Neurologic Disorders of the Larynx PDF

57 Neurologic Disorders of the Larynx Andrew Blitzer, Diana N. Kirke KEY POINTS diffuse and bilateral representation of laryngeal structures in the...

57 Neurologic Disorders of the Larynx Andrew Blitzer, Diana N. Kirke KEY POINTS diffuse and bilateral representation of laryngeal structures in the cortex, these lesions can result in aphasia, aphonia, dysarthria, Neurologic disorders of the larynx may be focal diseases dysphonia, and stridor. Extrapyramidal system defects are characterized or local manifestations of systemic disorders. by abnormal motor control, which may manifest as inappropriate Characteristic deficiencies found on clinical examination or excessive muscle tension, tremor, and involuntary spasmodic may aid in ascertaining the site of a lesion. muscle contractions, which vocally translates into strain, arrests, pitch breaks, and pitch instability. The dysfunction may be focal, Hyperfunctional disorders include dystonia, myoclonus, regional, or generalized. In addition to problems caused by tumors essential tremor, stuttering, and muscle tension or trauma, the extrapyramidal system is disrupted by conditions dysphonia. of uncertain etiology such as Parkinson disease (PD), tremor, and Hypofunctional disorders include focal disorders, such dystonia.1 Cerebellar lesions impair coordination of motor activities. as vocal fold paresis and paralysis, and central causes In that instance, problems are generalized rather than focal. such as Parkinson disease, multiple sclerosis, “Scanning speech” is regarded as characteristic of cerebellar neuromuscular junction disorders, poliomyelitis, involvement. Diagnosis is based on the presence of attendant myopathies, medullary disorders, and psychogenic physical signs, such as intention tremors, dysdiadochokinesia, disorders. dysmetria, ataxia, and nystagmus. Brainstem lesions result in flaccid Spasmodic dysphonia is an idiopathic focal laryngeal paralysis. Because the cranial motor nuclei are densely packed dystonia characterized by either halting or breathy within the brainstem, lesions at this level affect multiple outputs. speech breaks. Strokes and tumors of the brainstem produce severe dysfunction related to paralysis of the larynx, pharynx, or tongue and are Botulinum toxin is an important treatment for associated with sensory deficits. The site of the lesion is best spasmodic dysphonia and other dystonias. identified from the type of motor disruption, because observable Vocal fold paresis can result from trauma, tumor, or clinical signs are predominantly disruptions of motor acts (Table neurologic, idiopathic, or other medical diseases. Vocal 57.1). Diffuse central nervous system lesions result from specific fold positioning can vary on presentation. neurologic disorders, such as multiple sclerosis (MS) and amyo- trophic lateral sclerosis (ALS) and have a myriad of signs and symptoms. Patients with movement disorders have a paucity of movement (akinesia or bradykinesia), excessive or hyperfunctional Neurologic conditions that affect the larynx span a wide spectrum. movement (hyperkinesia), or a combination of the two. The They may be focal diseases or local manifestations of systemic hyperkinetic motor programming errors can produce spasms, disorders. These lesions can produce stereotyped patterns of tremors, jerks, or tics, and symptoms related to the body part abnormal function that the otolaryngologist should strive to involved. For those with laryngeal manifestations, a multidisciplinary recognize. Evaluation should include a complete head and neck approach that includes the involvement of an otolaryngologist, examination, neurologic examination, and visual recording of the neurologist, and speech pathologist is key to successful diagnosis functional disability for documentation. For systemic disorders, and management of hyperfunctional disorders of the larynx (see consultation with a neurologist is useful for diagnosis and optimizing also Chapter 57).1 medical management. In general, neurologic dysfunction results from one or more insults within the central or peripheral nervous system. HYPERFUNCTIONAL DISORDERS A few important generalized neurologic disorders are character- ized by specific patterns of involvement of the larynx and pharynx. Dystonia In early stages of involvement, patients with these disorders may Dystonia is a syndrome dominated by sustained contractions of consult otolaryngologists, because symptoms are located in the skeletal muscles that frequently cause twisting and repetitive head and neck region. At any stage of these disease processes, movements or abnormal postures that may be sustained or intermit- otolaryngologic consultation may be vital to differentiate manifesta- tent. Because the condition is rare, and the movements and resulting tions of the disease from problems caused by other concurrent postures are often unusual, dystonia is among the most commonly disorders to ensure appropriate management. The neurologic misdiagnosed neurologic conditions.2 The prevalence is unknown, disorders that affect the larynx are best understood when character- but an estimated 200,000 to 300,000 cases of idiopathic dystonia ized as either hyperfunctional or hypofunctional disorders (Box occur in the United States. Classification is important, because it 57.1). Although this is a general categorization, often both types can inform prognosis and the approach to management.3 The can exist concurrently, particularly when hyperfunctional activity, classification scheme is outlined in Table 57.2. such as muscle tension dysphonia, works to overcome a hypo- Dystonia can begin at nearly any age. Initial signs have occurred functional deficit. as early as 9 months and as late as 85 years. In general, onset has a bimodal distribution, with peaks at ages 8 and 42 years. As can LARYNGOLOGIC MANIFESTATIONS be seen in Table 57.2, patients are partly categorized according to symptom distribution. Focal dystonia involves one isolated body OF NEUROLOGIC DISEASES region, segmental disease involves two or more contiguous regions, Cortical lesions may result from strokes, tumors, or trauma and multifocal disease involves two or more noncontiguous regions, may impair the planning and execution of actions. Because of the hemidystonia involves half the body, and generalized dystonia is 832 Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  CHAPTER 57 Neurologic Disorders of the Larynx 832.e1 Abstract Keywords 57 Neurologic disorders of the larynx may be focal diseases or local Botulinum toxin manifestations of systemic disorders. Often these lesions produce dystonia stereotyped patterns of abnormal function that the otolaryngologist larynx should aim to recognize. Such disorders are best understood by neurology characterizing them as either hyperfunctional or hypofunctional pharynx disorders. Hyperfunctional disorders of the larynx include dystonia, tremor such as spasmodic dysphonia, pseudobulbar palsy, myoclonus, vocal fold paralysis essential tremor, stuttering, and muscle tension dysphonia. Hypofunctional disorders include polio, myopathy, medullary disorders, Parkinson disease, multiple sclerosis, and vocal fold paralysis/paresis. Each of these disorders are discussed, in turn, with a focus on the clinical features and current treatment options. Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  CHAPTER 57 Neurologic Disorders of the Larynx 833 widespread including the trunk plus two other sites. The more BOX 57.1 Hyperfunctional or Hypofunctional Disorders of common examples of focal dystonia are listed in Box 57.2.3 57 the Larynx History, physical examination, and laboratory studies may fail to identify the cause of a patient’s dystonic symptoms (idiopathic HYPERFUNCTIONAL dystonia). This is a diagnosis of elimination that requires a normal Dystonia perinatal and early developmental history; no history of neurologic Pseudobulbar palsy illness or exposure to drugs known to cause acquired dystonia (e.g., Myoclonus phenothiazines); normal intellectual, pyramidal, cerebellar, and Essential tremor sensory examination findings; and normal diagnostic study results. Stuttering Because up to 16% of patients with dystonia and primary Muscle tension dysphonia laryngeal involvement experience dissemination of the disease to HYPOFUNCTIONAL another body part, patients should be advised of this potential Central and should be reexamined on a regular basis for signs of other Polio dystonic involvement. Approximately 10% of patients with primary Myopathy laryngeal dystonia have a family history of dystonia.4 Medullary disorders In most cases of childhood-onset idiopathic dystonia, family Parkinson disease studies show an autosomal-dominant inheritance with reduced Multiple sclerosis penetrance. A marker for some cases of childhood-onset dystonia Psychogenic has been found on chromosome 9.5 Heterogeneous genetic patterns Vocal fold paralysis/paresis among patients with idiopathic dystonic symptomatology have been reported, including a linkage to the X chromosome and Parkinsonism,6–8 and a dopamine-responsive form.9 Family and linkage studies, as well as genomic research, have recently identified multiple subtypes of dystonia with different genetic bases. Inherited primary monogenic dystonia can be broadly categorized into three TABLE 57.1 Site of Lesion and Resulting Signs in Neurologic phenotypic variants: primary torsion dystonia, which exhibits Disorders of the Larynx dystonia as the only clinical sign besides tremor (DYT1, 2, 4, 6, Site of Lesion Signs Cortex Aphasia Aphonia BOX 57.2 Body Distribution of Dystonia Dysarthria Dysphonia Focal Stridor Blepharospasm (forced, involuntary eye closure) Extrapyramidal system Vocal strain and pitch breaks Oromandibular dystonia (face, jaw, or tongue) Tremor Spasmodic movements Torticollis (neck) Focal, regional, or generalized dystonia Writer’s cramp (action-induced dystonic contraction of hand Cerebellum Ataxia muscles) Dysmetria Spasmodic dysphonia (larynx) Tremor Segmental (cranial, axial, or crural) Incoordination Multifocal Brainstem Flaccid paralysis Never isolated Generalized (ambulatory, nonambulatory) TABLE 57.2 Classification of Dystonia Axis Dimension for Classification Subgroups Axis I: clinical features Age at onset Infancy (birth to 2 years) Childhood (3–12 years) Adolescence (13–20 years) Early adulthood (21–39 years) Late adulthood (40 years and older) Body distribution (see also Box 57.2) Focal (one isolated body region) Segmental (two or more contiguous regions) Multifocal (two or more noncontiguous regions) Hemidystonia (half the body) Generalized (trunk plus two other sites) Temporal pattern Disease course (static vs. progressive) Short-term variation (e.g., persistent, action specific, diurnal, or paroxysmal) Associated features Isolated (with or without tremor) Combined (with other neurologic or systemic features) Axis II: etiology Nervous system pathology Degenerative Structural (e.g., focal static lesions) No degenerative or structural pathology Heritability Inherited (e.g., sex linked or autosomal, dominant or recessive, or mitochondrial) Acquired (e.g., brain injury, drugs/toxins, vascular, or neoplastic) Idiopathic Sporadic Familial Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 834 PART V Laryngology and Bronchoesophagology 7, 13, 17, 21, 23, 24, 25, 27, and 28 phenotypes); dystonia plus, muscles, the later consequences of long-term injections are which can manifest with additional signs such as dopa-responsive unknown. Weakness and routine electromyography (EMG) changes Parkinsonism or myoclonus (DYT3, 5 [formerly 14], 11, 12, 15, in muscles distal to the site of injection have not been reported. 16, and 26 phenotypes); and paroxysmal forms of dystonia and However, abnormalities are detectable on single-fiber EMG.32 It dyskinesia (DYT8, 9, 10, 18, 19, and 20 phenotypes).5–11 is not known how long these abnormalities persist or whether Clinically, spasmodic dysphonia is an idiopathic focal dystonia they have any clinical significance. A paucity of data exists regarding of the larynx.12 Although the disease was initially described by use of BoNT during pregnancy; currently, injection is avoided in Traube13 in 1871, Fraenkel14 and Gowers15 later recognized the pregnant or lactating patients. Caution is warranted for the relationship with other dystonias, such as writer’s cramp. Approxi- management of patients with conditions such as myasthenia gravis, mately 80% of cases of laryngeal dystonia have adductor spasmodic Lambert-Eaton syndrome, and motor neuron disease, particularly dysphonia (ADSD), whereby spasmodic adduction of the vocal when large doses are required, such as in the management of folds during speech results in a strained and strangled voice. Fewer cervical dystonia. However, the amount of toxin that enters the patients, around 20%, have abductor spasmodic dysphonia (ABSD), circulation after injection is thought to be minute, and this theoretic with intermittent or sustained opening of the larynx during speech16 concern should be balanced against the severity of the hyperkinetic that leads to breathy voice breaks or a whispering voice. Some symptoms.32 patients display a combination of adductor and abductor signs In patients with ADSD, BoNT injection into the thyroarytenoid- and have been classified as having “mixed laryngeal dystonia.” vocalis muscle complex has been demonstrated to improve speaking Two other rare forms of laryngeal dystonia include adductor to 60% to 100% of normal function,33 with a mean of 90%; the breathing dystonia and singer’s laryngeal dystonia. In the former, duration of effect was between 3 