History
Mr. Ho was a 65-year-old gentleman who is a chronic smoker and regular drinker.
He has a past medical history of hypertension, hyperlipidemia, and non-ST elevation myocardial infarction 2 years ago, with percutaneous coronary intervention performed.
He presented with an acute onset of unsteady gait 10 days before the index admission. The gait disturbances were preceded by a 3-day history of abdominal pain and recurrent diarrhea without fever or vomiting. He received symptomatic medication from a private general practitioner 1 day before the gait symptoms.
Accompanying the unsteady gait were bilateral upper limb incoordination (the left being worse than the right), recurrent falls, and slowed verbal responses.
These neurological symptoms were of maximal severity at onset, with subsequent partial recovery over the ensuing days.
Of note, there was no fever, headache, seizure, or illicit drug use. He denied any family history of gait disorders or dementia.
Physical examination
The general examination was pertinent for a dulled verbal response, despite being fully oriented.
The neurological examination revealed asymmetrical ataxia with right upper limb intention tremor and dysdiadochokinesia. The patient displayed a broad-based gait and a failure to balance during tandem walking.
There were no features suggestive of a cord or peripheral nerve pathology.
Investigations
A CT of the brain demonstrated multiple bilateral lacunar infarcts, specifically at the left putamen and right cerebellum.
Baseline blood tests, including inflammatory markers, were unremarkable.
Thought process
The pathology was likely localized to the cerebrum and cerebellum. A cord pathology (bearing in mind the history of recurrent falls) or a peripheral nerve pathology (noting the prodromal diarrheal illness) would be unlikely to account for the altered mental state.
The etiology was likely to be ischemic given the acute onset of asymmetrical symptoms with subsequent recovery, CT brain findings, and the background vascular risk factors.
The acute presentation may also be accounted for by toxic (symptomatic medications prescribed by the general practitioner) or metabolic (Wernicke encephalopathy, history of alcohol use) causes.
The self-remitting clinical course was less typical for infectious or parainfectious etiologies.
Next steps
A contrast MRI brain with MRA head and neck was arranged to clarify the acuity of the infarcts, thalamic involvement, and features of Wernicke encephalopathy.
The medications were traced.
The patient was continued on aspirin and started on empirical thiamine replacement.