Spasmodic dysphonia - VOICE DISORDER

1. SPASMODIC
DYSPHONIA
BY-
DR.PRUTHVI RAJ
S
JUNIOR
RESIDENT
ENT - HNS

2. CONTENTS
• DYSTONIA
• SPASMODIC DYSPHONIA DEFINITION
• HISTORY & BACKGROUND
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOPHYSIOLOGY
• TYPES
• DIAGNOSIS
• TREATMENT
• FUTURES & CONTROVERSIES

3. DYSTONIA
• Hyper functional disorder .
• Dystonia is a syndrome dominated by sustained muscle
contractions of skeletal muscles that frequently causes
twisting and repetitive movements or abnormal postures
that may be sustained or intermittent.
• Because the condition is rare and the movements and
resulting postures are often unusual, dystonia is among the
most commonly misdiagnosed neurologic conditions.

6. SPASMODIC DYSPHONIA
• A form of focal adult - onset dystonia ; hyper functional
disorder.
• A neurological disorder involving voice muscles of the larynx
characterised by intermittent phonatory breaks secondary
to laryngeal muscle spasm .
• Spasmodic dysphonia (SD) is a chronic voice disorder of
unknown origin that is characterized by excessive or
inappropriate contraction of laryngeal muscles during
speech.

7. HISTORY & BACKGROUND
• TRAUBE , who believed the condition o be a form of nervous hoarseness ,
first described spasmodic dysphonia (SD) in 1871.
• DEDO first introduced recurrent laryngeal nerve section for treatment of
SD
• In 1980, ISSHIKI et al introduced a laryngeal framework surgery
(laryngoplasty) for patients with adductor SD . This technique permits
adjustment of position & tension in vocal folds .
• BLITZER et al applied botulinum toxin injection technique in 1987. This
has become treatment of choice for SD.
• Recent surgical advances include recurrent laryngeal nerve denervation &
reinnervation , thyroarytenoid and lateral cricoarytenoid myectomy etc.

8. EPIDEMIOLOGY
• Spasmodic dysphonia (SD) is not a rare disorder but rather frequently
goes undiagnosed.
• Incidence roughly one to four people per 100,000 people.
• Most studies show that this disorder affects females more commonly than
males, with a female-to-male ratio as high as 4:1.
• Onset is characteristically between 30 and 50 years of age, and 60 to 80% of
those affected are women.
• However, the condition may occur as early as the second decade of life in
rare exceptions and as late as the ninth decade of life.

9. ETIOLOGY
• Idiopathic
• Psychogenic
• Neurogenic
• SD caused by abnormal functioning of basal ganglia which consists of
cluster of nerve cells .
• It may also occur with other dystonias involving muscles of face , arms,
legs, eyes, body, jaws , lips, tongue , neck .
• Mutation in THAP1 gene is associated with whole body dystonia that
begins in childhood and appears with SD .
• Onset often follows an URTI , laryngeal injury or inflammation, a period of
excessive voice use, or occupational or emotional stress .

10. PATHOPHYSIOLOGY

12. • When we speak, air from the lungs is pushed between two
elastic structures called vocal folds or vocal cords with sufficient
pressure to cause them to vibrate, producing voice .
• In spasmodic dysphonia, the muscles inside the vocal folds
experience sudden involuntary movements called spasms which
interfere with the ability of the folds to vibrate and produce
voice.

13. PATHOPHYSIOLOGY
• SD is a focal dystonia that affects laryngeal muscle control during speech. Dystonia refers to
a syndrome of sustained muscle contractions.
• Dystonic movements are aggravated or become manifest during voluntary movement and
worsen with fatigue or physical and emotional stress.
• The preponderance of evidence suggests that idiopathic dystonias are due to an abnormality
of neurotransmitters in the basal ganglia (putamen, head of caudate, and upper brainstem).
Zweig et al suggested that the putamen and the striatopallidothalamocortical circuit are
disrupted in patients with focal dystonias.
• Evidence from both diffusion tensing imaging and neuropathological data show specific white
matter changes along the corticobulbar and corticospinal tracts and in the brain regions
contributing to them. Specifically, the genu of the internal capsule was found to have
decreased quality and density of axonal tracts.

