Toxic leukoencephalopathy is structural damage to the cerebral white matter as a result of exposure to a toxic substance. Damage occurs secondary to disruption of central nervous system myelin. Toxic leukoencephalopathy can occur after exposure to multiple agents including cranial radiation, chemotherapeutic agents, immunosuppressive drugs, antifungal agents, alcohol, illicit drugs, and environmental toxins such as carbon monoxide. Patients of any age can be affected after exposure to a leukotoxic agent. Symptoms may be acute and temporally related to a toxic exposure but are often chronic or delayed. Hypoxia from carbon monoxide poisoning, for example, can cause delayed posthypoxic leukoencephalopathy, as can drug overdoses, complications of general anesthesia, asphyxiation from strangulation, and hemorrhagic shock.

Patients may present with a variety of neurologic symptoms including behavioral or personality changes, memory impairment, and language and cognitive dysfunction. Focal symptoms are an uncommon finding. Due to nonspecific findings, patients may be misdiagnosed with psychiatric disease. Prognosis depends on the particular leukotoxin the patient was exposed to, the duration of exposure, and the degree of injury. While improvement often occurs, recovery is rarely complete.