughly investigated.
When to stop treatment
Though we do not have any literature on this issue, still,
for the short term insomnia, patient should be requested
to give drug holidays intermittently and to restart the
treatment when the symptoms appear again. CBT-I may
be discontinued once the sleep of the patient is stabilized
for at least 4 weeks, though this number has been chosen
arbitrarily.
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Special population
Pharmacotherapy should be cautiously advised to the
elderly because of the drug interactions and adverse
effect profile. This should also be cautiously used in
children and patients with other medical disorders for
the same reasons. CBT-I is not possible in patients with
neurocognitive deficits and non-compliant patients,
hence they should not be started it without assessing
their motivation.
Pregnancy: Duing first trimester it is best to avoid all
medications. In disabling cases, sedating antihistaminitcsmay
be used for the shortest possible period.
Lactation: Amount of psychotropicdrugs that is excreted in
milk varies from molecule to molecule. Reader is advised
to consult the pharmacology book for details regarding
individual molecule.
HYPEROSMNIA
Alertness is an integral necessity for learning, performance
and safety. Excessive daytime sleepiness impairs productivity
and exponentially increases the risk of accidents, particularly
in occupations like transportation, military, healthcare,
factory workers etc. excessive sleepiness is reported by
10-25% of the general population in different parts of the
world. However, as of now there are no prevalence studies
from India on hypersomnia/ excessive sleepiness.
International Classification of Sleep Disorder, 3rd edition
(ICSD 3) defines daytime sleepiness as: “the inability to
stay awake and alert during the major waking episodes of
the day, resulting in periods of irrepressible need for sleep
or unintended lapses into drowsiness or sleep”. Sleepiness
varies in severity and is more common during sedentary,
boring, and monotonous situations that require little
active participation. Some patients are aware of increasing
sleepiness before falling asleep, whereas others can fall asleep
with little or no prodromal symptoms (“sleep attacks”).
The most common cause of excessive daytime sleepiness
(EDS) in modern day world is the combination of suboptimal
duration of sleep, poor sleep hygiene, and changing
work schedules. In addition, various sleep disorders like
obstructive sleep apnea, circadian rhythm sleep disorders
and periodic limb movement disorder may be associated
with excessive daytime sleepiness.
Primary causes of hypersomnolence have been classified
under the heading of “Central disorders of hypersomnolence”
in ICSD 3. The various central causes of hypersomnolence
according to different classification systems is given in
the table 7 below and Algorithm to approach a case of
hypersomnia is given in Fig 3.
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 Gupta, et al.: CPGs for sleep disorders

Table 7: Comparative terminologies of causes of hypersomnolence between ICD‑10 and ICSD‑3

ICSD 3 ICD 10 ICD 10 code:
Narcolepsy Type 1 Narcolepsy With Cataplexy G47.411
Narcolepsy Type 2 Narcolepsy Without Cataplexy G47.419
Idiopathic Hypersomnia Idiopathic Hypersomnia With Long Sleep Time G47.11
Idiopathic Hypersomnia Without Long Sleep Time G47.12
Kleine‑Levin Syndrome Recurrent Hypersomnia G47.13
Hypersomnia Due to a Medical Disorder Hypersomnia Due to Medical Condition G47.14
Hypersomnia Due to a Medication or Substance F11‑F19
Hypersomnia Associated with a Psychiatric Disorder Hypersomnia due to other mental disorder F51.13
Insufficient Sleep Syndrome Insufficient sleep syndrome F51.12
Primary Hypersomnia F51.11
Other hypersomnia not due to a substance or F51.19
known physiological condition

Symptoms of Excessive insufficient sleep, inadequate Psychoeducation/ Sleep

Daytime Sleepiness sleep hygiene, job or familial Hygiene/ Behavior Therapy/
Yes
stressors and work schedules CBTi
from history

Recurrent hypersomnia, e.g. No

Klein Levin syndrome (usually
associated with behavioral
change, hyperphagia,
irritability)
Yes
Polysomnography Within
Normal limits
Episodic/ recurrent
Suggestive history for hypersomnia:
Yes No
Irresistable urge for sleep in daytime (or
in middle of activities)/ sleep attacks/
cataplexy/ hypnagogic or hypnapompic
Rating scales: hallucinations/ sleep paralysis/ REM
Epworth Sleepiness Scale behavioral disorders/ prolonged sleep
Sleep diary Yes time/ confusional arousals

Full night attended Level I

Polysomnography preferably Objective evidence of OSA/ Treat accordingly
with video recording CSA/ PLMD/ Parasomnias
Yes
Followed by Multiple Sleep
Latency Test next day With cataplexy or CSF
MSLT findings: Hypocretin 1 conc. either <=
MSLT: SL<=8 min, >= 2 SOREMPs Yes 110pg/mL or <1/3 of mean
reference values
MSLT findings:
MSLT: SL<=8 min, < 2 SOREMPs
Yes No
Narcolepsy Narcolepsy
Total 24 hr sleep time >=660 Type 1 Type 2
Idiopathic
mins by 24 hour PSG/ wrist Hypersomnia
actigraphy +sleep log Yes

Underlying medical
Yes Underlying medical condition Hypersomnia due to condition diagnosed by MRI/
judged to be directly causing a medical disorder SPECT/ Immunology etc.
the excessive sleepiness Yes
Yes
No
Attributable to sedative Hypersomnia due to a
Primary Narcolepsy
medications, alcohol or drugs medication or
Narcolepsy secondary to
of abuse Yes substance
(Type 1 or 2) medical
condition
(Type 1 or 2)
Attributable to underlying Hypersomnia
psychiatric conditions like associated with a
moods disorders, somatic Yes psychiatric disorder
symptom disorder etc.