14. • Postmortem histopathology also confirmed reduced axonal course and myelin content in
the right genu of the internal capsule. An increase in microglial activation in these
regions suggests a slow demyelination process.
• The changes in the Corticobulbar/corticospinal tracts suggest deficiency in connection
between the cortical and subcortical regions, which are essential for voluntary voice
production. Diffusion tensor imaging found changes in the common areas sited for focal
dystonias namely the basal ganglia, cerebellum, and thalamus.
• Similarly, Ali et al used H2
15 O PET to examine speech-related changes in regional
cerebral blood flow to assess patients both before and after botulinum toxin
injection. Their data demonstrate definitive patterns of cerebral activity in patients with
ADSD and neurologically normal controls. Their results suggest that the
pathophysiology of spasmodic dysphonia (SD) is related to sensory cortical areas as well
as motor areas.

15. • Using PET imaging, activity in the postcentral gyrus, inferior parietal lobule, and middle
temporal gyrus are found to be significantly reduced in patients with ADSD. Afferent
(proprioceptive/tactile) feedback mechanisms that are controlled in these sensory areas
are known to play a crucial role in coordinated oral-laryngeal movements. Hypoactivity
suggests that this sensory feedback is not being processed appropriately in ADSD.
Without sensory feedback, intracortical inhibitory mechanisms are deficient.
• Interestingly, botulinum toxin therapy resulted in a reversal of sensory hypoactivity 3-4
weeks after injection. The authors suggest that this process of renewed sensory feedback
can lead to reorganization in both sensory and motor areas. Motor regions as well as the
lateral premotor system (responsible for organizing and executing movements in
response to afferent signals) are found to have an increase in cerebral blood flow. This
suggests more efficient processing of sensory signals and possibly a return of normal
inhibition. This may translate to clinical improvement in speech and voice after
botulinum toxin injection.

16. TYPES
• ABDUCTOR TYPE
• ADDUCTOR TYPE
• MIXED TYPE
• OTHER SUBTYPES
MAJOR
TYPES

17. ADDUCTOR SD
• 85% Of the cases .
• Characterized by a strained /strangled quality to the
voice which cuts out at the onset of phonation.

18. Spasms that cause hyper adduction of vocal cords .
Intermittent rapid shortening and squeezing of vocal cords , which results in a
quick glottic closure that shuts the glottis and interrupts airflow through the
glottis .
Strained or strangled phonation with intermittent voice offsets on voicing of vowels.
PATHOLOGY

20. CLINICAL FEATURES
• Strained , strangled voice with abrupt breaks in phonation in the
middle of the vowels .
• Symptoms are worse when they are under emotional stress, when
they talk on the telephone, or when they speak publically .
• Only speech is affected ; singing is less affected and emotional
expression (laughter and cry) and shout are unaffected ; this is
often not the case with muscle tension dysphonia and helps to
clinically distinguish between the 2 disorders .

21. ABDUCTOR SD
•Less common , 15% of the cases .
•Characterised by breathy voice breaks or a
whispering voice.

22. PATHOLOGY
Spasms that cause vocal cords to open .
Vocal folds cannot vibrate completely as they are too far .
There is air escape during speech .
Weak , breathy , effortful voice with abrupt breaks .

24. CLINICAL FEATURES
• Intermittent or sustained opening of the larynx during speech
that leads to breathy voice breaks or a whispering voice .
• Prolonged vocal fold opening after voiceless sounds extending
into vowels (such as s, h, f, t, k) .
• Spasms are absent during laughing, crying , shouting .

