NEURORADIOLOGYTRUDY ROSS

RADIOLOGY DEPARTMENT

APPROACH TO THE CT BRAIN

• Ventricles and subarachnoid spaces• Basal cisterns• Asymmetry• Abnormal density• Grey-white matter differentiation• Bones and soft tissues

CHOOSE YOUR WINDOW

BASIC MR

• Basic features:• Fluid – T2 very bright• Haemorrhage – Varies with time, often hard to see,

blooming on GRE• Oedema – T1 dark, T2 bright• Fat – Bright T1 and T2• Can have Fat suppressed sequences (T2 FS bright =

oedema); or Fluid attenuated sequences (FLAIR – abnormal oedema is bright)

• FIR, STIR, FIESTA, GRE …….

IMAGING STRATEGIES – INDICATIONS FOR BRAIN IMAGING

• Non contrast for bleed, ventricles or stroke• Give contrast for masses, abscesses, dural venous sinuses.

Scan performed at approx 2min.• Angiogram – for assessment of arterial supply. High flow

rate, timed for opacification of the cerebral arteries. • MR – much better anatomical detail. More sensitive to

slight changes in tissue. Not as useful for bleeds or bone

HAEMORRHAGE

• Extradural• Subdural Extra-axial• Subarachnoid

• Contusion Intra-axial• DAI

DENSITY (HU)

Air < -500Fat -50CSF 0WM/GM 30/40ACUTE BLOOD 70Calcification >150Bone >500

BLOOD ON CT

• Acute: hyperdense• Subacute: Isodense• Chronic: hypodense• Hyperacute blood can be dark.

EXTRADURAL

• Lifts dura off inner table of skull• Fracture in 90% • Usually arterial from rupture of MMA. Can be venous

(10%).• Biconvex/lentiform. Doesn’t cross suture lines unless there

is diastasis.• 95% supratentorial

ACUTE EPIDURAL

T2T1

SUBDURAL HAEMORRHAGE

• Stretching/tearing of bridging cortical veins• 95% supratentorial, 15% bilateral• Cross sutures but not dural attachments (will never cross

midline)• Crescentic• Common in infants (child abuse) and elderly• Density change with age of haemorrhage.• Rebleeding may cause a heterogenous appearance ;

sediment level or haematocrit effect

Case courtesy of Dr Chris O'Donnell, Radiopaedia.org, rID: 16807

Case courtesy of Dr Lawrence Chia Wei Oh, Radiopaedia.org, rID: 24512

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 30404

SUBDURAL HAEMATOMA

T1T2PD

SUBDURAL HAEMATOMA

T2 T1 T1 + contrast

SUBARACHNOID HAEMORRHAGE• Aneurysm most common cause• Other causes

• trauma• Vascular malformation …

• Look for high density in CSF cisterns, interpeduncular fossa, sylvian fissure, sulci, ventricles. May be very tiny, especially in the setting of trauma.

• 95% positive in 1st 24 hours, < 50% by 1 week

RIGHT MCA BIFURCATION ANEURYSM

INTRA-AXIAL HAEMORRHAGE

• Diffuse Axonal Injury (DAI)- Significant cause of morbidity in severe closed head injury

- Axonal shearing injury and depolarisation

- Lobar WM-GW interface, CC, dorsolateral upper brainstem

- Only 20-50% abnormal on initial CT, petechial haem

INTRA-AXIAL HAEMORRHAGE

• Contusion- Brain striking bony ridge

- Acceleration/deceleration injury

- Occur in characteristic locations; temporal lobe, frontal lobe, parasagittal

- Coup + Contra-coup injury

• Hypertensive haemorrhage• 50% of nontraumatic ICHs caused by hICH

• Putamen/external capsule (60-65%)• Thalamus (15-25%)• Pons, cerebellum (10%)• Lobar (5-10%)• Multifocal "microbleeds" (1-5%)

• Heterogeneous density if coagulopathy or active bleeding• Other findings

• Intraventricular extension• Mass effect: Hydrocephalus, herniation

INTRA-AXIAL HAEMORRHAGE

DIFFERENTIALS• Cerebral Amyloid Angiopathy

• Lobar > > basal ganglionic• Usually elderly, often normotensive• But as HTN is so common it is still the most common cause of

lobar ICH• Vascular Malformation

• Patients usually normotensive, younger• Most common = cavernous malformation• Less common = thrombosed hemorrhagic AVM or dAVF

