Case Report:
A 70-year-old Caucasian male with a past medical history of hypertension, hyperlipidemia, benign prostatic hyperplasia, dementia, gastroesophageal reflux disease (GERD), and primary progressive multiple sclerosis (M.S.) presented to the emergency department from home for evaluation of progressively worsening dysphagia of one-week duration. His M.S. was diagnosed with lumbar puncture and MRI 37 years ago and has been progressing. He was previously on dalfampridine for 3-4 years until he became bedbound one year prior to this admission; it was at that time that his treatment was discontinued. He has also been treated in the past with steroids for multiple M.S. flares. The patient’s wife stated his ability to swallow food had become severely impaired over the past week. The patient frequently regurgitated and was also unable to adequately clear oral secretions on arrival.
His wife noticed an accelerated decline in his neurological status over the past year to the point that he was now bedbound, dysarthric, and intermittently cognitively impaired. Since being bed-bound, he also developed frequent episodes of chronic urinary tract infections (UTIs). At baseline, he was conversational, able to eat soft foods, and ingest medications in pureed foods. He did not have issues with clearing secretions until about 6 days prior to admission. It was 9 days before his presentation to our facility when he was started on carbamazepine by his neurologist for treatment of trigeminal neuralgia. The dosing was initiated at 200 mg daily for three days, followed by 200 mg twice daily for the 6 days leading up to presentation.
Upon admission, he was noted to have altered mental status as he was only oriented to person and place but not time or situation. He was afebrile and hemodynamically stable. Physical exam was notable for crackles in the upper and lower lobes of the right lung. His laboratory testing was unremarkable except for pre-renal acute kidney injury.
Imaging was significant for a chest x-ray that showed a small volume parenchymal opacity in the right lower lobe and suggested possible pneumonia (Figure 1). Brain CT did not show any new evidence for acute intracranial pathology (Figure 2). Brain MRI showed white matter disease in the periventricular areas, with no new changes in comparison to prior imaging (Figure 3). Echocardiogram showed normal systolic function, no regional wall motion abnormalities, with mild diastolic dysfunction and a moderately dilated left atrium.