25. MIXED SD
• Very rare.
• Combination of both abductor and adductor SD.

26. DIAGNOSIS & ASSESSMENT
• Best accomplished by a voice team including an otolaryngologist , a speech pathologist ,
a neurologist and a psychiatrist .
• A Extensive history including psychosocial history and complete examination including
IDL, nervous system .
OTOLARYNGOLOGIST NEUROLOGIST PSYCHIATRIST
vocal fold nodules, polyps,
carcinoma, cysts, contact
ulcers,
inflammation (laryngitis),
vocal fold paresis, or
paralysis etc.
amyotrophic lateral
sclerosis, Parkinson
disease, or supranuclear
palsy etc.
Psychogenic
dysphonia etc.

27. SPEECH TESTING
• Voice symptoms should be compared during following three tasks :
1) Prolonged vowel phonation usually manifests tremor if it is present. Prolonged vowel
production is affected only in the more severe forms of adductor and abductor SD.
2) Production of sentences in which most sounds are voiced and contact glottal stop at word
boundaries, for example, “We mow our lawn all year” and “We eat eels every day,” are usually
most difficult and demonstrate frequent breaks or voice arrest in adductor spasmodic
dysphonia.
3) Production of sentences with voiceless consonants (s, t, p, k, h), for example, “She speaks
pleasingly,” “Keep Tom at the party,” “When he comes home we’ll feed him,” are usually most
difficult in abductor spasmodic dysphonia. Sentences with predominantly voiced sounds are
much easier to produce and smoother for these patients.

28. FIBREOPTIC LARYNGOSCOPY
• Both speech and non speech tasks must be sampled to identify
(1) movement control abnormalities during vocal fold abduction (opening)
and adduction (closing) in speech .
(2) movement during non speech items such as respiration, sniffing, throat
clearing, whistling, and singing.
• Fiberoptic laryngoscopy is useful in evaluating patients with dysphonia
associated with neurological disorders for vocal fold movement during
speaking.

29. STROBOSCOPY
• Less helpful because patients with tremor or spasms do not have regular
phonatory cycles that can be tracked from the contact microphone or
electroglottographic signal.
• Further, in patients with other functional voice disorders, such as
muscular tension dysphonia, the severe signal aperiodicity similarly
interferes with tracking of the stroboscopy light source, rendering
stroboscopic interpretation meaningless.
• The emerging use of kymography and eventually high-speed video will be
particularly useful for examining vocal fold vibration in such patients, as
these techniques do not rely on signal periodicity .

30. ELECTROMYOGRAPHY
• The laryngeal muscles should be examined to determine which muscles contain spasms
concurrent with a patient’s voice symptoms during speech.
• In adductor SD, the thyroarytenoid is the most often affected muscle.
• In abductor SD, spasms can be seen either in the cricothyroid or the posterior
cricoarytenoid muscles as well as asymmetries in thyroarytenoid muscle activation during
speech.
• In others, no spastic activity is identifiable and the thyroarytenoid muscle is inactive
during vowels, that is, a “negative dystonia” .
• In vocal tremor, a variety of muscles can be involved. Most often the thyroarytenoid is
affected, but other muscles including the strap muscles can be affected including the
thyrohyoid, the sternothyroid, and in some patients with abductor tremor, either the
cricothyroid or posterior cricoarytenoid, or both.

31. • PRINCIPLE : By using a concentric EMG electrode connected to an amplifier with a dual
channel storage oscilloscope, one channel for the EMG and another for the speech
waveform, at a slow sweep speed, quick identification can be made of the muscles having
spasms during voice breaks.
• For the thyroarytenoid and lateral cricoarytenoid muscles, items to be examined for
spasmodic bursts concurrent with voice breaks include prolonged “ee,” repeated “ee,” and
all voiced sentences such as “We mow our lawn all year.”
• When examining abductor SD, while recording from the cricothyroid or posterior
cricoarytenoid, speech should include “see-see-see,” “pea-pea-pea,” “hehe-he,” “Kathy took a
potato,” and “Keep Tom at the party.”
• Muscles with bursts of activity before and during voice breaks can be considered for
injection with botulinum toxin injection.

