Chapter 27 - Cerebrovascular disorders

Questions

Define the following terms:

amaurosis fugax, homocystinemia, transient ischemic attack, large vessel disease, small vessel disease, hypercoagulability, emboli, ischemic penumbra, stroke in evolution, completed stroke.
Amaurosis fugax is a brief periof of abscuration of vision in one eye, usually described as "a curtain over the eye". It most often results from platelet emboli from an atheromatous plaque in the carotid artery and is a risk factor for stroke.
Homocystinemia is a risk factor for atheroma and stroke.
Transient ischemic attack is a brief (less than 24 hour) period of ischemic symptoms with complete resolution.
Large vessel disease refers to atheromatous disease of the major vessels supplying the brain.
Small vessel disease refers to damage to the small penetrating blood vessels.
Hypercoagulability refers to one of several conditions in which the blood shows abnormal tendency to clot.
Emboli are solid material (clots, pieces of atheroma, etc.) that get lodged in blood vessels and obstruct flow.
Ischemic penumbra is a region around a stroke where blood flow is compromised but which tissue has not (yet) died. This tissue may or may not be functioning.
Stroke in evolution is the evolution of deficit over several hours.
Completed stroke is an infarct of an entire region of supply of a major vessel with a fixed deficit.

27-1. How common is stroke (cerebrovascular accident - CVA)?

27-1. Over 700,000 people have strokes per year (it is the #3 killer).

27-2. Approximately what percentage of strokes are ischemic?

27-2. Ischemic strokes (due to occlusion of a blood vessel) is about 80% of strokes.

27-3. What is the pathology of atherosclerotic-thrombotic strokes?

27-3. Atherosclerotic plaques narrow blood vessels and often result in erosion of endothelium. At least 70% of the lumen must be occluded before it is hemodynamically significant. Platelet aggregation can trigger thrombosis with rapid occlusion of the residual lumen.

27-4. What are potential sites of emboli to the cerebral circulation?

27-4. Emboli arise from arteries, heart and aorta. A major percentage are caused by embolism of clot/atheromatous material from atherosclerotic plaques in the aorta, carotids or vertebrobasilar arteries. Cardiac sources include atrial fibrillation, severe valvular disease (including endocarditis), congestive heart failure (or ventricular dyskinesia, with pooling and clotting of blood), or recent myocardial infarction. Emboli may also pass from the venous side to the arteries via right to left shunts (such as a patent foramen ovale).

27-5. What is vasculitis and what causes it?

27-5. Vasculitis most often refers to arteritis, which is inflammation of the wall of blood vessels. It may be infectious, autoimmune, chemical (such as with stimulent abuse) or due to infiltration (such as with amyloid angiopathy).

27-6. What are the symptoms of stroke?

27-6. The symptoms of stroke are dependent upon the functions of the region of the brain that is involved.However, the symptoms are typically acute in onset.

27-7. What is a transient ischemic attack (TIA)

27-7. A transient ischemic attack is acute development of neurologic symptoms due to ischemia that completely resolve within 24 hours.

27-8. What are risk factors for small vessel disease?

27-8. There are several risk factors for small vessel disease. Lipohyalinosis is the most common pathology and hypertension, diabetes and age are the main risk factors. Vasculitis and stimulent abuse are other causes.

27-9. What is the treatment for small vessel ischemic disease?

27-9. In cases where no definitive treatment (such as for vasculitis), modify risk factors and use platelet antagonists.

27-10. What are risk factors for large vessel disease?

27-10. Risk factors for large vessel disease (i.e., atherosclerosis) include: hypertension, hyperlipidemia, family history, age, smoking and homocystinemia.

27-11. What is the treatment for large vessel cerebrovascular disease?

27-11. The treatment for large vessel cerebrovascular disease includes platelet antagonists, folic acid (helps decrease homocysteine), and carotid endarterectomy (if there is high grade carotid stenosis). There are ongoing investigations into intravascular procedures for intracranial atherosclerotic disease (but none are proven as of yet).

27-12. What are risk factors for embolic CVA?

27-12. Risk factors for embolic stroke include: atrial fibrillation, atrial septal defects (or other right to left shunts), severe valvular disease (such as endocarditis), myocardial infarction, ventricular hypokinesia (such as with congestive heart failure), ventricular aneurysm, hypercoagulability.

27-13. What is the treatment for embolic stokes?

27-13. Embolic stokes (at least those arising from the heart) may be prevented with anticoagulation.

27-14. What are some causes of stroke due to increased viscosity of the blood?

