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This is the second of a two part series on stroke syndromes. In last month’s EM:RAP column, we highlighted important differences among the various types of hemorrhagic strokes. This month, we turn our focus to ischemic stroke, which is more common, and by far the leading cause of severe disability in the developed world.

The overarching theme here is that strokes are not all the same. Although every emergency physician knows that hemorrhagic strokes are treated differently from ischemic strokes, we do tend to lump most ischemic strokes into the same category.

When we do sub-classify ischemic (sometimes called “bland”) strokes, it tends to be by general territory, either anterior circulation or posterior circulation. Anterior circulation strokes are a result of occlusion of the carotid artery and its branches, whereas posterior circulation strokes result from occlusion of the basilar artery and its branches. Although their clinical presentations may overlap significantly, anterior stroke syndromes most commonly result in contralateral hemiparesis and hemisensory loss, whereas posterior circulation strokes often affect the cranial nerves and may result in crossed findings (e.g. cranial nerves on one side of the body and paralysis or sensory loss on the other).

Perhaps, a more important distinction is the one between cortical and lacunar strokes. In fact, as we enter the next generation of interventional stroke therapy, it may become the most important basis by which to classify ischemic strokes.

Cortical strokes account for about 75% of ischemic strokes and involve the large arteries that supply the cerebral hemispheres: the anterior cerebral artery, the middle cerebral artery, and the posterior cerebral artery. Lacunar strokes, named after lakes because they appear as tiny lakes of CSF after they liquefy with time, involve occlusions of the tiny offshoots of the major vessels that penetrate into the deep structures of the brain such as the internal capsule, basal ganglia and thalamus.

The main issue here is size; whereas cortical strokes involve relatively huge chunks of brain tissue, everything supplied by one of the major vessels or its major branches, lacunar infarcts involve only a tiny area of brain that is supplied by a single, small, perforating end-vessel, one of hundreds that come off the main arteries of the circle of Willis.

Early signs of cortical stroke on CT include a blurring of the grey-white matter junction in the ribbon of cortex supplied by the affected vessel, and with time, many hours to days, they appear as hypodense wedges that extend to the margins of the brain. Lacunes are often too small to be seen on CT, but when they become old may appear as tiny black spots (pools of CSF) in the deep structures.

What is fascinating is that even though lacunar infarcts may affect just a tiny amount of brain tissue, when in a bad location, like the internal capsule that contains thousands of descending motor and sensory fibers all bundled together, they may look clinically just as bad as a large cortical stroke, at least initially.

Although emergency physicians aren’t generally preoccupied with distinguishing cortical from lacunar strokes, we should be. That is because their distinction carries major implications for therapy and disposition in the emergency department.

First, consider therapy with intravenous tPA. The major risk with tPA is that of intracerebral hemorrhage, a hemorrhagic transformation of the ischemic and infarcted tissue. This risk increases with the amount of tissue involved and is the reason why tPA is relatively contraindicated in strokes that involve more than one-third of the territory of the middle cerebral artery, as determined by the length of grey-white matter blurring on the CT or by a NIH stroke scale score >22. In contrast, because the volume of tissue involved in lacunar infarcts is so small, the risk of hemorrhage is also much smaller. This is an important factor in the decision to give tPA and one that should probably be a part of our risk vs. benefit discussion with the patient and their family prior to going ahead with IV thrombolysis. Although many EPs use the figure of 6% to quantify the risk for bleeding after IV tPA, this number may be many times higher than this in patients with large territory cortical strokes, especially if the tPA is given relatively late. In patients with lacunar strokes, this number is much lower.
Second, cortical and lacunar strokes differ with respect to the feasibility of interventional therapies, such as endovascular clot removal and stenting. These techniques are only available to patients with cortical strokes because they involve relatively large vessels that can be cannulated in an interventional radiology suite. This is completely analogous to percutaneous coronary intervention for ST elevation myocardial infarction. When small vessel disease is the culprit, as with lacunar disease, the catheterization suite is not the answer.

Third and lastly, the natural history of these two types of strokes is also different. Because of the large territories involved in cortical strokes, the amount of edema that ensues can quickly become life threatening. The mass effect of a cortical stroke, which begins within hours (e.g. in the ED) but usually peaks from 3 to 5 days, can cause hydrocephalus and herniation syndromes, both which may require neurosurgical intervention. So, if you have two patients in front of you, one with a cortical stroke and one with a lacunar stroke, all other things being equal, the cortical stroke should get the next available ICU bed. He or she has a real risk of dying in the hospital, many times higher than that of the lacunar stroke patient.

So, how does one tell a cortical stroke from a lacunar stroke clinically?
Sometimes, it may be difficult. At first glance, they may actually appear to cause identical deficits (e.g. a left sided arm or leg weakness). But there are several clinical features that distinguish the two. None are perfect discriminators, but together they can often point strongly toward one type of stroke or the other.

Progressive drowsiness and decreasing level of consciousness correlate with the mass effect of edema. These usually point to a cortical stroke. So do a combination of motor and sensory findings in the same distribution. Even though patients with cortical strokes may be able to feel the weak or paralyzed extremities, the presence of a change or decrease in sensation strongly suggests a cortical stroke. Lacunar strokes tend to cause classic syndromes, and the pure motor stroke syndrome is the most common, resulting from a lacune in the internal capsule. Other syndromes that suggest lacunar stroke include a combination of cerebellar findings with either hemiparesis or dysarthria and pure sensory stroke. Mixed motor and sensory lacunar strokes can occur, but they are extremely rare. Lacunar strokes also more commonly have a stuttering course, getting worse in small steps over the initial hours; whereas cortical strokes tend to begin suddenly and worsen progressively over time. Lastly and most importantly, the presence of a deficit in any higher brain function (e.g. cognitive function or thinking) by definition points to a cortical stroke. So, any patient that has a deficit with language comprehension or neglect has a cortical stroke – it can’t be lacunar.

So, the next time that you are faced with an acute ischemic stroke you should ask yourself, “Is this cortical or lacunar?” Your ability to distinguish the two is about to become a lot more important…

Dr. Swadron is an Associate Professor of Clinical Emergency Medicine at the Keck School of Medicine of the University of Southern California. He partners with Dr. Mel Herbert to bring you EM:RAP (Emergency Medicine: Reviews and Perspectives), the monthly audio program that can be found at http://www.EMRAP.org)

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