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      Isolated symmetrical bilateral basal ganglia T2 hyperintensity in carbon monoxide poisoning

      case-report

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          Abstract

          Carbon monoxide poisoning is not uncommon during the winter months. To make a diagnosis, strong clinical suspicion and acumen, and history of the exposure are necessary. Many a time, the presenting complaints may fail to help reach a diagnosis, in the absence of history. Imaging plays a role in the diagnosis of brain injury with the characteristic features, which are correlated with the clinical profile. Isolated bilateral basal ganglia injury revealing T2 hyperintensity in MRI may be observed in acute carbon monoxide poisoning.

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          Carbon monoxide poisoning.

          Carbon monoxide (CO) poisoning is common and frequently unrecognized since the signs and symptoms are relatively nonspecific. CO poisoning causes tissue hypoxia. Additionally, various animal studies have demonstrated that CO interferes with myoglobin, P450, and other enzyme function; causes lipid peroxidation through neutrophil activation; produces oxidative stress manifested by peroxynitrate deposition in endothelium; binds to cytochrome aa3, disrupting intracellular oxygen utilization; can cause neuroexcitotoxicity; and contributes to hippocampal cellular death through apoptosis. Emergency treatment for CO poisoning is 100% oxygen. Hyperbaric oxygen therapy (HBO2) is accepted in CO poisoning, although data from randomized clinical trials regarding the efficacy of HBO2 in CO poisoning is conflicting. CO poisoning, even when treated with supplemental oxygen can leave the patient with permanent neurocognitive or affective problems. Unfortunately, there appears to be no marker or constellation of signs or symptoms at presentation that predicts long-term outcome following CO poisoning. Given the neurocognitive sequelae following CO poisoning, increased awareness and prevention of CO poisoning is imperative.
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            The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning.

            To describe the magnetic resonance imaging (MRI) appearances of the brain in acute carbon monoxide poisoning, the commonest cause of accidental poisoning in Europe and the U.S.A. To attempt to correlate the imaging findings with patient outcome as an aid to prognosis. Brain MRI was performed on 19 consecutive patients, who had sustained acute carbon monoxide poisoning, as soon as possible after their referral to the regional Hyperbaric Unit at the Royal Hospital, Haslar. All patients were unconscious on arrival, and had received at least one treatment with hyperbaric oxygen by the time of first MR. The imaging findings were analysed independently by two experienced MR radiologists, with a third radiologist arbitrating on discrepant results. Thirteen male and six female patients, age range 21-70 years (mean 38.7 years) underwent MR an average of 35.6 h (range 6-126 h) following presentation at the referring centre. MR (at 0.5T) revealed abnormalities in the following areas: globus pallidus (n = 12); other basal ganglia [ n = 5: entire lentiform (globus pallidus and putamen), putamen alone, caudate nucleus, thalamus]; white matter (n = 6: periventricular, subcortical, other); cerebral cortex (n = 5), either localized or general; medial temporal lobe in the region of the hippocampus (n = 4). The majority of the patients with hyperintensity in the region of the hippocampus (n = 3) had no other area of cortical involvement. Two patients showed abnormalities in the cerebellum. Normal appearances were seen on the initial MR in seven patients. The appearances of the brain following acute CO poisoning are varied, and have previously been the subject of case reports or small studies, most of which have have addressed the delayed sequelae of this condition. This study, the first large series undertaken in the acute phase, confirms that, although the globus pallidus is the commonest site of abnormality in the brain, the effects of CO poisoning are widespread. The extent of damage correlates with clinical outcome, and therefore aids management and prognosis.
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              Carbon monoxide poisoning.

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                Author and article information

                Journal
                Ann Indian Acad Neurol
                AIAN
                Annals of Indian Academy of Neurology
                Medknow Publications (India )
                0972-2327
                1998-3549
                Oct-Dec 2008
                : 11
                : 4
                : 251-253
                Affiliations
                Department of Radiodiagnosis, Regional Institute of Medical Sciences, Imphal, Manipur, India
                [1 ]Department of Neurology, Regional Institute of Medical Sciences, Imphal, Manipur, India
                Author notes
                For correspondence: Dr. S. Subhaschandra Singh, Radiodiagnosis Department, Regional Institute of Medical Sciences, Imphal. Manipur-795004, India. E-mail: drsubhasc@ 123456yahoo.co.in
                Article
                AIAN-11-251
                10.4103/0972-2327.44563
                2771996
                19893684
                a2ebbcd1-a3ad-46bb-ad21-d270b0ad4cbf
                © Annals of Indian Academy of Neurology

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 06 February 2008
                : 15 May 2008
                : 14 July 2008
                Categories
                Case Report

                Neurology
                basal ganglia,t2- hyperintensity,carbon monoxide
                Neurology
                basal ganglia, t2- hyperintensity, carbon monoxide

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