Cranial Imaging

Goals of imaging

Guides acute interventions whether IV thrombolysis or mechanical thrombectomy

Confirming a stroke, excluding stroke mimics
Differentiating type of stroke: Ischaemic vs Haemorrhagic
Assess status of large cervical and intracranial arteries
Assess extent of ischaemic damage

Infarct core volume
Potentially salvageable brain tissue

Atherosclerosis

Carotid Duplex US

Carotid CTA

Contrast enhanced MRA

Vascular wall imaging

Components

Occlusion
Degree of stenosis
Plaque characteristics

CT scan

General

These principles do not apply to small lacunar infarcts, nor to hemorrhagic strokes (ICH).

CT is normal in 8–69% of MCA strokes in the first 24 hours.

Loss of grey-white matter differentiation, and hypoattenuation of deep nuclei

Cortical hypodensity with associated parenchymal swelling with resultant gyral effacement

Hyperdense vessel

Timing

Hyperacute (< 6 hours after stroke).

Early signs of infarction involving large areas of the MCA territory correlate with poor outcome. Early findings may include:

Focal low attenuation within the gray matter
Loss of the Gray-white interface
Attenuation of the lentiform nucleus
Mass effect

Early: effacement of the cerebral sulci (often subtle)
Late: midline shift in large territory infarction

Loss of the insular ribbon sign

Hypodensity involving the insular cortex, susceptible to ischemia due to poor collaterals

Enhancement with IV contrast:

Occurs in only 33%.
Stroke becomes isodense (called “masking” effect) or hyperdense with normal brain, and, rarely, may be the only indication of infarction

Due to

Increased water content resulting from the following:

Cellular edema arising from altered cell permeability, which produces a shift of sodium and water from the extracellular to the intracellular compartment, which also increases the extracellular osmotic pressure causing transudation of water from capillaries into the interstitium.

24 hrs

Most strokes can be identified as low density by this time.

Hyperdense artery sign:

The cerebral vessel (usually the MCA) appears as high density on unenhanced CT
Indicating intra-arterial clot (thrombus or embolus).
Seen in 12% of pts scanned within 24 hrs of stroke, and in 34% of very early CTs done to R/O haemorrhage.
Sensitivity for MCA occlusion is low, but specificity is high (although it may also be seen with carotid dissection, or (usually bilaterally) with calcific atherosclerosis or high hematocrit).
Does not have independent prognostic significance.

1–2 wks

Strokes are sharply demarcated.

In 5–10% there may be a short window (at around day 7–10) where the stroke becomes isodense, called “fogging effect.”

IV contrast will usually demonstrate these.

3 wks

Stroke approaches CSF density.

Mass effect

Common between day 1 to 25.

Then atrophy is usually seen by ≈ 5 wks (2 wks at the earliest).

Serial CT scans have shown that midline shift increases after ischemic stroke and reaches a maximum 2–4 days after the insult.

Calcifications.

Over a long period of time (months to years) ≈ 1–2% of strokes calcify (in adults, it is probably a much smaller fraction than this; and in peds it is higher).

Therefore, in an adult, calcifications almost rule out a stroke (consider AVM, low grade tumor…).

Alberta stroke program early CT score (ASPECTS)

To identify those who will benefit from thrombolysis (alteplase)

Derived from 2 noncontrast axial CT slices:

At the level of the the thalamus

Rostral to the basal ganglia.

MCA is divided into 10 territories that each get 1 point:

3 subcortical structures (caudate, lentiform nucleus, & internal capsule), and
7 cortical territories: insular cortex (ribbon) and M1 through M6
Starting with a normal score of 10, 1 point is subtracted for each of the territories that show signs of early ischemic change:

Swelling (evidenced by compression of sulci or ventricles) or
Hypoattenuation (relative to other areas of the brain) involving at ≥ 1/3 of the territory.

Outcomes

Score ≤7 is associated with a worse outcome from stroke.

Limitations

Only assesses MCA distribution infarcts
Cortical territories are not equally weighted

Advantage

Simple
Good interrater reliability
Can also be used on MRI

C: Caudate; IC: Internal capsule; L: Lentiform nucleus; I: Insular Cortex.

CT+C

Not routinely used in acute stroke

Many enhance by day 6, most by day 10, some will enhance up to 5 wks

Rule of 2’s:

2% enhance at 2 days
2% enhance at 2 mos

Gyral enhancement: AKA “ribbon” enhancement.

Common
Usually seen by 1 week (Gray matter enhances > white)
DDx:

Inflammatory infiltrating lesions such as lymphoma, neurosarcoidosis… (due to breakdown of BBB)

Rule of thumb: there should not be enhancement at the same time that there is mass effect

CT angiography

Do not delay IV tPA to get CTA

Indication

For patients with NIHSS score ≥10

Correlates with large vessel occlusion (LVO) to identify candidates for thrombectomy

To identify

For assessing the location and extent of vascular occlusion in acute ischemic stroke, and may identify the bleeding source in subarachnoid haemorrhage.
Suitable patients for thrombectomy
Can look for collaterals

If there is more collaterals then there is greater argument for thrombectomy as there is more brain to be saved

Findings can direct treatment towards endovascular options when a proximal or significant large vessel occlusion is seen.

To avoid delays in candidates for endovascular therapy, it is reasonable to proceed with CTA without waiting for serum creatinine if there is no history of renal impairment.

