CT scan of brain with pre- and post- intravenous contrast, and
 with multiplanar reconstruction:

1. Marked symmetric decreased densities in bilateral lentiform
   nucleus, predominant over bilateral putamina, possibly
   associated with encephalitis (figure 01).
2. Mild dilatation of left lateral ventricle temporal horn by
   compared with right side, significance unknown.

Impression:
1. Suspicious encephalitis with bilateral lentiform
   nucleus involvement.
2. Recommendation: Further evaluation with gadolinium-enhanced MRI.
   Thank you!

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MRI of brain with T1 weighted echo train spin echo, T2 weighted
 echo train spin echo, fluid-attenuated inversion recovery echo
 train spin echo, MR diffusion imaging, intravenous
 gadolinium-enhancement, and chemical shift MR imaging with
 metabolite map:

1. Symmetric long T1 and T2 change with marked restricted water
   diffusibility and without significant contrast enhancement
   in both cerebral and cerebellar deep grey matters, including
   bilateral lentiform nucleus, caudate nucleus (right head and
   bilateral bodies), posterior parts of thalami, and cerebellar
   dentate nuclei, suggesting extensive cytotoxic edema, but
   nature to be determined (figure 02-06).
   (Differential diagnosis: acute encephalitis such as Japanese
   encephalitis, inborn error of metabolism such as mitochondrial
   disorder,...,etc).
2. From the images of chemical shift MR imaging with metabolite
   map, presence of peaks of lactate in bilateral corpus striatum
   (figure 07,08), suggesting abnormal intracranial metabolism.
3. Presence of some mass effect of bilateral corpus striatum
   lesions with mild focal dilatation of left lateral ventricle
   temporal horn, in favor of mild early focal hydrocephalus.
4. Another symmetric long T2 lesions without restricted water
   diffusibility or contrast enhancement in bilateral substantia
   nigra of midbrain and posterior surface of medulla oblongata
   (figure 02,03), nature to be determined.

Impression:
1. Cytotoxic edema, both cerebral and cerebellar deep grey matters,
   suspicious encephalitis or inborn error of metabolism.
2. Recommendation: Please arrange feasible laboratory study
   and MRI follow up 3 months later. Thank you!

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Note: Because normal WBC and C.R.P laboratory data, inborn error of
 metabolism may be more considered!

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MRI of brain (1 month later) with T1 weighted echo train spin echo,
 T2 weighted echo train spin echo, T2 weighted fluid-attenuated
 inversion recovery echo train spin echo, MR diffusion imaging,
 intravenous gadolinium-enhancement, and single-voxel MR
 spectroscopy:

1. History of suspicious inborn error of metabolism or encephalitis,
   S/P conservative treatment.
2. Presence of enlargement of surface sulci and cisterns, suggesting
   brain atrophy (figure 09).
3. Multiple symmetric long T1 and T2 cystic changes without
   significant restricted water diffusibility in brain, including
   bilateral corpus striatum, thalami, cerebellar dentate nuclei,
   bilateral substantia nigra of midbrain, and both aspects
   of medulla oblongata, compatible with multiple encephalomalacia
   from previous brain insults, chief involvement over cerebral
   and cerebellar deep grey matters (figure 09).
4. Presence of some periventricular leukomalacia over bilateral
   parietooccipital white matter, around bilateral lateral ventricle
   occipital horns, compatible with another encephalomalacia
   (figure 09).
5. Some heterogeneous short T1 signals with faint contrast
   enhancement in bilateral caudate nucleus, suggesting
   tissue punctate hemorrhage from previous necrotic process
   (not showed).
6. From above findings, the brain condition is progressive extension
   by compared with previous MRI on 2008.01.21. But no new onset
   lesion could be detected.
7. From single-voxel MR spectroscopy (sampling from bilateral
   thalami and globus pallidus, marked reduced the ratio of
   N-acetylaspartate (NAA)/total Creatine (Cr) and elevated
   the ratio of choline (Cho)/total Creatine (Cr) by gross
   observation, compatible with previous neuronal damage with
   neuron loss (figure 10).
   No residual peak of lactate from this examination compared to
   previous high lactate contents noted on 2008.01.21, suggesting
   disease in subacute/chronic stage.

Impression:
1. Brain atrophy with extensive encephalomalacia, chief involvement
   over bilateral cerebral and cerebellar deep grey matters,
   suspicious inborn error of metabolism or encephalitis.
2. Disease in subacute/chronic stage without new onset lesion.