32. OTHERS
• Radiological studies ( CT with gadolinium or MRI)
• Electroglottograghy ( EGG )
• Voice range profile ( Phonetogram )
• Perceptual analysis (GRBAS Scale)
• Acoustics analysis (status of vocal function)
• Aerodynamic analysis (measurement of airflow & air pressure and their
relationships during phonation)
• Subjective evaluation by patient ( to determine deviance of voive quality &
severity of disability / handicap in daily & social life )

33. TREATMENT
• Medical therapy
• Voice therapy & Vocal hygiene .
• Botulinum toxin injection .
• Surgical treatment .

34. MEDICAL THERAPY
• Symptoms of SD often worsen during stress ; so there can be relative
improvement with benzodiazepenes , alcohol etc.
• Anticholinergic agents
• Dopamine antagonists
• Even when success is noticed with these agents , their use is often precluded
due to the well documented peripheral & CNS side effects .

35. VOICE THERAPY
• Voice therapy can assist mildly affected patients but may not
have long-lasting effects.
• When uncertain of the diagnosis of a patient’s voice disorder, a
trial of voice therapy is recommended. Usually within three
sessions, a speech pathologist experienced in voice therapy will
report whether or not voice therapy might be beneficial for a
patient.
• Voice therapy may also be helpful after botulinum toxin injection
by prolonging the benefit period.

36. • The aims of voice therapy sessions are:
1) to help the patient find a better voice quality which is stable,
reliable and less effortful to produce.
2) to make better use of vocal resonance and tonal quality.
3) to increase the flexibility of the voice by improving the pitch
range and loudness without undue effort.
4) to increase the stamina of the voice.

37. • Various techniques are used including one or more of the following:
1) vocal exercises with the aim of targetting and strengthening specific
muscle groups and improving glottal closure and efficiency.
2) increasing awareness of and reducing excessive tension in the muscles
around the larynx, neck and shoulders.
3) advice on posture and improving breathing during speech.
4) laryngeal massage.
5) general relaxation exercises and stress management.
6) psychological counselling.
7) remedial singing lessons.

38. • At present, voice therapy is recommended for the following types of patients
with spasmodic dysphonia (SD):
 Patients with mild, intermittent symptoms of adductor spasmodic dysphonia
(SD).
 Patients with a psychogenic dysphonia, psychogenic overlay, or symptom
exaggeration.
 Patients who request assistance with increasing benefit duration following
botulinum toxin injection.
 Patients with abductor spasmodic dysphonia (SD) who are receiving limited
benefit from botulinum toxin injections.
 Patients who develop significant muscle tension dysphonia while trying to
compensate for muscle spasms.

39. VOICE THERAPY PROTOCOL
• 6-8 sessions over 8-10 weeks.
• The key element in this treatment is the reduction of excessive pressure; the maintenance of a
non spasmodic phonation gives patients a sense of control over their treatment.
• Focus on reducing the effort associated with voice onset by using gliding phonation with
fricatives or vowels.
• Includes replacing short shallow inspirations with slow smooth inspirations, first without
phonation and then with phonation. Conscious awareness of lower thoracic breath control and
the rhythm of breathing are initiated. Patients are taught to use only the amount of breath
needed for a particular phrase. Emphasis is placed on coordinating the lower thoracic
exhalation phase of breathing with the onset of phonation.
• Phrasing of 3-6 syllables is emphasized. Voiceless phonemes are added to the voiced phonemes
to develop awareness in the patient that voicing is now produced more easily than in the past.
Exercises to improve resonance are added after treatment for airflow control and breathing is
established.

