Pathology sections of the brain in individuals with MS reveal well-demarcated lesions or plaques that appear pink or gray. Microscopically, the lesions are characterized by inflammation, demyelination, or gliosis. Inflammatory lesions have both perivascular and leptomeningeal infiltration of lymphocytes, mono-cytes, and macrophages. Histopathologic studies show that macrophages and CD4+ T cells are the most prominent cell types within lesions. There are fewer B cells and plasma cells. Lesions can be further characterized as active (acute), chronic active, or chronic inactive. In the acute lesion, perivascular and par-enchymal infiltration with mononuclear cells, such as T cells and macrophages, exists. Cells are mostly large, round, and lipid-laden macrophages. There are variable numbers of CD4 and CD8 cells present. MHC class II positive cells are abundant. Similar findings are seen in ADEM and animal models that have T cellmediated immune responses. In these cases, the demyelination that occurs with MS-type plaques is not present. This implies that there must be another factor present for demyelination to occur. Chronic active plaques have MHC class II cells and lipid-laden macrophages at the border of the lesion but not centrally. Chronic inactive lesions have few MHC class II-positive cells and are hypocellular. Recently evidence indicates that the pathologic process may vary between individuals. Lucchinetti and Lassmann described different types of pathological appearances based on immunohistochemical studies. The first type shows areas of demyelination with no oligodendroglia loss. There is local deposition of demyelinating antibodies and complement activation. The preserved oligodendroglia cells favor remyelination and recovery. A second type has demyelination; however, there is destruction and loss of oligodendroglia cells with the presence of T cells and macrophages in these areas. Local precipitation of antibody and complement is not evident. A third type involves primary demyelination and a gradient loss of oligodendroglia cells toward the center of an inactive plaque. In inactive plaques there is profound oligodendroglia loss. A fourth type describes primary oligodendroglia destruction in white matter near the plaque and resultant secondary demyelination. A fifth type describes demyelination with profound loss of axons, oligodendrocytes, and astrocytes. This is not likely to be due to different stages of the disease since individuals tend to have similar patterns of pathologic changes throughout the brain. Rather, the types of injuries may be the result of different immunologic mechanisms that occur between patients and not within a patient.

The irreversible disability of MS has been attributed to axonal injury, which is evident in autopsy specimens. Charcot recognized degeneration of axons in MS as early as 1877. Recently, axonal transection has been demonstrated even in the early stages of the disease. These findings suggest that accumulating axonal injury from early on may result in progressive disability. Attempts to prevent axonal damage may prevent long-term disability.

Breaking Bulimia

Breaking Bulimia

We have all been there: turning to the refrigerator if feeling lonely or bored or indulging in seconds or thirds if strained. But if you suffer from bulimia, the from time to time urge to overeat is more like an obsession.

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