EASTERN JOURNAL OF

PSYCHIATRY
OFFICIAL PUBLICATION OF THE INDIAN
PSYCHIATRIC SOCIETY: EASTERN ZONE
ISSN-0974-1313 Volume 13 Number 1&2 February- August 2010 ISSN (Online) 0976 – 0334

Journal Advisory Committee Eastern Journal of Psychiatry is the official

Chairperson publication of Indian Psychiatric Society –
Dr. Dipesh Bhagabati Eastern Zonal Branch. Eastern Journal of
Members Psychiatry publishes original work in all fields
Dr. Jiban Chakraborty (Tripura) of Psychiatry. All correspondence including
Dr. P.K. Mahapatra (Orissa) manuscripts for publication should be sent to the
Dr. Prabir Paul (West Bengal) Honorary Editor, Eastern Journal of Psychiatry,
Dr. Vinay Kumar (Bihar) L.G.B. Regional Institute of Mental Health,
Tezpur, Assam, 784001, E-mail:
Journal Committee drkpathak@gmail.com
Chairperson
Dr. Kangkan Pathak The material published in the Eastern Journal of
Members Psychiatry does not necessarily reflect the views
Dr. P.K. Singh (Bihar) of the Editor or the Indian Psychiatric Society –
Dr. S. Akhtar ( Jharkhand) Eastern Zonal Branch. The publisher is not
Dr. S. K. Das ( Orissa) responsible for any error or omission of fact.
Dr. Gautam Saha (West Bengal)
The appearance of advertisements or product
Ex-officio Members information in the Journal does not constitute
Dr. R. R. Ghosh Roy an endorsement or approval by the Journal and/
Dr. C. L. Narayan or its publisher of the quality or value of the said
product or of claims made for it by its
Editorial Board manufacturer.
Editor
Dr. Kangkan Pathak Published by
Associate Professor of Psychiatry Editor, Indian Psychiatric Society, Eastern Zonal
L.G.B.R.I.M.H. Branch
Tezpur, Assam, 784001
Assistant Editor Printed at
Dr. Sarada Prasanna Swain (Orissa) —————————
Members Distinguished Past Editors
Dr. Kamal Narayan Kalita (Assam) Dr. S. Akhtar: 1998-2000
Dr. N. M. Rath (Orissa) Dr. V.K.Sinha: 2001-2002
Dr. Sanjiba Dutta (Sikkim) Dr. Vinay Kumar: 2003-2005
Dr. Dhrubajyoti Chetia (Tripura)
Dr. Gajendra Singh (Manipur)
Online at: www.indianpsychiatryez.org
Dr. Dhrubajyoti Bhuyan (Assam)
Dr. Arabinda Brahma (West Bengal)
 EASTERN JOURNAL OF
PSYCHIATRY
OFFICIAL PUBLICATION OF THE INDIAN
PSYCHIATRIC SOCIETY: EASTERN ZONE
ISSN-0974-1313 Volume 13 Number 1&2 February- August 2010 ISSN (Online) 0976 – 0334

CONTENTS

Future of District Mental Health Programme : Kangkan Pathak

ORIGINAL ARTICLES

Insight into Schizophrenia: A comparative study between : S. Das , D. Bhagabati , U. Talukdar

patients and family members
Association of Anxiety and Depression in Postpartum Pe- : K N Kalita, H R Phookun, G C Das
riod: a Hospital Based Evaluative Study
A comparative study of thyroid hormone levels among the : S. G. Singh, S. Debbarma, N.Heramani
normal healthy persons, Depression and Schizophrenia Singh, Th. Bihari Singh, R.K.Lenin,
K.Shantibala Devi
An explorative study on Biomedical Waste Management in : J.Hazarika, A C Sarmah, M.Das
a Psychiatric Hospital of India
Efficacy of Psychosocial Intervention on Patients with : Shweta, K. S. Senger , A. R. Singh, M. Dutta
Schizophrenia
Visuospatial Working Memory Deficits in Patient with : K. Bala, M. Jahan, S. Sarkhel, A. Bakhla
Schizophrenia
A study of level of Depression, Anxiety and life satisfaction in : R. Kumar, D. K. Kenswar
acute and chronic schizophrenia
Psychopathology among primary caregivers of major psy- : S. K. Nayak, S. Kumari, M. Jahan,
chiatric patients A. R. Singh
A Comparative Study of Neuro-Cognitive Impairment in : N. A. Khan, A. Kanchan, A. Singh,
Elderly Patients with Schizophrenia and Elderly Normals K.S. Sengar, A.K. Nag

REVIEW ARTICLES

Legislation, Society and Substance Use - impact of NDPS Act,

1985 : M. Aggarwal, Umamaheswari V, D. Basu
Polypharmacy in clinical psychiatry-a brief review : G. P. Singh
Treatment Resistant Depression : M. Hembram, S. Chaudhury
Socio-Economic and Cultural Aspects of Suicide : Arabinda Brahma

VIEW POINT

Mindfulness and Mental Health : K. Nath Dwivedi

Era of Evidence Based Medicine: Is clinical expertise outdated : Y.P.S. Balhara, S. N. Deshpande

CURRENT THEME
: C.L. Narayan, Rajiv Jaiswal, Deepshikha
Towards A New Mental Health Act

CASE REPORT
Cerebral metastasis masquerading as late onset depression- A : S. G. Singh, N.H. Singh, L. Nelson, N. B.
case report Singh, K.S. Devi, L. R. Singh

BOOK REVIEW : Chris Nicholson

Kangkan Pathak
 EDITORIAL
EDITORIAL
Future of District Mental Health Programme
Kangkan Pathak
L.G. B. Regional Institute of Mental Health, Tezpur, Assam, 784001
BACKGROUND
India is the first developing country to formulate the
National Mental health Programme (NMHP) based
on the principle of decentralized and deprofessionalised
mental health care1. The approach was to integrate
mental health with general health services, also referred
to as community psychiatry initiative2. A model delivery
of community based mental health care at the level of
district was evolved and field tested in Bellary district
of Karnataka by NIMHANS during 1986-1995. The
Central Government launched the District Mental
Health Program (DMHP) as a 100% centrally
sponsored scheme for first five years, at the national
level during the 9th Plan as pilot project. It was
launched in 1996-1997 in four districts, one each in
Andhra Pradesh, Assam, Rajasthan, and Tamil Nadu,
with a grant assistance of 22.5 lakhs each. DMHP was
implemented in 27 Districts across 22 states/UTs in
the 9th Plan. The DMHP was extended to 7 districts
in 1997-1998, five districts in 1998 and six districts in
1999-2000. During the Tenth Five Year Plan, the
DMHP was extended to 127 districts in the country3.
During the 10th Five Year Plan, NMHP was restrategized
and it became from single pronged to multi-pronged
programme for effective reach and impact on mental
illnesses. DMHP was redesigned around a nodal
institution, usually the zonal medical college. The thrust
areas were to expand DMHP to 100 districts all over the
country, modernization of mental hospitals in order to
modify their present custodial role, upgradation of
Psychiatry wings of Govt. Medical Colleges/General
Hospitals and enhancing the psychiatry content of the
medical curriculum at the undergraduate as well as
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
Correspondence: Dr. Kangkan Pathak
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
LGB Regional Institute of Mental Health,
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
Tezpur, Assam, 784001
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
E-Mail: drkpathak@gmail.com
1234567890123456789012345678901212345678901234
postgraduate level, strengthening the Central and State
Mental Health Authorities with a permanent secretariat,
IEC Activities and Research & Training in the field of
community mental health, substance abuse and child/
adolescent psychiatric clinics for improving service
delivery4.
But 10th plan could not meet the objectives of NMHP
which necessitated adoption of revised national mental
health programme in 11th Plan. During the 11th Five Year
Plan, it has been proposed to decentralize the programme
and synchronize with National Rural Health Mission for
optimizing the results. The main components of NMHP
that have been proposed are 5, 6:
• To establish Centres of Excellence in Mental
Health by upgrading and strengthening of
identified existing mental hospitals for
addressing acute manpower shortage.
• To provide impetus for development of
Manpower in Mental Health
• Spill over of 10th Plan schemes for
modernization of state run mental hospitals and
upgradation of psychiatric wings of medical
colleges/general hospitals.
• District Mental Health Programme with added
components of Life Skills training and
counseling in schools, counseling service in
colleges, work place stress management and
suicide prevention services.
• Research in mental health
• IEC activities to remove stigma attached to
mental illnesses
• NGOs and Public Private Partnership for
implementation of the Programme to increase
the outreach of community mental health initiatives
under DMHP.
 • Monitoring at Central/State/District level to
facilitate implementation of various
components of NMHP and evaluation
DISTRICT MENTAL HEALTH PROGRAMME3
The Objectives of DMHP are:
1. To provide sustainable basic mental health services
to the community and to integrate these services
with other health services;
2. Early detection and treatment of patients within
the community itself;
3. To see that patients and their relatives do not have
to travel long distances to go to hospitals or
nursing homes in the cities;
4. To take pressure off the mental hospitals;
5. To reduce the stigma attached towards mental illness
through change of attitude and public education;
6. To treat and rehabilitate mental patients discharged
from the mental hospitals within the community
The strategies for achieving these objectives are: i. Training
programmes of all workers in the mental health team at
the identified Nodal Institute in the State. ii. Public
education in the mental health to increase awareness and
reduce stigma. iii. OPD and indoor services for early
detection and treatment. iv. Providing valuable data and
experience at the level of community to the state and
Centre for future planning, improvement in service and
research.
For DMHP funds are provided by the Govt. of India to
the state governments and the nodal institutes to meet the
expenditure on staff, equipments, vehicles, medicine,
stationary, contingencies, training, etc. for initial 5 years
and thereafter they should manage themselves.
Evaluation of DMHP 7
During 2008-2009 evaluation of DMHP covering 20 of
the 127 districts was carried out by Indian Council of
Marketing Research (ICMR), New Delhi to assess the
functioning of DMHP objectively and critically and to
suggest future expansion of the scheme along with
improvement in implementation if any, based upon the
evaluation. ICMR, a division of Planman Consulting
(India) Pvt. Ltd. visited 20 DMHP districts and 5 Non-
DMHP districts (as control). The DMHP beneficiary
Districts were chosen proportionately from 9th and the
10th Plan period. The following are the main findings of
the evaluation:
“One third of the districts under the 9th plan have
utilized over 99%, one third has utilized 63-91%, and
rests have utilized 37-47% of the total amount they
have received. This is mainly due to administrative
delay, difficulty in recruiting and retaining qualified
mental health professional, low utilization in training
and IEC components. In Case of the 10th plan districts,
most of the districts had received only the 1 st
installment under DMHP. Of the grant received one
third have utilized more than 90%, half of the districts
spent 51-87% and rests of the districts the programme
has recently started….. Most of the districts had not
utilized the full amount for training due to delay in
implementation. …..The expenditure on ... training and
IEC components which requires a lot of ground work,
coordination and networking in the community is
below par in most of the districts. This is mainly due
to lack of organizational skills in the DMHP team,
low community participation in the programme and
lack of coordination with the district health system
which comes under a different department. …..
Regarding availability of drugs, only 25% of the
districts reported that there has been a regular inflow
of drugs. …. This is because of lack of dedicated drug
procuring mechanism for DMHP and financial
authority to the nodal centre. …. About 61% of the
beneficiaries accessed the district hospital as their first
point of contact. The percentage of patients accessing
CHCs (12.7%) and PHCs (11.5%) were found to be
low”.
NORTH EASTERN EXPERIENCE
Mere allocation of fund has nothing to do with the
successful implementation of any programme. Now
we have enough evidence from the ongoing DMHPs.
We were part of the recent inspection of the Districts
under District Mental Health Programmes (DMHP) by
Central Mental Health institutions. What we have seen in
the DMHPs in the north eastern states is not at all
encouraging. The scenario is not different from other states
also as seen in the evaluation by ICMR.
The training of all categories of personnel is emphasized
in DMHP to face the challenge of shortage of
professional manpower. But many districts could not
train even 50% of the medical officers in the district.
The figure is 34.3% in Goalpara, 15.8% in Tinsukia ,
26.1% in Nalbari, 39.7% in Marigaon in Assam, 0% in
East Siang, 0.70% in Papumpare (Naharlagun) of
Arunachal Pradesh. Surprisingly, Papumpare district
where DMHP started in 1998-99 trained just a single
medical officer under DMHP out of 142 medical officers
at a cost of several lakh of rupees. He was sent to
NIMHANS for one year period but he is also no more
associated with the programme. For paramedical staff the
scenario is worse.
The basic tenet of DMHP was decentralization i.e.
appropriate mental health service should be made available
at the doorstep of the people. It should be accessible at
the sub-centre and village level. But in reality it is far from
truth even in those districts which have completed 5 year
term of central assistance and was taken over by state
government. The skeleton service of mental health care is
restricted to district hospital only. The non-psychiatrist
medical officers are hardly involved in the implementation
of the programme. The minimum training of the health
workers that is supposed to provide comprehensive health
care at the most peripheral level did not materialise in
most of the districts. Even the trained mental health
professionals are transferred from the DMHP to other
posts in state health services. In another case several lakh
of rupees were shown to be spent in training but there is
no record of the name of paramedical staff/ health worker
who were trained under DMHP, duration of training,
method of selection, their current place of posting, how
they have contributed to DMHP after the training etc.
According to norms DMHP team should be trained at
the nearest training institute. But some of the nodal
officers are ignorant about the training institutes which are
region wise identified for this purpose. There was no
communication from the ministry also. The identified
centres are NIMHANS, Bangalore for southern states,
IHBAS, Delhi for northern states, LGBRIMH, Tezpur
for northeastern states, Institute of Mental Health and
Neurosciences, Pune for Western states, CIP, Ranchi and
RINPAS for eastern states. It seems there is no
coordination among the Centre, the State Nodal officers
and the identified institutes. Because of which even the
paramedical personnel were sent to NIMHANS,
Bangalore for training at a huge cost.
The objectives of the programme are not achieved till today
after lapse of more than one decade. This indicates that
there is a poor commitment of the government,
psychiatrists, and community at large. The programme
has given more emphasis on the curative services to the
mental disorders and preventive measures are largely
ignored8. It is beyond doubt that more public awareness
programmes are required. A huge amount of money was
earmarked for IEC activities to increase public awareness
about mental illness. Here also the programme failed
abysmally in some districts. A classic example is this. In a
district where large majority of the people are illiterate,
pamphlets in English were printed as part of IEC activities.
The argument given was that there are many dialects in
that particular state so it is not possible to publish IEC
materials in each and every dialect. But the distribution
of materials in English to this group of people is unlikely
to serve any purpose. Moreover, as part of IEC activities,
Mental Health Act, 1987 was also printed. This must have
cost several thousands of rupees at the minimum if not in
lakh. This is sheer wastage of public money. This is
because MHA- 1987 is freely available in the market with
nominal price. Moreover this Act is hardly of use for the
laymen. So, huge stock of copies of MHA-1987 is lying
in the office of the nodal officer. It is not very difficult to
guess whose interest is served by such action.
According to the operational guideline9, states are required
to submit proposals under various schemes of the
programme. Based upon these proposals from the states
funds are released to the State Health Society for
implementation as per the scheme guidelines. State nodal
officer for NMHP will represent the programme in the
State Health Society and get the grant released for various
districts and institutions as per the scheme/guidelines. This
norm is also not followed by various state Governments.
Some state government took several years after the 1st
installment from the Central government to appoint the
state nodal officer. Obviously, there is long delay in
initiating the programme for which the utilization certificate
could not be provided within the stipulated time. As a
sequale of this, the programme did not receive the
successive installments and the programme had to be
withdrawn. There is an example of having practically two
State nodal officers, one, a senior official from state health
service, for those districts which already completed five
years term and are taken over by state government and
the other, a psychiatrist for those districts which are getting
central grants and yet to complete five years . There is no
coordination between the two nodal officers. Neither the
DMHP psychiatrists, nor the joint director of Health
services of the districts were ever taken into confidence
for the financial matter by the concerned official of the
directorate of health services of the state. In the district
level there was no documents related to financial matter
for monitoring. There is an allegation that there is frequent
change of officers in the centre who look after this
programme, because of which there is delay in issuing
subsequent installment even after submitting utilization
certificate repeatedly.
Another matter of concern in many DMHP is lack of
transparency and poor maintenance of record of
expenditure. There was no proper documentation of
the implementation of DMHP for the entire period in
a district. One peculiar aspect of handling grants from
centre for DMHP in one state is that the fund used to
be deposited in the state exchequer for a long time. The
1st installment of Rs. 26.2 lacs meant for East Siang
DMHP (located about 250 Km from the state capital)
was received in February, 2007. The grant was deposited
in state exchequer . Surprisingly it is not handed over to
the concerned district till date. This has prevented the
humble beginning even after 3 years. Keeping the money
of 1st installment for more than three years is violation of
guidelines of the programme9. If unspent, the money should
have been refunded with interest. Many programmes failed
to spend the 1st installment even after several years.
As DMHP is a district level programme, the financial
matters should be managed at district level. In most of
the DMHP, the people working at the district level are
totally unaware about the fund position and its utilization.
There is a case where the fund is managed not by the
nodal officer or DMHP team but by the member secretary
of State Mental Health Authority working in a diffferent
district. So, managing the programme from headquarter
of a different district becomes an obstacle for successful
implementation of the programme.
As per the scheme for strengthening the psychiatric
wings of general hospitals and medical col1eges in
the Government sector under revised NMHP, a one-
time grant of Rs.50 lakhs for upgradation of
infrastructure and equipment was received by many
districts hospitals which are nodal centers for DMHP.
The grant covers:
1. Construction of new ward.
2. Repair of existing ward.
3. Procurement of items like cots and tables.
4. Equipment for psychiatric use such as modified ECTs
The in-patient ward of a district hospital was renovated
several times with these central grants. But even after
expenditure of such a heavy amount the in-patient ward
is found to be in poor shape. The small cubicle like set
up is not suitable for hospitalization for psychiatric
patients. The dilapidated floor and dirty wall is tell-
tale evidence of utter neglect and mismanagement.
There was only a single patient in the ward on the day
of inspection. The arrangement in the ECT room
speaks volume about its utilisation. The ECT machine is
safely kept in locker. Layer of dust accumulated over the
Boyles’ apparatus. It seems it was never used since its
purchase. In another district hospital, the grant received
for development of psychiatric ward was spent for
construction of office building. Equipments like modified
ECT machine, Boyle’s apparatus were purchased with
the grant but never used as there is no indoor facility. The
erstwhile ‘Isolation ward’ was earmarked as in-patient
ward for psychiatric patient. Since no patient was treated
as in-patient, the existing psychiatry ward is being used
as ‘Burn Unit’. On the other hand, some DMHPs which
is doing a very good job is facing problem due to lack of
provision of in-patient ward in the district hospital. They
have to share beds with medicine department which
creates conflicts at times.
In most of the districts under DMHP, the supply of
psychotropic medicines is few and irregular. One DMHP
psychiatrist commented that supply of surgical items even
without indent is more regular (though often unused) than
psychotropic medicines. The reason behind this is well
understood. There was occasion when medicine supplied
was much more than required and hence major part of
the consignment expired. The medicines are dispensed
only in the district hospital. No essential psychiatric
medicines are made available or dispensed at primary
level.
There is another interesting case. As per record of
Ministry of Health and Family Welfare, Government
of India, there is a programme under DMHP in Darrang
District of Assam and Gauhati Medical College is the
nodal institute. But no such programme is going on in
Darrang District of Assam. Neither Principal of Gauhati
Medical College nor the State Nodal Officer received
any grant so far for this district. This matter was already
intimated to the Government of India by the State
Nodal Officer. But we were asked to inspect that
district recently by the Government of India.
Government of India should probe about allocation of
fund to Darrang DMHP. If no such sanction was made,
the money should be released immediately so that the
nodal institute can start the programme immediately.
At present the major issue of DMHPs which completed
five year term is the regularisation of services of the staff
working for DMHP by the state government. They were
given consolidated pay only without any increment or
allowances. For several years they worked without any
pay for which many member of DMHP team already left
the service. They were given infrequent financial assistance
in the form of lump sum amount by the state government.
But the staffs want their service to be regularised by the
state government with pay packages at par with other
state government employee which is very much justified.
In order to make the programme successful, their
grievances must be addressed by the concerned
government. As stated in the NMHP guideline, it is
mandatory on the part of the state government to take
over the programme on completion of central assistance
for a period of five years. But the genuine grievances of
DMHP team working in the field are not reaching the
officials sitting in state capital.
In all practicality, DMHP has become solely dependent
on the DMHP psychiatrist in most of the districts. The
medical officers who were trained under DMHP are
no longer recording and reporting the number of
psychiatric cases seen by them once it is taken over by
the state governments. This is probably because of lack
of communication. Even many nodal officers are not
receiving any guideline from the centre. So, it is not
surprising to know that there is no record of how many
medical officers who were trained under DMHP are
transferred to other districts or retired. No new training
programme is undertaken after it was taken over by
state government for lack of fund. In the monthly
meeting also, record from the psychiatry department
is hardly discussed.
The 11th Plan has a vision of district mental health
programmes that include community mental health
services like life-skill training and counselling in educational
institutions, workplace stress management and suicide
prevention services. Most of the DMHPs of this region
did precious little in this regard. DMHP in current form is
mostly focused on pharmacological management of
psychosis only.
There is a goal of providing short-term training to deliver
basic mental health services to the existing health staff in
the districts by the end of the 11th Plan. This goal is unlikely
to be achieved in the Plan period.
The role of State Mental Health Authority in
implementation of the programme needs to be defined.
In many states the state mental health authority is
defunct or it is not very much sure about their roles and
responsibilities. It should function as technical support
team to assist the state nodal officer.
REMEDIAL MEASURES
As a remedial measure for such anomalies and for success
of DMHP, frequent and timely monitoring is essential. In
many cases the official who was responsible for
implementation of the programme is no longer available
due to superannuation, death or transfer. Many queries
could not be clarified by the officials currently engaged
with the programme. There is no point of monitoring a
programme several years after it was completed. The idea
of monitoring is to find out the deficits so that timely
corrective measures can be taken in order to make the
programme successful. Continuous monitoring and
reporting as well as regular external evaluation is
recommended for mid-course correction. Utilisation
certificate should not be taken at their face value. The
staff working in DMHP should be regularized by the State
government and instead of consolidated pay they should
be given pay and allowances at par with other employees
of state government. The medical officers who are yet to
be trained under DMHP should be trained. There should
be thorough verification of expenditure in various heads
since inception of the programme. The programmes where
posts of supporting staff are lying vacant should be
recruited immediately and sent for training for stipulated
period in the identified nodal institutes for the region. The
in-patient ward should be made functional immediately.
There should be an effective and time specific monitoring
system. Periodic training of the health workers at primary
level on priority mental disorders and their day to day
supervision, along with monthly review of the mental health
programme during the regular review of other health
programmes will definitely play a significant role in proper
implementation of DMHP. By this process, the mental
health programme will not be seen as separate from the
other health programmes. Mental health services at
subcenter, PHC, CHC level should be strengthened so
that the services become more accessible to the patients7.
Most of the DMHP failed to provide disability certification
on a monthly basis. The involvement of Panchayat Raj
institutions and voluntary organizations for community level
rehabilitation of patients, including the setting up of support
to self-help groups is almost nonexistent.
Central Government in consultation with State
Governments should ensure continuity of DMHP
beyond the plan period by an undertaking to this effect
and integration of mental health services in State and
District Programme Implementation Plan (PIP). The
fund allotment should be regular and timely. Initiation
of programme should be ensured in time bound manner
after the receipt of funds7. The salary of staff should
be revised. The salary of DMHP psychiatrist and the
faculties under NMHP is so less that it is unlikely that
these posts will be filled up even if there is sufficient
manpower until and unless there is revision of the
remuneration. The DMHP psychiatrists are mostly from
state health cadre and therefore they are not spared from
other emergency duties. They do not get any incentive
also for working in DMHP. So, there is resentment and
some of them consider it to be an extra burden. The staff
of the DMHP should be exclusively engaged for
programme related works. Training should be imparted
regularly to all members of the DMHP team. Refresher
training and in-service training with the focus on local
challenges will boost up the morale of the personnel
implementing the programme. Training the DMHP team
in organizational skills, networking and involvement of all
stakeholders is also important. The trained personnel
should be retained in the district or if transferred it should
be to other DMHP districts only. The DMHP team needs
to be trained on Programme Management and
organizational activities7. It is recommended that in
addition to diagnosis and treatment involvement of family
members and community in the treatment process should
be stressed. Counseling should be an integral component
in each step. Proper mechanism should be evolved for
drop out cases by ensuring availability of psychiatric social
worker and community nurse to follow up the drop out
cases. The involvement of PRIs and local leaders can
make this much easier. The programme should emphasize
on promotive and preventive aspects rather than curative
only. So, suicide prevention, workplace stress
management, school and college counseling services etc
should be incorporated at each level. Though there is
enough discussion about integration/ coordination of
mental health programme with other health programme
like. ICDS, NRHM this is far from reality. There is urgent
need for regular inflow of medicines and availability at
primary level. Drug procurement mechanism should be
streamlined to reduce delay in procurement and achieve
economy of scale (e.g. Tamil Nadu model) 7.
There should be regular review of the case Records by
the DMHP officer/ team for completeness of the records;
correctness of the diagnosis, appropriateness of the
medicine used, appropriateness of the dosage of the
medicine, follow-up records-completeness,
appropriateness of changes in the treatment, Medicine
stock etc. The record and work of health workers should
be evaluated and their problem should be discussed. Ministry of Health and Family Welfare, New Delhi.Dtd.24
Most of the DMHP failed to initiate any programme for April 2009
support of the caregivers. Community resources like 7. Indian Council of Marketing Research, Evaluation of
District Mental health Programme-final report, 2009, New
families were not accorded due importance. Most Delhi
important is that the nodal officer should be a psychiatrist. 8. Srinivasa Murthy R and Wig N.N. Evaluation of the
Non Psychiatrist nodal officers overburdened with other progress in mental health in India since independence. In,
Mental Health in India (Eds) Purnima Mane and Katy
responsibilities and having no technical expertise failed to Gandevia) Tata Institute of Social Sciences, 1993; pp. 387-
give justice to their responsibilities particularly when the 405.
central guidance is inadequate. 9. http://www.mohfw.nic.in/Guidelines_NMHP_final.pdf
It was indeed a good idea to expand this programme
to each districts of the country during 11th five year
plan period. But it has not been possible due to flaws that
are discussed already. The core idea of integration with
the general health service is not implemented at the
operational level. With proper monitoring and active
involvement of all sections of people definitely DMHP
can lessen the sufferings of millions of mentally ill and their
families and promote mental health in the society.
REFERENCES
1. Government of India. National Mental Health Programme
for India. Ministry of Health and Family Welfare, New
Delhi.1982
2. Community Mental health News, District Mental health
Programme, 1988, Issue No.11 and 12, 1-16.
3. Government of India. In Annual report, National Mental
Health Programme for India. 2000 Ministry of Health and
Family Welfare, New Delhi.
4. http://nihfw.org
5. http://india.gov.in/sectors/health_family/mental_health.php
6. Government of India. Implimentation of National Mental
Health Programme during the Eleventh Five Year Plan-
approval of the manpower development component,
 ORIGINAL ARTICLE

Insight into Schizophrenia: A comparative study

between patients and family members
Shyamanta Das*; Dipesh Bhagabati**, Uddip Talukdar***
*Department of Psychiatry, Silchar Medical College Hospital, Silchar, Assam, ** Department of Psychiatry,
Gauhati Medical College Hospital, Assam,*** Department of Psychiatry, Himalayan Institute of Medical
Sciences, Jolly-Grant, Dehradun, Uttaranchal,

ABSTRACT

Background: Despite the recognition of the role that sociocultural factors play in the process of acquiring
insight, recent research on this issue is scare. Aim of the present study was to compare patients’ insight with
family members’ insight.
Method: 50 patients with schizophrenia (International Statistical Classification of Diseases and Related Health
Problems – Tenth Revision – ICD-10) undergoing treatment and members of their families were interviewed
using the Schedule for Assessment of Insight (SAI). It was a cross-sectional study.
Results: Family members performed better than patients in the total and partial SAI scores [total: 11 to 6.7 (p
< 0.0001); adherence: 3.84 to 2.7 (p < 0.0001); recognition of illness: 4.54 to 2.84 (p < 0.0001); relabeling of
psychotic phenomena: 2.62 to 1.16 (p < 0.0001)]. However, when the scores were correlated for each patient-
family member pair, the partial scores had positive correlations (adherence r = 0.07191; recognition of illness r
= 0.1632; relabeling of psychotic phenomena r = 0.2052).
Conclusion: There was a positive correlation between the scores of family members and patients regarding
adherence, recognition of illness and the ability to relabel psychotic phenomena as abnormal. This might be
understood as a stronger influence of sociocultural factors in these dimensions. The fact that family members
were not assessed for the presence of psychopathology is a limitation of this study.
Keywords: Schizophrenia. Awareness. Self concept. Family relations. Social environment.

INTRODUCTION

Insight is ability to understand the true cause and Schizophrenics (CCHS). In addition, lack of insight
meaning of a situation (such as a set of symptoms). has been included among the 12 symptoms that have
Impaired insight is diminished ability to understand the highest power to discriminate schizophrenia from
the objective reality of a situation 1. other psychoses and depression3. It has been shown
A lack of insight was the most prevalent symptom of that patients with better insight are more likely to
schizophrenia found in two seminal international present better adherence to treatment4, 5. Lack of
studies, the International Pilot Study of Schizophrenia insight has been correlated with worse outcome6, more
(IPSS) 2 and the Classification of Chronic Hospitalized admissions6, worse psychosocial functioning7, 8,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 reduced success rates in outpatient treatment of
12345678901234567890123456789012123456789012345
Correspondence:
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 relapses9, and longer interval between the onset of
12345678901234567890123456789012123456789012345
Dr. Shyamanta Das symptoms and the seeking of treatment10.
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Department of Psychiatry,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 The relationship between insight and psychopathology is
12345678901234567890123456789012123456789012345
Silchar Medical College Hospital, Silchar, Assam, India
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-Mail: drshyamantadas@gmailcom controversial. Some authors have proposed that insight
is independent of psychopathology11, 12 while others have
found a negative correlation between insight and the
general measures of psychopathology13.
The concept of insight is much larger than just knowing
whether one is ill or not, and if so, having a sensible view
regarding treatment. It is a quality that has been highly
valued by most mental health clinicians because a strong
link is assumed between having insight and better quality
of life14. Although, in psychiatry, we concentrate mostly
upon the narrow meaning of insight with regard to mental
illness, we need to retain this broader concept. Therefore
attempts in defining and measuring insight are potentially
of practical importance15.
In recent years, sophisticated instruments for quantifying
insight have been developed, in which different aspects of
insight can be considered independently. Within each of
these realms, insight is not an all-or-nothing phenomenon16.
A conflict about the nature of psychiatric symptoms and
disorders can arise between the interviewer and the patient.
Also, insight has to be assessed against the background
of knowledge of, and beliefs about, mental disorder; it is
not the same as complete agreement with the views of the
doctor 17.
The recent resurgence of interest in insight has had its share
of criticism. Medical anthropologists have criticized the
concept of insight for failing to recognize that people can
have various culturally shaped frameworks to explain their
illnesses, all possibly valid. From this point of view, the
concept of insight is ‘eurocentric and essentially arrogant’
18
as it dictates that patients should apart from agreeing
that they are mentally ill and requiring treatment, also agree
to re-construct their experiences within the terms and
concepts of western psychiatry.
In recent years, there has been consensus that insight is a
multi-faceted phenomenon. There is also recognition of
the need to operationalize the concept for clinical practice
and to devise scales to measure it. There are differences
in the number of dimensions of insight being studied even
among those not looking at the social and cultural aspects.
The latter aspects have not received sufficient attention15.
The scarcity of studies on the social and cultural influences
on insight arises in spite of the large number of works on
the role played by those factors in the onset, diagnosis,
treatment and prognosis of schizophrenia19, 20, 21.
According to Johnson and Orrell (1995)22, psychotic
patients disagree with their doctors as to their symptoms
and illness not only because they are ill, but also because
they have a different concept of their experience, which is
molded by their sociocultural context. There are
standardized ways of thought and action for reporting the
experiencing of illness that are guided by the local culture.
Patients use these standards, which may differ from the
physicians’ standards and from those of patients from
different cultures. Cultural influences on the self-evaluation
of mental illness are found when groups of psychotic
patients from different cultures are studied and compared.
In addition to the different conceptions of mental illness,
there are other important sociocultural factors. White et
al. (2000)23 found a strong association between the size
of the primary group (family and close friends) and insight.
They stated, as also postulated by Breier and Strauss
(1984)24, that broader social contact exerts a normalizing
function on the individual that leads to better insight.
Another sociocultural factor that could interfere in the
evaluation of mental illness by patients could be stigma,
which would be stronger in some specific cultures22. There
is evidence that patients’ denial of their illness could buffer
the impact of the stigma on patients’ self-appraisal25.
Aim of the study
The objective of this study was to:
Compare patients’ insight with family members’
insight.
Methods
Sample: 50 patients and 50 respective family members
were selected from those attending Psychiatry
Department of a General Hospital.
The inclusion criteria were:
Patients –
1. Diagnosis of schizophrenia according to the
criteria of the International Statistical
Classification of Diseases and Related Health
Problems, Tenth Revision (ICD – 10).
2. Only patients giving Informed Consent.
Family members –
1. Availability of family members to accompany the
patients to the interview and for application of the
scale. Family members (related by blood/
marriage) are key relatives having a relationship
 of parent/ sibling/ spouse/ off-spring with the
patient. Relatives are the primary caregivers
identified as the family member who provides the
most support and/ or assistance.
2. Only family members giving Informed Consent.
Patients who could not be interviewed because
of mutism, negativism or psychomotor agitation were
excluded.
Interview and Instrument
Demographic and clinical data were gathered and the
diagnostic inclusion criteria were assessed according to
the ICD – 10 criteria. The evaluation of insight was
carried out using the Schedule for Assessment of Insight
(SAI), for each participant (patient and family member)
separately. The interviews were carried out over four
months, between August, 2006, and November,
2006. Patients and family members were
interviewed on the same days.
Table 1. Demographic and clinical characteristics of the sample
The Schedule for Assessment of Insight (SAI) in
Psychosis was published in 199213 (David et al.), Demographic characteristics
variables, and correlations were performed using the
Spearman correlation test.
Results
The demographic and clinical characteristics of the two
groups are presented in Table 1.
It is evident from the table that there are significant
differences between the demography of patients and
family members, namely in the gender, age and marital
status. Multivariate analysis was done to find the
significance of these variations in the SAI scores. Two-
way ANOVA was done in the categories of gender and
age group. Marital status was not included for the test as
it is dependent upon the age. From the marital status table
we find that there are an increase number of married
persons in the family member group and that group has
of patients and family members
patients
(n = 50)
family
members
χ2/tt
test
p

(n = 50)
in which, apart from the recognition of mental Gender % (n)
illness and compliance with treatment, the ability Male
Female
44 (22)
56 (28)
66 (33)
34 (17)
4.040 0.0444

to relabel unusual mental events as pathological Age in years (95% CI) 34.4 42.34 2.558 0.0137
was also included. The SAI comprises three (31.290 – 37.510) (37.724 – 46.956)
Marital status % (n)
subscales that measure distinct components of Single 44 (22) 26 (13) 9.085 0.0106
Married 48 (24) 74 (37)
insight, namely adherence to treatment, Widowed/Separated 8 (4) -

recognition of illness and ability to relabel Religion % (n)

Hindu 80 (40) 80 (40) 0.00 1.00
psychotic phenomena as abnormal. The sum of Islam 18 (9) 18 (9)
the scores of the subscales yields a total score Christian 2 (1) 2 (1)

of up to 14 points. Years of education (95% CI) 9.26

(7.996 – 10.524)
8.68
(7.252 – 10.108)
0.6722 0.5046

Five demographic variables were recorded for Clinical characteristics

patients and family members: gender, age, marital Previous hospitalization % (n) 56 (28)

status, religion and number of years of education. Number of previous

hospitalizations,‡ mean (95% CI) 1.89 (1.493 – 2.293)
Seven clinical variables were recorded for
patients only. These were presence, number and Time spent hospitalized over
lifetime in weeks,‡ mean (95% CI) 6.35 (4.766 – 7.948)
duration of previous hospitalizations, duration of Duration of illness in years,
illness, family history of schizophrenia, suicide mean (95% CI) 9.28 (7.328 – 11.232)

attempts and age at onset of illness. Family history of

schizophrenia % (n) 20 (10)
Student’s t test, Welch t test and Mann Whitney
Patients who attempted
U test were used to compare means between Suicide % (n) 26 (13)

the two groups. The chi-squared test and two- Age at onset of illness in years, 25.12 (22.171 – 28.069)
mean (95% CI)
way ANOVA were used to compare category
‡ Refers to patients who had already been hospitalized;
CI = confidence interval.

high age compared to the patients.
From the ANOVA, it is concluded that a significant
difference exists between patients and family members
in the SAI scores but the interaction statistics shows
that gender does not influence that difference. So,
gender as a related factor for SAI score can be
discarded according to the test. Age was
another demographic variable that was found
significantly varying between patients and family
members and to test the influence of age on the SAI
scores another ANOVA was performed. The age was
divided into 7 equal groups and made into a category
variable for ease of calculation.
This again shows that the interaction between age
and SAI scores of patients and family members is
non-significant and hence age does not influence the
SAI scores.
Five patients had been admitted to the psychiatry
ward and the other 45 were under outpatient treatment
at the time of the interview.
The mean SAI score was 6.7 (95% CI: 5.897 to
7.503) for the patients and 11 (95% CI: 10.384 to
11.616) for the family members.
Family members performed better in the total and
partial SAI scores, as shown in Table 2.
However, when the scores were correlated for each
patient-family member pair, the partial scores had a
positive correlation (Table 3), though the correlation
coefficient was low.
Discussion
Family members scored significantly higher in all the
components of the scale, namely adherence (3.84
versus 2.7), recognition of illness (4.54 versus 2.84)
and relabeling of psychotic phenomena (2.62 versus
1.16) as well as in the overall score (11 versus 6.7)
than patients. These differences were statistically
Table 2. Mean and 95% confidence interval of total and partial scores for the Schedule for
Assessment of Insight in 50 patients with schizophrenia and 50 family members
Patients Family members t p
Adherence (95% CI) 2.7 (2.354 – 3.046) 3.84 (3.684 – 3.996) 5.947 p < 0.0001
Recognition of illness (95% CI) 2.84 (2.325 – 3.355) 4.54 (4.209 – 4.871) 6.097 p < 0.0001
Relabeling of psychotic 1.16 (0.8649 – 1.455) 2.62 (2.276 – 2.964) 7.685 p < 0.0001
phenomena (95% CI)
Total (95% CI) 6.7 (5.897 – 7.503) 11 (10.384 – 11.616) 9.402 p < 0.0001
Note: Maximum scores for adherence and relabeling of psychotic phenomena
= 4, and for recognition of illness = 6. CI = confidence interval.
The desired position of the Table 2 is in Results section
after the line “Family members performed better in the total
and partial SAI scores, as shown in Table 2.”
Table 3. Correlation of the components of insight between 50 patients with schizophrenia and 50
family members (Spearman Rho test)
Adherence Recognition of Relabeling of Total (P)
(P) illness (P) psychotic
phenomena (P)
Adherence (F) 0.07191
Recognition of illness (F) 0.1632
Relabeling of psychotic 0.2052
phenomena (F)
Total (F) 0.1365
Note: (F) = family members, (P) = patients.
significant (p < 0.0001). This may be due to the influence
of psychopathology.
In confirmation with findings of the present study, Sanz
et al. (1998)26 showed that there is an inverse correlation
between insight, the severity of psychopathology and
positive affective disturbance.
David et al. (1992)13 found that the ‘total insight score’
in their study had a moderate inverse correlation with the
Present State Examination27 total score, which was an
indication of the global severity of the illness.
In contrast to findings of the present study, McEvoy et
al. (1989a)28 reported that insight as measured by the
Insight and Treatment Attitudes Questionnaire (ITAQ)
did not correlate with either the severity of acute
psychopathology or the changes in psychopathology with
treatment. They speculated whether the mechanisms
underlying the production of positive symptoms and
disturbed insight were independent and whether the latter
was more resistant to the effective use of neuroleptic
medication.
The present study also exhibited positive correlation
between the scores of family members and patients in
adherence to treatment (r = 0.07191), recognition of
illness (r = 0.1632) and ability to relabel psychotic
phenomena as abnormal (r = 0.2052). Although these
correlations were not statistically significant
(adherence, p = 0.6197; recognition of illness, p =
0.2576 and relabeling of psychotic phenomena, p =
0.1529). The positive correlation can possibly be
understood as the effect of stronger influence of
cultural factors on these components of insight.
According to Kirmayer and Corin (1998) 29, the
individual’s capacity for self-knowledge stems mainly
from social processes, involving the observation of
others and the acquisition of ways to describe oneself
that are specific to the culture that the individual comes
from. Therefore, insight is not a mere act of the
patient’s self-perception that he or she is ill, but rather
a construction that depends on the sociocultural
context.
Johnson and Orrell (1995)22 stated that different
dimensions of insight are influenced in different ways
by psychosocial factors. The ability to relabel psychotic
phenomena as abnormal is influenced more by
psychopathological factors than by sociocultural ones.
Recognition of illness is the variable most affected by
the latter factors. This has also been suggested by Gigante
and Castel (2004)30.
Both David et al. (1992)13 and McEvoy et al. (1989c)
31
found that, as a group, involuntary (that is compulsorily
admitted) patients have less insight.
Moreover, compliance with prescribed treatment is a
much more complex phenomenon affected by social
factors and beliefs about health and sickness32.
David et al. (1992)13 found that treatment compliance
was not strongly related to the ability to recognize one’s
own delusions and hallucinations and to relabel them as
abnormal.
It is interesting that patients may comply with treatment;
even though they do not believe themselves to be ill, if the
social milieu is conducive31, 33. Startup (1996)34 suggested
that a relationship between cognitive deficits and insight
might only exist among some subpopulations of patients
and that there might be stronger influence of psychological
and sociocultural factors among those whose cognitive
functions but not insight are preserved.
Anthony S. David, Professor of Cognitive
Neuropsychiatry, Institute of Psychiatry, King’s
College, London, working on insight with colleagues
at the Christian Medical College and Hospital, Vellore,
consider the cultural factor is very interesting. What is
regarded as a symptom of an illness isn’t simply a
matter of biology and physiology. There are cultural
and social aspects to it as well. This is true especially
of psychiatric disorders. They feel that the biomedical
explanation is not the only explanation and are
currently trying to understand a more diverse culture
gives people a more flexible approach to understanding
illness. Some people argue that lack of “insight” is not
a brain disorder. It is simply a sensible approach, given
the stigma attached to mental disorders. They wonder
why anyone would want to admit that they have such
a problem. They would only be shunned. Maybe if the
person explains the hallucinations, mystical or religious
beliefs, and so on, rather than label it a medical
condition, some of the stigma would be avoided and
self-esteem preserved, and yet there is awareness that
something is different. It may be easier for them to
accept help. So, David and colleagues are looking at
the cultural as well as biological aspects.
Limitations
Family members were not assessed for personality traits
and neuropsychological deficits that could have influenced
their ability to recognize schizophrenia symptoms among
their relatives. With regard to the possibility of generalizing
the results of this study, there was a selection bias,
considering that the sample was recruited within a clinical
setting. Demographic and clinical characteristics may
influence study findings.
Conclusion
Since patients and members of their families share the
same cultural environment, the significant difference
 21. Redko C (1998) Cultura, esquizofrenia e experiencia. In: Shirakawa I, Chaves
regarding their insight can possibly be better explained AC, Mari JJ, editors. O desafio da esquizofrenia. Sao Paulo: Lemos Editorial.
by disease factors. Different degrees of insight, namely 22. Johnson S and Orrell M (1995) Insight and psychosis: a social perspective.
Psychological Medicine 25, 515-20.
adherence to treatment, recognition of illness and 23. White R, Bebbington P, Pearson J, Johnson S, Ellis D (2000) The social context
ability to relabel psychotic phenomena as abnormal, of insight in schizophrenia. Soc Psychiatry Psychiatr Epidemiol 35, 500-7.
seem to be strongly influenced by sociocultural factors. 24. Breier A, Strauss JS (1984) The role of social relationships in the recovery from
psychotic disorders. American Journal of Psychiatry 141, 949-55.
25. Lai YM, Hong CP, Chee CY (2001) Stigma of mental illness. Singapore
REFERENCES Medical Journal 42, 111-4.
1. Sadock BJ and Sadock VA (2003) Signs and Symptoms in Psychiatry. 26. Sanz M, Constable G, Lopez-Ibor I, Kemp R and DavidAS (1998)Acomparative
In:Synopsis of Psychiatry. Lippincott Williams & Wilkins, Philadelphia. study of insight scales and their relationship to psychopathological and
2. World Health Organization (1973) Report of the International Pilot Study of clinical variables. Psychological Medicine 28, 437-46.
Schizophrenia. Geneva: World Health Organization. 27. Wing JK, Cooper JE and Sartorius N (1974) Measurement and Classification
3. Carpenter WT, Strauss JS, Bartko JJ (1973) Flexible system for the diagnosis of Psychiatric Symptoms. Cambridge: Cambridge University Press.
of schizophrenia: report from the WHO International Pilot Study of 28. McEvoy JP, Apperson LJ, Appelbaum PS (1989a) Insight in schizophrenia:
Schizophrenia. Science 182, 1275-8. its relationship to acute psychopathology. Journal of Nervous and Mental
4. Buchanan A (1992) A two-year prospective study of treatment compliance in Disease 177, 43-7.
patients with schizophrenia. Psychological Medicine 22, 787-97. 29. Kirmayer LJ and Corin E (1998) Inside knowledge – cultural construction of
5. Cuffel BJ, Alford J, Fischer EP, Owen RR (1996) Awareness of illness in insight in psychosis. In: Amador XF and David AS, editors. Insight and
schizophrenia and outpatient treatment adherence. Journal of Nervous and Psychosis. New York: Oxford University Press.
Mental Disease 184, 653-9. 30. Gigante AD and Castel S (2004) Insight into schizophrenia: a comparative
6. Amador XF, Strauss DH, Yale S, Flaum MM, Endicott J, Gorman JM (1993) study between patients and family members. Sao Paulo Medical Journal 122,
Assessment of insight in psychosis. American Journal of Psychiatry 150, 146-51.
873-9. 31. McEvoy JP,Applebaum PS, Apperson LJ (1989c) Why must some schizophrenic
7. Amador XF, Flaum M, Andreasen NC, et al. (1994) Awareness of illness in patients be involuntarily committed? The role of insight. Comprehensive
schizophrenia and schizoaffective and mood disorders. Archives of General Psychiatry 30, 13-17.
Psychiatry 51, 826-36. 32. Bebbington PE (1995) The context of compliance. International Clinical
8. Lysaker PH, Bell MD, Bryson GJ, Kaplan E (1998) Insight and interpersonal Psychopharmacology 9 (Suppl. 5), 45-50.
function in schizophrenia. Journal of Nervous and Mental Disease 186, 432- 33. McEvoy JP, Freter S, Everett G (1989b) Insight and the clinical outcome in
6. schizophrenia. Journal of Nervous and Mental Disease 177, 48-51.
9. Heinrichs DW, Cohen BP, Carpenter WT (1985) Early insight and the 34. Startup M (1996) Insight and cognitive deficits in schizophrenia: evidence for
management of schizophrenic decompensation. Journal of Nervous and a curvilinear relationship. Psychological Medicine 26, 1277-81.
Mental Disease 173, 133-8.
10. Drake RJ, Haley CJ, Akhtar S, Lewis SW (2000) Causes and consequences
of duration of untreated psychosis in schizophrenia. British Journal of
Psychiatry 177, 511-5.
11. McEvoy JP, Freter S, Merritt M, Apperson LJ (1993) Insight about psychosis
among outpatients with schizophrenia. Hosp Community Psychiatry 44,
883-4.
12. Cuesta MJ, Peralta V (1994) Lack of insight in schizophrenia. Schizophrenia
Bulletin 20, 359-66.
13. David AS, Buchanan A, Reed A and Almeida O (1992) The assessment of
insight in psychosis. British Journal of Psychiatry 161, 599-602.
14. McGorry PD and McConville SB (1999) Insight in psychosis: an elusive
target. Comprehensive Psychiatry 40, 131-42.
15. Sims A (2003) Insight. Symptoms in the Mind. Saunders: An Imprint of
Elsevier. Philadelphia, Pennsylvania.
16. Kirkpatrick B and Tek C (2005) Schizophrenia: Clinical Features and
Psychopathology Concepts. In: Comprehensive Textbook of Psychiatry.
Lippincott Williams & Wilkins, Philadelphia Bebbington PE (1995) The
context of compliance. International Clinical Psychopharmacology 9 (Suppl.
5), 45-50.
17. Gelder M, Mayou R and Cowen P (2001) Signs and symptoms of mental
disorder. In: Shorter Oxford Textbook of Psychiatry, pp.26-27. New Delhi:
Oxford University Press
18. Perkins, R. & Moodley, P. (1993) The arrogance of insight? Psychiatric
Bulletin, 17, 233-234.
19. Fabrega H (1989) On the significance of an anthropological approach to
schizophrenia. Psychiatry 52, 45-65.
20. Salokangas RK (1997) Living situation, social network and outcome in
schizophrenia: a five-year prospective follow-up study. Acta Psychiatrica
Scandinavica 96, 459-68.
Appendices adequate understanding or “don’t know” = 1
SCHEDULE FOR ASSESSMENT OF INSIGHT (SAI)* Delusional explanation = 0
1a. Does patient accept (includes passive acceptance) 3a. Ask patient: “Do you think the belief that….
treatment (medication and/or admission and/ (insert specific delusion) is not really true/
or other physical and psychological therapies)? happening ?” or “Do you think that ….. (insert
Often = 2 (may rarely question need for specific hallucination) is not really true/
treatment) happening ?”
Sometimes = 1 (may occasionally question Often = 2 (thought present most of the
need for treatment) day, most days)
Never = 0 (ask why) Sometimes = 1 (thought present
If 1 or 2, proceed to 1b. occasionally, minimum once per day)
1b. Does patient ask for treatment unprompted? Never = 0
Often = 2 (excludes inappropriate requests for If 1 or 2 present, proceed to 3b.
medication, etc) 3b. Ask patient: “How do you explain these
Sometimes = 1 (rate here if phenomena (the belief that …. hearing that
forgetfulness/disorganization leads to voice/seeing that image, etc) ?”
occasional requests only) Part of my illness = 2
Never = 0 (accepts treatment after Reaction to outside event/s (eg,
prompting) tiredness, stress, etc) = 1
2a. Ask patient: “Do you think you have an Attributed to outside forces (may be
illness?” or “Do you think there is something delusional) = 0
wrong with you?” (mental, physical, Maximum score = 14.
unspecified) *Sajatovic, M. & Ramirez, L.F. (2003) Rating Scales
Often = 2 (thought present most of the in Mental Health, pp. 222-223. Hudson: Lexi-
day, most days) Comp.
Sometimes = 1 (thought present STATISTICS
occasionally) The study population consisted of 50 patients of
Never = 0 (ask why doctors/others psychosis and 50 of their relatives. In those 50 pairs
think he/she does) of patients and their respective relatives the distribution
If 1 or 2, proceed to 2b. of various demographic factors are depicted in the
2b. Ask patient: “Do you think you have a mental/ following table.
psychiatric illness?” Patient Relative Remarks
Gender
Often = 2 (thought present Male 22 33 Fisher’s test P=0.04
most of the day, most days) Female 28 17
Sometimes = 1 (thought Marital status
present occasionally, minimum once HM 2
22
2
35
Chi-statistic = 9.279
Df =3
per day) S 22 13 P = 0.0258
Never = 0 W 4 0
Religion
If 1 or 2, proceed to 2c. Christian 1 1 Comparison not done as both groups
2c. Ask patient: “How do you explain Hindu 38 38 had equal numbers.
your illness?” Islam 9 9
Reasonable account given based on M 2 2
plausible mechanisms (appropriate Age (mean years)
given patient’s social, cultural, and 34.4 42.34 Welch’s apprx. t = 2.87 Welch t test was performed as the
(+10.93) (+16.23) df = 85 SEMs were significantly different
educational background, eg, excess P = 0.0052 between the groups.
stress, chemical imbalance, family Edu (mean years)
history, etc) = 2 9.26 8.68 Mann Whitney U Statistic = 1198.5
Confused account given, repetition of (+4.44) (+5.02) U` = 1301.5
overheard explanation without P = 0.725
Comparison between patient and family members
Two-way ANOVA table for Patient-Family member and Gender variables.
group in the subscales and total scores of SAI. Mean
Treatment group is Patient-Family member and Blocks are gender
of SAI scores were compared by non-parametric test
Sum of Squares df Mean Square F P-value
for mean difference. The groups failed normality test
Patient-Family 423.18 1 423.18 65.61 <0.0001
and Mann Whitney U test was done to compare the
member (P-F)
groups. The table shows significant differences be-
Gender 1.34 1 1.34 0.21 0.6491
tween the scores among patient and their relatives
P-F * Gender 0.02 1 0.02 0.00 0.9572
in all subscales and also in the total score. Signifi-
Error 619.15 96 6.45
cance level were very high for all the tests
(p<0.0001). Total 1043.69 99
From the ANOVA table it is
SAI scores (Adherence concluded that a significant
subscale) difference exists between the Patient
2.7 3.84 MU statistic = 596.0 Mann Whitney U statistic
and Family members in the SAI
(+1.22) (+0.59) U`= 1904.04 was performed as the
P < 0.0001 groups failed normality test. scores but the Interaction statistics
shows that Gender does not
SAI scores (Recognition subscale) influence that difference. So, gender
as a related factor for SAI score can
2.84 4.54 MU statistic = 517.00 be discarded according to the test.
(+1.81) (+1.16) U`= 1983.0 -do
P < 0.0001
SAI scores (Relabelling subscale) Age was another demographic
variable that was found significantly
1.16 2.62 MU statistic = 596.0 varying between the patient and
(+1.04) (+1.21) U`= 1904.04 -do- family members and to test the
P < 0.0001
influence of age on the SAI scores
SAI Total Scores
another ANOVA was performed.
6.7 11 MU statistic = 272.50 The age was divided into 7 equal
(+2.82) (+2.17) U`= 2227.5 -do- groups and made into a category
P < 0.0001 variable for ease of calculation
It is evident from the first table that there are Two-way ANOVA table for Patient-Family member and Gender variables.
significant differences between the Treatment group is Patient-Family member and Blocks are gender
demography of patients and family members, Sum of Squares df Mean Square F P-value
namely in the gender, age and marital status. Patient-Family 368.97 1 368.97 60.24 <0.0001
Multivariate analysis was done to find the member (P-F)
significance of these variations in the SAI Age 47.10 6 7.84 1.28 0.2742
scores. Two-way ANOVA was done in the P-F * Age group 44.54 6 7.42 1.21 0.3080
categories of gender and age-group. Marital Error 526.73 86 6.12
status was not included for the test as it is Total 937.34 99
dependent upon the age. From the Marital
status table we find that there is an increase This table again shows that the interaction between
number of married persons in the family age and SAI scores of patient and family members is
member group and that group has high age non-significant and hence age do not influence the
compared to the patients. The following table SAI scores.
The following table states the correlation of the Two-way ANOVA table for Patient-Family member and Gender variables for
subscales of SAI to each other and also each other Adherence Subscale. Treatment group is Patient-Family member and Blocks
are gender
between patient and family members. Sum of Squares df Mean Square F P-value
Patient-Family 28.15 1 28.15 31.35 <0.0001
member (P-F)
Correlations: Spearman’s rho Gender 1.01 1 1.01 1.12 0.2921
Correlations P-F * Gender 0.00 1 0.00 0.00 0.9841
Error 86.21 96 0.90
PT_ADH PT_RECO PT_RELAB PT_TOTAL FM_ADH FM_RECOG FM_RELA FM_TOTAL
G B
Total 115.37 99
PT_ADH Correlation 1.000 .111 .199 .544 .072 .135 -.071 -.004 Two-way ANOVA table for Patient-Family member and Gender variables
Coefficient for Adherence Subscale. Treatment group is Patient-Family member and
Sig. (2-tailed) . .444 .165 .000 .620 .350 .623 .980
Blocks are age groups
N 50 50 50 50 50 50 50 50
PT_RECOG Correlation .111 1.000 .318 .807 -.031 .163 .099 .098 Sum of Squares df Mean Square F P-value
Coefficient Patient-Family 24.64 1 24.64 29.47 <0.0001
Sig. (2-tailed) .444 . .025 .000 .832 .258 .495 .497 member (P-F)
N 50 50 50 50 50 50 50 50 Age 7.85 6 1.31 1.56 0.1675
PT_RELAB Correlation .199 .318 1.000 .649 .115 .145 .205 .244 P-F * Age group 6.96 6 1.16 1.39 0.2292
Coefficient Error 71.90 86 0.84
Sig. (2-tailed) .165 .025 . .000 .426 .316 .153 .088 Total 111.34 99
N 50 50 50 50 50 50 50 50
PT_TOTAL Correlation .544 .807 .649 1.000 .021 .189 .111 .136 Two-way ANOVA table for Patient-Family member and Gender variables for
Coefficient Recognition Subscale. Treatment group is Patient-Family member and Blocks
Sig. (2-tailed) .000 .000 .000 . .888 .190 .441 .345 are gender
N 50 50 50 50 50 50 50 50 Sum of Squares df Mean Square F P-value
FM_ADH Correlation .072 -.031 .115 .021 1.000 .151 .109 .371 Patient-Family 64.82 1 64.82 27.61 <0.0001
Coefficient
member (P-F)
Sig. (2-tailed) .620 .832 .426 .888 . .295 .452 .008
N 50 50 50 50 50 50 50 50 Gender 1.31 1 1.31 0.56 0.4571
FM_RECOG Correlation .135 .163 .145 .189 .151 1.000 .403 .634 P-F * Gender 0.40 1 0.40 0.17 0.6798
Coefficient Error 225.36 96
Sig. (2-tailed) .350 .258 .316 .190 .295 . .004 .000 Total 291.88 99
N 50 50 50 50 50 50 50 50
FM_RELAB Correlation -.071 .099 .205 .111 .109 .403 1.000 .903 Two-way ANOVA table for Patient-Family member and Gender variables for
Coefficient Recognition Subscale. Treatment group is Patient-Family member and Blocks are
Sig. (2-tailed) .623 .495 .153 .441 .452 .004 . .000 age groups
N 50 50 50 50 50 50 50 50 Sum of Squares df Mean Square F P-value
FM_TOTAL Correlation -.004 .098 .244 .136 .371 .634 .903 1.000 Patient-Family 64.58 1 64.58 29.02 <0.0001
Coefficient member (P-F)
Sig. (2-tailed) .980 .497 .088 .345 .008 .000 .000 . Age 16.14 6 2.69 1.21 0.3098
N 50 50 50 50 50 50 50 50 P-F * Age group 20.16 6 3.36 1.51 0.1846
** Correlation is significant at the .01 level (2-tailed). Error 191.41 86 2.23
Total 292.28 99
* Correlation is significant at the .05 level (2-tailed).
Two-way ANOVA table for Patient-Family member and Gender variables for
Relabelling Subscale. Treatment group is Patient-Family member and Blocks
From the correlation table we can see that none of the are gender
scores of SAI and its subscales of patients haves any Sum of Squares df Mean Square F P-value
correlation with the same of family members (the blue Patient-Family 52.05 1 52.05 40.68 <0.0001
member (P-F)
shaded part of the table). However, there is significant Gender 0.98 1 0.98 0.76 0.3844
correlation of One Subscale score to another and also P-F * Gender 0.62 1 0.62 0.49 0.4868
to the total score in both patient and family member Error 122.86 96
Total 176.47 99
groups.
Two-way ANOVA table for Patient-Family member and Gender variables for
Relabeling Subscale. Treatment group is Patient-Family member and Blocks
SAI subscales scores adherence was similarly are age groups
subjected to ANOVA test keeping Gender and Age- Sum of Squares df Mean Square F P-value
group as the dependent variables. In both the ANOVA Patient-Family 38.55 1 38.55 28.29 <0.0001
test the difference in the score was significant in patient member (P-F)
and family members, but that was not for the gender. Age 3.20 6 0.53 0.39 0.8830
P-F * Age group 4.46 6 0.74 0.54 0.7726
The interaction between the variables was found Error 117.18 86
insignificant. Total 163.38 99
 ORIGINAL ARTICLE
Association of Anxiety and Depression in
Postpartum Period: a Hospital Based Evaluative Study
K N Kalita, H R Phookun*, G C Das**
Department of Psychiatry, LGB Regional Institute of Mental Health, Tezpur; * Department of Psychiatry,
** Department of Obstetrics & Gynaecology, Gauhati Medical College

