Tuberculous Meningoenchephalitis.
Must be considered in patients who present with a confused state, especially if there is a history of pulmonary tuberculosis, alcoholism, corticosteroid treatment, HIV infection, or other conditions associated with impaired immune responses. It should also be considered in patients from areas (e.g. Asia, Africa) or groups (e.g. the homeless and inner-city drug users) with a high incidence of tuberculosis.
Etiology
- Mycobacterium tuberculosis
- Inhalation
- Through the skin and by ingestion (rare causes)
Once introduced, the organisms undergo multiplication and hematogenous dissemination- during this stage the meninges are most likely to be involved. When the immune response fails, the subarachnoid space is infected by a rupture of meningeal tubercules followed by release of bacilli and the development of meningitis.
Clinical features
- Subacute or chronic onset over weeks - symptoms usually been present for less than 4 weeks at time of presentation
- Fever, signs of meningeal irritation, and a confused state are most common findings on physical examination, but all may be absent. Papilledema, ocular palsies, and hemiparesis or paraparesis are sometimes seen
- Meningoencephalitis (headache, lethargy, confusion, drowsiness, fever, stiff neck, K and Br, cranial neuropathies (usually oculomotor palsies, less often facial palsies and deafness))
- History of contact with an infected individual or a history of previous active tuberculosis
- In the early stages – anorexia, intermittent headache, lethargy, aching muscles, low-grade fever. Irritability and poor feeding may be the only evidence of the illness in infants.
- 2 weeks after initial febrile illness; persistent headache and stiff neck. Plus other signs of meningeal irritation, increased ICP (due to hydrocephalus) and focal neurological signs due to brain infarction from infectious arteritis (cranial nerve palsies, hemiparesis, etc) – weight loss, visual impairment, diplopia, focal weakness
- There is low progression over a period of week or months, with increasing drowsiness, evidence of progressive neurological dysfunction, and terminal coma and eventual death.
- In some cases the infection is confined to the spinal cord and presents as a radiculomyelopathy
- The course of the illness depends on the extent of the meningeal involvement, the immune response of a host, the virulence of the organism, and the stage at which treatment is administered
Complications:
- Cerebral infarction
- Hydrocephalus
- Seizures
- Focal motor deficit and impaired cognitive and intellectual functioning
- Hypopituitarism
- Hyponatremia
- Brain edema
Diagnosis
- CSF is under increased pressure, is clear or slightly cloudy and contains
- a predominance of lymphocytic and mononuclear pleocytosis (usually > 400/mm3),
- Increased protein (over 1g/l)