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Letter |
Key Words: Dementias (general) • Neuroleptics • Delirium
SIR: The neuroleptic sensitivity syndrome is a diagnostic criterion for Dementia with Lewy Body (DLB).1 Some reports suggest that sensitivity to atypical neuroleptics occurs less frequently and is less severe,2 and that antipsychotic agents with low D2 antagonism might ultimately prove appropriate in patients with DLB.3 We report a case of severe neuroleptic sensitivity to a single accidental dose of clozapine 175 mg; a low-level D2 antagonist:
An 86-year-old man was diagnosed with DLB on the basis of a 6-year history of progressive memory, language, gait, and functional impairment, parkinsonian signs, marked visual hallucinations, and fluctuating confusion. In 1999, he had been withdrawn from risperidone 0.5 mg daily because of the development of a sensitivity syndrome. He had not been able to walk and was unable to raise himself from a chair.
His medical history included an allergy to sulfa drugs, type 2 diabetes, stroke, deafness, myocardial infarction, pulmonary embolism, and osteoarthritis.
Two years ago, he was admitted to a long-term care hospital with agitation and functional decline. His medications on admission were L-thyroxin 0.1 mg, donepezil 10 mg, coumadin 3.5 mg po once daily, and trazodone 75 mg at bedtime. His admission vital signs, laboratory work, and general medical examination were unremarkable.
A few months after admission, and, while agitated, he received clozapine 175 mg in error, administered by mouth. Soon thereafter he became very confused and after 2 hours was obtunded. Examination revealed no spontaneous eye opening, no verbal response, and only a withdrawal motor response (Glasgow Coma Scale score: 6). He had pinpoint pupils, with sluggish reaction to light. He was transferred to the emergency room and monitored overnight.
When the neurological examination was repeated 4 days later, his coma showed only slight improvement. His pupils were now reactive; he raised his eyebrows in response to voice, and he grimaced in response to painful stimuli. His muscle tone was rigid in both arms, but he was able to move all limbs. Occasional myoclonus was noted. The remainder of the examination, laboratory evaluation, and special investigations to rule out other causes of coma were unrevealing, except for a serum creatine kinase of 327 IU/L. By Day 9, he responded to verbal stimuli. Full consciousness and mobility were regained only by Day 14.
This case is notable because the patient developed coma, a severe reaction, after the first dose of the low-level D2 antagonist clozapine. Given the sign of pinpoint pupils, it appears that the coma is not readily explained as part of an antihistaminic, anticholinergic adverse effect to clozapine. Other causes of coma were ruled out by examination and investigations, and the timing in relation to the clozapine dosing is highly suggestive.
If patients with DLB require a neuroleptic (for example, for hallucinations that do not respond to a cholinesterase inhibitor4) then this case, and others, suggest that extreme caution be used regardless of the class of neuroleptics. Dosing should be minimized, and careful monitoring should be instituted, preferably, perhaps, in the hospital.5 It should also be noted that previous response to atypical neuroleptics could be an unreliable indicator of future response.
REFERENCES
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