ABSTRACT:
Background: Postpartum period is associated with higher rates for depression, blue and psychosis. Anxiety is
also significant. These disorders may have serious implications in the cognitive development of the infant.
Many symptoms of both disorders overlap with each other. There is relative lack of data in this area. We tried
to estimate postpartum anxiety and depression in a group of women and tried to assess their correlation.
Material & Method: 100 women were assessed for depression and anxiety using Edinburgh Postnatal Depression
Scale, Hospital Anxiety and Depression Scale, ICD-10 criteria. They were selected on random basis. Analytical
statistical methods were utilized.
Result: 18% and 15% depression and anxiety were found respectively. Higher maternal age, parity, any post
operative history correlated with it significantly. It was found that anxiety and depression are not associated
significantly and are distinct categories. However 1% of variance of symptomatologies of depression can be
explained by anxiety and 20% of variance of symptomatologies of anxiety can be addressed by that of depression.
Conclusion: Depression and anxiety are separate clinical conditions having significant prevalence in postpartum
period. As anxiety, depression, psychosis all are increased in postpartum period a term ‘Postpartum mood
disorder’ may be proposed. Using easy screening tools by the paramedical workers will help early detection of
the cases and it will have long term effect on cognitive development of the infants.
Key words: anxiety, depression, postpartum

INTRODUCTION
Both anxiety and sadness are part of normal human are considerable. Again their co morbidity is of
behaviour. A person is said to be suffering from these particular interest. The associations between these
disorders if he/she exhibits significant distress and disorders are explained by interaction of three
impairment in functioning as a result of his/her systems of our body- neuroendocrine system,
symptoms for a specified period of time. The morbidity autonomic nervous system, and immune system. In
and mortality associated with anxiety and depression the WHO primary care study, prevalence of
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 depression and anxiety was 10.4% and 10.5%
Correspondence: Dr Kamal Narayan Kalita,
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 respectively as found by Sartorius et al. 1996. Even
Dept of Psychiatry, LGB Regional Institute of
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 if anxiety and depression are considered to be two
Mental Health, Tezpur, Assam, Pin 784001.
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 distinct disorders clinician frequently find that they
1234567890123456789012345678901212345678901234
E mail: knkalita@gmail.com
1234567890123456789012345678901212345678901234 are inter related. According to Clark, anxiety and
depression have been viewed as different points on
the same continuum1. In patients with lifetime
depression, prevalence of a lifetime anxiety disorder
is high (47% in Epidemiological Catchment Area
Study; 58% in National Co-morbidity Study; and 57%
in an earlier meta analysis)1,2,3. Although pure anxiety
without depression is more common than pure
depression without anxiety, the prevalence of
depression in anxiety is still high: 56% in the meta-
analysis found by Clark1.
Sichel and Driscoll, 1999 explained women’s increased
vulnerability to mood disorders at critical times in her
life, such as puberty, childbirth or menopause by using
his EARTHQUAKE MODEL for conceptualization
of woman’s mental health. Depression can result from
long-term ‘biochemical loading’ as a woman’s brain
responds to repeated stresses in her life. Altshuler et
al. remarked that, women in the childbearing age are
vulnerable to mood and anxiety disorders, and
physicians in all patient care specialties need to be
familiar with the prevalence and course of these
disorders, particularly during pregnancy and the
postpartum period 4. In a review Andrews 1999
discussed postpartum depression (PPD) as an irritable,
severely depressed mood occurring within 4 weeks of
giving birth and possibly as late as 30 weeks
postpartum. Murray et al. in his review on postpartum
depression commented that the growing interest in
postpartum mental disorders is due to the negative
impact on the child’s emotional and cognitive
development exerted by maternal psychiatric problem5.
Anxiety has received very little importance in the
postpartum period, however lately it is gaining
recognition. In a study Wenzel et al. 2003 found that
4.4% met DSM-IV criteria for generalized anxiety
disorder, and an additional 27.9% endorsed sub-
syndromal difficulties with generalized anxiety. Jones
et al. 2001 commented that anxiety disorders with or
without panic attack and obsessive symptoms might
develop during postpartum period. Researchers found
that 11% mothers met criteria for major depression
during the first 4 months postpartum, and an additional
13% met criteria for probable depression at 5 to 9
months postpartum6. In contrast 7.0% of the large
cohort had a visit or prescription for depression. Hence
a large population does not get attention to their
problem6.
Although few studies have been done in India in respect
to postpartum depression, studies in relation to
postpartum anxiety are scarce. Again in India for a
long time Reproductive Child Health Programmes are
going on but this aspect of maternal health and infant
health is neglected till now. Considering these facts
the present study was designed to find out the
prevalence of depression and anxiety in postpartum
period along with the association of these disorders to
each other.
MATERIAL & METHOD
This cross-sectional study was conducted in Gauhati
Medical College and Hospital, Guwahati, a premier
health institute in the north-eastern region of India.
The study sample comprised of 100 women giving birth
to their babies at Gauhati Medical College and Hospital
selected on simple random basis. The interview was
conducted at the outpatient department of obstetrics
and gynaecology when the mothers came for their
regular postnatal check-up and immunization of their
babies at 6 weeks postpartum.
Inclusion criteria
Study group
The subjects meeting the following criteria were
included in the study cohort-
1. Women of 18-42 years age giving birth to their
babies at Gauhati Medical College.
2. Women giving informed consent for the study.
3. Women were literate.
4. Married women.
Exclusion criteria
Women with the following criteria were excluded from
the study
1. Known chronic medical illness like asthma,
chronic painful condition, hypertension,
diabetes, neurological disorders, and chronic
 gynaecological condition like white discharge
per vaginum.
2. Known chronic psychiatric illness.
3. Known malignant condition.
4. Any history of substance dependence.
5. Any evidence of psychosis in the present
postpartum period.
6. Patients receiving some medication
continuously for last six months except for iron
and folic acid supplements.
7. Any disability causing functional impairment.
8. Birth of a congenitally malformed baby.
9. Death of the newborn.
10. Death of important family members in last six
months.
Sampling procedure
The women giving birth to their babies at Gauhati
Medical College and coming for the routine postnatal
check-up after discharge from hospital at 6 weeks
postpartum comprised the study sample. The samples
were taken as per systematic random sampling. In all
cases a detailed history and mental status examination
along with physical examination were carried out after
the gynaecological examination done by doctors from
department of obstetrics and gynaecology.
Tools used
1. A semi structured interview schedule for
collecting socio-demographic and obstetrical
data
2. Edinburgh Postnatal Depression Scale (EPDS):
EPDS was designed specifically to detect Post
Partum Depression, PPD7 . It contains 10 self
reported items, each scoring 0-3, depending
on severity. A score of 10 requires repeat of
the instrument in 2 weeks and a score above
13 requires further assessment for clinical
depression8. It has been validated in Assamese9.
3. The Hospital Anxiety and Depression Scale
(HADS): It is a self rating scale. This scale has
two subscales viz. HADS- Depression
(HADS-D) and HADS- Anxiety (HADS-A).
Each subscale has seven items with rating from
0-3. A cut-off score more than or equal to 11
for each subscale is considered a definite case
(Zigmond A, Snaith R 1983).
4. ICD-10 criteria for clinical description and
diagnosis guidelines: International
Classification of Diseases and Related Health
Problems, 10 th revision is the current
diagnostic guideline for diagnosing the health
problems across the globe adopted by the
World Health Organization. The chapter V(F)
is related to the behavioural problems.
Interview procedure
After a brief introductory phase informed consent from
the subjects were taken after explaining the nature
and purpose of the study. The EPDS was given to
the subjects while they were waiting for their
gynaecological examinations. After the gynaecological
examination they were evaluated as per the ICD
guidelines.
Analysis of data
The data obtained for the present study has been
analyzed by the Fisher’s exact test, chi square test, t
test using the instat statistical package.
RESULTS
A total of 100 women were assessed for depressive
and anxiety disorders. Of the 100 women 18 were
found to have depressive disorders while 15 had
anxiety disorders. The relationship of
sociodemographic variable and obstetrical variables
with these disorders has been shown in table 1.
Women with depressive and anxiety disorders were
significantly older than the non diseased group
(p<.05). Moreover mothers with some operative
history also had higher chances of getting these
disorders. Mothers with higher orders of pregnancy
were more prone to get depressive disorders. Both
the groups consisting of mothers with depressive
Table 1. Socio-demographic and obstetrical variables
disorders and anxiety disorders had
Depression Anxiety No diagnosis significance significantly higher score on EPDS. This
n=18 n=15 n= 67
association was found to be significant on
Religion Hindu 12 12 46 Fisher’s test. Again the mean score of EPDS
muslim 5 3 20 p>.05
in the three groups had significant differences
Family Joint 7 6 32 as shown in table 2. But the difference of
Nuclear 11 9 35 p>.05
mean value of EPDS in the group having
Locality rural 11 5 42 depressive and anxiety disorders was not
Urban 6 4 13
Semiurban 1 6 12 p>.05
significant.
Similarly Table 3 shows that the mean values
Age(mean) 28.05 29.0 23.43 Χ2=18.98 df 2 p<.05*
of depression and anxiety subscales in the
Education school 7 4 39 HADS differ significantly in the three
college 11 11 28 p>.05
groups. Again Table 4 shows that values in
m/o delivery spont 8 3 37 the depression and anxiety Subscale in the
CS 10 10 23 Χ2=6.64 df 2 p<.05*
Assisted 0 2 7 depressed group is correlated in a weak
manner. But the correlation is not significant
Male baby 9 7 32 p>.05
Female baby 9 8 35 (p>.05). In case of depression 1% variance
of symptomatologies can be explained by
b/o 1st baby 5 7 41
nd
2 baby 4 2 12 2
Χ =6.64 df 2 p<.05* anxiety. Similarly the correlation between
rd
3 baby 9 3 12 anxiety and depressive symptomatologies in
>3rd 0 3 2
the anxiety disorder group is not significant.
Table2: Scores on Edinburgh Postnatal Depression Scale In anxiety, from the co-efficient of determination we
EPDS Depression(n=18) Anxiety(n=15) No diagnosis(n=67)
found that 20% of the variance of symptomatologies
can be explained by variation in the depressive
>13 16 (88.89%) 9 (60%) 3 (4.48%) symptomatologies.
DISCUSSION
<13 2 (11.11%) 6 (40%) 64 (95.52%)*
Use of multiple self report inventories forced us to
Mean value 16.11±3.08 14.33±2.52 7.63±2.12 # exclude illiterate women from the study. So we
selected literate women above 18 years of age for
*p<0.001, Fisher’s test p<0.001, ANOVA # the present study. We found depression and anxiety
Table 3: Scores in subscales in Hospital Anxiety disorders in 18% and 15 % of the cases. Higher
Depression scale prevalence has been observed in many previous
Category No.of HAD- depression HAD- anxiety
findings both western and eastern10,11. Adewuya et
cases subscale subscale Table 4 : Relationships between depressive and anxi-
ety symptomatologies
Mean Std dev Mean Std dev Category No. of HAD score Co-efficient of Co-efficient of P value
Depression 18 13.78 1.44 7.67 1.88 cases co-relation( r ) determination
Depression Anxiety (r2)
Anxiety 15 9.40 3.58 11.73 2.84 (mean) (mean)

No diagnosis 67 7.48 1.74 7.01 2.36 Depression 18 13.78 7.67 0.12 0.01 >0.05

Anxiety 15 9.4 11.73 -0.45 0.20 >0.05

p<0.001, ANOVA
al. replicated similar results in Nigerian women12. In a
study done in India, it found higher prevalence of
postpartum depression and its significant association
with antepartum depression13. Anxiety disorders were
also higher in the postpartum period. Higher
prevalence has been reported by many
researchers,6,14,15. Findings from India are relatively less
in this regard. A researcher reported 11% of
generalized anxiety disorders in mothers attending a
postpartum clinic in India16. We also voice in similar
manner. Hence both anxiety and depressive disorders
are of concern in postpartum women.
These disorders are found in mothers with older age
group as compared with that in the younger mothers.
This goes against a previous finding that reported the
mean age for onset of depression to be 22.8 years17.
This contradiction may be the result of the sampling
procedure because we excluded the mothers below
18 years in our study.
The significant relationship of anxiety and depression
with operative history goes in line with previous
findings 18,19. This might be due to the somatic
symptoms found in postoperative women which
correspond to the somatic symptoms found in
depressive disorders. Another interesting finding of
the study is that as the birth order increases the chances
of depression also increases. A similar finding was
reported20. Again depressive disorder is said to have a
link with infantile development5. So we may encourage
our population to stick to small family norms.
On the other hand anxiety disorders were higher in
first time mothers. Maes et al had similar results21.
These results are self explanatory. In a poor country
like us the entry of a new born in the family carries
lots of economic burden so the mother may be
concerned with that. Our finding did not found any
significant relationship of the sex of the newborn to
these disorders. A researcher reported about higher
prevalence of depressive illness if the newborn was a
female in a study done in Goa,India 22. On the other
hand another study reported about no significant
relationship between maternal depression and her
preference for male or female baby17. This result can
be explained from cultural aspects of the north eastern
part of India. In this part of India boys and girls are
usually given equal weight.
Higher scores in the EPDS both in the anxiety and
depression group goes in line with previous findings23.
The sensitivity of 88.89% and specificity of 85.37%
of EPDS in detecting postpartum depression was
found in a regional language of India9. A researcher
commented that it can be regarded as a good tool for
assessing anxiety in postpartum period also23. In the
present study also mothers with anxiety disorders
scored significantly high than the non diseased group
in EPDS score. Hence we may consider it to be a good
tool to detect postpartum anxiety too. As the tool is
very easy to administer and can be given to even
illiterate persons with little aid, this can be utilized as
a screening tool for the new mothers so that the
conditions are recognized early. This will have long
term beneficial effect on the population. The newly
created accredited self help activists can be utilized
very effectively for this purpose.
In the HADS the scores for depression and anxiety
differed significantly. However no significant
correlation between the anxiety and depressive
symptoms was observed. In case of depression 1%
variance of symptomatologies can be explained by
anxiety and in anxiety, 20% of the variance of
symptomatologies can be explained by variation in the
depressive symptomatologies. It establishes that
anxiety and depression are separate categories of
disorders in postpartum period apart from psychosis.
Matthey et al voiced in similar manner and suggested
the term ‘postnatal mood disorders’ for the psychiatric
problems in the postpartum period24.
In the current study we looked into the problems of
anxiety and depression in postpartum period. Data in
relation to anxiety in postpartum period is scarce.
Again it gives an idea to integrate mental health
component in the Reproductive Child Health
Component of health policies prevailing in India. The
concept of ‘postpartum mood disorder’ is a timely one
at the time of revision of ICD and DSM. Our study
has the limitations of having smaller subjects for such a
common condition and there was no assessment done
in the ante partum period. A study that looks into
association of anxiety disorders both in antepartum and
postpartum period will be interesting.
REFERENCES
1. Clark LA. The anxiety and depressive disorders: descriptive
psychopathology and differential diagnosis. In Kendell PC,
Waston D.eds, Anxiety and Depression: Distinctive and
overlapping features. San Diego: Academic Press, 1989: 83-
129.
2. Kessler RC, Nelson CB, MC Gonagle KA etal. Co morbidity
of DS III R Major Depression Disorder in the general
population: results from the US National Co morbidity Study.
Br.J. Psychiatry 1996; 168:117-30.
3. Regier DA, Rae DS, Narrow WE etal. Prevalence of anxiety
disorders and their comorbidity with mood and addictive
disorders. Br J Psychiatric 1998; 173(suppl 34): 24-8
4. Altshuler LL, Hendrik V, Cohen LS. An Update on Mood
and Anxiety Disorders During Pregnancy and the Postpartum
Period. Prim Care Companion J Clin Psychiatry. 2000; 2(6):
217–222
5. Murray L. The impact of postnatal depression on infant
development. J Child Psychol Psychiat. 1992; 33(3):543-62
6. Coats AO, Schaefer CA, Alexander JL. Detection of
postpartum depression and anxiety in a large health paln. J
Beh Health Ser Res 2004 Apr- Jun 31(2): 117-33.
7. Cox JL, Holden JM, Sagovsky R. Detection of postnatal
depression. Development of the 10-item Edinburgh Postnatal
Depression Scale. Br J Psychiatry1987; 150:782-786
8. Murray L, Carothers AD. The validation of the Edinburgh
postnatal depression scale on a community sample. Br J
Psychiatry 1990;157: 288-90.
9. Kalita KN, Phookun HR, Das GC. A Clinical Study of
Postpartum Depression: Validation of the Edinburgh
Postnatal Depression Scale (Assamese version). Eastern J
Psychiatry 2008; 11: 14-18
10. Watson JP, Elliott SA, Rugg JA, etal. Psychiatric disorder in
pregnancy and the first postnatal year. Br J Psychiatry
1984;144:453-462
11. Yonkers KA, Ramins, Rush AJ, Navarrete CA, Carmody T,
March D, Heartwell SF, Levenon KJ: onset and persistence
of postpartum depression in an inner city maternal health
clinic system. Am J Psychiatry 2001; 158:1856-1863
12. Adewuya AO, Adekunle B, E, Lawal AM. Prevalence of
postnatal depression in Western Nigerian women : a
controlled study. Internat. J Psychiatry in Clin. Pract, 2005:
9(1): 60-64
13. Sood M, Sood AK. Depression in pregnancy and postpartum
period. Ind. J Psych. 2003; 45(1)
14. Stuart S, Couser G, Schilder K, O’Hara MW, Gorman L.
Postpartum anxiety and depression: onset and comorbidity
in a community sample. J Nerv Ment Dis 1998 Jul 186(7):
420-4
15. Adewuya AO, Afolabi OT. The course of anxiety and
depressive symptoms in Nigerian postpartum women. Arch
Women Mental Health 2005 Jan 17 (Epub ahead of print)
16. Kalita KN, Phookun HR, Das GC. Prevalence of anxiety
disorders in postpartum period: A clinical study. Eastern J
Psychiatry 2007; 10: 15-18.
17. Chandram M, Tharyan P, Mulijil J, Abraham S, Postpartum
depression in a cohort of women from a rural area of Tamil
Nadu, India. British J Psychiatry, 2002: 181: 499-504.
18. Johnstone SJ, Boyce PM, Hickey AR, Morris-Yatees AD,
Harris MG. Obstetric risk factors for postnatal depression
in urban and rural community samples. Aust NZ J
Psychiatry. 2001 Feb; 35(1):69-74.
19. Tambs K, Ebhard-Gram M,EskildA, Samwlsen SO,
Opjordsmoen S, Depression in postpartum and non
postpartum women : prevalence and risk factors. Acta
Psychiatr Scand, 2002; 106: 426-433
20. Forman DN, Videbech P, Hedegward M, Salving JD, Secher
NJ. Postpartum Depression: identification of women at risk.
British J obstet Gynecol,2000; 107:1210-1217.
21. Maes M, Bosmans E, Ombelet W. In the puerperium,
primiparae exhibit higher levels of anxiety and serum
peptidase activity and greater immune responses than
multiparae. J Clin Psychiatry. 2004 Jan; 65(1):71-6.
22. Patel V, Rodringe S, Desourza N: Gender, poverty and
postnatal depression: A study of mothers in Goa, India. Am
J Psychiatry, 2002; 159: 43-47
23. Ross LE, Gilbert Evans SE, Sellers EM, Rematch MK
Measurement issues in postpartum depression part 1:
anxiety as a feature of postpartum depression.Arch Women
Ment Health. 2003 Feb; 6(1):51-7.
24. Matthey S, Barnett B, Howie P, Kavanagh DJ. Diagnosing
postpartum depression in mothers and fathers: whatever
happened to anxiety? J Affect Disord. 2003 Apr;74(2):139-
47
 ORIGINAL ARTICLE
A comparative study of Thyroid Hormone levels
among the Normal Healthy Persons, Depression
and Schizophrenia

Senjam Gojendra Singh*, Sidhartha Debbarma*, N.Heramani Singh*,

Th. Bihari Singh*, R.K.Lenin*, K.Shantibala Devi**
*Department of Psychiatry, Regional Institute of Medical Sciences (RIMS), Manipur;
** J.N.Hospital, Porompat, Manipur.

ABSTRACT:
Background: Thyroid disorders can induce virtually any psychiatric symptom or syndrome, although no
consistent associations of specific syndromes and thyroid conditions are found. Abnormal thyroid hormone
levels are common in psychiatric disorders
Material & Method: T3, T4, TSH levels were measured in a sample of 90 (ninety) cases who attended
Department of Psychiatry, RIMS hospital. The sample consists 30 (thirty) cases each from three-group viz.,
Controls consisting of normal healthy persons, Schizophrenia, and Depression. Data was collected for a period
of 1 year from the subjects who were fulfilling the DSM IV TR diagnostic criteria of schizophrenia and
depression. All the study subjects were evaluated for socio demographic variables on semi structured Proforma.
Thereafter the laboratory assessments of T3, T4, TSH levels were conducted in the Dept. of Biochemistry,
RIMS.
Result: The blood level of T3 and T4 was seen highest among schizophrenic groups followed by control and
depressive groups. Highest level of TSH was noticed in the depressive groups followed by controls and
schizophrenia
Conclusion: This study shows that there is an abnormality in thyroid hormone levels in the psychiatric disorders
of depression and schizophrenia. In depression, T3 and T4 levels are lower but higher in case of schizophrenia.
TSH is higher in depression and lower in schizophrenia.

Key Words: Thyroid hormone depression and schizophrenia

INTRODUCTION
Thyroid disorders can induce virtually any psychiatric conditions are found. Hyperthyroidism is commonly
symptom or syndrome, although no consistent associated with fatigue, irritability, insomnia, anxiety,
associations of specific syndromes and thyroid
1234567890123456789012345678901212345678901234 restlessness, weight loss, and emotional lability;
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 marked impairment in concentration and memory may
1234567890123456789012345678901212345678901234
Correspondence: Dr. S.Gojendra Singh,
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
Dept. of Psychiatry, Regional Institute of
1234567890123456789012345678901212345678901234 also be evident. Such states can progress into delirium
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 or mania or they can be episodic. On occasion, a true
Medical Sciences (RIMS), Manipur.
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 psychosis develops, with paranoia as a particularly
E-mail: sgojendra@yahoo.co.in
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 common presenting feature. In some cases,
psychomotor retardation, apathy, and withdrawal are
the presenting features rather than agitation and
anxiety. Symptoms of mania have also been reported
following rapid normalization of thyroid status in
hypothyroid individuals and may co vary with thyroid
level in individuals with episodic endocrine
dysfunction. In general, behavioral abnormalities
resolve with normalization of thyroid function and
respond symptomatically to traditional
psychopharmacological regimens.
The psychiatric symptoms of chronic hypothyroidism
are generally well recognized. Classically, fatigue,
decreased libido, memory impairment, and irritability
are noted, but a true secondary psychotic disorder or
dementia-like state can also develop. Suicidal ideation
is common, and the lethality of actual attempts is
profound. In milder, subclinical states of
hypothyroidism, the absence of gross signs
accompanying endocrine dysfunction can result in its
being overlooked as a possible cause of a mental
disorder1.
Unlike in developed countries, endocrine and
metabolic disorders are predominantly caused by
environmental factors in India and perhaps in other
developing countries. Hence their prevalence is
several-fold higher in developing countries like India.
Kochupillai et al (2000) 2 have reported that thyroid
disorders are the most common endocrine and
metabolic disorders in India.
Nearly half of all cases of depression just like those
with adult onset diabetes, remain undetected for years
or inadequately controlled-both of which seen to lag
behind hypertension, in which early detection and
treatment have significantly reduced complications.
Akiskal HS et al (2005)3 reported that depressive
disorders are more common in women, more men than
women die of suicide.
Abnormal thyroid hormone levels are common in
psychiatric disorders. Subtle abnormality in thyroid
hormone levels without any clinical evidence of
hypothyroidism have been reported in depression
patients slightly higher levels of T4 with lower levels
of T3 and TSH4, decreased T4 along with lower levels
of T3 and TSH5 lower levels of T3 6 and lower T3 and
raised TSH and higher levels of T4 have been reported.
Approximately 5 to 10 percent of people evaluated
for depression have previously undetected thyroid
dysfunction, as reflected by an elevated basal TSH
level.
Hyperthyroxemia has been reported in variety of acute
psychiatric disorders eg. schizophrenia, functional
psychosis, major affective disorders, personality
disorders7.There was a high prevalence of (36.4%)
thyroid function test abnormalities in the study of 189
patients in a group of adult psychiatric in patients with
chronic schizophrenia8.
During the last 30 years a huge number of scientific
articles have appeared on the subject of relationships
between psychiatric disease and thyroid hormones.
These studies have demonstrated the presence of
numerous changes in the hypothalamo-pituitary-
thyroid (HPT) axis, mainly in patients with depression,
but also in patients with other psychiatric diseases9.
MATERIALS AND METHODS
The present case control study was conducted in the
Department of Psychiatry & Biochemistry, RIMS. The
data was collected in a period of 1 year period from
September 2007 to August 2008.
The study was based on a sample of 90 (ninety) cases
who attended Department of Psychiatry, RIMS
hospital either in the OPD or those who are admitted
in the ward. The sample consists of 30 (thirty) cases
each from three-group viz., Controls consisting of
normal healthy persons, Schizophrenia, and
Depression.
Inclusion criteria
Subjects of both sexes, age range between 18 to 65
years and cases of depression and schizophrenia
diagnosed according to DSM-IV TR10 diagnostic
criteria.
Exclusion criteria
Patients with any organic mental disorder, mental
retardation, epilepsy, substance use disorders or
subjects with concurrent medical illness.
Assessment tools
1. Semi-structured clinical and socio-
demographic data sheet
 2. DSM-IV-TR criteria for diagnosis of married (63.33%, 50% and 53.33%). Most of the
depression patients of depression and controls group have
3. DSM-IV-TR criteria for diagnosis of completed high school (66.66% & 73.33%) but only
schizophrenia 36.66% of schizophrenic groups have passed the exam.
4. Laboratory assessment of thyroid hormones The patients in all the groups were having income in
(T3, T4, TSH) the range of Rs 5,000-10,000/- per month.
Procedure
All the study subjects who fulfilled our inclusion Table-1. Age-wise distribution
criteria were assessed properly and the diagnosis of Age in years Group Total
depressive disorder and schizophrenia was made Control Schizophrenia Depression
according to DSM- IV TR diagnosic criteria. The 18 - 25 6 4 9 19
diagnosis of all the cases was reconfirmed again by 25 - 35 13 13 8 34
two consultant psychiatrists. An Informed consent was 35 - 45 9 8 8 25
taken from the patient as well from the informants 45 - 55 2 5 5 12
and the nature and purpose of the study was explained Total 30 30 30 90
to them. A Semi-structured clinical and socio- χ2=5.051; df=6; P=.537
demographic data sheet was administered to our study
groups. The laboratory assessment of thyroid Table-2.Religion-wise distribution
hormones (T3, T4, TSH) for all the participants were Religion Group Total
performed in Dept. of Biochemistry, RIMS. The T3, Control Schizophrenia Depression
T4, TSH level were compared for the depressive, Hindu 29 25 26 80
schizophrenia and matched control groups. Muslim 1 2 1 4
Analysis of data: Christian 0 3 3 6
The data was analyzed by using independent sample Total 30 30 30 90
t-test and person x2-test whenever found suitable and χ2=3.825; df=4; P=.43
necessary and interpretation was done accordingly. All
Table-3. Sex-wise distribution
tests were based on two-tailed and P < 0.05 and P <
0.01 were taken as significant and highly significant Sex Group Total
levels of significance respectively. Control Schizophrenia Depression
RESULT Male 17 18 11 46
The socio demographic characteristics of the subjects
Female 13 12 19 44
are summarized in table 1-6.
Majority of the patients in depression are belonged to Total 30 30 30 90
18-25 years age range whereas schizophrenia and χ2=3.824; df=2; P=.148
controls are in the 25-35 years of age group. In our
study population the average age of depression, Table-4. Marital status-wise distribution
schizophrenia and controls are 32.20 yrs, 33.96 yrs Marital status Group Total
and 32.70 yrs respectively. Females constitute a Control Schizophrenia Depression
majority (63.33%) in depressive group whereas in Unmarried 14 13 11 38
schizophrenia and control groups, males constituted Married 16 15 19 50
Divorce 0 1 0 1
majority of cases (60%) and (56.66%). Majority of
Widow 0 1 0 1
patients in depression, schizophrenia and controls were Total 30 30 30 90
Hindus (86.66%, 83.33% and (96.66%) and are
χ2=4.888; df=6; P=.558
Table-5. Literacy-wise distribution Table-7. Comparison of Mean±SD of parameters
of age, income, T3, T4, and TSH
Literacy status Group Total Parameters Control Schizophrenia Depression Total
Control Schizophrenia Depression Mean±SD Mean±SD Mean±SD Mean±SD
Illiterate 0 1 1 2 Age (yr.) 30.70±8.90 33.96±9.44 32.20±9.55 32.28±9.30
Under metric 4 15 9 28 Monthly Income(Rs.) 10533.33±5399.44 6633.33±3995.54 6433.33±4076.28 7866.66±4870.11
T3 1.033±.20 1.31±.62 .86±.86 1.07±.44
Intermediate 4 3 0 7
T4 5.86±1.29 7.91±3.18 5.40±1.30 6.39±2.37
Metric 6 9 10 25 TSH 4.57±2.06 1.62±1.74 4.58±1.60 3.59±2.27
Graduate 16 2 10 28
Total 30 30 30 90 est (7.91) followed by control (5.86) and
depression (5.40) respectively. On the contrary,
χ2=4.888; df=6; P=.558
depression group has highest mean TSH (4.58) and
Table-6 .Income-wise distribution next to highest is 4.57 for control group and lowest
1.62 pertains to schizophrenia (Table 7).
Income in group Group Total
Control Schizophrenia Depression Table 8. Comparison of Mean±SD of thyroid hormone
Below 5000 1 9 11 21 levels between control and schizophrenia
5000 - 10000 15 14 11 40 Parameter Control Schizophrenia t-value d.f. P
10000 - 15000 7 4 4 15 No. of cases Mean±SD No. of cases Mean±SD
15000 - 20000 2 3 4 9 T3 30 1.033±.20 30 1.31±.62 -2.288 58 .026
20000 - 25000 5 0 0 5 T4 30 5.86±1.29 30 7.91±3.18 -3.268 58 .002
Total 30 30 30 90
TSH 30 4.57±2.06 30 1.62±1.74 5.976 58 .000

χ2=20.517; df=8; P=.009 The comparison of thyroid hormone level between

The comparison of mean±SD of age, income, T3, T4, control and depression groups have shown that there
and TSH among the groups showed that the patients is a highly significant difference of T3 levels exist be-
belonged to schizophrenia groups are older (33.96 yr.) tween the groups whilst no significant difference is
than that of depression (32.20 yr.) and controls (30.70 observed for T4 as well as for TSH levels. These state-
yr.). The patients of controls group has higher monthly ments are supported by the corresponding P-values
income (average = Rs. 10533.33) than that of schizo- (Table 9).
phrenia (Rs. 6633.33), and depression (Rs. 6433.33). Table 9. Comparison of Mean±SD of thyroid
It was observed that schizophrenia group has higher hormone levels between control and depression
mean T3 (1.31) which is followed by control (1.03)
Parameter Control Depression t-value d.f. P
and lowest (0.86) belongs to depression group. A simi-
lar trend is witnessed in case of T4 too as schizophre- No. of cases Mean±SD No. of cases Mean±
nia group maintains highest (7.91) followed by con-
SD
trol (5.86) and depression (5.40) respectively. On the
contrary, depression group has highest mean TSH T3 30 1.033±.20 30 .86±.86 2.667 58 .010
(4.58) and next to highest is 4.57 for control group T4 30 5.86±1.29 30 5.40±1.30 1.380 58 .173
and lowest 1.62 pertains to schizophrenia (Table 7). TSH 30 4.57±2.06 30 4.58±1.60 -.018 58 .986
The comparison thyroid hormones between schizo- temperature, and are responsible for optimal
phrenia and depression groups have shown that there development and function of all body tissues. In
is a significant difference of T3, T4, and TSH between addition to its prime endocrine function, TRH has
them which is supported by the corresponding highly direct effects on neuronal excitability, behavior, and
significant P-values (shown in the table 10.). neurotransmitter regulation. During the last 30 years
Table 10. Comparison of Mean±SD of thyroid hormone a huge number of scientific articles have appeared on
levels between schizophrenia and depression the subject of relationships between psychiatric disease
and thyroid hormones. These studies have
Parameter Schizophrenia Depression t-value d.f. P
demonstrated the presence of numerous changes in
No. of cases Mean±SD No. of cases Mean± SD the hypothalamo-pituitary-thyroid (HPT) axis, mainly
T3 30 1.31±.62 30 .86±.86 3.556 58 .001 in patients with depression, but also in patients with
T4 30 7.91±3.18 30 5.40±1.30 4.004 58 .000 other psychiatric diseases9.
TSH 30 1.62±1.74 30 4.58±1.60 -6.851 58 .000
In the present study we found that majority of the
From the status wise distribution of thyroid hormone, subjects are from Hindu background perhaps it may
it is observed that there are 1, 3 and 5 no of cases of be due to the existence of the institute in the heart of
T3 level falls outside normal range for control, schizo- the Hindu dominated area and the sex-composition is
phrenia, and depression groups whereas in case of T4 almost similar in all the groups despite some variations.
level, 3 cases each in schizophrenia and depression Majority of our cases in depression group are females
falls outside the normal range while none exists in and this consistent with other studies for unipolar
control group. In case of TSH, 4 no of cases are no- depression. This gender difference begins in early
ticed outside the normal range in the controls whilst 2 adulthood, is most pronounced in people between the
cases in the schizophrenia group and only single case ages of 30 and 45 years11. Derik Herman et al 2004 12
was found in the depressive groups. However, each noticed that patients with thyroid disease were more
test value suggests that the variation of outside nor- likely to be female than male (82% vs 54%). The
mal cases among the groups is not significant statisti- majority of patients belong to lower group of income.
cally which is true for all thyroid hormone levels. This findings are consistent with that of Zoltan Rihmer
et al (2005) 11 and Robert W. Buchanan et al
Table 11. Thyroid hormone status-wise distribution (2005)13who also found that the lower socio economic
status and lower income as well as a rate of
Parameters Type of groups 2 d.f. P unemployment are common in schizophrenia and
Control Schizophrenia Depression
depression, irrespective of their thyroid profile.
StatusT3 Within normal 29 27 25 2.963 2 .227
Outside normal 1 3 5 In our study, schizophrenia group has higher T3 level
StatusT4 Within normal 30 27 27 3.214 2 . 200 which is followed by control and lowest among
Outside normal 0 3 3 depressions. A similar trend is witnessed in case of T4
Status TSH Within normal 26 28 29 .338 level as schizophrenia group maintain highest followed
Outside normal 4 2 1 by control and depression respectively. This finding is
2.169 2
consisted with other findings of Parshad O et al (1989)
Discussion 14
, Turianitsa I.M et al (1991)15, Smirnova LK et al
Thyroid hormones are involved in the regulation of (1993)16 who also reported that T4 & T3 is high in
nearly every organ system, particularly those integral schizophrenia. We also found that in depression, there
to the metabolism of food and the regulation of is lower in level of T3 & T4 which is consistent with
findings from other studies4, 5, 17, 18, 19, 20.
In the present study we have seen that in depressive
groups the level of TSH is highest followed by control
and lowest levels case of schizophrenia. This finding
is consistent with other finding that TSH is high in
depression by Wahby et al (1989) 19 and Roca RP et al,
(1990)21. We also noted that TSH level is decreased in
schizophrenia which also supported by other studies
like Parshad et al, (1988)14. The difference of means
of thyroid hormones level between control and
schizophrenia also shows that normal healthy person
has certainly lower levels of T3 and T4 than that of
those who are having schizophrenia but TSH level is
lower in schizophrenia than control group. Similar
finding has also been reported by Parshad et al, (1988)
14
. case of T4 levels. However, each test values suggest
The comparison of thyroid hormone levels between
control and depression shows that there is a highly
significant difference of T3 levels between two groups
(Table-9). The study did not report statistically any
significant difference of T4 as well as for TSH level
between the groups. This findings is supported by
Baumgartner et al, (1992) 4 and Bauer et al, (1994)5
studies.
The comparison of mean of all thyroid hormone levels
between schizophrenia and depression groups also do
not show any significant difference of T3, T4 & TSH
between the groups. In the group of schizophrenia
the levels of T3 and T4 is higher than depression group
which is supported by other studies by Sim K et al,
(2002)8 and Baumgartner A. et al, (2000)22. The
present study found that depressive groups have low
levels of T3 and T4 which is well supported by Gambi
F et al, (2005) 23, Kierkegaard C et al, (1991) 9 and
Baumgartner A et al, (1992)4. Our finding of high level
of TSH levels in depressive group is also reported by
Hickle I et al, (1996)24 and decreased in schizophrenia
is also found by Othman SS et al, (1995)25.
In this study, it is observed that the schizophrenia group
has 3 cases (10%) outside the normal range for thyroid
hormone for T3, 3 cases of T4 (10%) outside the normal
range and another 2 cases for TSH (6.66%) outside
the normal range. This finding is consistent with other
findings observed by Kelly DL et al (2005)26 who
reported that in schizophrenia the percentages of
randomized patients with abnormal values were 18%
for T3, 13% TSH and 9% for T4. In case of depression
with findings was 5 cases (16.66%) were found
outside the normal range for T3, 3 cases (10%) for T4
and 1 case in the TSH level (3.33%). Herman et al
(2004)12 observed the alteration of TSH in mood
disorders; TSH was elevated in 5.6%. There was no
literature available regarding the percentage of
abnormality in T3 & T4 levels. In the group of control,
one case (3.33%) falls outside the range for T3 level,
4 cases (13.33%) for T4 and no cases observed in the
that the variations of outside normal cases among the
groups are not significant statistically which is true
for all thyroid hormone levels.
This study shows that there is an abnormality in thyroid
hormone levels in the psychiatric disorders of
depression and schizophrenia. In depression, T3 and
T4 levels are lower but higher in levels in the case of
schizophrenia. TSH it is higher level in depression
patients and lowers in level in schizophrenia patients.
Therefore, thyroid dysfunction is common in
psychiatric disorders. Early detection of thyroid
abnormality should be considered for appropriate
management of psychiatric disorders especially in
depression and schizophrenia.
REFERENCES
1. Buchanan, R.W., & Carpenter, Jr. W.T.(2005). Concept of
Schizophrenia: Kaplan & Sadock’s Comprehensive
Textbook of Psychiatry. Sadock BJ and Sadock VA: Lippin
Cott Williams & Wilkins, Philadelphia, 8th Edn. I, 1329-
1331.
2. N, Kochupillai.(2000).Clinical endocrinology in India:
current science. 79; (8): 1061-1067.
3. Akiskal ,H.,S.(2005). Mood Disorders, Historical
Introduction and Conceptual Overview: Kaplan & Sadock’s
comprehensive textbook of Psychiatry, Sadock BJ and
Sadock VA. LippinCott Williams & Wilkins, Philadelphia,
8th Edn. I, 1559-1560.
4. Baumgartner, A., Barros, C.A., & Meinhald, A.(1992).
Thyroid hormones and depressive illness, implication for
 clinical and basic research. Acta Med. Austric. 19;
(Suppl.1): 98-102.
5. Bauer, M., Priebe, S.K., Utren, I., Graft, K.J.L., &
Baumgartner, A.(1994). Psychological and endocrine
abnormalities in refugee from East Germany: Part-1
prolonged stress, psychopathology and hypothalamic –
pituitary thyroid axis activity, Psychiatry research. 51;
(1): 61-73.
6. Bottai, T., Levy, C., Azorin, J.M., Grignon, S., Valli,M.
G., & Tissot, R.(1991). Plasma MHPG, peripheral non-
adrenergic marker and hormonal plasma levels of cortisol,
T3, T4, TSH in depressive syndrome. Encephale. 17;
(3): 203-211.
7. Spratt, D.I., Pont,. A, Miller, M.B., Mcdougall, Bayer.
MF., & Me, Laughlin.WT.( 1982). Hyperthyroxinemia
in patients with acute psychiatric disorders. American
Journal of Medicine. 73; 41-48.
8. Sim, K., Chong, S.A., Chan, Y.H., & Lum, W.M.( 2002).
Thyroid dysfunction in chronic schizophrenia within a
state psychiatric hospital. Ann Acad Med Singapore. 31;
(5): 641-644.
9. Carsten, Kirkegaard., & Jens, Faber. (1998). The role of
thyroid hormones in depression. European journal of
endocrinology. 138: 1-9.
10. American Psychiatric Association. Diagnostic and
Statistical Manual of Mental Disorders DSM-IV-TR
Fourth Edition (Text Revision).
11. Zoltan, Rihmer., & Jules, Angst.( 2005). Mood disorders;
epidemiology Kaplan and Sadock’s comprehensive
textbook of psychiatry, Sadock and Sadock: Lippincott
Williams and Wilkins, Philadelphia, 8th Edn. I, 1575-
1580, 2005.
12. Derik, Herman., Walter, Hewer., & Florian,
Lederbagen.(2004). Testing the association between
thyroid dysfunction and psychiatric diagnostic group in
an iodinic-deficient area. J Psychiatry Neurosci. 29;(6):
444-449.
13. Buchanan, R.W., & Carpenter, Jr. WT. Concept of
Schizophrenia: (2005). Kaplan & Sadock’s
Comprehensive Textbook of Psychiatry, Sadock BJ and
Sadock VA: Lippin Cott Williams & Wilkins,
Philadelphia, 8th Edn. I, 1329-1331.
14. Parshad, O., & Uppal, A. (1989). Thyroid-gonad
relationship in chronic schizophrenia. West Indian M ed
J. 38; (2): 83-87.
15. Turianitsa, I.M., Lavka, A., Shanich, M., Margitich, V.M.,
& Razhov, K.F.(1991). Status of the thyroid gland in
patient with schizophrenia. Zh Nevropatol Psikhiatr Im
SS Korsakova. 91;(1): 122-123.
16. Smirnova, L.K., & Zorenko, T.I.(1993). (1993).Thyroid
functional activity in schizophrenic patients with
aggressive sexual behavior. Zh Nevropatol Psikhiatr IM
SS Korsakova. 93;(4): 68-70.
17. Nakamura, T., & Nomura, J.(1992). Comparison of
thyroid function between responders and non-responders
to thyroid hormone supplementation in depression.
Japanese Journal of Psychiatric Neurology. 46; (4): 305-
309.
18. Bottai, T., Levy, C., Azorin, J.M., Grignon, S., Valli,
M.G., & Tissot, R.(1991). Plasma MHPG, peripheral
non-adrenergic marker and hormonal plasma levels of
cortisol, T3, T4, TSH in depressive syndrome. Encephale.
17; (3): 203-211.
19. Wahby, V., Ibrahim, G., Friendenthal, S., Griller, E.,
Kosten, T., & Merson, J. (1989).Serum concentrations
of circulating thyroid hormones in a group of depressed
men. Neuropsychobiology. 22;(1):8-10.
20. Tappy, L., Randin, J.P., Schwed, P., Wertheimer, J.,
Lemarchand, B., & Erand, T.(1987). Prevalence of thyroid
disorders in psychogeriatric in patients: A possible
relationship of hypothyroidism with neurotic depression
but not with dementia. Journal of Geriatric Society. 36;(6):
526-531.
21. Roca, R.P., Blackman, M.R., Ackerley, M.B., Harman,
S.M., & Gregerman, R.I.(1990). Thyroid hormone
elevations during acute psychiatric illness: relationship
to severity and distinction from hyperthyroidism. Endocr
Res. 16;(4): 415-447.
22. Baumgartner, A., Pietzcker, A. & Gaebel, W.(2000).The
hypothalamic pituitary thyroid axis in patients with
Schizophrenia. Schizophr Res. 44;(3): 233-243.
23. Gambi, F., De,Berardis. D., Sepede, G., Campanella, D.,
Galliani, N., Carano, A., La Rovere, L., Salini G, Penna
L, & Ferro, F.,M.(2005) Effect of mirtazepine on thyroid
hormones in adult patients with major depression. Int J
Immunopathol Pharmacol, 18;(4): 737-744.
24. Hicklel, Bennett, B., Mitchell, P., Wilhelm, K., & Orlay,
W.(1996). Clinical and subclinical hypothyroidism in
patients with chronic and treatment-resistant depression.
Australian and New Zealand Journal of Physiology.
30;246-252.
25. Othman, S.S., Abdul, K.K., Hassan, J., Hong, G.K., Singh,
B.B., & Raman, N. (1994). High prevalence of thyroid
function test abnormalities in chronic schizophrenia. Aust
NZJ psychiatry. 28 ;(4): 620-624.
26. Kelly, D.L., & Conley, P.R. (2005). Thyroid function in
treatment-resistant schizophrenia patients treated with
quetiapine, resperidone or fluphenazine. J Clin
Psychiatry.66 ;( 1): 80-84.
 ORIGINAL ARTICLE

An explorative study on Biomedical Waste

Management in a Psychiatric Hospital of India
J.Hazarika, A C Sarmah*, M.Das**.
Department of Microbiology,* Department of Pathology,
** Department of Biochemistry, LGB Regional Institute of Mental Health, Tezpur, Assam.

