Movement‐Induced Focal Motor Seizures and Choreoathetosis As‐ sociated with Nonketotic Hyperglycemia: A Case Report

Abstract

Case Report: We report the case of a diabetic woman who developed right‐sided reflex seizures and bilateral choreoathetosis during an episode of nonketotic hyperglycemia. The patient was a 67‐year‐old woman with a 14‐year history of HCV‐related liver cirrhosis who experienced polydipsia and polyuria in January 1998. She began to have episodes of abnormal hyperkinetic movements of the right upper extremity and tonic‐clonic seizures in the right arm triggered by voluntary movements of right or bilateral arms in the beginning of March 1998.The seizures increased in frequency and consequently left her disabled. She was admitted to our hospital with complaints of these abnormal motor phenomena on March 9, 1998. Neurological examinations revealed that she was alert, well‐oriented, and that cranial nerve functions were normal. Slight motor weakness of the right upper limb and deep tendon hyporeflexes were observed in all extremities. Sensations and cerebellar functions were intact. Choreic or athetotic involuntary movements were seen in the bilateral upper limbs and neck. These involuntary movements were increased by voluntary movement or posturing of the upper limbs. The focal tonic‐clonic seizures were easily triggered by voluntary movements such as knotting a cord. This seizure suddenly began by tonic movements in the right upper limb and gradually progressed to the right hemi‐face and neck without loss of consciousness.The average duration of seizures was about one minute. The laboratory data demonstrated mild leukocytopenia, thrombocytopenia, hepatic dysfunction, and hyperglycemia without ketosis. Fasting blood glucose was 41 I mg/dl, and HbAlc was 14.5%. Blood ammonia was within normal levels. Cranial CT revealed no abnormalities. Brain MRI on T I‐weighted images demonstrated bilateral high signal intensity in the putamen. An interictal EEG revealed a symmetrical slow background activity of 7–8 Hz. An ictal EEG recording showed a 2.5 4 Hz irregular sharp and slow wave discharge in the bilateral frontal‐central regions. Treatment with carbamazepine was ineffective for the seizures. However, the seizures completely disappeared after the administration of insulin on March 17. Under good control of the hyperglycemia, the abnormal involuntary movements decreased gradually and then completely disappeared; the patient became neurologically asymptomatic by March 30. The follow‐tip EEG demonstrated 9‐Hz alpha background activity without any epileptic discharges. Conclusions: Nonketotic hyperglycemia has been rarely reported to cause stimulus‐induced seizures or hyperkinetic involuntary movements such as hemichorea‐ballism. To our knowledge, this is the first reported case of both induced seizures and involuntary movements simultaneously caused by hyperglycemia. Movement‐induced seizures and choreoathetoid movements in this patient can be considered to result from transiently‐increased activity in the basal ganglia and/or cerebral cortex associated with metaholic disorders.