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MANAGEMENT of
POST-FACIAL
PARALYSIS
SYNKINESIS
This page intentionally left blank
     
MANAGEMENT of
POST-FACIAL PARALYSIS
SYNKINESIS
Edited by
BABAK AZIZZADEH MD, FACS
Associate Clinical Professor, David Geffen School of Medicine at UCLA
Diplomat, American Board of Facial Plastic & Reconstructive Surgery
Fellow, American Academy of Facial Plastic & Reconstructive Surgery
Fellow, American College of Surgeons

CHARLES NDUKA MB BS, MA(OXON), MD, FRCS, FRCS(PLAS)

Consultant Plastic Surgeon, Facial Palsy Unit
Department of Plastic & Reconstructive Surgery
Queen Victoria Hospital
East Grinstead, UK

London New York Oxford Philadelphia St Louis Sydney Toronto 2022

© 2022 Elsevier Ltd. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
mechanical, including photocopying, recording, or any information storage and retrieval system, without
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).

Notices

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using any information, methods, compounds or experiments described herein. Because of rapid advances
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Library of Congress Control Number: 2021939103

ISBN 978-0-323-67331-0

e_ISBN 978-0-323-75510-8

Content Strategist: Jessica McCool/Belinda Kuhn

Content Development Specialist: Trinity Hutton/Veronika Watkins
Project Manager: Julie Taylor
Designer: Bridget Hoette

Printed in the United States

Last digit is the print number: 9 8 7 6 5 4 3 2 1
Contents

Video Table of Contents, vi 7 Assessment and Grading of Synkinesis and

Preface, vii Facial Palsy, 51
Helen Hartley, Wendy Blumenow, Rebecca Williams,
Acknowledgements, viii Adel Fattah
Dedication, ix
Contributors, x 8 Objective Measurement of Outcomes in Facial
Palsy, 59
1 Facial Nerve and Muscle Anatomy, 1 Gerd Fabian Volk, Jovanna Thielker, Oliver Mothes, Orlando
G. Nina Lu, Patrick J. Byrne Guntinas-Lichius

2 Etiology, Epidemiology, and Pathophysiology of 9 Facial Neuromuscular Retraining for

Post-Facial Paralysis Synkinesis, 13 Synkinesis, 75
Kofi D.O. Boahene H. Jacqueline Diels

3 Psychosocial Impact of Facial Palsy, 19 10 Eyelid Rehabilitation in Post-Facial Paralysis With

Ietske J. Siemann, Carien H.G. Beurskens Synkinesis, 91
Amy Patel Jain, Yao Wang, Julia Kerolus, Babak Azizzadeh,
4 Facial Nerve Consultation, 25 Guy Massry
Stephanie Warrington, Sara MacDowell, Laura Hetzler
11 Surgical Management of Post-Facial Paralysis
5 Smile Analysis for Facial Nerve Disorders, 33 Synkinesis, 101
Scott R. Chaiet Mike Zein, Babak Azizzadeh

6 The Role of Botulinum Toxin in Facial Palsy Appendix: Instructions for Sonography of the ­Mimic
Management, 39 Musculature, 109
Ruben Yap Kannan, Charles Nduka Index, 135

v
Video Table of Contents
CHAPTER 1
Video 1.1 Levator labii superioris vector of pull
CHAPTER 3
Video 3.1 Alternatives for facial expressions
CHAPTER 4
Video 4.1 Flaccid paralysis
Video 4.2 Synkinesis
CHAPTER 7
Video 7.1 Example of iatrogenic synkinesis
Video 7.2 Post-operative rehabilitation therapy for
gracilis patients
Video 7.3 Additional assessments for bilateral facial
palsy patients
CHAPTER 8
Video 8.1 Example of a standard photo session
Video 8.2 Example of pathologic spontaneous activity
recorded by a needle-electromyography of the mus-
culus orbicularis oris
Video 8.3 Montage of video and electromyography
from a patient with synkinesis. Two needle-EMG -
electrodes are inserted in two different muscles:
channel 1 shows M. orbicularis oris; channel 2 shows
M. zygomaticus. Sound comes from channel 1
Video 8.4 Montage of video and electromyography
from a patient with synkinesis. Two needle-EMG -
electrodes are inserted in two different muscles:
vi
channel 1 shows M. orbicularis oris; channel 2 shows
M. zygomaticus. Sound comes from channel 2
Video 8.5 Montage of video and electromyography
from a participant without synkinesis. Two needle-
EMG - electrodes are inserted in two different mus-
cles: channel 1 shows M. orbicularis oris; channel 2
shows M. zygomaticus. Sound comes from channel 1
Video 8.6 Montage of video and electromyogra-
phy from a participant without synkinesis. Two
needle-EMG - electrodes are inserted in two differ-
ent muscles: channel 1 shows M. orbicularis oris;
channel 2 shows M. zygomaticus. Sound comes
from channel 1
Video 8.7 Sonography of the corner of the mouth
while patient with synkinesis is performing eye
blinks
CHAPTER 9
Video 9.1 Inhibition of oculi synkinesis during fNMR
Video 9.2 Inhibition of synkinesis using sEMG
feedback
Video 9.3 Movement acquisition during fNMR using
proprioception
Video 9.4 Dynamic demonstration of synkinetic inhi-
bition during evaluation
Video 9.5 Identifying botulinum toxin injection site(s)
for buccinator
CHAPTER 10
Video 10.1 Eyelid and periorbital reconstructive surgery
Preface
This book grew from the seed of an idea planted in 2017
at the 13th International Facial Nerve Symposium, orga-
nized and hosted by Babak Azizzadeh and colleagues.
It gathered over 500 professionals from over 40 coun-
tries in Los Angeles to share knowledge and research
about facial paralysis. There was an excellent panel
session on synkinesis with contributions from Jackie
Diels, Daniel Labbé, Mark Lucarelli, Guy Massry, Bill
Slattery, and Matt White. It was clear that there is im-
mense knowledge about the management of synkinesis
in the heads of the international faculty that needed to
be captured in one place. The result is this book, which
has drawn upon leading experts from across the world
to distill their knowledge within these pages.
vii
Acknowledgements
Acknowledgements from Charles Nduka
I would like to thank the thousands of patients affect-
ed by synkinesis who have allowed me to be part of
their care team. They have provided me with impor-
tant insights and inspiration. I am especially grate-
ful to the Facial Palsy UK community of patients,
their families, and supporters who have taught me
so much about the impact that facial paralysis has on
their lives.
I am grateful to my multidisciplinary colleagues at
the Queen Victoria Hospital in East Grinstead, includ-
ing facial therapists Trina Neville, Tamsin Gwynn, and
Karen Young, psychological therapist Beth Jordan, and
my plastic surgery colleague Ruben Kannan. I am also
grateful for the ongoing support of the oculoplastic
team led by Raman Malhotra and André Litwin, and
the facial nerve team at Guy’s Hospital in London.
Without the encouragement, patience, and support
of Veronika Watkins, Jessica McCool, and the Elsevier
team, this book would not have been possible.
Acknowledgements from Babak Azizzadeh
My personal journey as a physician has been so re-
warding, with my family, patients, mentors, and col-
leagues having an integral role in my passion for treat-
ing patients with facial nerve disorders. During the
very early part of my residency training, one of my
wife’s closest friends developed facial paralysis due to
a benign brain tumor and that started my deep curios-
ity into this most challenging of all medical and surgi-
cal disorders. During my early days as a resident in
Head & Neck Surgery at UCLA, Drs. Rinaldo Canalis,
Tom Calcatterra, Keith Blackwell, and Gerald Berke
were integral in my training in microsurgery, in-depth
viii
understanding of the facial nerve anatomy, and the
complexity of treating cranial nerve disorders. I was
privileged to train in facial plastic and reconstructive
surgery at the Massachusetts Eye & Ear Infirmary
which completely changed the trajectory of my career.
During my fellowship at Harvard Medical School, I was
fortunate enough to be trained by Dr. Mack Cheney
who had himself dedicated his life to microsurgery,
facial plastic surgery, and facial paralysis and, along
with Drs. Mark Varvares and Daniel Deschler, gave me
the necessary medical and surgical tools to further de-
velop my skills. After returning to Los Angeles, I was
privileged to be surrounded by a passionate team of
subspecialists who share the same desire, allowing us to
look at facial nerve disorders from a multidisciplinary
approach. Drs. Babak L ­ arian, Guy Massry, Bill Slattery,
Randy Sherman, Greg ­Lekovic, and Jackie Diels have
been inspirational and I have learned so much from
each of them almost every single day. I have also been
fortunate to have met so many pioneers of the field
such as Dr. Douglas Harrison who have mentored and
inspired me. I also want to thank my contemporaries
Drs. Tessa Hadlock and Patrick Byrne who continue
to push the envelope in this emerging field of study.
I would be remiss not to share how lucky I have been to
have Dr. Babak Larian as the most compassionate and
talented partner who has been with me every step of
the way for over two decades. He and I have operated
together, dreamed together, devised new approaches,
and managed the most challenging medical and sur-
gical cases. Finally, this book would not have become
reality without Jessica McCool, Veronika Watkins, and
the rest of the Elsevier team. They have been the ulti-
mate professionals in their own field.
 Dedication from Charles Nduka
To my wife Jules for her continued understanding and patience.
Dedication from Babak Azizzadeh
I dedicate this book to all my patients who have entrusted me to help them in their own journeys.

ix
Contributors

Babak Azizzadeh MD Adel Fattah PhD, FRCS(Plast)

Associate Clinical Professor, David Geffen School of Consultant Plastic Surgeon
Medicine at UCLA Regional Paediatric Burns and Plastic Surgery Service
Diplomat, American Board of Facial Plastic & Alder Hey Children’s NHS Foundation Trust
Reconstructive Surgery Liverpool, UK
Fellow, American Academy of Facial Plastic &
Reconstructive Surgery Orlando Guntinas-Lichius MD
Fellow, American College of Surgeons Professor and Chairman
ENT Department
Carien Beurskens PhD Jena University Hospital
Doctor Jena, Germany;
Physiotherapy Facial Nerve Center
Radboud University Medical Center Jena University Hospital
Nijmegen, Netherlands Jena, Germany;
Medical Faculty, Friedrich-Schiller-University
Wendy Blumenow Bsc (Hons), RCSLT, HCPC Jena, Germany
Principal Speech & Language Therapist
Alder Hey Children’s NHS Foundation Trust Helen Hartley MSc, BSc
Liverpool, UK Highly Specialist Paediatric Physiotherapist
Physiotherapy Department
Kofi Boahene MD Alder Hey Children’s NHS Foundation Trust
Professor Liverpool, UK
Department of Otolaryngology, Head and Neck
Surgery Laura Hetzler MD, FACS
Johns Hopkins University School of Medicine Associate Professor and Program Director
Baltimore Department of Otolaryngology – Head and Neck Surgery
MD, USA Louisiana State University
New Orleans
Patrick Byrne MD LA, USA
Chairman
The Cleveland Clinic Head and Neck Institute Ruben Yap Kannan MB, PhD, FRCS(Plast), DOHNS,
Cleveland DLM
OH, USA Consultant
Plastic & Reconstructive Surgery, (Facial Palsy)
Scott Chaiet MD, MBA Queen Victoria Hospital
Assistant Professor East Grinstead
Division of Otolaryngology, Department of Surgery West Sussex, UK
University of Wisconsin School of Medicine & Public
Health Julia Kerolus MD
Madison Assistant Professor
WI, USA Otolaryngology – Head and Neck Surgery
University of Illinois at Chicago
H. Jacqueline Diels OT Chicago
Facial Retraining Specialist IL, USA
Rehabilitation
Facial Retraining LLC G. Nina Lu MD
Madison Assistant Professor
WI, USA Otolaryngology
University of Washington
Seattle
WA, USA

x
 CONTRIBUTORS xi

Sara MacDowell PT, DPT Gerd Fabian Volk Priv. Doz. Dr. med. habil.
Doctor of Physical Therapy Senior Consultant
Our Lady of the Lake Hearing and Balance Center ENT Department
Baton Rouge Jena University Hospital
LA, USA Jena, Germany;
Head
Guy Massry MD Facial Nerve Center
Ophthalmic Plastic & Reconstructive Surgery Jena University Hospital
Beverly Hills, California, CA, USA; Jena, Germany;
Clinical Professor of Ophthalmology Medical Faculty, Friedrich-Schiller-University
University of Southern California, Keck School of Jena, Germany
Medicine,
CA, USA; Yao Wang MD
Diplomat, American Board of Ophthalmology; Fellow Physician
Fellow, American Society of Ophthalmic Plastic and Ophthalmology and Surgery
Reconstructive Surgery Cedars-Sinai Medical Center
Los Angeles
Oliver Mothes MSc CA, USA
Computer Vision Group
Friedrich Schiller University Stephanie Warrington MD
Jena Department of Otolaryngology – Head Neck Surgery
Thuringia, Germany LSU Health Sciences Center
New Orleans
Charles Nduka MB BS, MA(OXON), MD, FRCS, LA, USA
FRCS(Plas)
Consultant Plastic Surgeon, Facial Palsy Unit Rebecca Williams BSc (Hons)
Department of Plastic & Reconstructive Surgery Specialist Paediatric Physiotherapist
Queen Victoria Hospital Alder Hey Children’s NHS Foundation Trust
East Grinstead, UK Liverpool, UK