• Cocaine• Usually still basal ganglia, • Hypertensive mechanism

DIFFERENTIALS CONT..• Coagulopathy

• Elderly patients on anticoagulant therapy• Venous Thrombosis

• May have history of dehydration, "flu," pregnancy/OCP• Cause lobar hematomas• Look for hyperdense dural sinus (not always present)

• Deep Cerebral Venous Thrombosis• Less common than dural sinus or cortical vein thrombosis• Look for hypodense bilateral thalami• Look for hyperdense internal cerebral veins, intraventricular

hemorrhage• Hemorrhagic Neoplasm

• Secondary (metastasis) and primary (GBM)

COMPLICATIONS OF BLEEDS

• Hydrocephalus• Herniation• Vasospasm and infarct

HYDROCEPHALUS

HERNIATION

VASOSPASM

THROMBOEMBOLIC STROKE

• <12hrs : >50% norm, Hyperdense art• 12-24rs : Low dens, GW diff loss, Sulcal effacement• 1-3 days : mass effect, low density of G&W• 4-7 days : gyral enhancement, mass effect/oedema• 1-8/52: contrast enhancement, mass effect resolves• Months-yrs: encephalomalacia, volume loss, Calc rare

VASCULAR TERRITORIES

MCA

ACA

PCA

ACUTE SIGNS

• Hyperdense vessel• Insular ribbon sign• Obscuration of lentiform nucleus• Hypoattenuating brain• Loss of grey-white differentiation• Loss of sulcation

HYPOATTENUATING BRAIN LOSS OF SULCATION

• Failure of ion pumps cause increased brain water

• Irreversible damage

• Bad sign if seen in the first 6hrs

BLURRED BASAL GANGLIA

• Loss of definition of the basal ganglia

• One of the earliest and most frequently seen signs

• MCA infarction

INSULAR RIBBON SIGN

• Very sensitive to ischaemia

• A subtle but early sign• MCA territory

DENSE VESSEL

• Due to thrombus or embolus in the artery

IS IT OLD???

• Well defined• Hypodense• Negative mass effect• Ex vacuo dilation

CT PERFUSION

• CBF• CBV• MTT• Blue always low

value, red high value

MRI IN STROKE

• T2 and FLAIR hyperintensity = cell death • Will detect 80% in first 24hrs• Can be normal first 2-4hrs

• DWI• Normally water protons can diffuse between

compartments. Cytotoxic oedema disrupts this. “Restricted diffusion”.

• Most sensitive sequence for acute stroke

AGING BRAINS

SMALL VESSEL ISCHAEMIC CHANGES• Grade 1 is

normal.• 2 and 3 are

pathologic but can be seen in normal functioning people.

• Strong predictor of rapid global functional decline

RING ENHANCING LESIONS

RING ENHANCING LESIONS

• Long differential• Abscess• Tumour (primary or secondary)• Haematoma• Stroke• Tumefactive MS• Radiation necrosis• Resection cavity

SPINE

SPINAL IMAGING - APPROACH

• As for plain films, but more components visible in CT/MR• Alignment + number of vertebral bodies• Vertebral body and intervertebral disc heights• Joints – Atlanto-occipital, Atlanto-axial, Facet joints• Spinal canal• Spinal cord –

• conus termination; • cord signal, • nerve roots• If mass lesion – intra-axial (Cord) or extra-axial (Dural, bony)

GET THE MODALITY RIGHT

NORMAL DISC

DEGENERATIVE DISC

• Decreased height• Bulging• Gas bubbles• Endplate change• Happens from an early age• Osteophytes• Facet joint changes

FOCAL VS BROAD BASED BULGE

• Protrusion vs extrusion

• • Migration vs • sequesteration

• Central • Paramedian/lateral recess – most common• Foraminal – 5-10% but cause severe pain• Lateral - uncommon

DISC HERNIATION

FORAMINAL DISC PROTRUSION

TERMS

• Spondylosis – degenerative change between vertebral bodies or at zygopophyseal joints

• Spondylolysis – a pars interarticularis defect, usually a stress fracture.

• Spondylolisthesis – slipping of vertebrae, often due to spondylolysis

• Spondylitis – inflammation of the vertebrae eg AS

CERVICAL SPINE STENOSIS DUE TO CERVICAL SPONDYLOSIS

OSTEOARTHRITIS SPINE

• Uncovertebral joints• Facet joints• Intervertebral discs

• Compression on nerves can be just disc herniation, just productive OA changes or a combination of both (disc osteophyte complex)

FINISHED!!!