GAYLE E. WOODSON, MD
 Neurologic
dysfunction of the larynx is difficult to diagnose, even when it is part
of a generalized disease process. A major reason for this is that patients
with symptoms of laryngeal dysfunction are more likely to present to otolaryngologists
than to neurologists. Otolaryngology training in physical diagnosis emphasizes
anatomic inspection rather than functional evaluation. Thus, otolaryngologists
may not detect key neurologic signs and symptoms. Neurologists are also
prone to miss the diagnosis. Although neurologists do focus on functional
assessment, they generally lack the equipment and techniques for observing
the larynx and pharynx. When no organic cause for the symptoms can be found,
it is commonly assumed that the patient has a functional or psychogenic
problem. Some patients may even receive well-intentioned but ineffective
psychotherapy.
There is often no effective treatment for neurogenic laryngeal dysfunction.
For example, amyotrophic lateral sclerosis (ALS) is a relentlessly progressive
disease. In some disorders, such as myasthenia gravis, treatment can provide
substantial improvement. But no matter how limited the therapeutic options,
a patient's best interests are served by an accurate diagnosis and a realistic
prognosis.
To detect neurologic dysfunction of the larynx, the clinician must be
aware of this possibility and familiar with the salient signs and symptoms
of specific disorders and lesion sites. Neurologic dysfunction should be
considered in the differential diagnosis whenever a patient has symptoms
of upper airway dysfunction that cannot be explained by anatomic evaluation.
Neurogenic dysfunction may also coexist with morphological disorders, or
even be responsible for the genesis of anatomic lesions. This lecture will
review the salient features of the several neurologic disorders, and present
a systematic clinical approach to their detection.
It is not practical for an otolaryngologist to be familiar with all of
the pathological processes that disrupt laryngeal function. But a conceptual
framework based on the site of lesion can encompass the most frequently
encountered problems.
The cerebral cortex is susceptible to damage from strokes, tumors, and
trauma. The cortical areas that project to the larynx are diffuse, and
each side is controlled bilaterally. Therefore, lesions of the cortex do
not produce laryngeal paralysis. Instead, characteristic signs include
aphasia or speech apraxia. Sometimes, transient sustained abduction of
the vocal folds is observed after diffuse emboli. In other cases, the vocal
folds adduct instead of abducting during inspiration, and the result is
stridor.
Extrapyramidal system lesions are characteristically manifested by abnormal
motor control, including rigidity, tremor, or intermittent spasm. The best
known extrapyramidal disorder is parkinsonism, with cogwheel rigidity,
resting tremor, and shuffling gait. The laryngeal manifestations of parkinsonism
can be similar to the manifestations of limb involvement, with a strained
and strangled voice due to laryngeal rigidity and spasm. Conversely, the
larynx may be affected by paucity of motion, with vocal muscle atrophy
that results in a breathy voice. Spasmodic dysphonia is widely regarded
as an extrapyramidal disorder, with vocal strain, voice arrests, and pitch
breaks due to involuntary muscle contractions. Tremor and muscle spasms
are frequently not isolated to the larynx, but may also involve the palate
and pharynx. Some patients have a regional dystonia, with associated blepharospasm,
torticollis, oromandibular involvement, or facial grimacing.
Cerebellar lesions impair motor coordination, and usually
present as problems with balance or gait. The classic speech disturbance
associated with cerebellar pathology is "scanning speech." However,
the dysarthria involves both ataxic and spastic components. (l) Many
patients present with vocal strain due to excessive glottal closure. The
speech may similar to that of spasmodic dysphonia but with sustained, rather
than intermittent spasms. With disease progression, speech becomes slurred
and unintelligible.
Brain stem lesions can produce flaccid paralysis of the larynx, manifested
by a breathy voice and aspiration during swallowing. Such nuclear paralysis
is invariably associated with other motor signs, such as pharyngeal or
tongue weakness. Isolated laryngeal paralysis at this level is extremely
unlikely, because other motor neurons are in such close proximity.