and 4 months. Adverse effects patients adduct their vocal cords while inspiring. The glottic include a mild breathy dysphonia for less than 2 weeks (45%), adduction causes stridor and dyspnea, but this is typically self- mild choking on fluids for the first several days (22%), hyperventila- limited, does not cause hypoxia, and does not warrant surgical tion and dizziness when trying to speak while hypophonic, a sore airway management. Singer’s dystonia is the presence of symptoms throat or hemoptysis, and itching (without rash).34–37 In patients only during singing. These patients have almost always been with ABSD, injection of BoNT into the posterior cricoarytenoid performing professionally as singers, and in some, the symptoms (PCA) muscle produces marked improvement, with a return to progress to also involve their speaking voice.17 Patients with more mean maximal functional performance of 70% of normal. Adverse generalized dystonia, which also involves the larynx, have vocal effects include mild dysphagia without aspiration and mild stridor dysfunction that is clinically indistinguishable from idiopathic on exertion. spasmodic dysphonia. Meige syndrome, a regional dystonia of the The effective treatment dose is variable for each patient and head and neck, may be evident in those with blepharospasm, for each muscle injected; therefore injections are individualized.38 oromandibular dystonia, torticollis, or spasmodic dysphonia. The dose range for ADSD is 0.05 to 20 units of BoNT, with an In all types of laryngeal dystonia, patients have anecdotally average dose of less than 1 unit per vocal fold.39,40 In general, a reported that symptoms momentarily improve when they pinch starting dose of 1.0 unit in 0.1 mL of saline is used for bilateral the nares, press the hand against the back of the head, press the thyroarytenoid injections. Subsequent doses are varied according hand into the abdomen, pull on an ear, or touch the clavicular to clinical response and adverse effects, but over time the dose notch. Many patients observe that they speak better after a yawn range of BoNT appears to be stable in the majority.41 Injections or sneeze or when they sing or yell; these sensory tricks or “geste are given by means of a tuberculin syringe with a 27-gauge antagoniste” are also common for patients with other craniocervical monopolar Polytef-coated hollow EMG recording needle. EMG dystonias.2,18 There is no current cure for spasmodic dysphonia guidance has the advantage of controlled administration into the but a variety of treatments exist. Dedo and Izdebski19 described more actively contracting regions of the muscle.42 dramatic relief of symptoms with sectioning of the recurrent Adductor laryngeal injections are performed percutaneously laryngeal nerve. The initial favorable reports were temporized by through the cricothyroid membrane and into the thyroarytenoid– a review of 33 patients by Aronson and DeSanto20 that addressed vocalis muscle complex, with use of EMG guidance for optimum surgical management. Three years after surgical treatment, only placement (Fig. 57.1). Injections for ABSD are administered to 36% of patients had some persistent improvement, and only 3% the PCA muscle (Fig. 57.2). The physician reaches the muscle by achieved a persistent normal voice. Selective laryngeal adductor manually rotating the larynx, placing the EMG needle behind the denervation-reinnervation (SLAD-R) surgery for ADSD has posterior edge of the thyroid lamina, and advancing the needle shown outcomes similar to those with botulinum toxin (BoNT) to the cricoid cartilage to arrive at the PCA muscle. Alternatively, for surgeons experienced with the procedure.21 However at a transcricoid injection can be made. When the patient is instructed present, the symptoms are most consistently managed with use to sniff, which maximally uses the PCA muscle, a burst of activity of an individualized regimen of chemodenervation with BoNT is seen on the EMG, and the toxin is administered.34,35,40,42 Some into the involved muscles.21,22 patients, particularly with ADSD, may present with supraglottic squeeze during the course of their treatment. In this instance, if nonresponsive to voice therapy, the supraglottic portion of the Botulinum Toxin Therapy lateral cricoarytenoid muscles can be injected via a thyrohyoid The bacterium Clostridium botulinum produces eight immunologi- approach.43 cally distinct toxins that are potent neuroparalytic agents: A1-8, The adverse effects previously described are transient and are B1-8, C1,D, Dc, E1-12, F1-8, G, and H.23–29 BoNT exerts its effect at caused by an extension of the pharmacology of the toxin. If the the neuromuscular junction by inhibiting the release of acetyl- patient has a strong response to therapy, and too much weakness choline, causing a flaccid paralysis.30,31 Botulinum toxin type A, occurs, strength gradually returns. Follow-up therapy is carefully onabotulinumtoxin A (Botox; Allergan, Irvine, CA), abobotulinum- individualized, and the response to therapy should be meticulously toxin A (Dysport; Galderma, Fort Worth, TX), or incobotulinum- documented.32 toxin A (Xeomin; Merz Pharma GmbH, Frankfurt, Germany), is most commonly used. Botulinum toxin type B, rimabotulinumtoxin B (Myobloc; Solstice Neurosciences, San Francisco, CA) is also Pseudobulbar Palsy commercially available for clinical application. Pseudobulbar palsy (PBP) results from bilateral lesions of the Although BoNT has been used therapeutically in humans since corticobulbar tracts. Patients have muscle spasticity and hyper- the mid-1970s without evidence of a direct effect on uninjected reflexia of the pharynx, palate, lips, tongue, and larynx. The voice Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  CHAPTER 57 Neurologic Disorders of the Larynx 835 57 A SPA RECORD 16:30:10 500 µV FOOT SWITCH STATUS: HOLD RUN TRIG. –489 µV 500 ms 500 µV DELAY: 1 DIV 5 ms C B Fig. 57.1 (A) Anterior approach to the thyroarytenoid muscle through the cricothyroid membrane. The injection needle is passed into the airway and directed laterally and superiorly into the thyroarytenoid muscle. (B) Model depicting placement of 27-gauge injection needle into the thyroarytenoid-vocalis muscle. An acute angle places the injection into the anterior belly of the thyroarytenoid muscle. (C) Electromyogram obtained during injection of the thyroarytenoid muscle. The patient is asked to say “ee,” which results in recruitment and increased motor unit activation and confirms accurate placement of the electrode before injection. in the patient with PBP is harsh, strained, and strangled, and it that heard in laryngeal dystonia or tremor (personal observation). sounds somewhat like that of a patient with spasmodic dysphonia. Examination of the vocal cords often shows slow rhythmic adduction Patients with PBP