ABSTRACT
Background: In accordance with Bio-Medical Waste(management and handling)Rules,1998,it is the duty of
every ‘‘occupier” i.e. a person who has the control over the institution and or its premises, to take all steps to
ensure that waste generated is handled without any adverse effect to human health and environment. To improve
hospital waste management, it is important to begin by surveying the facility of current hospital waste practices.
A waste survey should therefore be undertaken about the information of the waste planning process.
Methods: A waste survey was undertaken about the information of the waste planning process; as to improve
hospital waste management, it is important to begin by surveying the facility of current hospital waste practices.
This survey should provide information on types and quantity of wastes, which are arising at each point of
production, and methods of storage, handling, treatment and disposal.
Results: In our survey it is seen that, management, handling and treatment of Biomedical Waste are done as per
Bio-Medical Waste Rules, 1998.
Conclusion: After analyzing the study it was felt that the healthcare waste management should go beyond data
compilation, enforcement of regulations and acquisition of better equipment. It should be supported through
appropriate education, training and the commitment of the healthcare staff, management and healthcare managers
within an effective policy and legislative framework.
Key words: Biomedical waste management (BMW), Psychiatric Hospital

INTRODUCTION:
The waste produced in the course of health care of 1998 but also associated with many health and
activities caries a higher potential for infection and environment hazards, if not managed properly.
injury than any other type of waste1.The proper Bio- However, very few health institutions are implementing
Medical Waste Management in the hospital is not only them properly because of lack of awareness and
the statuary (legal) obligation because of the Bio- difficulties at the institutional as well as operational
Medical Waste (Management and Handling) Rules2 level such as lack of resources, including personnel,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 space and equipment, lack of technical knowledge for
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence: Dr J Hazarika, scientific waste disposal. In addition, waste disposal is
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Department of Microbiology,
12345678901234567890123456789012123456789012345 monitored by Pollution Control Board and
12345678901234567890123456789012123456789012345
LGB Regional Institute of Mental Health, Assam-
12345678901234567890123456789012123456789012345 Environmental Ministry, which has no linkage with the
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
784001,E-Mail:drjhazarika@gmail.com
12345678901234567890123456789012123456789012345 Health Department3. Bio-Medical Waste means ‘‘any
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 solid, fluid or liquid waste, including its container and
any intermediate product, which is generated during
its diagnosis, treatment or immunization of human
beings or animals, in research pertaining thereto, or in
the production or testing of biological and the animal
waste from slaughter houses or any other like
establishments”. Hospital waste refers to all waste,
biologic or non biologic that is discarded and not
intended for further use. Medical waste is a subset of
hospital waste; it refers to the material generated as a
result of diagnosis, treatment or immunization of
patients and associated biomedical
research .Biomedical waste(BMW) is generated in
4
hospitals, research institutions, health care teaching
institutes, clinics, laboratories, blood banks, animal
houses and veterinary institutes5.According to WHO
report, 85% of hospital waste is non hazardous
waste6.The average quantity of hospital solid waste
produced in India ranges from 1.5 to 2.2kg/day/bed7.
Handling, segregation, mutilation, disinfection,
storage, transportation and final disposal are vital steps
for safe and scientific management of BMW in any
establishment8.It is a collective initiative and shared
responsibility of all viz. doctors, nurses, paramedical
staff, cleaning staff, all employees and administrators.
All personnel should be made aware and trained
regarding biomedical waste. To improve hospital waste
management, it is important to begin by surveying the
facility of current hospital waste practices. A waste
survey is therefore being undertaken about the
information of the waste planning process. The
purpose of the study is to review the current status of
Waste Management in the Hospital on types and
quantity of wastes, which are arising at each point of
production and methods of storage, handling,
treatment and disposal; and provide recommendation
to aide in achieving the optimal Hospital Waste
Management.
MATERIALS AND METHOD
Present study was carried out in a Psychiatric
Hospital in the year of 2009.Methods of storage and
segregation at ward/department level, internal
transportation, kerb site storage, external
transportation and on site final disposal/offsite disposal
were studied by direct observation and infrastructure
for the same were studied. Types of waste generated
and quantity of waste are estimated by discussion,
interviews and by physical checks. The average values
are presented in the prescribed from. The study was
carried out as a plan of development; leading to
comprehensive, safe and eco-friendly management &
disposal. Each step or part of the study led to another
step in seriatim ultimately culminating in a
comprehensive system of waste management.
RESULTS
The practical operational aspects regarding
management of Bio-Medical Wastes at a Psychiatric
Hospital has been described under each step starting
with the generation and ending with final disposal of
wastes. Since the studies were done in a Psychiatric
Hospital, so the waste generated in the Hospital is
very less in compared to other type of Hospitals.
Pathology, Microbiology and Biochemistry
departments generate sizable amount of biomedical
waste. Studies carried out have indicated that about
1.1kg of solid wastes generated per day which gives
an idea about the volume of waste generated on day
to day basis. Hospital Waste management committee
looks after the overall activity of Bio-medical waste
management process.
(A)Generation of Waste: About 85% of hospital wastes
are non-hazardous, whereas 10% are infectious and
5% are non-infectious but they are included in
hazardous wastes. Non-hazardous wastes generated
from office, kitchen, Pantries in wards etc. And
hazardous wastes generated from Laboratories, Wards,
Treatment Room, Nursing station etc.
(B)Segregation of Waste: Segregation or the
separation of different types(categories) of waste by
sorting at the point of segregation has been considered
as the ‘‘key” for the entire process as it allows special
attention to be given to the relatively small quantities
of infections and hazardous waste, thus reducing the
risks and cost of waste management. Conversely small
errors at this stage can create lot of subsequent
problems. Category No.1 (Human anatomical waste) in this study. Segregation of waste is done properly as
and Category No.2 (animal waste) waste are not found per BMW rules 1998 as mentioned in schedule I (Table 1).
Table 1(Schedule I)
CATEGORIES OF BIO-MEDICAL WASTE
Option Waste Category Treatment & Disposal
Category Human Anatomical Waste Incineration @/deep
No. I burial*
(human tissues, organs, body parts)
Category Animal Waste Incineration @ / deep
No. 2 burial*
(animal tissues, organs, body parts carcasses,
bleeding parts, fluid, blood and experimental animals
used in research, waste generated

by veterinary hospitals colleges, discharge from

hospitals, animal)
Category Microbiology & Biotechnology Waste local autoclaving / micro-
No 3 waving / incineration@
(wastes from laboratory cultures, stocks or specimens
of micro-organisms live or attenuated vaccines,
human and animal cell culture used in research and
infectious agents from research and industrial
laboratories, wastes from production of biologicals,
toxins, dishes and devices used for transfer of
cultures)
Category Waste sharps disinfection (chemical
No 4 treatment @ 01/auto
(needles, syringes, scalpels, blades, glass, etc. that claving / micro- waving
may cause puncture and cuts. This includes both used and mutilation/
and unused sharps) shredding"
Category Discarded Medicines and Cytotoxic drugs Incineration @/destruct
No 5 ion and drugs disposal in
(wastes comprising of outdated, contaminated and secured landfills drugs
discarded medicines) disposal in secured

Category Solid Waste Incineration @

No 6 autoclaving / micro-
(Items contaminated with blood, and body fluids waving
including cotton dressings, soiled plaster casts, lines,
beddings, other material

contaminated with blood)

Category Solid Waste disinfection by chemical
No. 7
(wastes generated from disposable items other than treatment @ @
the waste shaprs such as tubings, catheters, autoclaving/micro-
intravenous sets etc). waving and mutilation/

@@ Chemicals treatment using at least 1%
hypochlorite solution or any other equivalent
chemical reagent. It must be ensured that
chemical treatment ensures disinfection.
## Multilation/shredding must be such so as to prevent
unauthorised reuse.
@ There will be no chemical pretreatment before
incineration. Chlorinated plastics shall not be
incinerated.
• Deep burial shall be an option available only in
towns with population less than five lakhs and
in rural areas.
+ Options given above are based on available
technologies. Occupier/operator wishing to use other
State-of-the-art technologies shall approach the
Central Pollution Control Board to get the standards
laid down to enable the prescribed authority to consider
grant of authorization. (Schedule I; adapted from Bio-
Medical Waste (Management and Handling) Rules,
1998)
(C)Collection of Waste: Collection of Bio-medical Laboratories, Pharmacy and Nursing Station. The pro-
Wastes is done as per biomedical waste (Management cess of collection is documented in a register, the
and handling) rules in colour coded plastic bags/con- coloured polythene bags are replaced and the garbage
tainer. The container for collection is strategically lo- bin is cleaned with disinfectant regularly. The quan-
cated at all points of waste generated site like Indoor tum of waste produced in a period of one year in dif-
Patient Department, Outdoor Patient Department, ferent sections of the Hospital is detailed in Table: 2.
Table 2:Category-wise quantity of waste treated along with treatment facility in the year 2009.
Colour Coding Category wise Waste from Quantity of Treatment facility
Indoor/outdoor patient department, waste treated
Laboratory, Pharmacy & Yearly basis
anaesthesia department.

Cat. 1, Cat. 2, Nil

Incineration
Yellow Cat. 3, 4 8.4kg/Year
Cat. 6

Red Cat. 3, Cat. 6, Cat.7. 245.7 kg/ Chemical

Year Treatment

Blue/White Cat. 4, Cat. 7. 98.6 kg/ Year Chemical Treatment

translucent and
destruction/shredding

Black Cat. 5 5 kg/ Year Disposal in secured

Cat. 9 landfill
Cat. 10. (solid) 0.6 kg/ Year

-- Cat. 8, Liquid waste 38520 liters/ chemical treatment

Cat. 10, Liquid waste Year and discharge into
drains

(D)Storage and transport of Waste: Wastes are kept
at the site of generation and transit to the point of
treatment and final disposal. Usually wastes are finally
disposed within 12-24 hours in the Hospital. The
transport is done though covered trolleys from
different area of waste collected site and deposited in
area near the incinerator site. Personal protective
equipment and accessories are provided to the workers
according to the requirement. The general waste is
deposited at the municipal dumps which are
transported in the vehicle by Municipality authorities.
(E)Treatment and Disposal of Hospital Waste: Most
of the waste (about 80%-90%) generated in this
Psychiatric Hospital are general waste which is similar
to the waste generated in house and offices. These
waste is non toxic and non infectious, and comprise
of paper, leftover food, peels of fruits, disposable and
paper container, card board boxes, outer cover or
wrapping of disposable items like syringes etc. These
general wastes are put into green coloured polythene
bags are deposited at the municipal dump. It is
subsequently collected by the local municipal
authorities for disposal in every day. The waste
collected in yellow coloured bags is transported to
the site of incineration. The incinerator is maintained
by the Engineering services department and is manned
by supervisor and workers. The ash produced by
incineration is sent for secured land filling. Regular
monitoring of the process is carried out by the
engineers as per Pollution Control Board norms and
feedback provide to officer in charge. The waste
collected in blue bags is transported to the site of
autoclaving and shredding for treatment. Autoclaving
and Chemical treatment are done for Category3,
Category 6 and Category7 waste. Secured sanitary
landfill is considered for medical for medical wastes
which do not require incineration or disinfection.
Category 5, Category 9 and Category 10(solid) wastes
are disposed in secured landfill. Liquid and chemical
wastes are disinfected and then discharged into drains/
sewers where it is taken care of by the principle of
dilution and dispersal. Needles and syringes are
destroyed with the help of needle destroyer and syringe
cutters at the point of generation. Sharps are kept in
puncture resistant containers to avoid injuries and
infection to those handling them. After disinfection and
mutilation of sharps they are disposed in secured
landfills.
DISCUSSION
The current waste management practice has
been observed in one of the Psychiatry Hospital of
India. After analyzing the study it is felt that the
healthcare waste management should go beyond data
compilation, enforcement of regulations and
acquisition of better equipment. It should be supported
through appropriate education, training and the
commitment of the healthcare staff, management and
healthcare managers within an effective policy and
legislative framework. Hospital having defunct/
defective incinerators should be made to utilize central
incineration facility; as efforts of Govt. are towards
reducing the number of incinerators in cities to prevent
rise in air pollution. Since the cost of setting waste
management facility is too high, the only way is to
have a common disposal facility. There are many private
waste management facilities being set up now in most
cities and entered into an agreement with the private
company. Incinerators, which do not confirm to the
design and emission norms as per rules, must be
modified and air pollution control system may be
retrofitted to minimize the emission level. No
incinerator shall be allowed to operate unless equipped
with Air Pollution Control Device(APCD).Installation
of individual incineration facility by a healthcare unit
shall be discouraged as far as possible but approval
may be granted only in certain inevitable situations
where no other option available. The liquid waste
management needs more attention and effluent
treatment facilities need to be viewed seriously.
General awareness among the hospital staff regarding
Bio-medical waste is lacking. Regular training and
workshops should therefore be conducted. Recycling
of disinfected waste needs to be emphasized. Hospital
Waste Management committee formulate the details
plan of action in regard to segregation, collection,
storage and transport of waste from all patient care
areas as well as other activity in relation to Hospital
Waste. A policy need to be formulated based on reduce,
recover, reuse and dispose.
In conclusion, to improve the waste
management system, the medical staff should be more
involved in waste management system and importance
of this subject should be emphasized on everyone
including public, patients and hospital staff. Media can
also generate awareness amongst the citizens about
various types of waste and their safe disposal and
treatment.
REFERENCES
1. Park K.Hospital Waste Mangement.Park’s Textbook of Preventive
and Social Medicine.M/s Banarasdias Bhanot Publication,
Jabalpur.20th Edition, 2009:694-699.
2. Bio-medical Waste (Management and Handling) Rules,
1998.Ministry of Environment and Forests Notification,New
Delhi.
3. Bio-medical waste management at Community Health Centre
August 12, 2007.Available at http;//cbhihsprod.nic.in/
searnum.asp?PNum=164.
4. Rutala WA,Weber DJ.Disinfection,Sterlization and control of
hospital Waste.In:Mandell,Douglas and Bennett’s Principle and
Practice of Infectious diseases.Elsevier Churchill Livingstone
Publication.6th Edition,2005;3371-47.
5. Sharma M: Hosital waste management and its monitoring. Jaypee
brothers Medical Publication.1st Edition, 2002.
6. Pruss A,Cirouit E and Rushbrook P.Safe management of waste
from healthcare activities,WHO;1999.
10. Kumar M:Hospital Waste Disposal,a planning consideration,
National seminar on hospital architecture,planning and
enginerring,1995;IV:40-450.
11. Acharya DB,Sing Meeta.The book of Hospital Waste
Mnagement.Minerva Press,New Delhi2000;15,47.
ORIGINAL ARTICLE

Efficacy of Psychosocial Intervention

on Patients with Schizophrenia
Shweta*, K. S. Senger **, A. R. Singh**, M. Dutta*
*Department of Clinical Psychology, LGBRIMH, Tezpur, Assam.
**Department of Clinical Psychology, RINPAS, Ranchi.

ABSTRACT

Aim: To study the efficacy of psychosocial intervention on patients with schizophrenia. Schizophrenia is a
disorder that affects about 1% of the human population with a relatively uniform distribution throughout the
world. Pharmacotherapy alone is being considered critical for the successful management of patients with more
severe positive symptoms of schizophrenia. The integration and coordination of psychosocial treatment including
pharmacotherapy and rehabilitative services is widely advocated. The present study was designed to examine
the relationship between the administration of antipsychotic medication and responsiveness to psychotherapeutic
interventions.
Methodology: The study was based on experimental design. The sample of 20 (experimental-10& control- 10)
was selected on the basis of purposive sampling technique. Fisher’s exact test and t test were used to analyze
the data.
Results: The findings suggest that the marked differences have been found in both groups in all the areas i.e.
personal, social, occupational, physical, and general.
Conclusion: In the absence of psychosocial measures alone or with pharmacotherapy the target to return to the
premorbid level of functioning or community rehabilitation cannot be attained.

Key Words: Psychosocial intervention, Pharmacotherapy, Schizophrenia.

INTRODUCTION
The schizophrenic disorder is characterized in general
by fundamental and characteristic distortion of
thinking and perception and by inappropriate or
blunted affect1. Schizophrenic patients with the due
course of time manifest a number of behavioral and
cognitive changes which cause the impairment in the
functioning of the individual’s daily routine life
resulting in occupational efficacy, interpersonal deficits
and ability to take up the responsibility per se. The
schizophrenic individuals often exhibit a wide range
of impairments in effective functioning, and there is
frequently no single behavioral problem that can be
isolated as the sole target for intervention. Some
schizophrenic patients are highly deficient in the skills
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
Correspondences : Sweta
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
Dept. of Chmical Psychology
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
LGBRIMH, Tezpur
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
E. Mail: shweta727@ymail.com
123456789012345678901234567890121234567890123456
needed to solve everyday living problems effectively.
Executive function is the most impaired domain of cognition
in schizophrenia, which may explain the many functional
deficits of these patients .Whereas, moderate impairment
in distractibility, delayed recall, visuo-motor skills,
immediate memory span and working memory and mild
impairment in perceptual skill, delayed recognition,
confrontation naming and verbal and full scale IQ also
characterize the illness among schizophrenic patients.
Decreased motivation, self esteem, social interest and
diminished emotional range and experience of emotions
are also common. Disorganization of thought process and
behavioral mood symptoms along with impairment in
social functions are also generally present in schizophrenic
patients.
Despite the advent of number of claimed miraculous
antipsychotic, the expected results could not be achieved
as the antipsychotics mainly focused on neurotransmitters
which possibly produce such problems to certain extent.
Pharmacotherapy alone is being considered critical for
the successful management of patients with more severe
positive symptoms of schizophrenia. According to this
view, control of symptoms is considered to be requisite
for participation in psychotherapeutic and rehabilitative
measures. There is extensive evidence that social skills
training and family therapy are effective interventions
in rehabilitation.
A number of studies provide strong support for the
effectiveness of social skill training in improving the
outcome for patients with schizophrenia who are living
in hospital as well in the community. Twamley et al
(2003)2 and Dickerson et al (2005)3 has stated that a
variety of psychosocial intervention , such as social
skill training , vocational rehabilitation , psychotherapy
and token economy all have effective components that
hold promise for improving cognitive performance,
symptoms and everyday functioning. To see the effects
of cognitive behavioral therapy on work outcomes in
vocational rehabilitation for participants with
schizophrenia spectrum disorders Lysakera et. al.
(2008)4 conducted a study and results suggested a
connection between cognitive-behavioral interventions
and higher levels of work performance in people with
schizophrenia.
Another study attempted by Horanab et al (2009)5
on Social cognitive skills training in stabilized
outpatient schizophrenics and their results support
the efficacy of a social cognitive intervention for
community-dwelling outpatients and encourage
further development of this treatment approach to
achieve broader improvements in social cognition and
generalization of treatment gains. Wykesab et al.
(2009)6 suggested that younger people benefited more
from cognitive remediation in two of the three
cognitive domains tested. Further they concluded
younger group showed improvements in the context
of CRT but the older group did not. When older people
did show a cognitive advantage in memory following
therapy this cognitive improvement benefited social
behaviour.
The impact of one specific psychosocial intervention
alone on the lives of patient with schizophrenia is
difficult to analyze, partly because psychosocial
therapies are so broad and diverse in their scope. When
outcome of all therapies (psychosocial intervention &
pharmacotherapy) are clustered together, there are
encouraging results. So the present is design to see the
efficacy of psychosocial intervention on patients with
schizophrenia .The objectives were to identify the level
of severity of the symptoms, impairment of different level
of functioning and to see the difference on the recovery
of the schizophrenic patients by using the different
modalities of treatment such as pharmacotherapy with
psychosocial intervention and vice versa. The hypothesis
of the study is that there will be no difference in group A
(psychosocial intervention with pharmacotherapy) and
group B (only on pharmacotherapy).
Methodology
Present study consisting of 20 inpatients males age
range of between 20 -30,diagnosed of schizophrenic
disorder and the duration of illness not more than 1 ½
were purposively selected for the study from different
wards of RINPAS Ranchi.
All the subjects selected for the study were interviewed
and then assessed with the help of semi-structured
clinical data sheet and socio-demographic details. Brief
Psychiatric Rating Scale was administered
subsequently to rate the severity of clinical symptoms.
However, the patients falling in severe level were
excluded. The patients were screened on Brief
Psychiatric Rating Scale and were assessed with
Disability Assessment Scale7 (Here in this study the
concept of disability has been taken as impairment
occurred by due course of schizophrenic illness). It
was administered to know the severity level of
disability of each subject in all the areas viz. Personal,
Social, Occupational, Physical and General.
After completion of assessment sample was divided
into two groups on random basis namely group A
(psychosocial intervention with pharmacotherapy),
which is experimental group and group B (only on
pharmacotherapy) is control group. The group A was
subjected to psychosocial intervention in addition to
pharmacotherapy whereas the group B remained on
pharmacotherapy without any specific psychosocial
intervention. Both groups were kept on same drug
composition and were again assessed after the
completion of intervention package (after six months)
by same disability assessment scale. The group selected
for psychosocial intervention was subjected to
following target behaviour and therapeutic package. between 20-25 years and duration of illness is below
Intervention target focuses to motivating subject’s one year. In most of the cases (13%) there is improvement
participation in therapeutic program, to enhance their in the progress of the illness and there is no history of past admission
personal hygiene, organize daily routine for in majority of the cases (14%).
enhancement of interpersonal communication and to
join occupational therapy unit regularly. Therapeutic
package includes supportive Table: 1. Comparative assessment of disability between group A & B of pre and
psychotherapy, behaviour therapy, post intervention
cognitive therapy and group
Group A Group B
therapy.
The whole therapeutic package After the
was scheduled in several VariablesN=20 Pre Post P completion of
sessions, initially five sessions intervention intervention value Initial stage the study P
was given on regular daily basis assessment assessment of the study (6 months) value
and fifteen sessions were given Mean (SD) Mean (SD) Mean (SD) Mean (SD)
on alternatively. Last ten Personal 13.7 (3.4) 5.7 (1.6) 0.0001* 13.8 (3.8) 10.4 (2.9) 0.0373*
sessions were twice in a week Social
14.5 (4.7) 7.0 (1.8) 0.0002* 13.9 (4.1) 12.2 (3.6) 0.3378
basis after the discharges of
patient were advised to Occupational 11.7 (2.9) 6.4 (1.3) 0.0001* 9.7 (2.6) 9.0 (2.4) 0.5394
report the therapist whenever Physical 5.8 (2.1) 3.5 (1.6) 0.0130* 4.4 (2.1) 0.0118*
they come on follow-up. General 6.6 (2.4) 3.1 (1.2) 0.0006* 6.5 (2.9) 0.5638
Response of psychosocial
* P<0.05
intervention was reported satisfactory on follow up. The
total duration of therapy was six months. It was based That, group A shows statistically significant difference
on gradual manner from less difficult to more difficult in all five area of pre and post assessment whereas, group
way. B exhibits merely in two area i.e. personal and physical.
Statistical analysis
Data were coded, entered and analyzed manually. Table: 2. Post assessment of disability between
Fisher’s exact test was used for evaluating association experimental and control group
between gender and socio-demographic
Variables Group A Group B T value
characteristics and Paired t test was used to establish
the relationship between two groups. ‘P’ value less n=10 n=10 (DF) P value
than 0.05 was considered statistically significant. N=20 Mean (SD) Mean (SD)
Personal 5.7 (1.6) 10.4 (2.9) 4.49 (18) 0.0003*
Results and Interpretation of Data Social 7.0 (1.8) 12.2 (3.6) 4.09 (18) 0.0007*
Socio demographic characteristics of the sample Occupational 6.4 (1.3) 9.0 (2.4) 3.01 (18) 0.0075*
reveal no significant difference (Pe”0.05) between Physical 3.5 (1.6) 2.3 (1.1) 1.95 (18) 0.0664
both groups. Majority of the patients were Hindu, General 3.1 (1.2) 5.8 (2.4) 3.18 (18) 0.0052*
married, male between the age range of 20- 25. Most
of them were educated up to secondary level either *P<0.05
with a servicemen profile, student or unemployed.
Mostly belongs to urban area and nuclear families, Table two envisages overall significant difference
between both groups in all area except one i.e. physical
where family history of mental illness was absent. In
area.
majority of the patient’s age of onset of illness
Discussion
Although pharmacotherapy is effective in controlling
active / severe symptomatology emergent in nature and
to some extent helping to improve the cognitive
functions too. A variety of psychosocial treatment can
be beneficial to patients in such areas as improving
coping ability to decrease vulnerability to stress,
preventing relapse, improving social and vocational
functioning and quality of life, and coping with residual
schizophrenic symptomatology.
Results show statistically significant difference (P<0.05)
between pre and post assessment of group A. Before
intervention the mean (SD) of group A in personal area
was 13.7(3.4) and after therapy it was markedly reduced
to 5.7(1.6). However, group B also show significant
difference (P<0.05) between pre and post assessment.
Whereas, it was found that before intervention group B
also had similar mean (SD) 13.8 (3.8) and after six
months, reduction in mean average was found 10.4 (2.9).
The difference of 4.7 points in group A and B shows the
definite higher level of improvement in the area of
personal skills. It shows the efficacy of psychosocial
intervention that who received continuous 6 months
therapeutic package, shown the markedly improvement
in personal skills like personal hygiene, desire to talk,
inferiority complex etc when it was compared to those
who did not received the therapeutic package (group
B). The similar findings were reported by Frank et al
(1990)8, Herz et al. (1996)9, Andres (2000)10 and Malm
(1982) 11. Results further suggests the efficacy of
supportive psychotherapy in enhancing the personal care,
housing needs general medical care and help in solving
day to day problems and positive reinforcement for
healthy behavior. The importance of group approach
(including the supportive therapy, cognitive therapy,
psycho education and social skills training) to enchasing
the personal as well as social skill has been found
effective for the recovery and maintenance of
schizophrenic disorder.
Similarly, as in personal area the mean (SD) of group A
(pre treatment) in social area was found 14.5 (4.7) and
after treatment it was reduced on only 7 (1.8), which
shows the significant difference. At the same time no
significant difference noticed on group B (after the
assessment of the subjects).Although the mean (SD) was
observed 13.9(4.1) and after six months of medication
alone it was found 12.2 (3.6). Again it indicates that on
comparison to group A and group B, which did not
receive psychosocial intervention shows the some
improvement in social functioning but improvements
occur is not of that level as it is found in Group A who
received the medication with adjunct of package of
psychosocial interventions.
Similar finding was reported by Spencer et al. (1983)12.
Bellack and Mueser (1993)13 have also advocated a
number of psychosocial strategies available to assist the
re-integration of the patient into society. Our results are
also supported by William P. Horanab et al (2009)5.
In occupational area the results show significant
difference (P<0.05) on pre and post assessment of group
A. Before intervention the mean (SD) of group A was
11.7 (2.9) and after 6 months of intervention it was
assessed 6.4 (1.3) that indicates, there is marked
difference found between pre and post treatment.
Whereas, no significant difference was noticed in group
B. The mean (SD) was 9.7(2.6) and after six month it
was still found 9.0(2.4), indicates the subjects could not
develop occupational skills without proper intervention.
Researches in this area indicate that there is an advantage
to placing patients as rapidly as possible into competitive
employment setting .The finding of the study is
supported by the study of Cook (1995)14 and Bond et al
(1995)15. It was found in the results of various studies
that the effectiveness of supported employment and
nearly all have found substantial gains in work outcomes.
Those who received supported employment were twice
as likely to be employed as individuals in control groups.
Individuals who work tend to have better self-esteem,
even if work is only part time. The findings of Bellab
et al. (2008)16 also favour our findings.
In group A both physical and general area were noticed
to be significant in pre and post intervention assessment
wear as in group B physical area seem to be insignificant
but general area it was not so. Before intervention the
mean (SD) of physical and general areas of group A
was noted 5.8 (2.1) and 6.6 (2.2) respectively. When
compared with the results obtained after getting package
of therapeutic intervention marked improvement was
noticed that is 3.5 (1.6) and 3.1(1.2) respectively.
Whereas, after the assessment of the subjects (group B)
the mean (SD) was found 4.4 (2.1) and 6.5 (2.9) and
after six month, improvement was seen but it was not
very encouraging as the scores are 2.3 (1.1) and 5.8
(2.4) respectively for physical and general area.
Overall comparison between group A and B envisaged
that only physical area remained statically insignificant
(Pe”0.05) .It is only because of the reason that both
group took the medicinal benefit and improved there
physical health condition. The remaining areas
registered significantly.
At the same time it was also noted that the patients of
early onset has shown better and faster recovery
pattern when it was compare to later onset. Those
who were having the onset prior to age 20-25 were
shown better prognosis in comparison to onset was
the age group of after 25.The results is also supported
by findings of Marder and Wirshing (1996)17, that those
subjects whose onset of illness was less than 24 years,
they improved significantly. Wykesab et al (2009)6 also
concluded that negative symptoms showed a
moderating effect of age on CRT. This finding may be
due to early onset schizophrenia having more severe
social and interpersonal deficits than later onset
schizophrenia, and that this more severe presentation
may be more amenable to social skills training. This
indicates that one of the predicator of the positive
outcome for social skill training is early onset patient
with more fundamental social, interpersonal skill
deficits. Similarly the time duration of illness was also
found important factor on the recovery process. The
results of the study suggests that those who were
having the illness since below one year shown better
results on both modality of treatment when it was
compared to more than one year.
Conclusion
The findings of the index study suggests that the
marked difference has been found in group A and group
B in all the areas e.g. personal, social, occupational,
physical and general. Study also focuses the light on
the relationship of the age of onset / duration of illness
and level of effectiveness of the therapy. On the early
onset of the illness with / and less duration was found
positively correlated with quick and sustainable
improvements.
Study further suggests that the potential of
pharmacotherapy alone is not corresponding to
attainment of normal functioning of the patients
suffering from schizophrenia. The results of this study
convincing that the treatment toto / target to return to
the premorbid level of functioning or community
rehabilitation can not be conceptualized in the absence
of psychosocial measures alone or with the
pharmacological treatment.
REFERENCES
1 W.H.O. (2002). The ICD-10 Classification of Mental and Behavioural Disorders.
(First Indian Edition).
2. Twamely, Elizabeth W et al (2003). A review of cognitive training in schizophrenia.
Schizophrenia Bulletin,2003,vol.29,359-382.
3. Dickerson, FB. et al. (2005).the token economy for schizophrenia: review of the
literature and recommendations for future research. Schizophrenia Research.
2005, (June). vol.75 (2-3) 405-416
4. Paul H. Lysakera, Louanne W. Davisa, Gary J. Brysonb, Morris D. Bellb
(2008). Effects of cognitive behavioral therapy on work outcomes in vocational
rehabilitation for participants with schizophrenia spectrum disorders.
Schizophrenia Research, vol, 117:2 (Feb), 186-191.
5. William P. Horanab, Robert S. Kernab, Karina Shokat-Fadaib (2009) Social
cognitive skills training in schizophrenia: An initial efficacy study of stabilized
outpatients. Schizophrenia Research, vol, 107:1 :47-54.
6. Til Wykesab, Clare Reedera, Sabine Landaua, Pall Matthiassonc, Elke Haworthd,
Chloe Hutchinsond (2009) Does age matter? Effects of cognitive rehabilitation
across the age span .Schizophrenia Research , vol ,113:2-3(sep) , 252-58.
7. Behere PB, Tiwari K (1991).Disability assessment scale , Dept. of psychiatry
.Institute of medical sciences. BHU, Varanasi.
8. Frank AF, Gunderson JG (1990). The role of the therapeutic alliance in the
treatment of Schizophrenia: relationship to course and outcome. Arch Gen
Psychiatry; 47: 228-236.
9. Herz MI , Lamberti JS (1996).Psychotherapy, relapse prevention, and management
of relapse in Schizophrenia in Schizophrenia , vol.1. New York.
10. Andres K, Pfammatter M et al. (2000). Effects of a coping -oriented group therapy
for schizophrenia and schizoaffective patients: a pilot study [In Process Citation].
Acta Psychiatry Scand; 101:318-322.
11. Malm U (1982). The influence of group therapy on schizophrenia. Acta Psychiatr
Scand; 65 (suppl 297).
12. Spencer PG, Gillespie (1983). A controlled comparison of the effects of social
skills training and remidal drama on the conversational skills of chronics
schizophrenic inpatients.Br.J. Psychiatry, 143; 165-72.
13. Bellack AS, Mueser KT (1993). Psychosocial treatment for schizophrenia.
Schizophr Bull; 19:317-336.
14. Cook JA, Razzano L (1995). Discriminant function analysis of competitive
employment outcomes in transitional employment program; 5: 127-139.
15. Bond GR, Dietzen L et al. (1995). Accelerating entry into supported employment
for persons with severe psychiatric disabilities. Rehab Psychol; 40: 75-94.
16. Morris D. Bellab, Wayne Zitoab, Tamasine Greigb, Bruce E. Wexlerb (2008).
Neurocognitive enhancement therapy with vocational services: Work outcomes
at two-year follow-up. Schizophrenia Research , vol 107,1-3(sep), 252- 258.
17. Marder SR, and Wirshing (1996). behavioural skills training verses group
psychotherapy for out patient with schizophrenia : two year outcome. Am J
Psychiatry; 153:1582-1592.
 ORIGINAL ARTICLE

Visuospatial Working Memory Deficits

in Patient with Schizophrenia
Kiran Bala*, Masroor Jahan**, Sujit Sarkhel***, Ajay Bakhla***
* Department of Clinical Psychology, Central Institute of Psychiatry, Kanke, Ranchi,
**Department of Clinical Psychology, RINPAS, Kanke, Ranchi, *** Central Institute of Psychiatry, Kanke, Ranchi

ABSTRACT

Background: Review of Literature suggests that cognitive deficits of patients with schizophrenia can be attributed
to an inherent deficit of working memory. Hence, present study was conducted to assess the spatial working
memory in schizophrenic patients, to compare it with normal control and to find out clinical and socio-
demographic correlates of spatial working memory deficit.

Material & Method: The sample consisted of 25 schizophrenic patients (diagnosed according to DCR of
ICD-10) and 25 normal participants. Psychopathology was rated on Brief Psychiatric Rating Scale. Normal
participants were screened using General Health Questionnaire-12. The Rey–Osterrieth Complex Figure Test
was used to assess visuo-spatial working memory.

Result: Result shows that schizophrenic patient performed poorly on all the trials of ROCFT than normal
control. Increased severity of psychopathology was correlated with poor visuo-spatial working memory.

Conclusion: Since severity of psychopathology was correlated with poor immediate recall trial and delayed
recall trial, longitudinal studies will be important to know whether these deficits improve with improvement in
psychopathology. Findings will help in framing cognitive rehabilitation strategies for management of the
schizophrenic patients.

Key Words: visuospatial working memory, schizophrenia

Schizophrenia is associated with a broad array of memory impairments may be liability and vulnerability
cognitive impairments, including impaired attention/ markers and may be used to define schizophrenia
information processing, reasoning and problem- phenotypes. A number of investigations have demonstrated
solving, social cognition, processing speed, verbal and that many of the cognitive deficits of schizophrenic patients
visual learning and memory, and working memory can be attributed to an inherent deficit of working memory,
functions. Attention, language, memory, and and at least some of the cognitive deficits of schizophrenic
processing speed impairments are critically important patients can be attributed to a dysfunction of the pre-
and account for much of the variance in poor social frontal cortex1. Spatial working memory (SWM), the
and occupational functional outcomes. On a theoretical temporary storage and manipulation of spatial information
level, attention, working memory, and, possibly, verbal in the service of “higher” cognitive processing, has been
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456 proposed as a potential locus of dysfunction in the
123456789012345678901234567890121234567890123456
Correspondence : Dr.Masroor Jahan
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456 pathophysiology of schizophrenia. Cognitive processes
Dept. of Chmical Psychology
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456 that involve spatial working memory are compromised
RINPAS , Kanke, Ranchi, Jharkhand
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456 by a number of mental illnesses; symptoms (absence of
E-mail: masroorjahan@hotmail.com
normal traits) include affective and motivational deficits,
emotional and social withdrawal, disorganized speech and
anhedonia.
Many studies indicate that schizophrenia patients show
working memory deficits, transcending differences in
specific paradigms or tasks employed2-8. There is partial
evidence for the trait-marker hypothesis of working
memory deficit. In the current study, we examined one
component of the working memory system i.e., spatial
working memory. Park et al. (1992, 1995)2, 9 reported
SWM deficits in the non affected first degree relatives
of schizophrenic patients as well as schizophrenic
patient. Schizophrenic patients exhibit impaired
performance in spatial working memory tasks (spatial
oculomotor tracking tasks) that involve eye or manual
movements toward the remembered direction of a
visual target presented a few seconds earlier or that
require them to keep track of the locations of visual
stimuli presented or sampled in sequence. They also
concluded that schizophrenia is causally associated
with an inherent (genetic) impairment of spatial
working memory that is probably associated with
dysfunctions of the pre- frontal cortex 10.
Schizophrenic patients are similarly impaired in
antisaccade tasks which are a measure of spatial
working memory, requiring an eye movement in the
direction opposite to a visual target, and to smooth-
pursuit eye movements, tracking a moving visual
stimulus11,12. Impairment of spatial working memory
performance has been observed in patients with both
negative and positive symptoms of schizophrenia,
including those with psychosis, those who are
medicated and unmediated, those in the acute phase
of illness or in relapse, and even in undiagnosed
relatives of schizophrenic patients6, 9, 13, 14 and it may
be at the root of the cognitive fragmentation associated
with a propensity towards psychotic symptoms15.
Joyce et al (2002)16 found significant deficits in spatial
working memory, short-term spatial memory and long-
term episodic memory in 136 patients with
schizophreniform disorder (with less than 12 weeks’
medication) compared with 81 healthy controls. Some
studies done on schizophrenic to know
neuropsychological profile also found that
schizophrenic patients performed worst on Ray-
Osterrieth Complex Figure test17-22.
Review of literature shows that there is lack of study on
spatial working memory in Indian context. The purpose
of the present study was to assess the spatial working
memory in schizophrenic patient, to compare it with normal
control and to find out clinical and socio-demographic
correlates of spatial working memory deficit.
MATERIALS AND METHOD:
SAMPLE:
This is a hospital-based cross sectional study done at
Central Institute of Psychiatry, Ranchi. The sample
comprised of 25 patients of schizophrenia and 25
normal participants. These individuals fulfilled the
criteria for schizophrenia according to DCR of ICD-
10 (WHO, 1992)23. Patients with any co-morbid
psychiatric disorder and any significant neurological
disorder, head injury, epilepsy, major physical illness,
and using any substance were excluded from the study.
The mean age was 29.32 ± 5.49 years for patient group
and 26.68 ± 5.44 years for patient group. Minimum
education of all participants was 10 years. Majority of
participants of both groups were Hindu and belonged
to rural background.
TOOLS:
Socio-demographic and Clinical Data Sheet:
A socio-demographic and clinical data sheet was
specially designed for this study. It contained
information about socio-demographic and clinical
variables.
Brief Psychiatric Rating Scale (Overall & Gorham,
198824):
The Brief psychiatric rating scale (BPRS) is a widely
used scale that measures major psychotic and non-
psychotic symptoms in individuals with a major
psychiatric disorder, particularly schizophrenia. This
scale contains 18 items and it is rated on 7 point scale.
General Health Questionnaire-12 (Goldberg &
Williams 198825):
It consists of 12 items and is used to screen probable
psychiatric morbidity.
The Rey–Osterrieth Complex Figure Test (ROCF;
Rey, 194126):
It was developed by Rey in 1941 and standardized by
Osterrieth in 1944, is a widely used neuropsychological
test. The ROCF consists of three test conditions: Copy,
Immediate Recall and Delayed Recall and measures visuo-
spatial, constructional functions, and nonverbal memory.
PROCEDURE:
After screening participants were selected. Socio-
demographic data sheet was filled up. BPRS was
administered on patient group and GHQ-12 was
administered on normal group. Rey–Osterrieth
Complex Figure Test (ROCF) was administered on all
participants individually.
To find out socio-demographic correlates of the
performance correlation was computed. Significant
positive correlation has been found between education
of schizophrenic patient and copy trial of ROCFT (p
<.05), residence of schizophrenic patients and
recognition trial of ROCFT (p <.05), and family
income and all the trials of ROCFT (Table 2). In clinical
variables, BPRS Score was significantly negatively
correlated with immediate recall trial and delayed recall
trial of ROCFT (p <.01) suggesting that increased

STATISTICAL ANALYSIS: Table 2: Correlation between socio-demographic

To compare the performance of patient and control variables and performance on ROCFT
groups t-test was used. Correlation between ROCFT Variable ROCFT ROCFT ROCFT ROCFT
variables and socio-demographic and clinical variables copy trial Recognition
Immediate Delayed trial
was computed using Pearson’s r and point biserial recall
correlation. Statistical Package for Social Sciences recall
(SPSS), version 13.0 was used for the analysis of the Age - 0.12 -0.02 0.03 -0.27
data. Education 0.41* 0.33 0.34 0.26
Total no of family -0.23 0.15 0.16 0.28
members
RESULTS Marital status .27 .06 0.03 .26
Sex -.09 .21 .17 .21
The performance of schizophrenic patients and normal
Occupation -.12 .12 .11 -.23
control was compared on Ray Osterrieth Complex Residence -.33 -.27 -.28 -.40*
Figure Test (ROCFT) copy trial, immediate recall, Family income .39** .32* .32* .29*
Delayed recall, recognition total correct. Normal Religion .12 .06 -.05 .03
control scored higher on all the trials of ROCFT than
schizophrenic patients (Table 1). Statistically significant Significant at *p<0.05
difference (p <.01) was found which indicates that severity of psychopathology was correlated with visuo-
schizophrenic patient performed poorly on all the trials spatial working memory (Table 3).
of ROCFT than normal control. Table 3:Correlation between clinical variables
and performance on ROCFT
Table 1: Performance of patient and normal Variable ROCFT ROCFT ROCFT ROCFT
group on ROCFT copy trial Recognition
Immediate Delayed trial
Variable Schizophrenic Normal control t (df=48)
recall
patients Mean ±SD
recall
Mean ±SD ( N=25)
(N=25) Duration of 0.15 0.03 0.03 0.18
treatment
ROCFT copy trial 33.52 ±3.58 36.00± 0.00 03.46** BPRS Score -.17 -.66** -.66** -.14
ROCFT immediate recall 12.80 ±5.70 28.14 ±4.19 0.84**
Family history .21 .17 .20 .01
ROCFT Delayed recall 12.52 ±5.50 28.18 ±4.46 11.06**
Course of illness .15 .14 .16 .20
ROCFT recognition total 17.32 ±2.70 19.96 ±2.05 03.89**
correct Progress of illness .25 .37 .32 .30
Significant at ** p<0.01 Significant at ** p<0.01

DISCUSSION:
The aim of the present study was to see visuo-spatial
working memory deficit in schizophrenic patients.
Visuo-spatial working memory was assessed by Ray
Osterrieth Complex Figure Test (ROCFT) copy trial,
immediate recall, delayed recall, and recognition trial.
Schizophrenic patients showed significantly poor
performance on ROCFT than normal control
suggesting significant deficit in visuo-spatial working
memory of schizophrenic patients. Present results are
consistent with the findings of previous studies.
Bozikas et al. (2006)17 found significant difference (p
value<0.01) between normal control and schizophrenic
patients on immediate, delayed and recognition trial
of ROCFT. White et al. (2006)18 also reported that
normal control scored high on copy trial, and
immediate and delayed recall of ROCFT than
schizophrenic patients. Deficit in visuo-spatial working
memory of schizophrenic patients have been reported
by Snitz et al. (1999)19, Hoff et al. (1999)20, Krishnadas
et al. (2007)21 and Brodeur et al. (2010)22.
Correlation between BPRS score and ROCFT
suggests that increase severity of psychopathology was
correlated with poor immediate recall trial and delayed
recall trial. Clinical correlates of ROCFT performance
is less studied area. Krishnadas et al. (2007)21 found
that there was no significant meaningful correlation
between the scores on the tests of ROCFT and the
scores on SANS, BPRS and HRSD, however, it is
important to note that most of these patients were in
remission phase.
In order to generalize present findings study should
be replicated on a large sample. Since severity of
psychopathology was correlated with poor immediate
recall trial and delayed recall trial, longitudinal studies
will be important to know whether these deficits
improve with improvement in psychopathology.
Findings will help in framing cognitive rehabilitation
strategies for management of the schizophrenic
patients.
REFERENCE:
1. Goldman-Rakic, P. S. (1994). Working memory dysfunction in
schizophrenia. Journal of Neuropsychiatry and Clinical Neurosciences,
6, 348–57.
2. Park, S. & Holzman, P. S. (1992). Schizophrenics show spatial working memory
deficits. Archives of General Psychiatry, 49, 975–82.
3. Park, S. & Holzman, P. S.(1993). Association of working memory deficit and eye
tracking dysfunction in schizophrenia. Schizophrenia Research, 11, 55– 61.
4. Spitzer, M. (1993). The psychopathology, neuropsychology and neurobiology of
associative and working memory in schizophrenia European Archives of Psychiatry
and Clinical Neuroscience,243(2),57–70.
5. Keefe, R. S. E., Roitman, S. E. L. & Harvey, P. D. (1995). A pen–and– paper human
analogue of a monkey prefrontal cortex activation task: Spatial working memory
in patients with schizophrenia. Schizophrenia Research, 17(1), 25–33.
6. Carter, C. S, Robertson, L. C., Nordahl, T. E., Kraft, L., Chaderjian, M. & Oshora-
Celaya, L. (1996). Spatial working memory deficits and their relationship to
negative symptoms in unmedicated schizophrenic patients. Biological Psychiatry,
40, 930–2.
7. Gold, J. M., Carpenter, C. & Randolph, C. (1997). Auditory working memory and
Wisconsin Card Sorting Test performance in schizophrenia. Archives of General
Psychiatry, 54(2), 159– 165.
8. Spindler, K. A., Sullivan, E. V. & Menon V. (1997). Deficits in multiple systems of
working memory in schizophrenia. Schizophrenia Research, 27(1), 1–10.
9. Park, S., Holzman, P. S. & Goldman-Rakic, P. S. (1995). Spatial working memory
deficits in the relatives of schizophrenic patients. Archives of General Psychiatry,
52, 821–8.
10. Okada, A. (2002). Deficits in spatial working memory in chronic schizophrenia.
Schizophrenia Research, 53, 75-82.
11. Ettinger, U., Kumari, V., Crawford, T. J., Corr, P. J., Das, M., Zachariah, E. others.
(2004). Smooth pursuit and antisaccade eye movements in siblings discordant for
schizophrenia. Journal Psychiatry Response 38:177–84.
12. Reuter B, Kathmann N, Ettinger U, Kumari V, Crawford TJ, Corr PJ, and others.
(2004). Using saccade tasks as a tool to analyze executive dysfunctions in
schizophrenia. Acta Psychol (Amst) 115:255–69.
13. Park S, Puschel J, Sauter BH, Rentsch M, Hell D. (1999). Spatial working memory
deficits and clinical symptoms in schizophrenia: a 4- month follow-up study.
Biological Psychiatry 46:392–400.
14. Wood, S.J., Pantelis, C., Proffitt, T., Phillips, L.J., Stuart, G.W.& Buchanan, J.A..
(2003). Spatial working memory ability is a marker of risk-for-psychosis.
Psychological Medicine, 33, 1239–47.
15. Braff, D. L., Grillon, C. & Geyer, M. A. (1992): Gating and habituation of the startle
reflex in schizophrenic patients. Archives of General Psychiatry, 49, 206–215.
16. Joyce, E., Hutton, S.,& Mutsatsa, S. (2002) Executive dysfunction in first-episode
schizophrenia and relationship to duration of untreated psychosis: the West London
Study. British Journal of Psychiatry, 181(suppl.43),38–44.
17. Bozikas, V. P., Kosmidis, M. H., Kiosseoglou, G. & Karavatos, A. (2006).
Neuropsychological profile of cognitively impaired patients with
schizophrenia. Comprehensive Psychiatry, 47, 136– 143.
18. White, T., Ho, B., Ward, J., O’Leary, D. & Andreasen, N. C. (2006).
Neuropsychological Performance in First-Episode Adolescents with
Schizophrenia: A comparison with first-episode adults and adolescent
control subjects. Biological Psychiatry, 60, 463–471.
19. Snitz, B. E., Curtis, C. E, Zald, D. H., Katsanis, J. & Iacono, W. G. (1999).
Neuropsychological and oculomotor correlates of spatial working memory
performance in schizophrenia patients and controls. Schizophrenia Research, 38,
37–50.
20. Hoff, A. L., Sakuma, M., Wieneke, M., Horon, R., Kushner, M. & DeLisi, 25. Goldberg, D. P. & Willium, P. (1988). Auser guide to general health questionnaire.
L.E.(1999).Longitudinal neuropsychological follow-up study of patients with Windsor, NFER-Nelson.
first-episode schizophrenia.American Journal of Psychiatry,156,1336- 41. 26. Rey, A.(1941). L’examen psychologique dans les cas d’encephalopathie
21. Krishnadas, R., Moore,B.P., Nayak, A.& Patel, R.R.(2007). Relationship of traumatique. (The psychological examination in cases of traumatic
cognitive function in patients with schizophrenia in remission to disability: a encephalopathy). Archives de Psychologie 28, 215–285
cross-sectional study in an Indian sample.Annals of General Psychiatry, 6-19.
22. Brodeur, M., Pelletier, M., Bodnar, M., Buchy, L. & Lepage, M. (2010). The effect
of viewpoint on visual stimuli: A study of episodic memory in schizophrenia.
Psychiatry Research xxx xxx–xxx.
23. World Health Organization (1992). The ICD- 10 Classifications of Mental and
Behavioral Disorders. Diagnostic Criteria for Research, W.H.O., Geneva.
24. Overall, J. E. & Gorham, D. R. (1988) The Brief Psychiatric Rating Scale (BPRS)
Recent Developments in Assessment and Scaling. Psychopharmacological
Bulletin, 24, 97-9.
 ORIGINAL ARTICLE
A study of level of Depression, Anxiety and Life
Satisfaction in Acute and Chronic Schizophrenia
Ranjan Kumar, D. K. Kenswar*
Department of Clinical Psychology, LGBRIMH, Tezpur, Assam, * Department of Clinical Psychology,
RINPAS, Kanke, Ranchi-834006.