40. VOCAL HYGIENE
• The areas covered may include:
1) an explanation of how the voice works.
2) the links between lifestyle, phonatory and nonphonatory vocal activities and stress on voice
disorders.
3) the potentially traumatic effects to the vocal folds of 'vocally abusive behaviours', such as
talking or singing too loudly, talking too fast, shouting, throat clearing and harsh coughing.
4) communicating effectively without raising or straining the voice, for example using a whistle
in the school playground or using amplification devices where practical and conserving the
voice where possible or in extreme situations discussing the possibility of changing jobs.
5) the importance of adequate hydration for vocal fold function, i.e. by drinking water, use of
steam inhalations and avoiding excessive amounts of drinks containing caffeine, i.e. coffee, tea
and colas.
6) smoking cessation, reducing alcohol and social drug consumption (particularly spirits,
cannabis and cocaine) and avoiding exposure to fumes, dust and dry air.
7) diet and reflux reduction, for example avoiding eating late at night, large or fatty meals.

41. BOTULINUM TOXIN INJECTION
• This approach was developed in 1987.
• Clostridium botulinum ( Gram + , rod shaped, anaerobic, spore forming ,
motile bacterium)
• Toxins – A, B, C1, C2, D, E, F, and G.
• MOA : 1) It causes a chemical denervation of muscle fibers by blocking the
release of acetylcholine at neuromuscular junctions leading to flaccid
paralysis.
2) The toxin is found to not only affect extrafusal muscle fibers but also
the afferent muscle spindle output. Muscle activity is known to be regulated
by afferent feedback, so a decrease in muscle spindle output can lead to
decreased muscle effectiveness.

43. BOTULINUM TYPE A TOXIN

44. • Typically, the commercially available botulinum toxin is reconstituted with
preservative - free 0.9% sodium chloride before injection.
• Traditionally, this reconstituted solution is injected within 4 hours. A recent
study, however, shows no significant difference in efficacy or side effects
between this freshly reconstituted BOTOX® and reconstituted BOTOX®,
which is stored frozen for 4-8 weeks. This cost-effective measure allows the
otolaryngologist a longer period of use without sacrificing quality.
• The patient is placed in either a nearly supine position with a pillow
underneath the upper back and with the neck extended or a seated position in
an examination chair with the neck extended. The thyroid and cricoid
cartilages are palpated, and the midline of the Cricothyroid membrane is
identified.

45. DOSAGE & INJECTION
• Injection is given with a tuberculin syringe with a 27 G monopolar hollow
polytetrafluoroethylene (Teflon) – coated EMG needle connected to an EMG
recorder.
• The effective treatment dose is variable for each patient and for each muscle
injected; therefore injections are individualized.
• The dose range for adductor spasmodic dysphonia is 0.05 to 20 units of
Botox, with an average dosage of less than 1 unit per vocal fold.
• In general, a starting dose of 1.0 units in 0.1 mL of saline is used for
bilateral thyroarytenoid injections.
• Subsequent doses are varied according to clinical response and adverse
effects.

46. INJECTIONS
UNILATERAL BILATERAL
large doses of unilateral injections producing
unilateral vocal fold paresis.
small bilateral injections which do not alter
vocal fold mobility.
DA : large dosage of toxin must be
administered, and immobility of the injected
fold often results.
A : much smaller dosages of botulinum toxin
can be used, reducing the cost, and effective
symptom control can be obtained without any
observable change in range of motion.
DA : injections and needle insertions are
performed on both sides of the larynx. With
repeated injections over many years, damage
might result to both sides of the larynx.

47. TECHNIQUES
• Percutaneous method .
• Indirect laryngoscopic peroral method .
• Transcartilaginous method .
• Injection using a flexible catheter through a channeled
laryngoscope .

48. DOSAGE
INJECTION
TECHNIQUE EMG GUIDED PERORAL
TRANS -
CARTILAGINOU
S
ENDOSCOPIC
UNILATERAL
(Units)
15 2.5 6
BILATERAL
(Units per side)
2.5 2.5 2 2
Usual Dosages Used for Unilateral and Bilateral Injection of the
Thyroarytenoid Muscle in Adductor Spasmodic Dysphonia

49. PROCEDURE
• In adductor spasmodic dysphonia (SD), the needle is passed through the skin that lies over
the superior edge of the cricoid, just lateral to midline. The needle is then advanced through
the Cricothyroid membrane and superiorly and laterally directed into the right or left vocal
fold to reach the Thyroarytenoid muscle.

