**4.3.2 Imaging features suggesting cortical hemorrhage**

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

### **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 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

Neuroimaging Studies in Carbon Monoxide Intoxication 367

Fig. 12. Planar view of technetium-99m-sestamibi (99mTc-MIBI) in the evaluation of muscle

Compared with muscle 99mTc-MIBI of a normal control (12A), a 59-year-old man showed decreased 99mTc-MIBI uptake in the thigh muscles two months after CO intoxication (12B).

Damage to the neurological system after CO intoxication includes the basal ganglia, cerebral WM, cortex and muscles. The mechanisms of damage can be identified by MRI and correlated with clinical features. Apart from MRI, functional imaging can provide information about brain perfusion and metabolism in CO intoxication. With muscle MIBI,

The study was supported by grants CMRPG 880951, 890871 and 860171 from Kaohsiung

Adam, J., M. Baulac, et al. (2008). Behavioral symptoms after pallido-nigral lesions: a clinico-

Akaiwa, Y., I. Hozumi, et al. (2002). [A case suspected of acute gas poisoning by carbon

Ashburner, J. and K. J. Friston (2001). Why voxel-based morphometry should be used.

Atlas, S. W., R. I. Grossman, et al. (1988). Calcified intracranial lesions: detection with gradientecho-acquisition rapid MR imaging. *AJR Am J Roentgenol* 150, 6: pp. 1383-1389.

associated with marked brain edema]. *No To Shinkei* 54, 6: pp. 493-497. Arbuthnott, K. and J. Frank (2000). Trail making test, part B as a measure of executive

monoxide (CO), presenting with progressive diffuse leukoencephalopathy

control: validation using a set-switching paradigm. *J Clin Exp Neuropsychol* 22, 4:

mitochondrial function can be assessed in patients with CO intoxication.

pathological case. *Neurocase* 14, 2: pp. 125-130.

injury in a patient with carbon monoxide intoxication.

**6. Conclusion** 

**7. Acknowledgments** 

**8. References** 

Chang Gung Memorial Hospital.

pp. 518-528.

*Neuroimage* 14, 6: pp. 1238-1243.

the hypometabolism state of the involved regions (Tengvar, Johansson et al. 2004). In a study of serial [18F] FDG-PET follow-up scans, persistent hypometabolism of bilateral frontal lobes was found in a 29-year-old woman who demonstrated impaired responsiveness to stimuli for one year after CO poisoning (Shimosegawa, Hatazawa et al. 1992). In another case report on a 21-year-old woman who had coma, seizure and cortical blindness within three days after CO poisoning, the neurological deficit of cortical blindness remained. A subsequent [18F] FDG-PET four years later still showed hypometabolism of bilateral posterior temporal and occipital lobes (Senol, Yildiz et al. 2009).

Fig. 11. [18F]fluorodeoxyglucose positron emission tomography of two patients after carbon monoxide intoxication.

One month after CO intoxication, a patient's (age: 30) PET revealed reduced uptake of FDG in bilateral temporal and occipital lobes (11A, arrows), while the brain CT (11B) did not detect any hypodense lesions over the corresponding areas. One month after CO intoxication, another patient's (age: 58) PET revealed reduced uptake of FDG in bilateral frontal and parietal lobes (11C, arrows) with negative findings on the CT scan (11D).
