2004
DOI: 10.1159/000076536
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Diffusion-Weighted MRI and <sup>99m</sup>Tc-HMPAO SPECT in Delayed Relapsing Type of Carbon Monoxide Poisoning: Evidence of Delayed Cytotoxic Edema

Abstract: Background: Carbon monoxide (CO) is a common cause of poisoning, and its sequelae include a progressive (25%) and a delayed relapsing form (75%). We report the diffusion-weighted MRI (DWI) findings in the delayed relapsing form of CO poisoning and characterize the types of edema. Methods: From November 1, 2000 to June 1, 2003, 5 consecutive patients (2 men, 3 women, range of age: 54–67 years), who had the delayed relapsing type of CO poisoning, underwent DWI, conventional MRI, MR angiography and SPECT. CO pois… Show more

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Cited by 53 publications
(36 citation statements)
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“…It is difficult to determine the time course of change in ADC. For stroke, transition from decreasing to increasing ADC values seems to occur between 18 h and 7 days after stroke onset (Copen et al, 2001), while delayed cytotoxic edema with restricted ADCs was described up to 6 months, after carbon monoxide poisoning (Murata et al, 2001;Chu et al, 2004), and heroin abuse (Chen et al, 2000). Only one article was published with ADC measurements in heavy ecstasy users, and showed increased ADC values in the globus pallidus (Reneman et al, 2001b).…”
Section: Introductionmentioning
confidence: 99%
“…It is difficult to determine the time course of change in ADC. For stroke, transition from decreasing to increasing ADC values seems to occur between 18 h and 7 days after stroke onset (Copen et al, 2001), while delayed cytotoxic edema with restricted ADCs was described up to 6 months, after carbon monoxide poisoning (Murata et al, 2001;Chu et al, 2004), and heroin abuse (Chen et al, 2000). Only one article was published with ADC measurements in heavy ecstasy users, and showed increased ADC values in the globus pallidus (Reneman et al, 2001b).…”
Section: Introductionmentioning
confidence: 99%
“…Hypoperfusion (Sesay, Bidabe et al 1996;Watanabe, Nohara et al 2002;Chu, Jung et al 2004) and hypoxia (Opeskin and Drummer 1994) still play an important role. Demyelination (Murata, Kimura et al 2001;Kamijo, Soma et al 2007;Ide and Kamijo 2008), cytotoxic edema (Kim, Chang et al 2003;Chu, Jung et al 2004;Kwon, Chung et al 2004), hemorrhage (Ramsey 2001) and infarction (Schwartz, Hennerici et al 1985;Sung, Yu et al 2010) have also been associated with delayed neurological deficits. Hypoperfusion and cytotoxic edema in delayed CNS injury have been noted in WM areas and the cerebral cortex (Chu, Jung et al 2004), and ischemia and necrosis have been noted in the globus pallidus (Chang, Han et al 1992).…”
Section: Chronic Cns Injurymentioning
confidence: 99%
“…Demyelination (Murata, Kimura et al 2001;Kamijo, Soma et al 2007;Ide and Kamijo 2008), cytotoxic edema (Kim, Chang et al 2003;Chu, Jung et al 2004;Kwon, Chung et al 2004), hemorrhage (Ramsey 2001) and infarction (Schwartz, Hennerici et al 1985;Sung, Yu et al 2010) have also been associated with delayed neurological deficits. Hypoperfusion and cytotoxic edema in delayed CNS injury have been noted in WM areas and the cerebral cortex (Chu, Jung et al 2004), and ischemia and necrosis have been noted in the globus pallidus (Chang, Han et al 1992). Although demyelination and axonal damage might co-exist in CO intoxication, demyelination more than axonal damage is suggested in the literature (Chang, Han et al 1992;Murata, Kimura et al 2001;Kamijo, Soma et al 2007;Ide and Kamijo 2008).…”
Section: Chronic Cns Injurymentioning
confidence: 99%
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