Peripheral nerve injury results in more focal paralysis and paresis. In
recent years, it has become apparent that complete recurrent laryngeal
nerve paralysis is uncommon. Partial lesions are frequent. Additionally,
the recurrent laryngeal nerve has a very strong propensity for regeneration,
although reinnervation rarely results in normal involvement.
It is important for otolaryngologists to be familiar with the clinical
presentation of several neurologic diseases that can affect the larynx.
In some disorders, the initial impairment is frequently localized to the
head and neck region, so that the initial presentation is to an otolaryngologist.
The otolaryngologist may also be consulted when a patient with a known
neurologic problem develops laryngeal symptoms. Familiarity with the diseases
will permit the otolaryngologist to evaluate such patients more efficiently.
An expected manifestation is easier to detect, even when subtle. Sometimes,
the laryngeal problem is due to another disorder, unrelated to the neurologic
disease.
Multiple sclerosis is a progressive demyelinating disease that causes
fluctuating sensory and motor disturbances, primarily visual disturbances,
vertigo, tremor, limb weakness, and paresthesias. Speech and voice may
be significantly impaired by cerebellar involvement. Muscle weakness affects
swallowing.
Poliomyelitis is virtually never seen in clinical practice
today, because of the effectiveness of immunization. However, the postpolio
syndrome occurs in long-term survivors of acute poliomyelitis. (2) Progressive
weakness occurs, and is probably due to the inevitable loss of motor neurons
with aging. Acute poliomyelitis destroys motor neurons. Survivors function
with residual neurons that have sprouted to supply very large motor units.
Thus, loss of even a few motor neurons with aging can have very significant
functional impact. Bulbar poliomyelitis affects pharyngeal and laryngeal
muscles, causing hoarseness, dysphagia, and aspiration. Management of these
patients depends on identification of the specific functional defect. For
example, a patient with dysphagia may have insufficient pharyngeal strength
to propel the bolus, inadequate laryngeal elevation to open the upper esophageal
sphincter, and/or cricopharyngeal dysfunction, due to fibrosis or excess
muscle tone.
Pseudobulbar palsy is characterized by spasticity and hyperreflexia of
the pharynx, palate, lips, tongue, and larynx. Patients have thick, slurred
speech, dysarthria, and hypernasality. Dysphagia is mild to moderate, since
there is not a complete paralysis, but often includes nasopharyngeal reflux.
Spastic paresis of the jaw muscles is often present. A characteristic feature
of the disorder is emotional lability, with sudden and inappropriate laughing
or crying. Cognitive impairment is sometimes noted. Jaw, snout, and sucking
reflexes are brisk. The syndrome is caused by bilateral lesions of the
suprasegmental pathways as they descend into the bulbar nuclei. Damage
may be secondary to stroke, encephalitis, multiple sclerosis, or neoplasm.
Amyotrophic lateral sclerosis involves progression degeneration
of both upper and lower motor neurons, with muscle wasting and fasciculations.
Physical signs include muscle weakness, as well as difficulty in making
repetitive motions or rapid motor adjustments. Symmetric facial weakness
with preservation of ocular muscles is a common presentation that helps
to differentiate these patients from those with myasthenia gravis. In some
ALS patients, limb muscle involvement predominates, while others have more
cranial nerve involvement. As many as 25% of ALS patients initially present
with complaints related to speech and swallowing. The voice has a characteristic
change in resonance due to hypernasality. The speech is slurred, with poor
vowel and consonant definition and velopharyngeal incompetence. (3) Muscle
fasciculations are most easily observed in the tongue, classically described
as having the appearance of a "bag of worms."
The management of upper aerodigestive tract involvement in ALS is essentially
palliative and supportive. A palatal lift prosthesis is sometimes helpful
in improving articulation and in diminishing nasopharyngeal regurgitation
during swallowing. Nasogastric feeding is eventually required in most patients,
for both nutritional support and prevention of aspiration pneumonia. Tracheotomy
is often indicated, for pulmonary toilet, to decrease upper airway resistance
and respiratory dead space, or to permit mechanical ventilation. Death
from ALS usually results from Palatal myoclonus causes rhythmic 1- to 2-Hz
contractions of the soft palate, larynx, and pharynx.