Figure 3: Algorithm for the diagnosis of Hypersomnia

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 Gupta, et al.: CPGs for sleep disorders
Hypersomnias of central origin
Narcolepsy type 1: caused by a deficiency of hypothalamic
hypocretin (orexin) signaling. Excessive daytime sleepiness
and signs of REM-sleep dissociation are the characteristic
features of narcolepsy, however, the most specific feature
is cataplexy (defined as more than one episode of generally
brief (< 2 minutes), usually bilaterally symmetrical sudden
loss of muscle tone with retained consciousness). There
are repeated daily episodes of an irrepressible need to
sleep or lapses into sleep (sleep attacks). Most patients
awaken refreshed after a sleep episode but begin to feel
sleepy again after variable times. Many narcolepsy patients
have lapses in vigilance, sometimes in combination
with automatic behavior, such as writing gibberish or
interrupting a conversation with a completely different
topic. Apart from cataplexy and sleep attacks, 33% to 80%
of narcolepsy patients have hypnagogic hallucinations and/
or sleep paralysis. Hypnagogic hallucinations are defined
as vivid dreamlike experiences occurring at the transition
from wake to sleep. Typically, hypnagogic hallucinations
have a multimodal or “holistic” character, often combining
visual, auditory, and tactile phenomena. Hypnopompic
hallucinations are similar but occur at sleep to wake
transitions. Sleep paralysis describes the disturbing
temporary inability to move voluntary muscles at sleep-
wake transitions. Despite being awake and conscious of
the sleeping environment, it is impossible for subjects to
move their limbs or even open their eyes. The experience
may last for several minutes and can be very distressing.
Other symptoms may include ptosis, blurred vision, and
diplopia, presumably as a result of sleepiness. Obesity is
another common symptom of narcolepsy.
Narcolepsy type 1 due to a medical condition: This condition
is primarily associated with central nervous system (CNS)
disorders, including autoimmune or paraneoplastic
disorders associated with anti-Ma2 or antiaquaporin4
antibodies, and tumors or other lesions of the hypothalamus
or severe head trauma.
Narcolepsy type 2: is characterized by excessive daytime
sleepiness and abnormal manifestations of REM sleep on
polysomnography/MSLT [mean sleep latency less than or
equal to eight minutes and two or more sleep onset REM
periods (SOREMPs) on an MSLT (or one SOREMP on an MSLT
and one on the preceding nocturnal polysomnogram)].
Cataplexy is absent, although some atypical sensations of
weakness triggered by unusual emotions such as stress
and anger may be reported. Refreshing daytime naps are
characteristic. Sleep paralysis, hypnagogic hallucinations,
or automatic behavior, memory lapses, automatic behavior,
ptosis, blurred vision, and diplopia may be present.
Narcolepsy type 2 due to a medical condition:  Neurologic disorders
associated with narcolepsy type 2 include tumors or sarcoidosis
of the hypothalamus, autoimmune or paraneoplastic disorders
S124
associated with anti-Ma-2 or anti-aquaporin-4 antibodies,
multiple sclerosis, myotonic dystrophy, Prader-Willi syndrome,
Parkinson disease, and head trauma.
Idiopathic hypersomnia: is characterized by excessive
daytime sleepiness that occurs in the absence of cataplexy,
is accompanied by no more than one SOREMP on MSLT and
preceding polysomnogram combined, and is not adequately
explained by another disorder. Sleep drunkenness,
consisting of prolonged difficulty waking up with repeated
returns to sleep, irritability, automatic behavior, and
confusion may be present. Subjects typically do not easily
awaken to alarm clocks and frequently use special devices
or procedures to wake up. Naps are generally long, often
more than 60 minutes, and described as unrefreshing by
46% to 78% of patients. Associated symptoms which suggest
a dysfunction of the autonomic nervous system may be
present. These symptoms include headache, orthostatic
disturbance, perception of temperature dysregulation, and
peripheral vascular complaints (Raynaud-type phenomena
with cold hands and feet).
Recurrent Hypersomnia: Kleine-Levin syndrome is
characterized by recurrent episodes of excessive
sleepiness,however, associated cognitiveand behavioral
disturbances are not uncommon. A typical episode
lasts a median 10 days (range, 2.5–80 days), with rare
episodes lasting several weeks to months. Usual reported
triggering factors for the first episodes are infection or
alcohol intake, with further episodes recurring every
1–12 months (median three months) for years. During
episodes, patients may spend as long as 16 to 20 hours
per day in sleep, and they usually wake-up only for the
natural calls (incontinence is not observed). They remain
arousable, but are irritable if prevented from sleeping.
When they are awake during episodes, most patients
appear exhausted, indifferent, confused with psychomotor
retardation. Anterograde amnesia is typical and most of the
patients report derealization. A larger chunk of patients eat
ravenously (66%, although one third eat less), nearly half of
them turn hypersexual (53%, principally men), may show
childish behavior and nearly half appear depressed (53%,
predominantly women). They often become anxious when
left alone and after seeing strangers, and nearly third of them
experience hallucinations and delusions (30%). Importantly,
patients are completely asymptomatic in between episodes.
Hypersomnia Due to a Medical Disorder:Patients with
this disorder have excessive nocturnal sleep, daytime
sleepiness, or excessive napping that is attributable to
a coexisting medical or neurological disorder. Daytime
sleepiness may be of variable severity and may resemble
that of narcolepsy (i.e., refreshing naps) or idiopathic
hypersomnia (i.e., long periods of unrefreshing sleep).
Other symptoms of narcolepsy e.g., sleep paralysis,
hypnagogic hallucinations and automatic behavior may
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 Gupta, et al.: CPGs for sleep disorders
be present. Hypersomnia due to a medical disorder is only
diagnosed if the medical condition is judged to be directly
causing the excessive sleepiness. Hypersomnolence has
been described in association with a number of conditions
e.g., metabolic encephalopathy, head trauma, stroke,
brain tumors, encephalitis, systemic inflammation (e.g.,
chronic infections, rheumatologic disorders, cancer),
genetic disorders, and neurodegenerative diseases.
Hypersomnia due to a medication or substance:Patients
with this disorder have excessive nocturnal sleep, daytime
sleepiness, or excessive napping that is attributable to
sedating medications, alcohol, or drugs of abuse. This
diagnosis also includes hypersomnolence associated
with withdrawal from amphetamines and other stimulant
drugs.
Subtypes
Hypersomnia due to sedating medications:  desired or regarded as the societal norm ie. share a common
Hypersomnia due to substance abuse:  underlying chronophysiologic basis.
Hypersomnia due to stimulant withdrawal:  1. Time Zone Change (Jet Lag) Syndrome
Hypersomnia associated with a psychiatric disorder:
Patient may report increased duration of nocturnal sleep
associated with daytime sleepiness or excessive napping.
In addition, they often complain of poor quality and
nonrestorative sleep. Patients are often intensely focused
on their hypersomnolence, and psychiatric symptoms
may become apparent only after prolonged interviews or
psychometric testing. Associated psychiatric conditions
include mood disorders, conversion or undifferentiated
somatoform disorder, and less frequently other mental
disorders such as schizoaffective disorder, adjustment
disorder, or personality disorders.
Subtypes:
Hypersomnia associated with mood disorder
Hypersomnia associated with a conversion disorder or somatic
symptom disorder
Insufficient sleep syndrome:Many people curtail a small
portion from their normal sleep duration for prolonged
periods owing to societal or professional demands. Since
sleep deprivation has cumulative effect, they remain in a
state of chronic partial sleep deprivation that is insufficient to
maintain normal levels of alertness and wakefulness. Physical
examination reveals no medical explanation for the patient’s
sleepiness. A detailed history of the sleep pattern reveals that
patient is not spending adequate time in sleep and that he
has curtailed his sleep in past few days/months. Sleep time
that is markedly extended on weekend nights or during
holidays compared to weekday nights is also suggestive
of this disorder. Individuals with this condition may show
cognitive and behavioral symptoms e.g., irritability, attention
deficits, distractibility, reduced drive, anergia, dysphoria,
fatigue, impatience, incoordination, and tiredness.  consists of varying degrees of difficulties in initiating or
Indian J Psychiatry 59 (Supplement 1), January 2017
Management
A. Pharmacotherapy: Pharmacotherapeutic options for the
management of hypersomnia are depicted in Table 8.
B. Behavioral Treatment:
• Education about type of hypersomnia, course, prognosis
and management principles
• Regular frequent nap times of 10-20 mins at 2-4 hour
intervals during the day
• Emphasize need for a regular nocturnal sleep schedule
• Try to obtain 9 hours of nocturnal sleep
CIRCADIAN RHYTHM SLEEP DISORDERS
The circadian rhythm sleep disorders comprise of following
disorders having major feature is a misalignment between
the patient’s sleep pattern and the sleep pattern that is
2. Shift Work Sleep Disorder
3. Irregular Sleep-Wake Pattern
4. Delayed Sleep-Phase Syndrome
5. Advanced Sleep-Phase Syndrome
6. Non-24-Hour Sleep-Wake Disorder
7. Circadian Rhythm Sleep Disorder Not Otherwise
Specified
Diagnostic subtypes can be specified with the diagnosis of
intrinsic type (due to neurologic disease) or extrinsic type
(due to environmental or social circumstances) Severity
Criteria: Mild: Moderate: Severe:
Duration Criteria: Acute: Subacute: Chronic:
Major problem among all CRSDs is the inability to fall asleep or
staying awake when desired or expected. Since sleep episodes
occurring at inappropriate times, the corresponding wake periods
also seen at undesired times. Therefore, the patient complains
of insomnia or sleepiness but importantly both of them are
occurring at inappropriate times. For most of the CRSDs, once
sleep is initiated, the major sleep episode is of normal duration
with normal architecture. However, if any other sleep disorder
appears to influence the sleep timing, diagnosis of CRSD should
be deferred.For example patients with inadequate sleep hygiene
may show some degree of shift in sleep and wake timing. Hence,
CRSD should be diagnosed only when the symptoms can be
ascribed to the major shift in timing of sleep.
1. Time Zone Change (Jet Lag) Syndrome: Synonyms and
Key Words: Jet lag, transmeridian flight desynchronosis, air
travel, transmeridiandyschronism.
Essential Features: Time zone change (jet lag) syndrome
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Table 8: Pharmacotherapy for Hypersomnia

