21 Spasmodic Dysphonia
Nupur Kapoor Nerurkar
Spasmodic dysphonia (SD) is a focal laryngeal dystonia that
is an action-induced laryngeal movement disorder. The
action that triggers the spasms in the voice is speaking itself.
Only the volitional cortically driven system is affected in SD.
Dystonias are generally classified into two groups,
generalized and focal, and may be primary (idiopathic) or
secondary to birth injury, hypoxia, infection (encephalitis/
meningitis), toxicity (drugs), or stroke. The most common
types of focal dystonia are laryngeal dystonia, blepharospasm,
torticollis, and writer’s cramp. Laryngeal dystonia, also
called SD, is a focal, primary dystonia, affecting the muscles
of the larynx.
SD patients classically have a spasmodic speech pattern
with adductor or abductor spasms. Adductor spasms give a
strained and choked quality to the voice and this is referred
to as adductor spasmodic dysphonia (ADSD).There is an
abrupt initiation and termination of voicing, resulting in
short breaks of phonation. In contrast, abductor spasms
give a breathy quality to the voice referred to as abductor
spasmodic dysphonia (ABSD). It is possible to have a
combination of both these types of SD referred to as mixed
SD. A study by Cannito and Johnson1 suggests that all patients
have a mixed SD, with one type of an activity predominating
the other. Approximately one-third of persons with SD also
have voice tremor, which makes the pitch and loudness of the
voice waver at 5 Hz during vowels and is most evident when
“/a/” as in the word “all” is produced for at least 5 seconds.2
Historically, various terminologies have been used to
describe SD including spastic dysphonia,3 spastic aphonia,4
and coordinated laryngeal spasm.5 It was Aronson who helped
establish SD as an organic disease and also described two
distinct types of SD, the adductor and the abductor varieties.6
Though SD is today thought to be a completely distinct entity
to psychogenic dysphonia, there is a worsening of patients’
symptoms noticed in the presence of strangers, in crowds,
and over the telephone. There is often an improvement of the
SD patient’s voice with whispering, singing, and shouting or
after an alcoholic beverage is consumed. This is in fact one of
the mysteries of SD, that it is task specific. Spasms only occur
during speaking and not during emotional expressions such
as laughter, crying, and shouting. This may be explained by
Kuypers’ study (1958), which indicates that only humans
have a direct corticobulbar pathway from the laryngeal
cortex to the nucleus ambiguus.7 Possibly, neural systems
involved in learning speech are likely affected in SD, while
those involved in emotional vocalization are not. To identify
the neural abnormalities in SD, differences between these
two neural systems (one for emotional vocalization and the
other for speech) must account for symptoms being absent
in the former and present in the latter.8
LARYNGOLOGY_Ch21.indd 187
Occasionally, patients with ADSD compensate by
producing a breathy voice referred to as compensatory
abductor dysphonia. Similarly, ABSD patients may try to
tightly contract the vocal folds producing compensatory
adductor dysphonia, though this is more uncommon.9,10
Historical Anecdotes
• Traube used the term spastic dysphonia in 1871 while
describing a patient with nervous hoarseness.
• Aronson in 1968 helped establish SD as an organic and not
a psychiatric condition and also in later studies described
Downloaded by: Washington University. Copyrighted material.
the two types of SD, i.e., adductor and abductor SD.
• Dr. Herbert Dedo in 1976 introduced recurrent laryngeal
nerve (RLN) sectioning as a treatment for ADSD.
• Dr. Andrew Blitzer performed the first laryngeal injection
of botulinum toxin (BTX) for SD in 1984.
• Isshiki, in 1998, reported treating a case of ADSD with
type 2 thyroplasty.
• In 1999, Dr. Berke described the denervation–
reinnervation surgery.