When it was originally described, only the palate contractions, the tip
of the iceberg, were clinically appreciated; hence, the clinical term only
reflects involvement of the soft palate. Since the advent of flexible laryngoscopy,
it is easy to observe the motor function of the entire aerodigestive tract,
and the abnormal motion of the larynx and pharynx are also appreciated.
The presenting symptoms are primarily related to speech and voice problems.
The voice may be disrupted rhythmically by the spasms. Other patients may
sound as though they have spasmodic dysphonia, because of excessive compensatory
muscle contraction. Some patients note rhythmic clicking in the ears, which
is often audible to others. This is due to opening of the eustachian tube
by the contractions in the tensor veli palatini. There is rhythmic jerking
of the vocal folds, in synchrony with the palate motion.
Palatal myoclonus is virtually always the result of a
specific lesion in the central tegmental tract, involving the "Guillain-Mollaret
triangle" (dentate nucleus of the cerebellum, the red nucleus, and
the inferior olivary nucleus). Enlargement of the inferior olivary nucleus
in the medulla may be seen on magnetic resonance imaging. (4)
The presence of the syndrome indicates that the patient has had a stroke,
even if there is no other historical or physical evidence to support the
diagnosis. Therefore, all patients with palatal myoclonus should be evaluated
and treated to prevent future strokes. (5)
Parkinsonism is usually recognized because of its classic presentation:
resting tremor, bradykinesia, "cogwheel" rigidity, flat facial
expression, and shuffling gait. The specific definition of parkinsonism
is any combination of tremor at rest, rigidity, bradykinesia, and loss
of postural reflexes. (6) ln some patients, the bradykinesia
profoundly affects speech, with sluggish articulation. The voice sounds
breathy and flat because of diminished laryngeal muscle activity and atrophic
vocal folds. In other patients, laryngeal muscle rigidity predominates,
and the voice sounds tight and strained, as in spasmodic dysphonia. In
either situation, tremor can cause vocal instability. Dysphagia is not
a common presenting problem, although patients may drool because of decreased
voluntary swallowing. With progression of disease and generalized weakness,
swallowing ultimately becomes more of a problem.
Parkinsonism may be primary and idiopathic, or secondary
to stroke, drug effects, or encephalitis. The responsible lesion is in
the substantia nigra. Multiple system atrophy (MSA) encompasses a cluster
of degenerative neurologic disorders, previously referred to as Shy-Drager
syndrome, olivopontocerebellar atrophy, and striatonigral degeneration.
Shy-Drager syndrome consists of progressive autonomic nervous system failure,
with Parkinson's disease-like symptoms and orthostatic hypotension. Other
autonomic symptoms include impotence, anhidrosis, and sphincter dysfunction.
Some MSA patients, particularly those with the Shy-Drager variant of the
disorder, have stridor due to impaired abduction of the vocal folds. Histologic
analysis indicates that muscles are atrophic, but not denervated, indicating
that the responsible lesion is supranuclear. (7) An early
sign of vocal fold abductor weakness in MSA is nocturnal inspiratory stridor
during sleep, which appears to be due to inappropriate active adduction
during inspiration, and not merely failure of abduction. (8)
Essential tremor is a common problem, with oscillatory movements that
cause shaking of the hands, head, and/or voice. Tremor can be observed
in the larynx, pharynx, and soft palate, and sometimes the cervical strap
muscles. In contrast to the resting tremor of parkinsonism, essential tremor
is an action tremor. Essential tremor is a postural tremor of slower frequency
than physiological tremor and can disrupt motor tasks. (9) It
is exacerbated by emotional stress and improves with drinking alcohol.