Amy Patel Jain MD Mike Zein MB, MSc

Oculoplastics Bascom Palmer Eye Institute
Cedars-Sinai University of Miami
Los Angeles Miami
CA, USA FL, USA

Ietske Siemann MSc

Medical Psychology
Radboud University Medical Center
Nijmegen, Netherlands

Jovanna Thielker MD
ENT Department
Jena University Hospital
Jena, Germany;
Facial Nerve Center
Jena University Hospital
Jena, Germany;
Medical Faculty, Friedrich-Schiller-University
Jena, Germany
This page intentionally left blank
     
Facial Nerve and Muscle Anatomy
G. Nina Lu, Patrick J. Byrne
INTRODUCTION
The facial nerve, also known as the seventh cranial
nerve, combines motor, general sensory, special sen-
sory, and autonomic (visceral) components. The intri-
cate course of the facial nerve as it runs intracranially,
intratemporally, and extratemporally is essential for
any surgeon operating in the head and neck to under-
stand. The facial nerve innervates the muscles derived
from the second branchial arch and carries sensory and
parasympathetic fibers of the nervus intermedius. The
facial muscles, also known as mimetic muscles, func-
tion to protect the eye, maintain the nasal airway, pro-
vide oral continence, and articulate speech. Equally
as important, these mimetic muscles provide humans
the means for emotional expression and interpersonal
communication. This chapter details an anatomic de-
scription of the facial nerve and musculature with a fo-
cus on anatomy and physiology as they relate to facial
nerve disorder and treatment.
FACIAL NERVE
The facial nerve provides a diverse range of functions
via efferent and afferent innervation to structures of
the second branchial arch. The most well-associated
function of the facial nerve is its innervation of striated
muscles of facial expression. These functions will be
the focus of this chapter. However, additional effer-
ent motor fibers provide innervation to the stapedius
muscle, the stylohyoid muscle, and the posterior belly
of the digastric. Collectively, these motor fibers repre-
sent the special visceral efferents comprising the majority
of the facial nerve fibers. The remaining efferent fibers
of the facial nerve are general efferent fibers and form au-
tonomic contributions. These autonomic nerves travel
via the greater superficial petrosal nerve (GSPN) to the
lacrimal gland and seromucinous glands of the nasal
cavity and via the chorda tympani to the subman-
dibular and sublingual glands. Traveling with this au-
tonomic system, visceral afferent fibers supply visceral
sensation to the mucosa of the nose, pharynx, and pal-
ate. Additional afferent inputs include special sensory
fibers and somatic sensory fibers. Special sensory fibers
for taste to the anterior two-thirds of the tongue, ton-
sillar fossa, and palate originate from the geniculate
1
ganglion cell bodies and travel within the chorda tym-
pani and GSPN. Somatic sensory fibers provide touch
sensation to the external auditory canal and conchal
skin of the auricle as well as proprioceptive informa-
tion from the facial muscles (Fig. 1.1).
INTRACRANIAL
Facial muscle movement starts with a conscious or un-
conscious impulse in the motor cortex of the precentral
gyrus of the cerebral hemispheres. The majority of ce-
rebral fibers then project to the contralateral facial mo-
tor nucleus via the corticobulbar tract through the thal-
amus along the posterior limb of the internal capsule.
However, a subset of cerebral fibers controlling move-
ment of the frontalis and upper orbicularis oculi proj-
ect to both the ipsilateral and contralateral facial motor
nuclei. A central lesion will thus cause frontalis-sparing
facial paralysis due to the bilateral contributions to the
upper face. The precentral gyrus fibers synapse in the
facial motor nucleus, residing in the pontine tegmen-
tum. Postsynaptic fibers then travel dorsally within the
brainstem, loop around the floor of the fourth ventricle
at the facial colliculus, and exit the ventrolateral aspect
of the brainstem at the caudal border of the pons in the
cerebellopontine angle (Fig. 1.2).
Collectively known as the nervus intermedius, pre-
ganglionic fibers of the superior salivatory nucleus
and sensory fibers from the nucleus of tractus solitari-
us exit the brainstem directly lateral to the facial nerve
motor root. Together, the facial nerve motor root and
nervus intermedius enter the internal auditory canal
(IAC) at the porus acusticus. For the purposes of this
chapter, the facial motor root and nervus intermedius
will be collectively referred to as the facial nerve.
INTRATEMPORAL
Meatal
The facial nerve travels through the temporal bone via
a bony channel, the fallopian canal. The first segment of
the fallopian canal is the meatal segment or IAC. The
facial nerve travels in the superior anterior aspect of
the IAC. The transverse (falciform) crest separates the
facial nerve from the cochlear nerve inferiorly and
Bill’s bar, a lateral ridge of bone, and separates the fa-
cial nerve from the superior vestibular nerve posteri-
orly. Within the IAC, the nerve lacks a fibrous sheath
1
2 CHAPTER 1 Facial Nerve and Muscle Anatomy
Geniculate ganglion
Gustatory portion of the solitary nucleus
Superior salivatory nucleus
Nervus Greater petrosal nerve
intermedius Pterygopalatine ganglion
Lacrimal gland
Nasal mucous
glands
Taste fibers
Submandibular and
sublingual glands
Submandibular ganglion
Chorda tympani
Main facial nerve
Fig. 1.1 The Nervus Intermedius Branches and Functional
Targets. Blue and pink arrows indicate the direction of nerve
impulse. (From Mtui E, Gruener G, Dockery P. Fitzgerald’s
Clinical Neuroanatomy and Neuroscience. 7th ed. Oxford: Elsevier;
2016:218-221.)
or endoneurium and is surrounded by a thin layer of
arachnoid.1
Labyrinthine
Exiting the IAC, the facial nerve turns gently anteri-
orly within the otic capsule bone between the cochlea
and superior semicircular canal into the labyrin-
thine segment. This portion is on average 3 to 6 mm
in length—the shortest and narrowest section of the
fallopian canal. In this segment, the facial nerve is at
its thinnest and particularly vulnerable to injury. The
vascular supply is a watershed between the terminal
arterioles of the vertebrobasilar system (via the laby-
rinthine branch of the anterior inferior cerebellar ar-
tery [AICA]) and the external carotid artery (via the
petrosal branch of the middle meningeal artery). There
is also a lack of epineurium vascular plexus along the
labyrinthine segment.
At the distal end of the labyrinthine segment, the
nerve travels superior to the cochlea and opens into
the geniculate fossa. The geniculate fossa is separated
from the middle fossa floor by a thin layer of bone,
which is dehiscent in about 25% of cases. Here the first
Solitary nucleus
Spinal nucleus of
trigeminal nerve
Facial colliculus
Abducens nucleus
Facial nucleus
Superior salivatory
nucleus
NI
Main facial
Corticopontine and nerve
corticospinal fibers
VI
Fig. 1.2 Transverse section of the brainstem showing the intrapontine
course of the facial nerve from the facial motor nucleus, superior
salivatory nucleus, and solitary nucleus. NI, Nervus intermedius. (From
Mtui E, Gruener G, Dockery P. Fitzgerald’s Clinical Neuroanatomy and
Neuroscience. 7th ed. Oxford: Elsevier; 2016:218-221.)
fibers leave the facial nerve as the GSPN. The GSPN
carries preganglionic parasympathetic innervation to
the lacrimal gland and nasal mucosa. These fibers join
the deep petrosal nerve from the carotid plexus to be-
come the Vidian (or pterygoid) nerve. The thin bone
above the geniculate and anterior attachment of the
GSPN exerting intraneural traction place the nerve at
increased risk of traumatic injury at this location. After
the geniculate fossa, the facial nerve makes an acute
posterior and slightly inferior turn, nearly 180 degrees,
to enter the tympanic segment or horizontal segment.
Tympanic (Horizontal)
The tympanic segment is located along the medial
wall of the anterior attic, travels superomedial to the
cochleariform process, and forms the superior wall of
the oval window niche posteriorly. On average 8 to 11
mm in length, dehiscence of the horizontal fallopian
canal occurs in up to 20% of patients, with 80% above
the oval window and 12% anterior to the cochleari-
form process.2 At the pyramidal eminence, the facial
nerve makes a second genu anteroinferior to the lateral
semicircular canal and enters the mastoid or vertical
segment.
Mastoid (Vertical)
Greater anatomic variability is seen in the vertical
segment prior to exiting the stylomastoid foramen
than any other segment of the fallopian canal. In this
 Facial Nerve and Muscle Anatomy CHAPTER 1 3

Stapedius
Facial nerve [VII]
Geniculate ganglion

Stapedius, tendon

Stapes

Tensor tympani, tendon

Incus

Lesser petrosal nerve

Malleus

Nerve to stapedius

Greater petrosal nerve

Pyramidal process

Tensor tympani
Facial nerve [VII]

Canal for tensor tympani

Chorda tympani

Auditory tube,
bony part

Internal carotid artery

Mastoid process
Auditory tube, Petrosphenoidal Tympanic
cartilaginous part fissure membrane

Chorda tympani Stylomastoid

foramen

Stylohyoid branch Posterior auricular nerve

Digastric branch

Stylohyoid

Digastric, posterior belly

Fig. 1.3 Intratemporal Course and Branches of the Facial Nerve. (From Paulsen F, Waschke J. Sobotta Atlas of
Human Anatomy, Vol. 3. 15th ed. Munich, Germany: Urban & Fischer; 2012:133-160; Gleeson M. External and middle
ear. In: Standring S, et al., eds. Gray’s Anatomy. 41st ed. Oxford, UK: Elsevier; 2016:624-640.e1.)

segment, the facial nerve becomes more superficial
as it travels within the mastoid bone. Between 9 and
18 mm in length, the mastoid segment contains the
chorda tympani and stapedial branches (Fig. 1.3). The
chorda tympani has a variable take off from the mas-
toid segment but typically exits 6 mm above the stylo-
mastoid foramen. Coursing superiorly nearly parallel
to the facial nerve, the chorda angles anteriorly as it en-
ters the mesotympanum. It exits the temporal bone via
the petrotympanic fissure and joins the lingual nerve
to convey taste information to the anterior two-thirds
of the tongue and supplies preganglionic parasympa-
thetic innervation to the submandibular, lingual, and
minor salivary glands. This final segment ends at the
stylomastoid foramen, which is lined by the aponeuro-
sis of the posterior belly of the digastric muscle. This
aponeurosis directly supplies blood to the facial nerve
as it exits the fallopian canal.
EXTRATEMPORAL
The facial nerve exits the stylomastoid foramen cov-
ered in tough connective tissue. At the stylomastoid
foramen, the posterior auricular branch exits the facial
nerve and supplies general sensory innervation to the
posterior ear canal and concha, as well as motor inner-
vation to the auricular muscles and occipitalis muscle.
The digastric branch supplying motor innervation
to the posterior belly of the digastric muscle and the
4 CHAPTER 1 Facial Nerve and Muscle Anatomy

1 1
2 2
1
2 3

3 3 II
IV
3 4

4
5
VI 5

4 1
1
1
2
5
2
2

3
I
V 3
III 3
4

4
5
I Type I, 13% 1 temporal branch 5
4
II Type II, 20% 2 zygomatic branch
5
III Type III, 28% 3 buccal branch
IV Type IV, 24% 4 mandibular branch
V Type V, 9% 5 cervical branch
VI Type VI, 6%

Fig. 1.4 Branching Patterns of the Extratemporal Facial Nerve. (From Holmes S. Face and scalp. In: Standring S,
et al., eds. Gray’s Anatomy. 41st ed. Oxford, UK: Elsevier; 2015:475-506.)

