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.