Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4506_Библиотеки_им_академика_М_И_Перельмана.pdf
126 The Voice and Voice Therapy
FIGU RE 53. The vagus nerve.
CHAPTER 5 Neurogenic Voice Disorders 127
functions of the SLN and the RLN. The vagus nerve originates in the nucleus ambiguus in the
medulla, from which it emerges laterally and courses its way, continually branching along the
way, with particular branches terminating at the various innervation sites from the pharynx to the
abdominal viscera (Ardito et al., 2004). Affecting voice are the sensory components of the vagus,
with sensory innervation of the pharynx and larynx. Motor aspects affecting voice include innervation of the velum; the base of the tongue; superior, middle, and inferior pharyngeal constrictors;
larynx; and autonomic ganglia of the thorax (affecting the respiratory aspects of phonation).
As the vagus nerve leaves the nucleus ambiguus and exits laterally from the superior medulla
and descends, it soon begins a series of branches (see Figure 5‒3). The first and most superior nerve
branch off the vagus is the pharyngeal branch, which contains both sensory and motor branches
that supply the mucous membrane and selected muscles of the pharynx and soft palate (see
Chapter 10). The second branch is the SLN, which transmits sensory information from the base
of the tongue and the mucous membrane of the supraglottis; it also transmits motor innervation
to part of the lower pharyngeal constrictor and to the cricothyroid muscles. The third branch is the
RLN, which transmits sensory information from the subglottis; it also transmits motor innervation to all the intrinsic laryngeal muscles except the cricothyroid. In the following list, we review
the anatomy and physiology of the SLN and the RLN (see also Chapter 2), and we summarize
the major laryngeal and voice findings with paresis or paralysis of these nerves.
Superior Laryngeal Nerve. The SLN branches from the vagus nerve just inferior to the
nodose ganglion, which contains the sensory cell bodies of the SLN. As can be seen in Figure 5‒3,
the SLN travels inferiorly along the side of the pharynx, medial to the carotid artery, and splits into
two branches about the level of the hyoid bone. The internal division of the SLN penetrates the
thyrohyoid membrane with the superior laryngeal artery and supplies sensory innervation to the
larynx. The external division of the SLN lies close to the superior thyroid artery, although its exact
relation to the artery is variable. The SLN is vital to the tensing–relaxing of the true vocal folds, as
it penetrates the cricothyroid membrane and provides motor innervation to the cricothyroid (CT)
muscle (see Chapter 2). Inability to elevate vocal pitch is the primary symptom of CT disease or
trauma; in the case of unilateral CT paralysis, there may also be extreme hoarseness and occasional
diplophonia (because of the disparate tension between the two vocal folds).
Recurrent Laryngeal Nerve. The nuclei of the RLN axons lie within the nucleus ambiguus
in the medulla of the brainstem. As can be seen in Figure 5‒3, the RLN axons travel with the
vagus nerve down the neck until they branch off at the level of the aortic arch on the left and the
subclavian artery on the right. On the left, the nerve passes inferior and posterior to the aortic
arch and reverses its course to continue superiorly into the visceral compartment of the neck. The
right RLN loops behind the right subclavian artery and ascends superiorly and medially toward
the groove between the trachea and the esophagus. Both RLNs travel just lateral to or within this
groove and enter the larynx posterior to the cricothyroid joint. The positions of the nerves in the
neck make them susceptible to iatrogenic injury during surgery. Low in the neck, the course of
the left RLN is more oblique and lateral and probably more prone to injury than that of the right
RLN (Joliat et al., 2017). The RLN is vital to the abductory–adductory function of the true vocal
folds because it innervates four of the five intrinsic muscles of the larynx (see Chapter 2). Paralysis
of the thyroarytenoid muscle (TA) resulting from cutting or trauma to the RLN will in time lead to
128 The Voice and Voice Therapy
vocal fold atrophy, which in turn results in weakness in vocal fold approximation, mid–vocal fold
bowing, and dysphonia. Subtle changes of pitch variation required in normal talking and singing
are compromised with lack of TA innervation. The primary symptom of posterior cricoarytenoid
(PCA) paralysis is the inability to open the glottis on the involved side, creating a unilateral
abductor paralysis. The primary symptom of lateral cricoarytenoid (LCA) paralysis is vocal fold
paralysis in the fixed, paramedian, abducted position.
