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glossopharyngeal or vagus cranial nerves, and because of the rapid onset, the neurological damage
is prob ably vascular in origin. As often happens when neurologists cannot pinpoint the site of the
lesion, “possibly psychogenic in origin” is also stated.
You enter the patient’s room and greet him. Mr. Manterolla is sitting on the side of the bed.
He has a suction tube in his right hand and a towel folded on his lap. He returns your greeting
articulately and with no indications of dysarthria. His voice quality is normal; in fact, his voice
is strong and resonant. When he walks to the dresser to replace the towel, he moves normally.
You ask several general questions and then ask him to explain what brought him to the intensive
care unit.
He describes yesterday’s medical emergency in vivid detail. He was working in his garden early
in the morning to avoid the midday heat. He had just dug several holes and planted potatoes. At
about 8:30 a.m., he noticed drool escaping from his mouth and could not seem to swallow. (At
this point, he places the suction tube in his mouth, removes the accumulated liquid, and wipes his
chin with the towel.) He tried several times to swallow and realized that something was wrong.
He drove himself to the hospital, was promptly admitted, and has since been examined, probed,
scanned, and evaluated. He spent a sleepless night suctioning and wiping liquid from his mouth.
No one in the hospital would take the time to tell him what was wrong, and he was getting very
frustrated.
You explain that a firm diagnosis has yet to be made. In addition, you describe your role in the
diagnostic pro cesses and explain that therapies exist to help him regain the ability to swallow. You
also note that his isolated swallowing disorder is unusual.
The clinical/bedside screening reveals nothing remarkable about the oral intake and
transportation stages of his swallow. Mr. Manterolla accepts ice chips and creates a bolus. There is
good lip seal and mastication, and his dentition is unremarkable. There is no apparent pocketing
in his cheeks. Tongue mobility and sensation are normal. He has no difficulty propelling the bolus
along the palatal vault. Salivation is adequate to lubricate the bolus.
At the pharyngeal and esophageal- laryngeal levels there is no gag ref lex, and possibly mild
sensory deficits to the base of the tongue and posterior pharyngeal wall. However, no firm
determination of sensation can be made due to the patient’s inconsistent responses. He cannot
initiate a swallow voluntarily or automatically, and there is no laryngeal elevation or apparent
velopharyngeal closure. He has no concurrent motor speech disorders and no indications of
apraxia of speech or the dysarthrias. His speech musculature shows no signs of f laccidity,
spasticity, ataxia, hyperkinesis, or hypokinesia. At the conclusion of the clinical/bedside
evaluation, the neurologist enters and beckons you to the nurses’ station. Apparently, she wants
to discuss Mr. Manterolla’s case.
The neurologist is as perplexed about Mr. Manterolla’s dysphagia as you are and explores
several neurological possibilities. Lower motor neuron damage is ruled out because, as it is the final
common pathway for motor movements, there would likely be accompanying f laccid paralysis or
paresis. You confirm that there are no indications of f laccid dysarthria. Both of you agree that
the site of the lesion must be above the glossopharyngeal- spinal accessory nucleus where the cell