stylohyoid branch to the stylohyoid muscle also exit
the facial nerve prior to its entrance into the parotid
gland. Within the parotid, the facial nerve branch-
es into a larger zygomaticotemporal division and a
smaller cervicomandibular division at the pes anseri-
nus and terminates in five classic branches: temporal,
zygomatic, buccal, mandibular, and cervical. In reality,
the branching pattern of the facial nerve is highly vari-
able with multiple communications and the majority
of variations existing among the zygomaticobuccal di-
visions.3–5 Through the parotid gland, the nerve runs
at the level of the retromandibular vein and separates
the superficial and deep lobe of the parotid gland. As
it exits the parotid, the nerve has on average 8 to 15
branches making up the five divisions6 (Fig. 1.4). The
nerve runs deep to the superficial musculoaponeurotic
system (SMAS) and innervates the majority of facial
muscles from their deep surface. The mentalis, bucci-
nator, and levator anguli oris are innervated on their
superficial surface as these are the deepest layer of fa-
cial muscles.
Temporal Division
The temporal division, also known as the frontal divi-
sion or frontotemporal branch, consists of three to four
branches traveling obliquely in between the tempo-
roparietal fascia and the superficial layer of the deep
temporal fascia.7 Branches entering the frontalis mus-
cle at the level of the supraorbital ridge are located up
to 3 cm above the lateral canthus. Branches entering
the upper orbicularis oculi run along the undersurface
for 3 to 4 mm before entering the muscle to innervate it.
One common estimate of the frontotemporal branch
is Pitanguy’s line, defined by a line draw from 0.5 cm
inferior to the tragus to 1.5 cm superior and lateral to
the eyebrow. Numerous cadaveric studies have at-
tempted to further define the course and branching
patterns. Ishikawa demonstrated that three to four
branches of the FTN were consistently found between
3.8 and 6.0 cm posterior to the lateral canthus along
the superior zygomatic arch in both straight-line and
curved trajectories.8
Zygomaticobuccal Division
The zygomaticobuccal division consists of five to eight
branches with significant overlap of muscle innerva-
tions. These nerves innervate the midfacial muscles
spanning the lip elevators to the lower orbicularis
oculi. Connections between the lower branches and
marginal mandibular division also exist. Dorafshar
et al. describe “Zucker’s point” as a reliable surface
landmark for identifying the zygomaticobuccal nerve
as it exits the parotid.9 The authors found that the mid-
point of a line drawn from the root of the helix to the
oral commissure predicted the nerve location within
an average of 2.3 mm.
Marginal Mandibular Division
The marginal mandibular division consists of one to
three branches beginning up to 2 cm below the ramus

of the mandible and arcing upward to cross the man-
dible halfway between the angle and mental protuber-
ance. Branches lie on the deep surface of the platysma
and cross superficial to the facial vessels 3.5 cm from
the parotid edge. There are separate branches to the
depressor angularis, depressor labii inferioris (DLI),
and mentalis, and variable superior ramus supplying
upper platysma and lower orbicularis oris.
Cervical Division
The cervical division consists of one branch leaving
the parotid and running on the deep surface of the pla-
tysma. The point of entry into the muscle is 2 to 3 mm
caudal to the platysma muscle branch of the facial ves-
sel. It enters the muscle at the junction of its cranial and
middle thirds.
MICROSCOPIC ANATOMY
The microanatomy of the facial nerve reveals a het-
erogenous organization that explains in part the dif-
ficulty of facial nerve repair. As described by Captier
et al., the facial nerve lacks fascicular organization as
well as epineural or perineural covering from its exit
at the brainstem to the geniculate ganglion.10 Prior to
the geniculate ganglion, the nerve is surrounded only
by an arachnoid sheath. A thin epineural sheath arises
within the tympanic segment and thickens as the nerve
travels towards the stylomastoid foramen. The peri-
geniculate facial nerve demonstrates one or two fascic-
ular bundles that increase in number and decrease in
size as the nerve travels distally through the fallopian
canal. The number of fascicles and their spatial organi-
zation changes every 2 mm within the fallopian canal.
At the stylomastoid foramen the facial nerve has on
average 11 fascicles and up to 16. As individual fibers
emerge, they are surrounded by perineurium and en-
doneurium. In the horizontal segment, the upper mo-
tor division has been reported to be more superficial
(or lateral), whereas the lower motor division has been
reported to lie deeper (or medial).11 The nerve bundles
have a spatial organization as they traverse the mastoid
segment: branches to the lower division lie within the
anterior portion of the nerve and branches to the upper
division course posteriorly within the epineurium.11
From the brainstem to the mastoid segment, an aver-
age of 7800 myelinated nerve fibers are maintained. A
single neuron can innervate up to 25 muscle fibers.
VASCULAR ANATOMY
The intracranial (brainstem and IAC) facial nerve re-
ceives blood supply from branches of the AICA aris-
ing from the vertebrobasilar system. The labyrinthine
artery, a branch of the AICA, provides vascular input
within the IAC segment. However, the remaining in-
tratemporal segments receive blood supply through
the middle meningeal artery, a branch of the maxil-
lary artery from the external carotid. As described
Facial Nerve and Muscle Anatomy CHAPTER 1 5
previously, the transition zone of vascular supply be-
tween the AICA and the external carotid centers on the
labyrinthine segment and creates a watershed or weak
zone of arterial supply.
The extrinsic vascular network consists of one or
two main arterial trunks and accompanying venae co-
mitantes running between the periosteum of the fal-
lopian canal and the epineural sheath of the nerve. An
intrinsic vascular network also exists within the epi-
neurial sheath consisting of small arterioles, capillar-
ies, and venules.12
FACIAL MUSCLES
The striated muscles of facial expression derive from
the second branchial arch mesoderm and reside within
the SMAS layer. The SMAS layer continues superiorly
with the galea aponeurotica and inferiorly with the
platysma muscle. A total of 17 paired and 1 unpaired
sphincter muscle constitute the facial musculature.
These originate from the periosteum of the facial bones
and insert into the skin, allowing for a limitless num-
ber of facial expressions (Fig. 1.5).
The facial muscles possess a three-dimensional rela-
tionship to one another and exist in four layers based
on muscle origin as demonstrated by Freilinger et al.13
The orbicularis oculi, depressor anguli oris (DAO), and
superficial aspect of the zygomaticus minor are most
superficially located as the first layer. The platysma,
risorius, zygomaticus major, deeper portion of the zy-
gomaticus minor, and levator labii superioris alaeque
nasi compose the second layer. The levator labii supe-
rioris and orbicularis oris represent the third layer. The
deepest layer is composed of the levator anguli oris,
the mentalis, and the buccinator—these three muscles
are also the only muscles innervated from their super-
ficial surface, as explained by this relationship.
Distinct from most skeletal muscles, facial muscles
are flat, strap-like muscle sheets with interdigitations
to the skin, short or absent tendons, and an absent fas-
cial covering. A comprehensive list and description of
facial muscles are detailed in Table 1.1. The most clini-
cally relevant facial muscles are described in further
detail in the following sections.
FRONTALIS
The frontalis muscle is a broad, thin, bilateral muscle
originating from the galea aponeurotica near the coro-
nal suture and inserting onto the superciliary ridge of
the frontal bone and interdigitating with fibers of the
orbicularis oculi, procerus, and corrugator supercilia.
Densely adherent to the overlying skin, the frontalis
glides over the underlying periosteum to provide brow
elevation. The resting tone of the frontalis also prevents
brow descent and ptosis. Left- and right-sided frontalis
bellies fuse in the midline caudally, often as a fibrous
junction. The frontalis and occipitalis bellies can be de-
scribed as distinct muscle bellies or as parts of a single
6 CHAPTER 1 Facial Nerve and Muscle Anatomy

Epicranial aponeurosis

Occipitofrontalis, frontal belly

Depressor supercilii
Procerus

Corrugator supercilii
Orbicularis oculi, palpebral part Levator labii superioris
alaeque nasi
Levator labii superioris Nasalis
alaeque nasi
Orbicularis oculi, orbital part
Levator labii superioris
Levator labii superioris
Zygomaticus minor
Zygomaticus minor
Zygomaticus major
Zygomaticus major
Parotid gland

Orbicularis oris, marginal part

Levator anguli oris
Buccal fat pad
Depressor septi nasi
Risorius Buccinator

Depressor anguli oris

Masseter, superficial part
Depressor labii inferioris Orbicularis oris, labial part

Depressor anguli oris

Mentalis
Depressor labii inferioris

Platysma

Fig. 1.5 Facial Musculature (Frontal View). (From Zuker RM, Gur E, Hussain G, Manktelow RT. Facial paralysis. In:
Neligan PC, ed. Plastic Surgery: Volume 3: Craniofacial, Head and Neck Surgery and Pediatric Plastic Surgery. 4th ed.
Philadelphia: Elsevier; 2018:329-357.e2.)

occipitofrontalis muscle connected by an intermediate
tendon within the galea aponeurotica.
ORBICULARIS OCULI
The orbicularis oculi muscle is a paired sphincter
important in eyelid closure. The pretarsal, preseptal,
and orbital subdivisions of the orbicularis oculi are
defined by the anatomic level of the muscle. The pre-
tarsal portion is closely adherent to the pretarsal skin,
covers the tarsal plate and provides reflexive blink
movement. The preseptal portion covers the orbital
septum and is under more voluntary control. It is less
closely adherent to the skin other than at the medial
and lateral canthi. Both the preseptal and pretarsal
components function together during blink. The or-
bital component forms a ring over the bony orbital
margin and is recruited during forceful eye closure
as well as brow depression. This component origi-
nates medially from the superomedial orbital margin,
the maxillary process of the frontal bone, the medial

Table 1.1   Facial Muscles.
MUSCLE ACTION
MUSCLES OF THE SCALP
Frontalis Raises forehead and eyebrow
Occipitalis Draws scalp backwards
Auricularis Anterior Draws auricle forward and
upward
Auricularis Superior Draws auricle upwards
Auricularis Posterior Draws auricle backwards
Temporoparietalis Tightens scalp, raises auricle
and temple
MUSCLES OF THE EYELIDS
Orbicularis Oculi Sphincter muscle of eyelid,
eye closure
Corrugator Supercilii Draws eyebrow inferior and
medial (vertical forehead
wrinkles)
Depressor Supercilii Depressor of eyebrow
MUSCLES OF THE NOSE
Procerus Draws medial eyebrow
downwards (transverse
wrinkles of nose)
Nasalis Transverse: depresses
cartilaginous part of nose and
draws ala toward the septum
Alar: enlarges nasal aperture
Depressor Septi Nasi Draws ala downwards,
constricts aperture
MUSCLES OF THE MOUTH
Levator Labii Superioris Raises the medial aspect of
upper lip
Levator Labii Superioris Raises the medial aspect of
Alaeque Nasi upper lip and dilates the nostril
Levator Anguli Oris Elevates angle of the mouth
Zygomaticus Major Elevates angle of the mouth
upward and backward
Zygomaticus Minor Elevates upper lip backward,
upward, and outward
Risorius Retracts angle of the mouth
laterally
Facial Nerve and Muscle Anatomy CHAPTER 1 7
ORIGIN/INSERTION DESCRIBED DIMENSION
O: Galea aponeurotica near the Width: 60.9 +/- 8.7 mm19
coronal suture Height: 31.7 +/- 7.5 mm19
I: Superciliary ridge of the frontal
bone (frontalis) and occipital
bone (occipitalis)
O: Galea aponeurotica
I: Auricular cartilage
O: Galea aponeurotica
I: Auricularis muscles
O: Frontal bone, maxillary bone, Length: 65 +/- 5.6 mm15
medial palpebral ligament Width: 60 +/- 9.6 mm15
I: Lateral horizontal raphae
O: Medial orbital rim and frontal Length: 38–53 mm15
bone
I: Frontalis, orbicularis oculi and
skin20
O: Frontal process of maxilla
above medial canthal tendon
I: Dermis superior to the medial
canthal tendon
O: Caudal nasal bone
I: Skin of glabella and medial
brow
O: Maxilla over lateral incisor
I: Procerus/Glabellar skin and
lower lateral cartilage
O: Incisive fossa of maxilla
I: Nasal septum
O: Inferior orbital rim and maxilla Length: 47 +/- 7.5 mm15
I: Orbicularis oris of upper lip Males: 33.67 +/- 4.13 mm13
Females: 35.5 +/- 6.69 mm13
O: Medial angle of orbital rim 61.6 +/- 7.6 mm13
I: Levator labii superioris Width: 7.2 +/- 1.7 mm15
O: Maxillary canine fossa Length: 42 +/- 2.5 mm15
I: Orbicularis oris of upper lip Male length: 37.83 +/- 4.38
and modiolus mm13
Female length: 38.33 +/- 8.02
mm13
O: Zygomatic Arch Length: 65.6 +/- 3.8 mm15
I: Modiolus Male length: 70.67 +/- 6.32
mm13
Female length: 69.50 +/- 6.48
mm13
O: Zygomatic Arch Length: 51.8 +/- 7.4 mm15
I: Modiolus
O: Parotid fascia
I: Modiolus
Continued
8 CHAPTER 1 Facial Nerve and Muscle Anatomy

Table 1.1   Facial Muscles—cont’d

MUSCLE ACTION ORIGIN/INSERTION DESCRIBED DIMENSION
Depressor Labii Inferioris Draws lower lip downward and O: Mandible inferior to mental Length: 29 +/-4.9 mm15
laterally foramen
I: Modiolus, orbicularis oris, skin
of lower lip
Depressor Anguli Oris Depresses angle of the mouth O: Mandible inferior to mental Length: 48 +/- 5.1 mm15
foramen
I: Modiolus, orbicularis oris
Mentalis Raises and protrudes lower lip, O: Anterior mandible
wrinkles skin of the chin I: Chin skin
Orbicularis oris Sphincter function of lips, closure Neither bony nor tendinous
of lips origin, integration with perioral
muscles
Buccinator Compresses/flattens the cheek O: Maxilla, pterygomandibular Length: 56 +/- 7.4 mm15
raphe, mandible
I: Modiolus
Platysma Tightening of the neck, O: Supraclavicular skin
downward pull on lower lip I: Continuous with SMAS
  I, Insertion; O, Origin; SMAS, superficial musculoaponeurotic system.