Etiology
The basal ganglion plays an integral role in movement. Inputs
from the cerebral cortex, especially the primary motor strip
and primary somatosensory cortex, are received in the basal
ganglia and the substantia nigra. The exact etiology of SD is as
yet unknown. However, research by Simonyan and Ludlow11 has
shown that the primary somatosensory cortex shows consistent
abnormalities in activation extent, intensity, correlation with
other brain regions, and symptom severity in SD patients and,
therefore, may be involved in the pathophysiology of SD. When
the brains of dystonic patients were studied pathologically,
although no consistent lesions were found, most frequently
mentioned lesions were in the basal ganglia.12
In ADSD, the lack of symptoms during whispering, when
the vocal folds are not vibrating, suggests that changes in
laryngeal sensory feedback either from the vocal fold mucosa
or from subglottal pressures in the trachea may play a role
in the pathophysiology of the disorder. Further research on
the role of laryngeal sensory feedback in the manipulation of
symptoms needs to be performed.8
A genetic component does seem to be involved in some
patients as 12.1% of Blitzer and Brin’s 1991 series of laryngeal
dystonia patients had a family history of dystonia.10 The DTY1
gene was first identified in one large non-Jewish family with
multiple family members presenting with dystonia and has
187
17/10/13 2:57 PM
 188 Laryngology
been responsible for childhood-onset dystonia in the Jewish
population.13
A few cases with single mutations in THAP1, a gene
involved in transcription regulation, suggest that a weak
genetic predisposition may contribute to mechanisms
causing a nonprogressive abnormality in laryngeal motor
neuron control for speech but not for vocal emotional
expression.8
Demographics
Though SD may be present in both males and females, it is
more prevalent among the female population, with some
estimates indicating the prevalence to be as high as 80%.14
It is uncommon to find SD in children, and 45 years is the
most commonage of presentation of SD. There seems to
be a progression of symptoms for 2 years following which
there is usually a plateau of symptoms, though the patient
may complaint of a progressive increase in effort required
to phonate.
SD is a relatively rare disorder; however, accurate
worldwide audited numbers are not available. Some
estimates are as low as 1 per 100,000 cases,15 although
accurate diagnosis is a significant roadblock to research.
With the increasing awareness regarding SD being created,
more cases are being accurately diagnosed and managed.
Diagnosis
Clinical
The provisional diagnosis of SD is made more often than
not within a couple of minutes of talking to the patient as
the diagnosis is based primarily on auditory-perceptual
features.
This is possible as ADSD patients have a typical choking
voice and the spasms are seen on vowels. This type affects
at least 80% of persons with SD and disrupts sentences such
as “we eat eggs every day.”16 This is because any sentence
that has a lot of vowels dramatically worsens the voice. On
asking the patient to whisper or sing, the spasms markedly
decrease. In the case of ABSD patients, a typical breathy
spasm is observed and is almost always accompanied by a
flaring of the alae nasi. These breathy bursts take place due
to prolonged voiceless consonants and while attempting to
start voice after voiceless consonants such as /s/, /f/, /h/, /p/,
/t/, and /k/.17 Disruption of sentences such as “he had half a
head of hair”18 is observed.
Flexible laryngoscopy allows an evaluation of the vocal fold
movements in normal physiological phonation. The patient
is asked to talk, sing, and whisper, and any change in the
severity of spasms is observed. In ADSD patients, the spasms
may be of only the true vocal folds or of true and false vocal
folds. In severe ADSD, a complete anteroposterior and lateral
compression of the supraglottis is observed. Stroboscopy
may be performed using the flexible laryngoscope. In ABSD
Book 1.indb 188
patients, a sudden abduction is observed corresponding
with the breathy spasm on phonation.
Stroboscopy confirms the spasms seen on flexible
laryngoscopy, and the amplitude of the mucosal wave is
seen to be decreased or occasionally absent. However,
when stroboscopy is done using a Hopkins telescope
through the mouth, the signs of SD may occasionally get
masked as this test does not allow for normal physiological
phonation.
A team approach in the diagnosis of SD is vital. Besides the
laryngologist, a speech therapist and a neurologist form the
core team in the diagnosis of SD. Occasionally, the opinion of
a gastroenterologist or a psychiatrist may be sought.
Clinical Insights
• In ADSD, voice improves with whispering, singing, or
shouting and after consuming an alcoholic beverage and
Downloaded by: Washington University. Copyrighted material.
worsens on the phone or in the presence of strangers.
