Home of Radiologists


Recent Topics

جاري التحميل ...

Stroke - overview

Stroke is a generic term that describes the clinical event of a sudden onset of neurologic deficit secondary to
cerebrovascular disease.
Stroke has 4 main etiologies, including
cerebral infarction (80%),
intraparenchymal hemorrhage (15%),
nontraumatic subarachnoid hemorrhage (5%),
venous infarction (approximately 1%).
Clinically, ischemic infarction is the most common etiology and will be the main topic of this introduction.
The principal cause of cerebral infarction is atherosclerosis and its sequelae.

Ischemic Infarction
There are 3 major clinical ischemic stroke subtypes based upon the classification from a multicenter clinical trial (trial of drug ORG 10172 in acute stoke treatment [TOAST]).
These 3  subtypes include
large artery/atherosclerotic infarctions,
cardioembolic infarctions,
small vessel occlusion (lacunar) infarctions.
Large artery/atherosclerotic strokes
represent approximately 40% of strokes and can arise from thrombosis at the site of a plaque or from emboli produced at the plaque that lodge downstream.
The most common site of atherosclerotic plaque is at the carotid bifurcation with involvement of the distal common carotid artery and the 1st 2 cm of the internal carotid artery.
The most frequently occluded intracranial vessel is the middle cerebral artery (MCA).
Other common locations for atherosclerotic plaque include the carotid siphon and proximal anterior and middle cerebral arteries.
The vertebral and basilar arteries are also commonly involved by atherosclerosis.
Cardioembolic disease
accounts for 15-25% of ischemic strokes.
Risk factors include myocardial infarction, ventricular aneurysm, atrial fibrillation or flutter, cardiomyopathy, and valvular heart disease.
Lacunar infarcts
are small in size (< 15 mm), typically in the basal ganglia and thalamus, and account for 15-30% of all strokes.
They are often multiple and are due to embolic, atheromatous, or thrombotic lesions in the single penetrating end arterioles that supply the deep gray nuclei, including the lenticulostriate and thalamoperforating arteries.
Other common locations for lacunar infarcts include the internal capsule, pons, and corona radiata.

Intraparenchymal Hemorrhage
Intraparenchymal hemorrhage represents ~ 15% of all strokes and includes multiple etiologies.
Hypertensive hemorrhage is the most common etiology, representing ~ 40-60% of all primarily intracranial hemorrhages.
Other etiologies include amyloid angiopathy in elderly patients, as well as vascular malformations, vasculitis, drugs, and bleeding diathesis.
Risk factors for hemorrhagic stroke include increasing age, hypertension, smoking, excessive alcohol consumption, prior ischemic stroke, abnormal cholesterol, and anticoagulant medications.
Although the MR physics related to hemorrhage are complex, the stages are generally accepted as hyperacute, acute, early subacute, late subacute, and chronic.

Nontraumatic Subarachnoid Hemorrhage
Nontraumatic subarachnoid hemorrhage is typically related to an aneurysm (75%) or a vascular malformation, such as an arteriovenous malformation or cavernous angioma
Nonaneurysmal "perimesencephalic" subarachnoid hemorrhage is uncommon.

Venous Infarction
Dural sinus or cerebral vein occlusion is rare, representing less than 1% of strokes.
Venous thrombosis risk factors include pregnancy, trauma, dehydration, infection, oral contraceptives, coagulopathies, malignancies, collagen vascular diseases, and protein C and S deficiencies.
Venous infarcts occur in only ~ 50% of venous thrombosis cases, and can be differentiated from arterial infarcts by the location of the ischemia.
Superior sagittal sinus thrombosis typically results in T2/FLAIR hyperintense parasagittal lesions, while thrombosis of the transverse sinus often results in T2/FLAIR hyperintensities in the posterior temporal lobe.
Additionally, venous infarcts more commonly present with associated hemorrhage.
Contrast-enhanced CT is useful to identify the "empty-δ" sign representing thrombus within a major dural sinus, typically the superior sagittal or transverse sinus.