ABSTRACT
Background: The present study focuses upon studying the level of depression, anxiety and life satisfaction in acute and
chronic schizophrenics. Schizophrenia is known to be a heterogeneous disorder characterized by positive symptoms,
negative symptoms, disorganized state and cognitive deficits. Acute schizophrenia is a disorder consisting of various
degrees of psychosis, characterized by the sudden onset of personality disorganization
Methods: Thirty acute and thirty chronic schizophrenic patients were taken within the age range of 18 to 55 years of
male sex only. A self developed socio-demographic and clinical data sheet was used to assess the socio-demographic
correlates. The Beck Depression Inventory (BDI), the Hindi Version of Cattell’s Self Analysis Form or IPAT Anxiety
Scale Questionnaire (A.S.Q) and the Life Satisfaction Scale were used to assess the levels of depression, anxiety and life
satisfaction respectively.
Results: Significant differences were found between Acute and Chronic Schizophrenics in depression which was due to
the four factors: Sense of Failure, Crying Spells, Social Withdrawal, and in Work Inhibition. No significant differences
were found in anxiety (both covert and overt). On Life satisfaction, in the acute and chronic schizophrenia groups, the
level of life satisfaction is more among the acute schizophrenia group in comparison to chronic schizophrenia group.
Conclusion: The acute schizophrenia group appears to be having relatively higher level of depression than as compared
to the chronic group. But at the same time the acute group seems to have better life satisfaction than the chronic schizophrenia
group.

INTRODUCTION include disturbances in thought, mood, and behavior.

Schizophrenia is known to be a heterogeneous disorder Positive symptoms include delusions, hallucinations,
characterized by positive symptoms, negative especially auditory; disorganized speech; inappropriate
symptoms, disorganized state and cognitive deficits. affect; and disorganized behavior.
The schizophrenia disorders are characterized in The common signs of chronic schizophrenia are social
general by fundamental and characteristic disorders withdrawal, under activity, depression and odd behavior.
of thinking and perception, and by inappropriate or These symptoms are often known as
blunted affect. ‘negative’ symptoms and hallucinations and delusions
Acute schizophrenia is a disorder consisting of various are also common. Sometimes in chronic schizophrenia,
degrees of psychosis, characterized by the sudden the person appears to become used to these disordered
onset of personality disorganization. Symptoms thoughts.
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
Correspondence: Ranjan Kumar
1234567890123456789012345678901212345678901234 Schizophrenia and Depression:
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
Dept. of Clinical Psychology, LGBRIMH,
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 The individual experiencing depression is deeply
Tezpur, Assam, 784001
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
E-mail: ranjan.counsellor@gmail.com
1234567890123456789012345678901212345678901234 unhappy and finds little pleasure in life. This state is
1234567890123456789012345678901212345678901234 accompanied by at least some of the following: increased
or decreased sleep, increased or decreased appetite,
loss of interest in sex, loss of energy or excessive
energy, difficulties concentrating and making decision,
and sometimes suicidal thinking and actual attempts.
Depressive symptomatology as a feature of
schizophrenia has been recognized since Bleuler first
introduced the term in 1908. He described depressive
symptoms as either directly triggered by the disease
process in the acute stages or occurring as secondary
symptoms.
Knights and Hirsch (1981) 1 found depressive
symptoms in nearly two thirds of patients admitted
with schizophrenia, and Johnson ascertained that 70
per cent of a sample of 30 subjects with schizophrenia
had a depressive episode over a two year period.
Depression may occur independently of the symptoms
of schizophrenia and several months after recovery
from an acute episode, i.e., post-psychotic depression,
in up to 30 per cent of cases. Many investigators have
examined the prevalence of depression at different
phases of the schizophrenic illness. In particular,
Knights and Hirsch (1981) found depressive symptoms
in nearly two thirds of patients admitted with
schizophrenia, and Johnson ascertained that 70 per
cent of a sample of 30 subjects with schizophrenia
had a depressive episode over a two year period.
Depression may occur independently of the symptoms
of schizophrenia and several months after recovery
from an acute episode, i.e., post-psychotic depression,
in up to 30 per cent of cases. A similar rate of
depression was found in the longitudinal study of
Birchwood et al (2000)2 who found no significant
associations between depressive symptomatology and
negative schizophrenia symptoms. Tarrier et al. (1991)
concluded from their analysis of prodromal symptoms
that psychotic relapses can be predicted in 75 per cent
of cases on the basis of increasing scores for
hallucinations and depressive symptoms in the two
months preceding a relapse.
The character of depression in acute schizophrenia was
examined by Leff et al. (1988)3 found that the full
spectrum of depressive symptoms was present in
varying proportions in their group of drug-free acutely
ill schizophrenic patients. In the majority of cases, the
psychotic and depressive symptoms followed a similar
time course.
Depression is an integral feature of schizophrenia;
during the prodromal phase or the first episode of
schizophrenia and the major risk factor for suicide
among patients with schizophrenia. It is generally
acknowledged that depressive symptoms represent an
important and distinct symptoms domain in
schizophrenia. Mood state, energy loss, impaired
concentration and reduced self-confidence are
depressive dimensions that materially contribute to the
loss of social and vocational capacity experienced by
schizophrenic subjects, thus reducing their quality of
life. The importance and severity of depression in
schizophrenia is sustained by the high 10-15% rate of
suicide, which is the leading cause of premature death
among schizophrenics. Some authors suggest that
depressive symptoms may be related to schizophrenia
when the full-blown psychosis is most evident (so-
called “revealed depression”) 4, thus suggesting that
the depression may be associated with the psychotic
state itself or a subjective reaction to the experience
of psychotic decomposition.
Schizophrenia and Anxiety:
Anxiety is a construct and used to explain behavior.
It refers to a subjective experience of the individual a
“painful uneasiness state of mind” (Webster’s
Dictionary, 1960). Sigmund Freud first conceptualized
anxiety neurosis in 1895 and his position was that
neurotic anxiety resulted from the discharge of
repressed libido, his term for accumulated somatic
sexual tension. He later enlarged his view to relate
anxiety to the conflict between the ego and the id,
between mediation with reality and instinctual drives.
Later on, he modified this view and conceived it as a
signal indicating the presence of a danger situation
and differentiated between “objective anxiety”,
“neurotic anxiety” and “moral anxiety” largely on the
basis of whether the source of the danger was from
the external world or from the internal impulses.
Strian et al.5 describes the prevalence and distribution
of anxiety symptomatology and anxiety disorders in a
sample of hospitalized patients with schizophrenia, the
estimated level of agreement between a clinician
diagnostic measure and anxiety symptom status
measures, and their internal consistency based on the
average inter item correlations. Seventy inpatients
receiving treatment for schizophrenia were assessed
before discharge using a face-to-face diagnostic
interview and structured questionnaires, namely the
Mini International Neuropsychiatric Interview, the
Hospital Anxiety and Depression Scale, the Hamilton
Anxiety Scale, the Spielberger Anxiety Inventory, and
the Stein Generalized Anxiety Disorder (GAD) Scale.
About a quarter of patients met criteria for an anxiety
disorder, with GAD and social phobia occurring most
commonly. There was poor agreement between the
Mini International Neuropsychiatric Interview and a
diagnosis of anxiety based on symptom status
measures. The Stein GAD scale demonstrated the
highest internal consistency (0.85) followed by the
Hamilton Anxiety Scale (0.76). Anxiety disorders and
anxiety symptomatology are highly prevalent in
schizophrenia.
Schizophrenia and Life Satisfaction:
Life satisfaction is one of the indicators of subjective
wellbeing. It has been conceptualized as an assessment
of life as a whole the basis of the fit between personal
goals and achievements. Life satisfaction is a particular
effective predictor of psychiatric morbidity .It is not
surprising that life dissatisfaction is much more
common in psychiatric patient than in the general
population regardless of the level of psychopathology.
For the chronically mentally ill with schizophrenia, the
concept of life quality differs from that used to describe
physical and less-debilitating psychiatric illnesses.
People who are chronically ill with schizophrenia have
particular needs that exert a profound influence on their
existence and subjective well-being. These patients
must deal with the stigma associated with a mental
illness.
Persons with schizophrenia usually rate their life
satisfaction higher than persons with other psychiatric
disorders. Among patients with schizophrenia, severity
of psychopathology, especially the non negative
symptoms, correlates negatively with subjective life
satisfaction but not with objective aspect quality of
life. Schizophrenic disorders impose severe hardships
on patients and their families and challenge society in
the development of public policies that both preserve
the public welfare and afford patients a decent quality
of life.
METHOD
Objectives of the study:
1. To study the severity of depression level in
acute and chronic schizophrenics.
2. To study the level of anxiety in acute and
chronic schizophrenics.
3. To study the level of life satisfaction in acute
and chronic schizophrenics.
Hypotheses:
1. There is no significant difference between level
of depression in acute and chronic
schizophrenics.
2. There is no significant difference between level
of anxiety in acute and chronic schizophrenics.
3. There is no significant difference between level
of life satisfaction in acute and chronic
schizophrenics.
Sample of the study:
The sample consisted of 30 male acute schizophrenic
patients and 30 male chronic schizophrenic patients.
All the subjects were selected from the Ranchi Institute
of Neuro Psychiatry and Allied Sciences, Kanke,
Ranchi. The purposive sampling technique was used
in the selection of the sample.
Inclusion criteria:
• Patient who are diagnosed as schizophrenic
patients according to ICD – 10 diagnostic
criteria for research.
 • Duration at least 2 years or more than 2 years.
(For chronic Schizophrenic patients).
• Duration less than 6month (For acute
schizophrenic patients).
• Patients who are in the age range of 18 to 55
years.
Exclusion criteria:
o Patient’s with active psychopathology.
o History of severe physical illness in
near past.
o History of alcohol or substance abuse.
o Psychopathology that was interfering
in eliciting reliable information.
Tools for assessment:
Personal and Clinical Data Sheet was used to gather
information like name, age, sex, education, religion,
marital status, age and mode of onset, course and
duration of illness etc.
Beck Depression Inventory (BDI, developed by A.T.
Beck (1961) was used for assessing the level of
depression present among the acute and chronic
schizophrenic group. is a 21 item Scale, in which
evaluates key symptoms of depression including mood,
pessimism, sense of failure, self-dissatisfaction, guilt
punishment, self-dislike, self-accusation, suicidal ideas,
crying, irritability, social withdrawal, indecisiveness,
body image change, work-difficulty, insomnia, and
fatigability, loss of appetite, weight loss, somatic
preoccupation, and loss of libido. Individuals are asked
to rate themselves on a 0 to 3 spectrum (0-least, 3-
most) with a score range 0 to 63. Total Score is a sum
of all items. The most recent guideline suggests the
following interpretation of severity of score: 0-9,
minimal; 10-16, mild; 17-29 moderate; and 30-63,
severe. Subscale scores may be calculated for a
cognitive-affective factor and a somatic- performance
factor.
Hindi Version of Cattell’s Self Analysis Form or
IPAT Anxiety Scale Questionnaire (A.S.Q) was
originally developed by R.B. Cattell in 1963; translated
and adopted by permission into Hindi and printed and
published in India by Dr. S.D. Kapoor in 1970 and
introduced as ‘Self Analysis Form’. IPAT Anxiety scale
is a 40 items scale which evaluates key symptoms of
anxiety, including two types of anxiety; first is covert
and second is overt anxiety. As so far, scoring is
concerned the scorer simply adds 2 and 1 for each
answer. The higher score always means more anxiety.
Life Satisfaction Scale has been developed by
Q.G.Alam and Dr. Ramji Srivastava, 2001 6. This is
60 items related to six areas, viz., Health, Personal,
Economic, Marital, Social and Job. The scale has 60
items. Every item is to be responded either in yes or
no and yes responses indicate the satisfaction. Every,
‘yes’ response is assigned 1 mark. The sum of marks
is obtained for the entire score.
Procedure of the study: 30 acute schizophrenic
patients and 30 chronic schizophrenic patients were
selected from RINPAS, Kanke, Ranchi, who was
fulfilling the inclusion criteria of the study, constituted
the sample. Individual settings were arranged with all
selected patients. Beck Depression Inventory, IPAT-
anxiety Scale and Life Satisfaction Scale were
administered on them according to the all procedure
given in the manual. Each individual session took
approximately two hours to complete.
Statistical analysis:
The obtained data was analyzed using frequency,
percentage and chi-square test.
Results and discussion:
The study was carried out in the month of October
2008 to February 2009. The study was carried out in
the month of October 2008 to February 2009.
Table A. Distribution of the sample
Sl. No. Groups N Total
1 Acute Schizophrenics 30 60
2 Chronic Schizophrenics 30
The groups, the chronic schizophrenic and the acute Table B2: Item wise distribution of patients with
schizophrenic group were matched in terms of sample acute and chronic Schizophrenia on Beck Depres-
size and socio-demographic domains. sion Inventory
No of Subjects on Statements
Table B1: Level of depression in Acute & Chronic Item

Moderate
Schizophrenia

(Score3)

(score0)
(score2)

(score1)

square
Absent
Severe

Chi-
Mild
Group Level of Depression Acute 2 13 12 3 6.29
A. Mood
Chronic 4 10 6 10 NS*
Minimal Mild Moderate Severe Chi- 6
Acute 2 11 11 1.07
square B. Pessimism
Chronic 2 7 8 13 NS*
Acute 5 (16.66%) 11(36.66%) 12 (40%) 2(6.66%) 15.162 , Acute 8 0 11 11 12.98
C. Sense of failure
Chronic 10(33.33%) 5 (16.66%) 11(36.66%) 4(13.33%) S** Chronic 5 10 5 10 S*
Acute 4 5 10 11 2.98
D. Lack of satisfaction
Chronic 3 2 16 9 NS*
S**= significant at .01 level 10 6 12 2.09
Acute 2
E. Guilt feeling
Chronic 1 6 9 14 NS*
The above table shows that there is significant Acute 2 13 6 9 3.3
F. Sense of punishment
difference between acute and chronic Schizophrenics Chronic 2 7 6 15 NS*
group in so far depression is concerned. Acute 4 5 13 8 4.87
G.. Self hate
Chronic 1 8 8 13 NS*
It has been found that in acute Schizophrenia group, Acute 1 7 9 13 4.28
H. Self Accusation
83.33% are having mild to severe level of depression Chronic 0 15 7 8 NS*
Acute 2 6 5 17 2.71
and in chronic Schizophrenia group 66.66% are having I. Self punitive wishes
Chronic 0 7 7 16 NS*
mild to severe level of depression which reflects that Acute 4 3 14 9 9.97
among acute schizophrenia patients the depression is J. Crying spells
Chronic 3 5 5 17 S*
high in comparison to that in chronic schizophrenia. Acute 2 6 4 18 4.66
K. Irritability
Chronic 4 1 6 19 NS*
In a cohort study carried out with the Beck Depression Acute 1 3 10 16 13.09
L. Social withdrawals
Inventory of Schneiderian first rank symptoms, 24% Chronic 3 5 9 13 S*
Acute 5 1 4 20 7.27
depression rate were reported among schizophrenic M.Indicisiveness
Chronic 1 7 4 18 NS*
patients7 . It has found in acute Schizophrenics 16.66% Acute 5 2 4 19 5.54
N. Body image
of patients are having minimal depression which reflects Chronic 1 5 8 16 NS*
Acute 1 1 6 22 19.28
no depression in the subjects, 36.66% are mild, 40% O. Work inhibition
Chronic 0 2 12 16 S*
are moderate and 6.66% are having severe depression. Acute 2 1 4 23 5.28
P. Self disturbance
Chronic 4 6 3 17 NS*
In chronic Schizophrenics, 33.33% of patients are Acute 1 8 8 13 2.13
having minimal depression which reflects no depression Q. Fatigability
Chronic 2 4 11 13 NS*
in the subjects, 16.66% are mild, 36.66% are moderate Acute 0 5 4 21 7.32
R. Loss of appetite
Chronic 1 5 4 20 NS*
and 13.33% are having severe level of depression.
Acute 0 0 4 26 3.83
S. Loss of weight
Difference between acute and chronic Schizophrenics Chronic 1 3 3 23 NS*
Acute 1 4 5 20 1.35
are significant, reveals that both groups are having T. Somatic preoccupation
Chronic 1 3 4 22 NS*
different level of depression. Acute 1 6 15 8 2.06

Results reflect that depression is an integral feature of NS*=not significant at .05 level
Schizophrenics and distinct domain in Schizophrenics. S*= significant at .05 level
 The above table shows that there is significant
difference between the groups with respect to sense
of failure, crying spells, social withdrawal, and in work
inhibition items.
Results reflect that the depressive symptoms are
quantitatively and qualitatively among the most
important characteristics of Schizophrenics.
Table C: Level of anxiety in Acute & Chronic
Schizophrenics
Group Level of Anxiety Chi-
Low Average High square
Anxiety Anxiety Anxiety
Acute 0 (0%) 13(43.33%) 17(56.66%) 2.10,NS*
Chronic 2(6.66%) 13(43.33%) 15(50.00%)
NS*=not significant at .05 level
The above table shows that there is no significant
difference between the groups with respect to their
anxiety level. In acute Schizophrenics group 43.33%
had average level of anxiety, 56.66% of patients had
high level of anxiety and in chronic Schizophrenics
group 43.33% had average level of anxiety, 50% of
patients had high level of anxiety.
Statistically, there is no significant difference between
acute and chronic Schizophrenia in so far as their level
of anxiety is concerned. Thus both the groups have
same level of anxiety.
Table C.2: Overt and covert of anxiety in Acute &
Chronic Schizophrena
Group Dimension of Anxiety Chi-
Mainly Mainly Mixed square
Overt Covert
Acute 14(46.66%) 12(40.00%) 4(13.33%) .292,NS*
Chronic 12(40%) 13(43.33%) 5(16.66%)
NS*=not significant at .05 level
The above table shows that there is no significant
difference between the groups with respect to overt
and covert anxiety.
The scale measures two type of anxiety, overt and
covert anxiety. Covert anxiety which measures
unrealised anxiety and overt anxiety which measures
realised anxiety. For acute group, 46.66% cases are
showing mainly overt anxiety, 40% are showing mainly
covert anxiety and 13.33% are showing equal level of
overt and covert anxiety.
For chronic group, 40% cases were had mainly overt
anxiety, 43.33% had mainly covert anxiety and 16.66%
had equal level of overt and covert anxiety.
Table D1: Level of life satisfaction in Acute &
Chronic Schizophrenia
Group Level of Life Satisfaction Chi-
Low Average High square
Acute 3(10.00%) 13 (43.33%) 14 (46.66%) 10.184, S*
Chronic 7(23.33%) 20 (66.66%) 3 (10.00%)
S*=Significant at .05 level
The above table shows that there is significant
difference between the groups with respect to their
level of life satisfaction.
In the present study, out of 30 acute cases of
schizophrenia only 3 cases i.e. about 10% of total cases
were not satisfied with their life. Whereas 7 out of 30
cases of chronic schizophrenia which is about 23.33%
were not satisfied with their life and both the groups
statistically differ significantly in their level of life
satisfaction.
On the other hand out of 30 acute cases 14 cases i.e.
about 46.66% of total cases was highly satisfied with
their life. Whereas only 3 out of 30 cases of chronic
schizophrenia which is about 10% was highly satisfied.
Difference between acute and chronic Schizophrenics
on level of life satisfaction was significant. It has been
found that acute schizophrenic reported more life
satisfaction in comparison to chronic Schizophrenics.
It is concluded that better understanding of the
combining effects of psychopathology and
psychosocial factors on subjective life satisfaction
will be beneficial for effective intervention and
rehabilitation.
CONCLUSION:
The conclusion of this study can be summarized as
follows:
• There is significant difference between
level of depression in acute and chronic
schizophrenia.
• There is no significant difference between
level of anxiety in acute and chronic
schizophrenia
• There is significant difference between
level of life satisfaction in acute and
chronic schizophrenia
REFERENCES
1. Knights, A. & Hirch, S.R., (1981) ‘Revealed’ depression
and drug treatment of schizophrenia. Archives of General
Psychiatry, 38, 806-811.
2. Birchwood, M., Iqbal, Z., Chadwick, P., Trower, P. (2000).
Ontogeny of post-psychotic depression. British Journal of
Psychiatry, 177, 516-21.
3. Leff, J., Tress, K., Edqards, B. (1988). The Clinical course
of depressive symptoms in schizophrenia. Schizophrenia
Research, 1, 25-30.
4. Hirsh, S.R., Jolley, A., Barnes, T., (1990). Are depressive
symptoms part of the schizophrenic syndrome? In: DeLisi,
L.E., (Ed). Depression in schizophrenia. American
Psychiatric Press, Washington D.C., pp. 27-37.
5. Strian, F. & Klicpera (1983). Anxiety in schizophrenia
psychosis. European Archives of Psychology, 233, 247-257.
6. Alam, Q.G. & Srivastva, R. (2001). Life Satisfaction Scale.
(LSS). National Psychological corporation. 4/230, Kacheri
Ghat, Agra.
7. Johnson, D.A.W. (1981). Depression in schizophrenia some
observation on prevalence, etiology and treatment. Acta
Psychchiatrica Scandinavica, 63(Suppl. 291), 137-144.
 ORIGINAL ARTICLE

Psychopathology among Primary Caregivers of

Major Psychiatric Patients
Sanjay Kumar Nayak*, Surekha Kumari**, Masroor Jahan***, Amool R. Singh***

* Deptt. of Psychology, Jagadguru Rambhdracharya Handicapped University, Chitrakoot, U.P.**Deptt. of

Psychiatric Social Work, *** Deptt. of Clinical Psychology, Ranchi Institute of Neuro-Psychiatry and Allied
Sciences, Ranchi (Jharkhand).

ABSTRACT
Background:Perceived stigma and experiencing different kinds of burden for long time by primary caregivers
during caring family member suffering from major psychiatric illness may affects their mental health. Present
study was conducted to find out the nature of psychopathology experienced by primary caregivers of major
psychiatric patients.
Material & Method: Forty-four caregivers of major psychiatric patients were selected from outdoor psychiatric
unit of Ranchi Institute of Neuro-Psychiatry and Allied Sciences, Ranchi and forty-one normal controls were
selected from different location of Ranchi district. They were assessed on Symptoms Checklist–90–Revised
(SCL-90) and General Health Questionnaire – 28 (GHQ-28). Statistical analysis was done using SPSS (13.0
ver.).
Result: The result suggests that primary caregivers experience psychopathology, namely, somatization, obsessive
compulsive symptoms, interpersonal sensitivity, depression, anxiety, anger hostility, phobic anxiety, paranoid
ideation and social dysfunction while caring someone family member suffering from major psychiatric illness
and the number of caregivers in family definitely has an impact on severity of the caregivers’ psychopathology.
Total duration of patient’s treatment and total duration of patient’s illness also affect caregiver’s phobic anxiety
and number of patient’s hospitalization affects caregivers’ social dysfunction as well.
Conclusion:Findings suggest that mental health issues of caregivers should also be addressed while formulating
management plan for patients suffering from major psychiatric disorders.
Key Words: perceived burden, mental illness, stigma, depression.

INTRODUCTION

Caregivers provide unpaid assistance to care recipients Supporting someone with measure psychiatric illness
who have difficulty with daily functioning due to is a difficult, lifelong effect that can be very stressful.
physical, cognitive, emotional or other psychiatric The presence of someone with measure psychiatric
problem. Although giving care varies with severity of illness in the home can result in many kinds of burden
a recipient’s problems. affect the work and social life of family members or
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence: Dr. Masroor Jahan,
12345678901234567890123456789012123456789012345 the caregivers. Caregivers’ burden can include physical,
12345678901234567890123456789012123456789012345 psychological, social and financial problems,
12345678901234567890123456789012123456789012345
Deptt. of Clinical Psychology,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 embarrassment, overload and resentment. There is an
Ranchi Institute of Neuro-Psychiatry and Allied
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 ever going literature with consisting findings of the
12345678901234567890123456789012123456789012345
Sciences (RINPAS), Kanke, Ranchi 834006
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-Mail: masroorjahan@hotmail.com;
12345678901234567890123456789012123456789012345
burden experienced by families of patients with
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345 psychiatric disorders1, 2. 45% of primary caregivers of
masroorjahan@gmail.com
12345678901234567890123456789012123456789012345
chronic psychotic patients reported high level of
burden and high psychological impairment (High GHQ
score) was related to family atmosphere, and previous
admissions and duration of illness were also found to
predict burden3.
The psychopathological severity of the patients has a
negative impact on their caregivers’ mental health4,
family routines and general quality of life5. Studies have
shown that 43% to 92% of caregivers of people with
mental illness report feeling stigmatized6 and that
perceived stigma is associated with reports of
depressive symptoms7. Taj et al. (2005)8 reported that
depression is high among caregivers of schizophrenic
patients in their study conducted on 40 schizophrenic’s
caregivers. On the other hand depressive symptoms
were reported by 74% of caregivers of patients with
chronic mood disorders9. Perlick et al. (2007)10
conducted a study on 500 primary caregivers of
patients with bipolar disorder. They found that
perceived stigma was positively associated with
caregivers’ depressive symptoms.
A study conducted by Hou et al. (2008)11 on caregivers
of schizophrenia patients in Taiwan to investigate the
burden of the primary family caregiver and the factors
that affect caregivers’ burden. They reported moderate
level of burden among them, and caregivers anxiety
was the highest followed by dependency of the patient
feeling shame and guilt, and family interference.
Sandy et al. (2007)12 found that between 12% and
18% of general population of Mexican Americans meet
the cut-up for being at risk depression however 40%
of the caregivers of adult schizophrenic patients were
to be found to meet these criteria. Further they reported
that younger caregivers’ age, lower level of caregivers’
education and higher level of patient’s mental illness
symptoms were predictive of higher levels of
caregivers’ depressive symptoms and caregivers
perceived burden mediated the relation between
patient’s psychiatric symptoms and caregiver’s
depression.
As reported by Parabiaghi et al. (2007)13, 51% of
caregivers of schizophrenia experienced significant
emotional distress. Further they reported that higher
patients’ psychopathology, higher numbers of patient-
rated needs, patient’s lower global functioning and
patients’ poorer quality of life were related to the
severity of family burden.
Pinquart & Sorensen (2003)14 found in a meta-analysis
of 84 articles that caregivers of older had higher level
of depression, perceived stress and lower levels of self-
efficacy than non-caregivers.
Apart from caregivers of psychiatric patients,
psychopathology was to be found among caregivers
of chronic medical patients too. For example, mood
and anxiety disorders were common in the primary
caregivers of children with asthma. Brown et al.
(2006)15 reported 26.9% of caregivers were diagnosed
with a current depressive episode and 20.6% of
caregivers were with an anxiety disorder. Similarly,
Mahoney et al. (2005)16 found that 23.5% caregivers
were anxious and 10.5% caregivers were depressed
of Alzheimer’s disease patients.
Despite the fact that caring someone with chronic
psychiatric patient is difficult that may lead to
psychopathology among caregivers sometimes up to
diagnostic level. Still it is not elaborated the ranges
and nature of psychopathology among caregivers. The
present study attempted to find out the nature of
psychopathology experienced by primary caregivers
of major psychiatric patients and their associations with
different clinical variables i.e. total duration of patient’s
illness, duration of last episode, number of patient’s
hospitalization, total duration of treatment, duration
of care giving and number of caregivers in family.
METHODOLOGY
Sample – The sample for the present study consisted
of forty-four primary caregivers of major psychiatric
patients (suffering from schizophrenia – 21,
schizoaffective – 3, bipolar affective ‘manic’ – 18, and
depressive disorder -2) attending outdoor psychiatric personal inadequacy or inferiority), depression,
unit at Ranchi Institute of Neuro-Psychiatry and Allied anxiety, hostility, phobic anxiety, paranoid ideation and
Sciences, Ranchi and forty-one normal controls (the psychoticism. The respondent rates each item on 5-
persons who do not have psychiatric patient in the point scale which assesses the severity of the symptom.
family and do not care psychiatric patient) were
selected from different location of Ranchi district. The General Health Questionnaire-28(GHQ-28) – The
mean age of caregivers and normal control was 39.25 GHQ-28 scale was derived by factor analysis of the
± 9.53 and 36.07 ± 6.78 years respectively. The original 60-item version17 and prepared mainly for
difference was statistically non-significant (t value= research purposes. The GHQ-28 incorporates four
1.75; df= 83). Other socio-demographic subscales: somatic symptoms, anxiety and insomnia,
characteristics of caregivers are given in Table 1. social dysfunction, and severe depression. Rating is
Comparison shows that caregivers who participated done on 4-point rating scale. The cut-off score is 5.
in the study did not differ statistically from normal Table 1 Socio-demographic characteristics of he
participants. The age range of patients (to whom participants
caregivers were providing care) ranged between 18
years to 54 years (mean age = 30.88 ± 8.02). Mean RESULT
duration of illness was 7.16 ± 5.09 years. For most of Socio-demographic variables Group χ2
the patients apart from primary caregiver, care giving Caregivers Normal
(df)
was shared by other members of the family also N (%) N (%)
(27.3% patients had single caregivers, 27.3% had Sex Male 34 (77.3) 28 (68.3) 0.867
Female 10 (22.7) 13 (31.7)
double caregivers, 27.3% had three caregivers, 6.8% (1)
had four caregivers, 6.8% had five caregivers 2.3% Primary 15 (34.1) 6 (14.6)
had six caregivers and 2.3% had seven caregivers Secondary 15 (34.1) 12 (29.3) 6.683
Education Higher secondary 4 (9.1) 9 (22.0)
consequently in their family). Graduation and above 10 (22.7) 14 (34.1)
(3)

Married 37 (84.1) 31 (75.6)

Tools – The following tools have been used for the Marital Status Unmarried 6 (13.6) 9 (22.0) 1.025
collection of data in the present study: Widow/Widower 1 (2.3) 1 (2.4)
(2)
Farming 17 (38.6) 7 (17.1)
Socio-demographic and clinical data sheet – This
Service 14 (31.8) 14 (34.1) 6.884
data sheet was designed and used to gather Source of Unemployed 0 (0.0) 2 (4.9)
income (4)
information about sample characteristics and clinical Business 7 (15.9) 10 (24.4)
variables i.e. name, age, sex, education, socioeconomic Others 6 (13.6) 8 (19.5)
status, no. of patients hospitalization, duration of care Lower 16 (36.4) 9 (22.0)
Socioeconomic Middle 27 (61.4) 30 (73.2) 2.348
giving, no. of caregivers, duration of patient’s illness Status Upper 1 (2.3) 2 (4.9)
etc. (2)
Hindu 38 (86.4) 34 (82.9)
Religion Islam 1 (2.3) 1 (2.4) 1.261
Symptoms Checklist-90-R (SCL-90-R) – The SCL-
Christian 1 (2.3) 3 (7.3)
90-R (Derogatis, 1994) is a 90-item, multidimensional Sarna 4 (9.1) 3 (7.3)
(3)
self-report inventory designed to screen for a broad Types of Family Nuclear 18 (40.9) 17 (41.5) 0.003
range of psychological problems and symptoms of Joint 26 (59.1) 24 (58.5)
(1)
psychopathology. There are nine primary symptom Living Rural 26 (59.1) 17 (41.5)
dimensions that are measured: somatization Background Urban 8 (18.2) 12 (29.3) 2.763
(perception of bodily dysfunction), obsessive- Semi urban 10 (22.7) 12 (29.3)
(2)
compulsive, interpersonal sensitivity (feelings of
Psychopathology was assessed using symptoms Further, the severity of the psychopathology among
checklist-90-R and General Health Questionnaire-28. caregivers may be associated with different clinical
To compare psychopathology of caregivers and normal variables. Results (Table 4 and Table 5) show
participants on the different variables of SCL-90-R significant negative correlation between number of
and GHQ-28 t-test was applied. Result shows that caregivers in family and all variables of SCL-90-R and
both groups were statistically different on all variables GHQ-28 suggesting that if care giving is shared among
of SCL-90-R (Table 2) and GHQ-28 (Table 3) except more caregivers it has less negative impact on
psychotism in SCL-90-R which suggest that primary caregivers’ mental health. Significant negative
caregivers experience psychopathology, namely, correlation was also found between total duration of
somatization, obsessive compulsive symptoms, patient’s illness and phobic anxiety, total duration of
interpersonal sensitivity, depression, anxiety, anger treatment and phobic anxiety, and number of patient’s
hostility, phobic anxiety, paranoid ideation and social hospitalization and social dysfunction.
dysfunction while caring family member suffering from
major psychiatric illness. Table 4 –Correlation between clinical variables
Table 2 –Comparison of caregivers and normal and SCL-90
group on SCL-90 DISCUSSION
Clinical Total duration Duration of Number of Total duration of Duration of Number of
Group t variables → of patient’s last episode patient’s treatment caregiving caregivers in
SCL-90 variables Caregivers Normal illness hospitalization family
(df=83) SCL-90 (in month) (in month) (in year)
variables (in year)
(N=44) (N=41)
Mean SD Mean SD ↓
Somatization 8.636 7.767 4.048 4.398 3.318*** Somatization -.217 -.155 .089 -.190 -.085 -.390**
Obsessive-Compulsive 9.477 6.374 3.951 3.177 5.001*** Obsessive- -.169 -.134 -.117 -.098 -.038 -.568**
Compulsive
Interpersonal Sensitivity 8.545 5.824 3.926 3.836 4.284*** Interpersonal -.146 -.268 -.302* -.061 -.043 -.489**
Depression 15.590 10.399 6.609 5.774 4.873*** Sensitivity

Anxiety 9.159 7.100 3.609 2.528 4.731***

Depression -.259 -.167 -.142 -.204 -.043 -.542**
Anxiety -.239 -.310* -.151 -.181 -.192 -.468**
Anger Hostility 4.045 3.277 2.219 2.067 3.046**
Anger Hostility .004 -.206 -.109 .097 .081 -.440**
Phobic Anxiety 3.613 3.597 2.170 2.011 2.260*
Phobic Anxiety -.441** -.333* -.129 -.409** -.295 -.421**
Paranoid Ideation 7.340 6.313 3.780 4.356 3.005** Paranoid .021 -.158 -.142 .123 .134 -.525**
Psychotism 2.840 2.701 2.170 3.412 1.007 Ideation
Additional Scale 5.704 4.958 2.682 2.454 3.520*** Psychotism -.003 -.275 -.331* .030 .099 -.386**
Total Score on SCL 74.704 49.986 34.414 25.442 4.631*** Additional -.220 -.208 -.147 -.193 -.059 -.426**
Scale

***= p< 0.001 level (2-tailed),**= p< 0.01 level (2-tailed), Total Score on -.211 -.245 -.153 -.138 -.058 -.564**
SCL
*= p<0.05 level (2-tailed) **= p< 0.01 level (2-tailed), *= p<0.05 level (2-tailed)
Table 3 –Comparison of caregivers and normal Table 5 –Correlation between clinical variables
group on GHQ-28 and GHQ-28
GHQ-28 variables Group t Clinical Total duration Duration of Number of Total duration Duration of Number of
variables → of patient’s last episode patient’s of treatment caregiving caregivers
Caregivers Normal illness hospitalization in family
(df=83) GHQ-28 (in month) (in month) (in year)
variables (in year)
(N=44) (N=41)
Mean SD Mean SD ↓

Somatic Complain 2.500 2.236 1.170 1.547 3.165** Somatic -.021 -.153 -.333* -.055 .067 -.565**
Complain
Anxiety & Insomnia 2.590 2.234 0.951 1.203 4.169*** Anxiety & -.107 -.225 -.259 -.025 -.035 -.545**
Insomnia
Social Dysfunction 1.909 1.762 1.024 1.823 2.274* Social .007 -.225 -.389** .119 .180 -.443**
Severe Depression 1.977 2.415 0.609 1.222 3.256** Dysfunction
Severe -.117 -.162 -.160 .030 .095 -.460**
Total Score on GHQ-28 8.886 7.098 3.756 3.858 4.097*** Depression
Total Score on -.068 -.158 -.326* .019 .096 -.611**
GHQ-28
***= p< 0.001 level (2-tailed),**= p< 0.01 level (2-tailed),
*= p<0.05 level (2-tailed) **= p< 0.01 level (2-tailed), *= p<0.05 level (2-tailed)
The present study examined the nature of
psychopathology experienced by primary caregivers
during caring someone family member suffering from
major psychiatric illness. The data demonstrated that
despite belonging from similar socio-demographic
status caregivers experienced enormous amounts of
psychopathology than normal participants. The
caregivers experienced more somatization, obsessive-
compulsive symptoms, interpersonal sensitivity,
depression, anxiety, anger hostility, phobic anxiety,
paranoid ideation, and socially dysfunction than normal
participants. Previous studies also reported that
depressive symptoms was higher among caregivers of
schizophrenic patients8, 12, , caregivers of mood
disorders9, 10, and caregivers of people with mental
illness7,3. Similarly, anxiety11 and other emotional
distress 13 were reported among caregivers of
schizophrenia patients.
The present study suggested that the number of
caregivers in family definitely has an impact on severity
of the psychopathology found in primary caregivers.
The possibility of such psychopathology among single
or lesser caregivers of psychiatric patient might be
because of single or lesser caregivers feel more
stigmatized and have to bear more burden compare to
multiple caregivers in the same condition. However,
no review literature could be found such finding and
need further study to elaborate the reason. Although
previous studies suggested that perceived stigma is
associated to depressive symptoms7, 10. Perceived
burden is associated to caregivers’ anxiety and
depression12, 11. Apart from this, total duration of
patient’s treatment, and total duration of patient’s
illness also affect caregiver’s phobic anxiety. And
number of patient’s hospitalization affects caregivers’
social dysfunction.
Since cross-sectional assessment was done in the
present study, causal inferences could not be drawn.
However, literature suggests that stigmatization,
caregivers’ burden might engender feelings of
depression 7, 6, 10 , anxiety 11 and psychological
impairment 3. Nature of psychopathology among
primary caregivers found in the present study may be
explained. One of the possible explanations for the
findings of the present study could be the very nature
of the sample. The majority of the patients (care-
recipients) in the present study were bipolar affective
disorder ‘mania’ (18) and schizophrenia (21) that
experiences a number of psychological problems that
might have enhanced the caregivers’ distress. Secondly,
it has been argued in the literature that sharing the
same household as the patient may increase the burden
on caregivers18. Given that the all of caregivers in the
present study were close relatives, it is more likely
that they were living in the same house as the patient,
thereby feeling more distressed.
CONCLUSION
Findings suggest that primary caregivers experience
psychopathology, namely, somatization, obsessive
compulsive symptoms, interpersonal sensitivity,
depression, anxiety, anger hostility, phobic anxiety,
paranoid ideation and social dysfunction in the process of taking
care of mentally ill family member. Findings also suggest that apart
from primary cargivers, if other family members also participate in
caregiving, it reduces the severity of psychopathology of primary
caregiver. However, further studies are needed to ascertain causal
factors responsible for the psychopathology of caregivers. Most
important clinical implication of this study is that clinicians should
be aware of the high rates of psychopathology in primary caregivers
of patients having major psychiatric disorder so that they can make
appropriate plan for caregivers also.
REFERENCES
1. Ostman, M. & L. Hansson (2004). Appraisal of caregiving,
burden and psychological distress in relatives of psychiatric
inpatients. European Psychiatry, 19, 402-407.
2. Kalra, H., Kamath, P., Trivedi, J.K. & Janca, A. (2008).
Caregiver burden in anxiety disorders. Current Opinion in
Psychiatry. 21(1), 70-73.
3. Madianos, M., Economou, M., Dafni, O., Koukia, E., Palli,
A. & Rogakou, E. (2004). Family disruption, economic
hardship and psychological disress in schizophrenia: Can
they be measured. European psychiatry : the journal of the
Association of European Psychiatrists, 19(7), 408-414.
4. Lee, T.C., Yang, Y.K., Chen, P.S., Hung, N.C., Lin, S.H.,
Chang, F.L. & Cheng, S.H. (2006). Different dimensions
of social support for the caregivers of patients with
schizophrenia: Main effect and stress-buffering models.
Psychiatry and Clinical Neurosciences, 60(5), 546-550.
5. Lueboonthavatchai, P. & Lueboonthavatchai, O.
(2006). Quality of life and correlated health status and social
support of schizophrenic patients’ caregivers. Journal of
the Medical Association of Thailand, 89 (3), 13-19.
6. Struening, E.L., Perlick, D.A., Link, B.G., Hellman, F.,
Herman, D. & Sirey, J.A. (2001). Stigma as a barrier to
recovery: The extent to which caregivers believe most
people devalue consumers and their families. Psychiatric
Services, 52, 1633-1638Derogatis, L.R. (1994). Symptom
Checklist-90-R: Administration, scoring and procedures
manual, 3 rd edition, National Computer Systems, Inc.,
Minneapolis, MN 55440.
7. Phelan, J.C., Bromet, E.J. & Link, B.G. (1998). Psychiatric
illness and family stigma. Schizophrenia Bulletin, 24, 115-
126.
8. Taj, R., Hamed, S., Mufti, M. Khan, A. & Rehman, G.
(2005). Depression among primary caregivers of
schizophrenic patients. Annals of Pakistan Institute of
Medical Sciences, 1(2), 101-104.
9. Heru, A.M., Ryan, C.E. & Madrid, H. (2005).
Psychoeducation for caregivers of patients with chronic
mood disorders. Bulletin of the Menninger Clinic, 69(4),
331-340.
10. Perlick, D.A., Miklowith, D.J., Link, B.G., Struening, E.,
Kaczynski, R., Gonzalez, J., Manning, L.N., Wolff, N. &
Rosenheck, R.A. (2007). Perceived stigma and depression
among caregivers of patients with bipolar disorder. The
British Journal of Psychiatry, 190, 535-536.
11. Hou, S.Y., Ke, C.K.K., Su, Y., Lung, F.W. & Huang, C.J.
(2008). Exploring the burden of the primary family caregivers
of schizophrenia patients in Taiwan. Psychiatry and Clinical
Neurosciences, 62(5), 508-514.
12. Sandy, M., Jorge, I., María, G. & Raymond, C. (2007).
Psychological distress among latino family caregivers of
adults with schizophrenia: The roles of burden and stigma.
Psychiatric Services, 58, 378-384.
13. Parabiaghi, A., Lasalvia, A., Bonetto, C., Cristofalo, D.,
Marrella, G., Tansella, M. & Ruggeri, M. (2007). Predictors
of changes in caregiving burden in people with schizophrenia:
a 3-year follow-up study in a community mental health
service. Acta Psychiatrica Scandinavica, 116(suppl. 437),
66-76.
14. Pinquart, M. & Sorensen, S. (2003). Associations of stressors
and uplifts of caregiving with caregiver burden and depressive
mood: A meta-analysis. Journal of Gerontology:
Psychological Sciences & Social Sciences, 58B, 112-128.
15. Brown, E.S., Gan, V., Jeffress, J. Gingrich, K.M., Khan,
D.A., Wood, B.L., Miller, B.D., Gruchalla, R. & Rush, J.
(2006). Psychiatric symptomatology and disorders in
caregivers of children with asthma. Pediatrics, 118(6), 1715-
1720.
16. Mahoney, R., Regan, C. & Katona, C. (2005). Anxiety and
Depression in Family Caregivers of People With Alzheimer
Disease: The LASER-AD Study, American Journal of
Geriatric Psychiatry, 13(9), 795-801.
17. Gilleard, C.J., Gilleard, E., Gledhill, K. & Whittick, J. (1984).
Caring for the elderly mentally infirm at home: A survey of
the supporters. Journal of Epidemiology and Community
Health, 38(4), 319-325.
18. Goldberg, D.P. & Hillier, V.F. (1979). A scaled version of the
General Health Questionnaire. Psychological Medicine, 9,
139-45.
 ORIGINAL ARTICLE
A Comparative Study of Neurocognitive Impairment
in Elderly Patients with Schizophrenia and
Elderly Normals
Nawab Akhtar Khan*, Amrita Kanchan**, Archana Singh***, K.S. Sengar**, A.K. Nag****
* Clinical Psychologist, DMHP, Gumla; (Jharkhand), ** Department of Clinical Psychology, ***Department of
Psychiatric Social work, **** Department of Psychiatry, RINPAS, Kanke, Ranchi

ABSTRACT
Background: Cognitive impairment has been known to be a feature of Schizophrenia since the illness was first
described in a systematic manner. The course of cognition and functional status in schizophrenia remains an
area of significant controversy and is marked by conflicting findings. One of the reasons for this controversy is
that cognitive and functional changes occur with normal aging in the population.
Method: Total number of samples in the study were 80 (experimental and control), out of which 40 were
elderly schizophrenic patients and 40 were normal elderly individuals. Elderly patients with schizophrenia were
selected from the inpatient department of RINPAS, Ranchi. Normal elderly people were selected from near by
areas of the hospital. On both the groups the Post Graduate Institute- Battery for Assessment of Mental Efficiency
in Elderly (PGI- AMEE) test was administered.
Result: Significant differences were found in mental efficiency between normal elderly group and elderly
schizophrenic patients. The mean score of normal population is 52.90 and for schizophrenic group 40.20.
Conclusion: The findings of the index study suggests that the marked differences in cognitive functioning has
been found between elderly patient with schizophrenia and normal elderly people .Areas of impairment were
difficulty in recalling names of different things ,general orientation and visuo-spatial coordination.

