Abstracts

Rationale: Myoclonus is a rarely-discussed side effect of pregabalin (PGB). Risk factors include renal dysfunction and history of epilepsy. Most case reports in the literature have been associated with subcortical myoclonus. Although the myoclonus may be disturbing to patients and families and may result in unnecessary testing, it is reversible with removal of PGB. Myoclonic status epilepticus (MSE) is prolonged periods of myoclonic jerks occurring continuously or in clusters for > 30 minutes. MSE is associated with generalized epilepsy syndromes, post anoxic brain injury, and other toxic-metabolic syndromes. Rare cases of MSE have been reported with PGB. We present a case of MSE in a patient with acute on chronic kidney disease without a history of epilepsy. Methods: A 90-year-old female with history of Parkinson’s disease, hypertension, chronic kidney disease and peripheral neuropathy initially presented with generalized weakness and encephalopathy secondary to hypertensive encephalopathy. Her cognition improved to baseline with treatment of blood pressure. Upon admission she was started on PGB for neuropathy with a total dose of 100 mg administered. The following day she developed generalized myoclonic jerks. Neurologic exam showed myoclonic jerks of bilateral upper and lower extremities every 5-10 seconds. Additionally, she was noted to have symmetric resting tremor in both hands. Electroencephalogram (EEG) with video showed abundant (1-4 discharges every 10 seconds) generalized spike and polyspike-and-wave discharges lasting 100 msec- 400 msec, clinically correlating with positive myoclonus. She was loaded with levetiracetam and PGB was discontinued. Myoclonus then resolved and levetiracetam was weaned over several weeks. Results: Video EEG revealed abundant generalized spike/polyspike-and-wave discharges. There was brief generalized background attenuation immediately following the discharge. In addition to this, generalized irregular theta > delta activity was noted with an absence of posterior dominant rhythm. Serum creatinine was 2.10 mg/dL and blood urea nitrogen (BUN) was 36 mg/dL on admission. On day 2 of admission, creatinine rose to 3.60 mg/dL and BUN to 51 mg/dL. Rest of the lab work was essentially unremarkable. CT head showed chronic lacunar infarctions in basal ganglia, thalami, and left cerebellar hemisphere. MRI brain revealed chronic infarctions as seen on CT head and no acute intracranial abnormalities. Conclusions: Pregabalin is an analog of gamma-aminobutyric acid which acts as an inhibitor at the voltage-gated calcium channel receptors to limit cell excitability. The mechanism by which PGB induces myoclonus is unknown, however, it is thought to be related to the lactam ring. Myoclonic status epilepticus has rarely been reported, notably in elderly females with renal dysfunction. This case demonstrates the potential for myoclonic status epilepticus on low dose of PGB in a patient with renal dysfunction with no underlying epilepsy. Caution should be used in prescribing PGB particularly in elderly patients with renal dysfunction. Patient should be counseled accordingly and PGB withdrawn if MSE should occur. Additional research is needed to determine how PGB can evoke MSE. Funding: No funding