Approach to Stroke Imaging
Cerebral ischemia results from significantly decreased blood flow to selected areas or the entire brain.
Stroke progresses in stages from ischemia to actual infarction.
 In the most common situation, MCA occlusion, there is a densely ischemic central core and a less densely ischemic "penumbra."
The central core is usually irreversibly damaged unless reperfusion is quickly established, whereas the cells within the penumbra may remain viable but at risk for several hours.
Current stroke therapies attempt to rescue the "at-risk" cells.
Currently, acute stroke protocols vary among different institutions.
The exact protocol is often based on the availability of CT vs. MR, technology/software, time of stroke,
physician expertise, and the possibility of neurointervention.
Typically, stroke neurologists work with neuroradiologists to devise a plan that best serves the patient's needs.

Most stroke protocols begin with a noncontrast head CT to evaluate for hemorrhage or mass, which directly affects treatment decisions. Additionally, > 1/3 MCA territory hypodensity at presentation is considered by most to be a contraindication to thrombolysis, as it is associated with a greater risk of fatal hemorrhage.
CTA is useful to evaluate for large vessel occlusion.
When available, CT perfusion is an excellent way to evaluate for large vessel ischemia.
MR with diffusion-weighted imaging (DWI) is particularly useful for acute ischemia when CT perfusion is negative and the clinical suspicion for stroke remains.
MR is also the primary imaging tool when the clinical question includes a posterior fossa or brainstem lesion.
MR with perfusion imaging (PWI) has been found extremely helpful in guiding therapy when available.
Most stroke protocols use 3-hour and 6-hour windows for treatment of nonhemorrhagic ischemic stroke.
If the patient presents within 6 hours after the initial onset of symptoms, an unenhanced CT is typically the initial study of choice to exclude a mass or hemorrhage.
If there is a hemorrhage or mass, no thrombolytic therapy is initiated.

If there is no hemorrhage or mass and the patient is within 3 hours after onset of symptoms, the patient is eligible for intravenous (IV) thrombolysis.
If the patient is between 3 and 6 hours of onset, either a CTA with CT perfusion or an MR with DWI and PWI is performed to determine if they are eligible for treatment.
If the patient has an intracranial thrombus with a penumbra intraarterial (IA) thrombolysis or IA thrombectomy is recommended.
If there is no penumbra, IA therapy may notbenefit the patient, so each case is evaluated individually.
The effective therapeutic window for the posterior circulation is thought to be longer than the 3-6-hour window, but the exact time is variable and depends on collateral circulation.
Therefore, patients with vertebrobasilar thrombosis are evaluated individually for risk vs. benefit of IA thrombolysis or thrombectomy.

Ischemic Penumbra
Ischemic stroke results in a core of tissue that has undergone irreversible injury.
The ischemic penumbra is the area of brain that may be salvageable with appropriate therapy.
The penumbra typically surrounds the ischemic core and is supported by collateral circulation.
The ischemic penumbra can be identified by a combination of MR diffusion (DWI) and perfusion imaging (PWI).
DWI is the most reliable estimate of the ischemic core and generally correlates with irreversible injury. However, with early reperfusion following thrombolysis, some reversal of DWI can be observed.
PWI evaluates the presence of a penumbra.
With MR, the mismatch between the DWI and PWI defines the penumbra.
This model provides a practical means to estimate the ischemic penumbra.
In general, if there is no diffusion/perfusion mismatch, therapy may be ineffective.

With the newer CT perfusion techniques, an ischemic penumbra may also be measured with CT.
With the urgency of acute stroke, MR may be impractical.
However, with new faster MR protocols and the superiority of MR to CT in detecting small vessel ischemia and brainstem ischemia, MR may be a preferred technique.

CT Perfusion (pCT)
Cerebral perfusion refers to the tissue-level blood flow in the brain.
This flow is evaluated by 3 main parameters at pCT:
Cerebral blood flow (CBF),
cerebral blood volume (CBV),
mean transit time (MTT).
CBF is defined as the volume of blood moving through a given unit volume of brain per unit time.
CBF uses units of milliliters of blood per 100 g of brain tissue per minute.
Studies suggest that CBF is a reasonable marker for the ischemic penumbra.
CBV is defined as the total volume of blood in a given unit volume of brain.
This includes blood in the tissues as well as blood in the large-capacitance vessels, such as arteries, arterioles, capillaries, venules, and veins.
CBV uses units of milliliters of blood per 100 g of brain tissue.