are easily distinguishable clinically because and abduction of the vocal cords at the same timing and frequency they have associated signs of hypernasality; slow, labored articula- as the palatal, pharyngeal, and occasional diaphragmatic contrac- tion; emotional lability; and subcortical cognitive impairments. tions. This causes the broken speech pattern and a respiratory dysrhythmia. Although oculopalatolaryngopharyngeal myoclonus is usually unresponsive to pharmacotherapy, isolated cases have Myoclonus reportedly responded to serotonin,45 carbamazepine,46 clonazepam,47 Oculopalatolaryngopharyngeal myoclonus is an uncommon disorder tetrabenazine,48 and trihexyphenidyl.49,50 Several patients whose that consists of rhythmic contractions of the soft palate, pharynx, symptoms were unresponsive to drug therapy have been managed and larynx at a rate of one or two contractions per second. This with local injection of BoNT into the thyroarytenoid muscles. condition may affect only the palate, all of the laryngopharynx, and even the eyes, and it is caused by a lesion in the central tegmental tract that may result in speech that sounds like a choppy Essential Tremor voice with intermittent hypernasality. The palate and vocal folds Tremor is an involuntary, purposeless rhythmic movement of a may be treated with injections of BoNT to decrease the severity part of the body. It causes a 6- to 8-Hz shaking of the hands, head of the contractions and thereby reduce the symptoms. A patient titubation, and a tremulous voice. The current proposed underlying complaint of clicking in the ears, thought to be caused by involve- neural bases for tremor include dysfunction in the central networks ment of the eustachian tube and tensor veli palatini muscles, was of the basal ganglia and the cerebello-thalamo-cortical system.51 first noted in the 19th century by Müller and then Politzer.44 The Tremors, like dystonia, are classified along two axes: Axis 1, which clicking can often be heard by family and examiners. Laryngeal includes clinical characteristics, and Axis 2, which defines etiology involvement may produce a broken speech pattern, simulating (acquired, genetic, or idiopathic).52 Essential tremor is typically Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 836 PART V Laryngology and Bronchoesophagology SPA RECORD Forced Insp. 04:34:2 1 µV FOOT SWITCH STATUS: HOLD / RUN TRIG. µV 1 s 1 µV DELAY: –1 DIV 10 ms A C B Fig. 57.2 (A) Lateral approach to the posterior cricoarytenoid (PCA) muscle. The thyroid cartilage is rotated laterally with simultaneous anterior displacement, exposing the posterior lateral border of the thyroid cartilage. The 27-gauge injection needle is inserted into the posterior lateral aspect of the cricoid cartilage. (B) Model depicting placement of the injection needle into the PCA muscle using a posterior lateral approach. (C) Electromyogram obtained during injection of the PCA muscle. Vertical arrows indicate volitional “sniff” maneuvers with recruitment of PCA motor units. absent at rest, maximal during maintenance of a posture, attenuated decreasing the amplitude of the tremor and making speech more during movement, and often accentuated at the termination of fluent. If there is both vertical and horizontal tremor, injections movement.1,53,54 Of patients with essential tremor, 60% have a can be alternated 3 to 8 weeks apart to avoid dysphagia and family history.55 Pitch breaks (octave breaks to a lower frequency) aspiration. Although the toxin does not eliminate the tremor, it and phonation arrests have been reported in some cases of essential decreases the amplitude and thereby reduces the severity of the tremor56 and have been associated with visible vertical oscillations symptom. Finally, tremor can also accompany spasmodic dysphonia of the larynx.57 When present, this is termed vocal tremor and has and other focal dystonias. been described perceptually as “tremulous voice,”58,59 “wavy voice,”60 or “tremulous, quavering speech”60 and has been associated with, in addition to essential tremor, other neurologic disorders, including Stuttering PD, cerebellar ataxia, and flaccid dysarthria.16,61 Stuttering might best be considered a movement disorder because Vocal tremor may parallel the onset of other symptoms or may it characteristically includes abnormal, involuntary, and inappropri- have a sudden onset that can cause rapid deterioration in speech ate use of the muscles of speech production that results in dysflu- intelligibility.59 It has been reported to be greater with emotional ency. The abnormal movements are task specific and may be stress or fatigue. Vocal tremor can also present in isolation and repetitive and stereotyped. Stuttering occurs in three subsystems when it does, unlike essential tremor, it is generally seen at rest of speech—respiratory, phonatory, and articulatory—and it is a with quiet inspiration on examination of the larynx. result of increased muscle tension in these subsystems, which Propranolol and primidone have been established as effective causes the muscles to move too quickly and too far.64 This increased treatments for essential tremor.62 Deep brain stimulation (DBS) muscle tension results in postures that are sustained for longer and thalamotomy may also be effective.62 However, the effect of than expected or in quick repetitive movements of the same posture. medication on reducing vocal tremor is equivocal. Local injection In addition, other cranial musculature may inappropriately contract, of BoNT in the management of vocal tremor has shown benefit, including the eyelids and other muscles of facial expression.65–67 with injections being given into the muscles that seem to be most One report describes stuttering followed by the development of tremulous.63 If the patient has a predominately horizontal glottic jaw-opening dystonia.68 tremor, the bilateral thyroarytenoid muscles are injected with an As in other movement disorders, competing stimuli—such as initial dose of 1 unit per side. If the patient has a predominately emotional arousal; sensory stimuli; motor actions, such as walking; vertical laryngopharyngeal tremor, the bilateral strap muscles are and the use of rhythmic patterns (e.g., a metronome)—increase injected with an initial dose of 2.5 to 5 units per side. This fluency. Communicative pressures such as audience size, listener diminishes the up-and-down motion of the larynx, thereby reactions, concern about social approval, time pressure, and Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  CHAPTER 57 Neurologic Disorders of the Larynx 837 the extent to which the stutterer is responsible for conveying a weakness. The exact cause of postpolio syndrome is unknown, meaningful message to a listener are found to increase stuttering.69 but it is thought that the syndrome is derived from the natural 