Advanced neuroimaging of carbon monoxide poisoning

Abstract

Carbon monoxide (CO) inhalation is nowadays the most common cause of fatal poisoning worldwide. CO binds to haemoglobin 230-270 times more avidly than oxygen, thus leading to formation of carboxyhaemoglobin with subsequent reduction of tissue oxygenation. Brain is mainly affected due to its high oxygen requirement. Up to two-thirds of patients who survive the acute phase of this pathology present a delayed leukoencephalopathy, usually in a period ranging from two to 40 days. White matter damage closely relates to long-term prognosis of these patients. On the other hand CO seems to play a fundamental role as a possible neuro-protective agent in ischaemic stroke. Diagnostic imaging, with computed tomography and magnetic resonance imaging, especially magnetic resonance spectroscopy, is very useful to depict the presence and extension of this pathology, in both acute and late phase. Nevertheless, a correlation of imaging studies with clinical history and laboratory data is fundamental to perform the correct diagnosis. The purpose of this article is to highlight the imaging features of brain CO poisoning in acute and late phase, describing a case report of a 56-year-old man found unconscious at home.

Keywords: Brain CO poisoning; diffusion magnetic resonance imaging; leukoencephalopathy; magnetic resonance spectroscopy.

Figure 1.

Suggested emergency management of patients with suspicion of carbon monoxide poisoning. CO: carbon monoxide; GCS: Glasgow coma scale; EKG: electrocardiogram; COHb: carboxyhaemoglobin

Figure 2.

(a) and (c): mildly hypodense areas bilaterally affecting globus pallidus; no relevant findings in the centrum semiovale. (b) and (d): Six weeks follow-up showing malacic evolution of the bilateral and symmetrical hypodensities in the globus pallidus. Appearance of microlacunar lesions bilaterally involving centrum semiovale.

Figure 3.

(a) and (b): T1- and T2-weighted sequences showing bilateral and symmetrical infarctions in the globus pallidus. (c) and (d): H-MR spectrum in the right centrum semiovale showing increase in choline/creatine ratio, slight reduction of N-acetylaspartate and evidence of lactate peak. These findings show demyelination, loss or degeneration of neurons and activation of anaerobic metabolism.

Figure 4.

(a) to (d): axial and coronal FLAIR sequences bilaterally showing infarction of nucleus pallidus and multiple lesions involving the periventricular white matter of corona radiata and centrum semiovale.

Figure 5.

(a) to (c): diffusion weighted images showing multiple, bilateral areas of restricted diffusivity involving the periventricular white matter and centrum semiovale as a result of cytotoxic oedema and progressive demyelination. (d): apparent diffusion coefficient map values bilaterally confirm the decreased diffusivity of these areas compared with normal white matter.