SIR: Delayed sequelae of carbon monoxide intoxication are characterized by diminished memory, psychotic symptoms, parkinsonism, and so on.1 We report a case with psychotic symptoms and parkinsonism due to delayed sequeale of carbon monoxide intoxication but successfully treated with aripiprazole after failed trial of both olanzapine and quetiapine.
Case Report: A 44-year old, woman was exposed to CO Mar. 2004 but she returned to her daily routines as usual after 2 hours stupor. But after 20 days after the accident, she showed abrupt cognitive decline, parkinsonism, visual and auditory hallucination, and persecutory delusion. Those symptoms brought her to admit in our department by her family. The patient had no family history of Altzheimer’s disease and no past history of medico-surgical, neurological and psychotic disorders. There was no evidence of substance use. Upon admission, the patient failed to perform neuropsychological tests. Her minimental status examination score totaled 3 while not losing orientation to person and with the ability to name objects. All laboratory tests were normal. The brain MRI showed no definite abnormality (image not shown), while the brain PET-CT showed a reduced metabolism in the area of the frontal cortex, caudate nucleus, thalamus, globus pallidus, temporal cortex and the posterior cingulate gyrus. Five mg/day of olanzapine was administered to the patient for the first time. After 5 days of olanzepine treatment, the patient showed improvement in behavioral aspects and sleeping pattern. But the rigidity became worse, making walking impossible. Olanzapine was reduced to 2.5 mg/day without improvement of parkinsonism and psychotic symptoms. Consecutive switch to quetiapine of 150 mg/day also failed to improve her psychotic symptoms and parkinsonism and developed severe postural hypotension and sedation. Thus, quetiapine was directly switched to aripiprazole of 10 mg/day and continued for a week, which increased up to 15 mg until she was discharged. After a week of aripiprazole treatment, abnormal behaviors derived from auditory and visual hallucinations significantly declined and her rigidity and dyskinesia were prominently restored, enabling her to walk around. She demonstrated a considerable improvement in cognitive ability and psychotic symptoms. She was discharged on day 77 after admission. The favorable outcome of aripiprazole in the patient is likely to be attributed to the role of aripiprazole as a dopamine-serotonin system stabilizer.2 The speculative hypothesis for this case might be a mixture of dopaminergic overstimulation in mesolimbic pathway and a deficient dopaminergic transmission in nigrostriatal pathway, which suggest partial agonistic activity would be a rational option.3 Although it is hard to explain effect of aripiprazole on cognitive aspects, aripiprazole has been found to restore cognitive function.4 Finally, spontaneous improvement as a natural course may not be relevant because the case history was relatively short. This case suggests that aripiprazole may be helpful to those developed psychotic symptoms and movement disorders associated with toxic brain injury such as carbon monoxide intoxication.