Levator labii superioris alaeque nasi

Levator anguli oris
Levator labii superioris

Zygomaticus minor

Zygomaticus major
Buccinator
Modiolus

Risorius

Platysma

Depressor anguli oris

Depressor labii inferioris Orbicularis oris

Mentalis
Fig. 1.6 Periorbital Muscles Including Lip Elevators and Depressors. (From Drake R, Vogl W, Mitchel A. Gray’s
Basic Anatomy. 2nd ed. Philadelphia: Elsevier; 2018:413-596.)

canthal tendon, the frontal process of the maxilla, and
the inferomedial margin of the orbit. Within the most
superficial layer of facial muscles, the orbital sub-
division laterally overlies the temporalis fascia, the
origins of the zygomaticus major, and levator labii
muscles.
LIP ELEVATORS
The perioral muscles contributing to lip elevation and
smile are of particular interest to patients and surgeons
in facial rehabilitation. The main lip elevators are the
zygomaticus major, the levator labii superioris, and le-
vator anguli oris (Fig. 1.6).
The zygomaticus major is the most superficial of the
three and originates from the zygomatic bone in front
of the zygomaticotemporal suture. It runs to the angle
of the mouth where superficial fibers form the modio-
lus together with the DAO, the risorius, the orbicularis
oris, the buccinator, and the levator anguli oris. The
modiolus represents the interdigitation of all the peri-
oral muscles. The deeper insertion of the zygomaticus
major fuses with the levator anguli oris and the me-
dial fibers line on the buccinator muscle. The caudal
fibers continue into the DAO. The zygomaticus muscle
elevates the commissure superiorly and laterally at an
approximately 45-degree angle.

The levator labii superioris arises from the lower
margin of the orbit above the infraorbital foramen,
more medially located compared to the zygomati-
cus major. Its medial and upper insertion helps
form the nasolabial sulcus with partial insertion
into this crease. Its lateral fibers descend superfi-
cial to the orbicularis oris and deeper fibers inter-
digitate with the modiolus. Medial levator labii su-
perioris fibers reach the upper lip philtral columns
and insert into the medial vermilion border as far
as the peak of Cupid’s bow. The levator labii su-
perioris elevates the lip vertically and laterally to
expose the upper teeth and deepen the nasolabial
fold (Video 1.1).
The levator anguli oris originates from the maxillae
below the infraorbital foramen, fills the canine fossa,
and runs vertically. It inserts into the modiolus and
is in the deepest layer of facial muscles. The levator
anguli oris serves to elevate the commissure vertically
and medially.
The origins and insertions for the zygomaticus ma-
jor, levator labii superioris, and levator anguli oris
determine the vectors of pull. The relative strength of
each muscle interdigitating in the modiolus and orbi-
cularis oris determines the smile configuration unique
to each patient.
ORBICULARIS ORIS
The orbicularis oris is the only unpaired muscle of fa-
cial expression and serves as a sphincter of the mouth
essential for oral competence in both speech and the
oral phase of swallow. Superficially, portions of the
muscle fibers insert into the philtra columns as well
as along the vermilion border to form the white roll.
Superficial components of the muscle can contract in-
dependently to provide nuanced expression of the lips
and the deeper component functions as the main con-
strictor. Upper and lower lip depressors interdigitate
with the orbicularis oris and work in concert for lower
facial expression.
LIP DEPRESSORS
The lower lip musculature is as functionally complex
as the upper lip. An intricate three-dimensional assem-
bly of muscular sheets control the shape of the mouth
and position of the lips. The DLI, DAO, and platysma
comprise the lower lip depressors (Fig. 1.7).
The DLI originates along the alveolar bone of the
mandible inferior and lateral to the mental foramen. It
travels laterally to insert into the orbicularis oris mus-
cle along its deep surface and attaches to the vermilion
and middle third lip skin through fibrous septa.14,15
The DLI acts to depress and lateralize the lower lip,
evert the vermilion, and produce lower dental show.
The DAO arises from the mandible lateral and su-
perficial to the DLI origin. It inserts directly into the
skin at the labiomandibular crease medially and into
the modiolus laterally. Its main action is to draw the
corner of the mouth down and medial during frowning.
Facial Nerve and Muscle Anatomy CHAPTER 1 9
Fig. 1.7 Lower Lip Depressors. Nerve depicted here is the mental
nerve, a branch of the third division of the trigeminal nerve. (From
Zuker RM, Gur E, Hussain G, Manktelow RT. Facial paralysis. In:
Neligan PC, ed. Plastic Surgery: Volume 3: Craniofacial, Head and Neck
Surgery and Pediatric Plastic Surgery. 4th ed. Philadelphia: Elsevier;
2018:329-357.e2.)
When acting in conjunction with the platysma
muscle, the DLI and DAO depress the entire lower lip
producing a full denture smile. The mentalis muscle
similarly originates from around the mental foramen
but passes medially or inferomedially. The mentalis
muscle is the deepest layer of the lower lip muscles
and acts to raise the chin with an indirect action of
lower lip elevation.
MICROARCHITECTURE
Most facial muscles exhibit muscle fiber density equal
to other skeletal muscles such as the biceps and tibi-
alis anterior.16 Fiber density varies between 1000 and
1400 fibers/mm2 for the majority of facial muscles,
with the orbicularis oculi and oris having the highest
density (over 2000 fibers/mm2). The total number of
muscle fibers varies between 5400 fibers (zygomaticus
minor) and 9630 fibers (DAO). Muscle fiber size varies
between facial muscles. The frontalis, orbicularis oris,
and orbicularis oculi contain smaller muscle fibers (less
than 400 μm2). The zygomaticus major, DAO, buccina-
tor, zygomaticus minor, DLI, and levator labii superi-
oris contain intermediate muscle fibers (between 400
and 500 μm2). The platysma, levator anguli oris, and
risorius contain large muscles (greater than 500 μm2).
Facial muscles also demonstrate a great variability in
fast- versus slow-twitch fiber composition, likely related
to the multitude of functions they exhibit. Predominantly
tonic or slow-twitch muscles contain a high percentage
of type 1 fibers and predominantly phasic or fast-twitch
muscles contain a high percentage of type 2 fibers. Facial
muscle compositions range from 14% to 67% type 1 mus-
cle fibers.17 The most phasically composed facial muscle
is the orbicularis oculi and the most tonically composed
facial muscle is the buccinator (Table 1.2).
Facial muscles have a unique microarchitecture
compared to other skeletal muscles in the body and a
complex pattern of innervation. Most human skeletal
muscles consist of muscle fibers up to 18 cm in length
10 CHAPTER 1 Facial Nerve and Muscle Anatomy
Tablev 1.2   Fiber Composition of Facial Muscles.
MUSCLE TYPE 1 (%)/TYPE 2 (%)
Orbicularis oculi 15/85
Zygomaticus major 28/72
Orbicularis oris 29/71
Levator labii superioris 31/69
Depressor anguli oris 37/63
Corrugator superioris 41/59
Depressor labii inferioris 46/54
Occipitofrontalis 57/43
Buccinator 67/33
Adapted from Freilinger G, Happak W, Burggasser G, Gruber H. Histochemical
mapping and fiber size analysis of mimic muscles. Plast Reconstr Surg.
1990;86(3):422-428.
with a single motor end plate (MEP) in the middle of
the fiber.15 These MEPs form a narrow band that tra-
verses across the central zone of the skeletal muscles,
known as a motor band. Facial muscles differ signifi-
cantly from skeletal muscles in innervation pattern,
location of motor bands, and arrangement of MEPs.
These differences may be partially attributed to the
elaborate branching pattern of the facial nerve. Within
the parotid gland, the facial nerve divides into multiple
branches with an elaborate network of anastomosis and
interlaced branches before entering the facial muscles.
Each facial muscle is innervated by multiple terminal
branches of the facial nerve without an accompany-
ing vascular pedicle. Happak et al. demonstrate that
upon entrance into the muscle, round or oval-shaped
clusters of MEPs are found in the immediate vicin-
ity of the nerve entrance, described as motor zones.
Unlike the central motor band architecture of skeletal
muscles, motor zones are spread over facial muscles in
a de-centralized fashion with considerable variability
determined by pattern of facial nerve branching. The
orbicularis oris, orbicularis oculi, and buccinator mus-
cles demonstrate a great number of small MEP clusters
spread evenly over the muscle. The zygomaticus ma-
jor demonstrates a dominant motor zone with two to
three additional smaller motor zones. The levator labii
superioris contains two to four large motor zones in ec-
centric positions.
In experimental studies, facial muscle fibers dem-
onstrate a “multiply innervated muscle fiber pattern”
with multiple MEPs within a distance ranging from
25 to 500 μm on a single muscle fiber. This pattern of
innervation is also found in laryngeal muscles, per-
haps pointing towards a system capable of fine adjust-
ments.18 It is not yet known if multiple end plates on
a single facial muscle fiber are innervated mono- or
polyneuronally. The plexus of the facial nerve and high
branching pattern suggest a polyneuronal innervation
could be present. Further studies are needed to under-
stand the mechanisms of emotional expression and
neural control.
CONCLUSION
Facial nerve and muscle anatomy elegantly demon-
strates the complexities of the head and neck region.
Comprehensive understanding of the anatomic course
and contributions of the facial nerve is critically im-
portant for physicians treating facial nerve disorders
both surgically and medically. Further research and
understanding of nerve and muscle microarchitecture
is critical in understanding the nuances of facial move-
ment and emotional expression.
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ple motor endplates. Anat Rec. 1997;249(2):276–284.
16. Ito J, Moriyama H, Shimada K. Morphological evaluation of
the human facial muscles. Okajimas Folia Anatomica Japonica.
2006;83(1):7–14.

