ke/sb/nl/rg.
/29 Date : 00.00.00

Name of the Patient : Abc Xyzh Pilmn / M / 50 yrs.
Referred by : Dr. Abc Xyzikhalikar.
Examination : M.R.I. of the Brain and
Intracranial and Neck M.R.A.

CLINICAL PROFILE :

Known C/O Parkinsonism.
C/O excessive sleep since 2 months.

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 and Fast Scan (T2 *) coronal images.

5 mm thick T1 Weighted sagittal images.

Intracranial and neck MRA were performed with 3D TOF and 2D TOF sequences, respectively.

OBSERVATION :

BRAIN :

There is no focal area of altered signal intensity within the brain parenchyma.

There is mild fullness of both the lateral and third ventricles. There is slight prominence of the cerberal cortical sulci and cerebellar folia bilaterally.

The fourth ventricle is normal. The basal cisternal spaces are prominent. There is no shift of the midline structures.

Incidental note is made of left maxillary sinusitis.


INTRACRANIAL MRA :

The A1 segment of the left anterior cerebral artery appears hypoplastic and the left vertebral artery is smaller in calibre as compared to the right.

The petrous, cavernous and supraclinoid segments of the internal carotid arteries bilaterally show normal signal and calibre. The visualized right anterior cerebral, middle cerebral, basilar, right vertebral and posterior cerebral arteries also show normal signal, calibre and wall margins. No obvious aneurysm or vascular malformation is identified.

NECK MRA :

Small filling defects are seen along the posterior walls of the internal carotid artery just distal to the common carotid bifurcation, bilaterally and could be due to atherosclerotic plaques.

The common carotid arteries and their extracranial branches appear normal bilaterally. The left vertebral artery is hypoplastic.

IMPRESSION :

1. Filling defects along the posterior walls of the internal carotid artery just distal to the common carotid bifurcation, bilaterally, could be due to atherosclerotic plaques.

2. No significant abnormality is detected within the intracranial MRA or the brain parenchyma on this study.