Abstract
Multiple sclerosis (MS) is a chronic inflammatory graphics. disease of the central nervous system (CNS), leading to demyelination within the CNS, and is responsible for the progressive neurological deficits associated with MS (Stinisen et al., 1997). One of the best animal models of MS is the demyelination induced by Theiler's virus. The early events that occur during Theiler's virus infection are crucial in the effective clearance of virus from the CNS. Failure to clear virus results in the establishment of persistent infection of the CNS and subsequent demyelination (Brahic et aI., 1981 ; Rodriguez et aI., 1996). A growing body of evidence indicates that physical and psychosocial stressors compromise immune function (Ader et aI., 1991). An individual's response to a stressor is manifested in physiological, hormonal, behavioral, and immunological changes. Since the earliest descriptions of multiple sclerosis, stress has been considered a controversial, but potentially important, factor in the onset and course of the disease. Recent studies using standardized assessment of life events have begun to shed light on the idea that psychological stress precedes both the onset and recurrence of MS symptoms in 70-80% of cases (Warren et aI., 1982). The mechanism involving the role of stress in MS appears to be quite complex. Because of the autoimmune nature of this disease, along with evidence that stressful events exacerbate symptoms, it is prudent to begin to investigate how stress might effect the course of MS by studying the effect of restraint-stress on the neuropathogenesis of Theiler's virus-infection.
Campbell, Ted Ryan (1998). The effect of stress on the neuropathogenesis of Theiler's virus-infection in the central nervous system. Master's thesis, Texas A&M University. Available electronically from
https : / /hdl .handle .net /1969 .1 /ETD -TAMU -1998 -THESIS -C362.