17. Freilinger G, Happak W, Burggasser G, Gruber H.
Histochemical mapping and fiber size analysis of mimic
muscles. Plast Reconstr Surg. 1990;86(3):422–428.
18. Rossi G. From the pattern of human vocal muscle fibre in-
nervation to functional remarks. Acta Oto-laryngologica
Supplementum. 1990;473:1–10.
Facial Nerve and Muscle Anatomy CHAPTER 1 11
19. Jeon A, Kim SD, Han SH. Morphological study of the occipi-
tal belly of the occipitofrontalis muscle and its innervation.
Surg Radiol Anat. 2015;37(9):1087–1092.
20. Hwang K, Lee JH, Lim HJ. Anatomy of the corrugator mus-
cle. J Craniofac Surg. 2017;28(2):524–527.
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Etiology, Epidemiology, and Pathophysiology
of Post-Facial Paralysis Synkinesis
Kofi D.O. Boahene
The neural activity responsible for voluntary facial ex-
pression relies on an intricate set of interconnections
distributed across multiple cortical facial motor areas,
the amygdala, and other subcortical areas.1 The tar-
get end-organs for this intricate neural system are the
facial muscles directly innervated by last order post-
synaptic axons in the facial nerve. The muscles of the
upper and lower face are controlled by anatomically
distinct motor areas reliant on distinct patterns of neu-
ral activity. Disruption of this intricate neural network,
when followed by spontaneous recovery or surgical
repair, is commonly associated with abnormal facial
movements such as synkinesis. Synkinesis is the unde-
sired synchronization of an involuntary muscle group
triggered by a desired voluntary contraction of another
muscle group. Synkinesis can occur in any functional
muscle group in the body but is commonly seen after
facial nerve injury. A typical example of facial synki-
nesis is seen when a voluntarily blink is accompanied
by co-contraction of lower facial muscles around the
lips (ocular-oral synkinesis) and when narrowing of
the palpebral fissure occurs when smiling (oral-ocular
synkinesis). In its mildest form, facial synkinesis is tol-
erable and often ignored by patients but can be very
debilitating when severe.
The pathological mechanism of synkinesis is not
completely elucidated and as a result, current treat-
ment options have mixed efficacy. Presently, synkinesis
treatment is targeted towards peripheral facial nerves
and muscles in the form of chemodenervation, selec-
tive myectomy and selective neurectomy.2 To mini-
mize the sequelae of synkinesis post facial nerve injury,
and to offer more effective rehabilitative and therapeu-
tic treatment, it is necessary to better understand the
response of peripheral nerves to injury, the process of
nerve regeneration, electrophysiologic changes in pe-
ripheral facial nerves post injury, and any associated
cortical adaptations.
ETIOLOGY AND EPIDEMIOLOGY
Faulty regeneration is the norm and not the exception
following facial nerve injury of any cause. Facial syn-
kinesis has been reported in a wide range of ages from
infants to elderly patients and does not appear to be
limited to a specific demographic. The most common
2
causes of facial paralysis, such as Bell’s palsy, Ramsey
Hunt syndrome, trauma, and postsurgical injury, have
all been associated with synkinesis to varying degrees.
In one study, synkinesis was clinically observed in 55%
of patients.3 Using electrophysiologic criteria, synki-
netic movement can be detected in nearly all patients
with proximal facial nerve injury.4 In one of the larg-
est studies evaluating the natural course of idiopathic
peripheral facial nerve palsy, synkinesis was recorded
in about 16% of patients.5 In a retrospective study of
102 patients with untreated Ramsay Hunt syndrome,
all patients who initially developed complete paralysis
also developed synkinesis, whereas synkinesis was re-
corded in 10% to 15% of those with incomplete paraly-
sis.6 Pregnancy, advanced age, and diabetes have been
studied as potential risk factors for Bell’s palsy but
have not shown to be linked with severity of synkine-
sis. However, there is a clear relationship between the
severity of facial palsy and the degree of synkinesis.
This link is further supported by electrophysiologic
studies showing that patients with a prognostic elec-
troneurography (ENoG) value of less than 10% have
higher risks of aberrant regeneration and moderate-to-
severe synkinesis than those with an ENoG value of
10% to 20%.7
THE FACIAL NEUROMUSCULAR NETWORK
The facial nerve is a mixed motor and sensory nerve
composed of approximately 10,000 neurons. About
7000 of these neurons are motor and innervate the
muscles of facial expression. The motor fibers originate
from the motor face area of the frontal lobe and project
via the corticobulbar tract and the internal capsule to
the facial nucleus. These afferent motor fibers synapse
with nuclei within the facial nucleus arranged into four
major subgroups: dorsomedial, ventromedial, inter-
mediate, and lateral. Each nuclei subgroup projects to
a specific group of facial muscles and explains, in part,
the intricate voluntary control of facial muscle move-
ment. The degree of nuclei representation and projec-
tion to muscle groups are related to the functional and
behavioral importance of each muscle. For example,
the subnuclei representing the orbicularis oris and oc-
uli are prominently represented compared to those of
less important muscles such as the depressor septi nasi
13
14 CHAPTER 2 Etiology, Epidemiology, and Pathophysiology of Post-Facial Paralysis Synkinesis
or auricularis muscles. Much of what is known about
this facial nucleus sub-innervation in humans is ex-
trapolated from tracer injection studies in primates.8,9
The corticobulbar projections were defined by inject-
ing anterograde tracers into the face representation of
each motor cortex, and the musculotopic organization
of the facial nucleus was defined by injecting fluores-
cent retrograde tracers into individual muscles of the
upper and lower face. Following these injections, the
facial nucleus was noted to received input from all face
representations. Injections in all cortical face represen-
tations labeled terminals in all nuclear subdivisions
(dorsal, intermediate, medial, and lateral). However,
significant differences occurred in the proportion of
labeled boutons found within each functionally char-
acterized subdivision.
Once the facial nerve exits the brain stem, the dis-
crete compartmentalization of motor neurons destined
for specific muscle groups is lost.10 Consequently, the fi-
bers to all facial muscles are distributed throughout the
nerve at all levels before peripheral branching occurs in
the parotid. Within the parotid gland, the facial nerve
divides into a superior (temporofacial) and an inferior
(cervicofacial) division, interconnected but containing
fibers destined to specific muscle groups. The delicate
musculotopic arrangement of the facial nucleus and fa-
cial nerve is disrupted following facial nerve injury and
explains in part abnormal motor recovery.10
WHEN A NERVE IS INJURED
The axons that make up a motor nerve are myelinated
and arranged in a fascicular architecture that is both
protective and suited for rapid nerve conduction. The
myelin sheath is made and maintained by Schwann
cell membranes wrapped compactly around the axon.
Myelin is in turn coated by a basal lamina, outside of
which lies the endoneurium, which contains fibro-
blasts, blood vessels, and a few macrophages, which is
ultimately surrounded by a multilayered cellular tube,
the perineurium. This assembly of axons, Schwann
cells, and connective tissue makes up a nerve.11 Injury
to the facial nerve may disrupt the nerve architecture
to varying degrees depending on the extent of insult.
Seddon and Sunderland classified the fundamental
types of nerve injury based on the extent of disruption
of the endoneurium and perineum as well as the integ-
rity of the axon.2 The imperfect response of peripheral
nerves to injury underlies the clinical manifestation of
synkinesis.
In response to injury, both neurons and Schwann
cells switch to a cell state suited for nerve repair and
regeneration.11 In damaged neurons, the signal switch
to repair mode is heralded by the activation of an ex-
tensive gene program that facilitates axonal regen-
eration, a response classically referred to as the cell
body response.11–15 Similarly, Schwann cells change
into a phenotype primed for repair to facilitate nerve
regeneration. This transformation to a repair-sustain-
ing Schwann cell phenotype is mediated by a complex
cellular process that is time dependent. Early after
nerve injury, the Schwann cells distal to the damaged
area lose contact with axons as they degenerate. The
loss of contact is by itself a trigger for Schwann cell
transformation. Invading macrophages secrete bio-
active factors which, together with the loss of axonal
contact, influence the change in surrounding Schwann
cells toward a repair type cell.10
Within their original basal lamina tubes, these
transformed repair type Schwann cells aid in clearing
degenerated myelin by autophagy. The released cyto-
kines call in macrophages for further myelin clearance.
The Schwann cells elongate forming regeneration
tracts, Bunger bands, which guide regenerating ax-
ons towards their target. Axons that successfully grow
across the regeneration zone induce transformation of
the repair Schwann cells back to the myelin phenotype
and become ensheathed in a new myelin membrane.
This remarkable, adaptive injury response of neurons
and Schwann cells is clinically inadequate in severe
and long-lasting injuries. There are several reasons
for this inadequacy.16,17 First, the early regeneration-
enabling environment that enables nerve regeneration
is unstable as the number Schwann cell dwindles. The
number of cells that can be isolated from nerves after
6 months of chronic denervation is only 10% to 15% of
that obtained at 4 weeks. Second, with prolonged de-
nervation, the remaining Schwann cells become less ef-
fective with surviving cells gradually down-regulating
their repair phenotype, followed by the death of cells
that have by that time lost most of their regeneration-
supportive properties.16 Clinically suboptimal rein-
nervation of the facial muscles manifest as hypotonus,
hypertonia, myokymia, or synkinesis.
PROPOSED MECHANISMS FOR SYNKINESIS
Three main theories—aberrant regeneration of facial
nerve fibers, ephaptic transmission of impulses, and
somatotopic reorganization of the facial nucleus—
have been forwarded as potential mechanisms for
synkinesis. More recently, there has been increasing
understanding of the potential role played by electro-
physiologic changes in the peripheral nerve and corti-
cal adaptations in postinjury synkinesis.
ABERRANT REGENERATION
Injuries that disrupt the endoneurium can result in
interrupted and misaligned regeneration tracts. In
addition, mechanical barriers at the injury segment
compounded by the slow growth of proximal axonal
stumps limits the number of axons that successfully
cross, resulting in misrouting and reinnervation errors.
Misrouted axons meant for the orbicularis oris muscle
end up in the orbicularis oculi muscle and result in
ocular-oral synkinesis. Recent studies have suggested
 Etiology, Epidemiology, and Pathophysiology of Post-Facial Paralysis Synkinesis CHAPTER 2
that the opportunity for misdirection of axons does not
only occur at the injury site, but that aberrant axonal
growth occurs throughout the length of the nerve.18
The most commonly observed clinical patterns of
synkinesis are predictable rather than random, with
mouth and eyelid coupling the most common occur-
rence. The mechanism of misrouted axons is the most
commonly stated reason for synkinesis and underlies
the treatment method of selective neurectomy, che-
modenervation, and myectomy.
PERIPHERAL EPHAPTIC TRANSMISSION
The ability of Schwann cells to restore myelin sheath in
extensively degenerated nerve is imperfect and incom-
plete. Consequently, regenerated axons with defective
myelin membranes can result in “short circuiting”
with cross-excitation of adjacent axons meant for dif-
ferent target muscles. Ephaptic coupling of transmis-
sion between adjacent axons is distinct from impulse
spread across synapsis. Rather it is the spreading of
impulses along and across adjacent axons such that
action potential propagating along one axon fires up
an adjacent axon. The term ephaptic was coined from
the Greek word “ephapse” signifying the act of touch-
ing (as opposed to “synapse” or linking) by Arvanitaki
in a study of nerve conduction in giant axons of Sepia
officinalis (common cuttlefish).19 Since then, the term
ephaptic interaction has been used to refer to com-
munication between neuronal cells via electrical con-
duction through the surrounding extracellular space,
as opposed to communication mediated by chemical
synapses or gap junctions. Ephaptic transmission is
usually inhibited by myelination but can occur when
remyelination is incomplete. The coexcitation of differ-
ent muscle groups will, as a result of ephaptic impulse
transmission, result in synkinesis. The concept of ep-
haptic coupling of adjacent axons was investigated by
Katz and Schmitt in 1940, who showed nonsynaptic
electrical interaction between adjacent nerve fibers.20
In their work, two large parallel nonmyelinated axons
were isolated from the crab limb nerve. They demon-
strated that: (1) the passage of an impulse in one fiber
causes subthreshold excitability changes in the adjacent
fiber and (2) when impulses are set up simultaneously
along both fibers, a mutual interaction occurs that can
lead to speeding up or slowing down of the impulses
and also possibly to synchronization between the two
impulses, depending on the initial phase relationship.
In 1984, ephaptic interactions were suggested to play a
role in hemifacial spasm pathophysiology by causing
“cross-talk” between facial nerve fibers.21
NUCLEAR HYPEREXCITABILITY
Enhanced excitability of the facial nucleus has also
been suggested as a possible mechanism for synkine-
sis following facial nerve injury. This is supported by
the predictable and nonrandom pattern of synkinesis
and the clinical observation of synkinesis early in the
15
postinjury period within a time line that is neither ex-
plained by aberrant nerve regeneration or ephaptic im-
pulse transmission given that axons grow at a rate of
only 1 mm/day. Nuclear hyperexcitability is believed
to occur when inhibitory signals to the facial nucleus
are lost in response to peripheral facial nerve injury.
Stripping of synaptic input into the facial nucleus has
been observed within days of facial nerve injury.22 The
time line for this synaptic stripping matches the obser-
vation of synkinesis as early as 4 to 8 weeks following
the onset of idiopathic facial palsy.22,23
The first evidence for disconnection of synapses fol-
lowing peripheral nerve injury in humans was report-
ed in an autopsy study of a 77-year-old man who died
from an unrelated cause 3 months after developing left
facial paresis from otitis media.24 Microscopic evalu-
ation and immunohistochemistry revealed a striking
reduction in the number of afferent synaptic contacts
and marked chromatolytic changes in the left facial
nucleus. Immunocytochemistry for synaptophysin re-
vealed a marked loss of afferent synaptic contacts from
somatic and stem dendritic surface membranes of all
chromatolytic motor neurons. Wrapping of a number
of neurons by newly formed glial fibrillary acidic pro-
tein-positive astrocytic cell processes could be detected
in the regenerating facial motor nucleus. These chang-
es were absent from the contralateral, normal-appear-
ing facial nucleus. The marked occurrence of synaptic
stripping, preferentially of inhibitory nerve, can ex-
plain enhanced nuclear hyperexcitability and poorly
controlled bursts of undesired muscle contraction.
AXONAL HYPEREXCITABILITY
Fundamental to nerve conduction is the maintenance
of a resting membrane potential and rapid impulse
propagation due to the exchange of sodium (Na+) and
potassium (K+) across ion channels in response to depo-
larizing and hyperpolarizing stimuli. The arrangement
of myelin around nerves, with myelin free segments at
the node of Ranvier and the electrophysiologic char-
acteristics of ion channel distribution at the nodal and
internodal segments, facilitates the speed of impulse
conduction. Traditionally, nerve conduction studies
that measure impulse conduction velocity, latency, am-
plitude, and F-waves have been used clinically to as-
sess the gross status of peripheral nerves. More recently,
axonal excitability study has emerged as a noninvasive
technique that offers complementary information to
that provided by conventional nerve conduction stud-
ies, to gain more insight into axonal function with de-
tailed information about the axonal membrane potential
and ion channel properties.25 The key axonal excit-
ability parameters commonly measured after delivery
of impulse to a test nerve include threshold, strength-
duration time constant, rheobase, t­hreshold electroto-
nus, recovery cycle, and current/­ threshold relation-
ship. Changes in these axonal biophysical parameters
have been attributed to aberrant ionic conductance,
16 CHAPTER 2 Etiology, Epidemiology, and Pathophysiology of Post-Facial Paralysis Synkinesis
particularly pertaining to Na+ and K+ exchange, and
has been characterized for a diverse range of conditions
including toxic, metabolic, both acquired and inherited
demyelinating neuropathies, and neurodegenerative
disorders such as amyotrophic lateral sclerosis (ALS),
as well as providing insight into pathophysiologic
changes occurring at the peripheral nerve level in dis-
orders of the central nervous system such as stroke, spi-
nal cord injury, and multiple sclerosis.26,27 Using axonal
excitability techniques, recent studies have explored the
possible contribution of electrophysiologic changes in
peripheral facial nerves following injury that may pre-
dispose to ectopic activity such as spasms and synki-
nesis. In one study, facial nerve excitability parameters
were compared between patients with synkinesis and
those without following facial paralysis.28 Synkinesis
patients demonstrated marked alterations in a number
of excitability parameters compared with normal con-
trols. Specifically, there was depolarized resting mem-
brane potential in the synkinesis group predisposing to
axonal hyperexcitability hyperkinesis and myokymia.
As in ALS, the alteration in resting membrane poten-
tial of injured facial nerves was attributed to changes in
the distribution of Na+ channels in the injured nerves.
Acute Na+ channel dysfunction has been directly im-
plicated in the pathophysiology of virus-induced facial
palsy and has been linked to the hyperexcitability ob-
served in postinjury facial nerve.26,27 In one study, the
neurotropic virus implicated in Bell’s palsy, herpes sim-
plex type 1 (HSV-1), was found to inhibit the excitabil-
ity of the facial nerve by an elective, precipitous, and
complete internalization of voltage-activated sodium
channel proteins from the plasma membrane of the
neurons.29 This change in the transmembrane sodium
channel was RNA-mediated and occurred directly at
the axonal site of virus transfection. This ability of an
axon to modify protein transcription at the site of the vi-
ral exposure or injury has emerged as a key mechanism
in the response of peripheral nerves to injury. Axonal ex-
citability studies in Bell’s palsy patients shows a pattern
that lends further support to the role of Na+ channels in
the sequelae of facial nerve injury.28 This evolving un-
derstanding of the pathophysiology of peripheral facial
nerve injury offers opportunities for preventative and
therapeutic intervention. For example, medications that
stabilize membrane potential through their effect on
Na+ channels may be considered early in the recovery
of idiopathic facial nerve paralysis even before synkine-
sis becomes clinically evident. Additionally, excitability
parameters may be used to select appropriate nerves
for reanimation procedures or selective neurectomy.
CORTICAL ADAPTATION
The fine voluntary control of facial muscles begins in
the motor cortex. The previously described mecha-
nisms for synkinesis all pertain to the facial nerve from
the nucleus in the pons to the extracranial nerve. Given
the known ability of the brain to undergo plasticity, the
role of cortical changes following facial nerve injury
as a potential cause of defective motor control is be-
ing investigated. The development of sophisticated
noninvasive neuroimaging techniques over the past
decade has made it possible to study cortical changes
in response to peripheral nerve injury. In a study of pa-
tients with facial synkinesis, functional magnetic reso-
nance imaging (fMRI) demonstrated that the distance
between motor cortical subsites activated on ipsilateral
blinking and smiling tasks was decreased on the affect-
ed half of the face compared with the unaffected side.30
In another study investigating resting state fMRI pa-
rameters in post-facial paralysis patients, there was an
abnormal state of hypercompensation in motor control
areas in patients with compared with patients without
facial synkinesis.31,32 Together, these studies support
the role of a functionally aberrant motor control sys-
tem in facial synkinesis. Facial retraining therapy with
biofeedback is an integral aspect of the management
of facial synkinesis. Recent reports indicate that people
are able to develop control over the activity of specific
brain areas when provided with real time–fMRI bio-
feedback.33,34 The use of real time–fMRI biofeedback
in the treatment of facial synkinesis is an interesting
research tool that may hold therapeutic potential.
SUMMARY
Faulty facial nerve regeneration manifesting as syn-
kinesis is a challenging sequelae of facial nerve injury
for both clinicians and patients. The varied patho-
physiologic mechanisms of synkinesis, encompassing
misdirected axons, ephaptic coupling, synaptic strip-
ping with neuronal hyperexcitability, axonal excit-
ability from altered ion channel function, and cortical
adaptation, underscores the difficulty in establishing a
universally effective preventative and therapeutic in-
tervention. However, improved understanding of the
electrophysiologic alterations that accompany periph-
eral nerve injury and new clinical tools available for
characterizing the excitability parameters of individual
nerve branches offer a selective and targeted rebalanc-
ing of the disorganized facial neuromuscular circuit
using cortical retraining therapy, effective pharmaco-
therapeutics, selective myectomy, and neurectomy.
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Psychosocial Impact of Facial Palsy
Ietske J. Siemann, Carien H.G. Beurskens
INTRODUCTION
“Societal interest in appearance has a long history,”
and today this seems more important than ever.1
Social media, the importance of “the perfect picture,”
and the desire and possibilities to change and enhance
the body create more unrest and discomfort. Older
studies2 show that physical attraction is an important
predictor in entering relations and dating. Physical at-
traction is also associated with success, happiness, and
better job prospects.3
Rojas et al. believed that the face plays a crucial
role in social interaction.4 People with facial palsy feel
that their face is no longer “right” due to asymmetry
and negative physical side effects such as incomplete
eye closure, limited mouth movement, and synkine-
sis. Additionally, facial palsy is mentally burdening;
patients often indicate they prefer not to look in the
mirror because their face startles them. Moreover, they
find it difficult when other people look at them and
they cannot express their emotions. Because of the
latter, emotions can often be misunderstood, result-
ing in miscommunication. For example, patients want
to show their happiness, but due to asymmetric and
paradoxical facial movements they may seem sad or
angry.
It is of great importance that clinicians take into ac-
count the impact of facial palsy. Research has been per-
formed on facial palsy patients concerning self-percep-
tion, difficulties with social encounters, and depressive
disorders.5–10 Although facial palsy has been recog-
nized to influence patient-perceived quality of life, the
psychosocial disability may not be related to the sever-
ity of the condition.5 In 2000, evidence was found of a
large individual variation in adaptation to facial palsy.
At the same time, a strong relation between the degree
and severity of the limitations and levels of stress was
not found.6 Recently, the literature has shown that even
a condition we qualify as minor may have severe psy-
chosocial consequences, and that a patient with severe
facial palsy or disfiguring synkinesis may not neces-
sarily experience any problems.5 Health care providers
need to be aware of the fact that patients are distressed
but that it may not correlate with the severity of the
palsy. Patients with low self-esteem, younger patients,
and women suffer more from distress.7
3
According to several studies, facial palsy is signifi-
cantly correlated with not only reduced quality of life
but also significant rates of depression and psychologi-
cal distress.8,9 Significant correlations have also been
found between perception of facial palsy and level of
psychological distress. The authors also found that fe-
male patients with facial palsy were more severely im-
pacted with depression. Etiology of the facial paralysis
also appears to play a part in the degree of depressive
disorders. For instance, patients who develop facial
paralysis secondary to a tumor are simply glad to be
alive and often accept the paralysis more readily.
Coulson et al. also showed that 50% of facial palsy
patients are unable to accurately express one or sev-
eral emotions (happiness, anger, fear, sadness, disgust,
surprise).11 The partners of these patients also consid-
ered their expressions more difficult to read. There
were also some significant correlations between the
duration and the timeline and emotional representa-
tion subscales of the Illness Perception Questionnaire-
Revised (IPQ-R), as well as the Hospital Anxiety and
Depression Scale.12,13 This indicated that the dura-
tion of the facial palsy affected participants’ levels
of distress.9 In a sample of patients with facial palsy,
Bradbury et al. also found distress levels of 11.4% for
depression and 35% for fear.14
PSYCHOSOCIAL CONSEQUENCES OF FACIAL PALSY
The face is where all social interactions begin. Within a
fraction of a second assumptions are made concerning
age, gender, status, health, mood, and intentions—all
by looking at a person’s face for just nanoseconds. In
general, this is an efficient way of processing informa-
tion, as we learn to “read” complex social stimuli from
a very early age.
Facial palsy disturbs this process and changes the
position of both the patient and the conversational
partner in the interaction. In the literature, it is men-
tioned that damage to the face may also cause damage
to “the self.”15 Various psychological mechanisms are
triggered, and patients and their partners in conversa-
tion need to look for a new balance.
As described earlier, the responses of patients vary
widely. Two factors play an important role: circum-
stances that caused the facial palsy and the existing
19
20 CHAPTER 3 Psychosocial Impact of Facial Palsy
Social isolation
Worrying
Reduced
confidence
Problems with Reactions of
relationships others
Reduced
Depression
quality of life
Social fear Shame
Stigmatization
Fig. 3.1 Impact of New Appearance.
personality traits such as self-esteem and intrinsic self-
worth.7 Factors surrounding the facial palsy such as
the etiology, age, gender, the manner in which the situ-
ation has been explained to them, and social support
also have significant influence in outcome. The over-
all impact of a new appearance therefore is extremely
diverse and the most important consequences are de-
pression and anxiety (Fig. 3.1).
DEPRESSION
The most common psychosocial response to facial pal-
sy is depression. At the onset, feelings and complaints
of depression may not be pathological per se. They can
be seen as a normal way of mourning the loss of some-
thing the patient held dear—a “normal” face.
If the depressive response is out of proportion and
continues for a very long time, it can become patholog-
ical. Sometimes, it may be the case that the patient was
familiar with feelings of depression before the facial
palsy occurred but managed to cope with them. Facial
palsy then becomes an amplifier for something that
had been there all along. The most obvious manifesta-
tions of depression are: worrying, loss of interest, feel-
ing useless, being unable to make decisions, despair,
and concentration problems.
Worrying
“I hardly recognize myself. Before, I never worried about
anything, but now I will think about everything that might go
wrong. I am no longer spontaneous; I worry about so many
things now.”
Patients indicate they worry a lot more than before
and they think about what other people might think
of them. They may also worry excessively about their
situation at school or work.
Loss of Interest
“When someone talks to me about silly things like shop-
ping or some television program, I may think to myself: yeah
right, big deal... I am extremely self-absorbed now.”
  