Used for: Drug Mechanism of action Dose range (mg/day) Pediatric use
Hypersomnia Amphetamine stimulants 5‑60 mg Not recommended in pts<3 years
in Narcolepsy, Methyphenidate stimulants 20‑40 mg in adults; Not recommended in pts<6 years.
Idiopathic 5‑20 mg in children Parameters of growth are should be
hypersomnia, etc. regularly monitored in children
Modafinil non‑amphetamine 100‑400 mg SECNE
wakefulness‑promoting
medication
Armodafinil  (R)‑ enantiomer of modafinil with 50‑250 mg SECNE
a longer half‑life.
Sodium oxybate rapidly acting sedative/hypnotic/ 4.5‑9 g per night SECNE
(also used for Cataplexy, anesthetic medication.
sleep paralysis, hypnagogic
hallucinations)
Selegiline MAO‑B inhibitor that is 5‑10 mg SECNE
metabolized to amphetamine and
methylamphetamine
Atomoxetine selective noradrenaline reuptake 10‑25 mg generally well tolerated in children and
inhibitor (NARI) adolescents
Reboxetine selective noradrenaline reuptake 10 mg SECNE
inhibitor (NARI)
Ritanserin 5‑HT2 antagonist 5‑10 mg SECNE
Cataplexy Fluoxetine Selective serotonin reuptake 10‑40 mg Safety and effectiveness assessed in
inhibitor (SSRI) children aged 8‑18 yrs with major
depressive disorder and 7‑18 yrs with
OCD
Venlafaxine# serotonin‑norepinephrine reuptake 75‑375 mg SECNE
inhibitor (SNRI)
Protriptyline Tricyclic antidepressant (TCA) 10 mg SECNE
Viloxazine selective norepinephrine reuptake 50‑200 mg SECNE
inhibitor (NRI)
Imipramine Tricyclic antidepressant (TCA) 25‑200 mg SECNE
Clomipramine Tricyclic antidepressant (TCA) 25‑200 mg Can be used in children aged 10 years
and above
Desipramine Tricyclic antidepressant (TCA) 25‑200 mg Not approved for use in children
Recurrent Lithium* Mood Stabiliser 300‑900mg Special caution advised
hypersomnia (Klein
Levin Syndrome)
SECNE – Safety and effectiveness in children not established; NE – Not established *Carbamazepine and valproate can also be used for KLS, some benefit noted
in behavioral symptoms, but no consistent benefit observed in hypersomnia #Duloxetine and desvenlafaxine can also be used to treat cataplexy, though there is
lack of formal research data at present.

maintaining sleep, excessive sleepiness, decrements in
subjective daytime alertness and performance, and somatic
symptoms (largely related to gastrointestinal function)
following rapid travel across multiple time zones.
2. Shift Work Sleep Disorder: Symptoms of insomnia or
excessive sleepiness are seen in association of work shifts.
These patients are often having work shifts that defy the
natural sleep-wake cycle and thus they feel sleepy or unable
to fall asleep at inappropriate time, e.g., while on work or
after reaching home, respectively.
3. Irregular Sleep-Wake Pattern: These patients have
inconsistent timings of sleep and wakefuleness, although
the total duration of sleep remains normal in 24 hours.
When their circadian rhythm is examined through sleep
diary or actigraphy, it appears constantly changing.
4. Delayed Sleep-Phase Syndrome: In this condition, sleep
time and wake time both are delayed in relation to the
environmental timing, however, total sleep time remains
adequate (Fig 1). These patients can’t fall asleep till late in the
night and wake up late in the morning having optimal duration
of sleep. If they go to bed early in the evening, they have a long
sleep onset latency and if they are made to wake up early in
morning, they have reduced awareness and feel sleep.
5. Advanced Sleep-Phase Syndrome: This is opposite of the
delayed sleep phase disorder. These patients starts feeling
sleepy early in the evening, spent optimal time in sleep but
wake up early. If they are made to stay awake till late in
night, they show reduced vigilance.
6. Non-24-Hour Sleep-Wake Syndrome
When seen through sleep diary and Actigraphy, these
patients have optimal duration of sleep, although the timing
of sleep appears delayed by 1-2 hours each day.

