Carbamate intoxication as a stroke mimic
Cheng-Ting Wu, MD 1 , Lien-Ying Lin, MD 1 , Li-Wen Huang, MD 2 , Yan-Chiao Mao, PhD, MD 2, 3 , Chin-An Huang, PhD, MD 1 ,
1 Department of Neurology, Neurological Institute, Taichung Veterans General Hospital
2 Department of Emergency Medicine, Taichung Veterans General Hospital
3 Division of Clinical Toxicology, Taichung Veterans General Hospital
Cheng-Ting Wu , MD
Department of Neurology, Neurological Institute, Taichung Veterans General Hospital
A 51-year-old male without past systemic disease history suffered from acute onset general weakness, headache, cold sweating, excessive oral secretions, chest pain and slow response on 7th, September 2020. He was sent to our emergency department. Vital signs showed hypertension with normal heart rate. Neurological examination revealed Glascow coma scale E3VTM6, bilateral miosis without light reflex, opsoclonus and skew deviation of eyes, quadriplegia (muscle power rating scale right side grade 2, left side grade 0). His National Institutes of Health Stroke Scale (NIHSS) score was 17. Brain CT showed no intracranial hemorrhage or obvious low density. He was admitted under the impression of posterior circulation ischemic stroke due to abnormal ocular movements. Neurological examination became normal the next day. Brain magnetic resonance angiography (MRA) and electroencephalogram (EEG) were normal. Tracing back, he had eaten passion fruits that had a weird taste few minutes before onset of his symptoms, and the emergency department doctor was alerted by this clinical presentation and had checked cholinesterase RBC and plasma quantitative test at the emergency department, which were both decreased, 3046 U/L and 2003 U/L respectively. The urine organophosphates test was negative. We repeated the cholinesterase RBC and plasma quantitative test 6 days later, which had returned to normal. After consulting the toxicologist, the final diagnosis of this case was highly suspect of carbamate intoxication.
Stroke mimics are clinical conditions where non-vascular etiologies cause acute onset neurological deficits that simulate a cerebrovascular accident. Carbamate intoxication causes excessive acetylcholine at the nervous system, therefore present with confusion, seizure, miosis or mydriasis, salivation and flaccid paralysis. In our stroke center from year 2006 to 2018, toxic/metabolic condition was the second most common stroke mimic (15.6%). Keeping carbamate intoxication in mind as a stroke mimic help doctors acquire the necessary clinical information.