Using stereological techniques we have estimated the volume density of melanin and counted the number of pigmented and non-pigmented neuronal cell bodies in the pars compacta of the substantia nigra of 12 autopsied patients with acquired immune deficiency syndrome (AIDS) who did not have inflammation or necrosis of the midbrain or clinical parkinsonism. The total number of neuronal cell bodies was 25% lower in AIDS (P less than 0.01) than in 12 age-matched controls, although the volume density of neuronal melanin did not differ from that of controls because the percentage of pigmented cell bodies was higher (P less than 0.01) and the cell bodies were more fully packed with melanin in AIDS. Also, the expected increase with age of the volume density of neuronal melanin (P less than 0.02) and the percentage of pigmented neurons (P less than 0.01) occurred in the controls but not in AIDS patients. Importantly, our histopathological examination showed unequivocal nigral degeneration with neuronal loss, small neuronal cell bodies packed with melanin, reactive astrocytosis and extra-cellular melanin in the AIDS patients but not in controls. Our study shows that a subclinical nigral degeneration is common in AIDS and could possibly explain the heightened susceptibility of some patients to drug-induced parkinsonism.

No abstract

Changes in the electromyograms and motor nerve conduction velocities in 12 patients with diabetic amyotrophy suggested mild distal and moderate proximal neuropathy in the lower limbs. Histological and histochemical findings in the vastus medialis muscles were consistent with denervation. Electron microscopical examination of the vastus medialis muscles in 6 patients revealed myofibrillar degeneration. One patient had abnormal mitochondria and tubular aggregates. The basement membranes of the intramuscular capillaries were thickened in all but 1 patient. Histochemical staining of the myoneural junctions showed changes consistent with degeneration and regeneration. We conclude that diabetic amyotrophy is a distinct clinical entity and is secondary to metabolic derangement rather than diabetic microangiopathy.