Discussion:
There are many possible precipitating factors that can lead to the
development of dysphagia; some of the causes include functional or
structural abnormalities of the esophagus, throat, or pharynx. The
barium swallow study helped to rule out these as causes. The results
demonstrated impaired coordination of swallow with reduced hyolaryngeal
elevation resulting in pharyngeal residue and decreased airway
protection. He appears at increased risk for tracheal aspiration with
thin liquids and was recommended to continue with puree texture foods.
Additionally, his echocardiogram did not illustrate a severely enlarged
left atrium. Cardiovascular dysphagia is another possible entity that
leads to dysphagia and typically occurs when there is a mechanical
obstruction by the proximity of the enlarged atrium and the esophagus
(2).
The patient had multiple overlapping conditions that may have masked the
true etiology of his dysphagia. His history of GERD and M.S. initially
obscured the diagnosis, but because of clinical suspicion and
correlation of time-course, we believe the likely trigger of his
dysphagia to be carbamazepine use.
The patient’s symptoms began several days after initiating carbamazepine
treatment and continued to progress until its discontinuation. Stroke
was ruled out, and he was only given 1 dose of 500mg methylprednisolone
in the emergency department before getting discontinued. Neurology did
not consider the dysphagia to be due to MS or a cerebrovascular
accident. After symptom improvement, the patient’s home medications were
restarted aside from carbamazepine, which did not cause a relapse in the
condition. The patient had a UTI on admission, but he has been
struggling with chronic UTIs for over 1 year and was asymptomatic.
Dysphagia was never a presenting symptom in any of his prior UTI
admissions.
Carbamazepine is known to decrease the electrochemical potential of
neurons by restricting sodium influx into cells, inhibiting
depolarization. It is well documented that known side effects of
carbamazepine are ataxia, dizziness, or drowsiness (3). It can be
postulated that an individual with MS is more sensitive to these types
of medications due to a decrease in myelinated neurons, which can lead
to motor dysfunction, particularly of the oropharynx. It is hypothesized
that carbamazepine triggers impaired oropharyngeal motor coordination
due to poor axonal signalling because of an underlying demyelinating
condition. We also suspect that the patient may have had more profound
and diffuse neuromuscular dysfunction had he not been bed-bound and
minimally mobile.