50. PROCEDURE
• By entering slightly off the midline, the injection can be
accomplished totally submucosally, without entering the
airway.
• The oscilloscope and auditory output of the EMG apparatus
are monitored to detect muscle activity.
• When crisp action potentials are obtained with phonation,
needle position in a Thyroarytenoid muscle is confirmed.
Once the position is confirmed, the toxin is slowly injected.

53. PROCEDURE
• Injections of abductor SD are given to posterior cricoarytenoid muscle (PCA) .
• The specialist reaches the muscle by manually rotating the larynx, placing the
EMG needle behind the posterior edge of the thyroid lamina at the junction of
the lower third and upper two thirds of the cartilage, and advancing the
needle to the cricoid cartilage and then slightly moved out (under EMG
guidance) to arrive at the PCA muscle.
• Alternatively, a transcricoid injection can be made.
• When the patient is instructed to sniff, which maximally uses the PCA
muscle (abduction of vocal cords), a burst of activity is seen on the EMG, and
the toxin is administered.

56. EVALUATION OF INJECTION
• After an injection, the patient typically reports improvement in voice within 24
hours; this is followed by a breathy, hypophonic period that lasts 1 to 2 weeks
(45%), occasionally causing hyperventilation and dizziness when the patient tries
to speak.
• In patients with adductor spasmodic dysphonia, botulinum toxin injection has been
demonstrated to improve speaking to 60% to 100% of normal function, with a mean
of 90%; the duration of effect was between 3 and 4 months.
• Adverse effects include a mild breathy dysphonia for less than 2 weeks (45%), mild
choking on fluids for the first several days (22%), hyperventilation and dizziness
when trying to speak while hypophonic, a sore throat or hemoptysis, and itching
(without rash)( may occur in the first 1 to 2 days after injection).

57. EVALUATION OF INJECTION
• In patients with abductor laryngeal dystonia, injection of botulinum
toxin into the posterior cricoarytenoid (PCA) muscle produces marked
improvement, with a return to mean maximal functional performance
of 70% of the normal.
• Adverse effects includes mild dysphagia without aspiration & mild
stridor on exertion.

58. COMPLICATIONS
• Dysphagia is related to the toxin's partial diffusion into the inferior
constrictor muscle when the target muscle is the PCA muscle. This adverse
effect is transient and usually resolves in 1 week.
• Breathy hypophonia is usually a transient adverse effect of a botulinum toxin
injection into the TA muscle and usually resolves within 1-2 weeks.
• Clinically significant aspiration is a very rare complication that is related to
the dose of botulinum toxin injected into the TA muscle. Aspiration is
transient and resolves in 1-2 weeks.
• Stridor is more serious in patients with abductor spasmodic dysphonia (SD)
because of PCA paralysis. Extent of paralysis is related to the botulinum toxin
dose.

59. EVALUATION OF INJECTION
• Only about two-thirds of persons with abductor SD are benefited and to a
lesser degree than those with adductor SD following TA muscle injections.
• The effects of vocal tremor on voice production can also be reduced by
botulinum toxin injection; however, the outcome is less predictable and not all
persons with vocal tremor are benefited.
• In those patients with tremor affecting only the vocal folds and involving just
the TA muscles, this treatment can be as effective as in adductor spasmodic
dysphonia. However, many patients with this disorder have involvement of the
strap muscles and have limited benefit even when these additional muscles
are injected. Great care should be exercised with strap muscle injections due to
signifi cant concerns over aspiration symptoms.

60. TREAMENT REGIMEN
• Because of differing sensitivity to botulinum toxin, the injection protocol and
dosage must be established for every patient on an individual basis.
• Each patient is started with a standard dose. This is then increased or
decreased based on the patient's side effects, symptom response, and
individual needs.

