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Cases

Module 1: Introduction to Stroke & Stroke Prevention

The Case of RS

R.S. had a large ischemic stroke that was produced when thrombi that originally formed on the mitral valve (vegetations) broke loose and showered her brain with emboli of different sizes. She died about 10 days later. 

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This is a microscopic section of the patient's cerebral cortex. Can you find a small artery that is plugged up with an embolus composed mainly of fibrin and platelets?  Regions of the cortex that this vessel normally supplies are swollen and pale. This pathology indicates that the tissue is dead.

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This is a microscopic section showing a large artery that was also occluded by embolus. It was the failure of circulation produced by this embolus that caused brain swelling and led to her death.

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This is R.S.' brain.  Can you find indications of some brain swelling here? Swelling in additional regions was responsible for her death.  Note that the swelling has pushed some brain structures toward the opposite side.

A.B. suffered the occlusion of several arteries following cardiac catheterization that dislodged debris from an ulcerated atherosclerotic plaque in his aortic arch. Three weeks later he had a second myocardial infarction and died.

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This is A.B.'s aorta which has been opened up so that you are looking at its inner surface. You can see extensive atherosclerotic changes. Many large plaques protrude into the lumen giving the surface a bumpy appearance. When you mouse over it, the arrow will indicate one of the largest plaques which has broken open, rupturing the endothelium that normally lines the aorta and exposing the cellular debris and lipid in the core of the plaque. You can also see many areas where thrombus has formed over ruptured plaques. The pathologic changes that you are looking at here evolved over a period of many years. 

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Some debris from a ruptured plaque must have traveled up A.B.'s vertebral artery and lodged in one of its branches that supplies the cerebellum.  Part of A.B.'s cerebellum is shown at the right. You can see its numerous small neurons that are called granule cells (blue). The granule cells have disappeared in the lower part of the image because they have been killed by an ischemic injury. Now look at the blood vessels on the outer surface of the cerebellum. Can you see a vessel that is plugged with elongated unstained crystal-like profiles? This embolus is a fragment of an atherosclerotic plaque; the crystal-like profiles are accumulations of cholesterol.

A More Advanced Case

In this patient, thrombus had formed on a plaque in the basilar artery, at the point where it branches to form the posterior cerebral artery. 

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Here is an angiogram in which an iodinated dye was injected into one vertebral artery. The dye fills the injected vertebral artery and has been carried into the basilar artery. However, dye seems to stop at the place where the basilar artery branches.  It looks like the basilar just ends! 

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If you look at the CT scan of this patient at the corresponding level, the bright spot at the arrow is actually the thrombus.At the time this patient had this CT scan he had an occluded basilar artery and showed major neurologic deficits. 

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This is his CT scan at a level that includes regions of the occipital lobes that are supplied by the basilar branches that have been blocked. The white spots in his ventricles are calcified regions of choroid plexi.

Question
Do you see any abnormality here?
Answer
  • No.  Even a trained neuroradiologist would not see anything abnormal here.

Now look at the next CT scan which is a similar level but was taken 36 hours later. 

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Remember that the basilar artery branches that have been blocked supply parts of both occipital lobes. At 36 hours after the vascular occlusion, can you now identify areas of ischemia?  

Module 4: Ischemia in Carotid Territory

Case 1. Blurry Vision

The patient was sitting watching television when his vision suddenly went "blurry and cloudy" for about 4 minutes and then returned to normal over the next 10 minutes.  He wasn't convinced that anything had really happened, but then later on that evening he had another episode. This time he tried checking one eye at a time, and discovered that his right eye was fine, but that the vision in his left eye was "blurry."  He called 911 because he remembered seeing something about this kind of problem on a Brain Attack poster in his doctor's waiting room.  

Diagrams 

Dx

Transient Monocular Blindness

Note

Expert Note Case 1.

Blurry Vision

This patient experienced a typical episode of transient monocular blindness (amaurosis fugax). Many patients describe a blackout, a cloud or a "gray fog" that obscures vision in one eye, or in part of one eye. Occasionally it may be likened to "a shade falling over the eye." Usually the attacks are very brief, lasting about 1- 5 minutes, and are followed by full restoration of vision. Some patients have many repeated attacks, but others have only one or a few.

Two major mechanisms are proposed to explain this type of TIA. (1) A tiny piece of thrombus formed on an ulcerated plaque at or near the carotid bifurcation, or a piece of the underlying plaque itself, breaks off and enters the ophthalamic artery and finally lodges in a retinal arteriole. Ophthalmoscopic observation of the retinal vessels during actual episodes of transient monocular blindness has shown bits of whitish material (small emboli) temporarily blocking the retinal arteries. (2) A low perfusion state resulting from ICA stenosis (and probably temporary formation of thrombus that further blocks the vessel) causes regions far from the site of stenosis (like the retina) to become briefly ischemic.

There can be a number of reasons for a transient loss of vision in one eye, such as inflammation of the arteries that supply the eye. However, in older patients the cause is often carotid occlusive disease, produced by significant atherosclerosis and plaque erosion in the extracranial carotid. In such a patient, transient monocular blindness may be a warning that a stroke is in the offing. Patients like this should therefore be evaluated immediately.

Module 5: Ischemia in Vertebral-Basilar Territory

Case 1. Suddenly Dizzy

The patient suddenly developed vertigo ("the room was spinning") while getting up out of his chair. He lost his balance, became nauseated, and vomited on the living room floor. He was able to call out for help, but when his wife came running in from the next room she immediately noticed that his speech was slurred and hard to understand. She immediately dialed 911. 

The EMTs arrived about 20 minutes later and took him to the local hospital. He began to improve in the ambulance. By the time he arrived in the emergency room, he was speaking clearly again and could sit up. An electrocardiogram revealed atrial fibrillation. He was observed closely for the next 18 hours, but there were no further events and his neurologic exam showed no lasting deficits. Anticoagulation therapy was initiated.  

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Dx

Brainstem TIA

Note

Expert Note Case 1.

Suddenly Dizzy

This patient had a brainstem TIA most likely produced by a cardiac embolus that initially lodged in one vertebral artery and then broke up.  The TIA lasted approximately an hour before the deficits began to clear. Like many patients with brainstem ischemia, he experienced problems related to malfunction of the vestibular system. Vertigo can have many causes, but the combination of vertigo and dysarthria suggests brainstem or cerebellar involvement.

Question
Why does atrial fibrillation increase the risk of TIA or stroke?
Answer
  • Ineffective contraction of the atrial muscle increases the likelihood that thrombus will form in the atrium. This is a potential source of emboli, which can travel to the brain producing a TIA, like this patient had, or a stroke.