57 The use of antidepressants does not improve fluency.70 Most loss of motor neurons during the aging process. Patients who individuals with a stuttering disorder respond to traditional speech have recovered from poliomyelitis function by virtue of a small therapy and training. For cases resistant to traditional therapy, pool of surviving neurons that sprout to supply expanded numbers chemodenervation of the thyroarytenoid muscles may be consid- of muscle fibers. Thus, these patients are particularly susceptible ered; in a group of patients with stuttering and glottal block, this to the loss of even a small additional number of neurons. Acute maneuver initially achieved promising results71 Small doses of bulbar polio causes pharyngeal and laryngeal paresis but spares onabotulinumtoxin A (1 unit or less, given bilaterally) have produced the cricopharyngeus muscle. The resulting symptoms are hoarse- improvement in 50% of patients. The number of glottal blocks ness, dysphagia, and aspiration.74 Because the cricopharyngeus and the duration of the glottal blocks significantly diminish with muscle retains tone, cricopharyngeal myotomy is often helpful in management. The most significant advances in treatment of the patient with recent onset of polio; however, in those with stuttering have been achieved with in-the-ear devices that provide postpolio syndrome, the effectiveness of myotomy has not been altered auditory feedback.72,73 With the use of both delayed and established. frequency-altered auditory feedback, significant improvement in fluency and normalcy of speech has been demonstrated. Improve- ment was demonstrated for both young and adult subjects, and Myopathies these devices are currently marketed under the trademark Examples of myopathies are dermatomyositis, muscular dystrophy, SpeechEasy (Janus Development Group, Greenville, NC). and metabolic myopathies. Dermatomyositis manifests as dermatitis in conjunction with muscle weakness. This disorder may be associated with lung cancer, systemic lupus erythematosus, or Muscle Tension Dysphonia poliomyelitis. The muscular dystrophies vary in age at onset and Muscle tension dysphonia is defined as a hyperfunctional posturing anatomic distribution of involvement. The infantile variety often of the vocal folds. This hyperfunction causes tightness and dys- presents with oculopharyngeal weakness. Metabolic myopathies phonia with harshness, breathiness, choppy vocal production, or may result from abnormalities in acid maltase, glycogen branching tremor. The condition can be primarily behavioral in nature but enzyme, and cytochrome c-oxidase. Also, some episodic myopathies may also be a result of inadequate compensatory strategies for with periodic paralysis are drug induced or caused by fluctuating genuine structural or functional disorders of the larynx. Patients electrolyte abnormalities. are best treated initially with speech therapy to suppress maladaptive phonatory mechanisms and learn voicing techniques designed to minimize muscular tension. Medullary Disorders Medullary disorders that affect motor neurons include ALS, primary lateral sclerosis, postpolio syndrome, Arnold-Chiari malformations, HYPOFUNCTIONAL DISORDERS and medullary strokes. ALS (also known as Lou Gehrig disease) is an idiopathic and progressive degeneration of upper and lower Central Causes of Vocal Fold Paresis motor neurons that results in muscle wasting, fasciculations, and Central nervous system disorders that may produce vocal fold weakness. Incidence in the United States has been estimated at 1 paralysis/paresis are syringobulbia, Arnold-Chiari malformations, to 2 per 100,000 people. Up to 25% of patients with ALS initially stroke (including Wallenberg lateral postmedullary syndrome and have complaints related to speech and swallowing. In many patients, posterior and/or inferior cerebellar artery occlusion), and other limb symptoms predominate. The clinical course varies in its rate lower motor neuron disorders. Vocal fold paresis as a result of of progression but inevitably leads to deterioration. Approximately peripheral nerve injury or compression is discussed separately 25% of patients survive from 5 to 10 years after the onset of the later in the chapter. disease. Death is most often related to respiratory insufficiency as a result of weak breathing muscles and aspiration pneumonia; therefore the prognosis for a more rapid demise is higher in patients Neuromuscular Junction Disorders with throat involvement. Neuromuscular junction disorders include myasthenia gravis and When ALS involves the upper airway, the voice is monotonous the less common Eaton-Lambert disease. In such disorders, muscles and raspy with abnormal hypernasal resonance. Speech is commonly fatigue quickly with use. The incidence of myasthenia gravis is dysarthric and labored and has velopharyngeal incompetence. The less than 10 per 100,000 people. Specific patient complaints may dysarthria is related to tongue involvement. Patients have slurred vary, depending on the distribution of the muscles involved. Many speech as a result of weakness and slowed activity of the tongue, patients have ptosis or double vision, because ocular muscles are and the tongue often has visible fasciculations. Weakness in the most commonly affected. General fatigue is also a common palate, pharynx, and larynx are evident, along with an inability to complaint. Sometimes the disease is localized to the throat, and make rapid muscle adjustments or repetitive motions. Secretions patients have difficulty speaking, breathing, or swallowing. Careful pool in the hypopharynx, and aspiration often occurs during examination of the larynx and palate in such patients may reveal swallowing. Certain characteristics distinguish ALS from myasthenia fatigue as a result of repetitive movements. For example, asking gravis: symmetric facial weakness is common in patients with ALS, the patient to repeat “ee-ee-ee” can elicit laryngeal fatigue. EMG although extraocular motion is preserved; this characteristic and an edrophonium test are used for rapid diagnosis and treatment contrasts with the proclivity of myasthenia gravis to involve the of myasthenia gravis. Blood testing is used to detect antibodies eyelids and extraocular muscles. ALS results in muscle wasting against acetylcholine. Early detection of this disorder is invaluable, and fasciculations that are most easily observed in the tongue and because medical treatment is effective and may be lifesaving.74 the intrinsic muscles of the hand. Tongue fasciculations have a classic “bag of worms” appearance. Therapeutic options for patients with ALS are essentially limited Poliomyelitis to supportive care. In some patients, a palatal lift prosthesis may Poliomyelitis is essentially eradicated today as a result of worldwide improve speech intelligibility