Chapter 27 - Cerebrovascular disorders
Each year approximately 700,000 adults in this country have a stroke. Cerebrovascular dysfunction, occlusive and hemorrhagic, is the third most common cause of death in this country and is very high on the list of disorders causing morbidity. Approximately 2 million people are now disabled from the effects of one or more cerebrovascular events. A great number of these individuals are in the working-age population.
Approximately 80% of all strokes are ischemic (due to occlusion of a vessel). Atherothrombotic occlusion, embolic occlusion and small vessel occlusion are the three major categories. While the pathophysiology of atherothrombosis is similar to the pathophysiology of occlusion in many other vascular beds, the small vessels of the brain appear to be particularly susceptible to the effects of aging, complicated by hypertension and diabetes. These vessel walls can undergo a change known as "lipohyalinosis" that can damage the wall and compromise the lumen. Also, tiny cerebral vessels can be damaged by accumulation of abnormal proteins in a condition called "amyloid angiopathy." This is a disorder resulting from progressive accumulation of amyloid on the walls of small arteries and arterioles over the surface of the cerebral hemispheres. It occurs with increasing frequency after age 65 and progressive arterial narrowing results in ischemic lesions. The affected vessels are fragile and may also give rise to intracerebral hemorrhage. The condition is frequently associated with Alzheimer's disease, adding an ischemic component to that disease's degenerative process. A small number of occlusive strokes are caused by inflammatory involvement or spasm of arteries. Also, trauma can result in the accumulation of blood in the wall of the artery, a condition called "dissection" because it separates ("dissects") the intima from the adventitia. This can compromise the lumen and even result in local thrombus and thromboembolus from the damaged area of blood vessel. In some patients with weak connective tissue this can happen spontaneously and can be a cause of stroke in young patients.
Although there are no clear-cut data on this point, there is increasing evidence that a major percentage of occlusive strokes are caused by embolism of clot or atheromatous material from cervical carotid or vertebrobasilar atherosclerotic plaques to the intracranial vessels. Complete occlusion of the cervical portion of the internal carotid or vertebral arteries is probably not, as once thought, the most common cause of cerebral infarction, although primary intracranial branch occlusion is still considered a relatively frequent cause of stroke.
The symptoms of ischemic stroke are typically the sudden, usually unprovoked onset of a neurological deficit referable to damage to brain in the distribution of a specific artery. There are individual differences in presentation based on the particular blood vessels affected (see below) and the particular pathophysiology. For example, embolic strokes typically reach maximum deficit within the first several minutes, while atherothrombotic strokes may present as transient deficits or the stuttering evolution of symptoms.
Not all ischemic strokes are due to occlusion of arteries. Cerebral vein occlusion can cause ischemia, although less commonly. This typically occurs in hyperviscosity conditions (such as dehydration or other hyperviscosity states, such as with high red or white blood cell counts or thrombocytosis), hypercoagulability and, occasionally, in otherwise healthy young women due to the effects of estrogen on coagulation. These strokes are more likely to present with headache, confusion and seizure, along with evidence of some intraparenchymal hemorrhage on scans.
Intracranial hemorrhage, excluding traumatic causes, accounts for approximately 20% of all strokes. Primary intracerebral hemorrhage in hypertensive individuals and subarachnoid hemorrhage from weak blood vessels (congenital or acquired arterial aneurysms or arteriovenous malformations, mostly) are the major categories. Amyloid angiopathy may be a major etiology in individuals over 65.
The brain, in contrast with other organs, localizes specific functions to particular regions. Therefore, occlusion of an artery supplying a small area of the brain has a profound and specific effect. Although regeneration or at least functional compensation by the remaining tissue is the rule with most organs, significant regeneration does not occur in the brain. Functional compensation does occur, but the margin of safety is not nearly so great as in the kidney or other organs. Therefore, vascular occlusion and focal injury is significantly more serious in the brain.
The brain makes up only 2% of total body weight but uses more than 10% of the oxygen metabolized by the body, uses almost 20% of the glucose, and receives almost 20% of the cardiac output. This amounts to about 50-80cc of blood per 100 grams of brain tissue per minute in gray matter and a third to a half of this in white matter. If blood flow falls below about 15cc per 100 grams per minute, dysfunction of neurons begins, and the longer the brain is ischemic the more likely there is to be cell death and necrosis. Neurons respire only aerobically and therefore are dependent on an uninterrupted supply of metabolic substrates. An illustration of this is that only three to eight minutes of cardiac arrest result in irreversible brain damage, emphasizing the striking dependency of the brain on an adequate blood supply for proper functioning.