Some studies suggest that CT perfusion-acquired CBV is a reasonably reliable marker of the ischemic core.
MTT is defined as the average of the transit time of blood through a given brain region. The transit time of blood through the brain parenchyma varies depending on the distance traveled between arterial inflow and venous outflow.
MTT equals CBV/CBF.
CBF/CBV mismatch correlates with stroke enlargement in untreated or unsuccessfully treated patients.
Those patients with a CBF/CBV match or those with early complete recanalization do not exhibit progression of the ischemic stroke.
The general treatment guidelines for pCT are as follows.
If there is a CBF/CBV mismatch, with a larger CBF suggesting an ischemic penumbra, the patient is likely a good candidate for therapy.
Many treatment guidelines suggest that a ≥ 20% CBF/CBV mismatch should be present to consider thrombolysis.
Some authors propose that if there is no mismatch between CBV and CBF, treatment is unlikely to benefit the patient.

CT Perfusion Interpretation Pearls
The MTT is the most sensitive parameter for perfusion deficits.
Although it is generally elevated due to a thromboembolic process, it may be elevated in a patient with
significant arterial atherosclerotic narrowing.
In early ischemia, MTT is elevated and CBF is decreased. However, the CBV can be preserved or even elevated due to capillary bed dilatation in very early ischemia.
Once a CBF threshold is reached, CBV starts to decline.
This results in the ischemic core, which has a matched decrease in CBF and CBV, whereas a mismatch
between CBF and CBV suggests a penumbra.

Differential Diagnosis
When considering stroke in a child or young adult, several possible etiologies should be addressed, including arterial dissection, vascular malformation with hemorrhage, drug abuse, or clotting disorder.
In young children, other possibilities include congenital heart disease with emboli and idiopathic progressive arteriopathy of childhood (moyamoya disease).
In a middle-aged or older adult, the typical stroke etiologies include arterial thromboembolism, hypertensive hemorrhage, and cerebral amyloid angiopathy.
When evaluating a hemorrhagic stroke, etiologies in children include vascular lesions, hematologic disorder, vasculopathy, and venous infarct.
In a young adult, considerations include vascular malformations, drug abuse, and less commonly venous occlusions or vasculitis.
In older adults, common considerations for intracranial hemorrhage include hypertensive hemorrhage, neoplasm, cerebral amyloid angiopathy, and, less commonly, dural sinus/cerebral venous occlusion and coagulopathy.

Imaging gallery

Graphic shows the cortical MCA distribution in red. MCA distribution typically involves the majority of the lateral surface of the hemisphere, including the frontal, temporal, and parietal lobes. In addition, the majority of the lenticulostriate arteries arise from the M1 segment and supplies the basal ganglia.

Axial CT shows a large left MCA distribution infarct with involvement of the basal ganglia , indicating involvement of the lenticulostriate perforating arteries, which typically arise from the M1 segment.

Graphic shows the ACA cortical vascular territories in green. The ACA supplies the medial anteroinferior frontal lobe, the anterior 2/3 of the medial hemisphere surface, and a variable amount of territory over the cerebral convexity. The corpus callosum is also typically supplied primarily by the ACA branches: Callosal perforating, pericallosalposterior splenial branches.

Axial DWI MR shows diffusion restriction in the left ACA distribution within the medial parafalcine frontal lobe.

Graphic shows the typical PCA vascular territory, including the occipital lobes, inferior temporal lobes, And medial posterior 1/3 of the interhemispheric brain. Patients with PCA ischemia most commonly present with visual complaints. Large vessel/atherosclerotic strokes represent ~ 40% of strokes. The carotid bifurcation is the most common site of atherosclerotic plaque.

Axial DWI MR shows diffusion restriction in the occipital lobe related to PCA ischemia. DWI is the most sensitive MR sequence for acute ischemia.