27-14. Some causes of stroke due to increased viscosity of the blood include: severe dehydration, dysproteinemias, polycythemia, thrombocytosis, leukocytosis (rarely and with severe elevations such as leukemia).

27-15. List major risk factors for stroke.

27-15. Major risk factors for stroke include: hypertension, age, cardiac disease, heredity, smoking, diabetes, hyperlipidemia, obesity, homocysteinemia (remember folate/B12/B6), hyperviscosity, alcohol excess, hypercoaguable states, sedentary lifestyle. Oral contraceptives may contribute to stroke in relatively young women, particularly if they are a smoker, with migraine. The stroke may be due to venous thrombosis of the sagittal sinus.

27-16. What are the general preventative measures for stroke?

27-16. Preventative measures for stroke include treatment of increased BP, stopping smoking, diet (eat antioxidants, fruits, veggies, whole grain products, red wine in moderation, etc), exercise, controlling diabetes. Prevention of stroke requires identification of risk factors and modification of those factors.

27-17. What is the treatment for a transient ischemic attack?

27-17. Because there is an increased risk of stroke within a year it important to treat. Treat with platelet antagonists, and investigate for a specific cause: carotid endarterectomy is indicated if the carotid on the affected side is mort than 70% occluded. If there is a cardioembolic source, full anticoagulation is necessary.

27-18. What major factors prevent the development of stroke with occlusion of cerebral blood vessels?

27-18. Collateral circulation is the major safety factor (dependent on anatomical variation, the condition of the vessels, the speed of occlusion).

27-19. What are the potential causes of stroke in young individuals?

27-19. There are several less common causes of stroke in young individuals. These include hypercoagulability or hyperviscosity, arterial dissection, cardiac abnormalities or paradoxical embolism (through right to left shunt).

27-20. Outside of risk factor modification, what are the roles for the different treatment options for stroke prevention?

27-20. Platelet antagonists for small or large vessel disease. Anticoagulation with Coumadin for cardioembolic disease. Carotid endarterectomy for high-grade symptomatic stenosis. Immune suppressives for vasculitis.

27-21. What are the therapeutic options for a stroke in progress?

27-21. What are the therapeutic options for a stroke in progress. Aspirin and oxygen may be helpful. Do not lower blood pressure excessively. Thrombolysis may be effective in treating patients in the very acute stage (less than 3 hours from the moment of onset). There are various invasive procedures and methods for cytoprotection (protection of cells from ischemic damage) are under investigation.

27-22. How can ischemic stroke result in death?

27-22. Ischemic stroke can cause cytotoxic edema, with swelling and ultimate brain herniation (this swelling can not be treated with steroids although osmotic agents may temporarily help. Large strokes may subsequently hemorrhage due to weakening of the blood vessels in the damaged tissue. There are many potential complications of general debility (pneumonia, pulmonary emboli, poor nutrition, decubiti).

27-23. What are the stages of recovery from stroke?

27-23. Recovery from stroke may be complete or incomplete. Some tissue is functionally damaged but not killed (ischemic penumbra) and this area may recover early on. There is some redundancy of function and other areas can take over. There is some resolution of cytotoxic edema (not treatable by steroids). There is some plasticity, even in the adult brain and this can be encouraged by rehabilitation. While there may be new neurons produced, we are not sure whether they are functionally important. Later recovery involved compensation, when other methods of recovery fail. Compensation requires recognition of deficits and the ability to incorporate strategies to get around the deficits.

27-24. What are the types of intracranial hemorrhage?

27-24. Intracranial hemorrhage (20% of strokes) can be epidural, subdural, subarachnoid or intraparenchymal.

27-25. What are some causes of intracranial hemorrhage?

27-25. The most common cause is hypertension (it can be acute due to stimulant abuse), and this is intraparenchymal. Aneurysms (berry aneurysm) and arteriovenous malformations may rupture into the subarachnoid space (often with some extension into the parenchyma). Trauma is the most common cause of epidural and subdural hemorrhage, although trauma can also produce intraparenchymal bleeding (contusion). Anticoagulation, either iatrogenic or secondary to pathological condition (like liver disease, thrombocytopenia, etc) can contribute to hemorrhage (especially subdural).

27-26. What are the potential complications of subarachnoid hemorrhage?

27-26. Repeat bleeding can be devastating if a cause can't be identified and treated. Cerebral vasospasm (spasm of cerebral vessels) can result in stroke. Diabetes insipidus and central neurogenic salt wasting can complicate subarachnoid hemorrhage.