Cerebrovascular disease and non-traumatic haemorrhage

CEREBRAL ISCHAEMIA

DEFINITION

Stroke

A sudden neurological deficit of vascular origin

• Diagnostic imaging plays an important role as an ischaemic or haemorrhagic stroke cannot be distinguished clinically (and also around 30% of stroke-like episodes have a non-vascular cause)

• Causes (after excluding a subarachnoid haemorrhage): ischaemia (85%) spontaneous intracranial haemorrhage (15%)

• Causes of an ischaemic stroke: atherothrombotic arterial occlusion or embolism cervical arterial dissection vasculitis venous thrombosis generalized hypoperfusion substance abuse

Transient ischaemic attack (TIA)

Neurology resolving within 24 h

PATHOPHYSIOLOGY

CLINICAL OUTCOME

Proximal occlusions

These cause infarcts of an entire arterial territory if sufficient collateral circulation exists there may be deep infarcts with cortical sparing

• Most carotid territory infarcts involve the middle cerebral artery

• The anterior cerebral artery (ACA) collateral flow is generally excellent and emboli are relatively rare the commonest cause of an ACA infarct is vasospasm following a subarachnoid haemorrhage

Emboli/occlusions of terminal branch

These cause cortical peripheral wedge-shaped infarcts

Perforator vessel occlusion

These cause lacunar infarcts

• Brainstem infarcts: these are commonly due to occlusion of a short perforating vessel

‘Top of the basilar’ syndrome: a combination of an infratentorial, thalamic and occipital infarct suggesting a distal basilar arterial occlusion

• Multiple infarcts within different arterial territories suggest a cardiac rather than a carotid embolic source (or a haemodynamic hypotensive stroke if the distribution conforms to the arterial border ‘watershed’ zones)

IMAGING STRATEGIES IN ACUTE STROKE

Benefits of urgent neuroimaging

This allows exclusion of a haemorrhagic stroke, allowing the reversal of any anticoagulation or the prescription of aspirin (which is beneficial if commenced within 48 h) it can also exclude an underlying mass or AVM

Radiological features

This is usually the first-line investigation, and is more widely available outside routine working hours

MRI

This is better at showing the extent of the ischaemic change

DWI

This is more sensitive for early infarcts, demonstrating a new infarct on a background of chronic ischaemic damage, or for diagnosing a TIA

MRA/CTA

These allow a full assessment of the arterial tree from the aortic arch to the circle of Willis (and beyond)

Angiography

This assesses the extracranial vessels for secondary stroke prevention

Treatment

IV thrombolysis is given within 3 h of symptom onset (if haemorrhage or an obvious large infarct is excluded)

CEREBRAL ISCHAEMIA

RADIOLOGICAL FEATURES

CT

• Earliest detectable change: the ‘dense artery’ sign: this is due to fresh thrombus occluding a vessel (as thrombus can rapidly disperse, this sign is not always present) if this is seen within the proximal MCA, it correlates with a large infarct

MCA calcification can also mimic this sign but it is often bilateral the basilar artery may also appear dense (particularly in the ‘top of basilar’ syndrome)

• Early parenchymal signs:

Cytotoxic oedema: reduced grey matter density brain swelling (sulcal effacement)

Early MCA infarcts: a reduction in the clarity of the lentiform nucleus and cortex

– ‘Insular ribbon’ sign: this is demonstrated if the insular cortex is involved

• Late signs: encephalomalacia and atrophy with enlargement of the adjacent sulci and ventricles

• A region of swelling without an area of associated low density (resulting from a compensatory increase in CBV) can be a sign of compromised perfusion that may be reversible

• A high mortality is associated with an area of hypodensity affecting > 50% of the MCA territory (an area of hypodensity affecting > 33% is commonly a contraindication to thrombolysis)

• CT is much more sensitive than MRI for detecting acute haemorrhage

MRI

• Early changes: thrombus can cause loss of the normal arterial flow void (arterial high SI may be seen with FLAIR imaging due to altered flow – this is a useful qualitative sign of reduced perfusion when the parenchyma still appears normal)