Keywords: Cognitive assessment, Cognitive Impairment, Schizophrenia

INTRODUCTION
schizophrenia are having impact on the development
of personality and cognition and it significantly affect
The current literature in psychiatry reveals many
the functioning of the individual. Cognitive
studies dealing with the relationship between
impairments are common in schizophrenia1 since long
schizophrenia and cognitive deficits. Since long back
back psychological and cognitive deterioration was
it was talked by researcher that patient with
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 the centre of the literature of schizophrenia. But the
1234567890123456789012345678901212345678901234
Correspondence: Dr. K. S. Sengar
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 cause of cognitive and functional status in
1234567890123456789012345678901212345678901234
Department of Clinical psychology, schizophrenia is stills a controversial issue. Age of
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
RINPAS, KANKE,
1234567890123456789012345678901212345678901234 onset of the illness, duration of the illness, and types
1234567890123456789012345678901212345678901234
RANCHI - 834006 (Jharkhand), India
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 of symptomatology has significantly contributed in the
1234567890123456789012345678901212345678901234
E-mail: drkssengar2007@rediffmail.com
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234 outcome, maintenance, relapse and psychosocial
1234567890123456789012345678901212345678901234 rehabilitation of the patients 2, 3. Although the
pathophysiological mechanism of the observed
progression of cognitive impairments in poor outcome
schizophrenia patients have not yet been elucidated,
rather risk factors for poor outcome have been
identified. Lower levels of education and poorer
premorbid adjustment are positively associated with a
poorer outcome at follow up. Educational status plays
a role in out come in late life as well. A prospective
study of the geriatric schizophrenic patient’s who
developed moderate to severe cognitive impairment
over a 30 months follow up revealed that patient’s with
lower levels of education were at significantly greater
risk for this decline. It has been demonstrated that early
intervention with antipsychotic medication may reduce
some of the long term morbidity associated with
Schizophrenia4.
Prior works related to present study shows cognitive
impairment takes place due to many reasons, Patients
who demonstrate more severe cognitive deficits have
been found to be more likely to be unemployed 5, 6, to
be chronically institutionalized7, to have impaired basic
self-care skills 8, 9, and to be unable to benefit from
psychiatric rehabilitation10, 11, 12. Similarly, negative
symptoms have been found to be associated with
functional disability and poor outcome 3, 9. Because
cognitive deficits and negative symptoms appear to be
correlated in their severity, the differential association
between negative and cognitive symptoms and
outcome requires close attention. In a longitudinal
study there were cross-sectional correlations between
the severity of negative symptoms and cognitive
symptoms13 but no longitudinal relationships between
these aspects of the illness was confirmed. In contrast,
there is little evidence of any appreciable relationship
between the severity of the positive symptoms and
negative and cognitive symptoms and aspect of
functional outcome.
The instrumental and social skills deficits were studied
and results reveal the strong correlation of instrumental
and social skills deficits with cognitive impairments
than with the severity of under controlled behavior.
Each of the cognitive measures was correlated with
global social-adaptive deficits, with minimal variation
in the magnitude of correlations14.
The outcome of schizophrenia in old age remains
among the most debated topics in schizophrenia
research. The debate between the Kraepelinian
pronouncement that the outcome is invariably bleak,
and the view that the outcome of schizophrenia in
old age is variable, focuses on the schizophrenic’s
cognitive capacities in old age and not on the
psychosis, which for many (but not all) patients
ameliorates. There is consensus among investigators
that nearly all young and middle-aged schizophrenic
patients suffer from moderate cognitive impairment,
and that a certain proportion of geriatric patients suffer
from a very severe form of cognitive impairment.
There is, however, no consensus on the proportion
of geriatric schizophrenic patients who suffer from
the severe form of cognitive impairment, on the
specific manifestations of the cognitive impairment
in old age, or on how moderate impairment of specific
cognitive aspects progresses, if at all, into severe and
possibly global cognitive impairment.
Thus, keeping in mind the studies regarding cognitive
and functional deficit in elderly patients with
schizophrenics and various controversies regarding
it; an attempt is made to study various cognitive
deficits in elderly patients with schizophrenics and how
is it different from normal elderly population.
METHODOLOGY
Sample
The present study consisted of 40 elderly patients with
schizophrenia and 40 normal controls. The study was
carried out at Ranchi Institute of Neuropsychiatry and
Allied Sciences (RINPAS), Ranchi, India. Patients
were diagnosed as case of Schizophrenia according
to International Classification of Disease-10 (ICD-
10, DCR Criteria, WHO, 1993). Patients falling in
the age range of 55 and above, and who were co-
operative and literate were included in the study.
Patients who had co morbid psychiatric disorder,
vision and hearing impairment, history suggesting
organic pathology, substance abuse and mental
retardation or significant physical illness were
excluded from the study. For normal control, 40
individuals who were literate, cooperative and falling
in the age range of 55 and above were chosen for the file wherever required. Further Positive and Negative
study. Individuals with significant physical problem, Symptoms Scale (PANSS) was administered to screen
having a history of seizure/ severe head injury or any patients with active psychopathology. Finally Post
other neurological problems, who had faced any Graduate Institute Battery for Assessment of Mental
traumatic event in last 3 months, illiterate and who Efficiency in Elderly (PGI- AMEE) was administered
were uncooperative were excluded from the study.
to assess the cognitive functioning of schizophrenic
Tools elderly patients. Similar procedure was applied for
Socio–Demographic and Clinical Data Sheet: normal elderly control group individuals; GHQ-12 was
It is a semi-structured proforma especially designed used to screen out persons who were physically and
for the study. It contains questions regarding details
mentally fit. Further PGI-AMEE was administered to
of the age, education, and brief family background,
assess the cognitive functioning of normal control
duration of stay in the institution and nature of illness.
individuals.
General Health Questionnaire-12 (David Goldberg
& Paul Williams, 1988)15:
RESULTS
The test consists of 12 questions. It was used to
The socio-demographic variables of the subjects are
identify and exclude the individuals for normal control
group. mentioned in Table 1. The results show that there was
Positive and Negative Symptoms Checklist no significant difference in any domain in both groups.
(PANNS, Kay et. al. 1987)16:
Table 1: Socio demographic variables
This checklist contains relevant areas to assess the
Patient
severity of the symptoms. It is 7 point scale divided S.No. Variables
Normal group
group χ2
in three sub-scales-Positive scale, Negative scale and (40)
(40)
General psychopathology scale. It was used to assess 55-59 16 17
the psychopathology of the patients. Individuals with 60-64 13 12
1. Age in years .13 NS
65 and 11 11
active psychopathology were excluded from the above
study. 2. Sex
Male 20 20
.04 NS
PGI- Battery for Assessment of Mental Efficiency Female 20 20
0-5 years 16 17
in the Elderly (PGI – AMEE, Kohli, Verma & 3.
Education in
6-9 years 16 15 .04 NS
Prasad, 1993). years
10and above 8 8
The Test is basically used to assess the cognitive 4. Marital status
Married 39 36
.03 NS
Unmarried 1 4
functioning of individuals falling in the age range of
Hindu 33 30
55 years and above. The important dimensions of this 5. Religion Muslim 7 7 1.8 NS
test are: Mental efficiency motivation and alertness, Christian 0 3
general information, general orientation to time and Rural 19 17
6. Domicile Urban 8 8 .24 NS
place, memory, concentration, perceptual- motor Semi urban 13 15
functions including depth perception and muscular Joint 37 34
7. Family type .2 NS
coordination, and finally depressive mood associated Single 3 6
with old age.
Table – 2 Mental Efficiency of Elderly Schizophrenic
Procedure: Group and Elderly Normal Control Group
After screening patients according to inclusion and
exclusion criteria, they were selected for the study. Group Mean Score χ2 Level of Significance
Clinical interview and required history was taken and Normal elderly population 52.90
socio-demographic and clinical data sheet were filled. Schizophrenic elderly 40.20 29.23 .01 level
Information was cross-checked from the case record population
 Above mentioned Table – 2 reveals the mental
efficiency of both groups. Significant difference was
found between the mental efficiency of normal elderly
individuals and elderly patients with schizophrenia. The
mean score of normal population is 52.90 and for
schizophrenic group 40.20, it shows that individuals
who are not suffering from schizophrenia illness has
scored better in the test, specially in the areas as
orientation, visuo-spatial movement and set test, which
indicates that the mental functioning of normal group
is better than the schizophrenia group.
DISCUSSION
It is evident that most component processes of
cognition decline with advanced age if the difficulty
level is sufficiently high. The examples will include
the processes involving attention, working memory
capabilities (the amount of information you can work
without losing track of any), understanding text,
making inferences, encoding (putting information into
memory) and retrieval 17, 18, 19. Severe cognitive
impairment have also been reported in large numbers
of geriatric chronic schizophrenic patients, this
impairment also being found related to severe negative
symptoms and adaptive deficits7, but the question
arises is, whether the cognitive impairment in
schizophrenic patients is the results of old age or the
result of chronic illness. The results of the present study
show that elderly schizophrenic patients have
significant cognitive impairment in comparison to
normal elderly population.
Poor performance of schizophrenia group may be due
to poor information processing, reduced interaction
pattern as well as lack of opportunity to interact with
external environment. Result reveal that cognitive
impairment in adaptive functioning in patient with aged
schizophrenia has strong predictor of poor outcome.
Samples of present study were institutionalized
patients and many past studies on institutionalized
patients conducted all over the world, also reveal
similar findings. Schizophrenic patients who reside in
chronic psychiatric hospitals, over 50% suffered from
sever impairment in more than one area of cognition
which affects their social functioning2.
The results of present study reveal severe cognitive
impairment among elderly schizophrenics in areas such
as visuo-spatial task, general orientation and recall of the
items of set test. It may be the results of
long term institutionalization, where schizophrenic patients
hardly interact with others, sit alone & aloof. They are
poorly motivated to take any initiative. So they are not
willing to gather information about the world and
excessively detached from the society and current events,
which is an essential phenomenon for improving their
orientation about time, place, person, day, dale, month,
year etc.
Long term institutionalization also affects their motivation
level. This can reduce their ability to take initiative, ability
to use mental functions and ability to generate new ideas,
which are required for better information processing and
development of new concepts. Poor performance on
visuo-spatial task may be because of poor ability, poor
ability to plan and organize information in a rational manner.
However poor vision and extra pyramidal symptoms may
be caused by antipsychotic, which might have cobbled
some of the patent’s performance.
Persistent institutional social environment contribute to the
cognitive impairment. But some researchers are not in
the favour of similar findings they found that long term
deinstitutionalization also has the causal relationship in
worsening the cognitive functions in patient with positive
symptoms. The possible cause might be the poor family
support, poor drug complaints, infrequent consultation
to therapist and poor job involvement2.
The type of the symptoms (positive & negative) persists
has the significant place in the cognitive impairment of
schizophrenic patient. As patient with negative symptom
has markedly poor personal care & hygiene, retarded
psychomotor activities, restricted or flat affect, increased
reaction time etc. They are unable to take care of
themselves and orient to the outer world. Due to long
term hospitalization they need more supervision than the
patient with positive symptoms. On the other side patients
with positive symptoms having active hallucination, are
least concerned with outer world and are always busy
with their hallucinatory content. They make their own
world, which significantly hamper their interaction with
the outer world, which further causes stimulation of
restricted area of the brain. Over all outcomes is that both
positive & negative symptoms of the illness have
impairment in both adaptive and cognitive functioning14.
In the light of decay theory of forgetting where the loss of
memory is due to lapse of time and absence of rehearsal
in that particular time period. Most aged patients with
schizophrenia and with long standing institutionalization
are not being exposed to the external environment, so
they don’t get the opportunity to rehearse their prior
retained information that may also be one of the causes
of memory impairment.
Conclusion
The finding of the index study suggests that the marked
differences in cognitive impairment have been found
between aged patient with schizophrenia and normal
aged. Areas of impairment were recalling names of
different things, general orientation and visuo-spatial
coordination which may be problematic for aged
population of schizophrenia because above mentioned
deficits may result in difficulty in finding their way to
their houses or work place and performing/executing
the function to deliver the assigned task.
REFERENCES
1. Gold, J.M. & Harvey, P.D. (1993) Cognitive deficits in schizophrenia;
Psychiatric. Clinic of North America; 16, 295 312.
2. Davidson, M. Harvey, P.D., & Powchik, P. (1995) Severity of symptoms
in geriatric chronic schizophrenic inpatients; Am. J. Psychiatry; 152, 197-
207.
3. Perlick, D., Mattis, S., & Statsny, P. (1992) Neuropsychological
discriminators of long-term inpatient or outpatient status in chronic
schizophrenia; J. Neuropsychiatry Clin. Neurosci; 4, 428-434.
4. Wyatt, R.J. & Hanter, I.D. (1998) The effects of early and sustained
intervention on the long term morbidity on schizophrenia.; J Psychiatr
Res; 32 :169-177.
5. Jaeger, J., & Douglas, E. (1992) Neuropsychiatric rehabilitation for
persistent mental illness; Psychiat. Quart; 63, 71–93.
6. Meltzer, H.Y. & McGurk, S.R. (1999) The effects of clozapine risperidone
and olanzapine on cognitive functioning in schizophrenia; Schizophrenia.
Bulletin., in press.
7. Harvey, P.D., Howanitz, E., Parrella, M., White, L., Hoblyn, J., Mohs, R.C.
& Davis, K.L., (1998) Cognitive adaptive and clinical symptoms in
geriatric patients with lifelong schizophrenia: A comparative study across
treatment sites; Am. J. Psychiatry; 155, 1080–1086Brink, T. L., Yesavage,
J.A., Lum, O., Heersema, P. H.,Adey, M., (1982) Screening tests for geriatric
depression; Clinical Gerontologist, 1,37-43.
8. Harvey, P.D., Sukhodolsky, D., Parrella, M., White, L. & Davidson, M.
(1997c) The association between adaptive and cognitive deficits in
geriatric chronic schizophrenic patients; Schizophrenia Research;
27, 211–218.
9. Velligan, D.I., Mahurin, R.K., Diamond, P.L., Hazleton, B.C., Eckert, S.L.
& Miller, A.L., (1997) The functional significance of symptomotology
and cognitive function in schizophrenia; Schizophrenia Research; 25, 21–
31.
10. Mueser, K.T., Bellack,A.S., Douglas, M.S., & Wade, J.H. (1991) Prediction
of social skills acquisition in schizophrenic and major affective disorder
patients from memory and symptomotology; Psychiatric Research; 37,
281–296.
11. Corrigan, P.W., Wallace, C.J., Schade, M.I., Green, M.F., (1994) Cognitive
dysfunctions and psychosocial skill learning in schizophrenia; Behaviour
Therapy; 25, 5–15.
12. Lysaker, P., Bell, M. & Beam-Goulet, J. (1995) Wisconsin Card Sorting
Test and work performance in schizophrenia; Psychiatric Research; 56,
45–51.
13. Harvey, P.D., Lombardi, J., Leibman, M., White, L., Parrella, M., Powchik,
P. & Davidson, M. (1996) Cognitive impairment and negative symptoms
in schizophrenia: A prospective study of their relationship; Schizophrenia
Research; 22, 223–231.
14. Harvey, P.D., Parrella, M., White, L., Mohs, R.C. & Davis, K.L. (1999a)
The convergence of cognitive and adaptive decline in late-life
schizophrenia; Schizophrenia Research., in press.
15. Goldberg, D. & Williams, P. (1988) Manual of the General Health
Questionnaire. winder; NFER-Nelson Park, D. C. (1992) Applied
cognitive aging research; Pp 449-93.
16. Kay,S.R., Opler, .L.A., Lindenmayer, .J.P. (1987) The Positive and Negative
Syndrome Scale (PANSS) for Schizophrenia; Schizophrenia bulletin;
13,261-276
17. Park, D. C. (1992) Applied cognitive aging research; Pp 449-93.
18. Craik, In., Fergus I. M. & Salthouse, T. A. (1992) The Handbook of Aging
and Cognition; Hillsdale, NJ: LEA; Pp 111-165.
19. Starr, J.M., Deary, I.J., Inch, S., Cross, S. & MacLennan, W.J (1997)
Age-associated cognitive decline in healthy old people; Age and
Ageing.
REVIEW ARTICLE

Legislation, Society and Substance Use - Impact of

NDPS Act, 1985
Munish Aggarwal, Umamaheswari V, Debasish Basu
Department of Psychiatry, PGIMER, Chandigarh, India

INTRODUCTION
Society can be defined as an organization of individuals
who lives together and controls the behavior of the
constituting members through law and customs.[1]
Drugs and drug trafficking is a social and legal
problem. Every civilized society irrespective of caste,
creed, culture and the geographical location has been
affected by the menace of substance use. During 18th
century attempts by Chinese government to resist
smuggling of opium into China by European powers
resulted in the infamous Opium War.[2] Drug use and
trafficking activities have sharply increased over the
years and there has been change in the socio-
demographic characteristics and type of substance
use.[2-5]
HISTORICAL BACKGROUND
The geographical location of India makes it vulnerable
to massive inflow of the dugs across the border from
“Golden Crescent” comprising of Iran, Afghanistan
and Pakistan in the west and in the North-Eastern side
of the country is the “Golden Triangle” comprising of
Burma, Laos and Thailand.[6]
There were acts which tried to control the illicit trade
of the narcotic drugs in India. The principal Central
acts were:
1. The opium act 1857
2. The opium act 1878
3. The dangerous act, 1930
Newer drugs had come into use and these laws were not
sufficient to cover them.
To Control and regulate the supply of opium and other
narcotic drugs, the following International Conventions
were entered:-
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
Correspondence: Dr. Debasish Basu
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
Dept. of Psychiatry
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
PGIMER, Chandigarh-160012
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
123456789012345678901234567890121234567890123456
E-mail: db_sm2002@yahoo.com
i. 1912: International opium Convention
ii. 1925: Agreement Re Manufacture,
international trade and use of prepared opium
iii. 1931: Concentration manufacture and
distribution of narcotic drugs
iv. 1936: Convention for the suppression of illicit
traffic in dangerous drugs
v. 1946: Protocol Amending the 1912, 1925,
1931, and 1936 instruments
vi. 1948: Protocol extending the 1931
convention to synthetic narcotic drugs
1953: Protocol Re cultivation of the opium poppy and
production trade and use of opium
UN Convention on Narcotic Drugs
A major convention “the United Nations Single
Convention on Narcotic Drugs,” took place in 1961,
India is also a party to this and other conventions i.e.
Psychotropic Substances, 1971, and the Protocol,
1972 amending the single convention on narcotic
drugs.
Under UN single convention, India had to take
measures to control drug trade including the
traditionally used cannabis and opium.[6] In order to
meet these demands and control the menace of drug
use, the Narcotic Drugs and Psychotropic Substances
Act of 1985 was passed by Indian Parliament. This
act came into affect from 14th November 1985.
THE NARCOTIC DRUGS AND
PSYCHOTROPIC SUBSTANCES (NDPS) Act:[7]
The act consists of six chapters; chapter II and chapter
V are further subdivided into II A and V A, which were
included after 1989 amendment.
Chapter I
This act is called Narcotic Drugs and Psychotropic
substances act, 1985 it extends to all citizens of India
Definitions: (important definitions under the act) psychotropic substances. As per Sec 5 NDPS Act, the
a. Addict: Any person who has dependence on central government shall appoint a narcotic
any narcotic drug or psychotropic substances commission to control cultivation of opium for medical
purposes. Under sections 4, 5 & 7, both the central
b. Illicit traffic- cultivation any coca or opium and state government are empowered to appoint
plant, cannabis or in the production and officers required to enforce the provisions of the act.
distribution of these drugs
Enforcement
c. Narcotic drug- coca leaf, cannabis, opium, A number of agencies, including the department of
poppy straw and includes all manufactured goods customs and central excise, the directorate of revenue
intelligence, the central bureau of narcotics, the central
d. Psychotropic substance- any substance, natural bureau of investigation and the border security force
or synthetic, or any natural material or any salt at the central level and state police and excise
or preparation of such substance or material departments at the state level. The union ministries of
included in the list of psychotropic substances Social Justice and Empowerment and Health cover
specified in the schedule health care, drug de-addiction, rehabilitation and social
e. Use- any kind of use except personal consumption reintegration of patients with substance dependence.
The Narcotics Control Bureau (NCB) was set up by
f. Commercial quantity- any quantity greater the central government in 1986, to carry out these
than quantity specified by the Central activities.
Government
The Narcotics Control Bureau (NCB)
g. Small quantity-any quantity lesser than the NCB was constituted with its headquarters at New
quantity specified by the central Government Delhi. The NCB came into effect from 17th March,
1986. It is the apex coordinating agency and also
Table–1: Definition of small and commercial quantities* functions as an enforcement agency. The Bureau has
to exercise the powers and functions of the Central
Government for taking measures to:[8]
i. Co-ordination of actions by various offices,
state governments and other authorities under the
S. Drug / psychotropic substance Small quantity Commercial quantity NDPS Act, Customs Act, Drugs and Cosmetics Act.
No ii. Implementation of the obligation in respect of
1. Cannabis 100gm 1 kg counter measures against illicit traffic under the various
2. Cocaine 2 gm 100 gm international conventions and protocols.
3. Codeine 10 gm 1 kg iii. Assistance to concerned international
4. Ganja 1 kg 20 kg organizations to facilitate coordination and universal
5. Heroin 5 gm 250 gm action for prevention and suppression of illicit traffic
6. Morphine 5 gm 250 gm in these drugs and substances.
7. Opium 25 gm 2.5 kg iv. Coordination of actions taken by the other
8. Opium derivatives 5 gm 250 gm concerned ministries, departments and organizations
9. Poppy straw 1 kg 50 kg in respect of matters relating to drug abuse.
10. Diazepam 20 gm 500 gm
National fund (Chapter II A)
* These were defined after the 2001 amendments After the 1989 amendment national fund for control
of drug abuse was set up. The central government is
Chapter II- Authorities and Offences: required to constitute the national fund.
As per Sec 4 of the NDPS Act, the central government The fund shall meet the expenditure incurred to
has to take measures for preventing and combating 1. Combat illicit traffic and controlling the abuse
abuse and illicit traffic of narcotic drugs and of drug
 2. Identifying, treating, rehabilitating of addicts Chapter V (SECTIONS 41 TO 68)- Procedure
3. Prevent drug abuse This section deals with the procedures and powers
4. Educate public against drugs involving search of building/ place/ conveyance, arrest
5. Supplying drugs to addicts where such supply of the individuals/ attachment of illegal crops/
is a medical necessity responsibility of the officers under the law.

Chapter III- Prohibition Control and Regulation Chapter VA- Specials Provisions Relating to
Licit Opium Cultivation Forfeiture of Property
The licit opium cultivation is regulated and controlled This chapter was introduced into the act in May 1989
by the narcotics commissioner of India in terms of the to provide for the investigation, freezing, seizure and
provisions of sections 8 and 9 of the NDPS act. forfeiture of property derived from or acquired
through illicit trafficking in narcotic drugs and
Chapter IV- Offences and Penalties (Sections 15 psychotropic substances.
To 40)
Sections 15 to 21 deals with punishment of various Chapter VI- Miscellaneous
narcotic drugs while section 22 deals with the Immunities in Drug Cases
punishment for contravention of psychotropic Addicts charged with consumption of drugs (section
substances (Table-2). 27) or with offences involving small quantities will be
immune from prosecution if they volunteer for de-
Table-2: Offences and punishments addiction. This immunity may be
Offence Penalty Sections withdrawn if the addict does not
Contravention in relation to poppy Small quantity- RI upto 6 months or fine upto Poppy straw- 15
straw/ prepared opium/ Cultivation Rs.10,0000 or both; More than small quantity Prepared opium- 17 undergo complete treatment
of opium but less than commercial quantity-RI upto 10 Cultivation of opium- 18 (section 64A).
Production, manufacture, years + fine Rs 1 lakh; Commercial quantity- Cannabis-20
possession, sale, purchase, transport, R.I 10 to 20 years + fine Rs.1 to 2 lakhs Manufactured drugs or
Minors: An offence committed
import, export or use of drugs (court can impose fine > Rs 2 lakh) their preparations-21 under any law by persons under
Psychotropic substances-
22
the age of 18 will be covered by
Import, export or transshipment of Same as above 23 the Juvenile Persons (care and
narcotic drugs and psychotropic protection) act. This act seeks
substances
Contravention in relation to Rigorous punishment upto 10 years +fine Coca-16 to reform such juveniles rather
cannabis/ cannabis plant without upto Rs. 1 lakh Cannabis- 20 than punish them under the
license or coca plants/ coca leaves
Embezzlement of opium by licensed RI for 10-20 years + fine Rs. 1-2 lakhs 19 respective acts. It prevails over
farmer (regardless of the quantity) any other act in respect of
External dealings in NDPS engaging R.I. 10 to 20 years + fine of Rs. 1 to 2 lakhs 24
in or controlling trade whereby (regardless of the quantity) persons below the age of 18.
drugs are obtained from outside Hence, such persons cannot be
India and supplied outside India
Knowingly allowing ones premise to Same as for the offence 25 prosecuted under the NDPS act
be used for committing an offence too.
Attempts abetment and criminal Same as for the offence Attempts-28
conspiracy Abetment and criminal
Establishment of the drug de-
conspiracy-29 addiction centers: The central
Preparation to commit an offence Half the punishment for the offence 30
Repeat offence One and half times the punishment for the 31
government has the power to
offence. Death penalty in selected cases* Death-31A establish centers for
Consumption of drugs Cocaine, morphine, heroin- RI upto 1 year or 27 identification, treatment, etc of
fine upto Rs.20,0000 or both Immunity-64A
Other drugs- imprisonment upto 6 months or addicts and for supply of
fine upto Rs.10,000 or both narcotic drugs and psychotropic
Addicts volunteering for treatment enjoy
immunity from prosecution substances under section 71 of
the NDPS Act.
*Included after 1989 amendment
AMENDMENTS
The Prevention of Illicit Traffic in Narcotic
Drugs and Psychotropic Substance Bill
(1989 Amendment)[7]
The Prevention of Illicit Traffic in Narcotic Drugs and
Psychotropic Substance Bill, 1988 was passed to
effectively immobilize persons engaged in any kind of
illicit traffic in narcotic drugs and psychotropic
substances. The following amendments were included-
a. A National Fund was created under Section
IIA (described previously)
b. Provisions for the forfeiture of property
derived from or used in illicit traffic have been
described under chapter VA.
c. Death penalty for repeated offence by a person,
in case he is convicted of the commission or
attempt to commit or abetment of or criminal
conspiracy to commit any of the offences
involving commercial quantity of any narcotic
drug or psychotropic substance had been
included (Section 31).
d. Special courts were constituted under section
36A.
e. Amendments were made so that no sentence
awarded under the Act should be suspended,
remitted or commuted (other than section 27).
f. Every offence punishable under the act shall
be cognizable and non-bailable (Section 37)
g. Empowering officers authorized under section
42 to order attachment/ destruction of illicit
crop
h. Provisions for destruction of seized narcotic
drugs and psychotropic substances (Section
52A)
Commencement of NDPS (Amendment) ACT
2001 (2001 Amendment)[7]
The following short comings were noted in the
NDPS Act after the 1989 amendment
 The criminalization of drug use and the
increasing rates of arrest for possessing small
quantities of drugs
 There were low conviction rates
 There were weak bail laws
 Drug addicts have difficulty in seeking the
treatment openly
As a consequence of such criticisms a reassessment
of the Act in 2001 resulted in amendments relating to
the length of imprisonment and the quantity and type
of drug seized
Following amendments were included in 2001
amendment of the Narcotics Drugs and
psychotropic substances act, 1985
1. Small and commercial quantities were
mentioned (described previously).
2. Small quantity was redefined, which implied
that possession of small quantity is for personal
consumption.
3. It rationalized the sentence structure
(described previously).
4. Bail provisions were made stringent for
offenders who indulge in serious offences e.g.
cases involving commercial quantities.
5. It made provisions for immunity of individuals
convicted for small quantities who volunteer
for medical treatment once in their life time.
6. The obligations of U.N conventions against
illicit traffic in NDPS specially in respect of
the concept of controlled delivery have been
incorporated
NDPS ACT AND IMPACT ON SUBSTANCE
USE
There has been mention of various psychoactive
substances in the ancient Indian literature. Atharva
veda mentions that cannabis was created by god as a
medicinal plant[9] and to protect against evil spirit.[10]
Devotees use cannabis to increase their concentration
for meditation. It is considered to be the preferred
decoction to be offered to lord Shiva. Use of cannabis
has been sanctioned for use in various festivals like
“Holi” and “Shivratri” and for spiritual uplifting.[11]
Opium has been used in India since 9th Century after it
was possibly introduced by Arab traders. Opium
initially was used by ruling class especially the
Mughals. Now, its use had spread beyond the ruling
class and socially sanctioned use.[12] Opium has also
been by peasants to make young infant sleep and
thereafter mothers can go to field for work.[13] In Islam,
use of alcohol has been prohibited, but cannabis and
opium has been used by the Muslim community in
India.[14] Similar to cannabis, it has been used for
medicinal purposes and in social events.[6]
The social control theory states that individuals have
a tendency to pursue individual pleasures if there is no
external control of society or there is an internal control
exhibited by the individual himself.[15] Each society has
developed measures to control individual’s behavior
to adhere to the societal rules and norms.[16] There were
prevalent socio-cultural norms and sanctions regarding
the form and mode of use, profile of users and the
occasions on which cannabis was used in India, which
limited the use of cannabis to specific occasions like
“Shivratri.” Use beyond these occasions was not
approved of. Though opium was not associated with
any religious occasions but, similar to cannabis there
were social norms and sanctions which controlled its
use e.g. used by males only and on occasions like
marriages or to greet the relatives.[6] Moreover, when
used in social gathering the amount of drug each
individual would consume was limited and this would
act as a means to strengthen the social bond.[17]
Imprisonment and/ or fine for those prosecuted for
possession of even small quantities for personal use
under NDPS Act seems to be impractical in India citing
prevalent cultural acceptability of opium and
cannabis.[6,18] An individual’s perception and concern
about social norms will determine his eventual drug
use.[19] Due to urbanization, exposure to newer drugs
through tourism, production of illicit drugs and less
risky trade in high potency drugs than traditional drugs,
there has been change in the drug use pattern in India,
with increase in the use of synthetic opioids and
injectable drugs.[2-6,20] There was a system to provide
opium through legal outlets which vanished after the
implementation of the NDPS Act, this has also
contributed to increase in the use of the newer drug of
use.[6,21] Research has suggested that cultural norms in
India have been far more effective means of drug
control, and have fewer negative side effects than
legislative measures.[22]
There is some evidence to suggest that legislation has
not been able to control the level of drug use. In
countries like Netherlands where at coffee shops
people can smoke cannabis, and legalization of
cannabis has not resulted in increase in the use of other
drugs like heroin. The rate of cannabis use in past
month in high school students in Netherlands is 5.4%
as compared to 29% in United States.[23,24] It is human
nature to use mood altering drugs. When one drug is
banned, a newer one is discovered. Such legislations
have not controlled the problem but have shifted it
from one to another.[25] Better control on source,
distribution and advertising of drugs than
criminalization of the drugs is required to control the
menace of drug use.[26] Experiments in Netherlands
have shown that some degree of decriminalization has
helped in managing the drug menace while the
prohibitionist policies have not yielded the desired
results.[24] Moreover, cannabis and opioids appears to
be less harmful than other drugs like tobacco and
alcohol,[25,26] and these drugs are excluded from the
preview of the NDPS Act. Because of the technical
and the legal difficulties in obtaining opioid analgesics,
pharmacies and hospitals tried not to keep opioid
analgesics. This resulted in decrease in use of morphine
by 97%, from 716 kg in 1985 to 18 kg in 1997.[27]
Addiction is not just a law and order problem. It
involves intense craving for the substance and desire
to obtain the substance even if it involves indulgence
in the criminal activities. There is considerable degree
of social stigma attached to the use of drugs this makes
many patients not to seek treatment for substance use.
The department of Social Welfare has been declared
as the nodal agency in several state governments in
India to co-ordinate all the measures and activities
being undertaken by various Governmental and non-
governmental agencies to prevent drug abuse and
rehabilitate patients. Apart from its legal role in
control of the drug traffic, NDPS Act made
recommendations for the identification, treatment and
rehabilitation of the persons dependent on the
drugs. [28,29] Ministry of Health funded various
governmental organizations while non-governmental
organizations were provided aid by Ministry of Social
Justice and Empowerment. In 1988, government
established treatment centers in 5 central institutes and
2 centers in state capitals. There were 34 government
de-addiction centers by 1994. By 2003, 369 de-
addiction and 90 counseling centers across the country
were provided financial aid by Ministry of Social
Justice and Empowerment.[29] There is some provision
for drug de-addiction centers under NDPS, but the
number of such centers is limited and the grant
provided to these centers is inadequate.[21] Also, among
the centers being funded by the Ministry of Health and
Family welfare only three centers have been notified.[21]
Under the NDPS Act patients can take treatment once
in their lifetime if they are caught with small quantity
of the substance. This respite for treatment only once
in lifetime is complete disregard to the natural history
of patients with substance use who have history of
multiple lapses and relapses.[21]
Despite its innumerous limitations NDPS Act has been
an important milestone for the control of trade and
use of illicit drugs. Between the year 1996 to 2006,
21,895 kg of opium, 10,147 kg of heroin, 8, 55,667
kg of ganja and 48,278 kg of hashish have been seized
under the NDPS Act by various enforcement agencies.
In cases involving these illicit traffic, a total of 1, 42,337
persons were involved including these foreigners. Out
of which 38,030 persons were convicted for various
offences while 44,656 persons were acquitted. The rate
of acquittal has varied from 27.7% to 59.1% annually
during this period.[2]
CONCLUSION:
A variety of drugs have been used in India since
centuries and the use was under the control because
of various socio-cultural factors. In the last century,
because of change in social factors there had been an
increase in the substance use. Numerous legislations
including NDPS, have attempted to control drug use.
Attempts should be made to understand the
sociocultural factors which plays crucial role in type
and pattern of substance use and the degree of harm
the drug in question causes. Other measures for control
of substance use, e.g., education about harmful
consequences, good coping skills, curbs on the
advertisements of the drugs should be emphasized
upon. Measures for treatment and rehabilitation of the
patient with substance use should take into
consideration the social factors leading to the substance
use.
REFERENCES:
1. Park K. Park’s textbook of preventive and social medicine. 18th
ed. Jabalpur (India). Banarsidas Bhanot; 2005. p. 490.
2. Sabharwal YK. Narcotic Drugs and Psychotropic Substances.
[online]. 2006; Available from:
URL:www.supremecourtofindia.nic.in/newlinks/NDPS.doc
3. World Health Organization. Trends in Substance Use and
associated health problems 1998. Fact sheet No 127. Available
from URL: http://www.int/infofs/en/fact127.html
4. Sachdev JS, Yakhmi RS, Sharma AK. Changing pattern of drug
abuse among patients attending de-addiction centre at Faridkot.
Indian J Psychiatry 2002;44:353-355.
5. Margoob MA, Majid A, Hussain A, Wani ZA, Yousf A, Malik
YA, Zahger A, Zehangir I, Geelani I, Mushtaq H. Changing
sociodemograhic and clinical profile of substance use disorder
patients in Kashmir Valley. JK-Practitioner 2004;11:14-16
6. Charles M, Bewley-Taylor D and Neidpath A. Drug policy in
India Compounding harm? Beckley Foundation drug policy
programme, 2005 Briefing Paper 10.
7. Narcotic Drugs and Psychotropic Substances Act (Act) (as
amended upto date), Ministry of Law and Justice, Government
of India.
8. Ministry of home affairs. Available from: URL: http://
www.mha.nic.in/uniquepage.asp?Id_Pk=511
9. Chopra RN, Chopra IC. Drug addiction with special reference
to India. New Delhi: Council of scientific and industrial research
1965.
10. Sharma HK. Sociocultural perspective of substance use in India.
Subst Use Misuse 1996;31:1689-1714.
11. Roy S, Rizvi SHM. Nicotine water to heroin. Delhi: BR
publishing cop. Royal Commission on Opium 1893 Report.
Shimla: Government of India. Central printing office 1986.
12. Purohit DR. Community approach to opium dependent subjects
in rural areas of Rajasthan. Journal of Community Psychiatry
1988;11:3.
13. Lakshminarayana J, Singh MB. Opium addiction among rural
population in desert districts of western Rajasthan: some
observations from the study. J Hum Ecol 2009;25:1-4.
14. Siddiqui HY. Extent of drug abuse in Faridabad, in H Singh
(Ed), Drug abuse: summaries of research studies. New Delhi.
National Institute of Social Defense, Ministry of Welfare 1992.
15. Gibbs J. Social control: views from the social sciences. Beverly
Hills, CA: Sage 1982.
16. Nagasawa R, Qian Z, Wong P. Social control theory as a theory
of conformity: the case of Asian/Paciûc drug and alcohol nonuse.
Sociological Perspectives 2000;43:581-603.
17. Charles M, Nair KS, Gabriel B. Drug culture in India- a street
ethnographic study of heroin addiction in Bombay; Jaipur:
Rawat Publishers 1999.
18. Ambekar A, Lewis G, Rao S, Sethi H. ‘South Asia Regional
Profile’. Vienna: UNODC, 2005.
19. Yang X, Xia G. Causes and consequences of increasing club
drug use in china: a descriptive assessment. Subst Use Misuse
2010;45:224-239.
20. Charles M. Drug Trade Dyanamics in India. [online]. 2004;
Available from: URL:htpp://www.drugstat@free.fr
21. Anuradha KVLN. A flawed Act. [online]. 2001; Available from:
U R L : h t p p : / / w w w. i n d i a - s e m i n a r. c o m / 2 0 0 1 / 5 0 4 /
504%20k.v.l.n.%20anuradha.htm
22. Charles M, Britto G. Culture and the Drug Scene in India, in
Christian Geffary, Guilhem Fabre, Michel Schiray, Scientific
Coordinators, Globalisation, Drugs and Criminalisation, Paris:
UNESCO MOST and UNDP 2002;1:4-30.
23. Morgan JP, Riley D, Chesher GB. Cannabis: legal reform,
medicinal use and harm reduction. In: Heather N, Wodak A,
Nadelmann E, and O’Hare P, eds. Psychoactive drugs and
harm reduction: from faith to science. London: Whurr, 1993
24. Smith R. The war on drugs: Prohibition isn’t working - some
legalization will help. BMJ 1995;311:23-30.
25. Editorial- Dangerous habits. The Lancet 1998;352:1565.
26. Editorial- Deglamorising cannabis. The Lancet 1995;346:1241.
27. Rajagopal MR, Joranson DE, Gilson Am. Medical use, misuse,
and diversion of opioids in India. The Lancet 2001; 358: 139-
43
28. Malhotra A, Mohan A. national policy to meet the challenge of
substance abuse: programmes and implementation. Indian J
Psychiatry 2000;42:370-377.
29. Ray R. Substance abuse and the growth of de-addiction centers:
the challenge of our times, in Mental health: an Indian
Perspective, 1946-2003. Edited by Agarwal SP. New Delhi.
Director General of Health Services/ Ministry of Health and
Family Welfare, 2004, pp 284-289.
 REVIEW ARTICLE

Polypharmacy in Clinical Psychiatry-a Brief Review

Gurvinder Pal Singh,
Department of Psychiatry,
G.G.S.Medical College and Hospital, Faridkot, Punjab, 151203

ABSTRACT

Psychiatrists in clinical practice choose polypharmacy as a therapeutic strategy to control the symptoms.
Polypharmacy is much more common than would be expected in contrast to the available treatment guidelines.
Higher rates of relapse in patients receiving monotherapy have been documented. Polypharmacy in general
clinical practice may be employed with some justification. Unwanted use of these practices may be avoided for
better patient care. Limited knowledge and the wide spread marketing has led to widespread acceptance of
polypharmacy practices. Some remedial measures are needed in reducing this practice of polypharmacy in our
country. In this article an attempt has been made to highlight this important clinical problem for awareness of
mental health professionals.

Key-words: Polypharmacy, psychiatry, clinical practice

INTRODUCTION
Use of two or more medications simultaneously is need to establish the optimal prescriptions of
called polypharmacy.1 The term polypharmacy psychotropic medications in today’s era of
contains two components, poly derived from the Greek polypharmacy.
word polus (many) and pharmacy from the Greek word Polypharmacy is making psychiatrists more like a
pharmakon (drug).2 The word polypharmacy first physician or clinical pharmacologist. Due to the recent
appeared in the psychiatric literature in 1969 in a trend of psychiatrists to prescribe more psychotropic
published article.3 Polypharmacy .is commonly medications, space for psychotherapeutic interventions
observed in clinical practice in India and other is limited. This practice will generate physician hood
developing countries and can be problematic for the concept among young generation psychiatrists. The
patients especially when same class of drugs are concomitant use of psychiatric drugs is probably based
prescribed together. It is a matter of concern for mental more upon experience than evidence. 5
health professionals and health planners and is a How common is poly-pharmacy?
debatable issue in clinical psychiatry. Some authors The study of the phenomenon of polypharmacy in
consider that the concept of adequate prescription is psychiatry is inherently complex. Excessive dosing and
almost as abstract as that of health 4. There is a strong
12345678901234567890123456789012123456789012345 poly-pharmacy is widely prevalent in psychiatry. 6 There
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence: Dr Gurvinder Pal Singh
12345678901234567890123456789012123456789012345 are numerous studies on prescription habits showing
12345678901234567890123456789012123456789012345 that polypharmacy is much more common than would
12345678901234567890123456789012123456789012345
H.No. 76, Medical Campus
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
G.G.S. Medical College and Hospital be expected in view of the available treatment
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Faridkot-Punjab, 151203.
12345678901234567890123456789012123456789012345 guidelines.6-14 Hiroto et al,6 in a study of schizophrenic
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-mail: gpsluthra@gmail.com, patients found that majority of the patients were on
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
gpsluthra@rediffmail.com
12345678901234567890123456789012123456789012345 polypharmacy. In this study, 179 patients gave consent
for participation. In 34 patients data was incomplete
and 6 patients were not on any antipsychotic
medication. Out of 139 patients, 102 (73.4%) were
on non standardized dosage while 32 (23.02%) were
on excessive dosage of medications. In another study
by Adi et al, 7 , 93.4% of bipolar patients received
polypharmacy. Patients who received fewer drugs
reported normal mood frequently and had fewer mood
swings. Sachs and Thase8 analyzed polypharmacy in
many clinical trials and revealed that 40% of patients
derived little or no benefit. Cuevas and Sanz9 in a
sample of 264 patients of various psychiatric disorders
found that the mean number of psychotropic drugs
used were 1.63 (range 1-7) and 41.9% of patients
received polypharmacy. Sernyak and Roserheck10
found the rate of polypharmacy in outdoor
schizophrenic patients in the range of 6.8-15% while
in indoor patients it was 50 %( a high figure).
In a study comprising a review of the clinical records
of 209 patients with schizophrenia, 55.5% of patients
were found on polypharmacy treatment record. The
patients received an average of 3.06 psychotropic
drugs upon discharge and an average of 1.61
antipsychotic agents.11 In a developing country survey
of 158 psychiatric patients, the
authors found the pattern of polypharmacy was
prevalent in 54% study subjects.12 In another study of
case records and a second phase confirmation strategy
through personal interviews, mean number of
psychoactive drugs prescribed was 2.22 (range 1-6).
The rate of polypharmacy was 67% with 34.1% of
patients receiving two drugs, 20.5% receiving three
drugs and 12.5% of the patients receiving four or more
psychoactive drugs.13 Johnson and Wright14 found that
in a teaching hospital, 34% of patients were on two or
more drugs while 17% were receiving four or more
medications. Antiparkinsonian drugs were given
regularly to 48% of patients and an antidepressant to
10% of the schizophrenic patients.
Justification for polypharmacy
Despite so many advances in treatment of psychiatric
patients, 30% of the patients do not respond or only
respond partially to pharmacological treatment.15 Lack
of response to treatment in psychiatric patients is a
clinical problem in psychiatric practice. Clinician
generally chooses polypharmacy as a therapeutic
strategy to control the symptoms. Combining multiple
agents is the most commonly used clinical practice for
treatment of resistant bipolar patients. 16-18 The
combination of medications in some controlled studies
has demonstrated greater efficacy than monotherapy.19-
21
Response rates for combination treatment of acute
mania generally exceed those of treatment with lithium
or valproate by 20-25%.20-21
Newer drugs generally have improved safety profiles.
Use of multiple medications with synergistic effect
and with one drug augmenting the effect of the other
can be beneficial for some group of patients. Discovery
of various receptors with action and specificity for
drugs supports the judicial use of combination of drugs
having different receptor affinity. Judicial use can
augment the desired action without increasing the side
effects of the drug. Most Psychiatric disorders are now
considered as complete syndrome with no single
hypothesis explaining the phenomenology of the
disorder. So chances are that monotherapy will not
produce the desired results. This may lead to
refractoriness of the disorder. Hence, treatment of
patient’s refractory to monotherapy with combination
of medications may be justified.
Associated comorbid disorders are not exception in
psychiatry. Combination of two drugs with different
action on multiple receptors has proven to be helpful
in managing co morbid psychiatric disorders. The large
number of medications is now available in the market
for the treatment of patients with psychiatric disorders.
Pharmaceutical company’s claims of safety of the new
agents and probably the pressures of pharmaceutical
industry have created new opportunities for the use
of multiple medications for a single condition. Medical
treatment is viewed as more effective, easier to deliver,
less expensive and consuming less time and thus all
the symptoms are treated medically. Successful use of
polypharmacy for other chronic illness such as infection
with HIV, Parkinson’s disease, cancer and epilepsy.is
a common routine clinical practice and has
revolutionized the treatment of such chronic illnesses.
Polypharmacy in depression
Large number of depressive patients does not respond
to monotherapy Lithium is a classical augmenting agent
for unipolar depression resistant to first line
antidepressants. It enhances the action of
antidepressant by acting synergistically22. Thyroid
hormone potentiates the effects of antidepressants23.
Similarly buspirone has been used as an augmenting
agent. Serotonin specific reuptake inhibitors along with
estrogen are used in premenopausal and
postmenopausal women with refractory depression.
This combination has been reported in case reports
and clinical trials conducted to assess the efficacy are
limited one.
Polypharmacy in bipolar affective disorder
Polypharmacy with two or more psychotropic
medications is the rule rather than exception in the
treatment of bipolar disorders. First line treatment is
with lithium or valproic acid or divalproex. If patient
fails to stabilize in manic phase on first line drugs,
preferred another line of agent is atypical antipsychotic.
With newer evidence, atypical antipsychotic are
becoming the first line treatment for mania. If lithium,
valporic acid or atypical antipsychotics are not
effective, they can be given in combination. If this is
not effective, benzodiazepine or conventional
antipsychotic can be added to first or second line
monotherapies. Neuroleptic should be used for most
disturbed and out of control patients but restricted to
acute phase only. For maintenance phase, failure to
first line antimanic agents(lithium, valproate,
divalproex) or atypical antipsychotics, a trial of other
anti convulsants(carbamazepine, lamotrigine,
gabapentin and topiramate). is given to the bipolar
patients
Therapeutic recommendation for maintenance
treatment of bipolar affective disorder patient is
undergoing rapid changes. Till few years back, lithium
was the hallmark of bipolar treatment with
antidepressant cotherapy for patients prone to
depression. Recently several newer therapeutic
molecules are available for treatment. Valproic acid or
divalproex is now considered first line choice along
with lithium. Atypical antipsychotic are becoming
another choice for maintenance therapy of bipolar
disorders When lithium or valproic acid alone or in
combination fails, atypical antipsychotics are even
becoming first line choice for bipolar maintenance With
risk of switch to mania or hypomania antidepressants
are rarely used these days. The trend today is to use
antidepressant sparingly in bipolar depression. This is
used only in the presence of robust mood stabilization
with mood stabilizers.
With strong evidence of efficacy of lamotrigine and
quetiapine in bipolar depression, the use of
antidepressant is gradually diminishing. Higher
prevalence of comorbidity with bipolar disorder such
as substance abuse 24, anxiety disorder 25 necessitates
the need for combination treatment. Inherent
complexity of the recurrent, episodic and phasic nature
of bipolar disorder and lack of understanding of
specific pathophysiology, a single drug may not control
all symptoms. in bipolar patients.
Antipsychotic polypharmacy
In routine clinical practice, a patient not responding
to conventional or atypical antipsychotic is switched
to other atypical antipsychotic. Schizophrenia has
positive symptopms, negative symptoms, cognitive
symptoms, and mood and behavior symptoms.
Probably there are multiple mechanisms leading to
different symptoms in these patients, and one can use
more than one drug targeting different mechanism.
Patients were more likely to receive antipsychotic
polypharmacy if they were younger, unmarried, had
schizophrenia rather than schizoaffective disorder.
Lack of response to treatment in patients with
schizophrenia is one of principal concern facing
clinician in clinical practice. There are two group of
patient with schizophrenia who could benefit from the
use of polypharmacy. One group comprises patient
presenting a partial response to clozapine. The other
group consists of patient who needs admission in
psychiatry ward, with acute psychotic processes and
with behavioural problems (markedly aggressive
patients). Patient given prescription for polypharmacy
were more likely to receive antiparkinson medications,
antianxiety agents, and mood stabilizers.
Risk of polypharmacy
Polypharmacy increases the chances of drug drug
interactions. Polypharmacy is associated with early and
sudden cardiac death. 26-27. Polypharmacy is strongly
associated with excessive dosing usage in clinical
practice 28. The excessive dosage and medications may
be dangerous for psychiatric patients and may put them
on higher death risk. Higher rate of hospitalization
can be attributed to polypharmacy prescription
practices. Unwanted use of polypharmacy does not
confer any therapeutic advantage, but tends to increase
the side effects.
The introduction of combination of antipsychotics with
antiparkinsonian agents, combination of various
antipsychotics, antipsychotics with antidepressants or
anxiolytics is one of the most unfortunate
developments in the pharmacotherapy of psychiatric
disorder. Asian patients are more vulnerable to side
effects and require less antipsychotic medication than
European patients 12. Polyphramacy can lead to
increased cost of treatment and poor drug adherence.
Can Polypharmacy be reduced?
Fifty years ago psychiatrists had to manage psychotic
patients without the help of psychotropic medications.
Nowadays good molecules are available for
management. In teaching department polypharmacy
practices happens because of a high turnover of staff
and where the patient is seen by a new doctor every
six months. The easiest thing for the new doctor is to
repeat the same medication.
Some measures can be adopted in reducing this
practice of polypharmacy. Patrick et al 29 estimated
epidemiological measures of polypharmacy and
identified the patients at risk for polypharmacy in order
to develop proper interventions that minimize the risks.
Regular internal auditing of drug prescriptions was
found to be quite useful in decreasing the polypharmacy
practices. Adequate knowledge with research literature
can help the mental health professionals in reducing
this unwanted use of polypharmacy. Educational
programmes detailing scientific advances can be
effective for health care professionals in the reduction
of this trend of polypharmacy. Many psychiatrists do
not fully understand the mechanism and advantages
of new psychotropic medications. They are reluctant
to change their prescribing patterns. Educating the
patient and their families about the illness, its treatment,
side effects are integral parts of scientific
pharmacotherapy. This may improve the compliance
to treatment programme. Supervised gradual reduction
of medication should be attempted over time. Patient
should be treated with flexible dose.
Future Pharmacy
Polypharmacy use should be evidence based 30.
Evidence is now available for district subtypes of
bipolar affective disorder patients responding to
specific types of mood stabilizers Genetic studies of
bipolar affective disorder patients require the ability
to precisely define a phenotype. Pharmacogenomic
studies in future will be quite useful and will provide a
new direction for pharmacy. Such types of studies have
demonstrated a significant influence of genetic
mechanisms on the efficacy of clinically prescribed
drugs. Prescribing guidelines and algorithms and their
application in clinical practice may be an essential part
of future pharmacy. Long term antipsychotic
polypharmacy should be reserved for more severely
ill patients with psychotic symptoms rather than mood
symptoms. Prescribing too many drugs is not a good
practice and should be discouraged.
Conclusions:
Polypharmacy should be judicially used in routine
clinical practice. Rational approach in its application
is essential for better patient care. Good information
about polypharmacy practices in developed and
developing countries is available in the literature and
steps in regulation of this practice is needed to decrease
the risks associated with this practice. Regular
monitoring of the prescription pattern is quite helpful
in checking the spread of this phenomenon.
Educational interventions are beneficial for
psychiatrists and other professionals and they must
follow treatment guidelines.
REFERENCES:
1 . Ghaemi N, editor. Polypharmacy in psychiatry. New York:
Marcel Dekker Inc., 2002.
2. Berube MS.; Neely DJ.; DeVinne, PB. American Heritage
Dictionary. 2. Boston: Houghton Mifflin Co; 1982.
3. Sheppard C, Collins L, Fiorentino D, Fracchia J, Merlis S.
Polypharmacy in psychiatric treatment. I. Incidence at a state
hospital. Curr Ther Res Clin Exp. 1969;12:765–7.
4. Harris, CM.;Heywood, PL.; Clayden, AD. The Analysis of
Prescribing in General Practice: A Guide to Audit and Research.
HSMO: London; 1990.
5. Stahl SM. Antipsychotic polypharmacy: evidence based or
eminence based? Acta Psychiatr Scand. 2002;106:321–322.
6. Ito H, Koyama A and Higuchi T. Polypharmacy and excessive
dosing: psychiatrists’ perceptions of antipsychotic drug
prescription British Journal of Psychiatry 2005 187: 243-47.
7 . Adli M, Whybrow PC, Grof P, Rasgon N, Gyulai L, Baethge C,
Glenn T, Bauer M. Use of polypharmacy and self reported
mood in outpatients with bipolar disorder. Int Journal Of
Psychiatry in clinical practice 2005, 9 :251-256.
8. Sachs GS, Thase ME. Bipolar disorder therapeutics: maintenance
treatment. Biol Psychiatry 2000, 48:573-81.
9. Cuevas C, Sanz EJ, de la Fuente JA, Cueto M. Polypharmacy
in psychiatric patients as an alternative to limited mental health
resources. Actas Esp Psiquiatr 2005, 33:81-6.
10. Sernyak MJ, Rosenheck R: Clinicians’ reasons for antipsychotic
coprescribing. Journal of Clinical Psychiatry 2004,65:1597–
1600.
11. Lerma-Carrilo I, Leonor del Pozo M, Pascual-Pinazo F, et al.
Polypharmacy and prescribing pattern s in patients with
schizophrenia in an acute unit in Spain. Schizophr Bull 2007;
33:475.
12. Ungvari GS, Pang AH, Chiu HF, et al. Psychotropic drug
prescription in rehabilitation. A survey in Hong Kong. Soc
Psychiatry Psychiatr Epidemiol 1996, 31:288-291.
13. Procyshyn RM, Kennedy NB, Tse G. et al. Antipsychotic
polypharmacy: a survey of discharge prescription from a
tertiary care psychiatry institution. Canadian Journal of
Psychiatry 2001, 46:334-339
14. Johnson DAW, Wright NF. Drug prescribing for schizophrenic
outpatient on depot injections. British Journal of Psychiatry
1990, 156:827-834.
15. . Kane JM. The current status of neuroleptic therapy. J Clin
Psychiatry. 1989; 50:322-328.
16 Anil Yagcioglu AE, Kivircik Akdede BB, Turgut TI, et al. A
double-blind controlled study of adjunctive treatment with
risperidone in schizophrenic patients partially responsive to
clozapine: efficacy and safety. Journal of Clinical Psychiatry
2005, 66:63–72.
17.. Small J, Klapper M, Milstein V, Kellams J, Miller M, Marhenke
J, Small I. Carbamazepine compared with lithium in the
treatment of mania. Arch Gen Psychiatry 1991; 48:915–921.
18. Emrich HM, Zerssen DV, Kissling W, Moller HJ, Windorfer A:
Effect of sodium valproate on mania: the GABA hypothesis of
affective disorders. Arch Psychiatr Nervenkr 1980; 229:1–16.
19... Pope H, McElroy S, Keck P, Hudson J. Valproate in the
treatment of acute mania. Arch Gen Psychiatry 1991, 48:62–
68.
20. Freeman TW, Clothier JL, Pazzaglia P, Lesem MD, Swann AC.
A double-blind comparison of valproate and lithium in the
treatment of acute mania. Am J Psychiatry 1992; 149:108–
111.
21. Burgess S, Geddes J, Hawton K, Townsend E, Jamison K,
Goodwin G: Lithium for maintenance treatment of mood
disorders. Cochrane Database Syst Rev 2001; 3:CD003013.
22. Price LH, Charney DS, Heninger GR. Variability of response to
lithium augmentation in refractory depression. Am Journal of
Psychiatry 1986, 143:1387-1392.
23.. Prange AJ, Loosen PT, Wilson IC, Lipton MA. The therapeutic
use of hormones of the thyroid axis in depression, in the
Neurobiology of mood disorders. Edited by Post R, Ballenger
J. Baltimore , William and Wilkins 1984 : 311-312.
24. . Goldberg JF, Garno JL, Leon AC, et al. A history of substance
abuse complicates remission from acute mania in bipolar disorder.
J Clin Psychiatry, 1999, 60:733-740.
25 Freeman MP, Freeman SA, McElroy SL. The comorbidity of
bipolar and anxiety disorders: prevalence , psychobiology, and
treatment issues. J Affect Disord 2002, 68:1-23.
26. Waddington JL, Youssef HA and Kinsella A. Mortality in
schizophrenia. Antipsychotic polypharmacy and absence of
adjunctive anticholinergics over the course of a 10-year
prospective study. British Journal of Psychiatry 1998, 173:325-
329.
27. Reilly JG, Avis SA, Ferrier IN et al. QTc-interval abnormalities
and psychotropic drug therapy in psychiatric patients. Lancet
2000, 355:1048-1052.
28. . . . Lelliott P, Paton C, Harrington M. Influence of patient
variables on polypharmacy and high dose of antipsychotic
drugs prescribed in patients . Psychiatric Bulletin 2002, 26:411-
414.
29. Patrick V Schleifer J.S..,.Nurenberg J R., Gill K J, Best Practices:
An Initiative to Curtail the Use of Antipsychotic Polypharmacy
in a State Psychiatric Hospital. Psychiatr Serv 2006, 57:21-
23.
30. Taylor D, Mir S, Mace S, et al. Coprescribing of atypical and
typical antipsychotics-prescribing sequence and documented
outcome. Psychiatric Bulletin 2002, 26:170-172.
 REVIEW ARTICLE
Treatment Resistant Depression
Mahesh Hembram, Suprakash Chaudhury
Department of Psychiatry, Ranchi Institute of Neuropsychiatry and Allied Sciences (RINPAS),
Kanke, Ranchi-834006.

ABSTRACT
Most of the literature on Treatment Resistant Depression (TRD) has based its definition of resistance on the
failure to respond to antidepressant drug treatment of adequate dose and duration. The prevalence of TRD is
lowest in primary care settings and progressively increases in outpatient psychiatry settings, inpatient psychiatric
settings, and academic/tertiary care settings. Strategies available for the treatment of TRD include optimization,
substitution or switching, combination, and augmentation therapies. Currently there are no clear guidelines on
when to substitute, combine, or augment therapies in the treatment of patients with TRD. Some new and novel
therapies that show promise for the future include addition of an atypical antipsychotic to the initial antidepressant;
newer pharmacologic interventions; and non-pharmacologic therapies such as vagus nerve stimulation (VNS),
repetitive transcranial magnetic stimulation (rTMS), and deep brain stimulation (DBS). The newer models of
interpersonal, cognitive, and behavioral therapies offer structured, pragmatic methods to work with such difficult
patients. Guidelines for psychotherapeutic intervention for TRD suggested that the therapy should be collaborative
and centered on the goal of teaching new skills to improve coping with a chronic illness. A better understanding of
the many facets of the etiology of TRD as well as the availability of new and effective therapies hopefully will
decrease the morbidity and mortality associated with this condition.