It is a familial disorder, with onset in adult life. Vocal tremor occurs
in 10% to 20% of patients with essential tremor, and is sometimes the first
or only sign of the disease. (10) Examination of the
larynx may reveal rhythmic abduction and adduction of the vocal folds or
vertical motion of the larynx. There is frequently associated tremor of
the palate or pharyngeal walls.
Dystonia consists of uncontrolled muscle contractions
that cause involuntary movements or posture. It may be diffuse, involving
muscles throughout the body, or localized to a specific region or muscle
group (segmental). (11) Writer's cramp is a segmental
dystonia that involves the arm and hand, and is taskspecific. Torticollis
affects several muscles to cause a "wry" neck posture. Blepharospasm
may occur as a focal dystonia of the eyelid muscles or as a component of
Meige's syndrome, which affects the head and neck region. Spasmodic dysphonia
is generally considered to be a focal dystonia of the larynx. It may occur
in isolation, in association with other regional dystonias, or as part
of systemic dystonia. Laryngeal Generalized dystonia is a familial disorder,
and so are some focal dystonias. Focal dystonia can also be secondary to
stroke, head injury, or drug toxicity.
Myasthenia gravis is a defect of the neuromuscular junction, presenting
as easy fatigue with muscle use. The ocular muscles are most commonly involved,
but many patients manifest complaints related to the throat, such as hoarseness,
dysarthria, dysphagia, aspiration, or stridor. Occasionally, laryngeal
involvement is the presenting complaint. (12) Weakness
of vocal fold abductors can cause acute respiratory failure. (13) The
cardinal physical sign of myasthenia gravis is fatigue with repetitive
movements. Fatigue of laryngeal and pharyngeal muscles with repetitive
motion is best documented by flexible endoscopy. Electromyography (EMG)
and/or administration of edrophonium chloride (Tensilon) are useful diagnostic
tests.
The history-taking should be thorough, with the patient questioned carefully
about specific signs and symptoms that may indicate neurologic dysfunction.
If a patient with hoarseness also complains of dysphagia or drooling, then
a neurogenic cause is quite likely. Sometimes, a patient who complains
of hoarseness actually has a speech or resonance problem, such as dysarthria,
stuttering, speech apraxia, aphasia, or hypernasality. Such problems reflect
defects in motor control, not laryngeal disease. Vocal fatigue most commonly
results from swelling of the larynx with prolonged voice use; however,
fatigue that develops rapidly with normal voice use may be due to a motor
end plate disorder, eg, myasthenia gravis.
The past medical history is important. Laryngeal symptoms may be additional
manifestations of a previously diagnosed neurologic disorder. Previous
medications or trauma may also be implicated. A family history is also
important. Some rare disorders, such as Huntington's chorea, are inherited.
On the other hand, essential tremor, which is a common and generally benign
disorder, is also familial.
The review of systems should identify possible signs of neurogenic dysfunction
in other parts of the body. These include numbness or weakness of the limbs,
tremor, gait or balance disturbances, and visual problems.
A systematic physical examination is important, including evaluation of
cranial nerve function. Sensory deficits and altered reflexes of the larynx
and pharynx are difficult to assess. Therefore, functional evaluation focuses
chiefly on motor function, with laryngeal and pharyngeal movements observed
during a range of activities. This is best accomplished by using fiberoptic
endoscopy. Much useful information can also be gained by listening carefully
to the voice and speech of the patient and paying attention to the pattern
of breathing during speech.
Altered vocal resonance, such as hypernasality or a "hot potato" voice,
may be a sign of impaired motor function. Hypernasality and nasal emissions
during speech reflect incompetence of the soft palate. A "hot potato" voice
and indistinct vowels result from impaired motion of the pharynx and/or
base of the tongue.
