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Neurologist Clinical Specialist in Movement Disorder Department of Neurology & Psychiatry Hospital BHB Eggenberg Bergstrasse 27 A-8021 Graz, Austria FAX 43-316-5989-2380 E-mail rm.bonelli{at}nextra.at
www.theannals.com, DOI
Case Report. A 32-year-old white woman with genetically confirmed HD of 6 years' duration was hospitalized because of continuous worsening of her motor abilities. She was not able to walk or eat without help, and she could not dress or undress without help. The patient was treated with increasing doses of olanzapine and responded well to 30 mg/d; her motor function improved significantly. The woman had undergone 4 electroencephalograms (EEGs) in the last 7 years prior to the event and had not shown any EEG abnormalities.
The last EEG was undertaken 1 year before the event, and no EEG had been performed while she received olanzapine. However, after 1 month of treatment with olanzapine, she developed a severe generalized tonicclonic seizure of sudden onset associated with urinary incontinence. These symptoms ceased spontaneously after 5 minutes, and postictal cognitive impairment disappeared after 1 hour. No other toxic, metabolic, or anatomic abnormalities were identified (e.g., trauma, neoplasm, vascular disease, alcohol or drug withdrawal). At the time of the seizure, the patient was receiving 1 comedication: minocycline 100 mg/d.
The seizure was a probable adverse drug reaction based on the Naranjo probability scale.5 The olanzapine dose remained at 30 mg/d and carbamazepine 400 mg/d was added. No further events occurred in this patient. After the seizures, 3 more EEGs were done (in addition to the EEG immediately after the seizure; this was not done in our institution). All of these EEGs were normal.
Discussion. Seizures are common in juvenile-onset HD but rare in adult-onset HD.6 The pharmacodynamics of olanzapine are similar to those of clozapine, which has been described to induce seizures in 14% of patients. An increased incidence of EEG abnormalities has been associated with clozapine, but not with olanzapine, although isolated cases of seizures during olanzapine therapy have been observed in high-risk patients.7 There was no difference in epileptiform activity between the conditions with and without olanzapine. However, EEG slowing was significantly more frequent during olanzapine treatment. Although epileptiform activity did not increase with olanzapine, nonspecific EEG abnormalities may be more frequent than with use of other neuroleptics. EEG surveillance of patients with HD receiving olanzapine is advisable, although HD is generally not considered a risky condition for seizures.
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