• Early parenchymal signs: there is structural breakdown and disruption of the blood–brain barrier with fluid leaking into the extracellular space this manifests as cortical swelling and T1/T2 prolongation (this is more obvious with T2WI and especially FLAIR imaging)

T2 hyperintensity is often absent or very subtle in infarcts only a few hours old

• Subacute stage: contrast enhancement is commonly seen on MRI (as well as CT) due to disruption of the blood–brain barrier it can have a variable pattern but gyriform enhancement is characteristic of a cortical infarct

This is seen with MRI in almost all cases by the end of the 1^st week and persists for several months

• Late signs: these are as for CT (MRI signal intensities and CT attenuation values approach that of CSF) Wallerian degeneration is sometimes visible as faint T2 hyperintensity within the isilateral corticospinal tract together with asymmetrical brainstem atrophy

• Haemorrhagic transformation: this follows secondary bleeding into areas of reperfused ischaemic tissue it occurs during the first 2 weeks in up to 80% of infarcts seen on MRI it is often seen within the basal ganglia and cortex (with possibly a gyriform pattern) the severity of the haemorrhage correlates with the size of the infarct and the degree of contrast enhancement in the early stages

T1WI: high SI T2WI: low SI

• Intravascular enhancement (due to sluggish flow): this may be seen within affected vessels on contrast-enhanced MRI and CT during the first few days after an infarct (becoming less obvious towards the end of the 1^st week)

Advanced techniques

Proton MR spectroscopy (MRS)

• Infarcted regions: increased lactate reduced N-acetylaspartate (a neuronal marker) and total creatine

Perfusion CT (CTP)/perfusion-weighted MRI (PW-MRI)

• This utilizes dynamic bolus tracking techniques

• PW-MRI produces maps of time-to-peak contrast (TTP), mean transit time (MTT), cerebral blood volume (CBV) and cerebral blood flow (CBF) – (CBF = CBV/MTT)

TTP: this provides a qualitative overview of brain perfusion a delay > 4 s seems to indicate tissue at risk

A reduced CBV: this indicates an inadequate collateral supply and a high risk of infarction a CBV defect seems to be the best predictor of the initial infarct size (and final size if it successfully reperfused)

MTT and CBF: this indicates the tissue at risk (i.e. the final infarct volume unless reperfusion occurs)

DWI

• This has a pre-eminent role in acute stroke imaging (with a high sensitivity within the first few hours when a T2WI is usually normal)

• Pitfalls:

Chronic lesions with very long T2 relaxation times: ‘T2 shine through’ may generate high SI on DWI – however in comparison to an acute infarct it will also generate high SI on an ADC map

Acute haemorrhage: this can generate high SI resembling an infarct – however there is often a low SI margin produced by susceptibility effects

Ischaemic stroke

	T1WI	T2WI	DWI	ADC
*Hyperacute (0–6 h)*	Isointense	Isointense	Bright	Dark
*Acute (6 h to 4 days)*	Hypointense (+ oedema mass effect)	Hyperintense (+ oedema mass effect)	Bright	Dark
*Subacute (4–14 days)*	Hypointense	Hyperintense	Dark (It may be bright secondary to T2 shine through)	Pseudonormalization
*Chronic*	A smaller area of low intensity + encephalomalacia	Hyperintense	Hypointense Dark (It may be bright secondary to T2 shine through)	Bright

Ischaemic stroke

	Vasogenic oedema	Cytotoxic oedema
*Cause*	Tumour abscess haemorrhage trauma	Ischaemia (e.g. stroke)
*Mechanism*	Disruption of the blood–brain barrier increased capillary endothelial permeability leads to fluid extravasation	Failure of membrane ATP-dependent sodium pumps accumulation of intracellular sodium and water
*Imaging*	Characteristic finger-like pattern with cortical sparing	Involvement of both cortex and white matter