ODP194 EPC (Epilepsia Partialis Continue)- as a presenting symptom of HHS (Hyperglycemic Hyperosmolar Syndrome)

CASE PRESENTATION: A 51 year old female with history of type 2 DM and hypertension presented with elevated blood glucose levels (>500 mg/dL) and a two day history of multiple episodes of numbness, tremors and weakness affecting the right upper extremity. These episodes lasted ∼10 seconds and resolved spontaneously. She had no history of seizures or prior similar symptoms. Extensive review of systems was negative. Neurological exam was normal except for decreased sensation and dysmetria affecting the right upper extremity. Labs included: serum glucose 616 (70-99 mg/dL), serum osmolarity 302 mOsm/kg (285-295 mOsm/kg), serum bicarbonate 19 (21-31 mmol/L), anion gap 18 (6-14 mmol/L), serum ketones 0.2 (normal <0.6 mmol/L), Stroke work up including CT head, MRI brain, CTA/MRA head and neck, and TTE were negative. EEG showed no epileptiform changes likely due to the episodic nature of symptoms. Endocrinology started basal-bolus insulin regimen with IVF therapy for hyperosmolar hyperglycemia without diabetic ketoacidosis. However, she continued to have multiple documented episodes of twitching of right thumb with tingling, numbness and cramping lasting 10-15 seconds while fully awake and followed by full return of function. These episodes coincided characteristically with periods of hyperglycemia (in range of 122-440 mg/dL). Neurology attributed her symptoms to partial focal seizures in the setting of non ketotic hyperglycemia. Seizures decreased in frequency with improved glycemic control. She was discharged on basal-bolus insulin regimen and showed continued improvement with tight regulation of glycemic control. DISCUSSION: EPC is a rare variant of simple focal motor status epilepticus characterized by recurrent focal epileptic seizures involving distal extremities lasting seconds to hours and occurring over prolonged periods of time. It may be preceded by aura continua, non-motor manifestations such as tingling and numbness, and followed by Todd's phenomenon, transient unilateral weakness. Etiologically, it is attributed to structural (stroke, trauma), infectious (encephalitis, prion disease), autoimmune (Sjorgen syndrome), neoplastic (gliomas) and metabolic (HHS) pathologies. HHS is a rare yet known cause of EPC. Glucose plays a crucial role in synaptic transmission, and hyperglycemia increases the metabolism of inhibitory neurotransmitters such as gamma-aminobutyric-acid (GABA) thus lowering seizure threshold. Diagnosis is clinical; EEG is supportive only. Management primarily entails correction of underlying cause, hyperglycemia. Review of literature suggests that HHS induced EPC can often be resistant to anti-epileptic agents and medications such as phenytoin and valproic acid may actually exacerbate this condition due to their hyperglycemic effect. Through this case, we wish to highlight the importance of recognizing HHS as a cause of EPC in clinical practice and also emphasize that the first line treatment is the correction of underlying hyperglycemia. Presentation: No date and time listed