KEY WORDS: Treatment resistant depression; antidepressant; atypical antipsychotic.

INTRODUCTION Stage 1 TRD has a prevalence of ~50% when “response”

Despite recent advances depression remains a
challenge for the practicing clinician. Almost one third
of patients with depression do not respond to
monotherapy with an antidepressant. Treatment
resistance confers an additional economic burden,
resulting in higher treatment costs than those
associated with the care of non–treatment-resistant
patients.
PREVALANCE OF TRD
Estimates of TRD prevalence are lowest in primary care
settings and progressively increase in outpatient psychiatry
settings, inpatient psychiatric settings, and academic/
tertiary care settings. Based on data from randomized
controlled trials (RCTs) conducted in a research setting,
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
Correspondence :Dr.Col(Retd.) S.
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
Chaudhury
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
Dept. of Psychiatry, RINPAS, Ranchi
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
12345678901234567890123456789012123456789012345678
E-mail: suprakashch@gmail.com
is used as the criterion outcome and at least 60% when
“remission” is used. Studies in clinical practice settings
have reported even lower remission rates of 15% to 35%.
In the Sequenced Treatment Alternatives to Relieve
Depression (STAR*D) study, conducted in both
psychiatric and primary care practice settings, patients
with nonpsychotic major depression (N=2876) were
treated in Stage 1 for 12 weeks with citalopram at a mean
final daily dose of 55 mg. Stage 1 response rates were
47% and remission rates were 28% 1 that suggests
prevalence for Stage 1 TRD of ~50% using response
criteria and of~70% using remission criteria. Recent
STAR*D data reported response rates of 26% to 28%
when switching to a second antidepressant (sustained
release bupropion [N=239], sertraline [N=238], or
venlafaxine-XR [N=250] after failure to achieve
remission (or intolerance) with initial citalopram treatment2.
Given a 12 month MDD prevalence estimated at 6.6%3,
the 12 month prevalence estimates are ~3% for Stage 1
TRD and ~2% for Stage 2 TRD. Adequately powered
and well controlled trials of TRD in Stages 3 to 5 in clinical
practice settings have not been reported, and thus no
estimates are available.
DEFINITIONS
Depression is considered resistant or refractory when
at least two trials with antidepressants from different
pharmacologic classes (adequate in terms of dosage,
duration, and compliance) fail to produce a significant
clinical improvement4. An adequate response is defined
as much or very much improvement on rating scales
or 50% improvement in depression rating scale scores.
Currently the recommended adequate dosages have
increased from 150 mg daily to between 250 and 300
mg daily of imipramine or its equivalent5. Adequate
duration of treatment also varied widely from 4 weeks
to 12 weeks in different studies with number of
Antidepressants taken for treatment resistant from 1
to 3, even upto 5. A TRD may be chronic, but a chronic
depression is not necessarily resistant to treatment—
for example, it may be that no treatment was
attempted. TRD also may remit spontaneously, further
differentiating the concepts of treatment resistance and
chronicity.
• Nonresponse: A lack of response or response
poor enough to require a change in treatment
plan [e.g., failure to achieve 50% reduction in
HAM-D score (or equivalent scale)].
• Response: Therapeutic response good enough
to indicate continuing present treatment plan
(e.g., 50% reduction in HAM-D score)
• Remission :Attainment of virtually
asymptomatic status (e.g., HAM-D 7) for at
least 2 consecutive weeks
• Recovery: Remission for 6 consecutive
months.
• Adequate antidepressant trial: is defined as
a trial in which an appropriate drug is given in
a dosage and duration sufficient to produce a
response. Nowadays, four to six weeks is
considered an adequate trial period to see
clinical response, although recent research
suggests that longer periods of up to eight or 12
weeks may be needed to achieve remission.
• Adequate dosage: Clinically, it is defined as the
minimum dosage that would produce the
expected effect/ the maximum dosage that a
patient can tolerate until the expected effect is
achieved.
• Pseudo-resistance: Nonresponse to treatment
that is inadequate in dosage and duration.
• TRD: Nonresponse despite two treatment
trials with drugs from different pharmacologic
classes, each used in an adequate dose for an
adequate period. However, there is no
universally accepted definition of TRD. A
review of ten years literature revealed more
than 15 definitions5. One can approach these
concepts from a categorical or a dimensional
perspective.
• The categorical approach is based on the
use of cutoff points. For example, some have
proposed that depression should be considered
resistant when two adequate trials of different
antidepressants have failed, while others
suggested a higher threshold that consisted of
nonresponse to three or more adequate trials,
one of which must have been a tricyclic.
• The dimensional perspective places a
greater emphasis on levels of resistance and
specifying the treatments to which the
depression does not respond, rather than
viewing resistance as an intransitive
phenomenon.
• Difficult-to-treat depression: “includes
depression that inherently does not respond
satisfactorily to one or more treatments that
are optimally delivered (TRD) and also
depression treated under circumstances
precluding the optimal delivery of potentially
effective treatments. Such circumstances
include the use of subtherapeutic doses,
nonadherence, intolerable side effects that
prevent an adequate dose or duration of
treatment, and concurrent axis I, II, or III
conditions that reduce the likelihood of
remission for adherence, pharmacokinetic, or
pharmacodynamic reasons.”
NEUROBIOLOGY OF TRD
Major depressive disorder (MDD) is accompanied by
alterations in serum, CSF or brain concentrations of
excitatory amino acids such as aspartate and glutamate,
and in serum concentrations of other amino acids, such
as serine, glycine and taurine. Brain glutamate
concentrations exceeding those normally are found in
the synaptic clefts can cause selective neuronal loss
and may be involved in a variety of chronic
neurological disorders. NMDA subtype of glutamate
receptors plays a role in the pathophysiology of
depression. However no study has examined whether
serum alterations in the amino acids are relevant to
pathophysiology of TRD. There is only sparse
literature examining the effect of ADs on amino acid
concentration. One study found that CSF levels of
glutamate and aspartate were not affected by ADs
whereas serine levels significantly increased in CSF of
patients treated with ADs. Another study reported that
(i)there are no significant differences in serum levels
of the amino acids measured between patients with
TRD and controls (ii) there is a significant association
between lower serum aspartate, asparagine, taurine,
thereonine and serine levels than a non response to
treatment with Antidepressants and (iii) treatment with
ADs have significant effects on the serum levels of
several of the above amino acid. Studies combining
behavioural, molecular, and electrophysiological
techniques reveal that certain aspects of depression
result from maladaptive stress-induced neuroplastic
changes in specific neural circuits.6
STAGING OF TRD
The classification of TRD in stages has been recently
proposed where increasing resistance is equated with
an increased failure to respond to antidepressant
strategies. The rationale behind this approach is the
clinical impression that the greater the degree of
treatment resistance, the lower the probability of
response to any new treatment.
Thase and Rush Staging Method7: This could be
useful in the classification of TRD, although its
predictive value with respect to treatment outcome
has not been systematically assessed.
Thase and Rush Staging Method (Table 1)
Stage 0: Any medication trials, to date,
judged to be inadequate
Stage I: Failure of at least 1 adequate
trial of 1 major class of
antidepressants
Stage II: Failure of at least 2 adequate
trials of at least 2 distinctly
different classes of
antidepressants
Stage III: Stage II resistance plus failure
of an adequate trial of a TCA
Stage IV: Stage III resistance plus failure
of an adequate trial of an MAOI
Stage V: Stage IV resistance plus a
course of bilateral
electroconvulsive therapy
Massachusetts General Hospital Staging Method8:
considers both the number of failed trials and the
intensity or optimization of each trial but does not
make assumptions regarding a hierarchy of
antidepressant classes. This method generates a
continuous variable reflecting the degree of resistance
in depression (Table 2).
Table 2 Massachusetts General Hospital Staging
Method
1 No response to each adequate (at least 6 weeks
of an adequate dosage of an antidepressant)
trial of a marketed antidepressant generates an
overall score of resistance (1 point per trial)
2 Optimization of dose, optimization of
duration, and augmentation or combination of
each trial (based on the Massachusetts General
Hospital or Antidepressant Treatment
Response Questionnaire) increase the overall
score (0.5 point per trial per optimization or
strategy).
3. Electroconvulsive therapy increases the
overall score by 3 Points.
The European Staging Method: TRD is defined as
a failure to respond to 2 adequate trials of different
antidepressants given in adequate dosages for a period
of 6 to 8 weeks.
A. Nonresponder to: TCA, SSRI, MAOI, SNRI,
ECT, Other antidepressant(s)
No response to one adequate antidepressant trial
Duration of trial: 6–8 weeks
B. TRD: Resistance to 2 or more adequate
antidepressant trials
Duration of trial(s):
TRD 1: 12–16 weeks
TRD 2: 18–24 weeks
TRD 3: 24–32 weeks
TRD 4: 30–40 weeks
TRD 5: 36 weeks–1 year
C. Chronic resistant depression: Resistance to
several antidepressant trials, including augmentation
strategy
Duration of trial(s): at least 12 months
ASSESMENT AND PREDICTORS OF
RESISTANCE
A basic requirement in assessing resistance in
depression is the accuracy of the diagnosis.It is
important to assess the duration of the current trial
and its interaction with the degree of response. As
shown by Nierenberg et al (1995),9 minimal response
after 4 weeks of antidepressant treatment predicts
poorer outcome at 8 weeks. These findings have
challenged the utility of an 8 to12 week trial in someone
with no early sign of improvement. Another important
step toward the assessment of resistance in depression
concerns the level of drug treatment adherence. Finally,
clinicians need to use reliable measures of outcome in
establishing resistance. While the use of clinician-rated
instruments is preferred, it is more common for
clinician to use clinician global assessments, often
combined with self-rated instruments.
• Predictors of Resistance to a Single
Antidepressant Treatment: The search of valid and
robust predictors of resistance to a single
antidepressant treatment has yielded inconsistent
findings. It is also not clear if predictors are
independent of the type of treatment.
Type of depression: Atypical depression is associated
with poorer response to treatment with TCAs, but not
SSRIs or MAOIs. Chronic forms of depression, such
as index depressive episodes lasting two years or more
or double depression is associated with poorer
outcome.
Comorbidity: Substance abuse, and even moderate
consumption of alcohol, is associated with poorer
response to antidepressant treatment. MDD, with
comorbid anxiety disorders, is also associated with
poorer response to antidepressant treatment.
Comorbid personality disorder is associated with
poorer outcome in some. Neuroticism was associated
with poorer antidepressant response in earlier studies,
but not more recent ones 10 . Specific medical
comorbidity (e.g., diabetes, coronary artery disease)
has been associated with poorer outcome.
Decreased subjective social support, poorer
social adjustment and interpersonal relationships have
been associated with treatment resistance in
some.Psychotic features in unipolar depression are
associated with poorer treatment outcome following
treatments with antidepressants alone. When such
features are detected, the addition of antipsychotics is
warranted. Finally, of course, failure to respond to
multiple prior trials of antidepressants is often a
significant predictor of poorer response to
antidepressant treatment.
• Predictors of Resistance to Multiple
Antidepressant Trials or ECT: Longer duration of
the depressive episode and relatively greater
personality disorder comorbidity were associated with
poorer response to lithium augmentation. On the other
hand, contradictory findings have been reported.
Similarly, TRD patients did not differ in degree of Axis
I psychiatric comorbidity from nonresistant depressed
patients in one study.
CORRELATES OF TRD
There is the possibility of considering TRD as a unique
subtype of depression as: (1) clinical characteristics

and course of TRD (behavioral phenotype), (2)
neurobiological profile (EEG, neuroimaging, genetics,
laboratory studies), and (3) the context and
environment in which TRD develops. The
identification of meaningful subtypes of depression is
vital to those fields of psychiatric research that are
beginning to establish that depressive disorders are
brain diseases with unique genetic, neurophysiologic,
and molecular features and that can eventually provide
us with much-needed etiologic information on which
to ground an ideal future classification system.
CLINICAL CHARACTERISTICS AND
COURSE (Behavioral Phenotype): Several
correlates for a worse outcome following an episode
of major depression have been identified.
Atypical depression is characterized by mood
reactivity, weight gain, increase in appetite,
hypersomnia, interpersonal sensitivity, and leaden
paralysis. Atypical depression may be relatively
resistant to TCAs but show a good response to MAOIs
and possibly to the SSRIs and bupropion.
Psychotic depression is characterized by the presence
of either delusions or hallucinations, which are often
but not always congruent with the depressive themes.
Bipolar depression: The response to treatment is often
poor and the process of recovery is frequently slow.
Some characteristics that distinguish bipolar depression
from unipolar depression include age of onset, number
of lifetime episodes, and gender distribution. A number
of investigators have suggested a greater incidence of
reverse vegetative signs (e.g., hypersomnia, increased
appetite, weight gain) and have pointed to the relatively
poor response to TCAs in this population. Lamotrigine
and antidepressants, mainly SSRI’s which have a lesser
propensity for hypomania may be used.
Depression with psychiatric comorbidity,
particularly anxiety, has been found to be associated
with chronicity, poorer response to antidepressants,
delayed response, greater severity of depression and
anxiety, functional impairment, and decreased
responsiveness to treatment. MDD with comorbid
panic disorder is associated with greater chronicity
and severity of anxiety and depressive symptoms,
higher rate of suicide, higher risk of recurrence, and
greater psychologic and psychosocial impairment than
either disorder alone. A retrospective study on 1471
depressed patients found that a comorbid personality
disorder is associated with a worse outcome. Several
symptoms of alcohol and substance abuse can
contribute to TRD.
Medical comorbidity represents another major factor
of treatment resistance. Hypothyroidism, stroke,
diabetes, coronary artery disease, Parkinson’s disease,
HIV infection, AIDS, cancer, and chronic pain can
play a major role in inducing and sustaining TRD
especially when the medical illness is irreversible.
Some of the medications used to treat comormid
medical conditions may induce or worsen a depressive
episode. A number of other variables have been
identified as indicators for nonresponse to
antidepressants such as female gender and older age.
Neurobiological Profile: A number of possible
biological correlates to depression, including TRD,
have been described. Data from ECT,
pharmacotherapy, and psychotherapy studies suggest
that some EEG changes may be predictive of treatment
nonresponse. Patients undergoing ECT treatment
(because of TRD or of severe depression with
psychotic features) tend to show: (1) severe sleep
disruption with several arousals. (2) early awakening.
(3) short rapid eye movement (REM) latency. (4) high
REM density and (5) sleep-onset REM periods (first
REM period within 20 min of falling asleep). Several
of the characteristics mentioned (total sleep time,
REM latency, and REM density) returned to normal
after the ECT course, whereas sleep-onset REM
periods (the first REM period within 20 min of falling
asleep) did not. Also, a relationship was observed
between the presence of sleep-onset REM periods
after the course of ECT and poor response to, or a
high rate of relapse after, ECT therapy. Shortened
REM latency has also been reported for patients who
fail to respond to psychosocial treatment.
Neuroimaging Findings: Several important findings
suggesting the possibility that different topographies
might be related to treatment response have been
described. Although neuroimaging studies have
focused primarily on MDD in general rather than on
TRD specifically, the findings may be usefully applied
in refractory depression. A number of abnormalities
have been found in depressed patients, including
• decreased glucose metabolism in the entire parietal
lobe.
• increased metabolism in the superior posterior parts
of the parietal lobe.
• decreased metabolism in the inferior part of the
parietal lobe
• reduced glucose metabolism and hypofrontality
bilaterally in the prefrontal cortex .
• decreased blood flow and metabolism in the
subgenual prefrontal cortex.
• decreased blood flow or metabolism in the caudate
nucleus.
• and decreased activity in the insula and in the
temporal lobe.
Structural neuroimaging: Studies have suggested a
relationship between TRD and:
• right frontostriatal atrophy,
• changes in the left hippocampus.
• reduction in the frontal lobe volumes,
• subcortical graymatter hyperintensities, and white
matter hyperintensities.
• Negative correlations have been reported
between chronicity of illness and ventricular-brain
ratio, right temporal volume and amygdala-
hippocampus volume.
• Several studies, most involving elderly
depressed patients, have suggested that pathologic
vascular changes (white or gray matter
hyperintensities) may play an important role in
treatment nonresponse and that vascular depression
may be classified as a specific subtype of
depression.
Genetics and Familial Patterns: Positive family
history is associated with early age of onset of
depression and with chronicity, which have both been
linked to resistance. Patients with TRD are more likely
to have a family history of affective illness in the first-
degree relatives than patient without chronic
depression. Candidate genes regularly include members
of the main neurotransmitter systems such as serotonin,
dopamine, and glutamate.
The serotonin transporter (5-HTT) is the selective site
of action of several antidepressants and the 5-HTT
gene is a strong candidate gene for affective disorders.
Two extensively studied polymorphisms of the 5-HTT
gene are the variable number of tandem repeats
(VNTR) in the second intron and the 44 base pair
insertion–deletion in the promoter region (5-HTT
linked polymorphic region [5-HTTLPR], two alleles:
l and s)11. Significant associations have been reported
in patients with major depression between the 5-
HTTLPR allele and the response to paroxetine12,13,
fluvoxamine14, and total sleep deprivation. Associations
with the response to paroxetine and fluvoxamine have
also been described for the s allele of the 5-HTTLPR
and for the ST in 2.12 allele in the VNTR15. However,
other pathways that have influence over several
neuroendocrine systems have recently received
considerable attention. One such pathway, the
hypothalamic– pituitary–adrenal (HPA) axis, plays a
major role in stress hormone regulation. Several
hypotheses that could link genetics to TRD have been
formulated. For instance, it has been observed that
genetically determined abnormalities in
pharmacokinetics (medication absorption, transport,
distribution, metabolism, and excretion) and
pharmacodynamics (tissue response) can play a role
producing vulnerabil ity to TRD.
Laboratory Findings: Laboratory variables
associated with poor outcome of depressive episodes
include blunted prolactin response to fenfluramine
challenge, impairment in immune function and HPA
axis overactivation. However, many of the results are
still inconclusive. For instance, it has been observed
that hypercortisolemia does not always predict acute
antidepressant failure, despite the fact that it can be
associated with severe symptoms such as insomnia,
psychotic cognitive impairment, anxiety, agitation, and
suicidality.
Context and Environment: Several “environmental”
factors have been related to poor treatment outcome,
including -
• lower socioeconomic status.
• nonsupportive social environment.
• family conflicts, chronic stressors , multiple loss
events, lower levels of education and work
dysfunction.
Nonadherence has been estimated to account for as
many as 20% of cases considered to be treatment
resistant and has been associated with younger age,
unmarried status, and intolerance of side effects.
Although nonadherent patients would be excluded
from many of the currently used definitions of TRD,
there is no doubt that they represent a group of
difficult-to-treat patients who are unlikely to
achieve complete remission.
ISSUES RELATED TO CHILDHOOD AND
ADOLESCENCE
Comorbidity is the rule rather than exception in TRD
children and adolescent. ADHD and dysthymic disorder
is common along with comorbid anxiety disorder and
disruptive disorder. Childhood sexual abuse and
parental depression are significant factors16. IPT is
useful to modify social and interpersonal functioning.
Role of comorbid medical condition is also important.
A significant risk factor is development of bipolar
disorder. Geller et al.17 reported 10-15% incidence of
bipolar disorder in children. Before being given
antidepressant the child should be properly evaluated
for avoiding later development of bipolar disorder.
Psychosocial issues and family environment should be
addressed properly. Effect of CBT on psychosocial
issue resolution is not clear. Nemaroff et al.18 predicted
good response to CBT. Kaminski and Graber19 reported
use of family therapy especially in parent child conflict
and parental depression. But studies examining efficacy
of combination treatment (pharmacotherapy and
psychotherapy) in children have at the best modest
benefits over pharmacotherapy alone20. In drug therapy,
studies have shown a better response rate in adolescent
than in children and adolescent tend to metabolize
SSRI faster than adults. One study found that TCA
shows no better effect than placebo in children. It was
also corroborated in later studies. A controlled study
found no significant active versus placebo response
difference is present while others found a significant
active versus placebo difference for SSRI. No clear
recommendations exist for when to switch or augment.
ISSUES RELATED TO GERIATRIC
RESISTANT DEPRESSION
There are few adequately controlled studies of TRD
in geriatric population. Most of the studies focus on
geriatric depression. Alexopolus et al.21 described rate
of medical comorbidity as high as 25-50%. A recent
study22 found anxiety among 67.0% of cases, medical
burden on 43.6% of cases and significant cognitive
impairment among 32.3% cases among TRD patients.
Among 1/3 of patients who failed on initial
antidepressant trial: augmentation strategies can not
be prescribed due to comorbid medical condition. One
must be careful not to view age related brain changes
as necessarily pathoetiologic, as there is always a
danger of mapping multiple colinear markers that may
bring us no closer to effective treatments.
Evidences for efficacy of psychotherapeutic
interventions in old age are few and most of the studies
are based on evidences in old age depression. Even
these studies were having difficulties. Scott et al.23
studied 100 studies of effect of psychotherapy and its
combination in late age depression found that, only
17 studies met minimum sample size of 25. Only 1
study followed up patients for 2 years. The data for
frail elderly and older adults with cognitive impairments
are nearly absent. The evidence for combined treatment
in late life depression is still preliminary, although good
results are reported in chronic or recurrent depression.
Majority of research on late life depression found
strong association with executive dysfunction, memory
deficit, slowed information processing speed and
visuospatial disturbances. No psychotherapy studies
addressed these options particularly. SSRIs are now a
day preferred over TCAs but most of the studies shows
comparable efficacy between two groups. Studies of
SSRI alone or in combination with antipsychotic drugs
in elderly psychotic depression are lacking and in
absence of it, data available from more young
population is generalized to older age group. In
summary, the only strategies for ‘resistant depression’
in later life for which there is at least reasonable
evidence are ECT and lithium augmentation, with
prolongation of the standard course of antidepressant
monotherapy as a third option for less severely
depressed patients.
MANAGEMENT STRATEGIES FOR
TREATMENT RESISTANT DEPRESSION
Strategies for the treatment of RD include
optimization, substitution or switching, combination,
and augmentation therapies. Currently there are no
clear guidelines on when to substitute, combine, or
augment therapies in the treatment of patients with
TRD; however, management should follow a stepwise
approach that allows treatment modification according
to the response achieved. If a patient has a partial
response, augmentation or combination therapies may
be the most sensible strategy. If no clinical response is
observed, switching may be indicated. With the
exception of the STAR*D project, most of the
literature on pharmacologic options focuses on short-
term efficacy.
Optimization: Prescribing antidepressant medication
in dosages that are too low and for lengths of time
that are too short are common causes of treatment
failure. Inadequate antidepressant dosage and duration
are particularly prevalent in elderly patients. Some
depressed patients who are resistant to treatment may
benefit from antidepressant dosages that are higher
than the usual recommendations.
Augmentation: Augmentation can be defined as the
use of a psychotropic agent that does not have an
indication for depression to enhance the effect of an
antidepressant. The theoretical rationale of
augmentation is to obtain a different neurochemical
effect by adding an agent affecting different
neurotransmitter systems. Additionally, an
augmentation agent can be used to broaden the
therapeutic effect (eg, by adding an antianxiety agent
to an antidepressant).
• Lithium: Among the most widely studied
augmentation agents is lithium augmentation
(>600 mg/d) of TCAs, MAOIs, and SSRIs. It
apparently enhances serotonin transmission by
reducing the activity of post-synaptic serotonin
receptors. This, in turn, reduces the negative
feedback to serotonin-releasing cells and thereby
increases serotonin levels in the synaptic cleft.
Lithium may also have effects on other
neurotransmitter systems and neuromodulators. A
starting dosage of 150 mg twice daily, with a
trough serum level obtained within one week, is a
practical starting point for augmentation therapy.
The lithium dosage should be adjusted to result in
a serum blood level between 0.4 and 0.8 mEq per
L (0.4 and 0.8 mmol/L). In clinical practice, aiming
for the lower limit is prudent, since there is
probably equal augmentative efficacy at serum
blood levels of 0.4 and 0.8 mEq per L (0.4 and 0.8
mmol per L). Attempting to enhance response by
increasing the dosage to higher serum blood levels
may only result in unwanted side effects24.
• Thyroid hormone augmentation:
Triiodothyronine (T3) appears to be a more
effective augmentation agent than
tetraiodothyronine (T4) and is effective in small
dosages; for example, 25 to 50 μg per day. T3 may
be used to augment response to tricyclic
antidepressants, monoamine oxidase inhibitors and
SSRIs. Beyond the observation that T3 potentiates
noradrenergic activity, its mechanism of action as
an augmentation agent is not clearly understood.
Although fewer controlled studies have focused
on thyroid hormone than on lithium, T 3
augmentation of TCAs has been shown to be
effective in approximately 50 to 60 percent of
patients.
• Buspirone, a 5-HT1A partial agonist, augment
SSRIs by blunting the negative feedback of
increased synaptic serotonin effects on the
presynaptic 5-HT1A receptor. The STAR*D study
compared buspirone with bupropion and found
 that both helped about 30% of patients who had
not reached remission25. One particular advantage
of buspirone is that it may be helpful in SSRI-
induced sexual dysfunction among women.
• Pindolol. The 5-HT1A postsynaptic antagonist
pindolol accelerates the onset of action of
antidepressants by preventing negative feedback
to the presynaptic 5-HT1A receptor which results
in higher levels of 5-HT in the synapse. Pindolol,
at dosages of 2.5 to 7.5 mg per day for a trial
period of up to six weeks, might prove to be an
effective augmentor of SSRIs.
• Dopaminergic agonists have been particularly
interesting because they bring in a mechanism of
action missing from antidepressants. Pergolide
(0.25–2 mg/d), amantadine (100–200 mg twice
daily), pramipexole (0.125–1 mg three times
daily), and ropinirole (0.5–1.75 mg twice daily)
have been found to be helpful in uncontrolled
studies in patients who had MDD. Disadvantages
include the side of effect of nausea (with the older
compounds) and a lack of controlled studies. An
advantage is that pramipexole, ropinirole, and
amantadine have been used to treat SSRI-induced
sexual dysfunction. Pramipexole and amantadine
also may have neuroprotective properties26,
consistent with the neuroprotective or
neurogenesis hypothesis of antidepressant
action27.
• Traditional psychostimulants that affect
dopamine as potential augmenting agents include
methylphenidate (10–40 mg/d) and
dextroamphetamine (5–20 mg/d). Their use has
been reported as augmentation of TCAs, MAOIs,
and SSRIs. The only two controlled trials in TRD
were negative28, and clinicians also may avoid
using them because of the potential for abuse by
patients who have a history of substance abuse, a
frequent comorbid condition with MDD29. On the
other hand, ADHD is a frequent comorbid
condition of MDD, and a psychostimulant
therefore could be quite helpful.
• Modafinil: A few open trials suggested the
efficacy of modafinil (in doses up to 400 mg/d). A
double-blind study was positive for the treatment
of residual fatigue and sleepiness on SSRIs30, but
its efficacy is unclear in patients who do not
experience fatigue and sleepiness.
• Folate and related compounds: These participate
in the transfer of methyl groups involved in
neurotransmitter synthesis and DNA regulation.
Open augmentation with methylfolate (15–30 mg/
d) resulted in a statistically significant improvement
in depression scores in one study. Open addition
of s-adenosylmethionine (SAMe, 800–1600 mg/
d) also had promise.
• Anticonvulsants: Lamotrigine (100–300 mg/d),
gabapentin (300–1800 mg/d), topiramate (100–
300 mg/d), carbamazepine (200–400 mg/d), and
valproic acid (500–1000 mg/d) have been studied
as augmentation agents. Disadvantages of this
approach include potential tolerability issues with
some of the anticonvulsants (eg, sedation or weight
gain) and the specific risk of Steven Johnson’s
syndrome with lamotrigine and carbamazepine that
necessitates a slow dose escalation. A potential
advantage is that anticonvulsants may help mitigate
anxiety symptoms.
• Benzodiazepines may treat anxiety and also help
with core depressive symptoms when added to an
antidepressant. Evidence exists for the efficacy of
lormetazepam in a double-blind, placebo-
controlled augmentation study of TCAs.
Clonazepam also was nonsignificantly superior to
placebo in augmenting fluoxetine, and zolpidem
was better than placebo in augmenting SSRIs for
sleep problems but not depression. The
disadvantages include potential sedation and, in
the case of benzodiazepines, the possibility of
abuse.
• Riluzole, a putative antiglutamatergic agent
indicated for the treatment of amyotrophic lateral
sclerosis, as add-on therapy for treatment-resistant
major depressive disorder.
Other augmentation agents have been added to
failed trials of antidepressants, but none have been
studied extensively. Inositol (up to 12 g/d) was
found to be no better than placebo in a double-
 blind study. Evidence for the opiates oxymorphone
and buprenorphine is mostly anecdotal. A small,
positive double-blind study supported the use of
dehydroepiandrosterone (up to 90 mg/d). Gonadal
hormones have limited support. One small, double-
blind study reported positive results from the use
of testosterone gel (1% gel, 10 g/d) in men, and
estrogen has limited support from mostly anecdotal
evidence.
Combinations
• SSRI plus bupropion: Despite its popularity,
the evidence for the efficacy of this combination is
minimal. Open trials of bupropion (150 mg SR/
XL daily or twice daily) initially suggested that
this combination would be helpful. In a small trial,
54% of 28 partial and nonresponders to SSRIs or
venlafaxine responded to an open-label trial of
bupropion SR augmentation. A disadvantage of
combining SSRIs or SNRIs with bupropion is
tremor. Advantages are the theoretical gain of
effecting changes in the dopamine, serotonin, and
norepinephrine systems and that the addition of
bupropion may help manage SSRI-induced sexual
dysfunction. Among citalopram nonresponders in
level 2 of the STAR*D study, bupropion combined
with citalopram was nonsignificantly more
effective than buspirone augmentation25.
• Mirtazapine with SSRIs: Another intriguing
combination of theoretical interest is the
dovetailing combination of mirtazapine with SSRIs
or with SNRIs. In a placebo-controlled trial of
mirtazapine (15–30 mg at night) plus SSRIs, more
patients improved with the combination than with
placebo addition. The considerable promise of the
combination resulted in mirtazapine plus the SNRI
venlafaxine as being used one of the two treatment
options in level 4 of the STAR*D study, in which
this combination showed a nonsignificant
advantage over tranylcypromine31. Disadvantages
are the weight gain and sedation associated with
the antihistaminergic effects of mirtazapine.
Advantages are that mirtazapine plus SSRI should
be synergistic: because of its alpha-2 antagonist
properties and 5-HT2 and 5-HT3 receptor
blocking, mirtazapine could decrease the adverse
effects (nausea, anxiety, and sexual dysfunction)
caused by SSRI stimulation of these receptors.
• In small case series the addition of trazodone or
nefazodone to SSRIs was found to result in a
positive response rate in patients who had TRD.
Disadvantages include somnolence (trazodone)
and risk of hepatotoxicity (nefazodone). An
advantage is that trazodone and nefazodone may
help insomnia.
• The combination of SSRIs and TCAs was first
reported in 1991 with fluoxetine and desipramine
(25–75 mg/d). Disadvantages are that several
SSRIs inhibit the CYP450-2D6 system, and TCAs
are substrates of this liver isoenzyme, resulting in
increased blood levels of the TCA that can cause
more adverse effects or toxicity. Another problem
is that low response rates were found in two
double-blind studies. There is evidence, however,
that this combination may produce a more rapid
onset of action. Also, remission rates were
significantly higher with desipramine plus
fluoxetine than with either drug alone.
• Similar to the combination of SSRIs NARI
(reboxetine) (8–12 mg/d), has shown some
promise in combination with SSRIs. Atomoxitin
(40–120 mg/d), a norepinephrine reuptake
inhibitor (NRI) approved for the treatment of
ADHD, was found to be no better than placebo in
a large, double-blind trial of TRD. Combining a
5-HT uptake inhibitor and a norepinephrine uptake
inhibitor may be useful in severely depressed
patients. Also, these NRIs have better safety and
tolerability than TCAs.
Switching Pharmacotherapy
If a treatment fails, either because of lack of efficacy
or intolerable adverse effects, it makes clinical sense
to switch to an alternative treatment. Several choices
exist: switching to an alternative pharmacotherapy,
switching to an evidence-based psychotherapy, or
switching to a neurotherapeutic device that delivers
energy to the brain. Switches can be classified as within
or outside of class. Within-class switching has the
pharmacologic rationale that each medication shares
a common mechanism of action, but each has its own
pharmacologic ‘‘fingerprint’’ with differential effects
on other neurotransmitters and receptors. Outside-of-
class switching is done with the hope that changing
the primary mechanism of action will prove more
effective.
• Switching from one SSRI to another is
supported by open trials of ‘‘historical failures,’’
showing 50% to 60% response rates when
switching from other SSRIs to citalopram32, from
sertraline to fluoxetine, or from one SSRI to
another. Switching from one SSRI to another may
be less effective than switching to a non-SSRI, as
suggested by a double-blind study of a switch to
paroxetine versus a switch to venlafaxine. The
results of level 2 of the STAR*D study showed no
significant advantage of switching to a non- SSRI
compared with a same-class switch in subjects who
had not responded to treatment with one SSRI
(citalopram)2. An advantage is that the immediate
switch from one SSRI to another seems to be well
tolerated. Switching from a TCA to a SSRI is an
option that has not received extensive coverage in
the literature. The disadvantage of a switch to a
SSRI is the well-known high rate of sexual
dysfunction in persons treated with SSRIs. An
advantage of a SSRI over a TCA is that SSRIs
typically are better tolerated than TCAs.
• Switching to SNRIs is certainly a reasonable
option in TRD. An open study showed 30% to
33% of 84 consecutive patients who had TRD
(defined as having not responded to three or more
trials) responded to 12 weeks of open treatment
with the SNRI venlafaxine (300–450 mg/d).
Similarly, 58% of 152 depressed patients who had
not responded to one previous antidepressant trial
responded to an 8-week open venlafaxine
treatment (75–375 mg/d). In a larger study, 52.6%
of 312 depressed patients who had either
‘‘absolute’’ or ‘‘relative’’ treatment resistance
responded to open venlafaxine treatment. Finally,
about 69% of 69 SSRI-resistant depressed patients
were considered as responders after venlafaxine
treatment. Even though a doubleblind study found
that switching to venlafaxine was significantly
superior to a switch to paroxetine in patients who
had TRD, the results of level 2 of the STAR*D
study did not show any significant advantage of
switching citalopram nonresponders to venlafaxine
as compared with sertraline2. Disadvantages of
venlafaxine are blood pressure elevations at higher
doses and discontinuation reactions with sudden
discontinuation. An advantage is that venlafaxine
may be more effective than SSRIs in severe or
melancholic depression.
• Switching to mirtazapine is yet another option.
Forty-seven percent of patients who had not
responded to or tolerated SSRIs showed response
to mirtazapine (15–45 mg/d), and 38% responded
in another study when patients either were
switched to mirtazapine or added it to ongoing
medication. The disadvantages of mirtazapine are
the adverse effects of sedation and weight gain.
The advantages of mirtazapine are that, by
blocking 5-HT2 and 5-HT3 receptors, mirtazapine
may prevent SSRI discontinuation–emergent
adverse events, and immediate switching seems
to be well tolerated.
• Switching to bupropion is an opportunity to
expose patients to the novel dual mechanism of
norepinephrine and dopamine uptake inhibition.
Among 30 TCA nonresponders, bupropion was
better than placebo in reducing depressive
symptoms. Sixtyone patients who had not
responded to at least one antidepressant and who
then took either citalopram or bupropion for 6
weeks and did not respond were switched to the
alternative medication or to citalopram combined
with bupropion. Switching resulted in a remission
rate of 7%; 28% reached remission with the
combination. A disadvantage of switching from an
SSRI to bupropion is that SSRI-induced
discontinuation reactions may occur. An advantage
 is that a switch to bupropion reduces the incidence
of weight gain and sexual dysfunction associated
with SSRIs.
• SSRI to TCA: Clinical lore suggests that the older
generation of TCAs may have greater efficacy than
SSRIs, but the literature on such a switch is small.
A few studies found some efficacy with a switch
to a TCA in patients who had TRD and in SSRI
nonresponders. The disadvantages are the usual
side effects and toxicity caused by TCAs: sedation,
anticholinergic side effects, weight gain, and
lethality in overdose. Advantages include a clear
dose–response curve, the low cost of some of the
generic TCAs, and possible superiority of some
TCAs compared with SSRIs in severe/melancholic
depression.
• Nefazodone and trazodone are two
antidepressants that are used frequently for
insomnia. In terms of switching, a retrospective
study of 20 depressed patients who had not
responded to or tolerated prior antidepressant
treatment suggested the usefulness of trazodone.
Patients who had discontinued an SSRI because
of ‘‘poor response’’ showed significant
improvement with nefazodone (300–600 mg/d).
The disadvantages are that these medications
frequently are underdosed, and nefazodone
requires twice-daily dosing. Furthermore,
nefazodone has a black box warning because of
the risk of fatal hepatic toxicity. Advantages
include less weight gain and sexual dysfunction
than seen with SSRIs.
• MAOIs are used less frequently but also can be
considered as alternative agents for switching. In
one study of patients who had not responded to
imipramine, 58% to 65% showed improvement
with MAOIs. Disadvantages include dietary
restrictions, risk of hypertensive crises and
serotonin syndromes, and the need for wash-outs
before starting and after ending treatment.
Advantages are that the MAOIs are useful in
atypical unipolar depression and anergic bipolar
depression. The considerable promise of the
MAOIs in TRD resulted in the choice of
tranylcypromine as one of the two treatment
options in level 4 of the STAR*D study, in which
it was found to be nonsignificantly less effective
than the mirtazapine/venlafaxine combination 31.
• The norepinephrine uptake inhibitors
reboxetine (4–10 mg/d) and atomoxetine (40–120
mg/d) also may have some usefulness as switching
agents. In one study, patients who had not
responded to an adequate trial with fluoxetine
showed significant improvement with open
reboxetine (8–10 mg/d). Disadvantages are that
switching from an SSRI with a short half-life
requires tapering and that no studies with
atomoxetine have been reported in TRD.
Advantages are that the norepinephrine uptake
inhibitors are potentially useful in SSRI
nonresponders who have a history of prior TCA
response and perhaps in patients who have MDD
with comorbid ADHD.
PROMISING NEW TREATMENTS
Some new and novel therapies show promise for the
future treatment of TRD. These include new
approaches to augmentation treatment, eg, addition
of an atypical antipsychotic to the initial antidepressant;
newer pharmacologic interventions; and
nonpharmacologic therapies such as VNS, rTMS and
DBS.
Augmentation Therapy: Atypical Antipsychotics
and Antidepressants: Evidence suggests that
risperidone (0.5–2 mg/d), olanzapine (5–20 mg/d),
ziprasidone (40–80 mg twice daily), quetiapine (25–
300 mg/d) and aripiprazole (15–30 mg/d) could be
efficacious as augmentation agents in TRD. The
benefits of augmentation with atypical agents,
especially newer agents such as risperidone and
olanzapine, include lower risk for extrapyramidal
symptoms and tardive dyskinesia than with standard
agents also these drugs may help manage anxiety and
agitation.
Risperidone Augmentation of SSRI Therapy: At
low doses, risperidone antagonizes the serotonin (5-
HT)2A receptor—approximately 100 times more
effectively than the dopamine (D2) receptor. Because
the 5-HT2A receptor acts in opposition to the 5-HT1A
receptor, its inhibition may enhance the effects of
serotonin at the 5-HT1A receptor and, thus, augment
the effects of SSRI therapy. The potential benefits of
augmenting SSRI with risperidone indicate the need
for a controlled study.
Olanzapine Augmentation of SSRI Therapy:
Olanzapine is similar to risperidone in that it binds with
high affinity and antagonizes several receptor
subtypes—dopamine (D1¡5), serotonin (5-
HT2A,B,C), alpha 1-adrenergic, histamine (H1), and
muscarinic (M1¡5) receptors. Yet, olanzapine differs
from risperidone by its higher affinity for the 5-HT2C
receptor and, in contrast to risperidone, possesses
higher affinity for alpha 1- than for alpha 2-
adrenoceptors. In a blinded comparative study,
olanzapine demonstrated significantly greater efficacy
in treating depression in patients with schizophrenia
than did haloperidol. Most (57%) of these effects on
mood were primarily direct effects of olanzapine. The
investigators suggest that pharmacodynamic synergy
between fluoxetine and olanzapine may cause a larger
rise in norepinephrine and dopamine levels than that
occurring with fluoxetine monotherapy. The robust and
persistent increase in neurotransmitter release achieved
with fluoxetine plus olanzapine suggests a unique
synergy between these two agents. This synergy
indicates a possible therapeutic mechanism for patients
with TRD: specific targeting of dopamine-innervated
prefrontal regions along with noradrenergic and
serotonergic enhancement. This multimodal profile is
a novel approach to TRD and one not observed with
other augmentation strategies. Coupled with the
encouraging results of the randomized, controlled
clinical study, these insights indicate that effective
augmentation therapy may be achieved with olanzapine
and fluoxetine.
Quetiapine: An antagonist of 5-HT1A, 5-HT2, D1, D2,
H1, á1 and á2 receptors, it has no appreciable affinity
at cholinergic musca-rinic and benzodiazepine
receptors. Quetiapine is known to have a positive effect
on depressive mood in patients with schizophrenia and
bipolar dis-order.
Ziprasidone: exhibits high in vitro binding affinity for
the D2, D3, 5-HT2A, 5-HT2C, 5-HT1A, 5-HT1D, and á1
adrenergic receptors, and moderate affinity for the H1
receptor. Ziprasidone func-tions as an antagonist at
the D2, 5-HT2A, and 5-HT1D receptors, and as an
agonist at the 5-HT1A receptor. Ziprasidone inhibits
synaptic reuptake of 5-HT and norepinephrine. Dunner
et al. 33 compared ziprasidone/sertraline with
sertraline monotherapy in patients resistant to 6 weeks
sertraline therapy and 4 their SSRI therapy. In this
study, 50% responded and weeks of prior therapy with
at least one SSRI or non-SSRI antidepressant. Patients
who prior received a non-SSRI therapy demonstrated
under augmentation with ziprasidone a significantly
greater improvement compared with those patients
who received sertraline monotherapy. Among patients
with a history of SSRI resistance only, improvement
with the combination therapy did not reach significance
versus sertraline monotherapy. The second small
study34 was performed in 20 patients who received
ziprasidone in addition to 28% achieved remission after
6 weeks of therapy.
Zotepine: has a high affinity for D1, D2, 5-HT2A, 5-
HT2C, 5-HT6, and 5-HT7 receptors. Furthermore, it
inhibits the reuptake of noradrena-line. Zotepine has
been shown to be effective in the treatment of
delusional depression in combina-tion with a TCA or
SSRI. No data are currently available for treatment of
TRD. However, like with quetiapine the latter studies
might be indicative for the effectiveness in TRD.
Amisulpride: a selective antagonist for dopamine D2
& D3 receptors acts preferentially on pre-synaptic
receptors increasing dopaminergic trans-mission at low
doses. A placebo-controlled trial showed that
amisulpride at a low dose (50 mg/day) is effective in
the treatment of primary dysthymia.
SOMATIC THERAPIES FOR TRD
ECT: The efficacy of ECT for depression has been
demonstrated in a large number of clinical trials. A
recent metaanalysis found that real ECT was
significantly more effective than simulated ECT (six
trials, 256 patients), and treatment with ECT was
significantly more effective than pharmacotherapy (18
trials, 1144 patients). Bilateral ECT was more effective
than unipolar ECT (22 trials, 1408 participants) 35.
Patients often require continued maintenance
treatment; however, significant side effects such as
memory loss are associated with ECT.
Ablative Limbic System Surgery: Neurosurgical
procedures for treatment of psychiatric disorders
include anterior cingulotomy, subcaudate tractotomy,
limbic leucotomy, and anterior capsulotomy. These
procedures have been found to be efficacious in
patients suffering from intractable mood and anxiety
disorders with response rates ranging from 35% to
70% over a period of several weeks to several months,
depending upon the response criteria.
Vagus Nerve Stimulation: Evidence supporting a role
for VNS therapy in depression came from early
observations of mood improvement in patients with
epilepsy who participated in early VNS
studies.Prospective evaluation of epilepsy patients
evaluated with standard depression symptom severity
rating scales revealed that VNS therapy was associated
with statistically significant improvements in mood that
was not related to reductions in seizure frequency. The
documented efficacy of anticonvulsants, such as
carbamazepine, lamotrigine, valproate, and perhaps
others, as mood stabilizers and/or antidepressants in
bipolar disorder and the anticonvulsant properties of
ECT are concordant with the hypothesis that VNS
therapy may be a useful therapeutic option for
depression. VNS results in markedly increased c-fos
expression in forebrain (lateral hypothalamus,
paraventricular nuclei, CA3 hippocampal fields, and
neocortex) and brain stem regions (NTS, nucleus raphe
magnus, PBN, A7 area, locus ceruleus, and
periaqueductal gray), resolution of some of the regional
cerebral blood flow (rCBF) abnormalities in limbic and
cortical structures (eg insula, dorsolateral prefrontal
cortex (DLPFC), temporal cortex) that are associated
with depression36.
Transcranial Magnetic Stimulation: The most used
rTMS strategy for the treatment of depression is high-
frequency rTMS (20-HZ) of the left DLPFC, but this
strategy has an important cost benefit ratio and it may
increase the risk of seizure. Therefore, lower frequency
rTMS (1-HZ) strategies are potentially advantageous if
clinical efficacy can be demonstrated. The rationale of
targeting the left DLPFC is that lesion and imaging studies
show that left prefrontal cortex dysfunction is
pathophysiologically linked to primary and secondary
depression. Because this dysfunction is associated with
a decrease in the left DLPFC activity, high-frequency
rTMS is used as it induces larger cerebral blood flow in
the stimulated area in the majority of subjects37. Indeed,
the vast majority of the initial rTMS studies applied high-
frequency rTMS on the left DLPFC. It has been
speculated that an inhibition of the right prefrontal cortex
(based on the inhibitory effects of 1 Hz rTMS and the
notion of laterality in prefrontal activity in depression)
might correct the interhemispheric imbalance of DLPFC
activity in depression. In a sham controlled blind trial
by Fitzgerald et al.38 in TRD patients found at the end
of study that 44% of patients in active group and 8%
of patients in sham group responded (p<0.05).
Magnetic Seizure Therapy: MST or convulsive
rTMS refers to the administration of rTMS to the scalp
to induce seizures under general anesthesia.
Hypothetically, such magnetically induced seizures can
replace ECT (and its associated adverse cognitive
effects) in patients with TRD. The feasibility of the
procedure has been demonstrated in a female subject
with a 3-year episode of TRD39. A decrease in the
HAM-D score from 20 to 13 was noted in the latter
following MST. A randomized, controlled trial
examined the procedure in eight patients with a major
depressive episode who were candidates for ECT and
found the procedure to be well tolerated40. The clinical
efficacy of MST in the treatment of TRD and whether
MST will be preferable to ECT remains to be
established.
Deep Brain Stimulation: In one clinical trial of DBS41
electrodes were placed in the subgenual cingulate
cortex (approximately Brodmann area 25) bilaterally
in six patients who had TRD. At 6 months, four of the
six patients were classified as responders. Depressive
symptoms also improved in the cohort of patients who
had intractable obsessive-compulsive disorder
undergoing DBS42. Clinical trials of DBS in the anterior
limb of the internal capsule for major depression are
currently underway. To date, this procedure remains
an experimental, not approved for general clinical use
for this indication.
Natural Remedies
St. Johns wort: There are 37 published trials including
26 placebo controlled studies and 14 with standard
antidepressant as the active comparator, but none of
these focussed on TRD.
S-Adenosyl Mehionine: There are 45 published
clinical studies for treatment of depression out of which
8 are placebo controlled and used an active comparator
but very few for TRD. One study examined the efficacy
of sAMe as an adjunct for partial and non responders
to SSRI and found response and remission rates of
50% and 43% respectively and treatment was well
tolerated. But still no published studies using placebo
control is available.
Omega 3 fatty acids: A randomized, placebo
controlled dose finding study of Eicosapentanoate
(EPA) as adjunctive therapy with inadequate response
on antidepressant trial reported that 1 gm/day of EPA
for 12 weeks showed response rate of 53% compared
to placebo of 29% with notable improvement of
depressed mood, anxiety, sleep disturbance, libido
suicidality43.
ROLE OF PSYCHOTHERAPY
Interpersonal, cognitive, and behavioral therapies offer
structured pragmatic methods to evaluate and work
with such difficult patients. Although some evidence
supports the use of these psychotherapies alone for
treatment-resistant depression (in lieu of further trials
of medication), data are emerging to suggest a
potentially more valuable role when they are combined
with pharmacotherapy. The newer depression-focused
psychotherapies are relevant and potentially valuable
strategies for patients with treatment resistant
depression.
Evidence that psychotherapy works: Much
of the evidence about the effectiveness of newer
antidepressants comes from studies either supported
by or directly conducted by the manufactures of those
medications. A large portion of these studies are
already convincing evidence that the new treatment
works, at least in comparison to placebo. Since
psychotherapy is not manufactured nor protected by
patents, there are no comparable corporate research
and development funds to sponsor research. Moreover,
a pill placebo group is not an adequate control group
for psychotherapy research. As a result, there will never
be the weight of evidence supporting the efficacy of
psychotherapy that can be marshaled for antidepressant
pharmacotherapy. Nevertheless, a sizeable number of
comparative studies have examined cognitive,
behavioural and interpersonal therapies in relatively
uncomplicated (without severe personality problems
or a large number of comorbidities) groups of
depressed outpatients and in aggregate, 4 conclusions
can be drawn.
1. Depressions focused psychotherapies (i.e.
cognitive, interpersonal, and behavioural
therapies), typically provided across 8 to 16 weeks,
are significantly more effective than waiting list
or minimal contact control conditions.
2. Depression-focused therapies typically produse
response rate comparable to those found with
antidepressant medications in randomize clinical
trials.
3. There is no compelling evidence that one form of
depression focused psychotherapy is superior to
another. It has been suggested that cognitive
therapy may have more enduring effects following
termination of therapy, but one controlled trial
directly comparing cognitive therapy and
interpersonal therapy did not reveal any advantage
for the cognitive therapy condition across a 24
month follow up.
4. The addition of cognitive therapy or interpersonal
therapy to ongoing pharmacotherapy increases the
likelihood of remission for patients with chronic,
severe recurrent or resistant or partially treatment
 responsive treatment resistant depression thus
represents an important indication for combining
psychotherapy and pharmacotherapy.
Suggested guidelines for psychotherapeutic
intervention for treatment resistant depression The
therapy relationship should be collaborative and centered
around the goal of teaching new skills to improve coping
with a chronic illness. The therapist must pair core
therapeutic skills (e.g. empathy and understanding) with
the ability to appropriately select specific, targeted
interventions (e.g. relaxation training, activity scheduling,
problem solving, or cognitive restructuring).
• The therapist may make judicious use of examples
from other medical models in which rehabilitative
interventions are used to enhance the outcome of a
chronic disorder (e.g. poststroke rehabilitation, pain
management, or orthopedic rehabilitation).
• The therapist may express cautious optimism that
problems can be addressed with varying degrees
of success. However, it is important to be
understanding of the patient’s pessimism and elicit
feedback from the patient about what has not
worked well in the past.
• Establish stepwise, short term goals specifically
addressing life problems and/or symptoms. Use
graded tasks or intermediate assignments to
approach more daunting or potentially
overwhelming problems.
• Meet frequently and, if necessary, shorten sessions
to enhance learning and retention. Keep sessions
active and avoid the “silent treatment. Obtain
feedback at beginning and end of treatment
sessions so that patient’s reactions to therapy can
be monitored and promptly addressed. Be vigilant
concerning subtle affective and behavioural
reactions within sessions as an in vivo source of
feedback.
• Use homework assignments and in session
rehearsal to facilitate development of new coping
skills. It is important to avoid implicit criticisms
about difficulties in therapy, such as homework
noncompliance. The therapist must address his or
her own dysfunctional cognitions blaming the
patient for “not wanting to get better”.
• Involve spouse or significant others to provide
psychoeducation and enhance alliance with family
members.
• Establish intermediate and long term goals as
symptomatic improvement and short term goals
are accomplished.
• Do not terminate therapy until the patient has
achieved a remission and sustained it for at least 4
to 6 months.
Managing the course of Therapy: The depression
focused psychotherapies are conducted in both individual
and group formats and typically range from 10 to 16
weeks in duration. Individual sessions are typically 45 to
60 minutes in length, whereas group sessions are usually
90 to 120 minutes long. Ideally, we would recommend
twice weekly sessions early on to facilitate the process of
therapy. Perhaps even more frequent sessions would be
helpful, but economic considerataions usually make this
impossible. We prefer to continue with twice weekly
sessions until the patient has achieved at least a 50%
reduction in symptom severity, shifting to weekly sessions
thereafter. If the patient has not obtained significant
symptom relief by the eighth week (i.e., 16th session), a
careful evaluation of the continued indications for
psychotherapy, as well as possible alternatives, should
be undertaken. A successful course of acute phase,
focused psychotherapy for treatment resistant depression
typically lasts 4 to 6 months. It appears that patients who
did not remit fully may benefit from less frequent,
continuation phase sessions over the next 6 to 9 months.
SEQUENCED TREATMENT ALTERNATIVES
TO RELIEVE DEPRESSION (STAR*D)
This study aims at determining the best subsequent
treatment strategies (i.e. identifying which
combinations and which sequences of treatment are
effective with minimal side effects). This multisite,
prospective, sequentially randomized controlled trial
targeted 4000 adults with nonpsychotic major
depressive disorder. Following treatment failure at each
of the 4 sequential levels, patients progressed to the
next level, where they were randomly assigned to the
various treatment options (Figure 1). Independent
evaluators, blinded to level and treatment, conducted
periodic clinical outcome assessments. These
additional results will provide information on symptom
severity, level of functioning, adverse effect burden,
patient satisfaction/quality of lif, and health care
utilization and cost. Once patients have obtained a
satisfactory response, follow up assessment will
determine the degree and timing of possible relapse.
Fig.1. The four sequential levels of STAR*D study
Level 1: Initial Treatment: citalopram
Switch to: bupropion (sustained-release),
cognitive therapy, sertraline, venlafaxine
Level 2: (extended-release)
Or augment with: bupropion (sustained-
release) or venlafaxine (extended-release)
Only for those receiving cognitive therapy in
Level 2
Level 2a: Switch to: bupropion (sustained-release) or
venlafaxine (extended-release])
Switch to: mirtazapine or nortriptyline
Level 3: Or augment with: lithium or thiodothyronine
(only with bupropion [sustained-release],
sertraline, or venlafaxine (extended-release)
Switch to: tranylcypromine or mirtazapine combined
Level 4: with venlataxine (extended-release)
The remission rates for step one was 36.8%,
for step two 30.6%, for steps three 13.7% and step
four 13.0%. Remission rate declined significantly after
step two. This might support the developing notion
that treatment resistant depression can be defined by
two prior treatment failure. High remission rates
during initial trial were seen in patients who were
female, employed or higher level of education and
income. The cause of declining remission may be that
the remission occurring due to nonspecific effects of
patient care, attention, care, reassurance, education
and can be called as placebo response, was declining.
Khan et al.44 showed that about 73% decrease in
HDRS score in the drug group could be accounted
by these factors. Rate of relapse increases with each
step 33.5%, 47.4%, 42.9%, 50.0%. Relapse was even
higher in patients who improved but did not achieved
remission. Intolerance rate increased after each
treatment step. 16.3%, 19.5%, 25.6%, 34.1%.
Cumulative sustained recovery was calculated at 43%
taking relapse into account and it does not include
patients opting out. It pastes a little grim picture in
outcome of TRD. Randomizataion was not done at
step 2. Only 1.5% of patients agreed for randomization,
so comparison between treatment strategies is
difficult.It was found later on that patients entering
cognitive therapy were having lower entry scores. It
may explain the higher remission rate. According to
Rush et al.2 the biggest surprise of this study was
comparable findings to SSRI-SSRI switch to switch
to Bupropion or velafexine. Questions were raised
weather longer duration of treatment is just as
important to choosing a drug.
The drawbacks of this study are: (1) Only
outpatient seeking medical care is included (2) Age
limit was restricted to 10-75 (3) Patents with bipolar
and psychotic disorder excluded (4) reliance on self
report QIDS-SR16 as primary outcome (5) neither
clinician nor participants were blind to treatment (6)
placebo control was not used (7) dropout rate was
quite high and most of the people who exited were
not in remission (8) very high quality of care was
delivered which may limit its generalibility.
CONCLUSION
Despite the numerous options available for the
treatment of depression, many patients do not achieve
a partial or full response with an adequate dose of
two or more medications of different antidepressant
classes, each given for a sufficient duration. Such
resistance to psychopharmacologic treatment options
challenges the practitioner. A staged approach to TRD
includes reevaluation of the initial diagnosis and, when
no correctable cause for TRD is found, optimization
of the initial regimen. Other pharmacologic treatment
approaches include switching antidepressant agents,
adding a second antidepressant with a different
mechanism of action, and augmenting the effects of
the initial antidepressant by adding an agent other than
an antidepressant. Although this treatment paradigm
provides several management alternatives, depression
in many patients remains resistant. Promising new
therapies now under investigation may soon be
validated and available for use in clinical practice.
Efforts to identify true TRD and its definitive clinical
diagnostic criteria continue. A better understanding
of TRD and the many facets of its etiology, as well as
the availability of new and effective therapies,
hopefully will decrease the morbidity and mortality
associated with depression.
REFERENCES
1. Trivedi, M.H., Fava, M., Wisniewski, S.R. et al. (2006). STAR*D
Study Team. Medication augmentation after the failure of
SSRIs for depression. N Engl J Med, 354, 1243-1252.
2. Rush, A.J., Kraemer, H.C., Sackeim, H.A., et al. (2006). Report
by the ACNP Task Force on response and remission in major
depressive disorder. Neuropsychopharmacology, 31(9), 1841–
53.
3. Kessler, R.C., Chiu, W.T., Demler, O., et al. (2005). Prevalence,
severity, and comorbidity of 12-month DSM-IV disorders in
the National Comorbidity Survey Replication. Arch Gen
Psychiatry, 62,617–27.
4. Berlim,M.T. and Turecki, G. (2007) Definition, Assessment,
and Staging of Treatment–Resistant Refractory Major
Depression: A Review of Current Concepts and Methods. Can
J Psychiatry 2007; 52: 46–54
5. Souery D, Lipp O, Massat I, Mendlewicz J.(2001). The
characterization and definition of treatment-resistant mood
disorders. In: Amsterdam JD, Hornig M, Nierenberg AA,
editors. Treatment-Resistant mood disorders. New York (NY):
Cambridge University Press; p 3–29.
6. Krishnan V. and Nestler. E.J.(2008) The molecular neurobiology
of depression. NATURE, 455:16
7. Thase & Rush, 1997
8. Petersan et al. (2005). Empirical testing of two models for
staging antidepressant treatment resistant resistance. J Clin
Psychopharmachol, 25(4), 336-341.
9. Nierenberg et al (1995),
10. Petersen, T., Papakostas, G.I., Bottonari, K., Iacoviello, B.,
Alpert, J.E., Fava, M. et al. (2002a). NEO-FFI factor scores
as predictors of clinical response to fluoxetine in depressed
outpatients. Psychiatry Res, 109, 9–16.
11. Bellivier, F., Roy, I., Leboyer, M. (2002). Serotonin transporter
gene polymorphisms and affective disorder-related
phenotypes. Curr Opin Psychiatry, 15, 49–58.
12. Pollock, B.G., Ferrell, R.E., Mulsant, B.H., Mazumdar, S.,
Miller, M., Sweet, R.A. et al. (2000). Allelic variation in the
serotonin transporter promoter affects onset of paroxetine
treatment response in late-life depression.
Neuropsychopharmacology, 23, 587–590.
13. Zanardi, R., Benedetti, F., Di Bella, D., Catalano, M., Smeraldi,
E. (2000). Efficacy of paroxetine in depression is influenced
by a functional polymorphism within the promoter of the
serotonin transporter gene. J Clin Psychopharmacol, 20, 105–
107.
14. Serretti, A., Zanardi, R., Rossini, D., Cusin, C., Lilli, R.,
Smeraldi, E. (2001). Influence of tryptophan hydroxylase and
serotonin transporter genes on fluvoxamine antidepressant
activity. Mol Psychiatry 6: 586-592.
15. Kim, D.K., Lim, S.W., Lee, S., Sohn, S.E., Kim, S., Hahn,
C.G., Carroll, B.J. (2000). Serotonin transporter gene
polymorphism and antidepressant response. Neuroreport, 11,
215–219.
16. Southam-Gerow MA, Kendall PC, Weersing VR.
Examining outcome variability: correlates of treatment
response in a child and adolescent anxiety clinic. J Clin
Child Psychol 2001;30:422–36.
17. Geller, B. Zimmerman, M., Williams, R., et al. (2001)
Bipolar disorder at prospective follow-ups of adults who had
prepubertal pubertal major depressive disorder. Am J
psychiatry. 158(1) pp. 125-127.
18. Nemeroff, C.B. et al (2003) Improving antidepressant
adherence. J. Clin. Psych. 64 (suppl)25-30.
19. Kaminski, K.M., and Garber, J.. (2002) Depressive
spectrum disorders in high-risk adolescents: episode duration
and predictors of time to recovery. J Am Acad Child Adolesc
Psychiatry;41: 410–8.
20. Goodyer, I.M.. (2006).Arandomised controlled trial of
SSRIs with and without cognitive behaviour therapy in
adolescents with major depression. Cambridge, England: NHS
Technology Assessment Programme.
21. Alexopoulos, G.S., Meyers, B.S., Young, R.C., Campbell,
S., Silbersweig, D., Charlson, M. (1997). ‘Vascular
depression’ hypothesis. Arch Gen Psychiatry, 54, 915–922.
22. Dew et al.,(2007) outcome of antidepressant therapy in old age
group. Am J Psychiatry. 163: 864-866.
23. Scott, M. et al. (2005). evidence based psychotherapeutic
interventions for geriatric depression. PCNA, 805-820.
24. de Montigny, C. (1994). Lithium addition in treatment-resistant
depression. Int Clin Psychopharmacol, 9(Suppl 2), 31-5.
25. Trivedi, M.H., Rush, A.J., Wisniewski, S.R., et al. (2006).
STAR*D Study Team. Evaluation of outcomes with citalopram
for depression using measurement based care in STAR*D:
implications for clinical practice. Am J Psychiatry, 163, 28-
40.
26. Du, F., Li, R., Huang, Y., et al. (2005). Dopamine D3 receptor-
preferring agonists induce neurotrophic effects on
mesencephalic dopamine neurons. Eur. J. Neurosci,
22(10),2422–30.
27. Duman, R.S., Role (2004) of neurotrophic factors in the etiology
and treatment of mood disorders. Neuromolecular Med,
5(1),11–25.
28. Patkar, A.A., Masand, P.S., Pae, C.U., et al. (2006). A randomized,
double-blind, placebo-controlled trial of augmentation with an
extended release formulation of methylphenidate in outpatients
 with treatment-resistant depression. J. Clin.
Psychopharmacol, 26(6),653–6.
29. Davis, L.L., Frazier, E., Husain, M.M., et al. (2006). Substance
use disorder comorbidity in major depressive disorder: a
confirmatory analysis of the STAR*D cohort. Am. J. Addict,
15(4), 278–85.
30. Fava, M., Thase, M.E., DeBattista, C. (2005). A multicenter,
placebo-controlled study of modafinil augmentation in
partialresponders to selective serotonin reuptake inhibitors
with persistent fatigue and sleepiness. J. Clin. Psychiatry,
66(1),85–93.
31. McGrath, P.J., Stewart, J.W., Fava, M., et al. (2006).
Tranylcypromine versus venlafaxine plus mirtazapine
following three failed antidepressant medication trials for
depression: a STAR*D report. Am. J. Psychiatry,
163(9),1531–41.
32. Thase, M.E., Feighner, J.P., Lydiard, R.B. (2001). Citalopram
treatment of fluoxetine nonresponders. J. Clin. Psychiatry,
62,683–7.
33. Dunner, D.A., Amsterdam, J.D., Shelton, R.C., Hassman, H.,
Rosenthal, M., Romano, S. (2003). Adjunctive ziprasidone
in treatment resistant depression: a pilot study. Poster
presented at: annual meeting of the American Psychiatric
Association. San Francisco, Calif.
34. Papakostas, G.I., Peterson, T., Worthington, J. (2003).
Ziprasidone augmentation for major depressive disorder
rfractory to SSRIs. Poster presented at: annu-al meeting of
the American Psychiatric Association, San Francisco, Calif.
35. Kessler, R.C., Berglund, P., Demler, O., et al. (2005). Lifetime
prevalence and age-of-onset distributions of DSM-IV disorders
in the National Comorbidity Survey Replication. Arch Gen
Psychiatry, 62(6),593–602.
36. Devous, M.D., Husain, M., Harris, T.S., Rush, A.J. (2002).
Effects of VNS on regional cerebral blood flow in depressed
subjects. Poster presented at the 42nd Annual New Clinical
Drug Evaluation Unit
37. Nahas, Z., Marangell, L.b., Husain, M.M. et al. (2005). Two-
year outcome of vagus nerve stimulation (VNS) for major
depressive episodes. J Clin Psychiatry, 66, 1097–1104.
38. Fitzerald,B.P., Benitez, J., DeCastella, A., et al.(2006). A
randomized, controlled trial of sequential bilateral repetitive
transcranial magnetic stimulation for treatment-resistant
depression. Am j Psychiatry, 163, 88–94.
39. Lisanby, S.H., Schlaepfer, T.E., Fisch, H.U., Sackeim, H.A.
(2001b). Magnetic seizure induction for the treatment of major
depression [letter]. Arch Gen Psychiatry, 58, 303–305.
40. Lisanby, S.H., Luber, B., Barroilhet, L., Neufeld, E., Schlaepfer,
T., Sackeim, H.A. (2001c). Magnetic seizure therapy (MST):
Acute cognitive effects of MST compared with ECT. J ECT,
17, 77. Abstract 4.
41. Mayberg, H.S., Lozano, A.M., Voon, V. et al (2005). Deep brain
stimulation for treatment-resistant depression. Neuron, 45, 651–
660.
42. Greenberg, B.D., Malone, D.A., Friehs, G.M., et al. (2006).
Three-year outcomes in deep brain stimulation for highly
resistant obsessive-compulsive disorder.
Neuropsychopharmacology, 31, 2384–93.
43. Puri, B.K..,Counsell, J.K., Hamilton, G. et al. (2001)
Ecosapentanoic acid in treatment-resistant depression associated
with symptom remission, structural brain change andreduces
neuronal phospholipid turnover. Int J Clin Pract. 55:560-563.
44. Khan et al. (2003) Placebo response and antidepressant trial
outcome. J Nerv Ment Dis 19: 211-218.
 REVIEW ARTICLE
Socio-Economic and Cultural Aspects of Suicide
Arabinda Brahma
Consultant Psychiatrist, UNMC&RI, SaltLake; G.S. Clinic, Kolkata & Hon. Lecturer,
Indian Psycho-Analytical Society, Kolkata

