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Intraoral lesions, abnormalities on the tongue or tissues in the mouth and throat, caused by infections have been associated with AIDS and HIV infection from the early stages of the epidemic. Increasingly, HIV disease is being defined by CD4+ and CD8+ T lymphocyte counts. This study examined if there is a relation between T lymphocyte counts and intraoral lesions. HIV-infected individuals, enrolled in a drug study, underwent oral examinations between January and December 1989. Up to four examinations were performed during the study period. T lymphocyte counts were averaged for a given time frame covering a period just prior to the first examination, and for later examinations, for a period between the prior and present examination. A total of 106 patients participated in the study and were examined at least once. Of the 106 participants, 88 percent participated in the second examination, 72 percent in the third, and 56 percent in the fourth. Oral lesions were seen in 38 patients (36 percent) at some point during the study. CD4+ and CD8+ counts did not differ significantly for patients who did not have lesions and those who did. At the first examination, oral lesions were seen in 25 percent of the patients. For subsequent examinations, the rates were 19, 15, and 20 percent. The most commonly seen lesions were ulcerative lesions and hairy leukoplakia. CD4+ counts were stable until after examination 4. CD8+ counts increased slightly by examination 4. When data on T lymphocyte counts performed before and after the examinations were compared with examination results, a relation was found between an elevated CD8+ count before the examination and the presence of an oral lesion at the examination. This relationship remained unchanged when smoking and alcohol use were considered. These results indicate that information on changes in CD8+ counts may be useful for preventing or managing HIV-related oral lesions. (Consumer Summary produced by Reliance Medical Information, Inc.)

Recovery of voluntary motor function after incomplete spinal cord injuries is attributed to a variety of physiological mechanisms, such as resolution of conduction block in injured axons, and neuroplasticity mechanisms in spared axons. To better understand these recovery mechanisms, we have examined motor recovery in one type of incomplete cord injury, the Brown-Sequard Syndrome. This syndrome is observed in patients with unilateral injury of the spinal cord and is manifested as asymmetric weakness and painjtemperature sensory loss contralateral to the weakest extremity. We have followed the course of motor recovery in two patients and reviewed the literature in an additional 59. Common features of this motor recovery include: 1) recovery of ipsilateralproximal extensor muscles before ipsilateral distal flexors, 2) recovery of any weakness in the extremity with pain / temperature sensory loss before the opposite extremity, and 3) recovery of voluntary motor strength and a functional gait by 1 to 6 months. We discuss these observations with respect to three hypotheses to explain motor recovery and suggest that neuroplasticity mechanisms functioning in spared descending axons may mediate much of the observed recovery after Brown-Sequard cord lesions.