• Vocal tremors may accompany spasms in almost 30% of
ADSD patients.
• In ABSD, flaring of the alae nasi is seen to accompany the
abductor spasms.
Differential Diagnosis
The differential diagnosis of SD includes muscle tension
dysphonia (MTD), vocal tremor, Parkinson disease, Wilson
disease, myasthenia gravis, motor neuron disease (MND),
pseudobulbar palsy, cerebellar disorders, laryngopharyngeal
reflux, laryngeal cancer, and functional voice disorders.
Muscle Tension Dysphonia
MTD may be occasionally mistaken as SD. The cardinal
differences between the two are that SD is task-specific
unlike MTD and in SD the strain in the voice is spasmodic
unlike MTD where the strain is continuous. MTD is often
associated with tenderness over the greater cornu of the
hyoid and in the thyrohyoid membrane. Obliteration and
tenderness in the cricothyroid membrane may also be
observed. A lidocaine block of the RLN improves the voice
of both ADSD and MTD patients. However, the primary
treatment of MTD is laryngeal massage and speech therapy.
Vocal Tremor
Vocal tremor is an involuntary, rhythmic, oscillating
movement of the vocal folds. Vocal tremors are not task-
specific and are present on talking, singing, and on a
sustained /eee/. This vocal tremor may be part of an essential
tremor known as “benign heredofamilial tremor.” This may
involve only the voice or other body parts such as the head
and neck also. Vocal tremor occurs in 10 to 20% of patients
with essential tremor. It is essential to rule out cerebellar
9/25/13 7:54 PM

disease, parkinsonism, thyrotoxicosis, and drug-induced and
psychogenic causes of the tremor. In 30% of SD patients, an
associated vocal tremor is present.
Treatment Options
Speech therapy as a modality of treatment in ADSD patients
does not meet with much success. However, it may be a viable
option in patients with very early ADSD. Speech therapy is
also of value in those patients who have developed wrong
compensatory techniques of a breathy voice in ADSD or
compensatory abductor dysphonia in ADSD.
In ABSD patients, speech therapy especially with a
biofeedback mechanism has shown promising results.
This has a very positive bearing in the treatment of ABSD
patients who typically respond to BTX poorer than their
ADSD counterparts. One of the key biofeedback techniques
used for the ABSD group is to ask the patient to stand in front
of the mirror and talk while making a concentrated effort in
controlling the flaring of the alae nasi that accompanies each
abductor spasm.
Medical treatment may benefit patients of essential
tremor or those who besides having SD have a generalized
dystonia. Patients of SD occasionally are also anxious or
depressed and may need psychiatric treatment for the same.
Role of Botulinum Toxin in the
Management of Spasmodic Dysphonia
Pharmacology of Botulinum Toxin
Clostridium botulinum is the bacteria that produce seven
serologically distinct botulinum neurotoxins that are
designated from A to G. These seven neurotoxins are
antigenically distinct but do have similar molecular weight
and a common subunit structure. These neurotoxins are
synthesized as single-chain polypeptides. However, this
single chain gets cleaved by trypsin or bacterial enzymes
to form a bichained (one heavy chain and one light chain)
molecule in which both the chains are linked by a disulfide
bond. It is in this form that the molecule becomes potent.
Clinical studies have shown that BTX does not affect the
synthesis or storage of acetylcholine. The toxin probably
modifies the release of synaptosomes from the microtubular
subsystem. Though the clinical effects of BTX are probably
due to its peripheral effects, the action of BTX on the laryngeal
muscle contractions cannot be assumed to have altered only
muscle spasms. There may be retrograde transport affecting
input to the laryngeal motor neurons.19 In addition, as the
muscle spasms are reduced not only in the laryngeal muscle
injected but also in other laryngeal muscles on the opposite
side of the larynx,20 the sensory feedback from the larynx
is altered by less mucosal compression and lower subglottal
pressures in the trachea due to reduced hyperadduction
during speech. The clinical effects are seen 24 to 72 hours
following the BTX injection.
