Case Presentation: A 42-year-old male with past medical history of morbid obesity and methamphetamine abuse presented to the ED with a chief complaint of the right hand and arm weakness, tremors, numbness, and tingling. Three days prior to the admission, the patient reported awakening nausea and vomiting. The following day, the patient stated his right arm was shaking intermittently, lasting for seconds to minutes with multiple episodes throughout the day. The patient denied any prior history of seizures, tongue biting, bowel/bladder incontinence, loss of consciousness, shaking in any other location of the body, slurred speech, visual changes, facial droop, falls, trauma, fevers, chills, and recent sick contacts. The patient did endorse polydipsia, polyuria, and weight gain.On admission, the patient’s blood glucose was 884 with a calculated osmolality of 307 mOsm/kg. Laboratory results showed an A1c of > 16, measured serum sodium of 125, normal arterial pH, no anion gap and ketones in the urine. CT and MRI brain were unremarkable. EKG showed sinus tachycardia. Neurology recommended starting levetiracetam, aspirin, and an Electroencephalogram (EEG) was ordered. EEG showed a possible partial seizure discharge emanating primarily from the left parietal region. The patient’s focal seizures improved with the correction of his hyperosmolar, hyperglycemic state with an appropriate insulin regimen. The patient was counseled on appropriate diabetes management upon discharge to prevent Epilepsia Partialis Continua (EPS) in the future.
Discussion: EPS is a condition in which focal, jerky movements occur every few seconds to minutes, specifically in distal extremities and episodes may continue for hours to days or even prolonged periods [1]. EPS is frequently caused by Rasmussen’s encephalitis, Cerebrovascular stroke, and viral encephalitis. Metabolic disorders such as Hyperosmolar Hyperglycemic Syndrome (HHS) rarely cause EPC [2]. Seizures caused by hyperglycemia are usually reversible. Studies on rats showed that an appropriate glucose level is required to enable proper synaptic transmission. Both hypoglycemia and hyperglycemia can lead to neuronal hyperexcitability [3]. Hyperglycemia increases the metabolism of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) which can potentially reduce the seizure threshold [4]. A review of recent literatures also noted a correlation between a degree of hyponatremia and EPS in hyperglycemic hyperosmolar condition. A limited number of cases reported the presence of focal brain damage on MRI in the EPS [5]. For the patients presenting with EPS, correction of metabolic abnormalities is the most significant treatment measure. Anti-epileptic medications like phenytoin can increase glucose levels and can predispose the diabetic patient to develop HHS and subsequently seizures [6].
Conclusions: EPS is a rare neurological presentation of HHS. Strict glycemic control is the key for the successful prevention of EPS and it needs a concerted approach of primary care provider and Endocrinologist. Anti-epileptic medications may benefit in controlling seizures, but their use should be limited under the guidance of Neurologist.