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Radiodiagnosis · Neuroimaging

Toxic encephalopathy

Encephalopathia toxica

Toxic encephalopathy is a severe brain injury caused by exposure to exogenous toxins (drugs, illicit substances, alcohols, or heavy metals). The condition manifests with specific neurological disorders and characteristic MRI patterns that depend on the type of agent involved.

Carbon monoxideCauses bilateral necrosis of the globus pallidus due to acute hypoxia.
MethanolFormic acid selectively affects the putamen, causing necrosis.
Heroin inhalationLeads to symmetrical leukoencephalopathy, while the dentate nuclei remain intact.
GadoliniumIn acute renal failure, it can accumulate in the cerebrospinal fluid.
3 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Drugs and medications

Toxic exposure to illicit substances is often accompanied by severe vascular catastrophes and demyelination.

  • Cocaine: Promotes ischemic and hemorrhagic strokes. Hemorrhages occur twice as often and are usually localized in the subarachnoid space or intracerebral structures (basal ganglia, thalamus). The mechanism is associated with a sympathomimetic spike in blood pressure, which can lead to the rupture of aneurysms or arteriovenous malformations. Adulterants play an important role: the anthelmintic drug levamisole causes multifocal inflammatory leukoencephalopathy (lesions are hyperintense on T2-FLAIR with a rim of restricted diffusion).
  • Opioids (heroin): Ischemic strokes are the most frequent complication. The globus pallidus is often the target. A specific variant is the "chasing the dragon" syndrome from inhaling heroin vapors. MRI shows extensive symmetrical hyperintensity of the white matter: the posterior limb of the internal capsule (crus posterius capsulae internae), medial lemniscus (lemniscus medialis), and pyramidal tracts. The cortex and cerebellar dentate nuclei (nucleus dentatus) remain intact.
  • Ecstasy (MDMA): Causes a massive release of serotonin, leading to severe vasoconstriction and necrosis of the most vulnerable zones—the occipital cortex and globus pallidus.

Alcohol and surrogates

Chronic alcohol abuse leads to diffuse and focal lesions.

  1. Brain atrophy: Begins with infratentorial structures (atrophy of the cerebellar vermis — vermis), then extends to the frontal and temporal lobes. If alcohol affects the fetus, it inhibits the maturation of Bergmann glial fibers, causing marked cerebellar atrophy.
  2. Marchiafava-Bignami disease: A rare complication associated with the consumption of low-quality red wine and B-vitamin deficiency. Demyelination and necrosis of the corpus callosum (corpus callosum) occur. In the acute phase, MRI shows hyperintensity on T2 and restricted diffusion; in the chronic phase, necrosis of the splenium and genu.
  3. Methanol poisoning: Toxicity is mediated by formic acid. The primary target is the putamen (putamen). Scans show zones of necrosis (hyperintense on T2), sometimes with hemorrhages.
  4. Ethylene glycol and diethylene glycol: Cause cerebral edema and white matter involvement (predominantly in the temporo-parieto-occipital region).
Test your knowledge on the topicTasks from the "Diagnostic Radiology" course bank — instant answers and explanations.

Carbon monoxide, metals, and solvents

Specific toxins have preferential locations in the central nervous system.

  • Carbon monoxide (CO): Has a very high affinity for hemoglobin, causing severe hypoxia. A characteristic sign is bilateral necrosis of the globus pallidus (globus pallidus). In severe cases, the white matter is affected.
  • Heavy metals:
  • Manganese: Accumulates in the basal ganglia (appears bright on T1 without contrast). Often found in alcoholic liver cirrhosis.
  • Mercury: Selectively affects the cerebellar vermis and visual cortex.
  • Organic solvents (toluene): Cross the blood-brain barrier upon inhalation. Cause diffuse demyelination and axonal loss (diffuse T2 signal hyperintensity).

Iatrogenic and metabolic encephalopathies

A rare complication is gadolinium-induced toxic encephalopathy. It occurs in patients with acute renal failure after intravenous contrast administration. Gadolinium crosses the blood-CSF barrier—a bright signal from the CSF is visible on T2-FLAIR. The prognosis is favorable.

Inherited metabolic disorders may debut in adults. For example, X-linked adrenoleukodystrophy (affecting the corticospinal tracts with restricted diffusion and contrast enhancement) or Krabbe disease (also affecting the corticospinal tract, but without involvement of the lower brainstem and without contrast enhancement).

How to memorize

Manganese lights up on T1, carbon monoxide targets the globus pallidus, and methanol targets the putamen.

Class and exam questions

Which structures remain intact in toxic leukoencephalopathy from heroin inhalation?

The cerebellar dentate nuclei and cerebellar cortex remain intact, while the white matter and internal capsules are affected.

How to distinguish Krabbe disease from X-linked adrenoleukodystrophy in adults on MRI?

In Krabbe disease, lesions of the corticospinal tract do not extend to the lower brainstem, and the lesions do not show contrast enhancement.

What is the mechanism of cerebral hemorrhage associated with cocaine use?

Cocaine causes a sharp sympathomimetic increase in blood pressure and heart rate. In 50% of such patients, pre-existing aneurysms or arteriovenous malformations rupture.

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What else to study on this topic

  • Pathogenesis of demyelination in Marchiafava-Bignami disease
  • Specifics of blood-CSF barrier impairment following gadolinium administration
  • Cannabis-induced strokes: the role of vasculopathy
  • Differential diagnosis of globus pallidus necrosis on MRI
  • Neurotoxicity of levamisole as a contaminant in illicit drugs

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