**6. Conclusion**

366 Neuroimaging – Cognitive and Clinical Neuroscience

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

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

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

Although peripheral neuropathy has been reported in CO intoxication (Choi 1982), only

Skeletal muscle injuries have been reported in CO intoxication. In one case report, skeletal muscle MRI was performed showing hyperintensity lesions in T2WI of the thigh muscles three months after CO intoxication (Chen, Huang et al. 2010). The muscle biopsy in this patient proved the diagnosis of heterotopic ossification selectively involving the iliopsoas, the tensor fascia lata, rectus femoris, sartorius and quadriceps muscles. Another study using Tc99m-sestamibi SPECT to evaluate the skeletal muscular injuries in 25 patients after CO intoxication showed decreased uptake in the patient group as compared with the controls (Huang, Chang et al. 2011). The low uptake was related to mitochondrial dysfunction.

frontal and parietal lobes (11C, arrows) with negative findings on the CT scan (11D).

electrophysiological studies but not neuroimaging studies are available (Choi 1982).

lobes (Senol, Yildiz et al. 2009).

monoxide intoxication.

**5. Nerves and muscles** 

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, mitochondrial function can be assessed in patients with CO intoxication.