There are well-developed safety factors that help to protect the brain when its blood supply is threatened. The brain vasculature is able to adjust its arterial perfusion over wide changes of blood pressure to keep a relatively constant and adequate blood supply. This self-adjustment or autoregulation causes cerebral vasodilatation when the mean blood pressure drops below normal levels and maintains an adequate blood supply until the mean arterial pressure reaches approximately half the normal levels (50-60 mm Hg); lower pressures are associated with focal and diffuse cerebral dysfunction. This safety factor can be of great importance during systemic hypotension and also at a local level can protect against flow changes caused by increased intracranial pressure or progressive atherosclerotic narrowing of cortical or cerebral arteries.
The cerebral arterial system, through a direct myogenic reflex contraction, responds to increasing blood pressure by constriction, thus keeping perfusion within normal ranges and avoiding the possible hemorrhagic consequence of excessive pressures. When mean arterial pressure rises above approximately 150 mm Hg for prolonged periods, however, autoregulation may break down. Segments of cerebral arterioles may dilate to an excessive degree, breaking down internal integrity and the blood-brain barrier allowing focal cerebral edema and dysfunction. This condition has been appropriately labeled hypertensive encephalopathy and occurs rarely, probably because extended periods of hypertension of such great degree are unusual.
During systemic hypoxia, the brain is able to extract oxygen from the blood in increasing amounts and thus compensate for arterial hypoxia down to a tension of 50 mm Hg. Beyond this, some vasodilatation probably occurs, possibly on the basis of tissue hypoxia and associated local tissue acidosis, which is a strong stimulant of cerebral arteriolar and capillary dilatation. Small changes in the arterial CO2 partial pressure cause marked changes in cerebral blood flow, presumably by changing the perivascular hydrogen ion concentration. High CO2 tensions such as occur with pulmonary disease result in a lower pH in tissue and cerebral vasodilatation, which is an indirect protection against the associated hypoxia to which the brain vasculature is less reactive. Low CO2 partial pressures, such as occur with hyperventilation, cause a decrease in the perivascular hydrogen ion concentration and subsequent vasoconstriction. This decreases the cerebral vascular bed and may decrease intracranial volume by as much as 2-3%. During central neurogenic hyperventilation caused by midbrain or pontine dysfunction (see Chapter 17), this decrease in volume may have some protective effect against progressive rostrocaudal deterioration though hyperventillation in an otherwise normal individual often produces light-headedness due to diminished cerebral blood flow.
Collateral circulation is the major safety factor that helps protect the brain from damage caused by occlusion of one or more of its major arterial inputs. In the human there are many potential channels for collateral circulation, but only a few are significant following cerebrovascular occlusion. The circle of Willis (Figure 27-1) is the most important channel for collateral circulation following occlusion of either the internal carotid system or the basilar system. It is occasionally developmentally incomplete, and even when complete is often an unsuccessful collateral channel unless vessel occlusion occurs gradually, which gives an opportunity for increased compensatory flow through the usually small posterior and/or anterior communicating arteries. Fortunately, a common cause of narrowing in the major cerebral vessels is gradual atherosclerotic thrombotic occlusion, which often allows time for adequate development of collateral flow to the distribution of the affected vessel. The most frequently occluded major vessel is the internal carotid artery in the cervical region just above the bifurcation of the common carotid artery. Following occlusion and despite frequent anomalous variations in the circle of Willis, collateral flow is possible in approximately 90% of the population from the opposite carotid system via a patent anterior communicating artery or from the vertebrobasilar system through a patent ipsilateral posterior communicating artery, or from both sources. This rather optimistic view of the compensatory potential of the circle of Willis is somewhat dampened by the realization that age and associated cerebral atherosclerosis can also affect these potential collateral channels. Also, if atherosclerosis predisposes to thrombus formation and subsequent embolus, and if the emboli lodge beyond the circle of Willis (such as in the middle cerebral artery or its branches), then the circle proves useless as a collateral supply. The rapidity of occlusion with embolism also tends to preclude a useful development of collateral from other sources.
There is some anastomosis between the distributions of the main cerebral arteries and the main cerebellar arteries. These anastomoses largely occur at the arteriolar level in the pia over the respective hemispheres. These channels are variable and also limited by the same factors that limit the effectiveness of the circle of Willis, i.e., anatomical variability, difficulty responding to rapid occlusion, and the condition of the vessels. The penetrating arterial branches that reach the deeper structures of the brain anastomose to some degree at a capillary level with neighboring arterial branches, but this collateral circulation by itself is rarely of functional significance following an occlusion and the penetrating vessels therefore act essentially as end arteries.
