Mycobacterium tuberculosis central nervous system infections take a variety of

forms, including an acute fulminant meningoencephalitis, a subacute meningitis,

tuberculoma, and vertebral tuberculosis (Pott disease). Infection with M.
tuberculosis is acquired by inhalation of aerosolized droplet nuclei. Tuberculous
meningitis does not develop acutely from hematogenous spread of tubercle bacilli
to the meninges. Rather, isolated miliary tubercles form in the brain parenchyma or
the meninges during hematogenous dissemination of bacilli and subsequently
enlarge and are usually caseating. Subependymal caseous foci may remain
quiescent for months or years but then may discharge bacilli and tuberculous
antigens into the subarachnoid space, causing meningitis. The neurologic
complications of tuberculous meningitis are initiated by the intense inflammatory
reaction to the discharge of tubercle bacilli and tuberculous antigens into the
subarachnoid space. The inflammatory reaction leads to the production of a thick
exudate that fills the basilar cisterns, obstructing the flow of cerebrospinal fluid
(CSF) and surrounding the cranial nerves. Vasculitis typically involves the major
blood vessels at the base of the brain, resulting in cerebral ischemia and infarction.
Tuberculous meningitis may manifest as a subacute meningitis or as a fulminant
meningitis, resembling bacterial meningitis. When the presentation is that of a
subacute meningitis, headache, fever, and lethargy are often present for 4 weeks or
longer before the patient presents for evaluation. Patients present for evaluation of
unrelenting headache, night sweats, stiff neck, and lethargy. Cranial nerve
abnormalities occur in approximately one fourth of patients. The diagnosis of
tuberculous meningitis is made by examination of the spinal fluid. The classic spinal
fluid abnormalities in tuberculous meningitis are as follows: (1) elevated opening
pressure, (2) lymphocytic pleocytosis, (3) an elevated protein concentration in the
range of 100 to 500 mg/dL, and (4) a decreased glucose concentration. A CSF
glucose concentration between 45 and 35 mg/dL in combination with a lymphocytic
pleocytosis and an unrelenting headache, stiff neck, fatigue, night sweats, and fever
is highly suspicious for tuberculous meningitis. At an early stage in the clinical
illness, polymorphonuclear leukocytes may predominate in the spinal fluid, but
typically lymphocytes become the predominant cell type within 48 hours. The CSF
glucose concentration is only mildly decreased. The last tube of fluid collected at
lumbar puncture is the best tube to send for smear for acidfast bacilli. Culture of
CSF takes 4 to 8 weeks to identify the organism, except in cases of fulminant
tuberculous meningitis where culture is often positive in 1 to 2 weeks. There is a
polymerase chain reaction (PCR) available for M. tuberculosis ribosomal ribonucleic
acid (rRNA). Neuroimaging abnormalities are nonspecific and include enhancement
of the meninges postcontrast administration, communicating and/or obstructive
hydrocephalus, and infarctions typically in the basal ganglia. Patients should have
chest radiographs and intradermal tuberculin skin test. The tuberculin skin test may
be negative because patients with central nervous system (CNS) tuberculosis are
immunosuppressed. With treatment, the skin test may become positive. Treatment
of tuberculous meningitis includes a combination of isoniazid, rifampin,
pyrazinamide, ethambutol, and pyridoxine. Dexamethasone therapy is

recommended for patients who develop hidrosefalus. This complication may also
require a ventriculostomy or a ventriculoperitoneal shunt. Tuberculomas manifest as
spaceoccupying lesions. On computed tomography (CT) scan, they often have the
appearance of a central nidus of calcification surrounded by a ring of enhancement
and/or edema. Tuberculomas may develop during the course of therapy for
tuberculous meningitis. The treatment of tuberculomas includes a three or fourdrug
regimen similar to the treatment of tuberculous meningitis. Superficial
tuberculomas can be surgically excised if they do not respond to antituberculous
chemotherapy. Pott disease refers to vertebral tuberculosis or tuberculous
spondylitis. Two or more adjacent vertebral bodies are often involved, and infection
can spread to the disk and/or the epidural space. The thoracic and lumbar spine are
the most commonly affected areas, and thus the clinical presentation is with back
pain in the thoracic or lumbar area and fever. When the epidural space is involved,
signs and symptoms of progressive spinal cord compression can develop. Diagnosis
is made by stereotactic aspiration of the lesion. Treatment includes antituberculous
chemotherapy and surgical decompression if spinal cord compression is present.