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There are many infectious processes that induce an in ammation of the leptomeninges of lesser intensity and more chronicity than the acute forms described above Included here are some bacterial and most mycotic infections, tuberculosis, syphilis, Lyme disease, human immunode ciency virus (HIV) infection, and presumed noninfectious causes, such as lymphoma, sarcoidosis, Wegener granulomatosis, and others As pointed out by Ellner and Bennett (their experience coincides with that of Swartz and our own), the clinical syndrome comprises cognitive disorders, seizures, and absence of lateralizing and focal cerebral signs, with or without headache and mild stiffness of the neck In some cases there is little or no fever or other manifestation of infection As with acute bacterial meningitis, the CSF will usually divulge the causative agent, but not so readily as in acute bacterial meningitis, since the organisms are usually by nature more dif cult to detect and culture The main identi able forms of subacute and chronic meningitis are described below The approach to the complicated problem of chronic meningitis (aseptic variety) in which no cause can be found is addressed in Chap 33, which should be referred to along with this section

In the United States and in most western countries, the incidence of tuberculous meningitis, which parallels the frequency of systemic tuberculosis, has until recently decreased steadily since the Second World War At the Cleveland Metropolitan General Hospital, for example, the incidence of tuberculous meningitis during the years 1959 to 1963 was between 44 and 84 per 10,000 admissions (a decade earlier it was 58 to 129 per 10,000 admissions) By contrast, at the K E M Hospital in Bombay during the period 1961 to 1964, the incidence of this disease (in children) was 400 per 10,000 admissions, and similar gures have been reported from other parts of India Since 1985, however, there has been a moderate increase in the incidence of systemic tuberculosis (and tuberculous meningitis) in the United States a 16 percent annual increase compared to an average annual decline of 6 percent during the preceding 30 years (Snider and Roper) This increase is due mainly though not exclusively to the HIV epidemic In fact, tuberculosis may be the rst clinical manifestation of HIV infection (Barnes et al); among patients with full-blown AIDS, the incidence of tuberculosis is almost 500 times the incidence in the general population (Pitchenik et al) In developing countries, particularly in sub-Saharan Africa, recent estimates of the incidence of tuberculosis suggest that it is 25 times more frequent than in the United States, again largely because of the prevalence of HIV infection

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Pathogenesis Tuberculous meningitis is usually caused by the acid-fast organism Mycobacterium tuberculosis and exceptionally by Mycobacterium bovis or Mycobacterium fortuitum The emergence of AIDS has led to a marked increase in cases caused by both the classic organism and also by these last two atypical mycobacteria Rich described two stages in the pathogenesis of tuberculous meningitis rst a bacterial seeding of the meninges and subpial regions of the brain with the formation of tubercles, followed by the rupture of one or more of the tubercles and the discharge of bacteria into the subarachnoid space Whether the meningitis always originates in this way is, in our opinion, unlikely It can be said, however, that the meningitis may occur as a terminal event in cases of miliary tuberculosis or as part of generalized tuberculosis with a single focus (tuberculoma) in the brain Pathologic Findings Small, discrete white tubercles are scattered over the base of the cerebral hemispheres and to a lesser degree on the convexities The brunt of the pathologic process falls on the basal meninges, where a thick, gelatinous exudate accumulates, obliterating the pontine and interpeduncular cisterns and extending to the meninges around the medulla, the oor of the third ventricle and subthalamic region, the optic chiasm, and the undersurfaces the temporal lobes (Fig 32-2) By comparison, the convexities are little involved, possibly because the associated hydrocephalus obliterates the cerebral subarachnoid space Microscopically, the meningeal tubercles are like those in other parts of the body, consisting of a central zone of caseation surrounded by epithelioid cells and some giant cells, lymphocytes, plasma cells, and connective tissue The exudate is composed of brin, lymphocytes, plasma cells, other mononuclear cells, and some polymorphonuclear leukocytes The ependyma and choroid plexus are studded with minute glistening tubercles The exudate also surrounds the spinal cord Unlike the pyogenic meningitides, the disease process is not.

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