Neurogenic
Disorders of Mouth and Pharynx
The motor innervation to the pharynx and almost
all of the sensory supply is through the pharyngeal plexus, which is formed by
branches of cranial nerves IX and X. Disturbances to the neural conduction of
both of these cranial nerves will be reviewed together because anatomically and
functionally there is considerable overlap in their conductive patterns.
Normally, the uvula hangs
in midposition, and in case of a unilateral paralysis, it deviates to
the healthy side. This can be demonstrated when the patient utters “A-AH.” In
bilateral, peripheral, or nuclear (bulbar) palsy, the uvula does not move at
all on attempted phonation or reflex stimulation. On the other hand, in
supranuclear (pseudobulbar) palsy, the lower motor neuron reflex is preserved,
and the uvula will move on tickling or stimulation with a tongue depressor, but
it will not move on willful effort. The loss of pharyngeal reflex can be tested
by irritation with a tongue depressor. Deglutition can be examined by having
the patient swallow a few mouthfuls of water and observing the upward excursion
of the larynx. In paralysis of the soft palate, nasal regurgitation or
spasmodic coughing is noted because the fluid is propelled into the nasal
cavity, which is incompletely closed during the act of swallowing (nasal
regurgitation). Nasal and palatal speech, aphonia and dyspnea, and
difficulty in swallowing are the essential signs of a vagus paralysis. Because vagal
paralysis leaves the superior pharyngeal constrictor muscle without
innervation, retention of barium and distention of the involved piriform fossa
can be demonstrated with a modified barium swallow. Further-more, it is
possible to observe pooling of the saliva in the postcricoid region and in the
involved piriform fossa by mirror laryngoscopy or during a fiberoptic
endoscopic evaluation of swallowing. The vagal paralysis may be peripheral, as
in a postdiphtheritic condition or from a surgical resection; it may be part of
a jugular foramen syndrome; or it may have an intracranial origin, as occurs in
amyotrophic sclerosis, thrombosis of the posterior inferior cerebellar artery,
syringomyelia, or true bulbar palsy. Paralysis may also result from
supranuclear involvement (upper motor neuron), as seen usually in multiple
vascular lesions producing so-called pseudobulbar paralysis. Normally, the
tongue, which is innervated by the 12th hypoglossal nerve, can protrude
far out in the midline. In unilateral paralysis of this nerve, the
tongue deviates to the paralyzed side. In complete bilateral paralysis. the
tongue cannot protrude at all and lies flat in the mouth. Unilateral or
bilateral paralysis may be associated with atrophy and fibrillation, both
indicative of peripheral involvement. Articulation, except for the
pronunciation of labials, is impaired. In vagal paralysis the recurrent
laryngeal nerve on the same side is always involved. This produces hoarseness
owing to fixation of the vocal fold. In bilateral paralysis, the fold’s
extrinsic pressure most often assumes the cadaveric position or may become
fixed in the midline, producing dyspnea and requiring emergency tracheotomy.
Recurrent laryngeal nerve paralysis is most often attributed to surgical
trauma, extrinsic compression from enlarged lymph nodes, and local spreading of
regional cancers.
