American Journal of Therapeutics | 2021
Olanzapine Treatment for Chorea in a Patient With Delayed Neuropsychiatric Syndrome After Carbon Monoxide Intoxication.
Abstract
To the Editor: Delayed neuropsychiatric syndrome (NPS) after acute carbon monoxide (CO) intoxication, usually developed 14–45 days after the intoxication, which includes deficits in attention, memory impairment, disorientation, motor dysfunction, such as chorea and parkinsonism, urinary incontinence, and even psychosis.1 We hereby report a successful treatment by olanzapine for chorea in a patient with delayed NPS. A 46-year-old woman with depression and who attempted suicide with CO intoxication and was sent to our emergency department (ED) for hyperbaric oxygen therapy (HBOT) at 2.5 atmosphere (atm) absolute for 60 minutes soon after ED admission and 2.5 atm absolute for 100 minutes on the second day. She regained full consciousness. However, 30 days after ED discharge, she developed psychomotor retardation, mutism, poor response, incontinence, unsteady gait, and the impaired cognitive function tests. She was then hospitalized for further evaluation and management. The muscle power of the limbs was grade 5, deep tendon reflexes were normal, and Babinski’s sign was absent. Brain MRI showed symmetrical T2hyperintensities in the bilateral globus pallidus, bilateral cerebral white matter on fluid attenuated inversion recovery and T2WI, suggestive of carbon monoxide intoxication with leukoencephalopathy. We added piracetam 1200 mg/d and Madopar (benserazide 50 mg + levodopa 200 mg) 0.25 tablet QIDAC and administered HBOT for her. On day 7, she started to exhibit restlessness and persistent, rapid, irregular, involuntary choreic movements involving the whole body. The EEG which showed as essentially normal except for the increased beta activities with amplitude attenuation. 99mTcTRODAT-1 single-photon emission computed tomography showed relatively decreased radio-uptake on the bilateral putamen and caudate nuclei, advanced at the left striatum. We stopped Madopar for the generalized chorea, but the chorea persisted. We then prescribed olanzapine between 5 and 10 mg/d and clonazepam between 0.5 and 1.5 mg/d for the chorea. Although the symptoms of generalized chorea gradually alleviated, cognitive impairment, mutism, the urinary incontinence, and the rigidity of the limbs remained unchanged even after the HBOT for 20 sessions at 2.5 atm. She was discharged on day 36. CO intoxication is the leading cause of fatal poisoning worldwide, and delayed onset parkinsonism, gait disturbance, speech problems, cognitive impairment, seizure, memory impairment, and apraxia are neuropsychiatric symptoms.2 Furthermore, chorea after CO intoxication is extremely rare, and the mechanism is still unclear,3,4 which may be associated with excessive dopaminergic output on the receptors of the striatum since the choreic movement was relieved by neuroleptics,1 after hypoxia,5 related to globus pallidus necrosis, and overactivation of the positive feedback to the precentral motor cortex.6 In this case, the chorea in CO intoxication-related delayed NPS has a poor response to piracetam and Madopar. The chorea in this delayed NPS vanished after the olanzapine treatment. There are several case reports and small open-label studies assessing the treatment of olanzapine on improving symptoms of chorea.7–10 The efficacy of olanzapine on chorea has been between 0% and 60% reduction.11 In the United Kingdom, olanzapine is the most often prescribed antipsychotic for the management of around 55% of patients with Huntington’s disease.12 The possible mechanism of choreic movements may arise from hypoactivity in the indirect pathway from the basal ganglia–thalamocortical motor circuits.13 In our case, we see the compatible MRI images of symmetrical T2-hyperintensities in the bilateral globus pallidus. On 99mTc-TRODAT-1 single-photon emission computed tomography image, we see relatively decreased radio-uptake on the bilateral putamen and caudate nuclei. Clonazepam, one of the benzodiazepines, targets the cerebral gamma-aminobutyric acid-benzodiazepine receptor complex to enhance the gamma-aminobutyric acid activity. It may probably suppress hyperkinesia in American Journal of Therapeutics 0, 1–2 (2020)