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 Gupta, et al.: CPGs for sleep disorders
In January of 2014, the FDA approved the melatonin agonist
HetliozTM (tasimelteon) for the treatment of N24SWD among
the blind. This is the first FDA-approved drug for any CRSWD.
Diagnosis of CRSD
Polysomnography and Morningness-Eveningness
Questionnaire is not routinely indicated for any of the
CRSDs. Actigraphy is recommended for the delayed sleep
wake phase disorder and advanced sleep wake phase
disorder but may also be used to diagnose other CRSDs.
Sleep diary must be maintained to diagnose all CRSDs.
Actigraphy is a good tool to measure the progress.
Management
Planned naps are recommended for Shift worker disorder.
Timed bright light therapy is useful for shift worker disorder
and delayed sleep wake phase disorder. Jet lag disorder can
be managed by timed melatonin administration. Hypnotics
may be used to induce sleep in Shift worker disorder,
however, stimulants are usually not recommended for the
management of CRSDs.
RESTLESS LEG SYNDROME
Restless legs syndrome/Willis-Ekbom disease (RLS/
WED) is characterized by an urge to move legs that
is often accompanied by dysesthesias in the muscles.
The urge improves with the movement of the legs or
application of a counterirritant. Symptoms are seen only
in the evening and rest worsens the symptoms.A number
of conditions like nocturnal leg cramps, habitual leg
movement, varicose, arthralgia, positional leg discomfort
and leg edema must be excluded before making the
diagnosis of RLS. This condition interferes with the sleep
significantly. In some patients, significant sleep fatigue
or poor concentration is reported in absence of RLS,
but with polysomnographic evidence of periodic limb
movements during sleep (PLMS), in all such cases the
term periodic limb movement disorder (PLMD) is used.
It is an autosomal dominant, sensorimotor disorder in
which patient complains of a peculiar creepy or crawling
sensation in the extremities Prevalence varies between
2-11% across different studies depending upon the
geographical locations and populations included.
Assessment & evaluation in case of RLS
The diagnosis of restless leg syndrome is primarily
based on the symptoms reported by the patient or the
observer. Nocturnal polysomnography may help in the
diagnosis by having PLMs in the recording. Serum iron
level estimation may be helpful as iron is a co-factor
for tyrosine hydroxylase which is essential for synthesis
of dopamine.The Cambridge Hopkins RLS diagnostic
questionnaire(CHRLSQ )and its Hindi version can be
used during surveys and epidemiological studies.
Looking for risk factors viz - elderly population, low iron
Indian J Psychiatry 59 (Supplement 1), January 2017
level, Parkinsonism disorder, end stage renal disease is
important.
Management
The selection of therapy depends upon a number of
factors, including disease severity, patient age, co
morbidities (e.g., pain, depression, anxiety and history of
impulse control behaviours), drug side effects and patient
preferences.
1. Non – pharmacological
Proper maintenance of sleep hygiene, exercise, restriction
of coffee beverages, pneumatic compression stocking help
in the symptom reduction
Behavioral strategies — Use of the following interventions
is supported primarily on the basis of clinical experience in
some cases, and small randomized trials
• Avoidance of aggravating factors, including
consideration of withdrawal of possibly predisposing
medications
• Moderate regular exercise
• Reduced caffeine intake
• For symptomatic relief – walking, bicycling, soaking the
affected limbs, and leg massage, including pneumatic
compression
• Short daily hemodialysis for patients with end-stage
renal disease.
Avoidance of aggravating factors — Sleep deprivation is
known to aggravate symptoms of restless legs syndrome/
Willis-Ekbom disease (RLS/WED) in many patients, and
general principles of sleep hygiene should be reviewed.
Psychotropic drugs e.g., antidepressants, antipsychotics
and other dopamine-blocking antiemetics such
as metoclopramide, and sedating antihistamines (including
those found in nonprescription medications) may lead to
emergence of RLS/WED or worsening of prior symptoms.
Most antidepressant classes have been associated withRLS/
WED, including tricyclics, selective serotonin reuptake
inhibitors, and serotonin-norepinephrine reuptake inhibitors.
Discontinuation of antidepressantsmay not be possible
among all patients. In all such cases, symptoms of
secondary RLS/WED should be treated in the same
way as primary RLS/WED. Bupropion is an alternative
antidepressant that may be less likely to induce or
worsenRLS/WED.
Iron replacement
Serum ferritin concentration lower than 45 to
50 mcg/L (ng/mL) has been associated with an increased
severity of restless legs syndrome. If the serum ferritin
level is lower than 75 ng/ml, iron replacement is
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suggested. However, care must be taken not to induce
iron overlaod.
Both oral iron therapy as well as intravenous iron have been
found effective in treatment of RLS.
2. Pharmacological
The major classes of drugs used include dopaminergic
agents, alpha-2-delta calcium channel ligands, opioids, and
benzodiazepines
Chronic persistent symptoms  relief is obtained. Most patients require at least 2 mg,
 Chronic persistent restless legs syndrome is defined as RLS
that is frequent and troublesome enough to require daily
treatment, with symptoms usually occurring at least twice
a week on average and resulting in moderate or severe
distress.
Choice of therapy — Patients who do not respond to non
pharmacologic therapy and correction of iron deficiency,
pharmacologic treatment with a dopamine agonist or an
alpha-2-delta calcium channel ligand is recommended.
• For patients with very severe  RLS/WED,  co morbid
depression, or obesity / metabolic syndrome, a dopamine
agonist is preferred over other drugs as initial therapy.
• For patients with comorbid pain, anxiety, or insomnia
or a history of impulse control disorder or addiction
associated with use of a dopamine agonist an alpha-2-
delta calcium channel ligand. Is preffered
• Most other patients, initial trial an alpha-2-delta calcium
channel ligand because of the of augmentation with
dopamine agonists, but other potential side effects of
the various drugs should also be considered. In general,
older patients are more prone to side effects of alpha-
2-delta ligands. If the first drug chosen is ineffective
or poorly tolerated, then a drug of the other class
should be tried , including levodopa, benzodiazepines,
and opioids, but generally these are reserved for
intermittent use or in patients with more refractory
symptoms.
Dopamine agonists — A number of dopamine agonsits are
available in market e.g., cabergoline, lisuride, pergolide,
pramipexole, ropinirole,rotigotine, and sumanirole. All
except sumanirolehave been found superior to placebo. In
two trials, cabergoline and pramipexole were superior to
levodopa for improvement in disease severity as measured
by the International Restless Legs Syndrome Study Group
(IRLS) rating scale.
Pramipexole and Ropinirole — Action of pramipexole and
ropinirole  usually starts 90 to 120 minutes after intake.
Therefore, these medications should be started two hours
before RLS/WED symptoms start. The recommended doses
are as follows:
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• Pramipexole  0.125 mg once daily. The dose may be
increased by 0.125 mg every two to three days until
relief is obtained. In a clinical trial, all three doses
of pramipexole (0.25, 0.50, and 0.75 mg daily) were
equally effective, and some patients responded to the
initial dose of 0.125 mg daily. However, side effects
were more common with the 0.50 mg and 0.75 mg
daily doses. Therefore, it is expected that 0.25 mg daily
has the best therapeutic margin. Most patients require
0.5 mg or less, but doses up to 1 mg may be needed.
• Ropinirole  0.25 mg once daily. The dose may be
increased by 0.25 mg every two to three days until
and doses up to 4 mg may be needed. The maximum
recommended dose is 3 mg in patients with end-stage
renal disease on hemodialysis.
Rotigotine — Rotigotine is a non-ergot dopamine
agonist that is formulated as a 24-hour transdermal patch
.Transdermal rotigotine is a once-daily patch that is
typically started at 1 mg/24 hours and titrated upwards to a
maximum dose of 3 mg/24 hours. Application site reaction
is the most common adverse effect of rotigotine, reported
by 40 to 50 percent of patients.
Alpha-2-delta calcium channel ligands — Gabapentin
enacarbil, gabapentin, and pregabalin are alternative
choices for patients with chronic persistent RLS.
Gabapentin enacarbil — Several randomized, placebo-
controlled studies have demonstrated that gabapentin
enacarbil is effective in reducing RLS/WEDsymptom severity.
The recommended dose of gabapentin enacarbil for
RLS/WED is 600 mg, taken in the early evening
Gabapentin —Limited data suggest gabapentin may be
effective in RLS/WED.
Pregabalin — Pregabalin in the doses of 75-300 mg/day
found effective in treatment of RLS.
Duration of therapy 
RLS/WED is often a lifelong disease, but the optimal and
safe duration of pharmacologic therapy has not been well
established. Most of the supporting data are based on
relatively short (≤12-week) randomized trials, with fewer
long-term extension studies supporting efficacy for 6
to 12 months of therapy with either a dopamine agonist
or gabapentin enacarbil.
Special populations
Pregnancy and lactation — Management of restless
legs syndrome during pregnancy should be individualized
based on symptom severity, comorbidities such as
depression or anxiety, and patient preferences. Many
patients can be managed successfully with education,
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reassurance, iron supplementation if indicated, and
nonpharmacologic strategies. Pharmacologic therapies such
as clonazepam or carbidopa-levodopa may be considered
for severe symptoms.
End-stage renal disease — The management of RLS/WED in
patients with end-stage renal disease is similar to that in
patients with normal renal function. However, medication
doses may need to be adjusted, especially if the patient is
not yet receiving dialysis, as dopamine agonists and alpha-
2-delta ligands are all excreted by the kidneys. Careful
attention to iron status is especially important in this group..
REM-SLEEP BEHAVIOUR DISORDER
Most parasomnias are benign unwelcome phenomenon
observed in and around sleep that seldom present alarmingly.
It is a common observation that more often than not, they are
a cause of least concern both to patient and clinician. One such
sleep-related phenomenon is REM-sleep behaviour disorder
(RBD) that was first systematically defined 30 years back. It
is a kind of parasomnia characterized by dream enactment
behaviour (DEB) that emerges during rapid eye movement
sleep and may lead to injury or disturbance of sleep. Behaviours
include excessive abnormal and/or purposeful motor activities
such as vocalization and simple limb twitching to flailing
and punching of arms, sitting up, and kicking. Occasionally,
patients climb out of bed, something akin to sleep walking.
More complex and violent behaviours may occur rarely or
many a times during the same night, most action occurring
in bed. Not keeping with their waking personality, the
vocalizations may be loud and full of abuse and obscenities.
The routine REM-sleep atonia is typically absent. It manifests
as sustained muscle activity or transient phasic muscle
twitches in either the chin or limb electromyography (EMG) on
polysomnography (PSG). Most cases arise after the age of 50.
Its usual presentation in a speciality clinic is like a 65-year old,
male whose partner expresses concern about some unusual
sleep behaviour or who had injured himself or assaulted his
partner during sleep while having vivid, action-filled dreams of
self-defence. The reported prevalence rates are 0.38%-0.5% in
general population and, probably higher (≥6%) in 70-90 year
olds. Even more interesting is the equally higher prevalence
of RBD in psychiatric population (5.8%). The early-onset
(<50y) variety (EORBD) has more atypical clinical presentation
showing female preponderance, less violent behaviour, may
occur early during the night, and may get out of bed more
frequently. There is preponderance of idiopathic cases and
more association is seen with narcolepsy, depression, anti-
depressants and parasomnia overlap disorder (POD).
Indian demographics regarding this illness are largely
unknown and the published evidence is limited to half a
dozen case reports, retrospective chart reviews, prospective
questionnaire-based study and a case control study. All
discuss RBD as part of PD except one (table 9).
The aetiology of RBD is still speculative. RBD may be either
primary idiopathic type (iRBD) or secondary (table 10) to
other disorders. It is unclear whether the idiopathic variety
is an independent entity or it is merely a precursor
‘cryptogenic’ prodromal syndrome anti-dating degenerative
brain disorders predominantly of α-synucleinopathy type
((Parkinson’s disease (PD), dementia of Lewybody(DLB),
Multiple system atrophy (MSA)). RBD patients are at higher
risk of having cognitive, motor and autonomic impairments
at baseline. It may be that spontaneous iRBD precede a
parkinsonian neurodegenerative illness by several decades
and thus have a prognostic and therapeutic relevance. The
risk of iRBD converting to parkinsonian disorder varies
between 40-80% over 5-15 years. There is now a growing
body of evidence that suggests that depression may also be
a preclinical marker of PD in iRBD cases and anti-depressants
simply unmask the underlying pathology. Following are the
environmental and behavioural risk factors associated with
RBD (in common with PD):
1. traumatic brain injury,
2. farming,
3. pesticide exposure, and
4. low education.