61. PRECAUTIONS & CONTRANDICATIONS
• Avoided in pregnant / lactating patients (paucity of data ).
• Caution is warranted for the management of patients with conditions such as
myasthenia gravis, Lambert- Eaton syndrome, and motor neuron disease,
particularly when large doses are required, such as in the management of
cervical dystonia.
• However, the amount of toxin that enters the circulation after injection is
thought to be minute, and this theoretic concern should be balanced against
the severity of the hyperkinetic symptoms.

62. ADVANTAGES OVER SURGERY
Regardless of technique, botulinum toxin injections have several
advantages over surgical therapy in the management of intractable
disease.
• The patient is awake for the procedure.
• Complications that would be involved with anesthesia are avoided.
• Graded degrees of weakening can be achieved by varying the dosage.
• Most adverse effects are transient and are caused by an extension of
the pharmacology of the toxin.

63. DISADVANTAGES
• Necessity of repeated injections.
• Continuos follow up to assess .
• With repeated injections over many years, damage might result to both sides of
the larynx. A few patients lose symptom control over a period of many years
with continued injections, although the mechanisms for the loss of benefit is
not clear. Some of these patients may be managed by switching injection sides
and beginning treatment in a previously noninjected muscle resulting in the
return of symptom control.
• muscle scarring and atrophy.

64. OTHER USES OF TOXIN
• Muscle spasticity disorders
• Cosmetics – wrinkles
• Blepharospasm
• Excessive sweating , neuropathic pain
• Cervical dystonia etc.

65. RECURRENT LARYNGEAL NERVE
SECTION
• Dedo first described unilateral removal of a short segment of the RLN below
the thyroid isthmus for the treatment of adductor SD in 1976.
• The procedure resulted in an initial dramatic reduction or elimination of voice
spasms, but symptoms may recur in up to 64% of cases.
• Recurrence of symptoms has been attributed to reinnervation of the operated
side based on electromyographic and histological studies.

66. • Those patients failing surgery may still respond to botulinum toxin
injections.
• Due to the high rate of symptom recurrence, the permanent
alteration in laryngeal function, and the requirements for subsequent
medialization surgery in some patients with excessive breathiness,
RLN section is less preferred to botulinum toxin injections at the
present time.

67. RECURRENT LARYNGEAL NERVE
AVULSION
• Netterville and his colleagues proposed a more extensive removal of the
recurrent nerve in an effort to reduce the risk of reinnervation into the distal
stump of the sectioned recurrent laryngeal nerve.
• After mobilization of the ipsilateral thyroid lobe, all branches of the RLN are
identified, traced, and avulsed from their muscular insertions deep to the
cricopharyngeus muscle.
• The total length of RLN removed averages 9 cm, in contrast to an average of 2
cm reported in previous RLN section studies.
• Long-term follow-up, 3 to 7 years, on 18 patients following recurrent
laryngeal nerve avulsion revealed that 16 patients (89%) were free of SD
symptoms at 3 years.

68. • Two of these patients, however, later developed recurrent spasms
following medialization laryngoplasty for treatment of a breathy voice.
• Thus, an overall success rate of 78% (14/18) was reported for this
series which compares favorably to long-term recurrence rates for the
more limited RLN section.
• Weed and colleagues recommend that RLN avulsion be reserved for
patients who do not benefit from or do not tolerate botulinum toxin
injections and for patients who have failed prior RLN section.

69. SELECTIVE LARYNGEAL ADDUCTOR
DENERVATION & REINNERVATION
• Berke and colleagues published preliminary results with selective bilateral
dennervation of the laryngeal adductor muscles in an attempt to achieve a
permanent bilateral adductor weakness that mimics the transient effects of
botulinum toxin injection.
• This procedure involves bilateral section of the adductor RLN branches to
the thyroarytenoid and lateral cricoarytenoid muscles while preserving the
natural innervation of the posterior cricoarytenoid muscle.
• In addition, the distal thyroarytenoid branches are reinnervated using
branches of the ansa cervicalis nerve.
• The aim of this directed reinnervation is to prevent unwanted reinnervation
by RLN efferents and to preserve adductor muscle tone.

