MACROSCOPIC APPEARANCES

Tuberculous meningitis is characterized by a gelatinous subarachnoid exudate. This may appear slightly nodular and is usually thickest in the sylvian fissures, over the base of the brain (Fig. 16.1a), and around the spinal cord. Sectioning of the brain usually reveals a similar exudate within the choroid plexus and lining the ventricles. Tubercles may be visible in the meninges, usually adjacent to sulcal veins, and in the ventricular lining (Fig. 16.1b). Small superficial tuberculomas are quite common (Fig. 16.2) and may be associated with an overlying meningeal exudate. Large tuberculomas occasionally occur, but are rare in patients with meningitis.

The ventricles are often moderately dilated, owing to the development of obstructive or communicating hydrocephalus. There may be infarcts.

MICROSCOPIC APPEARANCES

The meningeal and ventricular exudate contains lymphocytes, macrophages, and sparse plasma cells, admixed with necrotic material and fibrin (Fig. 16.3a). There may be accumulations of epithelioid cells and fibroblasts, multinucleated giant cells, and well-defined tuberculous granulomas (Figs 16.2, 16.3, 16.4) with central caseous necrosis.

The inflammation extends into the subpial and periventricular brain tissue, which shows reactive astrocytosis (Fig. 16.3a) and microglial proliferation. This may be associated with degeneration of white matter adjacent to the ventricles and in the spinal cord.

The inflammatory cells tend to infiltrate through the adventitia, into the media and even the intima, of blood vessels within the exudate (Figs 16.3b, 16.6). Thrombosis occurs in some blood vessels. In others, the inflammation provokes a subintimal intimal fibroblastic reaction that narrows and can occlude the lumen (Figs 16.3b, 16.7). Infarcts are therefore common (Fig. 16.8), particularly in the superficial cortex and, due to the involvement of perforating branches of the middle cerebral artery, in the basal ganglia.

MACROSCOPIC APPEARANCES

Tuberculomas appear as solitary encapsulated yellow or gray masses or multinodular aggregates of smaller masses. They are most often cerebral or cerebellar, but can occur anywhere within the neuraxis. The central tissue, though necrotic, has a firm consistency when cut.

MICROSCOPIC APPEARANCES

Histology reveals solitary or confluent tuberculous granulomas with central caseous necrosis surrounded by lymphocytes, epithelioid cells, Langhans’-type multinucleated giant cells, and an outer zone of collagen, fibroblasts, lymphocytes, and macrophages (Fig. 16.9). Older lesions may calcify. The adjacent parenchyma is usually markedly gliotic.

MACROSCOPIC APPEARANCES

There is usually extensive destruction, which may be associated with collapse of the affected vertebral bodies and intervertebral discs. This is associated with variable protrusion of gray multinodular granulomatous tissue into the epidural space (Fig. 16.10).

MICROSCOPIC APPEARANCES

The epidural mass shows typical granulomatous tuberculous inflammation with caseation. Changes in the spinal cord reflect a combination of focal compression by epidural inflammatory tissue or vertebral kyphosis, ischemia (see Chapter 9), and secondary long tract degeneration. Compression of the anterior spinal artery may produce a typical ‘watershed’ infarct (see Chapter 9) involving the upper and middle parts of the thoracic cord.

 Asymptomatic CNS involvement, associated with CSF pleocytosis and increased immunoglobulin concentration, and positive CSF syphilis serology.

 Syphilitic meningitis.

 Meningovascular syphilis.

 Parenchymatous neurosyphilis (general paresis and tabes dorsalis).

 Gummatous neurosyphilis.