and reduce nasal regurgitation during vaccination programs. However, some survivors of poliomyelitis speech. In most patients, no intervention can improve speech. experience postpolio syndrome with a recurrence of motor Intractable aspiration eventually mandates enteral feeding, and Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 838 PART V Laryngology and Bronchoesophagology tracheotomy is often necessary for airway protection, assisted may not involve the superior laryngeal nerve, and thus sensation ventilation, and pulmonary toilet.75 of the larynx is variably affected. The term paralysis implies a complete denervation of the vocal fold with no motor activity, as proven by EMG. Paresis implies that there is some residual nerve Parkinson Disease function, as is most often the case. Vocal fold immobility as a broad PD is an extrapyramidal syndrome caused by cell death in the term encompasses impaired motion from either a neurogenic or substantia nigra. It may be idiopathic or secondary and may be a rare mechanical cause such as arytenoid dislocation, joint fixation, caused by drugs, encephalitis, stroke, toxins, tumors, or head trauma. or web formation. The criteria for diagnosis require that a patient be first diagnosed The causes of vocal fold paresis can be divided into the broad with Parkinsonism, which is defined as bradykinesia in combination categories of trauma, idiopathic, tumor, and neurologic or other with at least one of resting tremor or rigidity. Following those medical diseases. Trauma can be surgical—such as from thyroid- criteria, the diagnosis needs to meet further strict criteria, which ectomy, anterior cervical spine surgery, or thoracic procedures—or can be found in the appropriate reference.76 Affected patients from endotracheal intubation. Skull base tumors, mediastinal typically have a flat facial expression and abnormal posture. Tremor lymphadenopathy, and esophageal cancers are examples of tumors is often present in the distal parts of the extremities and the lips that can impinge at various points on the vagus nerve or its recurrent when patients are at rest. “Pill-rolling” tremor of the hands is branch; for this reason, neck and chest imaging are obtained in typical. Speech abnormalities are nearly universal, manifesting as the evaluation of vocal fold paresis. Systemic neurologic diseases defects in articulation and voicing. Patients may have a hypokinetic that can cause vocal fold paresis are discussed earlier in the chapter; dysarthria (45%), with a reduced range of articulation for lingual vocal fold paresis can also manifest as a peripheral neuropathy in and labial sounds. They may also have decreased loudness, disorders such Charcot-Marie-Tooth disease, sarcoidosis, and Lyme monopitch, and prosodic insufficiency because of poor air presenta- disease. Up to one-third of cases of vocal fold paresis are diagnosed tion to the vocal apparatus (sound generator), which is due to by exclusion as idiopathic. decreased airflow from a bradykinetic bellows mechanism. The Clinically, the patient with vocal fold paresis comes to medical vocal folds may be adynamic and/or bowed. On testing, patients attention with an effortful, weak, breathy, and hoarse voice. Vocal with PD show an increased shimmer and jitter, a decreased fatigue is common, because lack of proper vocal fold closure (glottic harmonic/noise ratio, and a tremor. Less commonly, these patients insufficiency) as a result of paresis requires greater effort to create experience a predominant effect of rigidity of the larynx and produce subglottic pressure against a leaking laryngeal valve. This is a strained voice with frequent breaks, similar to the voice of a especially apparent when a patient makes unfruitful attempts to patient with spasmodic dysphonia. yell; increased subglottic pressure pushes the flaccid and paretic PD may also be accompanied by autonomic nervous system vocal cord even farther away. Dysphagia can also be present from dysfunction or failure of supranuclear functions. The Parkinson-plus glottic insufficiency and sensory deficits. Maximum phonation syndromes include progressive supranuclear palsy and multiple time, measured as the length of time that the patient can phonate system atrophy. In the latter, autonomic nervous system failure is a sustained vowel, is often decreased. accompanied by orthostatic hypotension, impotence, sphincter Vocal fold positioning can vary on examination. Despite prior dysfunction, and anhidrosis. One form of multiple system atrophy characterizations, it is now clear that the traditional terms for is Shy-Drager syndrome. Patients with this disorder have failure vocal fold position—intermediate, paramedian, and cadaveric—do of vocal fold abduction with inspiration that is worse during sleep. not adequately characterize glottic configuration, and the distance Many require tracheotomy for maintenance of the airway, and of the vocal fold from the midline is not a reliable indicator of progression of multiple system atrophy may be rapid and lead lesion site.79 The effect of an isolated superior laryngeal nerve to death.77 lesion on the level of the vocal fold and rotation of the glottis is also controversial. Some writers report rotation of the glottis to the side of the lesion in patients with unilateral cricothyroid muscle Multiple Sclerosis paralysis, although the preponderance of the evidence indicates MS is a diffuse demyelination process with an incidence of that the cricothyroid muscle does not appreciably influence the approximately 3 per 100,000 people in the United States. The spatial orientation of the vocal fold or the glottis as a whole. signs and symptoms are protean but basically consist of relapsing Clinically observed variations in glottal configuration are chiefly and remitting sensory and motor deficits. Visual problems, numb- determined by the extent of the nerve lesion (complete or incom- ness, and limb weakness are common. Up to 50% of patients with plete) and the extent and accuracy of nerve regeneration. Informa- MS have problems that lie within the domain of the otolaryngolo- tion on the cricothyroid joint structure now indicates that the gist. These problems include vertigo, tremor, scanning speech, two cartilages interact in a visor fashion, similar to a bucket handle, and dysphagia.78 The clinical course in some patients is intermittent with little translational movement. Thus, a unilateral cricothyroid and slowly progressive, whereas others experience a rapid and muscle paralysis may decrease the strength of motion along the inexorable decline. Some promising developments have been made arc of rotation but has no differential effect on one vocal fold.80,81 in experimental drug therapy for this disorder. When the cause of vocal fold paresis is not obvious from history, such as recent