Cranial Nerve XI, Spinal Accessory. Cranial nerve XI is a motor nerve that has innerva-
tion of the neck accessory muscles as its primary function. It is composed of two sections, the
cranial portion and spinal portion. The cranial branch originates in the nucleus ambiguus and
emerges from the side of the medulla with five successive small rootlets. Some fibers are distributed
to the superior branches of the vagus nerve, innervating the levator veli palatini and uvula. Fibers
from the spinal portion of the nerve originate from the anterior horn of the spinal cord and
merge with lower spinal portion fibers to innervate the major muscles of the neck, such as the
sternocleidomastoid and the trapezius muscles. Lesions to cranial XI can cause obvious problems
of resonance and in the contribution of neck accessory muscles to respiration.
Cranial Nerve XII, Hypoglossal. The hypoglossal nerve is a motor nerve innervating (as the
name suggests) the extrinsic and intrinsic muscles of the tongue as well as some of the neck strap
muscles. The nerve originates in its own nucleus, the hypoglossus nucleus, in the lower medulla,
exiting laterally and entering the hypoglossal canal in the occipital bone, descending and then
moving laterally into its many innervation sites. The muscles it innervates are the omohyoid, sternothyroid, styloglossus, hyoglossus, genioglossus, geniohyoid, sternohyoid, and all of the intrinsic
PluralPlus
Self-Check
5–2
muscles of the tongue. Cranial nerve XII has much to do with positioning of the larynx, that is,
depression or elevation of the total laryngeal body, and is essential for all intrinsic movements of
the tongue. Its primary impact on voice is on resonance and quality.
Conditions Leading to Neurogenic Dysphonia
Medical diagnoses associated with neurogenic dysphonia include vocal fold paralysis, laryngeal
dystonia, essential tremor, Parkinson’s disease (PD), Huntington’s disease, myasthenia gravis
(MG), multiple sclerosis, amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP),
multiple systems atrophy, and acquired brain injury (traumatic brain injury [TBI], CVA), to name
just a few. A complete review of all medical conditions leading to dysphonia is beyond the scope
of this text. The interested reader may refer to textbooks about neurogenic speech disorders by
Duffy (2020) and Abou-Kahlil and Webb (2023) for detailed information. For quick reference,
see Table5‒1, which summarizes the differential features in each dysarthria subtype.
In the following sections, we review the identification and management of the neurogenic
voice disorders most commonly seen by ENTs and SLPs in the voice clinic (Cohen et al., 2012b):
vocal fold paralysis (unilateral and bilateral); laryngeal dystonia, for example, spasmodic dysphonia;
essential tremor; PD; and acquired brain injury. Management of each requires cooperation among
ENTs, neurologists, and SLPs, and the synthesis of each discipline’s expertise becomes the genesis
for innovative treatment approaches (Boominathan et al., 2012; McFarlane & Von Berg, 1998).
After reading this section, watch Videos 5–1 and 5–2.
