MRI, Quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning

Abstract

Carbon monoxide (CO) poisoning has been shown to result in neuropathologic changes and cognitive impairments due to anoxia and other related biochemical mechanisms. The present study investigated brain-behaviour relationships between neuropsychological outcome and SPECT, MRI, and Quantitative magnetic resonance imaging (QMRI) in 21 patients with CO poisoning. Ninety-three per cent of the patients exhibited a variety of cognitive impairments, including impaired attention, memory, executive function, and mental processing speed. Ninety-five per cent of the patients experienced affective changes including depression and anxiety. The results from the imaging studies revealed that 38% of the patients had abnormal clinical MRI scans, 67% had abnormal SPECT scans, and 67% had QMRI findings including hippocampal atrophy and/or diffuse cortical atrophy evidenced by an enlarged ventricle-to-brain ratio (VBR). Hippocampal atrophy was also found on QMRI. SPECT and QMRI appear to be sensitive tools which can be used to identify the neuropathological changes and cerebral perfusion defects which occur following CO poisoning. Cerebral perfusion defects include frontal and temporal lobe hypoperfusion. Significant relationships existed between the various imaging techniques and neuropsychological impairments. The data from this study indicate that a multi-faceted approach to clinical evaluation of the neuropathological and neurobehavioural changes following CO poisoning may provide comprehensive information regarding the neuroanatomical and neurobehavioural effects of CO poisoning.

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

“…2 Cognitive sequelae include impairments in memory, executive function, attention, visual spatial skills, mental processing speed, and apraxia and dementia. 3 Formal neuropsychological tests have confirmed these impairments. 3,4 After acute CO intoxication, patients may develop progressive white matter (WM) demyelination.…”

“…3 Formal neuropsychological tests have confirmed these impairments. 3,4 After acute CO intoxication, patients may develop progressive white matter (WM) demyelination. 5 This damage is variable and ranges from discrete perivascular foci in the corpus callosum to extensive periventricular demyelination and axonal destruction.…”

“…[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.…”

Neurobehavioral Grand Rounds Introduction: Does near drowning in ice water prevent anoxic induced brain injury?

“…Similarly, brain MRI findings in anoxic patients who were not near-drowning accidents include lesions in gray (e.g., basal ganglia, hippocampus, etc) and white matter, and global and focal atrophy (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986). Whereas braining imaging was normal by radiologic report in Case 1, quantitative neuroimaging was not carried out (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Gale et al, 1999;Hopkins et al, 1995b). Nonspecific brain damage may result in general volume reduction manifested by reduced gyral volume, increased sulcal space, passive increase in ventricular volume (i.e., hydrocephalus ex vacuo), increase in whole brain cerebral spinal fluid (CSF; Graham et al, 2002), and structural atrophy (e.g.…”

“…Vulnerable brain regions include the neocortex, hippocampus, basal ganglia, cerebellum, primary visual cortex, frontal regions, and thalamus (Chalela et al, 2001). Anoxic brain injury results in focal and diffuse neuropathologic lesions and atrophy (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Gale et al, 1999;Hopkins et al, 1995b) including lesions in the hippocampus (Manns et al, 2003a;Manns et al, 2003b), basal ganglia, cerebellum (Mascalchi et al, 1996), subcortical and periventricular white matter lesions (Parkinson et al, 2002) and atrophy of the corpus callosum (Porter et al, 2002). Generalized brain volume loss leading to ventricular enlargement and sulcal widening (Caine & Watson, 2000) and hippocampal atrophy are also common (Hopkins et al, 1995b;Press et al, 1989).…”