Mechanisms of Ischemic Stroke
- Thrombotic. Stenosis/occlusion of a large extracranial or intracranial vessel typically due to atherosclerosis leading to regional hypoperfusion. Nonatheromatous causes of arterial stenosis/occlusion include dissection and vasculitis.
- Embolic. Approximately 20% of brain infarcts are due to emboli originating from the heart. Emboli may also arise from atheromatous plaques in the cerebral vessels (artery-to-artery embolism).
- Watershed infarcts develop after episodes of global hypoperfusion, such as seen in cardiorespiratory arrest and prolonged hypotension.
- Lacunar infarcts are small round infarcts in the internal capsules, thalami, and basal ganglia due to stenosis/occlusion of small penetrating vessels typically seen in the setting of chronic hypertension and diabetes.
Symptoms and Signs
It is important to determine precisely the temporal course and physical distribution of all neurologic symptoms. The symptoms of ischemic stroke have an all at once onset but may be either transient or permanent. TIAs due to stenosis are characteristically short in duration and highly stereotyped, often occurring in clusters. Artery-to-artery embolic TIAs may also be stereotypical and are usually more long lasting. Cardioembolic TIAs tend to be quite long lasting (from 1 to several hours), do not recur frequently, and may present with symptoms from different vascular territories in separate attacks. Vascular dissections may be neurologically asymptomatic, and may become symptomatic days to weeks after.
Carotid distribution TIA or stroke, suggestive symptoms:
- Contralateral paralysis, weakness, or clumsiness.
- Contralateral sensory loss: paresthesia and numbness.
- Dysarthria (disturbance in articulation), not in isolation.
- Ipsilateral amaurosis fugax (transient monocular blindness).
- Rarely, homonymous hemianopsia.
- Dysphasia (words not arranged in understandable way).
Vertebrobasilar distribution TIA or stroke, suggestive symptoms:
- Weakness, bilateral or shifting.
- Sensory loss, bilateral or shifting.
- Homonymous hemianopsia.
- Vertigo, diplopia, dysphagia, dysarthria, ataxia (two or more together).
- “Top of the basilar artery” related symptoms including cardiorespiratory compromise, coma, “locked-in syndrome”—considered life threatening.
When evaluating a patient within a time window feasible for thrombolytic therapy, a standard noncontrast computed tomography (CT) is obtained to exclude hemorrhage, tumor, or other structural lesions which can preclude thrombolytic therapy. The CT findings in stroke evolve with time. Within the first 6 hours, early signs of infarction can be identified only in 30-40% of cases. With time, infarcts become more conspicuous. After 24 hours most infarcts are visible. Posterior fossa and brain stem infarcts are difficult to identify on CT owing to their small size and prominent beam hardening artifacts.
Early infarct Normal: majority of patients within the first few hours. Subtle loss of gray-white differentiation: look at the insular ribbon and putamen. Subtle brain swelling: look for asymmetry of cerebral sulci. Hyperdense artery: indicates thrombus; look at the middle cerebral and basilar artery.
Acute/subacute infarct Well-defined hypoattenuation conforming to a vascular territory. Regional mass effect. Midline shift if a large area is involved. Hemorrhage into infarcted tissue.
Chronic infarct Tissue loss (encephalomalacia) and regional volume loss.
Magnetic Resonance Imaging
MRI provides a more comprehensive evaluation in the expense of time. Limited availability, longer study time, and artifacts limit the use of MRI in a stroke patient who is a candidate for thrombolysis. Diffusion weighted image (DWI) is the most sensitive and specific sequence for acute infarct. DWI becomes abnormal minutes after the ictus and stays abnormal for approximately 10 days. Perfusion weighted image (PWI) helps establish region of hypoperfusion and allows visualization of the penumbra which potentially can be salvaged. Magnetic resonance angiography (MRA) can establish patency/occlusion of a vessel which may directly affect treatment decisions.
Increased signal on DWI with corresponding decreased signal on ADC maps. Decreased perfusion within the DWI abnormality and often extending beyond the DWI abnormality. Increased signal on FLAIR and T2WI: appears hours after the ictus but generally before CT findings become abnormal. Sulcal effacement and local mass effect. Absence of flow voids on T2WI; indicates occlusion. Gyriform contrast enhancement in the subacute stage.
Magnetic Resonance Angiography
Time of flight (TOF) is the most frequently used technique. A three-dimensional (3D) TOF method is used for the intracranial vessels. For the neck vessels 2D or 3D TOF can be used as well as 3D contrast-enhanced MRA. In general, the 3D TOF sequence has better spatial resolution than 2D TOF. TOF overestimates the degree of stenosis.
Possible Findings for MRA
Decreased vessel caliber and/or discontinuity of vessel with nonvisualization of distal branches. In many cases, MRA can detect the site of stenosis or occlusion and distinguish between these possibilities.
Issues After Imaging
Even when the clinical diagnosis of stroke has already been made, a positive finding on CT or magnetic resonance (MR) examination can still be valuable to clarify the extension and the mechanism of the infarction. Tissue plasminogen activator (tPA) is administered for stroke only if subjects meet strict criteria. Neurologists determine the time from the onset of the symptoms; if less than 3 hours, then IV tPA is considered; if less than 6 hours, then intra-arterial tPA is considered; if posterior circulation stroke, then longer time periods might be allowed. Treatment of stroke with heparin is indicated in only specific cases, for example, vascular dissection and atrial fibrillation.