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Journal of Pediatric Neurosciences logoLink to Journal of Pediatric Neurosciences
. 2016 Jan-Mar;11(1):86–87. doi: 10.4103/1817-1745.181260

Tuberculous meningitis sequelae as basal cisternal calcifications

Nagarajan Krishnan 1,, Lakshminarasimhan Renganathan 1
PMCID: PMC4862301  PMID: 27195045

A 10-year-old female child who was diagnosed with tubercular meningitis and underwent shunting for hydrocephalus came with the complaints of a mild headache. She had completed 18 months of antitubercular treatment. Plain computed tomography (CT) showed hyperdense basal cisternal and left Sylvian fissure calcifications obliterating the cerebrospinal fluid spaces [Figures 1 and 2]. The bilateral ventriculoperitoneal shunts were functioning well, and there was no ventricular dilatation.

Figure 1.

Figure 1

Axial computed tomography sections at the level of basal cisterns show hyperdense calcified nodules in the regions of basal cisterns and left Sylvian fissure obliterating the cerebro-spinal fluid spaces. Mild perilesional edema is noted in the left temporal lobe

Figure 2.

Figure 2

Axial computed tomography section at the level of body of lateral ventricles shows shunt tubes without any ventricular dilatation

Tuberculous meningitis classically produces basal exudates, hydrocephalus, and infarcts of arteritis, and neuroimaging using CT and/or magnetic resonance imaging plays an important role in the diagnosis. The sequelae of basal cisternal exudates seen as calcifications were noted more commonly during the preimaging era probably due to delay in diagnosis.[1] Studies have shown that basal calcifications were noted mainly in children presenting with longer duration of symptoms (more than 10 days) before starting treatment.[2,3] Hence, it may be relatively less common now as empirical treatment may be instituted early in the course of the disease based on clinical, imaging, and laboratory features.

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References

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