Toxic Leucoencephalopathy Research Articles

Pathology of toxic leucoencephalopathy in drug abuse supports hypoxic-ischemic pathophysiology/etiology.

The histopathological features of leucoencephalopathy caused by illicit drugs (such as opioids and cocaine) are well documented in acute cases but not in long-survival cases. There are several hypotheses about the pathogenesis of this disorder, including hypoperfusion, direct drug toxicity resulting from the neurotoxic effects of the drug itself or contaminants in the illicit drug vehicle. We reviewed the post mortem findings in five males (aged 24 to 56years, with survival intervals ranging from 7days to 5months) with a history of illicit drug use and concomitant fatal white matter changes. The histological characteristics of leucoencephalopathy vary with survival period. Prominent axonal injury and axonal spheroids were observed with shorter survival and spongiform changes becoming apparent with longer survival (acute and chronic incomplete infarct pattern). Necrosis was present in all cases and its appearance changed with longer survival (acute and chronic complete infarct pattern). Significant primary demyelination was not observed. These observations suggest that the primary defect in this leucoencephalopathy is hypoxic-ischemic injury, predominantly in the white matter. Spongiform leucoencephalopathy likely represents the longer-survival incomplete infarct pattern and is observed with polydrug abuse.

Toxic Leucoencephalopathy Due to CHOP Therapy in a Patient with NonHodgkin’s Lymphoma

Toxic leucoencephalopathy is damage to cerebral white matter due to exposure to cranial irradiation, environmental toxins, drugs of abuse and chemotherapeutic agents. It results in wide variety of clinical manifestations like personality change, inattention, memory loss, abulia, stupor, coma and death. It leads to white matter demyelination which is visible on T2 weighted MRI as hyperintensity. We report a rare case of a 14-year-old boy with large B cell lymphoma who developed toxic leucoencephalopathy due to exposure to CHOP regimen.

CEREBRAL WHITE MATTER DISEASE IN PATIENTS WITH MALIGNANCY: PML VERSUS TOXIC LEUCOENCEPHALOPATHY DUE TO CHEMOTHERAPY

BackgroundSystemic malignancy and its treatment can produce a variety of cerebral abnormalities. Malignancy itself can lead to metastatic disease and paraneoplastic encephalomyelitis Patients on chemotherapy can develop the Posterior Reversible...

Delayed reversible methotrexate-induced leucoencephalopathy in a four-year-old child with acute lymphoblastic leukemia

Intravenous/intrathecal methotrexate (MTX) has been implicated as a major cause of treatment-related neurotoxicity particularly leukoencephalopathy in children with hematological malignancy. We report a 4-year-old boy who presented with apathy and aphasia for 1 day while on the maintenance-phase chemotherapy according to MCP 841 protocol. MRI of brain revealed bilateral symmetrical FLAIR hyperintensities in caudate and putaminal region with FLAIR hypersignal in subcortical U-fiber in left frontal lobe consistent with MTX-induced toxic leucoencephalopathy. There was spontaneous resolution of symptoms within 1 week of onset. So, in Pre-B acute lymphoblastic leukemia patients with subtle neurological deficit, this diagnosis should be kept in mind and further treatment with MTX should be carefully decided.