Clinical outcome and magnetic resonance imaging of carbon monoxide intoxication. A long-term follow-up study

Abstract

The clinical and neuroradiological outcome of carbon monoxide (CO) intoxication was evaluated prospectively in 30 patients over a follow-up period of 3 years. Among the patients studied, 22 had been acutely exposed to CO while 8 were chronically exposed. One month after CO poisoning, 12 of the 22 patients with acute intoxication showed magnetic resonance imaging (MRI) abnormalities: 6 also had neurological sequelae and 6 were asymptomatic. The remaining 10 patients showed neither MRI abnormalities nor neurological sequelae. During the 3-year follow-up, 4 of the patients with both MRI abnormalities and neurological sequelae improved in both clinical features and MRI findings. One of the 6 asymptomatic patients with MRI abnormalities developed a progressive cognitive impairment 2 months after acute intoxication, with a concomitant severe worsening of the MRI lesions. Among the 10 patients with neither MRI abnormalities nor neurological sequelae, only 1 developed neurological sequelae after a clear period of 4 months. In the group of patients who experienced chronic CO intoxication, only 1 presented with a neuropsychiatric syndrome which improved at follow-up. Brain MRI showed white matter lesions which remained unchanged at control scan after 1 year. In conclusion, we observed that some patients with severe CO poisoning and neurological sequelae may fully regain normal functions after approximately 1 year. The presence of MRI lesions 1 month after CO poisoning did not accurately predict the subsequent outcome. The observation of a clear period longer than the usual 2-40 day interval in 2 patients should be considered for careful planning of follow-up and for prognosis in CO-poisoned patients.

White Matter Damage in Carbon Monoxide Intoxication Assessed in Vivo Using Diffusion Tensor MR Imaging

“…[1][2][3][4][8][9][10][11][12][13][14][15] They include hindered executive function and slowed mental processing speed, which are often observed after frontal lobe damage, and altered visuospatial abilities, which are commonly observed after parietal lobe injury. 10 Central executive function involves corticocortical connectivity, 31 which depends mainly on complex WM networks.…”

“…8,9 With conventional MR imaging, WM lesions are identified in 12%-37% of patients, but the findings are not related to the severity of intoxication. 10,11 Imaging appears to be relatively insensitive for assessing the clinical consequences of neurotoxicity in these patients.…”

Neuroimaging Studies in Carbon Monoxide Intoxication

“…The largest study included 129 patients, and 33% of them had WM lesions on brain CT (Choi, Kim et al 1993). In patients with improvements of neurological deficits, resolution of WM changes have also been noted (Klostermann, Vieregge et al 1993;Matsushita, Takahashi et al 1996;Pavese, Napolitano et al 1999). Lesions of the WM area are believed to be associated with clinical outcomes (Miura, Mitomo et al 1985;Vieregge, Klostermann et al 1989;Choi, Kim et al 1993).…”

“…The study revealed no correlation between WM hyperintensities and carboxyhemoglobin level, or duration of CO exposure at any of the three scan times (Parkinson, Hopkins et al 2002). Hyperintensities in T2WI and fluid-attenuated inversion recovery (FLAIR) and hypointensities in T1WI often suggest WM demyelination or axonopathy (Chang, Han et al 1992;Pavese, Napolitano et al 1999;Parkinson, Hopkins et al 2002). From a pathological perspective, myelin damage is constant and can vary from discrete perivascular lesions to extensive periventricular demyelination and/or axonal destruction (Funata, Okeda et al 1982;Prockop and Chichkova 2007).…”

“…The latter is often termed as delayed neuropsychiatric sequela in CO intoxication. The lucid interval after acute CO poisoning, on average, is around 20 days, varying from one to 240 days (Choi 1983;Lee and Marsden 1994;Ernst and Zibrak 1998;Pavese, Napolitano et al 1999;Hsiao, Kuo et al 2004), with a prevalence of 0.2-40% (Hsiao, Kuo et al 2004;Otubo, Shirakawa et al 2007). Delayed neuropsychiatric sequelae include parkinsonism (Lee and Marsden 1994), chorea (Park and Choi 2004), akinetic mutism (Lee and Marsden 1994), increased irritability, verbal aggressiveness, violence, impulsiveness (Meredith and Vale 1988), mood disorders (Weaver 2009), dementia (Meredith and Vale 1988;Ernst and Zibrak 1998;Weaver 2009), psychosis (Ernst and Zibrak 1998), sleep disturbances (Weaver 2009), cortical blindness (Quattrocolo, Leotta et al 1987;Senol, Yildiz et al 2009) and incontinence (Ernst and Zibrak 1998).…”