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Table 2 Comparison of radiological findings between representative toxic and hypoxic-ischemic encephalopathies

From: Neuropsychological, neuroimaging and autopsy findings of butane encephalopathy

 

Toxic encephalopathy

Acute hypoxic-ischemic encephalopathy

Delayed hypoxic-ischemic

encephalopathy

Etiology

Drugs of abuse

(e.g. Butane, Heroin)

Cardiac arrest

Acute respiratory insufficiency

Other toxic causes (e.g., CO)

Cardiorespiratory compromise

Other toxic causes

MRI findings

- High FLAIR or T2 signal intensities in the thalamus, basal ganglia, cerebellum, or insula (Butane intoxication)

- High signal changes in the putamen, and occipital and frontal lobes in DWI (Butane intoxication)

- Symmetrically increased T2 and FLAIR signal intensity of the cerebellar and posterior cerebral white matter, posterior limb of the internal capsule with sparing of the anterior limb of the internal capsule and dentate nuclei (Heroin inhalation)

- Diffuse cortical injury on DWI

- Border zone distribution of ischemia

- Increased T2 and FLAIR signal intensity in the globus pallidus along with corresponding diffusion restriction

- Much less commonly increased T2 and FLAIR signal intensity in the caudate, putamen, thalamus, hippocampus, cerebellum, and brain stem than that in the globus pallidus

- High T2-FLAIR signal intensity in the periventricular white matter and centrum semiovale sparing the cerebellum and the brainstem tracts

Reference

[2, 7, 11, 22]

[10, 23]

[24]

  1. MRI, magnetic resonance imaging; FLAIR, Fluid-attenuated inversion recovery; DWI, Diffusion weighted image; CO, Carbon Monoxide