Patients indicate they are preoccupied with their own
feelings and their facial palsy. They find it difficult to
show an interest in other people and are mainly trying
to “survive”.
Feelings of Uselessness
“I can understand my boss is reconsidering my contract. I
mean, just look at my face... I am not exactly an ambassa-
dor for the company, am I?”
Patients often feel useless because they feel they can no
longer function as a full member of society.
Despair
“And then this doctor just says: you’ll have to learn to live
with it. Does he have any idea what he’s saying? Does he
even know what he’s talking about?”
The despair of patients can not only impact their cur-
rent situation but also future prospects. They will
doubt if they will ever see an improvement or if they
will ever be able to get better.
Concentration Problems
“I notice that since I have this condition I cannot concen-
trate anymore. I used to read books, but nowadays I can
hardly manage.”
As a result of the events surrounding the facial palsy
and the consequences for the patient, the patient may
be fully preoccupied with the new situation, and con-
centrating on other matters may be difficult. One might
say that the brain is completely preoccupied with the
condition, and there is no room for other thoughts and
feelings.
Dissatisfaction
Dissatisfaction can be characteristic of a patient with
feelings of depression. Patients may be dissatisfied
with the treatment, progress, and doctor’s statements.
They may demand certain interventions that have not
been recommended, such as surgical procedures, and
they may decide to go and see other physicians hoping
that they will give them want they want.
ANXIETY
In addition to depression there may also be feel-
ings of anxiety. It must be stated that anxiety is a
perfectly normal reaction in a threatening situation.
Anxiety is episodic and can be related to certain
situations. Anxiety, however, can become restric-
tive if it is considerable and protracted. If patients
develop a chronic anxiety of rejection and choose
exclusion or isolation for fear, the fear may become
pathological.

Beliefs
Physiology
Heart rates, palpitations,
rapid breathing, faintness,
sweaty, blushing
Feelings
Anxious, lonely, despairing, unhappy,
disgusted, ashamed, angry
Fig. 3.2 Cognitive Behavioral Model.
Reactions of Others
“I am always extremely alert: I notice people watching me
and wondering what could be wrong with me. I’m just very
sensitive about that...”
  
Patients fear facing social situations and may worry
about the possible reactions of other people. They may
also be afraid to engage in conversation, speak clearly, or
spray spittle when talking with someone. This may cause
them to be extra alert when encountering a new situa-
tion, which in turn means they will be even more wary
and sensitive about other people’s looks and remarks.
Social Fear/Social Isolation
“I always find new situations scary. People will look at me
and I am convinced they’re thinking: look at that droopy
face. I prefer to arrive a bit later and I make sure I sit or stand
at the back.”
Patients may decide to avoid social situations and re-
frain from making contact. The tension that precedes
an encounter may be too much, the fear that the other
person may say something—or nothing at all—may
be too big. They may become reserved and withdraw
from everyday life.
Shame
“I have never been very self-assured but that is even worse
now. I am simply very much ashamed of my face.”
  
Patients are ashamed of their appearance and extreme-
ly self-conscious when they walk into a room. People
with facial palsy indicate they can no longer be them-
selves: they have lost all spontaneity. Spontaneously
engaging in an unknown situation is a thing of the past;
they need to think about how they may be perceived,
Psychosocial Impact of Facial Palsy CHAPTER 3 21
“I must always look immaculate,
I don’t look like other people,
I’m deformed, to be successful
I must be beautiful……..”
Behaviors
Mirror gazing, social avoidance,
avoid intimacy; safety behaviors:
big jackets, makeup, excessive
grooming, asking for reassurance
what they are going to say, and how they can prepare
themselves for all this. This is very exhausting and
leads to patients being wary of social contacts in gener-
al. Overall, depression and anxiety can have important
consequences and can have a major impact on patients
with a facial palsy.
OTHER PSYCHOSOCIAL CONSEQUENCES
At a certain moment in time, patients will be told
that they are beyond recovery and that they will no
longer be treated surgically or otherwise and the re-
habilitation process has come to an end. This is the
moment patients need to fend for themselves and
think of ways to arrange their own life with the palsy.
“When I understood that we had run out of options for more
surgery, I arranged for a meeting with my company doctor.
He literally said: Maybe now it is time for you to work on how
all of this is affecting you.”
The consequences of the aforementioned may be
significant. Patients may avoid social contact or mini-
mize their social environment. Studies show that qual-
ity of life is reduced for patients with facial palsy.16
Fig. 3.2 summarizes the aforementioned consequences
within a cognitive behavioral model.
COPING MECHANISMS OF FACIAL PALSY
It is important to understand the various ways that in-
dividuals deal with the psychosocial impact of facial
palsy. Each person copes in their own unique manner,
depending on the strategies they employ.
Coping mechanisms refer to each person’s mecha-
nisms to deal with stress or problems. These are con-
scious efforts to regulate cognition, behavior, and
emotions as a result of stressful situations. Coping
mechanisms strongly depend on personality and dif-
fer according to circumstances and age.17
22 CHAPTER 3 Psychosocial Impact of Facial Palsy
The patient indicated she feels uncomfortable when people
watch her but do not say anything. However, when people do
say something, she also feels awkward. Therefore, in her treat-
ment attention has been paid to: what do you like in certain
situations, what can you say, and what would you want to say?
  
