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INFECTIONS OF THE NERVOUS SYSTEM AND SARCOIDOSIS
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ACUTE BACTERIAL MENINGITIS (LEPTOMENINGITIS) The Biology of Bacterial Meningitis
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The immediate effect of bacteria or other micro-organisms in the subarachnoid space is to cause an in ammatory reaction in the pia and arachnoid as well as in the cerebrospinal uid (CSF) Since the subarachnoid space is continuous around the brain, spinal cord, and optic nerves, an infective agent gaining entry to any one part of the space may spread rapidly to all of it, even its most remote recesses; in other words, meningitis is always cerebrospinal Infection also reaches the ventricles, either directly from the choroid plexuses or by re ux through the foramina of Magendie and Luschka The rst reaction to bacteria or their toxins is hyperemia of the meningeal venules and capillaries and an increased permeability of these vessels, followed shortly by exudation of protein and the migration of neutrophils into the pia and subarachnoid space The subarachnoid exudate increases rapidly, particularly over the base of the brain; it extends into the sheaths of cranial and spinal nerves and, for a very short distance, into the perivascular spaces of the cortex During the rst few days, mature and immature neutrophils, many of them containing phagocytosed bacteria, are the predominant cells Within a few days, lymphocytes and histiocytes increase gradually in relative and absolute numbers During this time there is exudation of brinogen, which is converted to brin after a few days In the latter part of the second week, plasma cells appear and subsequently increase in number At about the same time the cellular exudate becomes organized into two layers an outer one, just beneath the arachnoid membrane, made up of neutrophils and brin, and an inner one, next to the pia, composed largely of lymphocytes, plasma cells, and mononuclear cells or macrophages Although broblasts begin to proliferate early, they are not conspicuous until later, when they take part in the organization of the exudate, resulting in brosis of the arachnoid and loculation of pockets of exudate During the process of resolution, the in ammatory cells disappear in almost the same order as they had appeared Neutrophils begin to disintegrate by the fourth to fth day, and soon thereafter, with treatment, no new ones appear Lymphocytes, plasma cells, and macrophages disappear more slowly, and a few lymphocytes and mononuclear cells may remain in small numbers for several months The completeness of resolution depends to a large extent on the stage at which the infection is arrested If it is controlled in the very early stages, there may not be any residual change in the arachnoid; following an infection of several weeks duration, there is a permanent brous overgrowth of the meninges, resulting in a thickened, cloudy, or opaque arachnoid and often in adhesions between the pia and arachnoid and even between the arachnoid and dura From the earliest stages of meningitis, changes are also found in the small- and medium-sized subarachnoid arteries The endothelial cells swell, multiply, and crowd into the lumen This reaction appears within 48 to 72 h and increases in the days that follow The adventitial connective tissue sheath becomes in ltrated by neutrophils Foci of necrosis of the arterial wall sometimes occur Neutrophils and lymphocytes migrate from the adventitia to the subintimal region, often forming a conspicuous layer Later there is subintimal brosis This is a striking feature of nearly all types of subacute and chronic infections of the meninges but most notably of tuberculous and syphilitic meningitis (Heubner s arteritis) In
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the veins, swelling of the endothelial cells and in ltration of the adventitia also occur Subintimal layering, as occurs in arterioles, is not observed, but there may be a diffuse in ltration of the entire wall of the vessel It is in veins so affected that focal necrosis of the vessel wall and mural thrombi are most often found Cortical thrombophlebitis of the larger veins does not usually develop before the end of the second week of the infection The unusual prominence of the vascular changes may be related to their anatomic peculiarities The adventitia of the subarachnoid vessels, both of arterioles and venules, is actually formed by an investment of the arachnoid membrane, which is invariably involved by the infectious process Thus, in a sense, the outer vessel wall is affected from the beginning by the in ammatory process an infectious vasculitis The much more frequent occurrence of thrombosis in veins than in arteries is probably accounted for by the thinner walls and the slower current (possibly stagnation) of blood in the former Although the spinal and cranial nerves are surrounded by purulent exudate from the beginning of the infection, the perineurial sheaths become in ltrated by in ammatory cells only after several days Exceptionally, in some nerves, there is in ltration of the endoneurium and degeneration of myelinated bers, leading to the formation of fatty macrophages and proliferation of Schwann cells and broblasts More often, there is little or no damage to nerve bers Occasionally cellular in ltrations may be found in the optic nerves or olfactory bulbs The arachnoid membrane tends to serve as an effective barrier to the spread of infection into the brain substance, but some secondary reaction in the subdural space may occur nevertheless (subdural effusion) This happens far more often in infants than in adults; according to Snedeker and coworkers, approximately 40 percent of infants with meningitis who are less than 18 months of age develop subdural effusions As a rule, there is no subdural pus, only a sterile yellowish exudate In an even higher percentage of cases, small amounts of brinous exudate are found in microscopic sections that include the spinal dura When brinopurulent exudate accumulates in large quantities around the spinal cord, it blocks off the spinal subarachnoid space Hydrocephalus is produced by exudate in the foramina of Magendie and Luschka or in the subarachnoid space around the pons and midbrain, interfering with the ow of CSF from the lateral recesses of the fourth ventricle and cisterna magna to the basal cisterns and cerebral convexities In the later stages, brous subarachnoid adhesions are an additional and sometimes the most important factor interfering with the circulation of CSF An infrequent late sequela of bacterial meningitis is therefore chronic adhesive arachnoiditis or chronic meningomyelitis In the early stages of meningitis, very little change in the substance of the brain can be detected Neutrophils appear in the Virchow-Robin perivascular spaces but enter the brain only if there is necrosis After several days, microglia and astrocytes increase in number, at rst in the outer zone and later in all layers of the cortex The associated nerve cell changes may be very slight Obviously some disorder of the cortical neurons must take place from the beginning of the infection to account for the stupor, coma, and convulsions that are so often observed, but several days must elapse before any change can be demonstrated microscopically It is uncertain whether these cortical changes are due to the diffusion of toxins from the meninges, to a circulatory disturbance, or to some other factor, such as increased intracranial pressure Restated, the aforementioned changes are not due to invasion of brain substance
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