Based on this anatomy of anastomosis, there is an area of overlapping blood supply in the regions between major blood vessels. This becomes clear to you if you review the areas of blood supply, especially of the brain stem and deeper structures of the cerebral hemispheres. With ischemia in the distribution of a single-vessel system (e.g., the middle cerebral, Figure 27-2), these areas of overlap are often able to avoid major damage. However, if blood flow is affected diffusely (such as with severe systemic hypotension/shock), these areas, somewhat inappropriately called watershed areas, become the regions of the greatest damage. This is because they are at the farthest reaches of blood supply and therefore are the first to develop decreased flow with low systemic perfusion pressure.
A third group of potential collateral circulation channels consist of connections between the external and internal carotid arteries (e.g., external maxillary-ophthalmic-internal carotid). These potential channels are rarely significant as a sole source of collateral circulation in persons with acute stroke. However, they may give major collateral support and decrease the severity of or prevent ischemia with slowly progressive occlusions of major vessels. Individuals have been described who have minimal symptoms or signs of cerebral ischemia but have complete occlusion of three and even all four major cervical vessels (both internal carotids and vertebral arteries). In such patients, arteriograms reveal large collateral channels from the external carotid system that anastomose with the intracranial arterial systems through the orbit and/or foramen magnum. Very gradual and probably staggered carotid and vertebral occlusion allows these compensatory channels to enlarge and prevent major ischemia.
Almost 50% of persons who suffer a complete ischemic stroke have stenotic or occlusive disease in the cervical vessels. Also, approximately half of patients with completed ischemic stroke have a history of prodromal symptoms and signs referable to ischemia in the areas supplied by the involved vessels. These episodic signs and symptoms take the form of transient neurologic deficits (transient ischemic attacks, TIAs).
For therapeutic convenience and with some arbitrary delineation, the degree of cerebral arterial occlusive disease can be divided into (1) covert disease (i.e., asymptomatic with risk factors for disease), and (2) overt disease (i.e., symptomatic). In the latter case, symptoms may appear in three patterns: a. transient ischemic attack, b. stroke-in-evolution, and c. completed stroke.
It is critical to identify patients who are at risk for stroke and, where possible, institute programs to prevent them. There are different risk factors for different types of stroke. For example, small vessel damage is promoted by hypertension and diabetes mellitus. Hypertension is also a major risk factor for intracerebral hemorrhage. There are multiple risk factors for arteriosclerosis, a major predisposition for stroke due to large vessel occlusions. Embolic disease usually results from some cardiac abnormality (such as atrial fibrillation, cardiac valvular disease or large right to left shunts. Most of the above conditions are, to some extent, treatable in a manner that can decrease risk for stroke. Unfortunately, many of these interventions provide imperfect prophylaxis and some major risk factors for stroke are not modifiable, such as advancing age.
Hypertension is the major prospectively proven and modifiable predisposition to both ischemic and hemorrhagic stroke. The pulsatile trauma to arteries and turbulent flow caused by systemic hypertension presumably initiates the atherosclerotic process and also causes microscopic arterial wall trauma and aneurysmal ballooning in small penetrating vessels (a process called lipohyalinosis). The thickening of the wall due to this process presumably is the reason for most small vessel occlusions, and the fact that this process results in weakening and microaneurysmal dilations of the wall makes hypertension the source of most intracerebral hemorrhages. Most authorities now feel that treatment of even mild hypertension is useful prophylaxis against stroke. In the last 25 years the incidence of ischemic stroke, intracerebral hemorrhage and, to a lesser degree, heart attack have decreased (recent data suggest that a plateau has been reached). The major reason for this decrease appears to be the aggressive treatment of hypertension. Dietary modification (e.g., eating less red meat, less dairy products, and more fish and fowl, whole grains, vegetables and fruits) and decreased smoking have probably contributed to the decline, as well.
