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Extrapulmonary tuberculosis, part 2: CNS involvement

Extrapulmonary tuberculosis, part 2: CNS involvement

Tuberculosis can have a variety of extrapulmonary manifestations in addition to the classic pulmonary disease. In the August 2005 issue of The Journal of Respiratory Diseases, we reviewed the most common extrapulmonary manifestations of tuberculosis--pleural and lymph node involvement. In this article, we will focus on the presentation of neurologic tuberculosis.

OVERVIEW

Neurologic tuberculosis occurs in 10% to 15% of patients who have extrapulmonary involvement. It occurs more frequently in children than in adults and is most common in children aged 3 years or younger. The prognosis is generally poor in young children, children of any age who have not received BCG vaccination, and adults who are older than 50 years.

Neurologic involvement is 5 times more frequent in HIV-positive patients than in HIV-negative patients. HIV infection does not generally alter the clinical presentation or response to antituberculosis therapy, although a poorer prognosis can be expected in patients with CD4+ T-lymphocyte counts below 200/µL.1,2 Poor outcomes have also been associated with infection with drug-resistant mycobacterial strains.1

The 3 clinicopathologic categories of neurologic tuberculosis are meningitis, tuberculoma (intracranial and spinal), and arachnoiditis (basal, opticochiasmatic, and spinal).3

MENINGITIS

Almost 80% of patients with neurologic tuberculosis have meningitis. Tuberculous meningitis continues to be a significant public health concern in developing countries.

Pathogenesis

CNS tuberculosis is invariably secondary to tuberculosis elsewhere in the body. Meningitis is the result of the rupture of a subependymally located tubercle (Rich focus) that developed during primary hematogenous dissemination into the subarachnoid space.

The pathology includes inflammatory meningeal exudates, ependymitis, vasculitis, and encephalitis. The blockage of the basal cisterns by the exudate in the acute stage and adhesive leptomeningitis in the chronic stage results in the development of communicating hydrocephalus in most patients who have been symptomatic for more than 2 to 3 weeks.

The hydrocephalus is more severein children than in adults. Infrequently, the hydrocephalus is of the obstructive type.3,4

Clinical presentation

The clinical presentation of tuberculous meningitis has evolved in the past decade and includes an acute meningitic syndrome simulating pyogenic meningitis, progressive dementia, status epilepticus, psychosis, stroke syndrome, and movement disorders. The factors responsible for this changing patterninclude delay in the age at onset of primary infection, BCG immunization,and HIV infection.3,4

The prodromal phase of constitutional features (low-grade fever, anorexia, and lethargy) lasts about 3 weeks. Subsequently, headache and vomiting occur, and the patient has a more toxic appearance. Cranial nerve palsies (especially sixth nerve involvement) and seizures occur in approximately one third of cases.

The loss of vision (clinical and/or impaired visual evoked response) is a major complication of optic pathway involvement and is reported in almost 50% of patients. There is progressive deterioration in sensorium as a result of increasing hydrocephalus and tentorial herniation. The disease is usually fatal within 2 months, if it is untreated.

Encephalopathy is the result of a hypersensitivity reaction to tuberculoproteins. It typically occurs in children and is characterized by diffuse brain edema and white matter disease with minimal evidence of meningitis.

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