NEURORADIOLOGYINTERESTING CASES ROUND ON 21 MAY

15

PRESENTER: ELVIN LIM, MEDICAL OFFICER

PATIENT PROFILE (S219*****)68 year old female

Premorbid ADL independent, ambulant with walking frame

Poorly controlled DM, HL, IHD, gastritis

Chorea like movements of left upper and lower limb, able to follow commands, GCS 15, no neurological deficits

CT BRAIN (15 JUN 13) Mild hyperdensity of the basal ganglia, slightly more on the right side

MRI BRAIN (14 JUN 13) Bilateral basal ganglial T1w hyperintensity Affecting lentiform nucleus and caudate head,

right more than left Likely related to recent episode of non-ketotic

hyperglycemia

DIFFERENTIAL DIAGNOSIS

20 DIFFERENTIAL DIAGNOSISToxic poisoning

Systemic metabolic abnormalities Liver disease

Non ketotic hyperglycemia Hypoglycemia

Hypoxic ischemic encephalopathy Leigh disease Wilson disease

Osmotic myelinolysis Wernicke encephalopathy

Neurodegeneration with brain iron accumulation Creutzfeldt-Jakob disease

Fahr disease Deep cerebral venous thrombosis

Arterial occlusion Neuro-Behcet disease Flavivirus encephalitis Cerebral toxoplasmosis Primary CNS lymphoma Primary thalamic glioma Neurofibromatosis type 1

DIFFERENTIAL DIAGNOSIS1. Toxic poisoning CO, methanol, cyanide

2. Systemic metabolic abnormalities liver disease, hyper or hypoglycemia, Leigh disease, Wilson disease, osmotic myelinolysis, Wernicke encephalopathy

3. Degenerative conditions Huntington disease, neurodegeneration with brain iron accumulation, Creutzfeldt-Jakob disease, Fahr disease

4. Vascular abnormalities venous infarction, arterial occlusion

5. Inflammatory - Behcet disease

6. Infective Flavivirus encephalitides, toxoplasmosis

7. Neoplastic primary CNS lymphoma, primary bilateral thalamic glioma

T1 HYPERINTENSE BASAL GANGLIA (STATDX)1. Physiologic calcification

2. Neurofibromatosis Type 1

3. Hepatic encephalopathy

4. HIE

5. Wilson disease

6. CO poisoning

7. Hyper or hypoglycemia

8. Hypothyroidism

9. Hyper or hyperparathyroidism

10. Fahrs disease

11. Encephalitis

NON KETOTIC HYPERGLYCEMIA

Poorly controlled DM

Present with acute chorea, hemiballismus, AMS.

Follow up neuroimaging in 2-12 months later usually shows resolution of findings.

Characteristic hyperintense on T1w images, variable intensity on T2w images.

Hypothesis involves deposition of proteins, myelin breakdown products, blood or calcium minerals have been proposed.

CT BRAIN (2013 VS 2014)

PATIENT PROFILE (S722*****)41 year old male

Premorbid ADL independent, ambulant with walking frame

History of major depressive disorder

Attempted suicide by carbon monoxide (CO) poisoning, found unconscious in enclosed room with burning charcoal

CT BRAIN (8 JUL 13) Symmetrical hypodensity in the globus pallidi with

small focus of acute hemorrhage on the left, compatible with the given history of CO poisoning.

MRI BRAIN (10 JUL 13) There is mild T1 hypointensity and low T2/FLAIR signal

with hyperintense rim in the bilateral globus pallidi with susceptibility.

The globus pallidi are swollen. Abnormal T2 prolongation extends into the cerebral

peduncles. There is also mild T2/FLAIR hyperintense signal in the periventricular white matter and centrum semiovale.

CO POISONING

Presents with nausea, vomitting and headache.

Neuropsychological sequelae, delayed in 10-30% of victims.

Ischemia and infarct of globus pallidi most common, may involve caudate nucleus and putamen.