Table 9: Evidence base on RBD‑ Indian studies

Authors Year Title Type of study Journal
Vibha D et al. 2011 RBD in Parkinson’s disease: a clinical case control study from India Case control Clinical Neurology
&Neurosurgerry
Gupta R et al. 2013 REM sleep behavior disorder in Parkinson’s disease: A case from India Case report Journal of Neurosciences
confirmed with polysomnographic data in Rural Practice
Mahale R et al. 2014 Rapid eye movement sleep behaviour disorder in young ‑ and older ‑ onset Cross‑sectional Sleep Medicine
Parkinson disease ‑ a questionnaire‑based study
Yadav R et al. 2015 Is palmomental reflex an important clinical marker of REM sleep behaviour Cross‑sectional Movement Disorders
disorder in patients with Parkinson’s disease?
Gupta S et al. 2015 Idiopathic REM Sleep Behavior Disorder: A Report on Two Cases with Case report Indian journal of
Contrasting Features Psychological Medicine
Siddiqui M M et al. 2015 Detection of rapid eye movement behaviour disorder using short time frequency Experimental Biomedical Research
analysis of PSD approach applied on EEG signal (ROC‑LOC)
Prashanth R et al. 2014 Parkinson’s disease detection using olfactory loss and REM sleep disorder Experimental Engineering in Medicine
features and Biology Society

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 Gupta, et al.: CPGs for sleep disorders
Table 10: Secondary causes of RBD
Multiple System Atrophy Brain tumours
Dementia of Lewy Body Multiple sclerosis
Parkinson’s disease (PD) Guillain‑Barre syndrome
Mild Cognitive Impairment Stroke
Spinocerebellar Ataxia 3 Narcolepsy
Guadeloupean parkinsonism Obstructive sleep apnoea (Pseudo‑RBD)
Alzheimer’s disease Medications (anti‑depressants, beta‑blockers)
Progressive supranuclear Substance withdrawal (alcohol, barbiturate)
palsy
Huntington’s disease Limbic Encephalitis
Frontotemporal dementia
Studies on animal model suggest involvement of brainstem
REM-sleep regulating nuclei, namely dorsal pontinesublateral
dorsal nucleus and/or magnocellular reticular formation.
The role of several genetic links is under study at present.
The risk of sleep-related injury (SRI) is markedly increased in
RBD cases and their bed partners (33%-95%). DEB vary from
harmless actions like knitting, singing, etc., to injurious ones
and common injuries include bruises, abrasions, lacerations,
fractures and dislocations, attempt at strangulation of partner
and occasionally, subdural hematomas. Lifetime incidence of
head injury is around 20%. Risk factors for SRI are:
• Idiopathic RBD
• Severe limb movements during DEB
• Dream recall
• Falling out of bed during DEB
It is to be noted that as against the common wisdom,
DEB frequency has not been found to be associated
with the frequency and severity of SRI. Cases of PD-
RBD are less likely to injure themselves compared to
idiopathic RBD and injuries and falls are more common
in PD-RBD than PD alone. RBD is a progressive disorder
and spontaneous remissions are witnessed very seldom.
There can be a gradual reduction of RBD symptoms over
the years in approximately 30% of the patients and they
may remit spontaneously in 14-30% of RBD-PD patients
per year. These data are probably reflective of progressive
neurodegeneration. DEB is absent in up to 30% of reported
cases of RBD.
Assessment and evaluation
Despite the presence of RBD in a higher number of patients
with PD, less than 1% complain about it at the time of
presentation. The reasons can be
• RBD being considered not severe enough or infrequent
to consult a physician
• Symptoms being perceived not worthy of discussion
• Unaware of their presence
• Waiting for them to resolve with time
• Feel shy to discuss.
Even if the above hiccups get surmounted, the required
support may still elude the patient either because the
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physician is unaware of RBD or the case may be misdiagnosed
a more common ailment such as epilepsy or sleep-walking.
Thus, an elaborate history with direct questions to
confirm the presence or absence of the symptoms of some
parasomnia is a must [Figure 4].
In RBD, a careful interviewing of bed-/room-partner will help
in eliciting of a history of brief recurrent DEB that occur
chiefly in the latter half of the night with patient confined
to bed distinguishing it from non-REM sleep parasomnias
that predominantly occur during first half without any dream
mentation. Two major classificatory systems define the
criteria for RBD diagnosis- International classification of sleep
disorders- third edition (ICSD-3) criteria and DSM-5 (Table
11 & 12). The DSM-5 now classifies RBD as an independent
disorder. ICD-10 is yet to come up with its own criteria of RBD
though ICD-10 CM does include RBD (G47.52) as a billable
code for the purpose of reimbursement claims in America.
There are several disorders that can present in a fashion similar
to RBDs that one needs to rule out. It should be also kept in
mind that these conditions may co-exist with RBD (Table 13).
On such example is POD, a younger-onset variant of RBD.
A baseline neurological examination (NE) that involves
specific evaluation of cognition and screening for
extrapyramidal symptoms should be done once a diagnosis
of RBD is established (Table 14). RBD precedes parkinsonian
neurodegenerative disorders and is fairly prevalent (50-90%) in
α-synuclein disorders, while in rest of the neurodegenerative
disorders RBD follows (except spinocerebellar ataxia 3) other
neurological deficits and is uncommon.
Following investigations will aid to the diagnosis of RBD:
Specific
• PSG with time-synchronized video (vPSG) is the single
most important investigation.
• Electro-oculogram (EOG) monitoring
• EMG with multiple channels for chin, bilateral extensor
digitorum, and tibialis anterior muscles.
• Electrocardiogram (ECG)
• Nasal air flow
• Arterial blood oxygen saturation.
The revised scoring of PSG features of RBD has been detailed
in AASM Manual for the Scoring of Sleep and Associated
Events: Rules, Terminology and Technical Specifications,
Version 2.2. RBD is the only parasomnia that requires vPSG
for confirmation of diagnosis.
Others
To aid in diagnosis or monitor:
• Routine lab investigations
• Neuroimaging – currently used as research tools to
identify pre-clinical disease markers
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 Gupta, et al.: CPGs for sleep disorders

• Transcranialsonography (TCS)- substantianigra (SN) Scales/Questionnaires/Inventories

echogenicity, a disease marker
• Positron-emission tomography (PET)- to assess
severity and extent of neurodegeneration
• Single photon emission computed tomography
(SPECT)- to study the SN dopaminergic neuronal
status
• Post-mortem brain autopsy
Table 11: ICSD‑3 criteria
Criteria A‑D must be met
Repeated episodes of sleep related vocalization and/or complex motor
behaviours*
These behaviours are documented by PSG to occur during REM sleep
or, based on clinical history of dream enactment, are presumed to occur
during REM sleep
PSG recording demonstrates REM sleep without atonia (RWA)**
The disturbance is not explained more clearly by another sleep disorder,
mental disorder, medication, or substance use
On occasion, there may be patients with a typical clinical history of RBD
with DEB, who also exhibit typical RBD behaviours during vPSG, but do
not demonstrate sufficient RWA, based on the current evidence‑based data,
to satisfy the PSG criteria for diagnosing RBD. In such patients, RBD may
be provisionally diagnosed, based on clinical judgement. The same rule
applies when vPSG is not readily available.
*Dream enactment is not exclusive to RBD **In ‘Subclinical’ RBD, criteria C is
present in absence of dream enactment
Table 12: DSM‑5 criteria of RBD (327.42)
Recurrent episodes of arousal during sleep associated with vocalization
and/or complex motor behaviours
These behaviours arise during rapid eye movement (REM) sleep and
therefor usually occur more than 90 minutes after sleep onset, are more
frequent during the later portions of the sleep period, and uncommonly
occur during daytime naps.
Upon awakening from these episodes, the individual is completely awake,
alert, and not confused or disoriented.
Either of the following:
RWA on PSG
A history suggestive of RBD and an established synucleinopathy
diagnosis (e.g., parkinson’s disease, multisystem atrophy)
The behaviours that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning (which may
include injury to self or bed partner)
The disturbance is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical
condition
Coexisting mental and medical disorders do not explain the episodes
Since access to vPSG is limited, clinical interview and
questionnaires may come in handy in early screening of RBD
cases and related morbidities. Number of tools are available
for this purpose and to choose the right tool will depend on
whether it is required for rapid screening of RBD in general
population, or in specific specialized population such as
psychiatric cases and patients suspected of neurodegenerative
illness, or to monitor progress of illness or effects of some
intervention, and who is the source of information. It is to be
noted that despite their ease of availability and applicability,
screening tools are not a replacement for vPSG. RBD scales
help us point out probable RBD cases and thus to plan out
RBD specific assessment and targeted intervention services
without causing a resource crunch.
For RBD screening
1. RBD Questionnaire-Hong Kong (RBDQ-HK)
2. RBD screening questionnaire (RBDSQ),
3. Mayo sleep questionnaire (MSQ),
4. RBD1 questionnaire,
5. Innsbruk RBD inventory,
For RBD severity
1. RBD severity index (in Japanese),
2. Minnesota parasomnia injury scale,
For sleep
1. Epsworth sleepiness scale,
2. Pittsburgh sleep quality index
For baseline cognitive screening
1. Modified mini-mental state examination
2. Montreal cognitive assessment
For parkinsonian features
1. Unified Parkinson disease rating scale
Formulation of a treatment plan & Choice of treatment
setting [Figure 4]
Any treatment plan concerning RBD will involve reduction of
DEB and prevention of injury, irrespective of frequency and

