| Findings: MRI of brain with T1 weighted echo train spin echo, T2 weighted echo train spin echo, fluid-attenuated inversion recovery echo train spin echo, short inversion time inversion recovery echo train spin echo, MR diffusion imaging, single voxel proton MR spectroscopy, and with intravenous gadolinium-enhancement: 1. A midline cleft in narrowed midbrain, extending from interpeduncular cistern to aqueduct (fig1 and arrows in fig2), and incomplete separation between midbrain and thalamus (fig3), in favor of mesencephalic cleft, possibly due to congenital abnormal development. 2. Mild but diffuse enhancement of leptomeninx around bilateral cerebral hemispheres, predominant over suprasellar cistern (fig5), interpeduncular cistern (fig4), and ambient cistern, infectious process such as tuberculous meningitis may be first considered. 3. Diffused gyriform distribution of restricted water diffusibility in gray-white matter interfaces of bilateral cerebral hemispheres (fig6-10) without contrast enhancement, and preservation of bilateral corpus striatum, suggesting diffused cytotoxic edema, possibly due to diffuse cerebritis, but toxic, metabolic brain disorder, or during/immediately after severe seizure can not be excluded. Presence of relative effacement of bilateral cortical sulci. 4. Reduced NAA [N-acetylaspartate (NAA)/total Creatine (Cr)= 0.92 ], elevated choline [choline (Cho)/total Creatine (Cr)= 1.47], and presence of abnormal peak of lactate (fig11), sampling randomly from right posterior temporal lobe, suggesting neuronal damage and increased anaerobic glycolysis. Impression: 1. Mesencephalic cleft, possibly due to congenital abnormality. 2. Leptomeningeal enhancement, suspicious meningitis. 3. Diffused cytotoxic edema, neuronal damage, and increased anaerobic glycolysis in bilateral cerebral hemispheres, nature to be determined. |