Book 1.indb 189
Spasmodic Dysphonia 189
Preparation of Botulinum Toxin
BTX is commercially available as a powder in vacuum-sealed
vials. The quantity of active toxin is mentioned in mouse
units (mu/U) and it is essential that BTX be manufactured
in a standard fashion such that each subsequent vial is of an
equal potency to maintain both safety and efficacy. BTX(A)
is available as Botox manufactured by Allergan (Irvine,
California, United States) and also as Dysport manufactured
by Ipsen, Slough, United Kingdom. In India, BTX is available
in 50- and 100-mu vials, where 1mu is the median lethal
dose in mice. The exact lethal dose in humans is not known
but is postulated to lie near approximately 2700 U.
A 50-U vial of BTX when reconstituted with 2cc of
preservative-free saline gives a concentration of 2.5 U BTX per
0.1mL of reconstituted solution. It has been recommended
to use this reconstituted BTX within 4 hours of preparation.
BTX use is currently not recommended in pregnant or
lactating women. Patients with myasthenia gravis, Eaton-
Downloaded by: Washington University. Copyrighted material.
Lambert syndrome, and MND should be treated cautiously
with BTX as the neuromuscular junction is affected.
Aminoglycosides may potentiate the effect of BTX as they
effect neuromuscular transmission and thus are also a
contraindication to BTX use.
Prolonged use of BTX may lead to antibody formation,
which is seen more in the group of patients being treated by
BTX for torticollis as larger doses are being used. Dezfulian
et al21 have developed an enzyme-linked immunosorbent
assay that appears to be sensitive and specific in the
detection of antibody.
Procedure of Botulinum Toxin Injection
in Spasmodic Dysphonia Patients
Dr. Andrew Blitzer performed the first laryngeal injection of
BTX for SD in 1984.22
The key to a successful BTX injection for SD lies in
correct dose titration of BTX for every individual patient
and an accurate placement of the BTX. To accurately inject
the BTX in the affected muscle, most laryngologists use the
laryngeal electromyography (LEMG)system while injecting.
Some laryngologists, however, inject with the help of
flexible laryngoscopic guidance, occasionally in association
with LEMG. Dose titration is perfected once the response
to standard doses of BTX on the patient has been audited.
LEMG-controlled BTX injection in the management of SD is
considered the gold standard.
Laryngeal Electromyography
in Spasmodic Dysphonia
Electromyography (EMG) is a test measuring the
micropotential reaching the muscle fibers utilizing a needle
electrode placed in the muscle. When the needle is placed
in the laryngeal muscle, the test is referred to as LEMG.
The primary role of LEMG is in the injection of BTX in SD.
9/25/13 7:54 PM
 190 Laryngology

level was significantly greater on break than nonbreak

words in ADSD patients only for the thyroarytenoid muscle
(p < 0.001). No significant differences were found between
the ADSD and control subjects during nonbreak words for
any of the other laryngeal muscles studied. The results
demonstrated that only the thyroarytenoid, of the muscles
tested, was affected in ADSD.24

Botulinum Toxin in Adductor

Spasmodic Dysphonia
In the ADSD group of patients, BTX is injected into the
thyroarytenoid muscle bilaterally. The standard dose for the
first injection is 2.5 mu bilaterally. When a 50-mu BTX vial
is diluted with 2 mL of preservative-free saline, 0.1 mL of
BTX will contain 2.5 mu of BTX. The position of the patient
Figure 21.1 AccuGuide laryngeal electromyography system with
during this procedure may be supine with neck extension
AccuGuide cable, surface electrodes, and 27-gauge Teflon-coated
or sitting with neck extension. The neck of the patient and

Downloaded by: Washington University. Copyrighted material.

monopolar needle.
the skin over the mandible is cleaned with spirit. The EMG
surface electrodes are placed on the skin overlying the
However, the other therapeutic uses are in the injection of mandible on the side being injected (Fig. 21.2). As electrical
BTX in patients with cricopharyngeal spasm and contact activity interferes with the EMG signal, all mobile phones,
granuloma. The diagnostic role of LEMG lies in differentiating cautery, and suction machines should be switched off in the
between vocal fold paralysis and cricoarytenoid joint room. Initially, marking of the lower border of the thyroid
fixation and also in the diagnosis of various neurogenic voice and upper border of the cricoid cartilage is helpful, but this
disorders. It is essential that the diagnostic applications of is not necessary as experience in the procedure is gained.