Table 13: Differential diagnosis of RBD

Disorders of arousal Others
Primary Secondary
Sleep terror Periodic limb movement disorder Physiologic hallucinations of sleep
Sleep walking Nocturnal seizures (e.g., frontal lobe epilepsy) Dissociative/conversion disorder
Sleep talking Gastroesophageal reflux disease Malingering
Confusional arousals Obstructive sleep apnoea Domestic violence
Post‑traumatic stress disorder
Vertigo
Absence seizures
Epilepsy in mentally retarded
Other seizure disorders (e.g., juvenile myoclonic
epilepsy, benign epilepsy of childhood)
Hereditary quivering chin syndrome

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 Gupta, et al.: CPGs for sleep disorders

Table 14: Neurological history and examination‑salient severity of DEB. The choice of treatment setting will be largely
features determined by the presenting complaints. Hospitalization
Triad of impending Explore for Early bradykinesia Subtle signs on NE: may be required for assessment of RBD, treatment of SRI
neurodegeneration: • Difficulty in turning over • Affect and/or current medical condition. SRIs in RBD can be life-
• RBD with chronic in bed • Voice volume
threatening and may have medico-legal consequences.
unexplained • Slowing of eating or dressing • Speed of articulation
• Hyposmia • Above difficulties • Blink rate
• Constipation unilateral (u/l)/bilateral • Motor tone While formulating a treatment plan of RBD following should
• If, Impaired colour (u/l significant of • Cogwheel rigidity be included:
identification, rapid parkinson’s disease) • Gait testing: stride
conversion to PD • Change of hand‑writing length, arm swing,
• Non-pharmacological measures
•*psychiatric disorders • Lowering of speech volume number of steps to • Safety measures
(depression) may also • Whether ever felt feet stuck turn, freezing • Removal or minimization of aggravating factors
be a predating factor to the floor • Postural instability
• Counselling of patient and care-givers

No
Adequate opportunity for sleep Rules out insomnia

No
Difficulty in maintaining sleep Evaluate for other sleep disorders

No
Evaluate for OSA &/or other sleep
Abnormal behavioural activity during night sleep
disorders

Clinical features of a parasomnia

No
Assess for NREM parasomnias/ other
Suggestive of RBD
causes of insomnia

vPSG fulfilling diagnostic criteria

Assess for type of RBD

No
Assess & manage causes of secondary
iRBD RBD

Environmental & life style modifications

No
Try different drug &/or non-
Response
pharmacological measures

Yes
Continue indefinitely Response

No

Regular follow-up and monitoring for

appearance of any neurodegenerative disorder Review diagnosis

Figure 4: Diagnosis and management of REM-sleep behaviour disorder

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 Gupta, et al.: CPGs for sleep disorders

Table 15: Drugs used in treatment of RBD

Molecule t1/2 (hr) Dose (mg/d) Formulations Adverse effects
Benzodiazepines
Alprazolam 12‑15 1‑3 Tablet/extended Sedation, fatigue, dizziness, ataxia, confusion,
release/solution forgetfulness (B)
Clonazepam 30‑40 0.5‑2 Tablet (B) + blood dyscrasias, grand-mal seizures
Temazepam 8‑15 7.5‑30 Capsules (B) + hallucinations, mania, hypotension, hypersalivation
Triazolam 1.5‑5.5 0.125‑0.5 Tablet (B) + Anterograde amnesia, mania, dry mouth, hypersalivation
Non‑benzodiazepine
receptor agonist
Zopiclone 3.5‑6.5 7.5 Tablet Sedation, dizziness, ataxia, dose‑dependent amnesia,
hyperexcitability
Melatonin and
melatonin‑receptor
agonists
Melatonin 0.33‑0.83 (dose 3‑12 Tablet, capsule, Vivid dreams, nightmares, drowsiness, abdominal cramps,
& route cream, lozenges, headache, irritability, ↑depression, ↑risk of seizures in
dependent) intranasal spray children with severe neurological problems. RARE‑ ↓libido,
gynaecomastia, psychosis
Agomelatine 1‑2 25‑50 Tablet Nausea, dizziness, somnolence, hyperhidrosis. RARE‑ mania,
hepatitis
Ramelteon 2‑5 8 Tablet Sedation, dizziness, fatigue, headache
Anti‑depressants
Desipramine 24 50‑300 Tablet Blurred vision, constipation, urinary retention, increased
appetite, dry mouth, weight gain, sedation, sexual dysfunction.
RARE‑↑intraocular pressure, paralytic ileus, ↑QTc
Paroxetine 24 10‑40 Tablet‑IR & CR Sexual dysfunction, diarrhoea, constipation, insomnia,
sweating, tremors. RARE‑ hyponatremia, suicidality, mania,
bleeding
Pramipexole 8‑12 0.5‑1.5 Tablet Dizziness, Sleep attacks, somnolence, insomnia, nausea,
constipation, asthenia, peripheral oedema, impulse control
disorders, gambling, sexual urges, hallucinations & psychosis,
RARE‑ dyskinesias, rhabdomyolysis, peritoneal/pleural/
pulmonary fibrosis
Dopaminergic
L‑dopa 0.83‑1.5 250‑1250 Tablet, Agitation, delusions, hallucinations, confusion, tremors,
extended‑release, fainting; depression, blurring of vision, blepharospasm.
capsule RARE‑ hypertension, priapism, seizures, gastrointestinal
bleeding
Herbal
Yoku‑kan‑san/Yi‑Gan 1.72‑12.3 2.5‑7.5 Freeze‑dried granules Hypokalaemia (in old), drowsiness, tiredness, gastrointestinal
San (component upset. RARE‑ interstitial pneumonitis, dermatitis,
dependent) hepatotoxicity
Acetyl cholinesterase
inhibitors
Donepezil 70 5‑10 Tablet Nausea, diarrhoea, vomiting, ↓appetite, weight loss,
insomnia, abnormal dreams, muscle cramps. RARE‑ seizures,
syncope (B)
Rivastigmine 1‑2 6‑12 Capsule, liquid, (B) + headache, asthenia, sweating
transdermal
GABA agonist
Sodium Oxybate 0.5‑1 2500‑9000 Oral solution Swelling over face or extremities, weight gain, paraesthesias.
Anxiety, rash, perspiration, palpitation, tightness in chest,
seizures, coma.
Anti‑epileptic
Carbamazepine 12‑17 (repeated 400‑1200 Tablet, capsule, Sedation, dizziness, confusion, unsteadiness, headache,
doses) suspension nausea, vomiting, diarrhoea, rash. RARE‑ aplastic anaemia,
Anti‑psychotic
Clozapine 5‑16 N.A. Tablet ↑risk for diabetes/dyslipidaemias, ↑salivation, sweating,
sedation, constipation, weight gain. RARE‑ tardive dyskinesia,
agranulocytosis, seizures (dose‑dependent), neuroleptic
malignant syndrome, deep vein thrombosis and pulmonary
embolism, ↑risk of death and cerebrovascular events in elderly
patients with dementia‑related psychosis

