This report describes a new and reliable technique for producing experimental noncommunicating syringomyelia. In 30 rats, 1.2 to 1.6 microliters of kaolin was microinjected into the dorsal columns and central gray matter of the spinal cord at C-6. The inoculations caused transient neurological deficits in four animals and no deficits in 26 animals. Within 24 hours, kaolin and polymorphonuclear leukocytes entered the central canal and drained rostrally. The clearance of inflammatory products induced a proliferation of ependymal cells and periependymal fibrous astrocytes, which formed synechiae and obstructed the canal at the level of injection and at one or more levels up to C-1. In 22 animals followed for 48 hours or longer, the upper end of the central canal became acutely dilated and formed an ependyma-lined syrinx that enlarged to massive dimensions within 6 weeks. The rostral syrinxes did not communicate with the fourth ventricle and were not associated with hydrocephalus. The histological findings in acute noncommunicating syringomyelia were characterized by progressive stretching and thinning of the ependyma, elongation of intracanalicular septae, and the formation of periependymal edema. After 3 weeks, there was progressive compression of the periependymal tissues associated with stretching of axons, fragmentation of myelin sheaths, and the formation of myelin droplets. These findings and the sequence in which they evolved were identical in most respects to those occurring in acute and subacute noncommunicating hydrocephalus.

Medullomyoblastoma is a rare histologic variant of medulloblastoma. Of the 20 cases reported in the literature, 19 were in children ages 2.5 to 10.5 years and one was in a 26-year-old woman. In the reported adult case the myogenic component of the tumor was leiomyosarcomatous. The authors report a case of medullomyoblastoma with a rhabdomyosarcomatous component in a 40-year-old man with light microscopic, immunohistochemical, and ultrastructural findings. The histogenetic theories regarding this tumor include that it is a teratoma, or that the myogenic component arises from the perivascular or leptomeningeal ectomesenchyme, or pluripotential neuroectodermal cells, or endothelial cells. The authors' findings do not elucidate the histogenesis but argue against an endothelial origin of the rhabdomyoblastic component.

A survey of skeletal muscle pathology in 92 autopsied cases of AIDS revealed microscopic alterations in 64 cases. There were 40 cases of disuse atrophy, 8 of denervation atrophy, 2 of cryptococcal myositis, 1 of Mycobacterium avium intracellulare (MAI) infection and 2 of necrotizing myopathy associated with hyperkalemia. A second group of cases with changes of unknown etiology was found. These were tentatively ascribed to the direct or indirect action of HIV. This category includes 8 cases of inflammatory myopathy, 8 of necrotizing myopathy in absence of a known etiological factor, 3 of extreme atrophy and 4 of "regenerating" myopathy.