NEURORADIOLOGY

INTERESTING 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 DIAGNOSIS
Toxic 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 DIAGNOSIS
1.

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

CEREBRAL AMYLOID ANGIOPATHY

PARENCHYMAL METASTASIS

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.

Axial T2* GRE MR shows striking

"blooming" of innumerable
hypointense foci, particularly in
the subcortical white matter with
sparing of the deep nuclei.

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

DIAGNOSIS

Clinical history

MRI

Pathological
examination (Congo red
stain of evacuated
hematoma)

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.

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