dementia.docx

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No Name & NRIC Diagnosis 1 Mdm Ang Soo Lim S0861011H Dr P Yap Inpatient Stroke 2 Mr Tan Bok Her S0308446I Dr P Yap Inpatient White matter changes 3 Mr Tan Seng Keh S0252876B VaD 4 Mr Ong Kim Book G0498658Q Dr Chen SL ?NPH / marked atrophy 5 Mdm Wee Sek Eng S0675306Z Dr L Tan

Transcript of dementia.docx

Page 1: dementia.docx

No Name & NRIC Diagnosis  1

 Mdm Ang Soo LimS0861011H Dr P YapInpatient

 Stroke

  2

 Mr Tan Bok HerS0308446I Dr P YapInpatient

 White matter changes

  3

 Mr Tan Seng KehS0252876B 

 VaD

  4

 Mr Ong Kim BookG0498658Q

Dr Chen SL

 ?NPH / marked atrophy

  5

 Mdm Wee Sek EngS0675306Z Dr L Tan

 

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S0861011H : STROKE

84 YEAR CHINESE GENTLE MEN

Foci of restricted diffusion are noted in the left thalamus, left occipital lobe, posterior limb of the right internal capsule and in the mid brain in keeping with presence of small acute infarcts. No focus of susceptibility is seen to suggest presence of haemorrhagic products. Chronic lacunar infarcts are noted in the right corona radiata and bilateral striato-capsular regions. Age-related cerebral involution as well as periventricular and deep white matter chronic microvascular ischaemic changes are evident. . Absent flow signal is noted within the basilar artery and bilateral posterior cerebral arteries, raising concern for underlying thrombosis. Luminal irregularity and narrowing of the bilateral vertebral arteries, cavernous, clinoid and supraclinoid segments of both internal carotid arteries and distal M1 and/proximal M2 segment of the right middle cerebral artery is likely due to underlying atherosclerotic disease.

No sizeable aneurysm is seen in both the anterior and posterior circulations.

S0308446I ? WHITE MATTER CHANGES

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78 year Chinese gentleman

acute giddiness and dizziness with functional decline and insomnia.

A homogeneously enhancing extraaxial lesion arising from the right greater sphenoid wing noted measuring 40.9 x 17.4 x 29 mm. It appears predominantly hypointense on T1-weighted images and shows mixed signals (peripheral dark and central bright) on T2-weighted images. Few areas of gradient blooming seen inside the lesion, representing bleed.

Inferiorly the lesion extends along the medial aspect of the right middle cranial fossa abutting the antero- medial aspects of the right temporal lobe. Lesion also extends to the roof of the sphenoid sinus along the right medial aspect involving the planum sphenoidale , extend around the anterior clenoid process, optic foramen , superior orbital fissure and early extension into the right cavernous sinus posteriorly. There is mild indentation over the underlying frontal temporal brain parenchyma. there is minimal oedema of the brain parenchyma around the lesion. Mass effect over frontal horn of the right lateral ventricle noted. There is 5 mm midline shift towards the left side in the anterior cranial fossa with mild subfalcine herniation. The supraclinoid portion of the right internal carotid artery and M1 segment of the right middle cerebral artery are abutted by the lesion. Appearances are most likely related to right-sided greater wing sphenoid meningioma and there is no underlying marrow signal changes in the sphenoid wing to suggest dural based metastasis and less amount of vasogenic oedema in adjacent brain. No similar lesion noted elsewhere in the brain. There is a thin subdural haematoma in the left parietal region , Maximum thickness measuring approx 3 mm.

Extensive chronic microvascular ischaemic changes noted involving bilateral cerebral white matter, basal ganglia, capsular tracts and brainstem.

Chronic micro bleeds noted in the bilateral thalami

Moderate age-related involutional changes with ex vacuo dilatation of the ventricles are noted. Visualised sections of the orbits and paranasal sinuses appear unremarkable.

S0252876B : VASCULAR DEMENTIA

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There are few old lacunar infarcts in the bilateral basal ganglia.

Mild bilateral periventricular and deep white matter T2 FLAIR hyperintensities are related to chronic microvascular disease. These T2 hyperintensities are appears slightly more confluent in bilateral frontal lobes (Fazekas 1).

Also there are bilateral frontal lobes increased T2 signal which was suppressed on T2 FLAIR, larger in the left frontal lobe which measure 3.2cmx2.5cm on axial image and the right frontal lobe lesion measures 1.2cmx0.8cm. These may represent cystic encephalomalacia, with surrounding frontal gliosis: post infarction? Post trauma? but no evidence of old blood products. Not a typical appearance for arachnoid cyst

Age appropriate moderate global cerebral involutional changes are present.

There is no asymmetry cerebral atrophy including the hippocampi. Proportionate ventricles dilatation is noted.

CONCLUSION: 1 Suggestion of bilateral frontal lobes parafalcine scarring, with cystic encephalomalacia, larger on left side 2 Fezekas 1 chronic microvascular ischemic changes, slightly more prominent at bilateral frontal deep white matter 3 Bilateral basal ganglia and right hippocampus lacunar infarcts; No asymmetry cerebral atrophy ]

Paucity of white matter lesions

No infracts in strategic location

Absent bilateral thalamic infarcts.

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G0498658Q

Brain parenchymal atrophy: Global Cortical Atrophy: Present; moderate atrophy

Regional atrophy:

Disproportionate Temporal lobe Atrophy: - Present, MTA 2-3 bilaterally. Disproportionate Frontal lobe atrophy: Absent

Disproportionate Parietal lobe atrophy: - Present, right worse than left. Right: Koedam 3; left: Koedam 2.

Disproportionate Cerebellar or Pontine atrophy: Absent

White matter changes: Present; involving periventricular white matter extending to the subcortical and deep white matter, Fazekas 2-3.

S0675306Z

Bilaterally, periventricular and deep white matter subcortical signal changes are noted, graded Fazeka2.

They are compatible with chronic micro ischaemic small vessel disease.

No evidence of previous territorial or strategic infarction nor multi lacunar infarcts. Normal flow void seen in the main intracranial arteries.

Both parietal lobes are more atrophic and this can be considered as early sign of AD?. Reported to the age, there is appropriate diffuse atrophy of the rest of the brain. No significant disproportionate hippocampal atrophy.

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GCA scale is the mean score for cortical atrophy throughout the complete cerebrum:

0: no cortical atrophy 1: mild atrophy: opening of sulci 2: moderate atrophy: volume loss of gyri 3: severe (end-stage) atrophy: 'knife blade' atrophy.]

MTA

score 0: no atrophy score 1: only widening of choroid fissure score 2: also widening of temporal horn of lateral ventricle score 3: moderate loss of hippocampal volume (decrease in height) score 4: severe volume loss of hippocampus

< 75 years: score 2 or more is abnormal.> 75 years: score 3 or more is abnormal.

Koedam atrophy :

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