Acquired speech impairment in adults virtually always indicates a neurologic
problem. Dysarthria may range from slurring of speech to imprecise consonants
to completely incomprehensible speech. Fluency problems include stuttering,
stammering, and aphasia. Sometimes, a patient knows what he or she wants
to say, but either cannot get the words out, or says the wrong thing. These
symptoms
are frequently misdiagnosed as hoarseness. It is not easy to deduce neural disease by listening
to vocal quality. There are various mechanisms by which neurologic dysfunction
can impair phonation, and the resultant vocal defects are often indistinguishable
from those caused by inflammation or a mass lesion. For example, laryngeal
paralysis impairs glottic competence, leading to a breathy voice. But the
same voice can result from atrophy of laryngeal muscles, upper motor neuron
lesions, or any disorder that impairs closure of the glottis, such as tumor
or posterior glottic edema. Focal dystonia of the larynx is manifested
by a strained or strangled voice, often clinically indistinguishable from
that of a patient with parkinsonism, Huntington's chorea, or even psychogenic
dysphonia. (14)
Neural lesions can directly or indirectly alter the breathing pattern
during speech. When the glottis is incompetent, much air is wasted during
speech. The patient must pause frequently to inspire enough air. However,
patients with central dysfunction often have impairment of coordination
of breathing with speech. They may stop to take a breath at frequent intervals
in the middle of phrases or sentences when there is more than sufficient
air in the lungs.
After observation of the patient during speech, the motor function of
the upper aerodigestive tract should be systematically evaluated. It is
helpful to follow a systematic protocol, beginning with the lips, the tongue,
and the palate, and then moving on to the pharynx and larynx. At each level,
one should evaluate symmetry and abnormal movements, at rest and during
a range of activity.
Central control of the lips and tongue can be assessed during repetition
of the syllables "pa," "ta," and "ga." "Pa" involves
lip motion, while "ta" and "ga" invoke motion of the
tip and base of the tongue, respectively. A normal patient can maintain
a regular, fairly rapid rhythm. An upper motor neuron lesion decreases
the rate at which the syllable can be repeated, while a cerebellar lesion
will impair rhythm. A lower motor neuron lesion decreases the strength.
In myasthenia, the motion initially appears normal, but rapidly fatigues.
Traditionally, palate function is assessed by looking into the mouth while
the patient says "ah." The palate should rise symmetrically,
with the uvula remaining in the midline. In a unilateral weakness, the
uvula should deviate away from the affected side. But thorough evaluation
of the palate requires assessment from above with a flexible nasopharyngoscope.
Sometimes, a palate that appears totally paralyzed when viewed from the
mouth will exhibit significant motion when viewed from above. This is because
when the patient's mouth is open, articulation is limited to "ah." Flexible
endoscopy permits observation during other behavior, including swallowing
and utterances that require palate closure, such as "kitty cat" and "she." Further,
the completeness of velopharyngeal closure is most accurately assessed
from above. The palate should be observed during rapid repetitive motion,
such as utterance of "kitty-cat, kitty-cat..." to assess rate,
rhythm, and fatigue.
Advancing the tip of the endoscope just past the soft palate permits assessment
of the pharynx and base of the tongue. Pooling of secretions may result
from either sensory or motor impairment. Motion is assessed by asking the
patient to alternately utter "ee" and "ah," which should
result in forward and backward motions of the base of the tongue, as well
as slight constriction and relaxation of the pharynx. It is difficult to
assess strength in this area, as strong contraction, as during a swallow,
results in obliteration of the image. However, if one side of the pharynx
is completely flaccid, it remains patulous during a swallow, so that the
lumen may still be visible.
The larynx has a much larger repertoire of motion. The vocal folds abduct
with inspiration and adduct with expiration. The degree of motion depends
on the respiratory demand and the level of consciousness. With extreme
respiratory demand, inspiratory abduction persists into early expiration,
facilitating the outflow of air. During panting (maximal voluntary ventilation),
the vocal folds are maintained in a widely abducted position. The vocal
folds should adduct lightly for phonation. During a Valsalva maneuver or
the compressive phase of a cough, adduction is vigorous and includes supraglottic
constriction. Just before a cough, the vocal folds open widely. For a voluntary
cough, the degree of abduction varies with the intended force of the cough.
