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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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