Other forms of cns tuberculous infection


Tuberculomata may occur in cerebral hemispheres, cerebellum or brain stem with or without tuberculous meningitis, and may produce a space-occupying effect. They consist of caseating granulomas made up of epitheloid cells and macrophages containing mycobacteria. Lesions may be single or multiple. CT and MRI demonstrate lesions but appearances are not pathognomonic. Most resolve over a few weeks with antituberculous therapy.


Chronic epidural infection follows tuberculous osteomyelitis of the vertebral bodies. This arises in the lower thoracic region, can extend over several segments and may spread through the intervertebral foramen into pleura, peritoneum or psoas muscle (psoas abscess) - see page 390.


Infection of the leptomeninges results in an exudate that encases the spinal cord and nerve roots. This produces back pain, paraesthesia, lower limb weakness and loss of bowel and bladder control. Imaging may be normal while CSF shows high protein, lymphocytes and rarely acid fast bacilli. This disorder is now more frequent in AIDS patients. Differential diagnosis includes cytomegalovirus, cryptococcus, syphilis and lymphoma. Laminectomy and meningeal biopsy may be required to establish diagnosis. When suspected, empirical theory with antituberculous drugs is appropriate.


An autoimmune encephalopathy with features of acute allergic encephalomyelitis or haemorrhagic leukoencephalopathy (page 511) may complicate the course of tuberculous infection and contribute significantly to the neurological sequelae. Clinically, convulsions and deepening coma with extensor posturing characterise this complication.

Clinical features:

Clinical features:

Results in - Weakness

-Occasionally arises from rupture of local metastatic focus; resultant infection is confined to the spinal level.

Results in - Weakness

- pyramidal and segmental.

- Sensory loss.

- Sphincter disturbance.

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