surgery, further workup, including a detailed medical history and imaging, is needed to rule out other causes. Computed Psychogenic, Malingering, and Mixed Causes tomography of the neck and chest to examine the full course of Psychiatric voice disorders can mimic all of the preceding disorders the recurrent laryngeal nerve is usually indicated. Magnetic reso- and hence are very difficult to distinguish from neurogenic voice nance imaging can be considered when skull base or intracranial disorders. Complete aphonia is most often due to a conversion lesions are suspected. Blood tests such as rheumatoid factor and disorder. antinuclear antibody tests, Lyme titer, and measurement of erythrocyte sedimentation rate are not typically performed unless prompted by the clinical history.82 EMG can assist in estimating Vocal Fold Paresis the potential for recovery and this is discussed in Chapter 56. Vocal fold paresis is most commonly due to injury of the recurrent laryngeal nerve, which results in vocal fold immobility. It may or For a complete list of references, visit ExpertConsult.com. Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  CHAPTER 57 Neurologic Disorders of the Larynx 838.e1 REFERENCES motor nerves by acceptor-mediated endocytosis, J Cell Biol 103:535, 1. Brin MF, Blitzer A, Velickovic M: Movement disorders of the larynx. 1986. 57 In Blitzer A, Brin MF, Ramig LO, editors: Neurologic Disorders of the 31. Simpson LL, DasGupta BR: Botulinum neurotoxin type E: studies Larynx, ed 2, New York, 2009, Thieme. on mechanism of action and on structure-activity relationships, 2. Fahn S: The varied clinical expressions of dystonia, Neurol Clin 2:541, J Pharmacol Exp Ther 224:135, 1983. 1984. 32. Sulica L, Blitzer A: Botulinum toxin treatment of spasmodic dysphonia 3. Jinnah HA, Alberto A: The new classification system for the dystonias: and other laryngeal disorders. In Blitzer A, Brin MF, Ramig LO, editors: why was it needed and how was it developed, Mov Disord Clin Pract Neurologic Disorders of the Larynx, ed 2, New York, 2009, Thieme, 1(4):280–284, 2014. pp 196–203. 4. De Leon D, et al: Genetic factors in spastic dysphonia, Neurology 33. Blitzer A, Brin MF, Stewart CF: Botulinum toxin management of 40(Suppl 1):142, 1990. spasmodic dysphonia: a 12-year experience in more than 900 patients, 5. Ozelius L, Kramer PL, Moskowitz CB, et al: Human gene for torsion Laryngoscope 108:1435, 1998. dystonia located on chromosome 9q32-34, Ann Neurol 27:114, 34. Blitzer A, Brin MF: Botulinum toxin for abductor spasmodic dysphonia. 1990. In Jankovic J, Hallet M, editors: Therapy with botulinum toxin, New 6. Fahn S, Moskowitz C: X-linked recessive dystonia and parkinsonism York, 1994, Marcel-Dekker, pp 451–460. in Filipino males [abstract], Ann Neurol 24:179, 1988. 35. Blitzer A, Brin MF: Botulinum toxin in the management of adductor 7. Kupke KG, Lee LV, Müller U: Assignment of the X-linked torsion and abductor spasmodic dysphonia, Oper Techn Otolaryngol Head Neck dystonia gene to Xq21 by linkage analysis, Neurology 40:1438, 1990. Surg 4:199, 1993. 8. Wilhelmsen KC, Weeks DE, Nygaard TG, et al: Genetic mapping of 36. Blitzer A, Brin MF: Laryngeal dystonia: a series with botulinum toxin the “Lubag” (X-linked dystonia-parkinsonism) in a Filipino kindred to therapy, Ann Otol Rhinol Laryngol 100:85, 1991. the pericentromeric region of the X chromosome, Ann Neurol 29:124, 37. Brin MF, Blitzer A, Fahn S, et al: Adductor laryngeal dystonia (spastic 1991. dysphonia): treatment with local injections of botulinum toxin 9. Nygaard TG, Marsden CD, Fahn S: Dopa-responsive dystonia: long- (BOTOX), Mov Disord 4:287, 1989. term treatment response and prognosis, Neurology 41:174, 1991. 38. Meleca RJ, Hogikyan ND, Bastian RW: A comparison of methods of 10. Bressman SB, de Leon D, Kramer PL, et al: Dystonia in Ashkenazi botulinum toxin injection for abductor spasmodic dysphonia, Otolaryngol Jews: clinical characterization of a founder mutation, Ann Neurol 36:771, Head Neck Surg 117:487, 1997. 1994. 39. Blitzer A, Brin MF, Fahn S, et al: Local injections of botulinum toxin in 11. Fuchs T, Ozelius LJ: Genetics of dystonia, Semin Neurol 31(5):441–448, the treatment of focal laryngeal dystonia (spastic dysphonia), Laryngoscope 2011. 98:193, 1988. 12. Blitzer A, Schwartz JS: Spasmodic dysphonia: evaluation and manage- 40. Blitzer A, Brin MF, Stewart C, et al: Abductor laryngeal dystonia: a ment. In Fried M, Ferlito A, editors: The larynx, ed 3, San Diego, series treated with botulinum toxin, Laryngoscope 102:163, 1992. 2009, Plural Publishing. 41. Tang CG, Novakovic D, Mor N, Blitzer A: Onabotulinum toxin A 13. Traube L: Zur Lehre von den Larynxaffectionen beim Ileotyphus, Berlin, dosage trends over time for adductor spasmodic dysphonia: a 15 year 1871, Verlag von August Hirschwald. experience, Laryngoscope 126(3):678–681, 2016. 14. Fraenkel B: Ueber die Beschaeftigungsschwäche der Stimme: Mogi- 42. Blitzer A, Lovelace RE, Brin MF, et al: Electromyographic findings in phonie, Dtsch Med Wochenschr 13:121, 1887. focal laryngeal dystonia (spastic dysphonia), Ann Otol Rhinol Laryngol 15. Gowers WR: Manual of Diseases of the Nervous System, London, 1899, 94:591, 1985. Churchill. 43. Young N, Blitzer A: Management of supraglottic squeeze in adductor 16. Aronson AE: Clinical voice disorders, New York, 1985, Thieme. spasmodic dysphonia: a new technique, Laryngoscope 117(11):2082–2084, 17. Blitzer A, Brin MF, Simonyan K, et al: Phenomenology, genetics, and 2007. CNS network abnormalities in laryngeal dystonia: a 30-year experience, 44. Rondot P, Ben Hamida M: Myoclonus of the velum and skeletal Laryngoscope 128:S1–S9, 2018. myoclonus: clinical and anatomical study [in French], Rev Neurol (Paris) 18. Brin MF: Dystonia: genetics and treatment with botulinum toxin. 119:59, 1968. In Smith B, Adelman G, editors: Neuroscience year; supplement 3 to the 45. Williams A, Goodenberger D, Calne DB: Palatal myoclonus following encyclopedia of neuroscience, Boston, 1992, Birkhauser, pp 56–58. herpes zoster ameliorated by 5-hydroxytryptophan and carbidopa, 19. Dedo HH, Izdebski K: Intermediate results of 306 recurrent laryngeal Neurology 28:358, 1978. nerve sections for spastic dysphonia, Laryngoscope 93:9, 1983. 46. Sakai T, Murakami S: Palatal myoclonus responding to carbamazepine 20. Aronson AE, DeSanto LW: Adductor spastic dysphonia: three (letter), Ann Neurol 9:199, 1981. years after recurrent laryngeal nerve resection, Laryngoscope 93:1, 47. Gauthier S, Young SN, Baxter DW: Palatal myoclonus associated with 1983. a decrease in 5-hydroxy-indole acetic acid in cerebrospinal fluid and 21. Mendelsohn AH, Berke GS: Surgery or botulinum toxin for adductor responding to clonazepam, Can J Neurol Sci 8:51, 1981. spasmodic dysphonia: a comparative study, Ann Otol Rhinol Laryngol 48. Jankovic J, Pardo R: Segmental myoclonus: clinical and pharmacologic 121(4):231–238, 2012. study, Ann Neurol 43:1025, 1986. 