The pathogenesis of carbon monoxide encephalopathy in the acute phase?Physiological and morphological correlation

Okeda, Riki; Funata, Nobuaki; Takano, Takehito; Miyazaki, Y.; Higashino, Fumio; Yokoyama, Kazuaki; Manabe, Masanobu

doi:10.1007/bf00691327

Cited by 87 publications

(26 citation statements)

References 26 publications

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“…In man and animal it was shown that CO exposure initially increases arterial blood flow in cortex and white matter along with the concentration of Co Hb, followed by a rapid fall in blood flow and blood pressure mainly in the white matter [44], These changes occur within the first hour during CO intoxication and cannot be corre lated to the findings of the PET examinations that were performed weeks after the acute event. On the other hand, transient hyperemia, followed by delayed hypo perfusion has been described after prolonged cerebral ischemia in cats.…”

Section: Discussionmentioning

confidence: 86%

Delayed Neurological Deterioration following Acute Carbon Monoxide Poisoning: Comparison of Clinical Outcome, Neuro-Imaging and Positron Emission Tomography Findings

Reuck¹,

Aken

Decoo³

et al. 1991

Cerebrovasc Dis

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In 8 patients with delayed neurological deterioration, following acute CO poisoning, the clinical outcome, the neuroimaging and the positron emission tomography (PET) findings were compared. The severity of the neuropsychiatric sequelae correlated well with the changes of blood flow and oxygen metabolism and the CT scan findings in the brain. Nuclear magnetic resonance (NMR) appeared to have less predictive value on the clinical outcome. In the severe cases of post-CO encephalopathy, the ischemic nature of the metabolic changes could be demonstrated in the cortical regions by PET. However, it could not be determined whether the disturbances in the basal ganglia and cerebral white matter were only due to ischemia or to an additional cytotoxic effect of CO.

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Section: Discussionmentioning

confidence: 86%

Delayed Neurological Deterioration following Acute Carbon Monoxide Poisoning: Comparison of Clinical Outcome, Neuro-Imaging and Positron Emission Tomography Findings

Reuck¹,

Aken

Decoo³

et al. 1991

Cerebrovasc Dis

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“…This theory helps to explain why CO-Hgb levels do not correlate with the severity of clinical effects [50][51][52][53][54]. An outline of some of the proposed mechanisms is presented in Fig.…”

Section: Direct Cellular Toxicitymentioning

confidence: 95%

Carbon monoxide poisoning

Kao¹,

Nañagas²

2004

Emergency Medicine Clinics of North America

170

171

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“…9 Whereas hypotension adds to hypoxia, the hypoxic-hypotension process leads to ischemic changes in the arterial border zones in the brain. 10 Brain hypoxia increases the level of excitatory amino acids including glutamine, leading to elevated nitrite levels and causing subsequent injuries to the cerebral cortex. 11 Furthermore, hypoxia in the brain causes oxidative stress, cellular necrosis, apoptosis, and ongoing inflammation.…”

Section: Mechanisms Causing Brain Damage After Co Exposurementioning

confidence: 99%

The Role of MR Imaging in Assessment of Brain Damage from Carbon Monoxide Poisoning: A Review of the Literature

Beppu

2013

American Journal of Neuroradiology

105

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SUMMARY:The aim of this article is to review how MR imaging and associated imaging modalities provide clinicopathologic information on brain damage after carbon monoxide poisoning. Initially, many authors documented typical findings of conventional MR imaging in the gray matter structures such as the globus pallidus and in various regions of cerebral white matter. The focus of investigation has since shifted to observation of cerebral white matter areas that are more frequently detected on MR imaging and are more responsible for chronic symptoms than the gray matter. DWI has dramatically contributed to the ability to quantitatively assess cerebral white matter damage. Subsequently, DTI has enabled more sensitive evaluation than DWI and can demonstrate progressive pathologic changes in the early stage, allowing prediction of chronic conditions. In addition, MR spectroscopy reveals changes in metabolite levels, offering quantitative clinicopathologic information on brain damage after carbon monoxide poisoning.ABBREVIATIONS: CO ϭ carbon monoxide; CWM ϭ cerebral white matter; DNS ϭ delayed neuropsychiatric sequelae; FA ϭ fractional anisotropy; GP ϭ globus

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The pathogenesis of carbon monoxide encephalopathy in the acute phase?Physiological and morphological correlation

Cited by 87 publications

References 26 publications

Delayed Neurological Deterioration following Acute Carbon Monoxide Poisoning: Comparison of Clinical Outcome, Neuro-Imaging and Positron Emission Tomography Findings

Delayed Neurological Deterioration following Acute Carbon Monoxide Poisoning: Comparison of Clinical Outcome, Neuro-Imaging and Positron Emission Tomography Findings

Carbon monoxide poisoning

The Role of MR Imaging in Assessment of Brain Damage from Carbon Monoxide Poisoning: A Review of the Literature

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