Research publications - Association for Research in Nervous and Mental Disease最新文献

In this chapter, we have suggested that neurobehavioral phenomena in HIV-infected individuals can be usefully grouped according to underlying pathogenesis. Neurogenic phenomena are those that result from direct involvement of the brain either by HIV-1 (primary neurogenic disorder) or from opportunistic infection, neoplasia, or side effects of treatment (secondary neurogenic disorder). These phenomena should be distinguished from disturbances resulting from a second pathogenetic mechanism--the psychogenic disorders. We define psychogenic disorders as those that reflect primarily psychological responses to knowledge of HIV infection and/or progression of disease, and resultant of social ramifications. In proposing the neurogenic and psychogenic groupings, we do not intend to harken back to antique "mind-body" distinctions. We recognize fully that diseases of the brain can and do cause disturbances in mood, thought, and behavior, and that preexisting psychogenic disturbances might, in fact, be substantially worsened by onset of such neuropathology. Nevertheless, for the sake of clarity and also of determining appropriate treatment, we feel that the distinction we propose is a heuristically useful one. Challenges that lie ahead include defining more precisely the incidence and natural course of HIV-associated neurogenic disorder. Although there is little doubt that CDC IV individuals have higher prevalence of both subclinical and clinical "organic mental" symptomatology, the time of onset and rate of progression of such changes are not understood. At present, it seems likely that early in the course of HIV infection, the CNS is spared; at some point, however, rate of neuropsychiatric abnormality probably increases, and this may not be directly related to progression of the immunological aspect of the disease. In regard to psychogenic phenomena, it is clear that anxiety syndrome can occur as a direct product of knowledge of HIV serostatus and may be exacerbated by progression of disease. It is possible also that some subgroups of HIV + individuals (e.g., military samples) may be at heightened risk for suicide. These observations pose challenges for focused intervention with these groups. Accumulating data both on neurogenic and psychogenic phenomenology underscore also the importance of conceptualizing HIV infection in neurobehavioral as well as immunologic-virologic terms.

PM, IBM, and DM represent the commonly occurring inflammatory myopathies. In DM, the effector response appears to be predominantly humoral and directed against intramuscular blood vessels; a local humoral response may occur in muscle itself. Capillary lysis precedes other pathologic changes, suggesting that the capillary endothelium is an early and possibly primary target of the immune response. Questions remain about the role of immune complexes versus circulating antibodies, whether the muscle fiber injury can be explained by ischemia alone, and the possible role of endomysial CD8+ T cells. In PM and IBM, there is evidence for T-cell mediated cytotoxicity against the muscle fibers; however, muscle fiber destruction also could result from antibody-dependent complement-mediated lysis of the sarcolemma. Questions remain about the identity of the muscle fiber surface antigen(s) recognized by T cells and the molecular mechanisms of T-cell-mediated muscle fiber destruction.