The magnitude of the problem:
Everyday thousands of people commit and attempt
suicide all over the world. However, actual statistics
about suicide is difficult to obtain. Under-reporting,
legal issues and improper record keeping are a few
important factors why official statistics appear to
underestimate the true rates of suicide and attempted
suicide of any given society.
Suicide is considered as a major public and mental
health problem. In 2000, approximately 8, 15,000
person committed suicide i.e. 14.5 per 100000
populations 1. On the other hand, approximately 20
million people attempt suicide every year throughout
the world 1. In India, suicide is among the top ten
causes of death. The current national suicide rate for
India is 10.3 per 100000 populations 2. According to
the National Crime Records Bureau, West Bengal
(13.3%), Maharashtra (13.1%), Andhra Pradesh
(11.2%), Tamil Nadu (10.5%) and Karnataka (10.3%)
contributed 58.4% of total suicide in India 3 .
Interestingly, densely populated states like Uttar
Pradesh and Bihar contribute relatively less suicides.
Under-reporting may be an important cause for this
significant difference between different states.
The importance of suicide from the public health point
of view is persistently under-recognized even though
it is considered as a leading cause of mortality all over
the world. Besides biological (including genetic) and
psychopathological factors, it has been revealed in
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence: Dr. A. Brahma,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Uma Nalini Mary Clinic & Research Institiute, KB 16,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Sector III, Salt Lake, Kolkata 700098.
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-mail: drarabindabrahma04@yahoo.com
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
researches that the socio-economic and cultural factors
influence the risk of suicidal behavior.
Evolution of concept:
The instinct to survive is a very common human
behavior. However, the wish towards self-destruction
has been reported since the beginning of the civilization
in every part of the globe. This peculiar behavior has
been found in the ancient scriptures and historical
documents written in different languages. According
to Edwin Shneidman suicide is associated with
thwarted or unfulfilled needs, feelings of hopelessness
and helplessness, ambivalent conflicts between survival
and unbearable stress, a narrowing of perceived
options, and a need for escape; the person wants to
die shows signals of distress 4.
Human suicidal behavior has been considered as a
dreadful and puzzling behavior. The word
‘suicide’ originated from Latin ‘SUI’ (of one self) and
‘CAEDES’ (murder). According to the eminent French
Sociologist Emile Durkheim 5: “suicide is any death
that is the direct or indirect result of a positive or act
accomplished by the victim himself/herself which, he
/she knows or believes will produce this result”. The
study of suicide and its causes have come a long way
since the views of Durkheim. In the present days, it
has been revealed in different researches that the
personal factors along with the social dynamics play a
great role in the causation of suicide.
Suicide is considered as a peculiar behavior because
all suicidal people are not death seekers. Before 1950s,
not much distinction was made between people killed
themselves and who died after such an act. Stengel in
1952 first used the term ‘attempted suicide’ to
differentiate between completed suicidal act from
attempted one 6. It was Kessel and Grossman who
changed the concept in 1960, stating the fact that intent
was not an essential factor for attempted suicide as
most of the attempters did this with the knowledge of
their safety 7. Later, Kreitman and his colleagues
introduced the term ‘parasuicide’ to refer to the non-
fatal act 8. Further modification of terminology evolved
when Morgan in 1979 coined the term ‘deliberate self-
harm’ to provide a single term covering all non-fatal
suicidal attempts 9.
Historical background:
Suicidal behavior involves not only the individual
concerned; it also affects the community for the socio-
emotional dynamics associated with it. Historical
analysis of suicidal behavior has shown that it had
different meanings in different situations since the birth
of mankind. In the ancient world, the voluntary self-
killing was honorific and praised by the society. The
cause of such act was either personal (for moral value)
or collective (species survival value).
Descriptions of suicidal behavior is seen in the ancient
Indian epics i,e. in Ramayana and Mahabharata 10. In
the more modern times, Sati and Jaharbrata are the
two important ritualistic self-killings practised by the
females in the Indian society. Some author considers
these two are examples of altruistic suicide 11.
Religious background:
Bhagavat Gita is against the self-killing and self-
destruction. However, in many Indian mythologies,
self-killings were glorified by attaching religious and
spiritual values. The self-killing of Vishma and
Balarama (elder brother of Lord Krishna) in
Mahabarata are the classic examples. In the Vedic and
Upanishadic times, death at the confluences of holy
rivers by drowning for achieving ‘punnya’ (salvation
in the next life) was a cultural and religious code
prevalent in the society.
Islam clearly mentions that one should wait for his
destiny and not to snatch it from the hand of Allah.
Similarly, it was seen in Bible that Judas (one who
betrayed Lord Jesus) was cried and wept with guilt
and remorse before hanging himself. Researches have
revealed that suicidal behavior was less commonly seen
amongst Islam and Catholic communities than Jewish
and Protestants communities.
Cultural background:
Durkheim was the first to highlight the influence of
social and cultural factors in suicidal behavior. Cultures
include all the aspects of living and thus have a complex
influence on human behavior. Researches have shown
that cultural value system of gender roles and social
expectations influence the nature and rates of self-harm
behavior 12. Influences of media on suicidal behavior
in different countries have been depicted in various
researches 13. In the modern world, more concern for
children is seen in most of the nuclear families. At the
same time, neglect towards the elderly in the family
has been increasing and leads to a feeling of
meaninglessness in life, which in turn increases suicidal
acts amongst them.
Researches from different parts of the globe have also
revealed that suicide by chemical ingestion (e.g.
pesticides, insecticides and indigenous poisons like
Oleander seeds) may be an attempt to seek help by
the individual involved in a specified distressed
situation 14.
Immigrant population is always at greater stress that
involves mainly the struggle between old and new
culture – with its attendant problems of poverty, poor
housing, lack of social support and unmet expectations.
All these may lead to suicidal behavior, especially in
the younger age groups. This acculturative stress is
also evident even within one country where the
traditional groups (e.g. tribal population) are fighting
hard for their existence by clinging to there traditional
ethos in the face of engulfing dominating culture.
Imitative suicide is a mode of cultural communication
where an individual or a group exhibits this behavior
in extreme distress. This type of suicide is
predominantly seen in adolescent age groups. It
spreads through media publicity and gaining much
attention in the recent days 15.
It is a known fact that religion and social cohesion are
two cultural determinants that guide the social life in
a community. An important study amongst British
Columbia’s First Nations Women has revealed that
how the cultural identity and traditional native
spirituality has a healing effect on suicidal ideation and
intention 16.
Socio-economic factors:
Age and sex are two important social determinants
identified in different suicide researches. The younger
(15-30years) and the elderly (above 65 years) age
groups are at increased risk of suicide 17. The suicide
rates in India also peak for both men and women
between the age 18 and 29 18. In most of the countries
more males than females commit suicide17. However,
a few studies from China and India have shown higher
female suicides than their male counterparts mainly in
the rural areas 19, 20.
Studies have shown that the risk of suicidal behavior
increases among divorced, widow and single people
21, 22
. Marriage appears to be protective for males in
terms of suicide risk but not so for females.
Certain occupational groups like farmers, dentists and
medical practitioners are at a greater risk of suicide 23,
24
. Easy accessibility to lethal means, extreme work
pressure, social isolation and economic constraints may
be the causative factors that explain the higher suicidal
rates amongst them 25. Unemployment increases
poverty, social deprivation, domestic difficulties and
hopelessness, which in turn increases the suicidal rates.
Suicide of farmers in different states of India in the
recent days probably highlights this association 25.
Easy availability of the means of committing suicide
and stressful life events are other important social
factors in suicidal behavior. A recent study in the
remote rural areas of the Sundarban region of West
Bengal, India has revealed that the ready availability
and improper storage of pesticides in the households
as well as the greater life stresses of women both in
the outdoor works and in the domestic front increase
the chance of suicide amongst them 26.
Conclusion:
Suicide is a preventable cause of death and the means
of prevention is the ultimate goal of the art and science
of suicide research. Strengthening the poverty
alleviation projects, proper education for children,
ensuring job security and to guarantee economic
security for farmers are some of the important aspects
of primary prevention of suicide. Minimizing migration
related stressors and family conflicts as well as
expanding family support are also important socio-
cultural issues. Identification of high risk groups and
establishment of emergency help lines services
(involving the NGOs) may be a major step to reduce
the morbidity and mortality related to the suicidal
deaths.
REFERENCES:
1. World Health Organization. The World Health Report:
2001; Mental Health Report: New Understanding, New
Hope. Geneva: WHO; 2001.
2. Vijaykumar L. Suicide and its prevention: the urgent need
in India. Ind J Psychiat 2007;49:81-4.
3. National Crime Records Bureau. Accidental deaths and
suicide in India. Ministry of Home Affairs, Government of
India, New Delhi; 2006.
4. Shneidman ES. The suicidal Mind. New York: Oxford
University Press; 1996.
5. Durkheim E. Suicide. New York: Free Press; 1966.
6. Stengel E. Enquiries into attempted suicide. Proceedings
of the Royal Society of Medicine 1952;45:613-20.
7. Kessel N. & Grossman G. Suicide in alcoholics. Br Med J
1965;2:1671-2.
8. Kreitman N. Parasuicide. London: Wiley; 1977.
9. Morgan HG. Death wishes? The understanding and
management of deliberate self-harm. Chichester: Wiley;
1979.
10. Chowdhury AN. Culture and suicide. J Ind Anthrop Soc
2002;37:175-85.
11. Vijaykumar L. Altruistic suicide in India. Arch Sui Res
2004;8:73-80.
12. Prichard C. Suicide in the People’s Republic of China
categorized by age and gender: evidence of the influence
 of culture on suicide. Acta Psychiat Scand 1996;93:362-
67.
13. Stack S. The effect of media on suicide: Evidence from
Japan, 1955-1985. Sui Life Threat Behav 1996;26:132-
42.
14. Hodes M. Overdosing as communication: a cultural
perspective. Br J Med Psychol 1990;63:319-33.
15. Chowdhury AN, Brahma A, Banerjee S, Biswas MK.
Media influenced imitative hanging: a report from West
Bengal. Ind J Publ Health 2007;51:222-24.
16. Paproski DL. Healing experiences of British Columbia
First Nation women: moving beyond suicidal ideation and
intention. Can J Commun Met Health 1997;16:69-89.
17. American Psychiatric Association. Practice guideline for
the assessment and treatment of patients with suicidal
behaviors. American Psychiatric Association, nov,2003.
18. Venkoba Rao A. Suicidology: The Indian context. In:
Agarwal SP (ed) Mental Health: an Indian perspective
1946-2003. Directoriate General of Health Services/
Ministry of Health & Family Welfare: New Delhi, 2004.
19. Chowdhury AN, Brahma A, Banerjee S, Biswas MK.
(2005). Psychiatric Morbidity at Primary Care: Study from
a Community Mental Health Clinic at Sundarban, India.
Int Med J 2005;12:11-18.
20. Phillips MR, Li X, Zhang Y. Suicide rates in China, 1995-
1999. Lancet 2002;359:835-40.
21. Kaprio J, Koskenvuo M, Rita H. Mortality after
bereavement: a prospective study of 95647 widowed
persons. Am J Publ Health 1987;77:283-87.
22. Luoma JB, Pearson JL. Suicide and marital status in the
United States 1991-1996: is widowhood a risk factor? Am
J Publ Health 2002;92:1518-22.
23. Boxer PA, Burnett C, Swanson N. Suicide and occupation:
a review of the literature. J Occup Environ Med
1995;37:4424-52.
24. Stack S. Occupation and suicide. Soc Sci Q 2001;82:384-
96.
25. World Health Organization. Preventing suicide: a resource
for General Physicians. Geneva: WHO; 2000.Chowdhury
AN, Brahma A, Banerjee S, Biswas MK. Deliberate Self-
harm Prevention in the Sundarbans region needs
immediate public health attention. JIMA 2009;107: 88-
93.
VIEW POINT
Mindfulness and Mental Health
Kedar Nath Dwivedi
International Institute of Child and Adolescent Mental Health, Northampton, UK
‘Mindfulness involves intentionally bringing one’s
attention to the internal and external experiences
occurring in the present moment, and is often taught
through a variety of meditation exercises’1. It includes
a kind of meta-awareness, self regulation of attention
(to immediate experience) and a certain mindset e.g.
being non-reactive, non-judgemental and accepting.
This practice has been derived from Buddhism which
originated in India in the 6th Century BC2. The Four
Noble Truths in Buddhism include the presence of
suffering (Diagnosis), its cause (Aetiology), that it can
be ended (Prognosis) and the Eight-Fold Noble Path
(Prescription). The Eight-Fold Noble Path includes
Right Speech, Right Action, Right Livelihood, Right
Effort, Right Mindfulness (Sati), Right Concentration,
Right Aspiration, and Right View. Mindfulness is also
one of the seven factors of enlightenment. These
include Mindfulness, Investigation of reality, Energy,
Rapture, Tranquility, Concentration and Equanimity.
Mindfulness in the Buddhist practice is like overseeing
a situation (for example, a cowherd sits in a relaxed
manner and watches his cows over a distance). In the
practice of mindfulness there is also a sense of restraint
i.e. bare attention and avoiding to get carried away by
associations, projections, evaluations, proliferations etc
(distractions); focus on here and now and on being
non-judgemental. There should be no craving, ill will
or ignorance regarding the object of mindfulness. In
order to practice or develop mindfulness one could
focus on body e.g. breath, posture etc.; sensations or
feelings; mind (Chitta) e.g. mental states; and
phenomena (Dhammas) e.g. hindrances and
aggregates.
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence: Prof. K. N. Dwivedi
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Director, International Institute of Child and
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Adolescent Mental Health, Northampton, UK
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E.Mail: k.dwivedi@londonmet.ac.uk
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
As ‘Buddha was essentially a psychologist’3 ‘It is
possible to practice Buddhist-derived meditation, and
ascribe to aspects of the psychological view of the
mind from this perspective, and maintain one’s beliefs
and membership in other religious traditions’ 4. Thus,
mindfulness is being applied in a variety of fields
including Education and Therapy.
In Education, there is a movement for Mindful learning
and teaching5 with features such as, Active involvement
of the student in the learning process; Student and
teacher join each other as collaborative explorers in
the journey of discovery; Embrace both knowledge
and uncertainty with curiosity, openness, acceptance,
and kind regard; Disentangle the mind from premature
conclusions, categorizations and routinized ways of
perceiving and thinking; Open to novelty, alertness to
distinction, sensitivity to different contexts, awareness
of multiple perspectives, & orientation to the present.
Thus, learning becomes more enjoyable, stimulating
and effective.
Mindfulness based therapies and their effectiveness
In the late 1970s, Jon Kabat-Zinn (University of
Massachusettes Medical Centre) set up MBSR
(Mindfulness based stress reduction) clinics for a wide
range of medical conditions from backache to
psoriasis. These demonstrated reduction in subjective
states of suffering, improvement in immune functions,
acceleration in rates of healing, nurturing interpersonal
relationships, and overall sense of wellbeing6. This led
to the application of mindfulness for a variety of mental
health problems.
Mindfulness is already assimilated in psychodynamic
therapies at many levels. It is integral to well
established forms of psychotherapy, as there is an
emphasis on the quality of attention in psychotherapy.
For example, Nina Coltart (1992)7 emphasises the
healing potential of bare attention in psychoanalysis.
There has also been found an augmentation of
therapeutic effect i.e. a potentiating effect of
mindfulness training for patients on psychodynamic
exploration, as treatment times were significantly
reduced during the study 8. Epstein (1995)9, Brazier
(2003)10 and others have thus, promoted Buddhist
psychotherapy.
Similarly in Behaviour Therapy there have been 3
waves 11:
o 1 st Wave of Traditional Behaviour
therapy focused on overt behaviours
and their relationship with their
environmental events.
o 2 nd Wave of Cognitive Behaviour
Therapy with an emphasis on the role
of thoughts.
o 3 rd Wave with Mindfulness e.g.
Dialectical Behaviour Therapy (DBT),
Mindfulness Based Cognitive Therapy
(MBCT), Acceptance and
Commitment Therapy (ACT).
DBT involves becoming more aware, and hence more
accepting of ones emotional experiences. It has been
shown to be effective in treating symptoms of
borderline Personality Disorder 12; co-occurring
substance dependence 13; eating disorders14; and
emotion dysregulation15.
In MBCT, one learns to see thought as a process and
not as a fact, thus, leading to detachment. It has been
found to be effective in: prevention of relapse/
recurrence in major depression16 ; childhood disorders
e.g. conduct disorders, anger problems, attention
deficit hyperactivity disorder (ADHD), anxiety
disorders17; adolescent externalizing disorders e.g.
oppositional defiant disorder, ADHD, behaviour
problems in Autism Spectrum Disorder18 ; and parent
training19 .
ACT involves accepting of experience to reduce
avoidance of private experience and accomplishing
goals in life that serve higher values. It has been found
to be successful in: Substance abuse20; Coping with
psychosis 21; Stigma and burnout 22; and Worksite
stress23.
Other examples of the effectiveness of mindfulness
based therapies include:
• Mindfulness based eating awareness training
(MB-EAT:24)
• Mindfulness based relapse prevention (MBRP:
25
)
• Mindfulness based relationship enhancement
(MBRE: 26)
• Treatment of adolescent sex offenders 27
• Treatment of addictive behaviours 28
• MAP (Mindful Attention Program) for the
treatment of ADHD; a project of the Santa
Barbara Institute (UCLA) for Consciousness
Studies 29
There is also a study of the impact of therapist
practicing mindfulness oneself. In a randomised
comparative trial of the clinical outcomes of over 120
patients who received psychotherapy from 18
psychotherapists in training, patients seen by 9
therapists (with mindfulness training) did significantly
better symptomatically than the patients seen by the
other 9 therapists 30 .
Mindfulness based therapies have now been
demonstrated to be effective in a variety of mental
health problems such as, anxiety disorders (including
phobias, panic and obsessive compulsive disorder),
depression, anger and emotion dysregulation, binge
eating & other behavioural problems, substance
misuse, suicidal behaviour, trauma, relationship issues
and so on 31. However, there have also been reports of
adverse effects 32 as well such as, symptoms of
restlessness, anxiety, depression, guilt and hallucinosis
in vulnerable (e.g. traumatised) individuals in intensive
retreats.
The findings in a meta-analysis by Baer (2003)1 suggest
that mindfulness-based interventions may be helpful
in the treatment of several disorders. She also points
out that there are methodological flaws in the studies
on these interventions and because of their promising
nature, more rigorous studies are highly recommended.
Measuring instruments
There are already some scales available for measuring
mindfulness, for example, The Mindful attention and
Awareness Scale (MAAS: 33, The Toronto Mindfulness
Scale (TMS: 34), The Kentucky Inventory of
Mindfulness Skills (Kims: 35), and The Freiburg
Mindfulness Inventory (FMI: 36).
Mechanisms implicated
As regards the mechanisms involved in mindfulness
and its effectiveness there appear to be a number of
theories. Some of these are briefly outlined below.
• In a study on Zazen meditators, there was
a failure to respond to repeated clicks by
habituation of autonomic responses (e.g.
momentary blocking of alpha frequencies).
Thus, they seem to react to stimuli as if for
the first time 37.
• The act of becoming consciously aware of
the stream of awareness has the immediate
effect of rendering the dominant EEG
patterns stronger & more coherent 38.
Mindfulness leads to two, ordinarily
incompatible, developments: boost of the
fast wave activity that is associated with
alert states, along with particular kinds of
slow wave activity associated with
expansion of awareness, creativity and deep
relaxation 31. For example, while resting,
meditators (Tibetan method) were found
to have significantly greater gamma band
(40 c/s) activity relative to slower activity
and synchrony than controls.
• In the frontal lobes of the brain,
asymmetrical activation, favouring one side
more than the other, is consistently
associated with specific mental states in the
neurophysiology literature. For example,
greater left sided activation has been
associated with positive emotion
(happiness), enhanced immune function
and in those who participated in 8 week
training in MBSR i.e. mindfulness based stress
reduction 39 .
• There are reports that in subjects practicing
mindfulness meditation there is an increased
thickness of at least two parts of the brain i.e.
middle prefrontal area, bilaterally and a related
neural circuit, the insula (more on right side).
The degree of thickness correlated with the
time spent on practicing mindfulness
meditation40.
• There are individual differences in the neural
correlates of voluntary emotion regulation.
These are related to endogenous regulatory
processes in everyday life. Some individuals
when attempting to voluntarily downregulate
negative affect using cognitive strategies are
poor performers as reflected in less ventro-
medial prefrontal cortex activation and more
amygdala activation and show a flatter slope
of the cortisol rhythm, mainly due to higher
evening levels of cortisol 41. Chronic stress
can lead to several changes 42 e.g. increase in
the ability of the amygdala to learn and
express fear associations, deficiency in the
hippocampus function (depriving the subject
of the contextual information needed to
recognise an environment as safe), and
reduction in the ability of the prefrontal cortex
to control fear. Thus, a vicious cycle is created
in which increased fear and anxiety lead to
more stress, which leads to further
dysregulation. However, prefrontal activity
can be augmented pharmacologically,
physiologically (e.g. repetitive trans-cranial
magnetic stimulation, deep brain stimulation)
and psychologically such as through
mindfulness meditation.
• According to the ‘dynamicist’ view of top-
down control, spatio-temporal trajectories of
neural activity emerge from complex
nonlinear neural interactions and follow the
rules of dynamical theory 43. These large-scale
coherent neuronal ensembles (e.g. which
emerge during Focused Attention on breath)
can influence other local neuronal processes
 (e.g. evoked by an external distractor) by
entraining local ensembles 44, 45. The brain
goes through a succession of large-scale
brain states, with each state becoming the
source of top-down influences for the
subsequent state. Such large-scale
integrative mechanisms may participate in
the regulatory influence of meditative
states.
• Mindfulness leads to Dechaining i.e.
loosening of strong associations e.g. in
phobia 46. Mindfulness also leads to
Decentring or disidentification from the
activities of our minds as our relationship
to our experiences change 31.
• There are 7 common factors between
Mindfulness, secure attachment &
prefrontal functions: Regulation of body
systems, Balancing emotions, Attuning to
others, Modulating fear, Responding
flexibly, Exhibiting insight, and Empathy.
There are two other prefrontal functions
found in mindfulness but, so far, not studied
in secure attachment: Being in touch with
intuition and morality 4
• Other mechanisms implicated include
iimprovement in patterns of thinking,
reduction in negative mindsets, capacity to
combat emotional dysfunction, and
improved capacity to regulate emotion4, 31,
47.
REFERENCES
1. Baer RA (2003) Mindfulness training as a clinical
intervention: A conceptual and empirical review. Clinical
Psychology Science and Practice, 10, 125-143
2. Dwivedi, K N & Prasad, K. M. R. (2000) The Hindu, Jain
and Buddhist communities: Beliefs and Practices. In: A. Lau
(Ed.) Asian Children and Adolescents in Britain. London:
Whurr.
3. Germer CK (2005) Mindfulness: What it is/ What does it
matter? In cK Germer, RO Siegel & PR Fulton (Eds)
Mindfulness and Psychotherapy, New york: Guilford Press.
4. Siegel DJ (2007) The Mindful Brain. New York: WW Norton
5. Langer EJ (2000) Mindful learning. Current directions in
psychological science, 9(6): 120-123
6. Kabat-Zinn, J (1996) Full catastrophe living: How to cope
with stress, pain and illness using mindfulness meditation.
London: Piatkus
7. Coltart N (1992) Attention. In: Coltart N (Ed) Slouching
Towards Buddhism. London: Free Association Books, pp
176-93
8. Kutz I, Leserman J, Drington C, Morrison C, Barysenko J
& Benson H (1985) Meditation as an adjunct to
psychotherapy; an outcome study. Psychotherapy and
Psychosomatics, 43, 209-218.
9. Epstein M (1995) Thoughts without a thinker:
Psychotherapy from a Buddhist perspective. New York:
Basic Books.
10. Brazier C (2003) Buddhist Psychology. London: Robinson.
11. Hayes SC (2004) “Acceptance and Commitment Therapy,
relational frame theory, and Third wave of behaviour
therapy”, Behaviour Therapy, 35, 639-665
12. Linehan MM, Armstrong HE chronically, Suarez A, Allmon
D, Heard HL (1991) “Cognitive-behavioral treatment of
parasuicidal borderline patients,” Archives of General
Psychiatry, 48, 1060-1064.
13. Linehan MM, Dimeff LA, Reynolds SK, Comtois KA,
Welch SS, Heagerty P & Kivlanahan DR (2002) Dialectical
Behaviour Therapy versus comprehensive validation therapy
plus 12 step for the treatment of opioid dependent women
meeting criteria for borderline personality disorder. Drug
and Alcohol Dependence, 67(1), 13-26.
14. Telch CF, Agras WS, Linehan MM (2001) “Dialectical
behavior therapy for binge eating disorder,” Journal of
Consulting and Clinical Psychology, 69(6), 1061-1065
15. Fruzzetti AE, Shenk C, Lowry K, Mosco E (2003) “Emotion
regulation,” in W. O’Donohue, J Fisher & S Hayes (eds)
Cognitive Behaviour Therapy: Applying Empirically
supported techniques in Your Practice (pp 152-159), New
York: Wiley
16. Teasdale JD, Segal ZV, Williams JMG, Ridgeway VA,
Soulsby JM, Lau MA (2000) “Prevention of relapse/
recurrence in major depression by mindfulness based
cognitive therapy,” Journal of Consulting and Clinical
Psychology, 68(4), 615-623
17. Semple RJ, Lee J & Miller LF (2006) Mindfulness-Based
Cognitive Therapy for children. In: RA Baer (Ed)
Mindfulness Based Treatment Approaches. Amsterdam:
Academic Press.
18. Bogels S, Hoogstad B, van Dun L, de Schutter S, Restifo K
(2008) Mindfulness training for adolescents with
externalizing disorders and their parents. Behavioural and
Cognitive Psychotherapy, 36:193:209]
19. Dumas J (2005) Mindfulness-based parent training:
Strategies to lessen the grip of automaticity in families with
disruptive children. Journal of Clinical Child and Adolescent
Psychology, 34, 779-791
20. Gifford EV, Kohlenberg BS, Hayes SC, Antonuccio DO,
Piassecki MM, Rasmussen-Hall ML & Palm KM (2004)
Applying a functional acceptance based model to smoking
cessation; an initial trial of ACT. Behaviour Therapy, 35,
689-705.
21. Bach P & Hayes SC (2002) The use of acceptance and
commitment therapy to prevent the rehospitalisation of
 psychotic patients: a randomised controlled trial. Journal of
Counselling and Clinical psychology, 70, 1129-39.
22. Hayes SC, Bissett R, Roget N, Padilla M, Kohlenberg Bs,
Fisher G, Masuda A et al (2004) The impact of acceptance and
commitment training and multicultural training on the
stigmatising attitudes and professional burnout of substance
abuse counsellors. Behaviour Therapy, 35, 821-35.
23. Bond F & Bunce D (2000) Mediators of change in problem
focused and emotion focused worksite stress management
interventions. Journal of Occupational Health Psychology, 1,
156-163
24. Kristeller J & Hallett C (1999) An exploratory study of a
meditation based intervention for binge eating disorder. Journal
of Health Psychology, 4 , 357-63
25. Witkiewitz K, Marlatt GA and Walker D (2005) Mindfulness-
based relapse prevention for alcohol substance use disorders.
Journal of Cognitive Psychotherapy, 19, 211-28
26. Carson J, Carson K, Gil K et al (2004) Mindfulness based
relationship enhancement. Behaviour Therapy, 35, 471-94.
27. Derezotes D (2000) Evaluation of Yoga and meditation training
with adolescent sex offenders. Child and Adolescent Social Work
Journal, 17(2):97-113
28. Marlatt G, Witkiewitz K dillworth T (2004) Vipassana
meditation as a treatment for alcohol and drug use disorders.
In: S Hayes, V Follette and MM Linehan (Eds) Mindfulness
and acceptance: Expanding the Cognitive Behavioral Tradition.
New York: Guilford, pp. 261-87.
29. Zylowska l, Ackerman DL, Yang MH, Futrell JL, Horton NI,
Hale S, Pataki C, SmalleySL (2008) Mindfulness meditation
training in adults and adolescents with ADHD: a Feasibility
study. Journal of Attention Disorders, 11:737
30. Grepmair I, Mitterlehner F & Nickel M (2008) Promotion of
mindfulness in psychotherapists in training. Psychiatry
Research, 156, 265.
31. Mace C (2008) Mindfulness and mental health: Therapy,
Theory and Science. London: Routledge.
32. Albeniz A & Holmes J (2000) Meditation: concepts, effects
and uses in therapy. International Journal of Psychotherapy,
5, 49-58.
33. Brown K & Ryan R (2003) The benefits of being present:
mindfulness and its role in psychological well being. Journal of
Personality and Social Psychology, 84, 822-48.
34. Bishop S, Lau M, Segal Z et al (2003) Development and
validation of the Toronto Mindfulness Scale. In: International
Meeting of the Society for Psychotherapy Research. Weimar
35. Baer RA, Smith G and Allen K (2004) Assessment of
mindfulness by self-report: the Kentucky Inventory of
Mindfulness Skills. Assessment, 11, 191-206.
36. Buchheld N, Grossman P and Walach H (2002) Measuring
mindfulness in insight meditation (vipassana) and meditation-
based psychotherapy: the development of the Freiburg
Mindfulness Inventory (FMI). Journal of Meditation and
Meditation Research, 1, 11-34.
37. Kasamatsu A and Hirai T (1966) An electroe ncephalographic
study on the Zen meditation (zazen). In: C Tart (Ed) Altered
States of Consciousness (3rd Edition) San Francisco: Harper-
Collins, pp. 581-95.
38. Austin JH (1998) Zen and the brain. Cambridge MA: MIT
Press.
39. Davidson RJ, Kabat-Zinn J, Schumacher J, Rosenkranz M,
Muller D, Santorelli SF, Urbanowsky MA, Harrington A,
Bonus K & Sheridan JF (2003) Alterations in brain and
immune function produced by mindfulness meditation.
Psychosom. Med. 65, 564-570
40. Lazar SW, Kerr CE, Wasserman RH, Gray JR, Greve DN,
Treadway MT et al (2005) Meditation experience is associated
with increased cortical thickness. Neuroreport, 16(17), 1893-
1897.
41. Davidson, RJ, Fox, A, NH Kalin, NH (2007) Neural bases of
emotion regulation in nonhuman primates and humans. In: J J
Gross (Ed) Handbook of Emotion Regulation, New York:
Guilford Press
42. Mitra R, Vyas A, Garga Chatterjee G and Chattarji S (2005)
Chronic-stress induced modulation of different states of
anxiety-like behavior in female rats. Neuroscience Letters,
383(3), 278-283
43. Freeman WJ (1992) Tutorial in neurobiology: from single
neurons to brain chaos. Int. J. Bifurcat. Chaos 2, 451-482.
44. Varela F et al (2001) The brainweb: phase synchronisation
and large scale integration. Nat. Rev. Neurosci. 2, 229-239.
45. Engel AK et al (2001) Dynamic predictions: oscillations and
synchrony in top-down processing. Nat. Rev. Neurosci. 2,
704-716
46. Martin J (1997) Mindfulness: a proposed common factor.
Journal of Psychotherapy Integration, 7, 291-312.
47. Dwivedi, K.N. (2004) Emotion regulation and mental health.
In: K.N. Dwivedi and P.B. Harper (Eds) Promoting emotional
well being of children and adolescents and preventing their
mental ill health. London: Jessica Kingsley.
VIEW POINT
Era of Evidence Based Medicine: Is clinical expertise
outdated?
Y.P.S. Balhara, S. N. Deshpande
Department of Psychiatry & De-Addiction Services,
PGIMER- Dr. Ram Manohar Lohia Hospital, New Delhi.
Evidence Based Medicine (EBM) is a relatively recent
concept. However, it has more than made up for its
late entry by showing exponential growth over the past
two decades. Pioneered in early 1990s by Guyatt et
al, it represents the conscientious, explicit and judicious
use of current best evidence in making clinical decisions
about the care of individual patients1. Although new
to modern times, its philosophical underpinnings have
been traced back to China in older times2 .
In simple terms EBM helps the clinicians make
decisions supported by evidence. The philosophy of
EBM can be summed up as follows: if there is evidence
that something is of good and of benefit to the patient,
then use it; if there is evidence that something is not
good for the patient and can be harmful, then do not
use it3. In this context Evidence Based Practice (EBP)
would pertain to any practice that applies up-to-date
information from relevant and valid research about the
usefulness of various diagnostic tests or the predictive
power of prognostic factors or the beneficence of a
particular treatment method.
Multiple ongoing clinical trials, ever increasing number
of biomedical journals and thousands of articles
published every month have ensured floods of
information. Going by most conservative of estimates
this is likely to grow exponentially in the coming years.
Also growing use of the internet and other modes of
communication has ensured that most of this information
1234567890123456789012345678901212345678901234567
1234567890123456789012345678901212345678901234567
1234567890123456789012345678901212345678901234567
Correspondence : Dr. S.N. Deshpande
1234567890123456789012345678901212345678901234567
1234567890123456789012345678901212345678901234567
1234567890123456789012345678901212345678901234567
Dept. of Psychiatry
1234567890123456789012345678901212345678901234567
1234567890123456789012345678901212345678901234567
1234567890123456789012345678901212345678901234567
PGIMER- Dr. Ram Manohar Lohia Hospital, New Delhi
1234567890123456789012345678901212345678901234567
E-mail: smitades@vsnl.com
1234567890123456789012345678901212345678901234567
is easily accessible at the user end point4. As an integral
component of the professional development clinicians are
expected to keep themselves apprised of this enormous
amount of information. However, not all available
information is necessarily scientifically valid and reliable.
Thus the clinicians have a two-fold task: to go through
the available information and simultaneously screen it for
scientific validity, applicability and relevance before putting
it to practice.
With this explosion of ever evolving biomedical
information the age old practice of depending on a
combination of informed guesswork, unsystematic
observation, common sense, the consensus views of
clinical experts, and the so-called ‘standard and
accepted practice’ has been put to question. So does
this mean that clinical expertise and opinion is
unnecessary or obsolete for patient care? Does
acceptance of EBM to guide clinical decision making
preclude and forbid the use of clinical judgement and
expertise? Is what a clinician has gathered over the
years by his/her interaction with patients or
professional colleagues no longer relevant in patient
care?
We would be able to answer these questions better if we
revisit the concept of EBM and EBP. EBM aims at
evidence being the driving force behind clinical decision
making. If an intervention is supported by evidence for
its benefit, then EBM recommends its use. If an
intervention is not supported by evidence then EBM does
not recommend its use5. However, the practice of EBM
in no way refutes the importance and value of clinical
expertise in decision making. In fact, EBM goes a step
beyond. It not only recommends that clinical expertise
be integral to effective patient care, it also acknowledges
and recommends inclusion of ‘patient values’ in clinical
decision making. EBM is the integration of clinical
expertise, patient values, and the best evidence into the
decision making process for patient care6. These ‘patient
values’ include individual specific personal and social
issues, clinical settings etc.
EBM helps foster shared decision making. The
importance of shared decision making is of special
relevance to our setting where clinicians tend to rely
heavily on evidence generated in other populations and
settings (primarily Western) and need to extrapolate it
to a vastly different Indian patient population. The
differences are evident in terms of accessibility,
acceptability, affordability and applicability of these
interventions. As a result when a clinical decision has
to be taken for an individual patient, one has to keep
in mind certain additional factors along with the level
of evidence. At times applicability of intervention best
supported by evidence could be put to question
because of lack of availability or affordability. Neglect
of clinical expertise and ‘patient values’ could be
counterproductive in such scenarios and would defeat
the basic principle of patient care- provision of
effective, acceptable and affordable interventions. Such
a decision calls for sound clinical expertise based on
the clinician’s accumulated experience, education and
clinical skills. A related situation would be to choose
from two or more interventions with comparable
evidence base. Even in such a situation, clinical
expertise could play a key role. A decision guided by
astute clinical judgement would ensure judicious use
of resources and maximum benefit to the patient.
The process of practice of evidence based medicine
follows a systematic approach. It begins with
conversion of medical information in to competent,
searchable, focused questions7. Once the question of
interest is ready then one endeavours to search for best
evidence to answer the question. Subsequently one has
to critically appraise available evidence. This includes
ascertainment of the validity and clinical usefulness of the
evidence. Following this the evidence is put to clinical
practice. The job is not yet completely done and involves
a final step - evaluation of performance of the evidence
in clinical application.
In order to practice EBM the clinicians need to have
access to relevant literature as well as good
understanding of the correct strategy to search and
then critically evaluate it. However, the most important
pre-requisite and potential barrier to the practice of
EBM remains the attitudinal change of the clinicians8.
The clinicians need to realise that it is their
professional, moral and ethical responsibility to deliver
the most appropriate and effective care to their
patients. Also they have to acknowledge the ever
changing and evolving nature of the medical field.
What seems to be the most appropriate strategy might
not hold good if appropriate search for alternative
strategies is carried out. Thus the clinicians need to
be open to challenge their knowledge and be on the
look out for better alternatives. This would ensure
that they choose the most appropriate intervention
for their patients and in the process enrich themselves
as well.
To conclude, clinical expertise and EBM are
complimentary and go hand in hand. Rather, it would
be more precise to put clinical expertise as an integral
component of clinical decision making based on EBM.
EBP has evolved from the application of clinical
epidemiology and critical appraisal to explicit decision
making within the clinician’s daily practice. Practice
of EBM would ensure the judicious use of valuable
clinical expertise and hence help arrive at sound clinical
judgement. While EBM ensures the science of
medicine it is finally the experience, knowledge and
integrative capacity of the clinician which provides its in Clinical Curriculum. Ann Acad Med Singapore 2006;
art, and thus becomes the scaffold on which final clinical 35: 615-8.
decision rests. 5. Elstein, A.S. On the origins and development of evidence-
based medicine and medical decision making. Inflammation
Research 2004; 53(2): S184–9.
REFERENCES
6. Sackett, D. Evidence-based Medicine: How to Practice
1. Sackett, D. Evidence-based Medicine - What it is and
and Teach EBM. 2nd edition. Churchill Livingtone, 2000.
what it isn’t. http://www.cebm.net/ebm_is_isnt.asp 1996
7. Richardson, W.S., Wilson, M.C., Nishikawa, J., Hayward,
2. Guyatt, G. etal (EBM working group), EBM-A New
R.S. The well-built clinical question: a key to evidence-
approach to Teaching the Practice of Medicine., JAMA
based decisions. ACP J Club 1995; 123: A12-3.
1992; 268(17): 2420-25.
8. Zippoli, R. P., & Kennedy, M. Evidence-based practice
3. Tonelli, M.R. The philosophical Limits of Evidence-based
among speech-language pathologists: Attitudes, utilization,
Medicine. Academic Medicine 1998; 73(12):1234-1240.
and barriers. American Journal of Speech-Language
4. Wanvarie, S., Sathapatayavongs, B., Sirinavin, S., Ingsathit,
Pathology, 2005; 14, 208-220.
A., Ungkanont, A., Sirinan, C. Evidence-based Medicine