TABLE 51. Dysarthria Differential Features
Dysarthria
Type Site of Lesion
Neurophysiological
Impairment
Associated
Neurological Signs
Prominent AuditoryPerceptual Speech
Characteristics
Flaccid Lower motor
neurons for
speech (CNs, V,
VII, IX, X, XI,
XII) and cervical
and thoracic
spinal nerves
Spastic Upper motor
neuron (bilateral)
Hypokinetic Extrapyramidal
(substantia nigra)
Hyperkinetic Extrapyramidal
(basal ganglia)
Weakness Diminished reflexes Indistinct and
labored articulation,
hypernasality, and
breathy voice quality
Spasticity Loss of skilled
movement; hypertonia,
manifested as spasticity;
hyperreflexia; clonus,
Babinski sign; Hoffman
Rigidity, reduced
range of movement,
resting tremor
Quick-to-slow,
regular or irregular
involuntary
movements
Rigidity, bradykinesia,
akinesia, resting tremor,
postural abnormalities
One or more: of chorea,
dystonia, athetosis,
dyskinesia, myoclonus,
tics, tremor
Slow, imprecise
articulation harsh
voice; monopitch and
monoloudness; short
phrases
Reduced loudness,
monopitch, and
monoloudness; reduced
syllable stress, accelerated
rate and short rushes
of speech, palilalia,
inappropriate silences
Highly variable affecting
one or more components
of speech production,
often with rate and
prosodic abnormalities;
speech features
consistent with nature of
involuntary movements
Ataxic Cerebellum Dyscoordination;
possible intention
tremor
Unilateral
upper motor
neuron
Mixed Two or more of
Upper motor
neuron
(unilateral)
above
Weakness, spasticity,
lack of coordination,
singly or in
combination
Combinations of
above
Dyscoordination Excess and equal stress;
irregular articulacy
breakdown; rhythm
disturbances; sound
prolongations; excess
loudness
Hemiparesis and
hemiplegia, unilateral
central face and tongue
weakness
Combinations of above Combinations of above
Imprecise articulation,
irregular articulatory
breakdowns, slow
rate, harsh-strained or
breathy-hoarse voice,
reduced loudness
129
130 The Voice and Voice Therapy
Video 5–1. Phonation in this video example
reveals a longitudinal gap, diplophonia,
and extensive air escape. Grand Rounds:
Describe three behavioral approaches you
would probe to reduce air escape and
supraglottal interference and increase vocal
quality.
Video 5–2. Parkinson’s disease. Note in this
video the increases in respiratory support,
articulation accuracy, and phonatory volume
for the reading passage before and after
voice intervention. Grand Rounds: Describe
the changes in physiology for three subsystems of speech (respiration, phonation, and
articulation) that underlie these changes.
Vocal Fold Paralysis
Individuals who experience damage to cranial nerve X anywhere along its path, from the medulla
to the larynx, may have voice difficulties because of vocal fold paralysis. This pathology is also
called vocal fold impairment. The roles of the ENT and SLP are to confirm the diagnosis and to
be certain that the movement deficit is not a result of mechanical causes, such as arytenoid cartilage
dislocation or subluxation, cricoarytenoid arthritis or ankylosis, or a tumor (Hu et al., 2023). The
type and extent of dysphonia largely depend on the lesion site and whether damage is unilateral
or bilateral, and partial or complete.
Unilateral Vocal Fold Paralysis
The etiology of unilateral vocal fold paralysis (UVFP), also called unilateral vocal fold impairment,
can be broadly divided into four categories: neoplastic (compression or infiltration of the vagus or
CHAPTER 5 Neurogenic Voice Disorders 131
RLN), traumatic (surgical and nonsurgical), secondary to medical disease, and idiopathic (Nelson
et al., 2019).
Disease or trauma to the RLN on one side is the most common form of vocal fold paralysis
(Case, 2002; Hu et al., 2023; Prasad et al., 2017). As we see in Figure 5‒3, because of the extended
course of the left RLN, it appears to be more prone to traumatic or surgical injury than the right
RLN. Conceivably, any lesions along the RLN or the proximal vagus nerve could be the cause.
Bhattacharyya and colleagues (2002) reported that of 64 patients presenting with UVFP, 53 cases
were left-sided. In a retrospective review of patient cases, Hughes and colleagues (2000) reported
that isolated right vocal fold paralysis comprised only about 3% of laryngeal evaluation cases.
Surgical trauma predominated as an etiology, followed by viral and idiopathic causes. In a study
by Heman-Ackah and colleagues (2011), undiagnosed thyroid disease was discovered in about
50% of patients presenting to the ENT with UVFP and dysphonia. A 10-year review reported by
Nelson and colleagues (2019) identified causes of UVFP as surgically induced (46%), followed
by idiopathic causes (18%) and malignancy (13%). These findings were consistent with those of
Hu and colleagues (2023) who reported that the main cause of vocal fold paralysis is neck surgery,
most commonly thyroid surgery.
