Longitudinal study of carbon monoxide intoxication by diffusion tensor imaging with neurospsychiatric correlation

Abstract

115Background: White matter damage is common after carbon monoxide (CO) intoxication, but in vivo follow-up studies about the mechanism of white matter damage are not possible in pathology series. Diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) can quantify diffusion parameters and volumetric changes in white matter that can be correlated with neuropsychological performances in longitudinal studies. Methods: We examined 9 patients with CO intoxication using DTI, VBM and neuropsychologic tests at an average of 3 and 10 months after CO exposure. We used data from 18 age-and sex-matched controls for comparison. Results: We found that cognitive recovery at 10 months after CO intoxication was not significant, although it was after 3 months. The neuropsychologic tests correlated better for the fibre tract of the semicentrum ovale and not the periventricular fibres. Diffusion measures suggest increases in fractional anisotropy, mean diffusivity and axial eigenvalues over time, while increases in radial eigenvalue were evident at 3 months compared with controls. Periventricular white matter atrophy was observed 10 months after CO intoxication. Limitations: Our study included few cases, and the interpretation of the putative changes on neuroimaging findings cannot be confirmed by histology. Conclusion: Our study showed that the evolution of white matter injury in CO encephalopathy occurred over time. Cognitive recovery was not evident in the follow-up period because of white matter injuries.

The Role of MR Imaging in Assessment of Brain Damage from Carbon Monoxide Poisoning: A Review of the Literature

“…Selection of these areas was sensible because some reports have shown a relationship between damage in the centrum semiovale and cognitive disorder after CO poisoning. 48,59 Our previous study in which we used DTI with voxelbased analysis also showed that deep WM areas including the centrum semiovale were the most widely damaged regions in those patients presenting with chronic symptoms (Fig 4). 60 When the CO-damaged brain is assessed by DWI or DTI, it is important to emphasize that evaluations of deep WM, including the centrum semiovale, are indispensable.…”

Neuroimaging Studies in Carbon Monoxide Intoxication

“…A longitudinal study used diffusion tensor imaging (DTI) and compared the changes of diffusion measurements in CO intoxication patients including mean diffusivity, axial diffusivity and radial diffusivity with follow-up scans three months and 10 months later. Extensive changes found in the FA maps at both three and 10 months in the CO group were attributed to initial increments of radial diffusivities, while a decrement of axial diffusivities were found at 10 months follow-up (Chang, Chang et al 2010). The study suggested that changes in diffusion parameters might reflect WM demyelination at three months followed by subsequent axonopathy.…”

“…White matter insults after CO intoxication lead to transient or permanent injuries, which consequently lead to decreased WM volumes. Diffusion indices including mean diffusivity, axial diffusivity and radial diffusivity reflect WM injuries earlier than volume reduction, while the major regions of WM atrophy in one study were in the periventricular WM areas (Chang, Chang et al 2010). …”

“…Voxel based morphometry (Ashburner and Friston 2001) enables the quantification of grey and WM volume changes between groups. In one study using voxel based morphometry, no significant differences in the GM were found in the patient group compared to age-matched controls ten months after CO intoxication (Chang, Chang et al 2010), while atrophy of WM was evident in the periventricular areas. In another study of 13 patients with brain MRI studies 25 years after CO poisoning, the parieto-occipital region was most frequently involved, and six of the 13 patients had dilated temporal horns (Uchino, Hasuo et al 1994).…”

“…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). The cognitive deficits are often very diverse (Hurley, Hopkins et al 2001;Parkinson, Hopkins et al 2002;Raub and Benignus 2002) including impairment in verbal or visual episodic memory, language, visuospatial ability, executive function and calculation (Chang, Chang et al 2010). No specific neuropsychiatric battery has been designed for the cognitive deficits in CO intoxication.…”