**4.2.3 Imaging features suggesting WM hemorrhage**

In the acute phase, petechial hemorrhages of the WM, particularly the corpus callosum, are common (Funata, Okeda et al. 1982; Finelli and DiMario 2004; Weaver and Hopkins 2005). Gradient echo T2WI uses a shorter repetition time than spin-echo T2WI and can detect metal material such as ferritin and ferritin-containing substances such as hemosiderin, thus detecting hemorrhages and microbleeds (Atlas, Grossman et al. 1988; Bradley 1993). Susceptibility-weighted imaging (SWI) is a heavy T2\*-weighted gradient-recalled 3-D fast low-angle shot sequence with full flow compensation in all three directions (Sehgal, Delproposto et al. 2005). Microhemorrhages have been reported in patients with CO intoxication with the complimentary information provided by gradient echo T2WI and SWI (Finelli and DiMario 2004; Weaver and Hopkins 2005). In gradient echo T2WI, hemorrhages along the nerve fibers are distributed predominantly over the posterior WM (Finelli and DiMario 2004).

Fig. 8. Microhemorrhage shown on susceptibility-weighted imaging.

Four months after carbon monoxide intoxication, a 53-year-old woman with a low signal intensity lesion on susceptibility-weighted imaging (8A, arrow) suggesting microhemorrhage of white matter which was invisible on T1 (8B), T2 (8C), and fluidattenuated inversion recovery (8D).

#### **4.3 Cortex**

#### **4.3.1 Imaging features suggesting cortical injury and atrophy**

Pure cortical involvement without concurrent WM lesions in CO intoxication is not common (Choi, Kim et al. 1993). Using DWI, imaging features suggesting cortical cytotoxic edema were described in bilateral posterior temporal lobes and bilateral occipital lobes in one patient, bilateral posterior temporal lobes and left parietal lobe in

Neuroimaging Studies in Carbon Monoxide Intoxication 365

Fig. 10. Cortical atrophy after carbon monoxide intoxication revealed in T1-weighted image. A 47-year-old woman with rapid cortical atrophy after CO intoxication as revealed in T1WI

Hemorrhage in the cortical areas has also been reported in CO intoxication. One 28-year-old man had achromatopsia five months after CO intoxication (Fine and Parker 1996). Brain MRI revealed hemorrhage in the bilateral temporal and occipital lobes (Fine and Parker 1996). Another case demonstrated a 7-year-old boy who had generalized convulsions, coma and right hemiparesis on the day of CO intoxication (El Khashab and Nejat 2009). Brain CT on the same day revealed a left temporal hemorrhage (El Khashab and Nejat 2009). Microvascular impairment and brain reperfusion injury were the suspected pathogenetic

**4.3.3 Imaging features suggesting cortical hypoperfusion and hypometabolism**  Six studies have reported SPECT findings in the evaluation of cortical blood flow after CO intoxication (Choi, Lee et al. 1992; Choi, Kim et al. 1995; Watanabe, Nohara et al. 2002; Pach, Hubalewska et al. 2004; Huang SH, Chang Chiung Chih2 et al. 2005; Pach, Urbanik et al. 2005). The largest one included 20 cases with 85% of the patients showing hypoperfusion over the frontal-parietal cortex (Pach, Hubalewska et al. 2004). In a study on follow-up SPECT in patients with CO intoxication, six of seven patients had improvement of hypoperfusion throughout the cortex, while their clinical conditions also improved concomitantly (Choi, Kim et al. 1995). In a comparison between those with delayed neuropsychiatric sequelae and those without sequelae, significant hypoperfusion was noted over bilateral frontal lobes, bilateral insula and right temporal lobe in patients with delayed neuropsychiatric sequelae, whilst only bilateral frontal lobe hypoperfusion was noted in

three months (9A) and 20 months (9B) after CO exposure.

**4.3.2 Imaging features suggesting cortical hemorrhage** 

mechanisms causing the damage (El Khashab and Nejat 2009).

those without neuropsychiatric sequelae (Watanabe, Nohara et al. 2002).

To date, there have only been a limited number of reports on [18F] FDG-PET in the evaluation of metabolic dysfunction in the cortical areas of patients with CO intoxication (Tengvar, Johansson et al. 2004; Senol, Yildiz et al. 2009). One case report of a middle-aged man revealed hypometabolism of bilateral frontal lobes and anterior cingulate cortices (Tengvar, Johansson et al. 2004), and his neurological deficit of akinetic mutism was regarded as the consequence of

another patient, and right frontal, temporal and parietal lobes in another (Hon, Yeung et al. 2006). Hippocampal involvement has been linked with anterograde amnesia, with pathological findings of necrosis and apoptosis (Uemura, Harada et al. 2001; Mahmoud, Mestour et al. 2009).

Fig. 9. Cortical injuries after CO intoxication.

Four days after CO intoxication, a 37-year-old woman with hyperintensities in bilateral hippocampi in a T2-weighted image (9A). Six days after CO intoxication, a 42-year-old woman with hyperintensities in bilateral superior frontal gyrus in fluid-attenuated inversion recovery (9B). Another 28-year-old female five days after CO intoxication showed bilateral medial temporal region high signal intensity lesions (9C, diffusion weighted image, arrows) with corresponding low intensity lesions on apparent diffusion coefficient map (9D, arrows) suggesting cytotoxic edema.

Cortical volume reduction is a late consequence of CO intoxication. Significant ventricle and sulcus dilatation in comparison with the controls were found in all 34 patients evaluated during the chronic phase of CO intoxication in a study by Kono et al. (Kono, Kono et al. 1983), with a 19-year interval from CO intoxication. In a case report several months after CO intoxication, brain MRI revealed bilateral atrophy of lateral temporal lobes and the clinical deficits included severe cognitive impairment and a transient Klüver-Bucy-like behavior (Muller and Gruber 2001). 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).

another patient, and right frontal, temporal and parietal lobes in another (Hon, Yeung et al. 2006). Hippocampal involvement has been linked with anterograde amnesia, with pathological findings of necrosis and apoptosis (Uemura, Harada et al. 2001; Mahmoud,

Four days after CO intoxication, a 37-year-old woman with hyperintensities in bilateral hippocampi in a T2-weighted image (9A). Six days after CO intoxication, a 42-year-old woman with hyperintensities in bilateral superior frontal gyrus in fluid-attenuated inversion recovery (9B). Another 28-year-old female five days after CO intoxication showed bilateral medial temporal region high signal intensity lesions (9C, diffusion weighted image, arrows) with corresponding low intensity lesions on apparent diffusion coefficient map (9D, arrows)

Cortical volume reduction is a late consequence of CO intoxication. Significant ventricle and sulcus dilatation in comparison with the controls were found in all 34 patients evaluated during the chronic phase of CO intoxication in a study by Kono et al. (Kono, Kono et al. 1983), with a 19-year interval from CO intoxication. In a case report several months after CO intoxication, brain MRI revealed bilateral atrophy of lateral temporal lobes and the clinical deficits included severe cognitive impairment and a transient Klüver-Bucy-like behavior (Muller and Gruber 2001). 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

Mestour et al. 2009).

Fig. 9. Cortical injuries after CO intoxication.

suggesting cytotoxic edema.

(Uchino, Hasuo et al. 1994).

Fig. 10. Cortical atrophy after carbon monoxide intoxication revealed in T1-weighted image.

A 47-year-old woman with rapid cortical atrophy after CO intoxication as revealed in T1WI three months (9A) and 20 months (9B) after CO exposure.