LEMG be performed using a sophisticated, multichannel A 27 number Teflon-coated monopolar needle is used by
EMG system by the EMG technician in concert with the the author. The tip of this needle is not coated with Teflon.
neurophysician and not by the laryngologist alone. This needle is curved at an angulation of 30 degrees while
A conventional EMG machine or the AccuGuide system injecting male patients (Fig. 21.3). While injecting female
marketed by Medtronic Xomed (Jacksonville, Florida, United patients, the needle need not be angulated or may be
States) (Fig. 21.1),which is a portable, cost-effective, single- angulated by 10 to 15degrees. While injecting the right vocal
channel EMG device, may be used for the injection of BTX in fold, the needle is inserted 1 to 2 mm from the midline on
SD patients. Various needles are available commercially for the right side with the tip directed 30 degrees laterally. The
use in LEMG. A monopolar Teflon-coated 27-gauge needle patient is instructed to say “eeee” as phonation stimulates
is one of the most standard needle electrodes to be used.
In any EMG test, the parameters studied are insertional
activity, spontaneous activity at rest, response to minimal
voluntary contraction, and response to maximum voluntary
contraction. Rarely are laryngeal muscles at complete
physiological rest. With minimal voluntary contraction, 1
or 2 motor unit potentials can be recorded, which increase
with increasing strength of the contraction. Full interference
pattern is the normal response of the muscle to maximal
voluntary contraction where the entire screen gets filled up
with waves of large action potentials such that single motor
unit potentials cannot be distinguished from each other. In
the case of SD, there is a normal insertional activity. However,
there is a sudden increase seen in the muscle activity on
asking the patient to phonate. This sudden burst of action
potentials just precedes the voice spasms that are heard. If the
EMG signal is put on the same time as a voice spectrogram, a
greater-than-normal delay in the onset of voice production
is observed, particularly in patients with ADSD.23 In a study Figure 21.2 Surface electrodes applied on the skin over the surface
by Eric Nash and Christy Ludlow on laryngeal muscle activity of the mandible for right-sided injection in an adductor spasmodic
during speech breaks in ADSD, the mean muscle activity dysphonia patient.

Book 1.indb 190 9/25/13 7:54 PM


Figure 21.3 Insertion of the 27-gauge monopolar injection needle
which has been bent by 30 degrees (for a male adductor spasmodic
dysphonia patient), via the cricothyroid membrane, 1 mm to the
right of the midline, angulated 30 degrees to the right for the right
thyroarytenoid muscle injection.
the adductor group of muscles and a burst of activity is seen
on the monitor. Aspiration before injection is advisable and
the patient is instructed not to move or swallow during
the procedure. A tuberculin syringe is preloaded with the
amount of BTX to be injected. While using the AccuGuide
system, a burst of sound is heard from the EMG system
and an increasing number of bars get lit up on the liquid
crystal display. This AccuGuide system has the option of
being connected to the computer with a serial port interface
connector so that a graphical representation of the signal
may be studied on the monitor.
Botulinum Toxin in Abductor
Spasmodic Dysphonia
In the case of ABSD, BTX is injected into the posterior
cricoarytenoid (PCA)muscle, which is the only abductor of
the larynx. If a person is very sensitive to BTX, a bilateral
injection may result in stridor. Most laryngologists prefer
therefore to inject ABSD patients unilaterally. There are
two routes of approaching the PCA. One is through the
cricothyroid membrane, passing the needle through the
airway till the cricoid is hit, followed by gentle withdrawal
of the needle. The primary problem with this approach is
blocking of the luminal patency of the needle by pieces
of cartilage. The second approach, which is commonly
followed, is entering the PCA from the lateral side. If a line is
made marking the posterior edge of the thyroid cartilage and
another is made at the superior border of the cricoid cartilage,
a transection of the two lines takes place. The upper outer
quadrant of this transection is the surface marking for the
insertion of the needle. While injecting the PCA, the larynx
is rotated toward the side being injected (Fig. 21.4). When
Book 1.indb 191
Spasmodic Dysphonia 191
Figure 21.4 Larynx rotated toward side being injected in abductor
spasmodic dysphonia.