Single phase

Ideally arterial, but venous contamination is common
From arch to include circle of Willis
Identify/exclude large vessel occlusion
Secondary findings: Vasoconstriction, aneurysms, large AVMs
Large vessel vasculitis
Carotid web
Fibromuscular dysplasia
Post radiotherapy (H&N) carotid narrowing/pseudoaneurysm

Multiphase

Three phases

mCTA collateral score

Score	Multiphase CT Angiography
0	When compared with the asymptomatic contralateral hemisphere, there are no vessels visible in any phase within the ischemic vascular territory
1	When compared with the asymptomatic contralateral hemisphere, there are just a few vessels visible in any phase within the occluded vascular territory
2	When compared with the asymptomatic contralateral hemisphere, there is a delay of two phases in filling in of peripheral vessels and decreased prominence and extent or a one-phase delay and some ischemic regions with no vessels
3	When compared with the asymptomatic contralateral hemisphere, there is a delay of two phases in filling in of peripheral vessels or there is a one-phase delay and significantly reduced number of vessels in the ischemic territory
4	When compared with the asymptomatic contralateral hemisphere, there is a delay of one phase in filling in of peripheral vessels, but prominence and extent is the same
5	When compared with the asymptomatic contralateral hemisphere, there is no delay and normal or increased prominence of pial vessels/normal extent within the ischemic territory in the symptomatic hemisphere

Perfusion imaging (CT/MR perfusion)

CT perfusion

Perfusion = the flow of blood through the vascular/capillary bed of a tissue

Microcirculation, determined by CBF

Three parameters:

Mean transit time (MTT) or time to peak (TTP)
Cerebral blood flow (CBF)
Cerebral blood volume (CBV) = AUC (Tissue)/AUC (AIF)

Identifies

Infarct core
Salvageable brain tissue: a region of mismatch between CBF and CBV.
Degree of collateral circulation

Assumption:

The infarcted core (with no salvageable tissue) has decreased CBF within a region of decreased CBV (CBF/CBV match).
A mismatched area (decreased CBV without a decrease in CBF) represents potentially salvageable penumbra.

Implication:

Thrombolytics and interventional treatment modalities without mismatch will likely increase morbidity and mortality without clinical benefit.
DAWN and DEFUSE III trials
Selection of patient for mechanical thrombectomy

Core infarct volume: <30% threshold for CBF reduction
Penumbral volume: Tmax > 6 secs

EXTEND

Extend the time window for intravenous tPA administration

CT-Perfusion limitations

Patient factors

Cardiac output, AF, severe proximal stenosis, movement

Limited spatial resolution
Estimates
Time

Redder less blood flow or longer transit time. Prolonged MTT or Tmax, only moderately reduced CBF, near-normal/increased CBV (due to autoregulatory vasodilatation)

An area with prolonged MTT or Tmax, markedly decreased CBF and markedly reduced CBV

MRI perfusion

Arterial Spin Labeling (ASL) MRI perfusion

Non-invasive technique that measures cerebral blood flow (CBF) by using magnetically labeled water protons in arterial blood as an endogenous tracer.

Dynamic susceptibility contrast (DSC) MR perfusion

Relies on the susceptibility induced signal loss on T2*-weighted sequences which results from a bolus of gadolinium-based contrast passing through a capillary bed.

Dynamic contrast enhanced (DCE) MR perfusion

Calculates perfusion parameters by evaluating T1 shortening induced by a gadolinium-based contrast bolus passing through tissue.

Areas of matched DWI and Perfusion Weighted Imaging abnormality are thought to represent infarcted tissue.

PWI abnormalities that do not have a DWI correlate are thought to represent potentially salvageable penumbra.

MRI

Advantage

More sensitive than CT (especially DWI-MRI (p.247), and particularly in the 1st 24 hrs after stroke), and especially with brainstem or cerebellar infarction.

Newer scanners have faster acquisition time

Gradient echo or SWI sq high sensitive to haemorrhage

Disadvantage

More contraindications than CT.

Non contrast MRI

Cortical laminar necrosis

necrosis of cortical neurones in situations when the supply of oxygen and glucose is inadequate to meet regional demands

Acute phase: cytotoxic oedema causes a high signal on DWI with corresponding low apparent diffusion coefficient (ADC) values in the affected cortex,

Later in acute phase: cortical enhancement

Chronic phase (2-4 weeks): DWI hyperintensity reverses

Contrast MRI:

Not often used.

4 enhancement patterns:

Intravascular enhancement:

Seen in ≈ 75% of 1–3-day-old cortical infarcts
Due to sluggish flow and vasodilatation

Thus, it is not seen with complete occlusion).

May indicate areas of brain at risk of infarction

Meningeal enhancement:

Especially involving the dura.
Seen in 35% of cortical strokes 1–3 days old
Not seen in deep cerebral or brainstem strokes
No angiographic nor CT equivalent

Transitional enhancement:

Above two types of enhancement coexist with early evidence of BBB breakdown; usually seen on days 3–6

Parenchymal enhancement:

Classically appears as a cortical or subcortical gyral ribbon enhancement.
May not be apparent for the first 1–2 days, and gradually approaches 100% by 1 week.
Enhancement may eliminate “fogging effect” (as on CT) which may obscure some strokes at ≈ 2 weeks on unenhanced T2WI

Diffusion weighted imaging (DWI)