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[Tuberculous meningitis with hydrocephalus: a clinical and CT study]
Abstract:
Fourteen cases of tuberculous meningitis complicated by moderate or severe hydrocephalus identified by CT are reported. The accumulation and blockage of tuberculous exudate in the basic cisterns and ependymitis in the cerebrospinal drainage pathway are the important pathological features of this disease. There may be a correlation of hydrocephalus with hyponatraemia. Headache, vomiting, and impaired consciousness are common symptoms, although a few cases did not show obvious symptoms of raised intracranial tension. The study suggests a relation between the degree of hydrocephalus and the pressure on lumber puncture. If patients with impaired consciousness, especially in the chronic stage show no improvement during medical treatment, ventricular shunt may bring about remarkable improvement.
Insights
Tuberculous meningitis can cause hydrocephalus, leading to symptoms like headache and vomiting. Ventricular shunting offers significant improvement for patients with impaired consciousness unresponsive to medical treatment.
Area of Science:
- Neurology
- Infectious Diseases
- Neurosurgery
Background:
- Tuberculous meningitis (TBM) is a severe infection.
- Hydrocephalus is a common complication of TBM.
- CT scans are crucial for diagnosis.
Purpose of the Study:
- To report on 14 cases of TBM with hydrocephalus.
- To describe pathological features.
- To explore correlations and treatment outcomes.
Main Methods:
- Retrospective review of 14 TBM cases with hydrocephalus.
- CT imaging analysis.
- Clinical assessment and lumbar puncture data.
Main Results:
- Tuberculous exudate and ependymitis obstruct cerebrospinal fluid (CSF) pathways.
- Hydrocephalus may correlate with hyponatremia.
- Symptoms include headache, vomiting, and altered consciousness.
- Lumbar puncture pressure may relate to hydrocephalus severity.
Conclusions:
- TBM-induced hydrocephalus has specific pathological features.
- Ventricular shunting can significantly improve consciousness in non-responsive chronic TBM patients.