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/60 Date : 00.00.00

Name of the Patient : Abc Xyzai Blmn / F / 55 yrs.
Referred by : Dr. Abc Xyziram.
Examination : M.R.I. of the Brain & intracranial MR Venogram.

CLINICAL PROFILE :

C/O giddiness since 2 months with tremors in BUE and BLE and gait ataxia.
H/O seizures since 15 days.

EXAMINATION :

M.R.I of the brain was performed using the following parameters :

5 mm thick T1 Weighted, proton and T2 Weighted axial images.

5 mm thick FLAIR coronal images.

MR Venogram was also obtained.

OBSERVATION :

There are hyperintense areas in the head of the caudate nucleus, thalamus and the lentiform nucleus bilaterally on the proton, T2 Weighted and FLAIR images. These are hypointense to the normal white matter on the T1 Weighted images. Similar areas are seen in the right middle cerebellar peduncle, pons and bilateral cerebral peduncles.

Diffuse hypointense signal is seen in the fronto-parietal deep white matter with involvement of the internal and external capsules bilaterally as well as the periventricular deep white matter on the proton, T2 Weighted and FLAIR images. This is hypointense to the normal white matter on the T1 Weighted images.

Lacunar infarcts which are seen to follow CSF signal characteristics on all the pulse sequences are noted in the right cerebellar hemisphere.
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Both the lateral, third and the fourth ventricles are normal. The basal cisternal spaces are unremarkable. There is no shift of the midline structures.

MR Venogram :

On the MRV the visualized dural and deep venous sinuses show normal flow characteristics. No obvious venous thrombosis is evident on this scan.

IMPRESSION :

The MRI/MRV features are suggestive of :

1. Altered signal in the head of the caudate nucleus, thalamus, head of the lentiform nucleus bilaterally,
in the right middle cerebellar peduncles, pons and bilateral cerebral peduncles and in the fronto-parietal deep white matter with involvement of the internal and external capsules bilaterally as well as the periventricular deep white matter as described is not specific for a single etiology.

The possibilites to be considered are,

a. Demyelination.

b. Ischemia/infarction.


c. Gliomatosis Cerebrii.

2. Lacunar infarcts in the right cerebellar hemisphere.



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