Presentation Number: SAT-784
Date of Presentation: June 15th, 2013

Alejandra Borensztein*1 and Helena Abby Guber2
1SUNY Downstate, New York, NY, 2Brooklyn VA Med Ctr, Brooklyn, NY



             Autonomic and peripheral neurologic  manifestations of hyperglycemia are commonly seen in clinical practice; hyperglycemia-induced movement disorder is a rarer and lesser known entity. We report on a patient who manifested with epilepsia partialis continua as an initial presentation of diabetes mellitus.


            A 58 year-old man presented with weakness, blurred vision, polydipsia, polyuria and shaking of the left leg for 4 days.  On initial evaluation in the emergency department, the patient was found to have repeated episodes of myoclonic jerking of the left leg, described as simultaneous partial flexion of the hip and knee with dorsiflexion of the foot. The neurologic exam was otherwise normal.  Blood glucose at that time was 891mg/dl with a calculated serum osmolality of 313. Labs were significant for a creatinine of 1.4 mg/dl and potassium of 5.7 mmol/L [3.5-5 mmol/L], and elevated liver enzymes with alkaline phosphatase of 506 U/L [42-121 U/L], AST of 60 IU/L [10-42 IU/L], ALT of 76 U/L [10-40 U/L]. The patient was admitted to the medical ICU and treated with aggressive intravenous hydration and an insulin drip.  On the second day, the patient’s glucose decreased into the 300 mg/dl range. An electroencephalogram (EEG) performed that day showed diffuse cerebral dysfunction with no epileptogenic focus. After blood glucose normalized, the abnormal movements subsided and did not recur.  A brain MRI performed 1 month later revealed no focal enhancing abnormalities.  The patient was determined to have epilepsia partialis continua secondary to hyperglycemia.


            Though Hyperglycemia-induced movement disorder was first described by Bedwell et al in 1960, it continues to be an under-recognized manifestation of hyperglycemia.  It can manifest in a variety of ways, including epilepsia partialis continua(1). Though more commonly seen in patients with long-standing diabetes, it can also be the initial presentation of diabetes.  It is hypothesized that hyperglycemia increases metabolism of GABA thereby decreasing the seizure threshold(2). The treatment of these movement disorders varies from traditional movement disorders and focal seizures as it relies primarily on glucose control rather than anti-epileptic medication1.  It is important to recognize hyperglycemia as a possible cause of movement disorders so as to provide earlier treatment for potentially life-threatening conditions such as hyperosmolar nonketotic states and diabetic ketoacidoses.


Nothing to Disclose: AB, HAG