Teaching Case

A 45-year-old woman was admitted to the hospital in a stuporous state of three days duration. No history of suicide attempt or drug abuse was known. Blood gas sampling of the patient showed marked alteration of PaO2 and normal PaCO2 levels.

A 45-year-old woman was admitted to the hospital in a stuporous state of three days duration. No history of suicide attempt or drug abuse was known. Blood gas sampling of the patient showed marked alteration of PaO2 and normal PaCO2 levels. The patient had been using a coal heater in a poorly ventilated room. An MRI study of the patient, with 1.5 T MR scanner, in three planes with SE T1, FSE PD-T2 and FLAIR sequences and MRS was performed.

Carbon monoxide (CO) poisoning has been shown to result in neuropathologic changes and cognitive impairments due to anoxia and other related biochemical mechanisms. It most commonly occurs in the setting of attempted suicide or the use of coal heaters in poorly ventilated homes. CO attaches to the hemoglobin of the red blood cells and blocks their capacity to carry oxygen. The formation of carboxyhemoglobin (that cannot bind oxygen) causes hypoxia. The oxyhemoglobin dissociation curve shifts to the left, which decreases the release of oxygen to tissues. CO also has a direct toxic effect on mitochondria via binding to cytochrome a3. This interferes oxydative phosphorylation. The patients are often unconscious at presentation. Survivors present with affective changes including depression and anxiety and a variety of cognitive impairments, including impaired attention, memory, executive function, and mental processing speed. Later they may manifest movement disorders,hypertonia,short- term memory loss and mental deterioration. Cardiac arrhytmias also may occur (1st degree AV blocks mostly). The most affected area in the brain is the globus pallidus bilaterally, but abnormalities in the following areas may be observed too: entire lentiform nucleus, putamen alone, caudate nucleus, thalamus, white matter (periventricular, subcortical, other), cerebral cortex (either localized or general) and medial temporal lobe in the region of the hippocampus. The radiologic appearances of the brain following acute CO poisoning are varied. On CT imaging low-attenuation lesions may be observed whereas T2 hyperintensity and T1 iso-hypointensity may be observed on MRI. Proton MRS studies in the white matter reveals a persistent increase in choline in the early period, which is thought to reflect the course of progressive demyelination.The appearance of lactate and decrease in N-acetylaspartate reflects the point at which neuron injury becomes irreversible. Later, the findings of irreversible changes on MRI and single photon emission computed tomography occurs. The findings suggest that 1H-MRS may be a useful modality to determine neuron viability and prognosis, early in the course of the interval form of CO poisoning. The treatment of the disease includes 100 % hyperbaric oxygen. Prognosis varies with severity and duration of exposure.