Downloaded by: Washington University. Copyrighted material.
the needle is inserted into the PCA, a signal is observed with
every inspiration. The patient is asked to sniff deeply and
the response to maximum stimulation is observed. Usually
3.75 mu (0.15 mL) of BTX is injected unilaterally for the first
injection of BTX.
Response to Injection of Botulinum
Toxin in Spasmodic Dysphonia
Following BTX injection, there is no noticeable change
observed in the patient’s voice for 24 to 48 hours.
In ADSD patients, this is followed by a breathy voice for
a variable period of approximately 1 to 6 weeks. Though
the voice is breathy, it is spasm-free. If the voice becomes
very breathy, it is possible that the patient has an occasional
aspiration while swallowing water or clear liquids. This is
due to a large phonatory gap that has temporarily developed
following BTX injection. Drinking water with a straw or
spoon usually allows the patient to overcome this swallowing
difficulty that may be seen in 30% of the patients. The special
swallow technique is also taught to these patients. In the
special swallow, the patient is asked to take a deep breath
and hold it while swallowing twice before exhalation.
Following the breathy phase, the patient’s voice becomes
stronger and remains spasm-free. This golden period may
last from 6 to 24 weeks. Finally, a return of spasms is noticed
by the patient and this indicates that it is time for reinjection
of BTX. Patients of ADSD show a 90 to 95% improvement
following BTX injection.
In ABSD patients, a 30 to 70% improvement is observed.
This is possibly due to the fact that accurate insertion of the
needle into the PCA muscle is difficult coupled with the fact
that most of these patients receive unilateral injections.
Though a tremulous voice may also improve with BTX
injection, the results are better when the patient has both
ADSD and vocal tremor.
9/25/13 7:54 PM
 192 Laryngology
Surgical Options for Spasmodic
Dysphonia Patients
Dr. Herbert Dedo introduced RLN sectioning as a treatment
for ADSD in 1976.25 The phonatory gap thus created is the
basis of loss of adductor spasms and a breathy but spasm-free
voice. However, various studies have shown a regeneration
of the cut end of the RLN with a return of spasms within
3 years in 40 to 60% of the patients.
RLN avulsion was introduced by Weed et al where the
RLN was resected in the upper mediastinum and also avulsed
from its insertion into the muscle in an attempt to prevent
the return of spasms due to RLN regeneration seen with
just sectioning. Though 78% of the patients had no return
of spasm at 3 to 7 years,26 the voice in most was too breathy,
warranting a medialization procedure. However, following
medialization, most patients developed a return in spasms.
Selective denervation with reinnervation was described
by Berke et al in 1999. Here, the adductor branch to the
thyroarytenoid muscle is bilaterally denervated and the
distal stump is reinnervated to the ansa in an attempt to
retain muscle tone and prevent nerve regeneration.27
Thyroarytenoid-Myoneurectomy
In this surgery, a variable amount of thyroarytenoid muscle
fibers are destroyed in a bid to cause weakness of the
adductory action of the vocal fold. An attempt is made to
find and avulsion-cut the thyroarytenoid branch of the RLN.
This surgery may be performed unilaterally or bilaterally
using either the external or the endoscopic approach. When
the external approach is used, the surgery is performed
under local anesthesia. A window is made in the thyroid
ala cartilage, similar to that used for a type 1 thyroplasty.
The inner perichondrium of the thyroid cartilage window
is then incised and removed. A bipolar cautery is then used
to cauterize the thyroarytenoid muscle fibers (Fig. 21.5)
Figure 21.5 Thyroarytenoid muscle fibers being coagulated in
thyroarytenoid myoneurectomy surgery.
Book 1.indb 192
till the patient’s voice loses all its spasms and becomes
slightly breathy. The advantage of doing the procedure
under local anesthesia is that the voice can be tested and a
decision regarding necessity of performing the procedure
bilaterally can be made. An attempt is always made to find
the thyroarytenoid branch of the RLN at the posteroinferior
corner of the thyroplasty window. This branch is better seen
using the ocular loop or microscope and is avulsed and cut.