In UVFP, there is glottic incompetence due to the inability of the affected true vocal fold
to adduct completely and meet the normally mobile opposing true vocal fold. The paralyzed
vocal fold is fixed in the paramedian position, that is, neither fully abducted nor adducted.
The vocal fold remains at the paramedian position for both inspiration and expiration (including
attempts at phonation). UVFP often leads to significant morbidity that may include dysphonia,
dysphagia, and aspiration (Adessa, 2021; Dhar et al., 2022; Marques et al., 2021). With respect
to dysphonia, the voice in UVFP is markedly dysphonic or aphonic. Perceptual characteristics
include breathy, hoarse vocal quality; reduced phonation time; decreased loudness and monoloudness; diplophonia; and pitch breaks. The breathy vocal quality, reduced loudness, and short
phonation times result from air escape through an open glottis (glottal insufficiency) during
phonation. Hoarseness, pitch breaks, and diplophonia result from the reduced ability to adjust
the internal tension of the paralyzed vocal fold. Secondary muscle tension may contribute to the
perception of hoarseness (Schneider, 2019).
Behavioral Management of Unilateral Vocal Fold Paralysis
Because many traumatic vocal fold paralyses have spontaneous recovery within the first 9 to
12months after onset (Marques et al., 2021; Mau, 2021), permanent corrective procedures are
usually delayed until voice therapy has been tried. In many cases, strengthening the vocal muscles
and improving voicing technique result in very good voice quality, and surgery may be unnecessary (Eldsoky & Ismaiel, 2021; Mattioli et al., 2011; Schindler et al., 2008). Behavioral voice
therapy may be the only treatment required, or it may suffice as a temporary measure until
medical intervention is feasible. One study by Busto-Crespo and colleagues (2016) found that
voice therapy for individuals with UVFP was effective as measured by imaging, aerodynamic, and
perceptual measures. The researchers reported that voice improvements were sustained over time.
The voice facilitating approaches we normally introduce in clinic are focus, half-swallow boom,
head positioning, tuck-chin, digital manipulation, tongue protrusion /i/, yawn-sigh, pitch shift up,
and inhalation phonation (see Chapter 7). Each approach affords an anatomical and physiological
rationale for improving voice in individuals with UVFP.
132 The Voice and Voice Therapy
In addition to direct voice therapy, Helou and colleagues (2021) suggest that indirect therapy
plays an important role in management of vocal fold paralysis. Indirect therapy may include
education and counseling related to the anatomy and physiology of voice production and changes
in voice related to UVFP. Readers are encouraged to investigate Schneider (2019) for a comprehensive review of behavioral management of UVFP and paresis.
Medical Management of Unilateral Vocal Fold Paralysis
As noted earlier, classical management of UVFP typically involves a waiting period of up to
12months for spontaneous recovery before medical management is considered (Husain et al.,
2018). Voice therapy is a viable option, especially if the client is stimulable for improved vocal
quality and acoustic measures. However, for many, vocal fold paralysis is consistent with swallowing problems, along with weak and ineffective cough. Dhar and colleagues (2022) found
that as many as two-thirds of patients with UVFP have dysphagia, with one-third to one-half of
patients showing aspiration. For these clients, there are two main medical approaches: vocal fold
medialization and vocal fold reinnervation (Marques et al., 2021 ).
Medialization procedures include injection medialization laryngoplasty and laryngeal framework surgery. Several injectable materials have been used to medialize the vocal fold and improve
glottic competence. These can be categorized into short lasting/temporary (bovine gelatin,
collagen-based products, hyaluronic acid, and carboxymethylcellulose gel [Prolaryn]) and long
lasting (autologous fat, calcium hydroxylapatite, polymethyl-methacrylate, and polydimethylsiloxane) (Marques et al., 2021). Most ENTs agree that the use of injectable materials appears
to be (a) a temporary step for patients with UVFP who require immediate medialization, but
in whom some recovery is likely, or (b) a minimally invasive option for those patients whose
medical–surgical status precludes a procedure such as thyroplasty.