Microscopically demyelination, edema and hemorrhagic necrosis.

Treatment is hyperbaric oxygen therapy (within 6 hours for best effect).

CT BRAIN (22 days later)

MRI BRAIN (22 days later)

PATIENT PROFILE (S104*****)79 year old male

Premorbid ADL independent, community ambulant

No past medical history of note Witnessed fall, no head trauma, fell on buttocks

GCS 15, no focal neurological deficits

CT BRAIN (19 MAY 15) Multiple small 2-4mm hyperdense foci in the grey-white matter junction in the temporal and

parietal lobes.

Raises the possibility of malignancy

MRI BRAIN (17 MAY 15) Innumerable T2 hypodense foci with blooming are noted in the cerebrum and

cerebellum predominantly at the grey-white interface with relative sparing of the deep grey nuclei and corpus callosum.

May represent cerebral amyloid angiopathy.

MULTIPLE HYPERDENSE PARENCHYMAL LESIONS (STAT DX)Caused by: 1. Clotted blood 2. Non hemorrhagic hypercellular mass 3. Calcification

Trauma cerebral contusion, DAI (no trauma) Hypertension (not hypertensive, usually central > peripheral) Ischemic stroke with microhemorrhage (no neurological deficit) Hemorrhagic metastasis (possible, but not enhancing in this case) Cerebral amyloid disease (possible, microbleeds on T2*,

peripheral > central) Cavernous malformations

COMPARISON ON MRI

HYPERTENSION

Axial T2w MR shows old hemorrhage (black open arrow), multiple "black dots (microbleeds) are seem. Basal ganglia microhemorrhages are more common in hypertension than cerebral amyloid-associated microangiopathy.

CEREBRAL AMYLOID ANGIOPATHY

Axial T2* GRE MR shows striking "blooming" of innumerable hypointense foci, particularly in the subcortical white matter with sparing of the deep nuclei.

PARENCHYMAL METASTASIS

Axial T2w MR of a breast cancer patient shows multifocal white matter hyperintensities (white solid arrow). Several lesions enhanced with contrast.

CEREBRAL AMYLOID DISEASE

Amyloid beta peptide (B-amyloid) deposits within small to medium sized vessels of the brain and leptmeninges due to mutant amyloid precursor protein (autosomal dominant)

Can be primary/idiopathic or secondary/reactive (dialysis related amyloidosis)

Most common clinical presentation is spontaneous lobar hemorrhage (15-20% of spontaneous lobar hemorrhage in elderly)

May have stroke like clinical presentation, but classic case is >60 year old normotensive dementia patient with lobar hemorrhage(s) of different ages and multifocial cortical/subcortical black dots on T2/T2* MRI

Clinical history

MRI

Pathological examination (Congo red stain of evacuated hematoma)

DIAGNOSIS

TREATMENT

Avoid anticoagulants, antiplatelets

BP control (lower ICH risk)

Avoiding statins (lower ICH risk)

Immunosuppression (glucocorticoids, pulsed cyclophosphamides)

PATIENT PROFILE (S710*****)43 year old female

ADL independent community ambulant

History of endometrial cyst and adenomyosis

Giddiness for the past 3 days and sudden onset of headache

Expressive aphasia, otherwise no other neurological deficits

CT BRAIN (3 JAN 15) Acute left temporal intraparenchymal hemorrhage

with vasogenic edema and mass effect.