This neurectomy is believed to give a more long-lasting
result postoperatively. Some surgeons like to place fat or
connective tissue in the window before closure in an attempt
to decrease the postoperative phonatory gap that is created.
Laser-Assisted Thyroarytenoid
Myoneurectomy
The thyroarytenoid muscle fibers may also be destroyed
endoscopically with the help of a CO2 laser. Under general
Downloaded by: Washington University. Copyrighted material.
anesthesia, a microlaryngeal surgery is performed where the
CO2 laser is used to destroy the superolateral thyroarytenoid
muscle fibers along the length of the vocal fold. Following
this myectomy, the thyroarytenoid branch of the RLN is
looked for, lateral to the vocal process of the arytenoid. This
process is referred to as “fishing for the nerve” and is best
accomplished by taking a 24-cm long hook which is used to
hookup the nerve from posterior to anterior.
Thyroarytenoid myoneurectomy (TAMN) gives dramatic
results on the operation table, but the long-term results are
unpredictable. Spasms have been seen to return as early
as 1 year after surgery. In the authors’ series of six TAMNs
performed (all externally), a return of spasms was seen in
three patients within 1 to 2 years postoperatively. One of these
patients has restarted BTX injections with good response.
Laryngeal Framework Surgery
Isshiki, in 1998,28 performed what is now termed as a
lateralization laryngoplasty for ADSD. This type 2 thyroplasty
involves vertically incising the thyroid cartilage at the
junction of the two alae, taking care not to enter the larynx.
The vocal folds are held apart at the anterior commissure by
4-mm silicon shims (Fig. 21.6). The voice remains variably
breathy and a return of adductor spasms may take place at
an unpredictable time interval.
Figure 21.6 Diagrammatic representation of type 2 thyroplasty.
9/25/13 7:54 PM

Research is needed to address the basic cellular and
proteomic mechanisms that produce this disorder to
provide intervention that could target the pathogenesis of
the disorder rather than only providing temporary symptom
relief.4
Pearls and Pitfalls
• Botulinum toxin with laryngeal electromyography
control is till today considered the gold standard in the
management of spasmodic dysphonia (SD).
• Muscle tension dysphonia is one of the commonest
differential diagnoses of SD.
• A team of laryngologist, speech therapist, and neurologist
is the key in the accurate diagnosis of SD.
References
1. Cannito MP, Johnson JP. Spastic dysphonia: a continuum disorder. J
Commun Disord 1981;14(3):215–233
2. Schweinfurth JM, Billante M, Courey MS. Risk factors and
demographics in patients with spasmodic dysphonia. Laryngoscope
2002;112(2):220–223
3. Traube L. Gesammelte Beitrage zur Pathologie und Physiologie.2nd
ed. Berlin: Verlag Von August Hisschwald;1871:674–678
4. Schnitzler J, Hajek M, Schnitzler A. Klinischer Atlas der Laryngologie.
Nebst Anleitung zur Diagnose und Therapie der Krankheiten
des Kehlkopfes und der Luftrohre. Wein und Leipzig: Wilhelm
Braumuller;1895
5. Gerhardt P. Bewegunggsstoerungen der stimmbaender. Nothnagels
Spezielle Pathologie und Therapie.1896;13:307
6. Aronson AE. Clinical Voice Disorders. New York, NY: Thieme
Medical Publishers;1985
7. Kuypers HG. Corticobular connexions to the pons and lower brain-
stem in man: an anatomical study. Brain 1958;81(3):364–388
8. Ludlow CL. Spasmodic dysphonia: a laryngeal control disorder
specific to speech. J Neurosci 2011;31(3):793–797
9. Blitzer A, Brin MF, Fahn S, Lovelace RE. Clinical and laboratory
characteristics of focal laryngeal dystonia: study of 110 cases.
