Encephalopathy related to long term CO poisoning

Clinical History

We report the case of a 23-year-old male patient, who had had two partial complex seizures apparently caused by sleep deprivation and alcohol intake.

Imaging Findings

We report the case of a previously asymptomatic 23-year-old male patient, who had had two partial complex seizures apparently caused by sleep deprivation and alcohol intake. A brain magnetic resonance imaging (MRI) was performed in order to understand the causes of the seizures. On FLAIR sequences, hyperintensity of the temporo-occipital cortex and subcortical white matter (Fig. 1), with a normal signal of the basal ganglia (Fig. 2), was found. Bilateral atrophy and a high signal of hippocampi were seen on the FLAIR sequences (Fig. 3), associated with a hyperintense rim in the subcortical white matter of the cerebellar hemispheres (Fig. 4). The patient underwent a thorough clinical interview and he remembered having lost consciousness at the age of six, due to accidental carbon monoxide (CO) exposure. The standard blood examination which had been done three days after the exposure had shown high carboxyhemoglobin plasmatic levels. Subsequently, the patient had been treated with hyperbaric oxygen. His recovery had been complete and he had been healthy until the onset of the seizures.

Discussion

CO is a colourless, tasteless and odorless gas generated from the incomplete combustion of carbon-containing compounds. CO has a very high oxidizing power and a much greater affinity for heme than oxygen and causes neuronal damage by inducing hypoxia, membrane peroxidation, excitotoxicity, and apoptosis. The acute manifestations of CO poisoning may include nausea, vomiting, headache, weakness, dizziness, collapse, confusion, convulsions, loss of consciousness, coma and death. The late neuropsychiatric sequelae (seizures, Parkinsonian symptoms, gait disturbances, apraxia, mood and personality disorders, memory deficit, decreased attention, and cognitive impairment) are reported to happen years or decades after CO exposure, which makes the diagnosis difficult. The brain MRI is the most sensitive tool for the evaluation and follow-up of CO poisoning-related lesions of the central nervous system. The most frequent neuroradiological finding is represented by a bilateral signal alteration of the globi pallidi, showing hyper- or hypointensity areas on the SE T1-weighted sequences, as a result of hemorrhagic infarction and necrosis, respectively. This sign, although frequent, could not be found out in our case. On SE T2-weighted and FLAIR images, the globi pallidi are usually characterized by bilateral hyperintensity surrounded by a hypointense rim due to hemosiderin accumulation. The subcortical white matter is commonly affected and is characterized by multiple hyperintense areas on the SE T2-weighted and the FLAIR sequences, with a preferential distribution in the periventricular region and in the centrum semiovale. A similar pattern may be shown by the cortical gray matter, particularly that of the temporal and occipital lobes, and by the gray and white matter of the cerebellar hemispheres. The hippocampal involvement is a well-established hallmark of CO poisoning seen on histopathological examination but quite a rare finding on a brain MRI, consisting of bilateral atrophy and hyperintensity on T2-weighted and FLAIR sequences. The differential diagnosis must be made with Wilson disease, Japanese encephalitis, small vessel ischemic disease, Creutzfeldt-Jakob disease, and Leigh disease.

Differential Diagnosis List

Final Diagnosis

Encephalopathy related to long term CO poisoning.

URL:	https://www.eurorad.org/case/3538
DOI:	10.1594/EURORAD/CASE.3538
ISSN:	1563-4086