Abstracts

Rationale: An 83-year-old R-handed male presented with a two-day history of episodic jerking and “spasms” in the left arm, each lasting approximately 1 min, followed by weakness. He also described episodes of flashing colored lights in his left visual field, not always accompanied by arm jerking. The patient was also mildly confused with short-term memory impairment. His past medical history was significant for type-2 diabetes mellitus, dyslipidemia, hypertension, ischemic heart disease, cardiac pacemaker, and he was treated with prednisone for giant cell arteritis. There was no past history of seizures or migraine. Methods: On physical examination, the patient was disoriented to date. He had a visual deficit in the inferior fields of both eyes, but was unable to clearly describe the demarcation of the visual defect. He also had a mild left upper extremity weakness (4/5) with brisk biceps and brachioradialis reflexes and an extensor plantar reflex on the left. Several brief episodes of focal motor (clonic) seizure activity involving the left upper limb were observed. Results: Blood Glucose was 639 mg/dl and serum osmolarity 316 mosmol/l. Ketoacidosis was absent. Mg+ and Ca2+ were normal. There were mild abnormalities of Na+ and K+, which normalized with treatment in a few hours, however, clinical seizures continued for 24 hours. Two electrographic seizures from the left occipital region maximum at O1 with spread to P3 and T5 associated with visual symptoms were recorded. The ictal rhythm in both seizures was characterized by fast activity in the frequency of beta followed by post-ictal theta and then delta. CT head was normal. MRI was not obtained because of the pacemaker. The patient was treated with hydration and insulin and all the neurological symptoms including the seizures disappeared after 24 hours. In a subsequent follow up, four months later, the EEG was normal and the patient remained asymptomatic. Conclusions: This patient had clinical and electrographic seizures from the occipital region associated with hyperglycemia. He also suffered from other transient neurological symptoms associated with hyperglycemia that eventually disappeared with the correction of the metabolic problem. This is a unique complication of hyperglycemia with only few anecdotal reports over the years. Historically the presence of focal seizures, most frequently focal motor seizures, has been described during non-ketotic hyperglycemia, however, the description of occipital seizures is exceptional. It has been demonstrated that increased extracellular glucose, in a concentration dependent manner, increases neuronal excitability via decreasing the conduction of KATP channels. Also decreased GABA levels during hyperglycemia can predispose to seizures. More potential aspects of pathophysiology and EEG findings will be presented at the congress.