Laryngoscope 1988;98(6 Pt 1):636–640
10. Blitzer A, Brin MF. Laryngeal dystonia: a series with botulinum
toxin therapy. Ann Otol Rhinol Laryngol 1991;100(2):85–89
11. Simonyan K, Ludlow CL. Abnormal activation of the primary
somatosensory cortex in spasmodic dysphonia: an fMRI study.
Cereb Cortex 2010;20(11):2749–2759
12. Marsden CD, Obeso JA, Zarranz JJ, Lang AE. The anatomical basis of
symptomatic hemidystonia. Brain 1985;108(Pt 2):463–483
Book 1.indb 193
Spasmodic Dysphonia 193
13. Ozelius LJ, Kramer PL, de Leon D, et al. Strong allelic association
between the torsion dystonia gene (DYT1) andloci on chromosome
9q34 in Ashkenazi Jews. Am J Hum Genet 1992;50(3):619–628
14. Adler CH, Edwards BW, Bansberg SF. Female predominance in
spasmodic dysphonia. J Neurol Neurosurg Psychiatry 1997;63(5):688
15. Nutt JG, Muenter MD, Aronson A, Kurland LT, Melton LJIII III.
Epidemiology of focal and generalized dystonia in Rochester,
Minnesota. Mov Disord 1988;3(3):188–194
16. Erickson ML. Effects of voicing and syntactic complexity on sign
expression in adductor spasmodic dysphonia. Am J Speech Lang
Pathol 2003;12(4):416–424
17. Rodriquez AA, Ford CN, Bless DM, Harmon RL. Electromyographic
assessment of spasmodic dysphonia patients prior to botulinum
toxin injection. Electromyogr Clin Neurophysiol 1994;34(7):
403–407
18. Rontal M, Rontal E, Rolnick M, Merson R, Silverman B, Truong DD.
A method for the treatment of abductor spasmodic dysphonia with
botulinum toxin injections: a preliminary report. Laryngoscope
1991;101(8):911–914
19. Moreno-López B, Pastor AM, de la Cruz RR, Delgado-García JM.
Downloaded by: Washington University. Copyrighted material.
Dose-dependent, central effects of botulinum neurotoxin type
A: a pilot study in the alert behaving cat. Neurology 1997;48(2):
456–464
20. Bielamowicz S, Ludlow CL. Effects of botulinum toxin on
pathophysiology in spasmodic dysphonia. Ann Otol Rhinol Laryngol
2000;109(2):194–203
21. Dezfulian M, Hatheway CL, Yolken RH, Bartlett JG. Enzyme-linked
immunosorbent assay for detection of Clostridium botulinum type
A and type B toxins in stool samples of infants with botulism. J Clin
Microbiol 1984;20(3):379–383
22. Blitzer A, Brin MF, Stewart CF. Botulinum toxin management of
spasmodic dysphonia (laryngeal dystonia): a 12-year experience in
more than 900 patients. Laryngoscope 1998;108(10):1435–1441
23. Schaefer SD. Neuropathology of spasmodic dysphonia.
Laryngoscope 1983;93(9):1183–1204
24. Nash EA, Ludlow CL. Laryngeal muscle activity during speech breaks
in adductor spasmodic dysphonia. Laryngoscope 1996;106(4):
484–489
25. Dedo HH. Recurrent laryngeal nerve section for spastic dysphonia.
Ann Otol Rhinol Laryngol 1976;85(4 Pt 1):451–459
26. Weed DT, Jewett BS, Rainey C, et al. Long-term follow-up of
recurrent laryngeal nerve avulsion for the treatment of spastic
dysphonia. Ann Otol Rhinol Laryngol 1996;105(8):592–601
27. Berke GS, Blackwell KE, Gerratt BR, Verneil A, Jackson KS, Sercarz
JA. Selective laryngeal adductor denervation-reinnervation: a new
surgical treatment for adductor spasmodic dysphonia. Ann Otol
Rhinol Laryngol 1999;108(3):227–231
28. Isshiki N, Tsuji DH, Yamamoto Y, Iizuka Y. Midline lateralization
thyroplasty for adductor spasmodic dysphonia. Ann Otol Rhinol
Laryngol 2000;109(2):187–193
9/25/13 7:54 PM