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Improvement with steroids


Acute vasculitis, small cortical vessels, cortical infarct with multinucleated giant cells Lymphocytic infiltration, small vessels and larger vessels normal, no granulomas, multiple cystic, necrotic and gliotic areas in white matter with multinucleated giant cells Lymphocytic infiltration, small vessels and endothelial swelling Lymphocytic infiltration in small vessels of cortex and brainstem, small infarcts, cerebral edema with diffuse encephalomalacia Non-necrotizing leukocytoclastic vasculitis, neutrophils and mononuclear cells in venules Neutrophil infiltration and fibrinoid degeneration in small arterioles and veins

Stabilized after hematoma removed Improvement with steroids


Improvement with steroids Death

Improvement without steroids Partial recovery

Figure 2.4.9 This cross-section of tongue demonstrates the contusions that may be seen in drug-induced seizures. Parkinsonism

Parkinson's syndrome has been reported in addicts who receive the synthetic meperidine analog contaminated with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). MPTP is produced during the careless synthesis of MPPP (1-methyl-4-phenyl-4-propionoxypiperidene) often in clandestine laboratories. Neurotoxic symptoms include resting tremor, rigidity, bradyki-nesia, and other signs and symptoms of Parkinsonism. Neuropathologic examination has demonstrated substantia nigra degeneration confined to the zona compacta. There is astrocytosis, focal gliosis, and extraneuronal melanin pigment.47 MPPP contaminated with MPTP has been reported to produce Parkinson's syndrome within days of injecting this drug mixture.48 MPTP-induced Parkinson's syndrome can also result from snorting the drug.49 The severe rigidity that results from MPTP-induced Parkinonism has been implicated in the asphyxiation death of one victim who was unable to move his head from a suffocating posture.50 Postmortem neuro-pathologic examination also revealed severe neuronal loss in his substantia nigra. Anoxic Ischemic Encephalopathy

Drugs of abuse commonly produce anoxic-ischemic encephalopathy.51-53 This can occur from insufficient oxygen reaching the blood from the lungs, insufficient oxygen carriage, or inadequate cerebral blood perfusion. This is a common mechanism in drug abusers who have a delayed death after drug intoxication.

The morphology of anoxic-ischemic encephalopathy is variable with preferentially affected areas in the brain. In the gray matter, the watershed zones are commonly affected with laminar necrosis involving lamina zones III, V, VI. The h1 segment (Sommer's sector) and endplate in the hippocampus is commonly involved. Other vulnerable sites include the Purkinje cells of the cerebellum and the caudate and putamen. The brain is often swollen and soft with a pale or dusky gray matter. Laminar necrosis may be apparent if sufficient time has elapsed between the time of anoxia and death. Microscopic changes are not recognizable until 6 to 8 hours after the anoxic-ischemic insult. The affected neurons become shrunken with eosinophilic cytoplasm and nuclear pyknosis, and gradually disappear. There is also non- specific capillary proliferation with endothelial swelling, spongiform change, and gliosis in the affected neuropil.

Figure 2.4.10 Coronal section of brain with multiple necrotic abscesses in an intravenous drug abuser.

Figure 2.4.11 Within the necrotic cerebral cavities on the patient in this figure are branching, septated fungi (Gomori methanamine silver, 80x). Drug-Associated Central Nervous System Infections

Primary fungal cerebritis due to Rhizopus has been reported in cocaine,54 heroin,55-59 and amphetamine60 users with no other systemic foci identified at autopsy. The victims are usually men in their 3rd or 4th decades of life and present with hemiplegia, facial weakness, and headache. The brain lesions are usually multiple with frequent bilateral involvement of the basal ganglia. The phycomycoses are angiotrophic fungi that commonly occlude and invade the cerebral blood vessels causing hemorrhagic infarcts. Fungal cerebritis or meningitis have been reported in intravenous drug abusers (Figures 2.4.10 and 2.4.11) with HIV infection. In addition to fungal cerebritis, HIV-infected intravenous drug abusers can develop a large variety of central nervous infections and neoplasms (Table and thus fulfill the criterion for AIDS. Intravenous drug abusers may develop multifocal brain abscesses or cerebritis from embolic vegetations arising from valvular endocarditis.61 Nasal insufflation of drugs can also cause frontal sinusitis and overlying frontal lobe abscess.62

Central Nervous System Infections in Intravenous Drug Abusers with AIDS

HIV encephalitis

Progressive multifocal leukoencephalopathy Cytomegalovirus ventriculitis and cerebritis Toxoplasma cerebritis Cryptococcal meningitis and cerebritis Histoplasma cerebritis Nocardia cerebritis

Mycobacterium infections (including tuberculosis, avian-intracellulare)

Fungal meningitis and cerebritis (Candida, Aspergillus, Rhizopus


Entameba histolytica

Acanthameba castellani

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