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.