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 Gupta, et al.: CPGs for sleep disorders
• Others
• Pharmacotherapy
Non-pharmacological meassures
The primary goal of RBD treatment is SRI prevention.
Among the non-pharmacologic measures, modification of
sleep environment should be initiated as the first step.
A. Environmental modification may include:
Patient safety. e.g.,
lowering of bed
putting a mattress on the floor alongside bed
sleeping on the floor mattress itself
shift bed/ bedroom to the lowest floor of the house
barricading with pillows around the bed
using a bed with padded rails
minimize furniture around the bed
maximize the distance from ungrilled windows
soft-pad the sharp edges of furniture around the house
remove fire-arms or knives from within reach
(preferably lock away)
safety locking of windows and doors
physical restraint. e.g., sleeping bags, padded belts,
padded waterbeds
Partner safety
Bed partner should sleep separate from the patient
till the problem symptoms of RBD are brought
under control with treatment.
It is a matter of investigation whether environmental
manipulation is enough in itself for the management of RBD
or it has only an adjunct role to pharmacotherapy.
B. Patient or caregiver should be asked to maintain a sleep diary
C. Avoid sleep deprivation- maintain adequate total sleep
time with a fixed waking time.
D. Avoid alcohol and/or other recreational drugs.
E. Treat co-morbid sleep disorders, if any.
F. Reassure and counsel patient and family about need
of treatment, regular follow-ups, and the possibility of
onset of a neurodegenerative disorder.
G. Review ongoing medication charts. Remove or reduce
the dose of aggravating agent wherever possible.
Antidepressants can trigger RBD or expose RBD in up
to 6% cases of depression. Tapering off might result
in symptom reduction but not complete remission
in such cases. Bupropion is the only anti-depressant
not reported to be associated with RBD till date.
Thus, it might be considered for use in those where
pharmacotherapy is indicated for depression.
Along with these measures, pharmacological treatment
should be instituted. As no large randomized double-blind
or head-to-head controlled trials are available till date
to assess efficacy of medications, the current treatment
guidelines are largely expert consensus, based on evidence
of large case series or small clinical trials.
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Pharmacological treatment
The only REM-sleep parasomnia where pharmacotherapy is
clearly indicated is RBD. Many pharmacological agents have
been tried for this purpose, but there is marked variation
in their efficacy and there is lack of standardization of the
dose of medication and the duration of its continuation
(Table 15). Among all the medications utilized till date,
the most robust support is for clonazepam and melatonin.
A medication that improves sleep quality with minimum
day time effects and results in improvement of objective
measures of RBD such as RWA on PSG should be chosen.
Clonazepam
Recommended as first-line medication. The evidence
base is almost exclusively in terms of retrospective
case reports and case series in over 300 patients. Initial
response to low dose clonazepam (0.5-2mg) is seen in
upto 90% of patients but later tolerance and treatment
failures are reported. Because of its long half-life, it may
become a cause of concern if causing impaired alertness,
morning sedation and gait impairment in parkinsonian
disorders and elderly patients and can worsen concomitant
obstructive sleep apnoea (OSA). It vanquishes DEB but do
not re-establish REM sleep atonia. It helps markedly in
reduction of SRI, one study reporting a reduction from
80.8% pre-treatment events to 5.6% post-treatment levels.
Patients on clonazepam should be regularly monitored
for development of newer symptoms of dementia or gait
disorders. Clonazepam is metabolized by cytochrome p450
enzyme system (cyp2C19 & cyp3A4). Thus, the possibility
of drug-drug interactions should be kept in mind especially
in elderly population where polypharmacy is a rule rather
than exception.
Melatonin
The pineal gland secretion, melatonin when used
exogenously is said to be effective in RBD in few case reports,
case series and a small randomized controlled trial of eight
patients. Recent studies find melatonin as efficacious as
clonazepam in RBD with a better adverse effect profile
and re-establishment of REM atonia especially in those
with dementia or sleep apnoea. Efficacy is not known in
cases where RBD co-exists with both PD/dementia and
depression that requires treatment with anti-depressants.
Most patients respond to 3mg dose with minimal or no side
effects. The mechanism of action of melatonin in RBD is not
known, though calmodulin antagonism is suggested as a
potential mechanism and the effects probably go beyond
simple hypnosis.
Others
In cases where clonazepam and melatonin are not
indicated or are refractory to these medications, other
medications may be tried. But so far, the evidence in
their favour is inadequate or at times, contradictory.
e.g., there are just two case reports of successful RBD
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 Gupta, et al.: CPGs for sleep disorders
treatment with sodium oxybate. Acetylcholinesterase
inhibitors may be instituted in patients with dementia or
synuleinopathies.
Among all the tried medications, the only preparation that
is claimed to have some neuroprotective effects in in-vitro
and in-vivo animal studies is Yi-Gan San/Yoku-kan san. It
is a Chinese/ Japanese traditional kampo preparation that
consists of seven different herbs- Japanese Angelica root
(3g), Atractylodeslancea rhizome (4g), Bupleurum root (2g),
Poriasclerotium (4g), Glycyrrhiza root (1.5g), Cnidium rhizome
(3g), and Uncaria hook (3g). Its neuropharmacodynamic
actions include serotonergic, glutamatergic, cholinergic,
dopaminergic, adrenergic, GABAergic along with
anti-inflammatory, anti-stress, neuroplasticity, and
neuroprotective effects. It is through these mechanisms
it is supposed to exert its effects in its primary indication
for behavioural and psychological symptoms of dementia
including alzheimer’s disease, dementia of Lewy body, and
PD. There is one case report of successful management of
three RBD patients with Yi-Gan San.
Other Pharmacological Treatment Modalities
It is very ironic that currently there are no cognitive or
cognitive-behaviour therapies available for REM-sleep
“behaviour” disorder probably highlighting the
‘non-functional’ organic nature of the disorder. Two
therapies- one behaviour and one somatic- does require a
mention though.
Bed Alarm Relying on the brain’s ability to process complex
auditory stimuli during REM sleep similar to wake state and
low arousal threshold for external stimulus Howell et al. at
university of Minnesota developed a pressurized bed alarm
customized with a pacifying pre-recorded message in a
familiar person’s reassuring voice to calm down the patient at
the onset of dream enactment behaviour. This prevents bed-
exiting and averts potential injuries. It can be used in patients
who are refractory to pharmacotherapy or do not tolerate it.
Deep brain stimulation of subthalamic nucleus is
ineffective in RBD though it does improve the subjective
sleep quality.
Management as per different phases of illness & when to
stop
RBD is a progressive neurological disorder. Though
clonazepam is highly effective and works in almost 70-90%
of the cases, relapse rates are high on discontinuation so
pharmacologic treatment should be continued indefinitely.
Regular monitoring to assess risk for neurodegenerative
disorders should be taken up keeping in mind the strong
relationship of RBD as a prodrome of such illnesses.
At present, there are no treatment strategies available to
prevent or delay the development of PD in iRBD cases.
Indian J Psychiatry 59 (Supplement 1), January 2017
It should be noted that most patients who ultimately
developed neurodegenerative illness were on clonazepam
indicating clonazepam’s ineffectiveness as a preventive
agent. It is recommended that an annual neurological
examination should be done for the earliest detection and
management of PD.
Special populations
The basic tenets of diagnosis, assessment and management
of medicine are equally applicable to the special populations
of RBD. The following few things should be kept in mind
while dealing with them:
Children
Assessment of children will require a careful approach
depending on their ability to communicate which can be
limited given their age or co-morbidity. Idiopathic RBD in
this population is rare and is usually seen in context with
narcolepsy, epilepsy, brain tumours, or, medication effects.
Elderly
After the onset of idiopathic RBD almost half of the patients will
develop a parkinsonian disorder within a decade, and nearly
80-90% will develop some neurodegenerative disorder in their
lifetimes. Therefore, middle-aged or elderly people presenting
with RBD symptoms should be counselled and monitored
about these future possibilities. An opportunity to enrol them
in any ongoing research clinical drug trials for developing and
testing disease-modifying drugs can also be explored.
Women
RBD is infrequently reported in females. This may be
because firstly, they might be having less injurious and
less dramatic behaviours during dream enactment; and
secondly, they may outlive their partner (gender difference
in life expectancy) thus having less likelihood of coming
to the notice of family members and receive the required
medical attention. All medications require caution for use
during pregnancy and lactation and should be taken only
under expert guidance.
The paramount importance of recognizing RBD as a
treatable parasomnia lies in the fact that it can prevent
serious life-threatening injuries. Psychiatrists should
actively screen for the presence of RBD as patients usually
do not come forward to report these symptoms for a
variety of reasons. The population of India grew at 17.7%
between 2001-11. During the same period there was a
quantum jump in the population of those above 60 years- a
staggering 35.5%. With an all-time high elderly population
of 8.6%, it is high time we brace-up for the identification of
RBD and appreciate its importance as a pre-clinical marker
of neurodegenerative illnesses. The success of any future
neuroprotective and preventive interventions will, thus,
rely on early and reliable identification of illness in its
nascent stage.
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Table 16: Symptoms of Obstructive sleep apnoea (OSA) cerebrovascular disorders, diabetes mellitus, pulmonary
Somatic symptoms Cognitive and Behavioural symptoms hypertension, arrhythmias, systemic hypertension,
Daytime sleepiness Decreased concentration memory disturbances, cognitive dysfunction and sexual
Fatigue Memory loss problems.
Irritability Decreased libido
Snoring Learning difficulties In addition, psychiatric disorders and OSA are also
Gasping/choking at night Impaired cognitive functioning
Morning headaches Personality changes
frequently comorbid, especially depression.Mood
Non-refreshing sleep Depression disturbance may represent a consequence of sleep apnoea.
Nocturia Anxiety Psychiatric disorders associated with weight gain may
also contribute to and promote the development of sleep
apneas. Medications with depressent effect on CNS can
Table 17: Medical history to be taken in patients
worsen or exacerbate the symptoms of OSA.Patients with
with OSA
sleep apnea often have fregmatned sleep and thus they may
Depression
Sedatives
have daytime symptoms of poor quality sleep e.g., fatigue,
Parkinsonism lethary, poor appetite, poor concentration, memory lapses,
Narcolepsy headache, distressed mood that may be mistaken for
Restless leg syndrome/periodic limb movement disorder depression. Fregmented sleep often presents as multiple
Hypothyroidism
somatic symptoms during the daytime suggesting the
β‑blockers
Idiopathic hypersomnolence diagnosis of somatoform disorder.
Excess alcohol
Previous head injury The symptoms are the direct consequences of OSA and
DystrophicaMyotonica occur due to the repetitive collapse of upper air ways.
Stimulants (caffeine, theophyllines, amphetamines)
Thin and lean individuals with significant apnoea are likely
OBSTRUCTIVE SLEEP APNOEA (OSA) to show upper airway abnormalities. These include, e.g.,
hypertrophic tonsils and adenoids, a low-set palate or
Sleep apnoea is charcaterized by recurrent pauses (at least palatal webbing, a large uvula, a large tongue or a small
5/hour) in breath, each lasting at least 10 seconds and is mandible.
important for the Psychiatric practice as it can mimic or
exacerbate symptoms of psychiatric disorders such as Risk factors, Screening, Examination and Diagnosis of OSA
depression, anxiety and panic disorder. The prevalence of OSA is higher in patients who have a
combination of the following risk factors: obesity, neck
Three types of apnoeas have been described in literature. larger than 17 inches for men or 16 inches for women,
In obstructive sleep apnoea (OSA), cessation of breathing male gender, middle age, large tonsils, or recessed chin.
occurs despite persistent respiratory efforts. In central Besides anatomical factors, physiological factors that
apnoea, there is no respiratory effort. Mixed apnoea has influence the tone of the upper airway muslces play
initial part similar to central apnea but in the later part, equally important role in generation of OSA. It is prudent
effort to breath is seen with absence of airflow throughout to screen all patents who are at risk since untreated OSA
the period. Excessive daytime sleepiness, one of the major is an independent risk factor for mortality. In addition,
symptoms of OSA is seen in one-third of the patients and information regrading conditions as described in Table 17
many report mid-nocturnal awakenings due to chocking must be gathered.
which may be mistaken for panic. On the other hand, central
sleep apnea has subtle clinical manifestations and often Physical Examination
these patients present with chronic non-restorative sleep. Examination is very important to exclude other causes for
the patient’s symptoms mentioned below:
Obstructive sleep apnoea (OSA) is a common disorder
with an estimated prevalence in the general population of Following points should be kept in mind during physical
2–5% (Table 16). Apnoea during sleep leads to decrease in examination
blood oxygen level which leads to disturbance in sleep and
frequent arousals. Sleep apnoea severity is assessed with • Weight and height should be documented.
apnoea-hypopnoea index (AHI), which is the number of
apnoeas and hypopnoeas per hour of sleep. • Mandibular and tongue abnormality.
• Assessment of Nasopharyngeal abnormality.
Obesity is a major risk factor for OSA. Untreated OSA leads
to significant clinical problems including cardiovascular and • Measurement of Blood Pressure.