Patients try to make an initial assessment when their
face is paralyzed and will immediately think about
the consequences of the condition for their wellbeing.
They have a need for objective information from a phy-
sician as well as subjective information from friends
and family in order to compare themselves to others.18
It is not until later that patients will try to assess inter-
nal and external resources in order to determine what
they will need to expect from themselves and others.
They will adapt their behavior to the situation and de-
termine what might be helpful to help them adjust to
their facial palsy.
Two general coping reactions are classified: emotion-
oriented and problem-oriented. The emotion-oriented
manner of coping with stress relies on the individual
to transform or regulate their emotions with respect to
the problem. The problem-oriented manner of coping
with stress focuses on searching for potential causes of
the problem in order to transform the problem. Which
coping mechanism a patient chooses depends on their
past experiences and personality. Obviously, a combi-
nation of the two is also possible.
This certainly applies to patients with facial palsy.
Some of the patients concentrate on coping with the
situation and on self-examination, whereas others
actively investigate possible treatments. Some will
do both. Together with the psychologist, the situa-
tion can be examined to determine the patient needs
and appropriate course of action, as well as patient
response.
In most cases patients are advised to first attend to
the physical function such as facial asymmetry and
synkinesis and then concentrate on the cosmetic as-
pects, such as feelings of imperfection.
TREATMENT CONSIDERATIONS
The manner in which patients cope with facial palsy
differs significantly between individuals and there-
fore may result in varying outcomes. First of all, the
principle of “one size fits all” certainly does not apply.
Health care professionals and the patient will need to
work together to determine the nature of the issue that
needs to be addressed.
When the psychosocial consequences of facial palsy
are discussed, several subjects may be addressed:
• Psychoeducation: patients have a need for more in-
formation about their condition, prospects, possible
treatments, and psychological impact. Explaining
what it means to have facial palsy may indeed help
clarify emotional reactions and offer a context for
the patient.
• B eginning with mime therapy or neuromuscular
retraining (NMR) may be a good starting point for
dealing with functional problems.19,20 Positive feel-
ing is established when patients realize that there
is some improvement with appropriate exercises.
Attention can also be paid to hair, make-up, colorful
clothing, jewelry, and the use of nonverbal expres-
sions that divert attention away from the face.
• Behavioral therapy such as cognitive behavioral
therapy or acceptance and commitment therapy
(ACT) should be considered. Learning to cope with
thoughts and feelings concerning facial palsy may
improve a patient’s confidence.21 Cognitive behav-
ioral therapy assumes that it is not the events that
cause a person to have negative feelings and to
show a certain behavioral pattern, but rather the
biased view with which they see things. If a per-
son is taught to interpret these negative thoughts
differently, they will have a more objective take on
their own feelings and perceptions. This may cause
the negative feelings to disappear and will change
behavior. ACT may also be a useful approach as
patients learn to end their struggles with unpleas-
ant thoughts, emotions, and physical sensations.
This leads to them being able to focus their atten-
tion on the issues that really matter to them in life
(values).
• Interacting with other individuals who have a simi-
lar condition can be a powerful aid for patients with
facial palsy. Patients often indicate that they feel
isolated, partly because they do not know anyone
with a similar condition. Enabling contact among
patients who have facial palsy can have a very posi-
tive effect as they can now identify with each other.
• Patients often feel that other people stare at them. A
psychologist can explain that looking another per-
son in the eye (i.e., looking at their face) is the start-
ing point of any interaction.
• Discuss with the patients what they want and make
them aware of their preferred strategy: do they or
do they not want to mention the facial palsy when
interacting with others? If patients indicate they
would like to say something about their appear-
ance, practice sentences like “I can see you’re look-
ing, I do have a changed facial condition but let’s
talk about how you are doing.” They should say
these sentences out loud and practice them.
• For their own self-confidence, the patient should be
encouraged to look their best (clothes, make-up, hair).
• Utilize other body parts such arms, hands, and
shoulders more frequently to divert attention from
the face (Video 3.1).
• If the patient wears glasses, they may like to choose
a dark frame or a colorful frame to distract attention
from the facial palsy.
• Mime therapy or NMR can be utilized to reduce
the stiffness of the face so that patients will be less
aware of the fact that their face consists of two

separate halves. If patients do not feel their face, it
is less present and as a consequence the facial palsy
will also be less present.
• 
It may be useful to visualize stressful situations
(social interaction, unknown people) in advance.
Patients can think of what may happen and think of
how they will respond to possible looks or remarks.
CONCLUSION
Facial palsy is not only a physical condition, but also
a damage to “the self.” The most common psychoso-
cial response to facial palsy is depression. In addition
to depression there may also be feelings of anxiety.
Various psychological mechanisms are triggered, and
patients need to look for a new balance. A multidis-
ciplinary approach for patients with a facial palsy is
important, whereby a psychologist can make a contri-
bution concerning psychosocial problems.
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Facial Nerve Consultation
Stephanie Warrington, Sara MacDowell, Laura Hetzler
INTRODUCTION
Facial paralysis and its sequela is a complex medical
issue that can be both physically and emotionally dis-
tressing. Patients may present to us at any time along
the continuum of their recovery or lack of recovery.
In addition to the medical aspects of treatment, psy-
chosocial impacts are common and must also be ad-
dressed.1–6 Here we discuss our approach to the evalu-
ation and early management of patients with facial
nerve dysfunction.
HISTORY
Upon initial evaluation for facial nerve dysfunction,
there are a few key components of the history that
are invaluable in diagnosing and ultimately guiding
management. First, a timeline of the onset of facial pa-
ralysis is essential. It is important to understand if the
paralysis occurred immediately or over the course of a
few days or months. This needs to be followed up with
further questioning about the severity of the weakness,
to include partial or complete paralysis. If some time
has passed since the onset of facial paralysis, a timeline
of recovery is also needed. Certain etiologies, such as
Bell’s palsy, are supported by recovery of facial func-
tion within 2 to 3 months. Failure to recover function
within that period may indicate a different etiology
and further workup with imaging and nerve conduc-
tion studies may need to be initiated.7
The health care provider should also ask specific
questions that might indicate more clearly the etiology
of the dysfunction. Common causes are inflammatory
post viral, neoplasms, trauma, congenital, and infec-
tion including otologic pathology.3,7–10 Questions for
diagnostic purposes can include personal history of
past facial paralysis, family history, presence of vesicles
or rashes, travel history, or recent surgery or trauma.
The practitioner should also note other symptoms tem-
porally associated with onset of facial paralysis such as
hearing loss, dizziness, facial pain, facial twitching, or
facial swelling.
The next part of the history should discern if the pa-
tient has received any prior treatments for their paraly-
sis such as steroids or antivirals. Some patients may
have participated in facial exercises or electrical stimu-
lation to aid in their recovery.1,6,10 Questions regarding
4
past imaging are necessary and may direct further
workup. In the setting of tumor extirpation or onco-
logic causes of facial paralysis, radiation therapy may
have been performed or may be planned in the future.
As each patient has a unique perception of their fa-
cial deficit, it is imperative to ask each patient to ar-
ticulate what is most bothersome to them, as this may
not always correlate to the most notable deformity to
the clinician. Patient-driven care can be appropriate,
especially in the partially recovered facial paresis or
synkinetic patient.
THE ROLE OF PATIENT-REPORTED OUTCOME
MEASURES
Facial nerve dysfunction can take a great emotional
toll on patients, causing them to withdraw from social
interactions. The psychosocial impact of the individu-
al’s facial paralysis must be directly explored during
the initial evaluation. Patients often have a negative
self-image and low self-esteem. To the observers, these
patients can be thought of as displaying a negative
affect, which may lead to social isolation. Quality of
life studies have shown that facial paralysis is signifi-
cantly associated with depression.1–6 This profound
emotional component must be part of the assessment
of patients with facial nerve dysfunction. Some of the
patient-reported outcome measures (PROMs), such as
the Facial Disability Index (FDI) and Facial Clinimetric
Evaluation (FaCE), are very useful in aiding the cli-
nician in capturing additional and useful informa-
tion about the patient’s quality of life (Fig. 4.1).2,4,6,9,11
Furthermore, PROMs can be useful in research out-
come studies to evaluate the efficacy of our treatment
methods. It is useful to have resources such as online
or in-person support groups and counseling to offer
to facial nerve patients in addition to traditional treat-
ment modalities.5
PHYSICAL EXAMINATION
Once a thorough patient history is elicited, a detailed
physical examination assessing the function of the fa-
cial nerve must be completed. Traditionally, the House-
Brackmann scale has been an objective way to measure
facial dysfunction. However, this scale is more of a broad
overview of facial nerve function without assessing
25
26 CHAPTER 4 Facial Nerve Consultation

Facial Disability Index (FDI)

Please circle the most appropriate response to the following questions related to
problems associated with the function of your facial muscles. For each question,
consider your function during the past month.
Physical function:
1. How much difficulty did you have keeping food in your mouth, moving food around in
your mouth, or getting food stuck in your cheek while eating?

2. How much difficulty did you have drinking from a cup?

3. How much difficulty did you have saying specific sounds while speaking?

4. How much difficulty did you have with your eye tearing excessively or becoming dry?

5. How much difficulty did you have with brushing your teeth or rinsing your mouth?

(5) Usually did with no difficulty

(4) Usually did with a little difficulty
(3) Usually did with some difficulty
(2) Usually did with much difficulty
(1) Usually did not do because of health
(0) Usually did not do because of other reasons

Social function:
6. How much of the time have you felt calm and peaceful?

7. How much of the time did you isolate yourself from people around you?

8. How much of the time did you get irritable toward those around you?

9. How often did you wake up early or wake up several times during your nighttime sleep?

10. How often has your facial function kept you from going out to eat, shop, or participate
in family or social activities?

(6) None of the time

(5) A little bit of the time
(4) Some of the time
(3) A good bit of the time
(2) Most of the time
(1) All of the time

Fig. 4.1 Facial Disability Index (FDI) and Facial Clinimetric Evaluation (FaCE).

specific affected facial regions.4,6,8,11,12 A more detailed
characterization of the defect is warranted. It is good
practice to divide the face into five overall sections: fore-
head, periocular, midface, perioral, and cervical. From
there, documenting the deficits associated with each divi-
sion is ideal (Table 4.1). Once there is a more precise char-
acterization of deficits and symptoms, this will aid in the
decision-making process for rehabilitation and treatment,
as well as allowing for more precise assessment of treat-
ment results.
A complete head and neck examination is necessary
to evaluate prior incisions and deficits as well as the
status of other cranial nerves. Injury to candidate do-
nor nerves for reanimation may dictate the treatment
options for a patient. Presence of palpable and/or vis-
ible extratemporal causes of facial paralysis must be
ruled out. To the general practitioner, smaller parotid
tumors may elude a rudimentary physical examina-
tion. The presence or history of skin cancer can be a
concerning factor in patients with initially incomplete
but progressive facial nerve paralysis.
Another important aspect of assessing facial
dysfunction is facial tone. Abnormal facial tone is
evident to the casual observer, even when the pa-
tient is at rest, and therefore can have a profound
impact on the patient’s ability to participate in the
community. Facial tone may be either hypertonic or
hypotonic, both of which may exist in the same in-
dividual (Fig. 4.2) (Video 4.1). This distinction is im-
portant as there are different treatment approaches
for both.1,2,5,6,13
During a patient’s recovery from facial nerve inju-
ry they can experience aberrant neural regeneration,
which can lead to undesired facial tone and/or synki-
nesis. Synkinesis is uncoordinated facial motion that
occurs during abnormal facial nerve recovery. The
patient may experience a lack of perceived motion or
restricted movement that is due to poor coordination
of muscle activation rather than paralysis. For ex-
ample, during an attempt at normal smile, the zygo-
maticus complex is restricted in its movement from
synkinetic smile antagonists such as depressor anguli
 Facial Nerve Consultation CHAPTER 4 27

