Table 1. Neuroradiological abnormalities at baseline.
Tuberculous meningitis (n = 48) | ||
---|---|---|
Meningeal enhancement | 39/48 (81%) | |
Basal meninges | 25 | |
Sylvian fissure | 22 | |
Convexity | 18 | |
Ventricular | 3 | |
Hydrocephalus | 27/48 (56%) | |
Communicans | 27 | |
Non-communicans | 0 | |
Tuberculoma | 37/48 (77%) | |
Miliary | 35 | |
Non-miliary | 24 | |
Pseudo abscess | 1 | |
Brain Infarction | 29/48 (60%) | |
Acute, n = 26 (90%) | Chronic, n = 4 (14%) | |
Cerebrum, basal ganglia & thalamus | 22 | 2 |
Cerebrum, outside basal ganglia & thalamus | 22 | 2 |
Cerebellum | 2 | 0 |
Brainstem | 5 | 0 |
Cranial nerve enhancement | 9/48 (19%) |
Meningeal enhancement was defined as linear or nodular enhancement of meninges with contrast media [33] at one or more locations: the basal meninges (e.g. basal cistern, ambient cistern, quadrigeminal cistern, prepontine cistern, cerebellopontine cistern, suprasellar cistern, premedullary cistern), sylvian fissure, cerebral or cerebellar convexity/sulci and ventricular system [24]. Hydrocephalus was present if one or more of: dilated temporal horns of lateral ventricles, ballooning of frontal horns of lateral ventricle, ballooning of third ventricle, narrowed callosal angle, presence of flow void in T2W images at the Sylvian aquaducts [34]. Evans’ index [35] of every patients with and without hydrocephalus were measured and compared. Communicating and non-communicating hydrocephalus were defined based on the absence or presence of an obstructing lesion along the intraventricular CSF pathways[34]. Tuberculomas were defined as the presence of nodular or ring enhancement with contrast media [33, 36] and specified as milliary (<2mm) or non-milliary (>2mm) tuberculomas, or pseudo-abscesses [37]. Abscesses were defined as the presence of ring enhancement with restricted diffusion appearance on DWI-ADC [38]. Acute infarctions were defined as lesions with restricted diffusion on DWI-ADC, and increased T2-weighted and fluid-attenuated inversion recovery (FLAIR) signal intensity [39]. Cranial nerve neuropathy was defined as enhancement with or without thickening of the oculomotor nerve, trigeminal nerve, abducens nerve, facial nerve or vestibulocochlear nerve [40].