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 Gupta, et al.: CPGs for sleep disorders
• Perform routine respiratory, cardiovascular and
neurological examination to detect any coexisting disease.
Diagnosis
Certain questionnaires e.g., STOP-Bang, Berlin Questionnaire
have been developed to screen the OSA. However, the gold
standard for the diagnosis of OSA is polysomnography.
Ideally, in-lab attended video-synchronized full
polysomnography (level 1) is indicated for the diagnosis of
OSA, however, among high risk cases, limited channel level
3 polysomnography may also be used. This is also known as
Home Sleep testing.
Treatment
Depending upon the severity the various treatment options
is most appropriate for the management of OSA.
Treatment options can be broadly divided into:
1. Patient education
2. Behavioural interventions
3. Non-surgical options
4. Surgical options.
5. Treatment for comorbidities.
Patient Education
Patients and their attendants should be educated about the
pathophysiology, risk factors, clinical consequences and the
treatment of OSA.
Education should include behavioural modification like
weight loss, sleep position, alcohol avoidance, risk factor
modification, and medication effects.
Behavioural Interventions
Lifestyle changes can be very effective in mitigating the
symptoms of sleep apnoea. However, large control trials are
not available in this regard.
1. Weight loss is most important in all those who are
overweight. Weight reduction improves symptoms in
OSA
2. Exercise
3. Avoidance/Reduction of smoking and alcohol is
beneficial.
4. Sedatives or sleeping tablets should be avoided.
5. Snorers should be discouraged from sleeping on their
backs.
Non-Surgical Options
1. Positive Air Pressure (CPAP). This is the “gold standard”
treatment for OSA. Optimal pressure of the PAP should
be titrated as per the standard guidelines so as to
ameliorate all kinds of sleep related breathing events-
apnea/hypopnea, RERA and snoring. Automatic PAP has
limited application in these cases.
2. Oral Appliances: These are effective only in mild to
moderate severe cases of OSA.
Indian J Psychiatry 59 (Supplement 1), January 2017
I. Mandibular Advancement Splints (MAS). This works
by moving the mandible forward along with the
tongue and increasing the caliber of upper airway.
Surgical Options
The treatment of choice for moderate to severe OSAS is
continuous positive airway pressure (CPAP) devices , but
patient adherence to these devices has been a limiting factor.
In ‘selected cases’, surgical treatment on the upper airway
(UA) or on the facial skeleton may be beneficial in alleviating
this disease or improving the use of CPAP. Following surgical
procedures can be beneficial to patients with OSA.
Any of the single staged procedure has not been found
effective in management of OSA in large controlled trials.
Patient should be educated regarding possible recurrence
of OSA after 1-2 years of surgery, especially when it is done
on the soft tissues.
Treatment for comorbidities
Hypothyroidism, depression, etc, are more prevalent
.Obstructive sleep apnea (OSA) and hypothyroidism are
relatively common disorders that have similar clinical
features and are thought to be causally linked. The
mechanisms proposed to explain how hypothyroidism
might cause OSA include mucoprotein deposition in the
upper airway, decreased neural output to the upper airway
musculature, obesity, and abnormalities in ventilatory
control.
Treatment of hypothyroidism in the presence of sleep apnea
is potentially hazardous and may lead to cardiovascular
complications. Management by a combination of  Nasal
continuous positive airways pressure(CPAP) and low-dose
thyroxine is helpful in this situation.
OSA patients may have comorbid depression or any other
psychiatric illness. In such cases bothe the disorders must
be adequately and optimally treated.
Obstructive sleep apnea (OSA) leads to frequent arousals,
which are characterized by fragmented sleep. Persistent
sleep loss can lead to depressive symptoms. Patients may
be treated for depression, but if the underlying symptoms
are caused by OSA and the apnoea is not treated, depressive
symptoms can remain. We may be treating someone with
antidepressants when what we really should be doing is
treating their sleep disorder, which could in turn restore
their normal mood.
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2. Sharma SK, Kumpawat S, Banga A, Goel A. Prevalence and risk factors
of obstructive sleep apnea syndrome in a population of Delhi, India. Chest
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 Gupta, et al.: CPGs for sleep disorders
2006;130:149–56.
3. Rangarajan S, Rangarajan S, D’Souza GA. Restless legs syndrome in an
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Indian J Psychiatry 59 (Supplement 1), January 2017
Editor Dr. T. S. Sathyanarayana Rao. Printed and published by Wolters Kluwers (India) Pvt. Ltd. on behalf of Indian Psychiatric Society, Mysore and
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