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[Transitory cranial dyskinesias and tubercular meningitis. Report of three cases]
1Instituto Oftalmológico Santa Lucía, Quito, Ecuador.
Abstract:
Three patients who suffered transitory (from 18 to 49 days) cranial dyskinesias during the course of tubercular meningitis are described. The diagnosis was confirmed by the presence of acid-alcohol resistant bacilli in spinal fluid. Cranial tomography or magnetic resonance images failed to demonstrate anatomical lesions. The blink reflex and brain stem auditory evoked potentials were abnormal, indicating dysfunction of motor nuclei of the cranial nerves, possibly secondary to changes in their regulation by basal ganglia. No recurrences have been observed during follow-up (from 3 to 7 years).
Insights
Tubercular meningitis can cause temporary cranial dyskinesias in patients. Diagnostic tests confirmed the infection, and neurological assessments revealed cranial nerve dysfunction without anatomical lesions.
Area of Science:
- Neurology
- Infectious Diseases
- Neurophysiology
Background:
- Tubercular meningitis is a serious infection affecting the central nervous system.
- Cranial nerve palsies are known complications, but dyskinesias are less commonly reported.
Observation:
- Three patients with confirmed tubercular meningitis presented with transient cranial dyskinesias lasting 18-49 days.
- Clinical diagnosis was supported by identifying acid-alcohol resistant bacilli in cerebrospinal fluid.
- Neuroimaging (CT/MRI) did not reveal structural abnormalities in the brain.
Findings:
- Abnormalities in blink reflex and brainstem auditory evoked potentials indicated cranial nerve motor nucleus dysfunction.
- This dysfunction may stem from basal ganglia regulatory changes secondary to meningitis.
- No relapses of dyskinesias were noted during 3-7 years of follow-up.
Implications:
- Highlights a rare neurological manifestation of tubercular meningitis.
- Suggests the importance of neurophysiological assessments in diagnosing cranial nerve dysfunction in meningitis.
- Underscores the potential for reversible neurological deficits following treatment.