Facial Clinimetric Evaluation (FaCE) scale

You may have answered these or similar questions before. Please answer ALL QUESTIONS as best
you can. The following statements are about how you think your face is moving.
Circle only ONE number One side Both sides I have no difficulty
When I try to move my face, I find that I have difficulty on 1 2 0

If you have problems on BOTH sides, answer the questions in the remainder of the survey with regard
to the more affected side, or with regard to both sides if they are equally affected. In the past week:
Circle only ONE number on each line Not at all Only if I A little Almost Normally
concentrate normally
(1) When I smile, the affected side of
1 2 3 4 5
my mouth goes up
(2) I can raise my eyebrow on the
1 2 3 4 5
affected side
(3) When I pucker my lips, the affected
1 2 3 4 5
side of my mouth moves

The following are statements about how you might feel because of your FACE OR FACIAL PROBLEM:
Please rate how often each of the following statements applied to you during the PAST WEEK.
Circle only ONE number on each line All of the Most of Some of A little of None of
time the time the time the time the time
(4) Parts of my face feel tight, worn
1 2 3 4 5
out, or uncomfortable
(5) My affected eye feels dry, irritated,
1 2 3 4 5
or scratchy
(6) When I try to move my face, I feel
1 2 3 4 5
tension, pain or spasm
(7) I use eye drops or ointment in my
1 2 3 4 5
affected eye
(8) My affected eye is wet or has tears
1 2 3 4 5
in it
(9) I act differently around people
1 2 3 4 5
because of my face or facial problem
(10) People treat me differently
1 2 3 4 5
because of my face or facial problem
(11) I have problems moving food
1 2 3 4 5
around in my mouth
(12) I have problems with drooling or
keeping food or drink in my mouth or 1 2 3 4 5
off my chin and clothes

The following are statements about how you might have felt or been doing in the
PAST WEEK because of your FACE OR FACIAL PROBLEM. Please rate how much
you agree with each statement.
Circle only ONE number on each line Strongly Agree Don’t Disagree Strongly
agree know disagree
(13) My face feels tired or when I try to
move my face, I feel tension, pain, or 1 2 3 4 5
spasm
(14) My appearance has affected my
willingness to participate in social 1 2 3 4 5
activities or to see family or friends
(15) Because of difficulty with the way I
eat, I have avoided eating in 1 2 3 4 5
restaurants or in other people’s homes

Fig. 4.1, cont’d

oris, and platysma as well as other perioral muscles
including buccinator, and depressor septi nasi. In this
case, the patient often feels the lack of motion is relat-
ed to weakness but in actuality, it is the result of over-
active tone and contraction of antagonist muscles
restricting any meaningful motion (Video 4.2). This
must be recognized prior to effectively managing
these patients. Ocular synkinesis is another frequent
complaint in patients with aberrant facial nerve re-
generation, where attempts at movement such as
28 CHAPTER 4 Facial Nerve Consultation

  The Five Divisions of the Face to Be smile or speech can lead to contraction of the orbi-
TABLE 4.1 Evaluated and the Facial Deficits in Each cularis oculi and thus narrowing the eyelid aperture
That Should Be Documented. (Fig. 4.3).1,3,4,6,10,11,13 This is in direct contrast to lag-
ophthalmos that patients experience in fully dener-
FACIAL DIVISIONS FACIAL DEFICIT
vated facial and eyelid musculature.
Forehead Tone An objective assessment of facial tone, voluntary
Synkinesis
movement, and synkinesis should be performed at
Brow elevation
Brow ptosis
the initial evaluation and can be performed using a
myriad of available grading systems. The authors
Periocular Tone
consistently use the Sunnybrook Facial Grading
Synkinesis
Visual acuity
System during initial evaluation.6,10,12–14 In addition
Corneal integrity to descriptive documentation and objective grading
Tearing systems, it is also recommended that photographic
Bell’s phenomenon and video documentation of patients be captured
Lagophthalmos at each session.13,14 Patients should be recorded in
Lower lid laxity repose, brow elevation, gentle eye closure, firm eye
Lacrimal puncta position closure, closed mouth smile, open mouth smile,
Midface Tone snarl, pucker, wide mouth opening, lower lip de-
Synkinesis pression, and nasal base view. The authors also doc-
Oral commissure excursion ument a “puffing cheeks with air” photograph (Fig.
Nasal obstruction 4.4).14 Videos can be captured of dynamic move-
Perioral Tone ments and speech. This is a useful way to monitor
Synkinesis treatment outcomes and to allow patients to ob-
Oral incompetence serve progress. A subjective questionnaire that can
Articulation errors be used to determine a patient’s perception of syn-
Cervical Tone kinesis is the Synkinesis Assessment Questionnaire
Synkinesis (SAQ) (Fig. 4.5).4,6

A B
Fig. 4.2 (A) An example of the flaccid facial tone on the right. Note dependent oral commissure position and
generalized facial ptosis as well as nasal deviation. (B) An example of hypertonic facial tone on the left. In the
hypertonic face, you can see decreased ocular aperture, deepened nasolabial crease, and platysmal banding in
repose.

A B
Fig. 4.3 Example of Blepharospasm Synkinesis. Right (A) and left (B) facial paralysis with synkinesis resulting in eye
closure/blepharospasm upon smiling.
RADIOLOGY AND ELECTRODIAGNOSTICS
Imaging studies may play an important role in the
evaluation and treatment of facial palsy patients. In
the unrecovered patient with idiopathic facial paraly-
sis, imaging studies such as computed tomography
(CT) and magnetic resonance imaging (MRI) can be
useful to evaluate the presence of tumors along the fa-
cial nerve or to confirm inflammation in patient with
presumed Bell’s palsy.7
Some patients may require surgery to help with
their facial nerve recovery. For those who have facial
nerve injury due to previous surgery or trauma, a CT
scan can be useful preoperatively to help with surgical
planning.
When evaluating the need for or planning for spe-
cific facial reanimation procedures, the type of reani-
mation procedure an individual can receive depends
on the time since injury, the viability of the facial nerve,
and the status of the myogenic potential of the facial
muscles. Electroneuronography (ENoG) can help de-
termine the degree of injury to the nerve. However,
due to Wallerian degeneration, which takes place 3 to
5 days after injury, an ENoG cannot be performed un-
til after that time. It is recommended to be completed
between 3 days to 3 weeks after injury to the facial
nerve. ENoG can only assess early stages of acute fa-
cial paralysis and act as a prognostic indicator in facial
nerve regeneration. Electromyography (EMG) can be
performed acutely and in patients with chronic facial
paralysis and is typically the study of choice after 3
weeks post injury. Electric action potentials seen on
Facial Nerve Consultation CHAPTER 4 29
EMG can indicate reinnervation, fibrillations can indi-
cate muscle fibers are still viable but do not have inner-
vation, and no activity on EMG indicates the muscle
fibers no longer have myogenic ability and cannot
be reinnervated. This information can help direct the
available options for reanimation.7,8
MANAGEMENT
As mentioned earlier, allowing the patient to articu-
late their perception of the deficit is key. The smile is
considered a thumbprint of an individual’s personal-
ity and loss of this ability can be personally devastat-
ing.5,11 That being said, as clinicians, we must protect
from further harm such as loss of vision. Clear direc-
tion on how to protect the eye should be given and re-
ferral to an ophthalmologist who can follow the status
of the cornea is ideal.2,3
Expectation management is crucial in our recover-
ing patients. Whether the patients have had an attempt
at surgical dynamic reanimation or the treatment plan
is to allow for natural recovery, the timeline to a new
normal may be significant. Sharing that complete and
perfect recovery is not likely early on, but expressing
commitment to optimize their outcome will allow the
patient to both understand the need for patience and
the limitations of nerve recovery.
The paradigm of care in facial paralysis has shifted
over the past decade to a multispecialty model.11 Patients
with facial paralysis require multiple medical special-
ties to be involved in their care including neurologists,
30 CHAPTER 4 Facial Nerve Consultation

A B C D

E F G H

I J K
Fig. 4.4 Photographic Documentation of Patients Obtained at Each Evaluation. (A) Repose. (B) Brow elevation.
(C) Gentle eye closure. (D) Firm eye closure. (E) Closed mouth smile. (F) Open mouth smile. (G) Snarl. (H) Pucker. (I)
Wide mouth opening. (J) Lower lip depression. (K) Puffing cheeks with air.

neurotologists, neurosurgeons, oculoplastic surgeons,

and facial plastic surgeons/plastic surgeons, as well as
physical or occupational therapists, nurses, psycholo-
gists, and other support staff.6 This allows for a mul-
tidisciplinary plan of care to be determined which can
include: patient education, psychotherapy, soft tissue
mobilization, neuromuscular retraining, chemodener-
vation, and surgical facial reanimation.2,3,6,10,13 Some
treatment options, such as soft tissue mobilization or
neuromuscular retraining, will need to be reinforced at
home and therefore an understanding of the purpose
and goals of treatment is essential.6 Patient education
and psychosocial wellness may be improved by this
multidisciplinary approach to treatment.
CONCLUSION
Facial nerve dysfunction may have a complex and var-
ied presentation. Management of these patients requires
a comprehensive and directed facial nerve evaluation
with an individualized work up. The advent of multi-
disciplinary care teams to approach facial nerve dys-
function and recovery is likely to improve quality of life
for those we treat.5,6,11 Importantly, allowing the patient
to articulate their perception of facial deficit is integral to
their evaluation for both expectation management and
overall goals. Beginning with proper assessment, sub-
sequent evaluation and a proctored recovery can lead
to improved patient understanding, expectations, and
quality of life in those with facial nerve dysfunction.
 Facial Nerve Consultation CHAPTER 4 31

Synkinesis Assessment Questionnaire (SAQ)

Date:

Please answer the following questions regarding facial function, on a scale from 1 to 5,
according to the following scale:

1 = seldom or not at all

2 = occasionally, or very mildly
3 = sometimes, or mildly
4 = most of the time or moderately
5 = all the time or severely

Question Score
1 When I smile, my eye closes
2 When I speak, my eye closes
3 When I whistle or pucker my lips, my eye closes
4 When I smile, my neck tightens
5 When I close my eyes, my face gets tight
6 When I close my eyes, the corner of my mouth moves
7 When I close my eyes, my neck tightens
8 When I eat, my eye waters
9 When I move my face, my chin develops a dimpled area

Total synkinesis score: sum of scores 1 to 9 / 45 x 100

Fig. 4.5 The Synkinesis Assessment Questionnaire (SAQ) can be used to objectively measure the patient’s perception
of their synkinesis.

REFERENCES 8. Lee DH. Clinical efficacy of electroneurography. J Audiol

1. Fargher KA, Coulson SE. Effectiveness of electrical stimula-
tion for rehabilitation of facial nerve paralysis. Phys Ther Rev.
2017;22(3–4):169–176.
2. Henstrom DK, Lindsay RW, Cheney ML, Hadlock TA.
Surgical treatment of the periocular complex and improve-
ment of quality of life in patients with facial paralysis. Arch
Facial Plast Surg. 2011;13(2):125–128.
3. Ishii LE. Facial nerve rehabilitation. Facial Plast Surg Clin N
Am. 2016;24:573–575.
4. Mehta RP, Wernick Robinson M, Hadlock TA. Validation
of the synkinesis assessment questionnaire. Laryngoscope.
2007;117:923–926.
5. Nellis JC, Ishii M, Byrne PJ, Boahene KD, Dey JK, Ishii LE.
Association among facial paralysis, depression, and quality
of life in facial plastic surgery patients. JAMA Facial Plast
Surg. 2017;19(3):190–196.
6. Van Landingham SW, Diels J, Lucarelli MJ. Physical therapy
for facial nerve palsy: applications for the physician. Curr
Opin Ophthalmol. 2018;29(5):469–475.
7. Peitersen E. Bell’s palsy: the spontaneous course of 2,500
peripheral facial nerve palsies of different etiologies. Acta
Otolaryngol Suppl. 2002;549:4–30.
Otol. 2016;20(1):8–12.
9. Lee J, Fung K, Lownie SP, Parnes LS. Assessing impair-
ment and disability of facial paralysis in patients with
vestibular schwannoma. Arch Otolaryngol Head Neck Surg.
2007;133:56–60.
10. Pourmomeny AA, Asadi S. Management of synkinesis and
asymmetry in facial nerve palsy: a review article. Iran J
Otorhinolaryngol. 2014;26(77):251–256.
11. Kahn JB, Gliklich RE, Boyev KP, Stewart MG, Metson RB,
McKenna MJ. Validation of a patient-graded instrument
for facial nerve paralysis: the FaCE scale. Laryngoscope.
2001;111:387–398.
12. Neely JG, Cherian NG, Dickerson DB, Nedzelski JM.
Sunnybrook Facial Grading System: reliability and criteria
for grading. Laryngoscope. 2010;120:1038–1045.
13. Maria CM, Kim J. Individualized management of fa-
cial synkinesis based on facial function. Acta Otolaryngol.
2017;137(9):1010–1015.
14. Santosa KB, Fattah A, Gavilán J, Hadlock TA, Snyder-
Warwick AK. Photographic standards for patients with facial
palsy and recommendations by members of the Sir Charles
Bell Society. JAMA Facial Plast Surg. 2017;19(4):275–281.
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