**3.1 The diagnosis of CO intoxication**

The diagnosis of CO intoxication is based on the clinical history of exposure or elevated carboxyhemoglobin level (> 10%) (Handa and Tai 2005; Chang, Lee et al. 2009). There is currently no definition of clinical staging in CO intoxication in the literature, although the pathophysiology follows that of hypoxic–ischemic encephalopathy (Gutierrez, Rovira et al.).

Neuroimaging Studies in Carbon Monoxide Intoxication 357

prevalence differs among studies (Silver, Cross et al. 1996; O'Donnell, Buxton et al. 2000). One study showed 63% of abnormal lesions in the GP with 26% in the rest of the basal ganglia (O'Donnell, Buxton et al. 2000). Another study with 73 patients revealed only one patient (1.4%) with basal ganglia lesions scanned two weeks after CO poisoning (Parkinson,

Low density GP lesions, commonly seen in computed tomography (CT), are considered as characteristic findings in patients with CO intoxication (Kanaya, Imaizumi et al. 1992; Gotoh, Kuyama et al. 1993; Uchino, Hasuo et al. 1994; Chu, Jung et al. 2004; Kinoshita, Sugihara et al. 2005; Hopkins, Fearing et al. 2006). Low density lesions of the putamen and caudate nucleus, in contrast, have only been reported in one case (Ferrier, Wallace et al. 1994). The nature of GP lesions has been studied further by diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) mapping (Chu, Jung et al. 2004; Kinoshita, Sugihara et al. 2005). One case report interpreted low ADC values and high intensity GP lesions on DWI as restriction of water diffusion (i.e. cytotoxic edema) (Kinoshita, Sugihara et al. 2005). Vasogenic edema can also be visualized on ADC and DWI as increased signal intensity lesions (Chalela, Wolf et al.

Fig. 1. Magnetic resonance imaging study in the acute stage of carbon monoxide intoxication. Six days after CO intoxication, a 42-year-old woman with a globus pallidus interna lesion with hyperintensity in diffusion weighted imaging (1A), hypointensity in apparent diffusion coefficient (1B), hypointensity in T1 weighted image (WI) (1C), hyperintensity in T2WI (1D),

Imaging studies showing cavity-changes by T1 or T2WI often suggest necrosis of the GP (Mendelsohn and Hertzanu 1983; Pulst, Walshe et al. 1983; Ko, Ahn et al. 2004). Autopsies of patients with CO intoxication have confirmed the histology of necrosis and/or neuronal degeneration of the GP (Jones, Lagasse et al. 1994). The pathogenesis of necrosis is believed to be due to edema-induced ischemia or hemorrhage transformation (Chang, Han et al.

**4.1.1 Imaging features suggesting edematous change in the acute phase** 

2001). The high signal on DWI is due to the T2 shine-through effect.

and hyperintensity in fluid-attenuated inversion recovery (1E).

**4.1.2 Imaging features suggesting necrosis** 

Hopkins et al. 2002).

### **3.2 Symptoms in the acute phase**

Tightness across the forehead, headache, throbbing in the temples, nausea, vomiting, dimness of vision, dizziness, general weakness, syncope, convulsion, and coma are commonly found in patients with CO exposure within one day (Choi 2001). Cortical blindness with initially normal visual evoked potentials has also been reported in a case (Katafuchi, Nishimi et al. 1985). The pathogenesis contributing to the clinical manifestations includes change of blood flow (Penney 1990; Lo, Chen et al. 2007), hypoxia (Lo, Chen et al. 2007), and neurochemistry abnormalities (Penney 1990).