Axial graphic shows the major penetrating artery distributions.
The pontine and thalamic perforating arteries , as well as the medullary perforators  , arise from the
vertebrobasilar system.
The medial and lateral lenticulostriate arteries arise from the anterior circulation and supply the basal ganglia. The choroidal arteries are shown in magenta.

Axial DWI MR shows diffusion restriction related to acute ischemia in a pontineperforating artery distribution.

Axial graphic shows the cerebellar artery distributions.
The superior cerebellar artery (SCA) (green) supplies the superior cerebellum.
The posterior inferior cerebellar artery (PICA) (peach) supplies the majority of the inferior cerebellum and lateral medulla.
The anterior inferior cerebellar artery (AICA) (yellow) supplies the petrosal surface of the cerebellum.

Axial T2WI MR shows hyperintensity in the right inferior cerebellum and lateral medulla related to a PICA infarct from a vertebral artery embolus.

Axial T2WI MR showhyperintensity and local mass effect in the right superior cerebellum related to an acute SCA infarct. SCA infarcts may involve the superior cerebellum and the upper lateral pons.

Axial DWI MR image shows acute diffusion restriction in the anterior, inferior cerebellum
laterally in an AICA distribution.
AICA primarily supplies the ventral pons and
petrosal surface of the cerebellar hemispheres, the
brachium pontisflocculus, and inner ear as well as CN7 and CN8.

Whole brain graphics show the major arterial supply to the hemispheres.
The MCA (red) supplies the lateral aspects of the frontal and temporal lobes.
The ACA (green) supplies the medial hemispheres.
The PCA (purple) supplies the occipital lobes
and inferior temporal lobes.
The watershed zone is the border between the major vascular territories.

Axial DWI MR shows restriction in left MCA territory with preservation of the basal ganglia.

The MCA territory is the most common location for ischemic stroke.

Axial CT perfusion CBF color map shows a large area of decreased blood flow in the left hemisphere related to hyperacute MCA ischemia.

Axial CT perfusion CBV color map in the same patient shows a much smaller area of decreased blood volume. The CBV is a marker for the ischemic core.This CBF/CBV mismatch correlates with the presence of a large ischemic penumbra, which suggests the patient would benefit from intraarterial thrombolytic therapy or clot retrieval.

Lateral gross pathology shows a chronic MCA infarct with hemorrhage and encephalomalacia in the frontal operculum and temporal lobe .

Axial FLAIR MR shows multiple hyperintense foci in the watershed zones between the major cerebral artery territories (MCA, PCA, and ACA) related to acute ischemia from hypoperfusionThe posterior confluence where all 3 vascular distributions meet together at the vertex is especially vulnerable to cerebral hypoperfusion.

Coronal oblique graphic of the rostral basilar artery shows (left panel) the typical arterial supply to the medial thalami by multiple PCA and basilar tip perforators. Right panel shows the anatomicvariant, artery of Percheron , in which a single large perforating artery from P1 supplies bilateral thalami and the medial midbrain.

Axial FLAIR MR shows hyperintensity in the bilateral medial thalami related to an acute artery of Percheron infarct.Extension to the medial midbrain is often present.

Axial DWI MR shows hyperintensity related to acute ischemia in the posterior limb of the internal capsule in an anterior choroidal artery distribution. The anterior choroidal artery typically supplies the lateral midbrain, uncus, thalamus, posterior limb of internal capsule, and the optic tract.The posterior choroidal artery typically supplies the pulvinar, thalamus, medial temporal lobe, splenium, and choroid plexus.

Axial CT shows a classic thalamic hypertensive hemorrhage, the 2nd most common cause of stroke.

Axial CT shows bilateral thalamic hemorrhage related to deep venous thrombosis. Venous thrombosis risk factors include pregnancy, trauma, dehydration, infection, oral contraceptives, coagulopathies, malignancies, collagen vascular diseases, and protein C and S deficiencies.

Axial SWI MR image in an elderly patient shows extensive susceptibility artifact related microhemorrhages in the bilateral hemispheres. Pattern is typical of cerebral amyloid angiopathy.

عن الكاتب

دكـــــتور جدا


اتصل بنا

جميع الحقوق محفوظة