70. • The study presented 1- to 5-year follow-up on 21 patients with adductor SD
who underwent the procedure.
• In general, symptoms and overall severity of SD improved from moderate to
severe ratings preoperatively to mild to absent ratings postoperatively.
• All patients experienced severe vocal fold bowing and breathiness in the early
postoperative period that improved after 3 to 6 months.
• Aspiration of greater than 2 weeks duration was noted in 2 patients, one of
whom required hospitalization for aspiration pneumonia. Additional
treatments (botulinum toxin, voice therapy, collagen injection, thyroarytenoid
myotomy) were also performed in several patients to enhance the
postoperative voice result.

71. • These authors have subsequently published an analysis of the long-
term results of these procedures.
• The average follow-up was 49 months.
• A total of 83 patients filled out pre- and postoperative Voice Handicap
Index (VHI) scores with an improvement from 36 to 13.
• Eighty-three percent of the subjects showed improvement in the VHI.
• Perception evaluation of voice samples after surgery revealed voice
breaks in 26% of the subjects.

72. OTHER SURGERIES
• Isshiki et al proposed type 2 thyroplasty techniques for adductor spasmodic
dysphonia (SD). These techniques were successful in 5 of 6 patients. The
concept of these techniques is to change the thyroid cartilage shape to relax
and slightly lateralize the vocal folds.
• The advantages of the surgery include
(1) the ability to adjust optimal glottal closure for phonation.
(2) unlikely recurrence.
(3) no damage to the physiological function of phonation.
(4) intraoperative reversibility if ineffective.
(5) the ability to perform readjustments when needed.

73. • A retrospective study by Nomoto et al indicated that bilateral thyroarytenoid
muscle myectomy (TAM) and type 2 thyroplasty are each effective in
treating adductor spasmodic dysphonia, with both resulting in comparable
improvements on the voice handicap index.
• The study, in which 30 patients underwent TAM and 35 were treated with
type 2 thyroplasty, also found that TAM was better than type 2 thyroplasty
in improving strangulation, interruption, and tremor but that it tended to
worsen breathiness.
OTHER SURGERIES

74. • A final surgical option for adductor spasmodic dysphonia is a bilateral TA and
lateral cricoarytenoid myectomy staged a minimum of 6 months apart.
• This weakens the vocal folds bilaterally to prevent spasms.
• It is performed under local anesthesia and is titrated to breathiness to
eliminate the risk of overresection.
• Short-term results in 5 patients revealed improved fluency in all patients.
• Long-term studies are needed.
• Recurrence of symptoms or dysfunction due to muscular fibrosis or scarring.
• These surgical techniques are in their infancy and require wider evaluation
and long-term follow-up data before being considered as a standard treatment
for spasmodic dysphonia (SD).

75. FUTURE & CONTROVERSIES
• Surgical therapy is still controversial because the side effects can be severe, and
wide evaluation with long-term follow-up data is not available.
• To date, botulinum toxin injection is the standard therapy for spasmodic dysphonia
(SD). Unfortunately, this is just a treatment at the end organ and is not a cure.
• Current research, especially gene research, is progressing in the elucidation of the
cause of focal dystonia. Advances in the understanding of genetically determined
early-onset primary torsion dystonia are offering insight into the pathophysiology of
dystonia. An amino acid deletion in the DYT1 gene has been found to be responsible
for familial primary torsion dystonia. This defect results in an abnormality in the
protein torsin A, which is widely distributed in the CNS.

76. REFERENCES
• Scott brown’s otorhinolaryngology, head & neck surgery (7TH edition).
• Cummings otolaryngology & head & neck surgery (6th edition).
• Ballenger's Otorhinolaryngology Head and Neck Surgery (17th edition )
• https://www.nidcd.nih.gov/health/spasmodic-dysphonia
• http://emedicine.medscape.com/article/864079-overview

77. THANK YOU