Sulica and Louis (2010) performed a retrospective review of patients who underwent injection
laryngoplasty at seven university medical centers from July 2007 to June 2008. They found that
the most popular mode of injection delivery was by transcricothyroid, peroral, and transthyroid
membrane. Five-year data showed that injections in patients who were awake rose from 11% to
43%. Readers are encouraged to explore the latest literature to learn of the long-term effects and
voice outcomes of the various injection fillers and methods (Liao & Wang, 2022; Pan & Sadoughi;
2022). It appears that injections are a safe and largely durable treatment option for the management of glottal insufficiency in both children and adults (Liao & Wang, 2022; Marques et al.,
2021; Pan & Sadoughi, 2022).
Thyroplasty Type I, first described by Isshiki and colleagues (1975), is a surgical approach
to medialization of the paralyzed vocal fold, using a free-moving wedge to move the vocal fold to
midline (Dursun et al., 2008). The surgeon cuts a rectangular window out of the thyroid cartilage
on the side of the paralyzed vocal fold. The patient is conscious during the procedure and produces
voice when the surgeon places the wedge at various sites against the paralyzed vocal fold. When it
is confirmed that a certain site produces the best phonation, the wedge is fixed surgically at that
point. Thyroplasty in the hands of a competent surgeon produces excellent results, and patients
should expect “voice improvement as early as 1 month postoperatively and should remain stable
with slight fluctuations for at least 6 months” (p. 576). Dean and colleagues (2001) introduced a
modification of the thyroplasty technique by introducing a titanium implant with a micrometric
CHAPTER 5 Neurogenic Voice Disorders 13 3
screw that allows for secondary adjustment of medialization, if necessary. Sano and colleagues
(2020) reported on long-term treatment of titanium medialization thyroplasty with arytenoid
adduction for 16 patients with UVFP. Results showed significant improvements in maximum
phonation time, mean flow rates, the GRBS scale, the VHI, and the voice-related quality of
life (VRQoL) over the 12-month postoperative period. See Chapter 6 for these voice-related
assessments.
There are numerous reports on the long-term results of both injection and medialization
thyroplasty. One notable study by Morgan and colleagues (2007) reported a retrospective study
of 19 patients with UVFP who received either vocal fold injection with Radiesse or Thyroplasty
Type I. Outcome measures were laryngostroboscopy, perceptual analysis, and patients’ subjective voice handicap assessment. Results revealed that both approaches were comparable in their
improvements of subjective and objective voice outcomes at 3 months. In a follow-up study
from the same institution, Vinson and colleagues (2010) retrospectively assessed outcomes for
34patients with UVFP at 6 months and reported that both approaches were comparable in terms
of voice outcomes. A retrospective study by Sipp and colleagues (2007) compared outcomes for
three procedures (injection laryngoplasty, thyroplasty, and laryngeal nerve reinnervation) and
reported successful surgical and quality-of-life outcomes with all three procedures. See Bouhabel
and Hartnick (2018) for a comprehensive overview of injections, thyroplasty, and nerve reinnervation for UVFP.
While injection laryngoplasty, medializion thyroplasty, and arytenoid adduction are effective
in improving voice quality, they cannot prevent vocal fold atrophy. As a result, some researchers
have explored a variety of vocal fold reinnervation approaches, including primary neurorrhaphy
(nerve suture), ansa cervicalis to RLN anastomosis, vagus nerve to RLN anastomosis, and free
nerve grafting (Grover & Bhattacharyya, 2012). Recent literature reviews indicate positive laryngeal and voice outcomes for children, adolescents, and adults (Hoey and colleagues, 2022; Onifade
and colleauges, 2023). Torrecillas and colleagues (2024) reviewed 132 patients who underwent
ansa-recurrent laryngeal nerve reinnervation over 22 years. These authors reported that reinnervation significantly improved MPT and reduced scores on the VHI.