MRI BRAIN (5 JAN 15) Large hemorrhagic venous infarct of temporal lobe with

associated mass effect and 3mm rightward midline shift. This is secondary to a clot within the left transverse and sigmoid

sinuses, extending into the left upper internal jugular vein

DIFFERENTIAL DIAGNOSIS (STATDX)1. Arterial infarction territorial vascular distribution

2. Neoplasm- enhancing mass, DWI shows vasogenic edema instead of cytotoxic edema

3. Venous infarction nonarterial distribution, clinical history of trauma, hypercoagulable states, pregnancy, dehydration

4. Encephalitis / cerebritis strong restriction on DWI, nonvascular distribution

CEREBRAL ARTERIAL VS VENOUS TERRITORIES

CEREBRAL VENOUS INFARCTION

Sequelae of cerebral venous thrombosis high venous pressure which first results in cytotoxic vasogenic edema, then infarction and development of cytotoxic edema (arterial infarction has no vasogenic edema component)

Hemorrhage more frequent than arterial infarction due to high venous pressure

Other causes include trauma and surgical ligation

Arterial supply to infarcted tissue is not compromised

PATIENT PROFILE (S164*****)51 year old female

No past medical history of note

Vertical diplopia, ?space occupying lesion

No further clinical history available

MRI ORBITS AND BRAIN (18 MAR 15) Assymetric thickening of right side of nasopharyngeal

mucosa with adjacent enlarged retropharyngeal lymph node.

Right cavernous sinus is asymmetric on the right compared to the left.

Superior rectus complex thickened and hyperintense on T2 compared to contralateral side, with subtle equivocal prominence of the medial and inferior recti muscles.

Differential diagnosis include lymphoma, metastasis, sarcoid, pseudotumor. Atypical for Wegeners and Graves disease.

To exclude NPC

LR6 SO4 AO3

INVESTIGATIONS

T3 and T4 normal

Right post nasal space biopsy showed reactive lymphoid hyperplasia, negative for malignancy.

DIFFERENTIAL DIAGNOSIS (STATDX)1. Thyroid associated orbitopathy IM SLOW mnemonic for predilection, spares tendons

2. Idiopathic orbital inflammatory disease - painful

3. Lymphoproliferative disease - possible

4. Metastasis possible, from breast, lung, melanoma

5. Trauma no prior trauma

6. Cellulitis no sinusitis

7. Sarcoidosis isolated muscle disease rare

8. Rhabdomyosarcoma

PATIENT PROFILE (S050*****)64 year old female

ADL independent community ambulant

History of HTN, HL

Lethargy 2/52, unsteady gait 2/52, dizziness 1/52

No neurological deficits, no papilloedema

CT BRAIN (27 APR 15) Bilateral choroid plexus hyperdense lesions,

more on left side

Left thalamic invasion and adjacent perilesional edema

3mm midline shift to right

Differentials include choroid plexus lymphoma or metastasis (e.g. from renal cell carcinoma, breast or lung primary)

PROGRESS NOTES Planned for outpatient MRI with sterotactic

biopsy or left periventricular lesion

However AOR discharged and readmitted for increasing drowsiness and dizziness since AOR discharge

MRI brain performed on 6 May 15.

CT thorax, abdomen, pelvis performed on 7 May 15 showed no significant abnormalities. Hematological investigations and tumor markers were negative.

MRI BRAIN (6 MAY 15) There is a fairly homogenously enhancing lesion

involving the choroid plexus of the left temporal horn, subependymal and periventricular left crus of fornix and posterior aspect of the left thalamus, associated with focus of restricted diffusion and focal calcification (or small haemorrhage) in the posterior left thalamus. Significant perilesional oedema is noted.

A small separate subependymal enhancement at body of the right lateral ventricle with mild extension into the right thalamus.

Overall findings may suggest choroid plexus neoplasm with CSF spread, lymphoma or metastasis.

CHOROID PLEXUS LESIONS (STATDX)1. Choroid plexus cyst most common cause, hyperdense

2. Choroid plexus papilloma strongly enhancing

3. Meningioma - enhancing

4. Metastasis enhancing; commonly from breast, lung or melanoma

5. Ventriculitis enhancing

6. Sturge-Weber Syndrome enhancing angiomatous ipsilateral choroid plexus

7. Neurofibromatosis type 2 extensive choroid plexus calcification

8. Choroid plexus carcinoma enhancing intraventricular mass and ependymal invasion

9. Lipoma - extra-axial mass with fat intensity

THE END