CURRENT THEME
Towards A New Mental Health Act
C.L. Narayan*, Rajiv Jaiswal**, Deepshikha**
*Consultant Psychiatrist, Gaya, ** SRHC Hospital, Narela, New Delhi
INTRODUCTION
Mental health legislation was first enacted in India in
1858 three separate Acts - (1) The Lunacy (Supreme
Court) Act, 1858 relating to judicial inquisition as to
lunacy in presidency towns; (2) The Lunacy (District
Courts) Act, 1858 relating to proceedings outside
presidency towns; and (3) The Lunatic Asylums Act,
1858 relating to confinement of lunatics in asylums.
These were based on two English Acts namely the
English Lunacy Regulation Act, 1853 and the Lunatics
Act, 18531. The Indian Lunacy Act, 1912 was enacted
to amend and assimilate the law relating to custody of
lunatics in India with the English law on the subject
and to re-arrange and consolidate as far as possible
the whole law relating to lunatics (Statement of Objects
and Reasons of the Indian Lunacy Bill, 1911).
After Second World War the Universal Declaration
of Human Rights was adopted by the UN General
Assembly to ensure inherent dignity and the equal and
inalienable rights of all people. India was a signatory
to the Declaration. The need was felt to replace the
Indian Lunacy Act, 1912 and the Indian Psychiatric
Society (IPS) realized the need to enact new law in
this regard and submitted a Draft Mental Health Bill
to the Government of India in 1950.Dr. B.A. Bhagwat
took active part in preparation of the draft. In 1978 a
Mental Health Bill was introduced in the Lok Sabha
and was later referred to a JPC headed by Dr. Sushila
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence:
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Dr. C. L. Narayan
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Consultant Psychiatrist, Gaya-823001, Bihar
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-Mail : drclnarayan@gmail.com
12345678901234567890123456789012123456789012345
cccCURRENT THEME
Nayyar. The Bill could not be considered due to
dissolution of Lok Sabha. The Bill was again
introduced in 1981 in the Rajya Sabha and again
referred to a JPC headed by Shri Sukhdeo Prasad, M.P.
In 1982, National Mental Health Programme was
launched by the Government of India. In 1983 Indian
Psychiatric Society voluntarily submitted a
memorandum to the JPC and Dr. Jaya Nagaraj, the
then President of IPS and Dr. A.B. Dutta2 represented
the IPS before the JPC. The JPC, which was
reconstituted in 1985, submitted its report in May
1986. After being passed by both houses and receiving
the Presidential assent, it became Mental Health Act,
1987 in May 1987. It took another three years for the
Central Government to frame The State Mental Health
Rules, 1990 and The Central Mental Health Authority
Rules, 1990. The Government took a further period
of three years to issue notification that the Mental
Health Act, 1987 would come into force in all States
and Union Territories from April 1, 1993. Because of
a large number of very complicated procedures, defects
and absurdities in the Act and also in the Rules, it can
never be implemented properly3. The National Human
Rights Commission observed in 1999 that the Act was
not implemented in many States even in 1999. The
Indian Psychiatric Society voluntarily submitted its
recommendations on mental health legislation to the
Government of India in January, 2001 urging upon
the Government to declare its mental health policy and
to repeal the Mental Health Act, 1987 by a new Act
based on the mental health policy, modern concept of
psychiatry and recommendations of the international
bodies and the IPS. After occurrence of Erwadi tragedy
in August 2001, the Supreme Court of India initiated
a PIL (WP no.334/2001) and a second PIL was filed
by a NGO Sarthak (WP 562/2001). Indian Psychiatric
Society and Indian Association of Private Psychiatry
also represented themselves in these Writ petitions.
The Supreme Court in its interim order in April 2002
directed to examine the feasibility of formulating
uniform rules regarding public and private sector
psychiatric institutions. Human right activist group and
NGOs working in the field were also pressing for
revision of the Act to ensure protection of the human
right aspects of the mentally ill patients. One of them
commented “the Mental Health Act is a statute which
provides a procedure by which persons living with
mental illness can be denied their liberty”4.
Major objection of the IPS to the MHA, 1987 5,6
as summarized in IPS documents are as follows.
1. MHA, 1987 was not based on modern concept
of psychiatry with all the attendant scientific
and technological advancement which had
impacted the management of psychiatric
illnesses.
2. Definition of mental illness was unsatisfactory.
It excluded Mental Retardation.
3. Definition of Medical Officer and Psychiatrist
was unsatisfactory as it had to be either a
gazetted medical officer in service of the
Government in the case of former or any
medical practitioner to be declared so in the
case of latter.
4. Only Government run and not privately run
general hospitals providing psychiatrist service
were exempted from the provisions of MHA,
1987.
5. In MHA, 1987 legal considerations were given
too much weightage, whereas, medical
consideration was given too little importance.
6. A Judicial Officer could determine the presence
and nature of mental illnesses in people, by
personally ‘examining’ them (diagnosing
someone with mental illness requires special
training and anybody without that could not
be entrusted with that responsibility).
7. The licensing procedures were found
cumbersome.
8. Nonprofessionals had the access to the
confidential records of the patients in the name
of inspection.
9. Inspection and licensing was applicable to
mental hospitals and nursing homes even
where those admitted were under the
supervision of patient’s family, which was
consulted for all treatment decisions.
10. Central and State Mental Health Authorities
were constituted by the Government, which
had set up most of the mental hospitals mainly
providing custodial care. This was in conflict
with one of the objectives of the MHA viz. to
regulate the powers of the Government for
establishing, licensing and controlling
psychiatric hospitals and psychiatric nursing
homes for mentally ill persons.
11. No budgetary provisions were made available
for the functioning of Central or State Mental
Health Authority.
12. The Act had nothing to suggest the role of
family in the care of mentally ill subjects.
13. Although there were provisions for delegating
powers to the police officer with respect to
bringing the homeless wandering mentally ill
for treatment, there was no provision for
penalizing the police if it failed to do so.
PROPOSED DRAFT OF AMENDMENTS TO
MHA-1987 7,8
India signed United Nations’ Convention on Rights
of Persons with Disability (UNCRPD), which was
ratified by the Government of India in May, 2008. It
became imperative for the Government to revise all
related law on mental health and disability to bring
them in harmony with UNCRPD. A National
Consultation on the Mental Health Programme was
held on 22nd January 2010 with the objective to review
and identify gaps in the Mental Health Programme
and actions to fill up these gaps. It was felt that the
MHA 1987 needs amendments. It should move
towards supporting, promoting and protecting the
rights of persons with mental illness. Centre for Mental
Health Law & Policy, ILS College, Pune was given
the responsibility of preparing the draft of the proposed
legislation and present it to the Ministry of Health and
Family welfare after having nationwide consultation
on it. The first draft was circulated on 28-02-10 and
after seeking objections and suggestions on the draft,
a revised draft was released on 23-05-10. A series of
regional and national consultation is planned before
the final draft is presented to the Ministry. The salient
features of the proposed draft are as follows.
1. Persons with mental illness - The
nomenclature has been changed from ‘mentally
ill person’ to ‘person with mental illness’.
Similarly ‘mentally ill prisoner’ has been
replaced by ‘prisoner with mental illness’. It
is stated that language has a role in stigma
associated with any condition. Hence ‘persons
with mental illness’ is preferred to the term
‘mentally ill person’.
2. Statement of objects and reasons - By
definition the Act is stated to protect promote
the rights of persons with mental illness. It is
stated to create access to treatment, care and
rehabilitation and to fulfill the obligations under
the Constitution of India and obligations under
various International Conventions. It is also
stated to ensure that care, treatment and
rehabilitation is provided in the least restrictive
manner that does not intrudes on the right and
dignity of the person. One of the objects of
MHA -1987 which is dropped is ‘to protect
society from the presence of mentally ill
persons who have become or might become a
danger or nuisance to others’. Facilitation of
integration of persons with mental illness into
community life is also stated to one of the
objects.
3. Mental Health Facility - Psychiatric hospitals
and Psychiatric Nursing homes have been
described as ‘Mental Health Facility’. It is
defined to include all facilities either wholly or
partly meant for the care of the persons with
mental illness, where persons with mental
illness are admitted or reside at for care,
treatment, convalescence and/or rehabilitation,
either temporarily or otherwise and includes
general hospital or general nursing home
established or maintained by the Government
or any other person. It is obvious that
Psychiatric OPD services are not covered by
this definition. There is an exclusion criteria
which specifies that if the person with mental
illness resides with his family, the place will
not be regarded as mental health facility and
thus exempt from registration. The definition
is intended to cover non-medical institutions
also, if the persons with mental illness are
residing for care, convalescence or
rehabilitation.
4. Mental Health Professionals - A new
category of ‘Mental Health Professional’ has
been created which includes psychiatrist,
 clinical psychologist, psychiatric social worker
and registered mental health nurse. It is said
that the category is created to facilitate
involuntary admissions under section 19 of the
Act. But they can become professional
members in Mental Health Review
Commission (MHRC) and also in Central and
State Mental Health Authority.
5. Nominated Representative - A new concept
of ‘nominated representative’ has been
introduced and a person who has attained the
age of 18 years and is competent to do so has
the right to appoint a nominated representative
and it can be communicated either verbally or
in writing to the person in charge of the
person’s medical care. If no nominated
representative has been appointed, family
member as described in section 2 (t) will be
the nominated representative. If no family
members are available, ‘carer’ (who is not a
relative but who normally resides with the
person and/or predominantly responsible for
providing care to that person) will be the
nominated representative. In certain cases
nominated representative can be appointed by
MHRC also.
6. Mental Illness - It has been defined as a
substantial disorder of mood, thought,
perception, orientation or memory which
grossly impairs a person’s behavior, judgment
and ability to recognize reality or ability to meet
the demands of normal life and includes mental
conditions flowing from the use or abuse of
alcohol and drugs, but excludes mental
retardation. It is stated that the mental illness
has been defined for the purpose of the Act in
behavioral terms so that it can be understood
by non-professionals also. It is obvious from
this definition that if the disorder does not
involve gross impairment of patient’s insight
and reality testing, the provisions of MHA will
not apply and the disorders can be treated in
normal ‘doctor-patient’ relationship. Thus
neurotic and similar types of illnesses are
excluded. Mental Retardation has been
excluded from the ambit of the definition. It is
pertinent to note here that the National Trust
Act covers four illnesses i.e. mental
retardation, autism, cerebral palsy and multiple
disabilities. It was suggested that WHO
definition as given in ICD should be adopted.
But if it is adopted all psychiatric illnesses will
come into the ambit of MHA.
7. Registration of Mental Health Facility -
Licensing has been replaced with registration
and for registration, every mental health facility
shall fulfill the minimum standards of facilities,
minimum qualifications for the personnel,
provisions for maintenance of records and
reporting and any other conditions as may be
prescribed. The registration will be done by
State Mental Health Authorities and the
application may be furnished in person or by
post or online. The Authority within a period
of 10 days and without any inquiry issue a
provisional certificate of registration, which
shall be valid for 12 months from the date of
issue and shall be renewable. Permanent
registration, which shall be valid for 36
months, shall be granted only when a mental
health facility fulfills the prescribed standards
for registration by the State Government.
Mental health facility shall be classified into
different categories and different standards
may be prescribed for them. If at any time after
registration the SMHA is satisfied that the
conditions of registration are not being met
or the persons entrusted have been convicted
of an offence under this Act or persistently
violating the rights of the Persons with mental
illness, a show cause notice may be issued. If
even after giving reasonable opportunity to the
mental health facility, the Authority is satisfied
that there has been breach of Rules under this
 Act or persistently violating the rights of
persons with mental illness, the registration of
the mental health facility may be cancelled. The
Authority shall have right to cause an
inspection of or inquiry in respect of any mental
health facility, the result of which shall be
communicated to the mental health facility. The
Authority can issue any directions as it may
deem fit and the mental health facility shall have
to take action to the satisfaction of the
Authority. The Authority or any person
authorized by it may enter and search in manner
prescribed by the authority at any reasonable
time if there is any reason to suspect that
anyone is running a mental health facility
without registration. Any person aggrieved by
any order of the Authority may appeal to the
High Court of the State.
8. Inspecting officers and Visitors - Provisions
of inspection at anytime by the Inspecting
Officer (Sec 13), provisions of visitors for
every mental health facility (sec 37 and 38)
have been dropped in the draft.
9. Admission to a Mental Health Facility -
There are four types of admissions under the
proposed draft – Independent admission,
Admission of a minor, Supported Admission
up to 30 days and Supported admission beyond
30 days.
a) Independent admission – Any person
who is not a minor and consider
himself to have a mental illness may
request the medical officer in charge
of a mental health facility to be
admitted. The medical officer in
charge will admit him if he is satisfied
that person has a mental illness of
sufficient severity and he will benefit
from admission. An independent shall
not be given treatment without his/
her informed consent and he may
discharge himself from the mental
health facility without the consent of
the medical officer in charge. But a
mental health professional may
prevent discharge of an independent
patient seeking discharge for 24 hours
to allow assessment by two mental
health professionals necessary for
supported admission under sec 19 of
the Act, if the necessary conditions
are met.
b) Admission of a minor – A minor shall
be admitted only in exceptional
circumstances on application in
writing of the nominated
representative of the minor. Two
mental health professionals, at least
one of whom is a psychiatrist or one
psychiatrist and one registered
medical practitioner shall have to
independently examine the minor and
both conclude that the minor has a
mental illness of sufficient severity, it
is in the best interest of the minor, his
mental health care needs of the minor
cannot be met unless he/she is
admitted and all community based
alternatives have been shown to have
failed or demonstrably unsuitable to
the needs of the minor. It is also
specified that no irreversible
treatment can be provided for the
mental illness of a minor. If the
nominated representative of the
minor no longer supports admission
of the minor, he must be discharged.
All admissions of minors beyond 30
days must be informed to MHRC and
every subsequent 30 days
continuation of admission requires
approval from the MHRC.
c) Supported admission up to 30 days
– A person with mental illness may
be admitted in a mental health facility,
 if two professionals, one psychiatrist and
the other being a mental health professional
or a registered medical practitioner, each
of them have independently examined in
the preceding 7 days and both conclude
that the person has a mental illness has
recently threatened or attempted or is
threatening or attempting to cause bodily
harm to himself/herself and/or to another
person and/or recently behaved or is
behaving violently towards another person
and/or has recently shown or is showing
lack of competence to care for himself/
herself and the mental health professionals
certify that admission to the mental health
facility is the least restrictive option. The
admission under this section shall be
limited to 30 days. At the end of 30 days
he will cease to be admitted under this
section or continue to be admitted as an
independent patient or continue to remain
admitted under section 20, according to
whatever criteria are met at the end of 30
days. If it is assessed even earlier that the
criteria as described under this section are
no longer met, the medical officer in charge
will terminate the admission.
d) Supported admission beyond 30 days –
If the person is already admitted under
section 19 and the criteria of admission as
described above are still valid, the person
will have to be independently examined by
two psychiatrist in the preceding 7 days
and if both certify that admission in the
mental health facility is the least restrictive
option possible, the person will remain
admitted in the facility. But all admissions
under this section must be approved by the
MHRC within a period of 60 days from
such admission or renewal becomes
effective. Admission under this section will
be limited to 180 days. Further admission
beyond 180 days can be renewed for 180
days at each instance upon application of
the nominated representative and by
following procedures as above.
10. Emergency Treatment - Under section 20.1,
treatment can be initiated by any registered medical
practitioner with the consent of nominated
representative in certain specified emergency
situations, at any health facility or in the
community. But the treatment under this section
will be limited to 72 hours and ECT and irreversible
treatments shall not be provided under this section.
What constitutes irreversible treatment is not
specified.
11. Prohibited Treatments – ECT without the use
of muscle relaxants and anesthesia and sterilization
of persons with mental illness intended for
treatment of mental illness is prohibited in the
proposed draft. Psychosurgery may only be
performed on approval of SMHA
12. Restrains and Seclusions – It is stated that person
with mental illness cannot be chained in any manner
whatsoever. Restrains and may only be used if it is
authorized by the psychiatrist at the mental health
facility and may be used no longer than necessary.
13. Duties of police officers and order in case of
person with mental illness cruelly treated -
Police officers have been assigned duties to take
any wandering person with mental illness to the
nearest public mental health facility within a period
of 24 hours and the duty of police officer once the
person have been conveyed to the facility. In case
any person with mental illness is cruelly treated or
not under proper care, a police officer or any
private person may report the fact to a Magistrate,
who will pass appropriate order for proper care
of the person after following the specified
procedure or may order for conveying the person
to a mental health facility for assessment and
treatment as per other provisions of the ACT.
14. Mental Health Authorities – Central Mental
Health Authority established by the Central
Government, in addition to earlier function will
also maintain an all India register of mental health
 facilities and mental health professionals and
will also co-ordinate programs run by
different ministries. Similarly State Mental
Health Authority, in addition to earlier
functions, will be in charge of registration of
mental health facilities in the State. It has also
been assigned duty to register certain mental
health profession and make rules and criteria
in that respect.
15. Mental Health Review Commission – It
will be a judicial body established by the State
Government to perform various functions
under the Act. President of the MHRC will
be a person qualified to become a High Court
Judge. There shall be three types of members
– Judicial members, Professional members
(any mental health professional can be the
professional member) and representatives of
users or carers and their organizations or
NGO working in the field. MHRC may have
as many panels in districts depending upon
the workload. The panel shall be constituted
by the President of the MHRC and shall
consist of three members, judicial member,
professional member and representative of
users or carers or NGOs working in the field.
Appeal against the decision of the MHRC
shall lie to the High Court.
16. Protection of Rights of Persons with
Mental Illness – There is a separate chapter
dealing with these rights. It states that persons
with mental illness cannot be subjected to
cruel, inhuman and degrading treatment and
their living environment will be safe and
hygienic, with adequate provision of food,
facilities for recreation, privacy etc. They shall
not be subjected to physical or sexual abuse
or forced to compulsory work. There will be
non-discrimination in respect of medical
insurance and in respect of emergency
medical services or any other health services.
Free and informed consent is required from
them in case research works. If they are
unable to give free consent, permission will
have to be obtained from SMHA. Persons
with mental illness or their nominated
representative shall have right to information
and right to confidentiality and shall in general
be given access to their medical records. But
the psychiatrist may withhold information in
case of likelihood of harm to the person with
mental illness or to other persons.
17. Advance Directives – Every person has a
right to make written statement specifying
the way the person wishes to be cared for
and treated for a mental illness and the
individual or individuals he wants to be
appointed as his nominated representative or
special personal representative. The advance
directive should also be signed by a medical
practitioner certifying that the person is
competent and aware of what he is doing. It
may be amended or cancelled by the person
who has made it. An appeal can be made by
the MHRC for overruling the advance
directive.
18. Special Support Arrangements – MHRC
may require create special support
arrangements in case of persons with long
term mental illness requiring very high level
of support in decision making. MHRC can
also appoint the nominated representative as
Special Personal Representative if it is
satisfied that all conditions exist and it is in
the best interest of the person. Special
Personal Representative will be a time limited
arrangement, who will decide on behalf of
the person in his/her personal matters and
property except marriage, sexual relations
and voting rights.
CONCLUSION
Many objections were raised on provision of the
draft. Some of them insisted on adoption of the WHO
definition of the mental illness and inclusion of mental
retardation. The concept of nominated
representative, carer, inclusion of general hospital
psychiatry unit (GHPU) in mental health facility,
recognition of so many professionals as mental health
professional and prohibition of unmodified ECT were
also objected. Advance directive and special personal
representative were also the subjects of objection. IPS
also insisted for recognition of role of family in care
of persons with mental illness and introduction of open
and closed ward concepts. Constitution of Central and
State Mental Authority was seen to be heavily loaded
by non-professionals. In constitution of MHRC also,
psychiatrists are not given due weightage. Human right
activist groups protested about dismantling of specific
adjudicatory and monitoring power to judiciary and
abolition of board of visitors. One of them called it
‘Total Empowerment of Psychiatrist Act 2010’. The
Act is still in process of consultation at the time of
writing this article and comments to the draft may be
posted to amendmentstomha1987@gmail.com.
It seems that the objectives of the psychiatrists
and human right activist groups are at variance to each
other. But primary concern for everyone should be
the interest and welfare of the persons with mental
illness. Mental Health Act is the Act meant for the
persons with mental illness. Naturally, it should be
directed towards betterment of their conditions and
protection of their rights. But the protection should
not be so overstretched that their welfare and proper
care is endangered. It is in the interest of everyone if
in the new Act, the emphasis is on ensuring easy
availability of psychiatric treatment to all, finding ways
to promote opening of more and more psychiatric
inpatient facility, providing for better care of
wandering persons with mental illness and protecting
and promoting rights of persons with mental illness.
REFERENCES
1. Beotra, B.R (1965) Indian Lunacy Act, 1912
(Central & States) with 1971 supplement. Law
Book Co., Allahabad.
2. Dutta, A.B. (1987) – Mental Health Act, 1987: A
Critical Approach, Proceedings of Workshop on
Ethics in Psychiatry, 117-147, KG Medical
College, Lucknow.
3. Dutta, A. B. (2001) – The Long March of Mental
Health Legislation in Independent India; Dr. L. P.
Shah Oration delivered at IPS-WZ Conference at
Goa, published by Goa Psychiatry Society.
4. Dhanda, A (2010) - Status Paper on Rights of
Persons living with Mental Illness in the light of
the UNCRPD, in Harmonizing Laws with
UNCRPD, Report prepared by the Centre for
Disability Studies, NALSAR University of Law,
Hyderabad
5. Government of India (1987) – The Mental Health
Act; published by Delhi Law House in 2002.
6. Das, S.K. (2002) – The Mental Health Act –
1987 and Current Issues; Presidential Address
delivered at IPS – EZ Conference at Patna, 2002.
7. Pathare, S. and Sagade, J. (2010) – Working
Papers on Amendments to MHA-1987 prepared
on behalf of Ministry of Health, GOI, Centre for
Mental Health Law and Policy, Indian Law
Society, Pune.
8. Pathare, S. and Sagade, J. (2010) – Amendments
to MHA-1987 – Draft dated 23-05-10 prepared
on behalf of Ministry of Health, GOI, Centre for
Mental Health Law and Policy, Indian Law
Society, Pune.
CASE REPORT
Cerebral Metastasis Masquerading
as Late onset Depression- A Case Report
Senjam Gojendra Singh*, N.Heramani Singh*, L. Nelson*, N. Biplob Singh**,
K.Shantibala Devi***, L. Roshan Singh****
*Department of Psychiatry, Regional Institute of Medical Sciences (RIMS), Manipur;
** Dept. of Medicine, RIMS, ***J.N.Hospital, Porompat, Manipur,****Dept. of Psychology, RIIMS.

ABSTRACT

A case of a 63 year-old woman with no past psychiatric illness presented with 5 months history of depressive
symptoms but minimal neurological signs and symptoms is discussed. She met the ICD-10 diagnostic criteria of
depressive disorder. Chest radiograph revealed a radio-opaque lesion and CT scan brain showed a large frontal
lobe mass that was neurologically silent. This case demonstrates that intracranial metastasis can manifest as late
onset depression without significant accompanying neurological deficits.

INTRODUCTION
Metastasis to the brain is the most feared complication
psychiatric symptoms may be the initial presenting
of systemic cancer and the most common intracranial
features in patients with brain metastasis.
tumor in adults. The incidence of brain metastasis is
rising with the increase in survival of cancer patients. The case was brought by relatives to see the
Approximately 40% of intracranial neoplasms are psychiatrists because of the patient’s psychiatric
metastatic. Multiple, large autopsy series suggest in symptoms.
order of decreasing frequency that lung, breast, CASE REPORT
melanoma, renal, and colon cancers are the most
common primary tumors to metastasized to the brain.1 A 63 years old illiterate female from rural background
Metastatic spread to the brain occurs through blood presented to psychiatric OPD with features of lack of
circulation occurs mostly via arterial circulation; less sleep, sad feelings, decreased social interaction,
often, it occurs via the Batson venous plexus (pelvic feelings of hopelessness and suicidal thoughts for past
and GI tumors). Most metastases are round, well- 5 months. She also reported of gradual onset of
demarcated lesions located at the junction of gray forgetfulness for the same period. Patients relative also
and white matter.2 Cerebral tumors presenting with reported that she talks irrelevantly sometimes for past
symptoms of raised intracranial pressure, focal few days. Past history of the patient did not reveal
neurological signs, or epileptic seizures are usually first any significant psychiatric problems or any mental
seen by neurologist or neurosurgeons. Rarely, illness in her family. There was no history suggestive
12345678901234567890123456789012123456789012345 of DM/HT/TB/Cardiac problems/thyroid disorder. Her
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence: Dr. S.Gojendra Singh,
12345678901234567890123456789012123456789012345 illness was followed after she lost money in business
12345678901234567890123456789012123456789012345
Dept. of Psychiatry, Regional Institute of Medical
12345678901234567890123456789012123456789012345 and had constant family problems in the past 2 yrs.
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Sciences (RIMS), Manipur.
12345678901234567890123456789012123456789012345 She was a chronic smoker for many years but
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-mail: sgojendra@yahoo.co.in
12345678901234567890123456789012123456789012345 discontinued for many months.
Details physical and neurological examination did not
reveal any significant findings. On MSE, she was found
to be conscious, oriented, depressed mood and speech
occasionally irrelevant but coherent. On the basis of
positive clinical history, depressed mood and intact
cognitive function in MSE which was precipitated by
stressors before illness, we initially diagnosed the case
as “Severe depression with psychotic features”
After she was diagnosed as depression, we initiated
Escitalopam 5mg, antipsychotic Olanzepine 5 mg. Her
condition was deteriorated further within next 2 weeks
and she did not show any signs of improvement with
the above treatment rather she complained of sudden
onset of weakness on right side of body with difficulty
in walking. She was readmitted again for proper
evaluation and management.
All the routine investigations like Blood R/E, LFT,
KFT, and RBS were within normal limits. Chest X-
Ray revealed a mass occupying lesion on the right side
of Chest. The patient was referred to Radiotherapy
Dept for opinion. The USG whole abdomen and USG
of B/L Breast advised and reports were found to be
normal except Rt. Renal cortical cyst. CT scan brain
showed solitary metastatic lesion in left frontal lobe.
The final diagnosis was made as lung carcinoma with
intracranial metastasis. The patient was finally shifted
to Dept. of Radiotherapy for further management.
Figure 1. PA View Chest X-Ray showing a radio-opaque
lesion on right upper lobe of lung.
Figure2: A round, cystic space occupying lesions with cen-
tral hypodensity, perifocal edema, mass effect in frontal
region.
Discussion
Lung cancer has the greatest predisposition for brain
metastasis, the predominant type of intracranial
neoplasm found in adults. Approximately two thirds
of brain metastases are symptomatic at some point.
Symptoms primarily are caused by 1increased
intracranial pressure resulting in headache, nausea,
vomiting, confusion, and lethargy and 3focal irritation
or destruction of neurons resulting in hemiparesis,
visual field defects, aphasia, focal seizures, ataxia, and
other focal neurologic signs or deficits.
Suriya A & Anand (2008)4reported that Lung cancer
frequently causes neurological complications from
direct and indirect effects and brain metastatic tumours
may be associated with a greater incidence of mental
problems than primary tumours and may be probably
due to tumours being scattered throughout brain
substance. Similar findings is also been reported by
Michael L. Pearl et al5 (1998) who demonstrated
that majority of the patients with brain metastases may
present with neurological symptoms but a minority
may develop psychiatric symptoms.
The clinical manifestations of intracranial lesions are
generally dictated by the location of the metastases.
Increased intracranial pressure and mental changes are
symptomatic of a frontal metastatic lesion, visual field
defects and cortical blindness are indicative of an
occipital metastasis, motor weakness suggests a front
parietal lesion, and a cerebellar metastasis may manifest
itself as ataxia or symptoms related to hydrocephalus.
Madhosoodanan et al. (2006)6 also reported psychiatric
symptoms as a initial presentation in case of brain
tumour and similar findings are also reported by other
authors. In our case, the patient initially presented with
depressive symptoms like sad feeling, sleep
disturbances, hopelessness, suicidal ideation
precipitated by a stressor and since patient did not
have any abnormality in either positive and deficits in
neurological examination, we thought this a case of
clear cut depression without any organic origin.
Manic symptoms in a case of small cell carcinoma of
the lung with ectopic adrenocorticotropic hormone
(ACTH) production have been reported 8 but few
others are found only neurological symptoms in a case
of brain metastasis in case of lung carcinoma.9
Neuropsychiatric symptoms like cognitive impairment,
impaired memory for recent events, nominal aphasia
may be present in case of cerebral tumours and clinical
neurological examinations sometimes generally
unremarkable with no evidence of focal signs or
features of raised intracranial pressure. The factors
contributing to the psychiatric symptomatology of
cerebral tumours are raised intracranial pressure,
location of the tumour, nature of the tumour and the
individual constitution and response of the patient.10
This case demonstrates that intracranial metastasis can
manifest as late onset depression without significant
accompanying neurologic deficits. Therefore, clinician
should conduct extensive investigations for each and
every patient who presents with such symptoms
especially in old age. It is also suggested that thorough
and systematic physical, mental status examination is
necessary in every patient with late onset of mental
problems to prevent lapse in diagnosis and delayed
treatment which has potentially serious consequences.
Appropriate intervention may improve the patient’s
prognosis and quality of life, hence early and accurate
diagnosis is crucial.
REFERENCES
1. Posner, J.B. (1992).Management of brain metastases. Rev
Neurol (Paris),148; (6-7):477-87.
2. Hwang, T.L., Close, T.P., Grego, J.M.( 1996).Predilection
of brain metastasis in gray and white matter junction and
vascular border zones. Cancer, 15 ;77(8):1551-5.
3. Wen, P.Y.. Loeffler, J.S.(1999). Management of brain
metastases. Oncology (Huntingt), 13;(7):941-54, 957-61.
4. Suriya , A. Jeyapalan.,Anand, Mahadevan. (2008).
Neurologic Complications of Lung Cancer .Cancer Neurology
In Clinical Practice, VII: 397-421.
5. Michael, L. Pearl., Gulnaz, Talgat., Fidel,A. Valea., Eva,
Chalas.(1998). Psychiatric symptoms due to brain
metastases. Medical update for psychiatrists,3; 4:91-94.
6. Subramoniam, Madhusoodanan., Deepa, Danan., Ronald,
Brenner., Olivera. Bogunovic. Brain tumor and psychiatric
manifestations (2004). A case report and review. Annals of
Clinical Psychiatry, 16; 2 :111 – 113.
7. Adam, J. Goodman., Anand, Kumar.(2004). Case report:
Frontal lobe tumor presenting as late onset depression.
International journal of geriatric psychiatry, 7; 5: 377 – 380.
8. C, Collins., M, Oakley., browne.(1988). Mania associate
with small cell carcinoma of lung. Australian and New Zealand
Journal of Psychiatry, 22; 207 – 209.
9. K, W.,Lam., F,C. Cheung, K,M.,Ko. (2005).Case report:
pineal metastasis from lung cancer. Priory Lodge Education
Ltd.
10. S, M., Ko, L,P., Kok.(1989). Cerebral tumours presenting
with psychiatric symptoms. Sing. Med J, 30: 282-284.
 BOOK REVIEW
Transformative Tales: How Stories Can Change People
Parkinson, R. London: Jessica Kingsley, 2009, 327 pp. Pb £17.99
‘There is one story, and one story only / That will prove
worth your telling,’ wrote the poet Robert Graves.
He was referring to the idiosyncratic mythology of
The White Goddess. In this story, crystallised from his
fabulous ‘grammar of poetic myth’, Graves avows the
eternal feud between the God of the Waxing moon
and the God of the Waning mood who compete yearly
for the favour of the Goddess. Each successively wins
the Goddess only to be eventually betrayed by her and
supplanted by the other. Rob Parkinson would not
agree with this reductionist notion, nor Jungian
archetypes, nor the work of Northrop Fry (1957), nor
the current manifestation of this general point of view,
popularised by Christopher Bookers (2004). Seven
Basic Plots, that all the multitudinous stories available
world-wide are reducible to a single pattern, or
numerous archetypes, or in Brooker’s case, just seven
basic plots. He appears to despair of any such
Procrustean chopping up of stories to fit with systems
or formula.
Transformative Tales, as the subtitle suggests however,
does not see stories as mere forms of entertainment
that must never be formulised or theorised. The author
views stories as invested with therapeutic potential:
‘story metaphors can be used as powerful instruments
for inspiring change’ (18), and ‘present an important
means of overcoming limitations and developing
personal autonomy’ (31). Underlying this view there
seems to be a desire to display the author’s rich
explorations into the traditions of storytelling. Though
he claims to be merely presenting ‘a primer in the
language of story’ and not, as it were, the storytellers
worldview, ‘the philosophical and mystical traditions
that have used stories for centuries’ (20), Parkinson
cannot resist dangling these traditions before our jaded
Western eyes.
Despite the confusions of intentionality, the author
manages to squeeze in an incredible amount of
interesting material into the book’s 336 pages. After
chapter one’s discussion of the inherent story making
tendencies in human nature, the author moves on to a
chapter long-handbook on guided imagery and
visualisation and describes its positive effect upon
sufferers of post-traumatic stress disorder. Next
Parkinson sets out the business of telling stories,
defining their distinct, if dubious categories, how they
are constructed, and how to harness the psychological
dynamics between teller and audience. Chapter four
describes the main traditions of storytelling and a little
about traditional storytellers, for example, the Irish
seanachie, the Celtic filidh, French minstrels (the
jongleur, literally juggler), the Moroccan rawi qissas
and the tribal shaman. The next chapter, ‘Marvellous
Miniatures’ explores brief story types and includes
maxims, aphorisms, analogies, parables and vignettes.
Here Parkinson also includes allegories and satires, a
curious choice given the length of the better known
such as Gulliver’s Travels and Pilgrim’s Progress. For
the remaining twenty pages of this chapter Parkinson
turns rather abruptly to ‘reframing’ stories, stories
which can shift the often static frame through which
we view our experience, a technique he had first
mentioned on page 28! Chapter six returns to
theoretical issues as the author illustrates how stories
interact, change and develop. But first Parkinson
attempts to disentangle stories from Jungian archetypes
and Richard Dawkins tedious evolutionary ‘memes’.
This section marks a happy moment of acceleration in
which the author gives way to the brief ‘flow’ of
impassioned thought and feeling about his subject.
This leads more logically to a technical section about
transposing stories from one situation or culture to
another.
The final chapter is symptomatic of the text as a whole.
Rather worryingly in a last chapter of a book about
stories, it begins with an exploration of symbols and
metaphors including a breakdown of five traditional
symbols. The material here is fine, but seems
redundant by this stage. There is no marked out
conclusion to Transforming Tales as such, and this
chapter ends in a coda using three interwoven stories.
But there are what I took to be concluding remarks
made on pages 301-2 for the interested reader.
To compare Transformative Tales with other work
about therapeutic stories, for example the work of
Alida Gersie, seems unfair. What Parkinson lacks in
formal structure and theoretical strength – qualities
clearly found in Gersie’s work – he makes up for
through his lively and engaging style. The book does
contain moments of depth and brilliance, and the author
is incredibly generous with his knowledge of stories
and how they work. The reflective reader will learn a
good deal about themselves as well as the subject.
On the other hand Parkinson’s book is hopelessly
muddled. He presents a theoretical case for the
potential of stories to effect change in the listener, and
he illustrates his points using a dazzling variety of
stories from around the world. The argument is
dressed in modern clothing, especially utilising the
Human Givens approach, as well as research on
dreaming, trauma and neurology. In regard to the
function of dreaming for example, though the author
differentiates his approach to that of Freud, it does
not seem substantially different to the old notion of
wish fulfillment:
...strange stories in dreams can be traced to
emotionally arousing introspections occurring
specially during the previous day’s experience
– arousals that remained essentially unresolved
since they didn’t lead to actions. In other words,
dreams reflect unfulfilled expectations. (47)
Since he wishes to inhabit the similar ground as
psychotherapists, but, of course to inhabit it in a very
different way, Parkinson occasionally adopts a critical
stance towards the profession. On page 78, he gives
an extreme example of psychoanalytic interpretation,
where the therapist is quizzing the patient about why
she chose a particular seat in the waiting room.
Parkinson asserts: ‘This kind of spurious
‘’psychologising’’ and covert domination is what many
people mistrust in the therapy/counselling industry’.
He would not then agree with Camille Paglia (1992)
who suggested that every thought bears some
emotional burden: ‘Had we time or energy to pursue
it, each random choice, from the color of a toothbrush
to a decision over a menu, could be made to yield its
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence:Chris Nicholson
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
5 Birch Close, Brightlingsea, Essex,
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
CO7 0LE , UK
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-Mail:cnich@essex.ac.uk
12345678901234567890123456789012123456789012345
secret meaning in the inner drama of our lives’ (26).
There are more unresolved interactions with
psychodynamic approaches. Pakinson hi-lights the link
between hypnosis and the trance-state which he believes
can be induced by listening to stories. He is not the
first writer or storyteller to suggest this, but it is
interesting to view his argument in relations to Freud,
who is regularly accused of going too far in the art of
persuasion. The point is that Freud himself abandoned
hypnosis in favour of free association because, while
the patient was susceptible to suggestion and open to
change in a trance-state, they were not enough in control,
the executive self, the ego, was in abeyance and
consequently change could not be consciously owned.
However, the main difficulty with Transformative Tales
is that the author has not sufficiently worked out what
the book is intending to do. Is it making a case for the
centrality and necessity of stories in human life, is it a
theoretical argument about how stories work
therapeutically upon the individual, is it a manual for
would-be story tellers or, finally, is it a collection of
tales? As the author puts all of these chicks into the
same nest it becomes difficult to deduce the species of
the mother. The situation could have been rescued with
a little re-structuring. The history and nature of
storytelling and the case for its therapeutic potential
needed to be drawn properly and cohesively together
into sustained argument which might then be lightly
peppered with relevant story examples. Unfortunately
the author’s overuse of this pepper means we don’t
properly taste the food he offers us however good it
may be. After a clear section on technique (with relevant
examples) if a final section collected the majority of the
stories the author introduces then we would have a vastly
more memorable account which the student or
professional storyteller could easily use.
Having said this, I imagine that many professionals will
enjoy this book, and if you are happy to just go along
with the author, to follow his wayward tale, then his
not inconsiderable knowledge of both tales and telling
will repay you generously for the ride.
REFERENCES:
1. Paglia, Camille, (1992) Sexual Personae: Art and Decadence from
Nefertiti to Emily Dickinson. London: Penguin Books, p 26
2. O’Prey, Paul, (2001) Robert Graves: Selected Poems. London:
Penguin Books, p 158
Chris Nicholson
BOOK REVIEW
Children and Adolescent in Trauma: Creative Therapeutic Approaches
Edited by Chris Nicholson, Michael Irwin and Kedar Nath Dwivedi; ISBN: 978-1-84310-437-7,
Jesica Kingsley Publishers, UK, 2010, Pages: 251
Trauma in the formative years of life often leads to
deleterious consequences. Effective treatment of
traumatized children and adolescent is of paramount
importance. A mental health professional must be
equipped with special expertise to deal with this
problem. To work with traumatized children and
adolescent is difficult. It is often a team work
incorporating different approaches. A professional in
isolation will not be able to offer effective services to
these group of people.When a traumatized child, feels
that he has no control of a situation, he will predictably
get more symptomatic. If a child is given some choice
or some element of control in an activity or in an
interaction, he will feel safer, comfortable and will be
able to feel, think and act in a positive way. The book
“Children and Adolescent in Trauma: Creative
Therapeutic approaches” offers insight into this
baffling subject.
The editor of this book, Chris Nicholson, is a lecturer
in the Centre for psychoanalytic studies at the
University of Essex. Nicholson has vast experience
of working in a range of Children’s service. Michael
Erwin is Emeritus Professor of English at the
University of Kent. Kedar Nath Dwivedi is a visiting
professor at the London Metropolitan University and
Director of the International Institute of Child and
Adolescent Mental Health. Formerly he served as a
consultant child psychiatrist at Northampton General
Hospital. The contributors of this book also include
psychotherapist, psychiatric nurse and manager of in-
patient adolescent unit and art therapist. So, the vast
experiences of these professionals working with
traumatized children are put together in this
comprehensive book.
The book consists of thirteen chapters written by eight
different authors. For the benefit of the reader there is
an introduction followed by five main parts- Trauma,
Story, Self-harm, Art Therapy and Violence. Each topic
is discussed in different chapters so that the reader can
smoothly understand the subject. The authors described
the concepts that relate to psychodynamic and
therapeutic community principles through story, art,
film and biography and case studies
This book provides a new approach to understanding
traumatized children and adolescent and highlights a
variety of creative therapeutic approaches for this
group in different residential settings – children’s home,
secure or psychiatric units and special schools. The
approaches include art therapy, literature and story
telling. The authors explored how creative methods
are applied in cases of abuse, trauma, violence self-
harm and identity development. The authors discussed
the impact of abuse and maltreatment on mental health
drawing links between psychoanalytic theory and
practice and study of literature and the arts. The
potential of using the creative arts such as film,
biography, sculpture, painting, poetry and stories in
training to convey psychoanalytic concepts to those
working with traumatized children is stressed. The
book may be used as a training material as most of the
standard textbook on child and adolescent psychiatry
cannot afford to discuss this topic in such a detail and
pragmatic way. We would like to recommend this book
to all busy practitioners who are dealing with problems
of children and adolescents.
The contents of the book are clearly written. Chapter
one describes the problematic nature of traumatic
experiences, their effects and management. The second
chapter stressed upon predictability of an ordered daily
routine for traumatized young people. Using corollary
from the biography and poetry the author described
the early life traumatic war experience and subsequent
post-traumatic stress disorder of the poet Robert
Graves. Chapter three and four narrates neurobiology
of trauma and the impact of trauma on brain
development taking example from Hitchcock’s film
Marine. A range of treatment options like eye
movement desensitization and reprocessing (EMDR)
and their appropriateness is discussed. In chapter five
Christine Bradley discussed early trauma from
psychotherapist’s perspective using analogy from
children’s story, The Velveteen Rabbit. In chapter six,
Prof. K. N. Dwivedi from his vast experience of using
stories within a group setting based on long tradition
of story telling in India explores how story telling can
enable therapeutic change. Therapeutic benefit of story
telling is supported by a number of fascinating stories.
Chapter seven and eight deals with self-harm In these
chapters Chris Nicholson shows how self-harm can
also be seen as an attempt at recreating the self rather
than self-destruction using case examples. Episodes
of self-harm may be symbolic representations of early
abusive acts. Chapter nine and ten provides an
introduction to art therapy and its role in enabling
traumatized young people to work through severely
damaging life events such as neglect, violence and
sexual abuse with striking case examples. In chapter
eleven the factors implicated in childhood violence and
how these children can be helped within a therapeutic
community setting are discussed. In chapter twelve
Chris Nicholson explores adolescent violence and its
relationship with poor early attachment and parenting.
The attachment theory is re-examined in this chapter
using the children’s poetry of A.A. Milne.
The intention of the editor to promote innovative and
creative practice in working with traumatized young
people is mostly successful. This book can also serve
the purpose of training manual for the staff engaged in
this work. This book will be of immense help for
practitioners of various mental health traditions- social
workers, psychotherapists, art therapists, psychiatrists,
residential child care workers, teachers, counsellors,
psychologists and students in these fields as well as
parents, teachers and interested lay people. As the
Editor hoped in the preface, we also expect that
definitely the book will provide nourishment for all
those who are working often without thanks and in
very challenging circumstances, to provide therapeutic
care and education for the troubled young people.
Kangkan Pathak, LGBRIMH, Tezpur, Assam
 BOOK REVIEW
Managing Anger
Edited by: B. Sujatha, G. Sushuma; ISBN: 978-81-314-1891-8, The Icfai University Press, Hyderabad,
India, 2008, Pages: 223
“Holding on to anger is like grasping a hot coal with
the intent of throwing it at someone else; you are the
one who gets burned”. Buddha
The natural emotion of anger if uncontrolled often
becomes disastrous. At the same time this powerful
emotion could be helpful and it can motivate people
to succeed. In this competitive modern world
everybody is under some kind of stress which often
reduces their tolerance level. Anger irrespective of
whether expressed outwardly or inwardly often lead
to negative impact on the physical and psychological
well being of the individual and it also affect the
environment. So, anger management has become
crucial. Anger management commonly refers to
techniques and exercises by which someone with
excessive or uncontrollable anger can control or reduce
the triggers, degrees, and effects of an angered
emotional state. Not to speak of the lay people even
mental health professionals sometimes do not feel
comfortable while dealing with cases of problems
related to anger. This is because topic like anger
management is not given adequate importance in the
course curriculum of mental health.
In this compilation, the editor from management and
commerce background embodied articles from various
authors from diverse fields to cover mechanism of
anger, its expression in various contexts, understanding
anger and its causes, physical symptoms, strategies to
overcome anger and anger management for different
group of people.
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
Correspondence:Dr. Kangkan Pathak
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
LGBRIMH, Tezpur, Assam, India, 784001
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
E-Mail: drkpathak@gmail.com
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
1234567890123456789012345678901212345678901234
This well-organized book is divided into three sections-
“Understanding anger”, “Managing Anger- Strategies
and Techniques”, and “Managing Anger: Specific
Insights”. The first section deals with what is anger,
anger styles, causes and its effects with illustrative
examples. There is an article on Shakespearean
perspective on anger taking examples from the four
great tragedies. The second section contains articles
on managing anger using various tips and techniques-
cognitive behavioral,rational-emotive behavioral
therapy, meditative approach and multidimensional
approach. This section also has an article on spiritual
aspect drawing essence from Bhagavad Gita and other
scriptures. The value addition from different sources
of website containing signs of anger, cause for angry
feeling, how to react to those feeling and suggestions
of anger management activities has given the book a
different format from the conventional book on similar
subject. Definitely it will help the reader to have a better
grasp on the subject and they can practice some of it
in their life. The third section details anger management
in marital and other relationships, children and at
workplace.
The articles are already published in electronic and
print media and the editor reprinted it with permission.
The book is handy and useful not only for the general
public but also for the mental health professionals. But
the annexure on anger statistics is an overdose of
information.
Kangkan Pathak,
L.G. B. Regional Institute of Mental Health,
Tezpur, Assam
BOOK REVIEW
BOOK REVIEW
Psychiatry: An evidence-based text
Edited by Basant Puri and Ian Treasaden; ISBN: 9780340950050, Hodder Arnold, London, UK, 2010, Pages: 1323
Rapid progress in the basic and clinical neuroscience in
the recent years has led to information explosion. To keep
oneself abreast of the recent developments in the related
fields is a challenging task. The development in basic
sciences has helped in better understanding of many
clinical conditions. As a result of which clinicians are
expected to deliver ‘high quality cost-effective patient-
focused care based upon best evidence available.’ The
book “Psychiatry: An evidence-based text” is likely to
help the reader to achieve this goal.
This book attempts to provide an integrated overview of
current knowledge of Psychiatry. The contributions from
84 authors, some of whom are acknowledged
international leaders in their respective fields and pioneer
in shaping psychiatric research and practice, are complied
in this evidence based text book.
Evidence-based medicine (EBM) is defined as the process
of systematically finding; appraising and using
contemporaneous research data as the basis for clinical
decisions1. The debate for and against evidence based
practice is still going on. There has long been a tension
between research and clinical practice, which are viewed
respectively as inhabiting ‘an ivory tower’ and ‘the real
world’. EBM seeks to remedy this by joining research to
best clinical practice2. It emphasizes the importance of
sound scientific methods and the use of the best available
information, generally that derived from well-designed
and carefully interpreted research studies. The evidence-
based approach de-emphasizes intuition and unsystematic
clinical experience applied without integrating empirical
evidence. Treatments should not be whimsical, neither
should they be driven by fashion, tradition or advertising.
Perhaps the most compelling reason to adopt an evidence-
based approach is an ethical obligation to support patients
and families in making informed choices about medical
decisions 3. Rapid advancements in information
technology have facilitated the development of evidence-
based medicine. A clinician can now swiftly extract
information relevant to a clinical question. At the same
time to get rid of unwanted information is becoming a
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
Correspondence:Dr. Kangkan Pathak
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
LGBRIMH, Tezpur, Assam, India, 784001
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
E-Mail: drkpathak@gmail.com
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
12345678901234567890123456789012123456789012345
major concern in this era of information explosion. This
text book has made the task much easier. Though the
text book is based on the syllabus of MRCPsych in UK
and Ireland , this book will be useful for trainees of
psychiatry elsewhere. Basic sciences related to
psychiatry e.g. Research methodology, epidemiology,
psychology, neuroanatomy, neurophysiology,
neuroendicrinolgy, neurochemistry, neuropathology,
neuroradiology and genetics are presented in a succinct
manner in the initial chapters. Clinical disorders and their
various modalities of treatment are described
comprehensively emphasizing the evidence underlying
theory and practice. Though the book is written for the
trainees of MRCPsych, but it will be useful for all
students of psychiatry and allied disciplines around the
globe as well as for consultant psychiatrist for ready
reference.
The book is thoughtfully divided into 79 chapters under
8 parts for better organization. Chapters are standardized
and cross referenced and it includes important and up to
date references. The generous use of tables, figures,
boxes and pictures has made the book reader-friendly.
The major learning points at the end of the chapter will
help the students for recapitulation. Though the chapters
are written by a galaxy of authors, the overlapping in
content is negligible. But contents of few chapters
suffered for preference of brevity for which it may not
fulfill the expectation of some readers and they have to
consult some other source for detail. The chapter on Risk
assessment is helpful for all clinician. Topics like
assessment of disability and rights of mentally ill are
totally ignored. In a nutshell it is true that the editor
succeeded in the attempt to provide the sound foundation
of evidence- based theoretical knowledge required for
psychiatric practice.
REFERENCES
1. Evidence-based medicine working group. Evidence-based
medicine. JAMA 1992; 268: 2420-5.
2. Geddes JR, Harrison PJ. Closing the gap between research
and practice. Br J Psych 1997; 171: 220-5
3. Goldner EM, , Abbass A, Leverette JS, Haslam DR, Evidence-
Based Psychiatric Practice: Implication for Education and
Continuing Professional Development; Can J Psychiatry. 2001
Jun; 46(5):1
Kangkan Pathak,
L.G. B. Regional Institute of Mental Health,
Tezpur, Assam