Anoxic/Toxic Brain Injury

David Cheng, MD
Liangge Hsu, MD

September 8, 1997

Presentation

A previously healthy 29-year-old man was brought to the ER after being found in bed unconscious and difficult to arouse. He displayed abnormal posturing in the emergency room.

Imaging Findings

Noncontrast CT images of head

MR images of the brain (one week after CT)

The noncontrast computed tomograms (CT) of the head demonstrate symmetrical bilateral low attenuation areas in the globus pallidus (arrows). No other abnormalities are visible.

Follow-up magnetic resonance (MR) images of the brain (obtained one week later) demonstrate abnormal T2 hyperintensity bilaterally in the globus pallidus (black arrows), cerebellar hemispheres, and frontoparietal white matter.

Diagnosis

Anoxic/toxic brain injury

Discussion

Symmetrical low attenuation pallidal lesions in adults are compatible with a diffuse metabolic insult such as hypoxia, global ischemia, or exposure to toxins. Presumably the more metabolically active areas in the brain are preferentially injured. These include the putamen, caudate nucleus, thalamus, parahippocampal gyrus, hippocampus, cerebellar hemispheres, brainstem nuclei, and cerebral white matter (1,3). The underlying event can be hypotension, hypoxia, hypoglycemia, or exposure to carbon monoxide, cyanide, barbiturates, or hydrogen sulfide (2). In cases of carbon monoxide poisoning, pallidal hyperlucency on CT may persist for months, and MR findings, which are compatible with hemorrhagic necrosis, may persist for years (3,4). Although brain injury is generally associated with a poor prognosis, the extent of cerebral white matter lesions may be a better predictor of outcome (3).

This patient did not have documented hypotension, hypoxia, or carbon monoxide exposure. His toxic screen was positive for opiates, benzodiazepine metabolites, and amphetamines. Laboratory testing revealed acute renal failure, rhabdomyolysis, and liver injury with transaminitis. The overall clinical picture was compatible with exposure to 3,4-methylenedioxymethylamphetamine (MDMA), also known as "Ecstasy". Use of MDMA has been associated with the multiple organ injury seen in this patient, including hypoxic brain injury and hemorrhagic infarcts (5,6). Laboratory confirmation of MDMA use in this patient could not be obtained.

References

1. Osborne AG. Diagnostic neuroradiology. St Louis: Mosby, 1994:355-60, 766-69.

2. Yock DH Jr. Computed tomography of CNS disease: a teaching file. Chicago:Year Book Medical, 1985:153.

3. Miura T, Mitomo M, Kawai M, Harada K. CT of the brain in acute carbon monoxide intoxication: characteristic features and prognosis. Am J Neuroradiol 1985;6:739-42.

4. Silverman CS, Brener J, Murtagh FR. Hemorrhagic necrosis and vascular injury in carbon monoxide poisoning: MR demonstration. Am J Neuroradiol 1993;14:168-70.

5. Milroy CM, Clark JC, Forrest AR. Pathology of deaths associated with "Ecstasy" and "Eve" misuse. J Clin Pathol 1996 Feb;49(2):149-53.

6. Manchanda S, Connolly MJ. Cerebral infarction in association with "Ecstasy" abuse. Postgrad Med J 1993 Nov;69(817):874-5.

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