Case Presentation: A 59-year-old male presented to the emergency room with confusion, dysarthria, weakness, and diarrhea for 6 days. He reported taking colchicine for a gout exacerbation a week prior. Past medical history was significant for gout, non-Hodgkin’s lymphoma (in remission), and partial small bowel resection. Vital signs were within normal limits. Physical exam revealed dysarthria, bidirectional nystagmus, ataxia and dysmetria. Laboratory studies revealed the following electrolyte levels: potassium 2.0 mmol/L, calcium 5.7 mg/dL and magnesium < 0.3 mg/dL. CT scans of the brain, abdomen and pelvis were unremarkable, so were cerebrospinal fluid results. MRI brain demonstrated cerebellar hyperintensity. A diagnosis of Hypomagnesemia Induced Cerebellar Syndrome was made. He was initially treated with intravenous magnesium supplementation. Due to ongoing diarrhea and slow improvement in serum magnesium levels, peripheral parenteral nutrition (PPN) was initiated which resulted in much more rapid improvement. Calcium was also replaced intravenously. His gait, weakness and dysarthria improved as his electrolyte levels normalized. Subsequently he was discharged from the hospital. We called the patient three weeks later and he confirmed continued improvement in his symptoms with ongoing oral magnesium supplementation.
Discussion: Hypomagnesemia induced cerebellar syndrome is a rare condition which should be on the differential diagnosis for any patient with cerebellar symptoms and hypomagnesemia. Due to the low prevalence of this condition, it is very easy to misdiagnose it for a stroke or for Wernicke’s encephalopathy. The differentiating test is brain MRI; in Wernicke’s Encephalopathy we are more likely to find hyperintensity in the mamillary bodies or temporal lobes instead of in the cerebellum. On literature review, we identified 24 cases; ours is the 25th. We found that up to 50% of patients also presented with hypocalcemia and/or hypokalemia. These patients showed symptomatic improvement after magnesium replacement, but 50% showed significant sequelae, and 46% relapsed. The use of PPN was a creative way of managing our patient and has not been reported before. We recommend further investigation into its clinical utility in such cases. Also, in hindsight, we should have initially admitted the patient to the ICU given the risk of arrhythmias.
Conclusions: Hypomagnesemia Induced Cerebellar Syndrome is a rare manifestation of critically low serum magnesium levels and can easily be misdiagnosed Individuals with this condition are at high risk of ventricular arrhythmias, seizures, and other complications of severe electrolyte derangements and should initially be admitted to the intensive care unit