The vocal folds then close tightly for compression, and spring open widely
for expulsion. A voluntary cough is a very good means of assessing laryngeal
motion, since it generally recruits maximal motion, even in hysterical
aphonia patients who have limited phonatory adduction.
Vocal fold motion impairment is often difficult to accurately characterize.
Video recording permits evaluation of slow motion and permits repeated
viewing, which enhances accuracy. Complete laryngeal paralysis is much
less common than paresis. Careful viewing of an apparently immobile vocal
fold often reveals subtle arytenoid motion or spasmodic twitching. Conversely,
repetitive phonation may reveal subtle unilateral weakness in a larynx
that appears to move normally with breathing and sustained phonation. Paradoxical
motion resulting from inspiratory adduction can be difficult to distinguish
from bilateral vocal fold immobility. Such paradoxical motion may be neurogenic,
functional, or psychogenic.
Stroboscopy is useful for detecting subtle lesions of the vocal fold,
such as scarring, small cysts, or sulci. Thus, its role in the evaluation
of suspected neurogenic dysphonia is to rule out local anatomic causes
of hoarseness, not specifically to detect any neurologic signs.
Cineradiography is helpful in elucidating upper aerodigestive tract function.
The most common application is in the modified barium swallow study, wherein
a trained speech pathologist and a radiologist collaborate. The patient
swallows boluses of varying volume and consistency while swallowing function
is carefully observed. The test is useful in detecting and documenting
aspiration and identifying specific mechanisms of dysphagia. Cineradiography
is also used to study motion of the soft palate.
In patients with vocal fold immobility, laryngeal EMG may be helpful in
differentiating between joint fixation and nerve paralysis. Unfortunately,
EMG findings are often normal in a paralyzed vocal fold, either because
of an incomplete nerve lesion or because of partial regeneration of the
nerve. Such immobility in the presence of motor innervation has been attributed
to synkinesis, with misdirection of regenerated motor nerve fibers to the
wrong muscles. It is theorized that motor fibers distribute randomly, so
that intended activation simultaneously activates opposing muscles, abductor
and adductor. The muscle forces would then cancel each other out, resulting
in no net motion. This explanation is not entirely satisfactory, since
it would be quite a coincidence for the muscles to cancel each other out
so precisely. Nevertheless, synkinesis has been detected in paralyzed larynges,
evidenced by inappropriate EMG activation, and therefore must play some
role in the phenomenon. In any case, normal laryngeal EMG findings do not
rule out neural paralysis, and abnormal EMG findings do not rule out the
possibility of joint ankylosis. Hence, EMG is only one piece of evidence,
and the definitive determination requires palpation during direct laryngoscopy.
Electromyography provides some prognostic information in cases of laryngeal
paralysis. Total electrical silence indicates a complete nerve transection.
Fibrillation potentials are not often detected in laryngeal muscle, but
when present, clearly indicate denervation of 2 or more weeks in duration.
In either situation, there is a very poor prognosis for recovery of any
useful function. Electromyography can also detect evidence of reinnervation
(polyphasic action potentials), but cannot determine whether the reinnervation
is recent, remote, or still in progress.
Evoked EMG can be used to test for myasthenia gravis.
Decreasing amplitude of muscle activity with repetitive stimulation supports
this diagnosis, particularly when such fatigue is prevented by the administration
of edrophonium. Of course, one can also observe a repetitive voluntary
motor act before and after administration of edrophonium, but the use of
EMG provides an objective measure and record.
Sensory testing in the larynx is difficult, because the area is not accessible
to standard methods of tactile stimulation, such as light touch or pin-prick.
One can use the tip of the flexible scope to touch the epiglottis or larynx,
and normally this touch should cause a brisk gag or cough. A more sensitive
and quantitative test has been developed, using standardized puffs of air
delivered via the suction port of a flexible scope. The threshold for patient
awareness of sensation and the threshold for an observed laryngeal adductor
response can be compared to age-matched control data. (15)
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