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• We report the first published case (to our knowledge) of histopathologically documented acquired immunodeficiency syndrome-related cytomegalovirus (CMV) myelitis in which antiviral drug therapy was administered. Despite sensitivity of the patient's CMV isolate to therapy with both ganciclovir and foscarnet, use of neither of these agents halted progression of central nervous system CMV disease. Higher doses of these drugs or combination therapy may be required to treat acquired immunodeficiency syndrome-related CMV myelitis effectively.

• An unusual myopathy characterized by selective loss of thick filaments and widespread formation of rod bodies is described in two men, both seropositive for human immunodeficiency virus. We were unable to find any previous reports documenting this combination of morphological abnormalities, which we believe may be related to human immunodeficiency virus infection. Both patients responded to treatment: one, to steroid therapy; the other, to plasmapheresis.

STROKE has been previously described as a complication of chiropractic manipulation of the head and neck. The reported cases are notable in two respects. First, the affected patients are predominantly young (under 40 years of age) and have no demonstrable coexisting vascular disease. Second, premonitory symptoms of vertebrobasilar ischemia during neck manipulation were simply not recognized as an absolute contraindication to further mechanotherapy. We wish to reemphasize this avoidable syndrome. Report of Cases Case 1.— A 52-year-old woman complained of weakness on the left side of 24 hours' duration. One month earlier she had begun a series of chiropractic manipulations because of recurrent neck pain that had started after minor injury ten years before. During several of these treatments, she experienced transient vertigo associated with nausea, blurred vision, and scintillating scotomata without loss of vision or headache. Near the end of her last treatment, following a painful rotation of the

The clinical presentation and course of abetalipoproteinemia in two male patients, a child and an adult, are described. Apoprotein B was absent in both cases and each patient had > 50% acanthocytes present on peripheral blood smear. Family studies revealed normal lipid profiles in the parents of both patients, which is consistent with the usual autosomal recessive inheritance of this disorder. In addition to a low-fat diet, both patients have been maintained on high doses of vitamins A and E. In the adult patient, detailed evaluations over a five-year period have failed to show any progression of neurological disease while maintained on high-dose vitamins. The role of supplemental vitamins A and E in the therapy of abetalipoprotenemia is discussed.