Abstract Details

Downbeat nystagmus (DBN) can be severe to result in emergency department (ED) visits. Medications that cause DBN include lithium and anti-epileptics. We aim to highlight the importance of adequate history, thorough physical/neurological examination, and medication review in evaluating patients with DBN.

44-year-old woman with history of bipolar disorder on valproic acid, and LTG, presented with ‘bouncy vision’, sensation of ‘room spinning’, and tinnitus described as ’sounds of the ocean’. At her first ED visit, Head CT - unremarkable, MRI brain (without contrast) - nonspecific subcortical white matter changes. Valproic acid and LTG levels were 76 and 19 mcg/ml respectively. She was discharged with provisional diagnosis of Peripheral Vertigo and LTG dose was decreased, which was increased two months prior by her psychiatrist.

On her third ED visit, neurology was consulted, a complete neurological examination revealed DBN in primary gaze, left and right gaze, and downgaze. The nystagmus improved in upgaze. She also had bilateral upper extremity dysmetria on finger to nose with staggering gait. She was admitted for suspected LTG toxicity (serum LTG: 23·6 mcg/mL). LTG was discontinued and her symptoms resolved completely the next day. On follow-up she had normal neurological examination with no residual symptoms. 

DBN is a known sign of LTG toxicity; however, the mechanism of LTG-induced nystagmus is not fully understood. Our patient was taking valproic acid and LTG. Inhibition of LTG is maximal at approximately 500mg daily resulting in an approximate two-fold increase in serum LTG levels. LTG blocks voltage-gated sodium channels leading to decreased depolarization in regions with epileptogenic foci. The therapeutic range for the use of LTG varies in different disorders. The serum toxicity is at 20 mcg/mL. Due to the widespread use of LTG in psychiatry and neurology, drug interactions must be taken into serious considerations when prescribing medications that influence metabolism.