Buyukatalay and colleagues (2021) reported positive voice outcomes for both voice and
swallow function following laryngeal reinnervation for 22 patients with UVFP. In all cases, the
UVFP was iatrogenic, with paralysis occurring after neck surgery (thyroidectomy, cervical spine
or paraganglioma) in seven patients and after thoracic surgery in two patients and intubation in
one patient. Reinnervation techniques in this population were ansa cervicalis to RLN anastomosis
and neuromuscular pedicle. Postsurgical results reported statistically significant improvements in
both the VHI-10 and the EAT-10, the latter of which is a dysphagia assessment tool (Belafsky
etal., 2008).
Some patients, after injection or surgery, continue to display the hyperfunctional vocal behaviors they were using before treatment. Direct symptom modification can usually reduce problems
such as squeezing the words out, using pushing behaviors, and using excessive glottal attack.
Following injection or medialization, the SLP may help the patient reestablish a normal voice,
giving attention to adequate breath support and focused phonation free of effort (Schneider,
2019). On the other end of the spectrum, some patients complain of continued breathy voice, even
following reinnervation. For these patients, Kodama and colleagues (2022) offered postsurgical
vocal function exercises as an adjunct treatment. Thirty patients were enrolled in the study, with
134 The Voice and Voice Therapy
eight patients in the VFE groups and 22 patients as controls. After VFE therapy, amplitude, glottal
gap, mean airflow rate, pitch range, and several other parameters showed significant improvement
while the control group did not except for the VHI-10. The authors suggested that VFE could be
used as a follow-up behavioral therapy for patients with UVFP after reinnervation who are not
satisfied with their voice.
Bilateral Vocal Fold Paralysis
The pathophysiology of bilateral vocal fold paralysis (BVFP) includes two major categories: neurogenic paralysis and mechanical fixation (Kelchner et al., 2014; Trozzi et al., 2020; Woodson,
2011). BVFP is usually the result of lesions high in the trunk of the vagus nerve or at the nuclei of
origin in the medulla (see Figure 5‒3). If the lesion is above the nodose ganglion, other muscles
innervated by the vagus, as well as muscles supplied by other cranial nerves, will be affected as
well. These high lesions include tumors at the base of the skull, carcinoma, or trauma. In the
case of children, BVFP is a common cause of neonatal stridor (Shanthakunalan and colleagues,
2023). Many cases are associated with intracranial pathology such as meningomyelocoele, hydrocephalus, or Arnold-Chiari malformation. Trozzi and colleagues (2020) suggest that an MRI is
often required to evaluate the CNS to begin to determine the cause of the paralysis. BVFP can
also be acquired. Bathini and colleagues (2014) reviewed five cases of BVFP and found that four
cases were related to major cardiac surgery, while one followed a thalamic stroke. In their study of
86 patients with BVFP, Dixon and colleagues (2022) found that the most common etiology was
iatrogenic injury during thyroid surgery.
BVFP may be of the abductory or adductory type; both are life threatening. In bilateral
adductor paralysis, the vocal folds are at the paramedian position bilaterally, and neither vocal fold
is capable of moving to the midline, thus making phonation impossible and placing the individual
at risk for aspiration. In abductor paralysis, the vocal folds remain at the midline, causing serious
respiratory problems for which most patients will need a tracheostomy. Voice per se is of secondary
concern to respiratory survival and feeding.