22. Blitzer A, Brin MF, Stewart CF: Botulinum toxin management of 49. Jabbari B, Rosenberg M, Scherokman B, et al: Effectiveness of spasmodic dysphonia (laryngeal dystonia): a 12 year experience in trihexyphenidyl against pendular nystagmus and palatal myoclonus: more than 900 patients, Laryngoscope 125(8):1751–1757, 2015. evidence of cholinergic dysfunction, Mov Disord 2:93, 1987. 23. Simpson LL: Molecular pharmacology of botulinum toxin and tetanus 50. Jabbari B, Scherokman B, Gunderson CH, et al: Treatment of movement toxin, Annu Rev Pharmacol Toxicol 26:427, 1986. disorders with trihexyphenidyl, Mov Disord 4:202, 1989. 24. Simpson LL: The origin, structure, and pharmacological activity of 51. Hallett M: Tremor: pathophysiology, Parkinsonism Relat Disord 20(Suppl botulinum toxin, Pharmacol Rev 33:155, 1981. 1):S118–S122, 2014. 25. Evans GM, Williams RS, Shone CC, et al: Botulinum type B: its 52. Bhatia KP, Bain P, Bajaj N, et al: Consensus statement on the classifica- purification, radioiodination and interaction with rat-brain synaptosomal tion of tremors, from the task force on tremor of the International membranes, Eur J Biochem 154:409, 1986. Parkinson and Movement Disorder Society, Mov Disord 33(1):75–87, 26. Kozaki S: Interaction of botulinum type A, B, and E derivative toxins 2018. with synaptosomes of rat brain, Naunyn Schmiedebergs Arch Pharmacol 53. Marshall J: Observations on essential tremor, J Neurol Neurosurg 308:67, 1979. Psychiatry 25:122, 1986. 27. Kozaki S, Sakaguchi G: Binding to mouse brain synaptosomes of 54. Findley LJ: The pharmacology of essential tremor. In Marsden CD, Clostridium botulinum type E derivative toxin before and after tryptic Fahn S, editors: Movement disorders, ed 2, London, 1987, Butterworths, activation, Toxicon 20:841, 1982. pp 438–458. 28. Williams RS, Tse CK, Dolly JO, et al: Radioiodination of botulinum 55. Koller WC, Busenbark K, Miner K: The relationship of essential neurotoxin type A with retention of biological activity and its binding tremor to other movement disorders: report on 678 patients. Essential to brain synaptosomes, Eur J Biochem 131:437, 1983. Tremor Study Group, Ann Neurol 35:717, 1994. 29. Peck MW, et al: Historical perspectives and guidelines for botulinum 56. Lebrun Y, Devreux F, Rousseau JJ, et al: Tremulous speech: a case neurotoxin subtype nomenclature, Toxins (Basel) 9(1):38, 2017. report, Folia Phoniatr (Basel) 34:134, 1982. 30. Black JD, Dolly JO: Interaction of 125I-labeled botulinum neurotoxins 57. Massey EW, Paulson GW: Essential vocal tremor: clinical characteristics with nerve terminals II: autoradiographic evidence for its uptake into and response to therapy, South Med J 78:316, 1985. Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 838.e2 PART V Laryngology and Bronchoesophagology 58. Brin MF, Blitzer A, Stewart C: Vocal tremor. In Findley LJ, Koller WC, 71. Brin MF, Stewart C, Blitzer A, Diamond B: Laryngeal botulinum toxin editors: Handbook of tremor disorders, New York, 1994, Marcel-Dekker, injections for disabling stuttering in adults, Neurology 44(12):2262–2266, pp 495–520. 1994. 59. Brown JR, Simonson J: Organic voice tremor: a tremor of phonation, 72. Kalinowski J: Self-reported efficacy of an all in-the-ear-canal prosthetic Neurology 13:520, 1963. device to inhibit stuttering during one hundred hours of university 60. Hartman DE, Overholt SL, Vishwanat B: A case of vocal cord nodules teaching: an autobiographical clinical commentary, Disabil Rehabil masking essential (voice) tremor, Arch Otolaryngol Head Neck Surg 25:107–111, 2003. 108:52, 1982. 73. Stuart A, Kalinowski J, Rastatter M, et al: Investigations of the impact 61. Tomoda H, Shibasaki H, Kuroda Y, et al: Voice tremor: dysregulation of altered auditory feedback in-the-ear devices on the speech of people of voluntary expiratory muscles, Neurology 69–100, 1987. who stutter, Int J Lang Commun Disord 39:93–113, 2004. 62. Zesiewicz TA, Elble RJ, Louis ED, et al: Evidence based guideline 74. Younger DS: Neuromuscular disorders of the larynx. In Blitzer A, update: treatment of essential tremor: report of the Quality Standards Brin MF, Ramig LO, editors: Neurologic Disorders of the Larynx, ed 2, subcommittee of the American Academy of Neurology, Neurology New York, 2009, Thieme. 77(19):1752–1755, 2011. 75. Rubin AD, Griffin GR, Hogikyan ND, Feldman EL: A new member 63. Gurey LE, Sinclair CF, Blitzer A: A new paradigm for the manage- of the multidisciplinary ALS team: the otolaryngologist, Amyotroph ment of essential vocal tremor with botulinum toxin, Laryngoscope Lateral Scler 13(2):229–232, 2012. 123:2497–2501, 2013. 76. Postuma RB, Berg D, Stern M, et al: MDS clinical diagnosis criteria 64. Webster RL: Empirical considerations regarding stuttering therapy. In for Parkinson’s disease, Mov Disord 30(12):1591–1601, 2015. Gregory HH, editor: Controversies about stuttering therapy, Baltimore, 77. Lim YS, Kennedy NJ: Multiple system atrophy as a cause of upper 1979, University Park Press. airway obstruction, Anaesthesia 62:1179–1182, 2007. 65. Prins D: Personality, stuttering severity, and age, J Speech Hear Res 78. Woodson G: Management of neurologic disorders of the larynx, Ann 15:148, 1972. Otol Rhinol Laryngol 117(5):317–326, 2008. 66. Riley GD: A stuttering severity instrument for children and adults, 79. Sulica L, Blitzer A, editors: Vocal fold paralysis, New York, 2006, Springer. J Speech Hear Disord 37:314, 1972. 80. Pei YC, Fang TJ, Li HY, Wong AM: Cricothyroid muscle dysfunction 67. Smith A, Luschei E, Denny M, et al: Spectral analysis of activity impairs vocal fold vibration in unilateral vocal fold paralysis, Laryngoscope of laryngeal and orofacial muscles in stutterers, J Neurol Neurosurg 124(1):201–206, 2014. Psychiatry 56:1303, 1993. 81. Koufman JA, Walker FO, Joharji GM: The cricothyroid muscle does 68. Sveinbjornsdottir S, Pakkenberg H, Werdelin L: Developmental not influence vocal fold position in laryngeal paralysis, Laryngoscope stuttering followed by intermittent jaw opening dystonia, Mov Disord 105(4):368–372, 1995. 8:396, 1993. 82. Merati AL, Halum SL, et al: Diagnostic Testing for vocal fold paralysis: 69. Miller S, Watson BC: The relationship between communication attitude, survey of practice and evidence-based medicine review, Laryngoscope anxiety, and depression in stutterers and non-stutterers, J Speech Hear 116:2006, 1539. Res 35:789, 1994. 70. Stager SV, Ludlow CL, Gordon CT, et al: Fluency changes in persons who stutter following a double blind trial of clomipramine and desipramine, J Speech Hear Res 38:516, 1995. Downloaded for Andrea Trigueros ([email protected]) at Francisco Marroquín University from ClinicalKey.com by Elsevier on December 02, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.