Abstracts

Rationale: Epilepsia partialis continua (EPC) is characterized by recurrent focal motor seizures with retained awareness lasting for a prolonged period. We present a case of EPC caused by the combination of acute multifocal strokes and nonketotic hyperglycemia.

Methods: Case Report.

Results: A 65-year-old right-handed woman presented to the emergency room stroke stop with sudden onset right arm weakness and inability to speak. On arrival, she was observed to have frequent and rhythmic right orofacial twitches. She was otherwise awake, alert, and followed basic commands. She attempted to speak but was inhibited by the inability to swallow her saliva, which intermittently obstructed her airway. She urgently received intravenous lorazepam 2 mg and levetiracetam 3 mg and was intubated and sedated for airway protection. Point of care labs were remarkable for glucose 921 mg/dL, so she was started on continuous insulin drip. Video EEG revealed left frontocentral onset status epilepticus with right facial twitching (Figure 1). She then received one dose of intravenous lacosamide 400 mg, and her EEG later showed diffuse slowing along with focal left frontocentral and right parietal-occipital cortex slowing with epileptiform discharges. Following resolution of hyperglycemia and extubation the next day, she was alert and oriented and had fluent speech. She had full strength throughout and was able to walk with a walker. Her past medical history was significant for type 2 diabetes mellitus, hypertension, and heavy tobacco use. Multiple years ago, she had a generalized tonic-clonic seizure due to hypoglycemia, but otherwise no other history of seizures or stroke. MRI brain revealed multiple tiny acute and subacute infarcts involving the pons and bilateral cortical and subcortical regions (Figure 2), suspected to be embolic in origin. She was continued on oral levetiracetam 1500 mg twice daily.

Conclusions: EPC etiologies noted in Epilepsia partialis continua: A review published in Seizure 2017 44:74-80 include morphologic lesions, trauma, operations, inflammation, and metabolic causes. Hyperglycemia is thought to lower seizure thresholds by increasing extracellular glutamate supply and gamma-aminobutyric acid usage. This threshold is usually offset by ketones which are thought to counteract the hypoglycemia. For this reason, seizures are more likely to be found in nonketotic hyperglycemia as noted in Non‐ketotic hyperglycaemia presenting as epilepsia partialis continua from Epileptic Disorders 2016 18.2:201-203. Hyperosmolality with hyponatremia also increases the blood’s viscosity and can decrease the red blood cells’ oxygen-carrying capacity. The case above presents the rare and unfortunate combination of acute stroke and hyperglycemia as cause of EPC. In this case, we suspect that the patient gradually developed nonketotic hyperglycemia, which then presented as EPC once the acute multifocal strokes occurred. The ischemic infarct at the left frontal lobe then created a scar which served as a nidus for onset of focal motor seizures.

Funding: Please list any funding that was received in support of this abstract.: None.