In the largest study following patients with BVFP to date, Dixon and colleagues (2022)
conducted a retrospective review of 86 patients with BVFP over a 17-year period at a single
institution. Most patients (85%) did not recover any vocal fold motion, while 13 patients (15%)
recovered motion in at least one vocal fold. Sixty-seven patients (78%) underwent tracheotomy
placement, the most performed procedure. The authors further reported that age, gender, or
paralysis progression did not predict whether patients underwent tracheotomy or experienced
spontaneous vocal fold recovery. Belafsky (2011) reported surgical procedures to open the posterior glottis airway remain the current gold standard for treatment of BVFP. Surgical options
include open vocal fold lateralization, laser cordotomy with or without partial arytenoidectomy,
endoscopic vocal fold lateralization, bilateral selective reinnervation, and endoscopic arytenoid
abduction lateropexy (Lee et al., 2020; Marina et al., 2011; Trozzi et al., 2020; Woodson, 2011).
An alternative to surgery for some patients with abductor vocal fold paralysis that is not life
threatening may be inspiratory pressure threshold training. Baker and colleagues (2003) reported
reductions in dyspnea during speech and exercise for a 6-year-old child with congenital bilateral
abductor paralysis after 8 months of respiratory muscle strength training.
CHAPTER 5 Neurogenic Voice Disorders 13 5
Andrews and Summers (2002), Hoffman and colleagues (2008), Harvey-Woodnorth (2004),
and Kelchner and colleagues (2014) offer specific procedures for the SLP to use in working with
young children with BVFP — that is, how to manage the tracheostomy, the use of tracheal valves,
PluralPlus
Self-Check
5–3
and the need for minimizing the negative effects of the vocal fold dysfunction on the child’s
expressive language and speech development.
Spasmodic Dysphonia
Laryngeal Dystonia
Spasmodic dysphonia (SD), also called laryngeal dystonia (LD), is a task-specific focal dystonia
affecting the intrinsic muscles of the larynx (Sanuki, 2023). Although the terms SD and LD
are used interchangeably in practice and in literature (Simonyan et al., 2021), SD is the nomenclature used in this chapter.
SD is classified as a rare disease with a prevalence of 3.5 to 7 individuals in 100,000 (Sanuki,
2023). It usually occurs in middle age, between the fourth and sixth decades of life and has a
female preponderance with an overall ratio of 4:1 (Blitzer et al., 2018; Simonyan et al., 2021).
Dystonia is a neurological dysfunction of motor movements, either more generalized to major
body movements or seen in focal disorders, such as in the eyelids (blepharospasm), in the neck
(spasmodic torticollis), or in the larynx (SD). As such, it is a hyperkinetic movement disorder
(see Figure 5‒1). The site in the brain where a lesion might occur that in turn would result in
SD is still not definitively known, but researchers have suggested alterations in the basal ganglia,
structural changes in both gray and white matter, and abnormal functional connectivity within the
sensorimotor and frontal parietal networks (Sanuki, 2022, 2023; Yeung et al., 2022) . One of the
first studies using MRI, single photon emission computed tomography, or brain electrical activity
mapping for identifying possible SD lesion sites was reported by Finitzo and Freeman (1989), who
concluded that “SD is a supranuclear movement disorder primarily, but not exclusively, affecting
the larynx. Fully half of our subjects had evidence of isolated functional cortical lesions” (p. 553).
SD primarily affects the essential function of voice production (Yeung et al., 2022). The
patient with SD exhibits a strained and strangled and harsh voice with observable effort in pushing
the air out during most voicing attempts. Endoscopic examination shows that this voice results
from hyperadduction of the true vocal folds, often accompanied by tight closure of the false
vocal folds with supraglottal constriction of the aryepiglottic vocal folds and contraction of the
lower pharyngeal constrictors. The total laryngeal and lower pharyngeal airway appear to close
down. No wonder we hear a strained, strangled voice in such patients. Hirano and Bless (1993)
nevertheless caution that the voice clinician should not anticipate seeing one particular laryngeal
pattern. They suggest that SD presentation can be heterogeneous, ranging from spasmodic hyperfunction to hypofunction, to irregular twitching of the true vocal folds. It has been reported that
approximately one-third of patients presenting with adductor SD have an associated vocal tremor
(Ozgursoy et al., 2020).
In addition to the problem of voicing, patients with SD complain about the difficulties they
experience trying to force expiratory air out whenever they desire to phonate. Aronson (1990)