There are many factors, in addition to hypertension, that contribute to atherosclerosis. Obesity, hyperlipidemia, sedentary lifestyle, and cigarette smoking, are major factors (they are also implicated as causes of coronary atherosclerosis and insufficiency). Homocysteine, an amino acid by-product of the metabolism of methionine, an essential amino acid derived mostly from red meat, has been linked to the atherosclerotic process. It may interact with the "bad" form of cholesterol (low density lipoprotein: LDL) in the pathological process. If inadequate amounts of folic acid, Vitamins B12 or B6 are present in the diet, homocysteine accumulates and may be damaging. High red meat intake and low vegetable intake are prevalent in the western world, especially North America resulting in a folic acid deficiency in a significant portion of the population. Despite recognition of this risk factor, recent studies using folic acid (also B6 and B12) to try to prevent cardiovascular, cerebrovascular, and peripheral vascular events have had disappointing results. Nonetheless, epidemiological studies have clearly shown an association between low prevalence of atherosclerosis and vascular events in populations eating more whole grains, vegetables, and fruit. However, it not clear what specific ingredient or ingredients are involved or whether the effect is actually due to lower intake of animal products in this type of diet. Low-density lipoproteins (LDL) appear to be critical to the process (they are the major lipid component of the "plaque"). Treatments that lower LDL with newer drugs (statins, which decrease cholesterol production by the liver) are associated with a decreased incidence of vascular events, including stroke and myocardial infarction. However, it is not clear that this effect is directly due to the lipid lowering function and the statins may work by anti-inflammatory, antioxidant, or other means to lower stroke risk. This is an active area of research. It is clear that oxidation of LDL is a part of the process of atherogenesis, although prospective studies of antioxidant administration (e.g., Vitamins E, C, and beta carotene) have yielded disappointing results. Elevated high-density lipoproteins (HDLs) are inversely proportional to the risk of atherosclerosis. However, it is harder to elevate HDLs than to lower LDL and drug development and study is in its infancy.
Persons with diabetes mellitus are predisposed to atherosclerosis and occlusive stroke. It is suspected but not definitively proven that fastidious treatment of the glucose intolerance is useful prophylaxis against generalized atherosclerosis. It appears that the prime mechanism of damage is due to osmotic effects of glucose and its breakdown products on endothelial health so glucose control would be predicted to help.
For persons at risk for embolization from cardiac valves, fibrillating atria, or ischemic endocardium, chronic anticoagulation with antithrombin agents is considered the treatment of choice. Some antiplatelet agents appear also to be of use in persons with artificial heart valves. Of course, full anticoagulation conveys some risk of both intraparenchymal hemorrhage as well as hemorrhage around the coverings of the brain. However, in the above situations, this risk appears less than the risk from well-regulated anticoagulation in these patients with risk for repeated systemic embolizations. It is less clear what to do about patients with right to left shunts (such as a patent foramen ovale). These can be closed via transcutaneous catheter placement of an "umbrella", however, the precise criteria for considering such closure are not well-established.
A transient ischemic attack (TIA) is defined as a reversible episode of neurologic deficit caused by vascular insufficiency usually lasting no 5 to 30 minutes but occasionally persisting for 24 hours and rarely several days (the longer the TIA the more likely there is to be some actual tissue destruction seen by sensitive tests, such as MRI). The syndrome of TIA is defined by complete clinical recovery, despite the fact that there may be evidence of damage on MRI. Approximately half of all patients who develop completed ischemic destruction (infarction) of brain tissue have had premonitory transient ischemic attacks. This underscores the importance of recognizing the TIA, since this defines a patient who is at risk for stroke. In many instances, the risk of going on to have stroke is modifiable and identification of the TIA affords an opportunity to institute such treatment.
From 20-40% of patients with TIAs progress to ultimately develop a cerebral infarction. The prognosis for vertebrobasilar distribution attacks is somewhat better than that for carotid attacks, with approximately 20% and 40%, respectively, developing infarction on long-term follow-up, if untreated.
Most of what we will present in the following discussion of TIA will be relevant to later discussion of ischemic stroke, its symptoms and presentation. Therefore, we will address these issues in some detail before going on to consider the issue of stroke. First, we will discuss the symptoms of ischemia in several vascular distributions. Although these symptoms are transient in the syndrome of TIA, completed stroke in the particular vascular distribution will result in similar (albeit permanent) symptoms. Then we will consider the management of the patient presenting with TIA before continuing with discussion of stroke.
Disease in the carotid circulation results in one of several symptoms patterns. One classic pattern is transient monocular visual obscuration (amaurosis fugax) that is due to retinal ischemia. Amaurosis fugax usually results from internal carotid stenotic or ulcerative disease. Symptoms of damage to the cerebral hemisphere classically present as contralateral hemimotor, hemisensory, and hemivisual deficits, while dysphasia may be present if the dominant hemisphere is involved. Cerebral symptoms alone may be caused by either cervical carotid disease, hemispheric small-vessel disease or embolization from the heart (atrial fibrillation, valvular disease or ischemic wall) or aortic arch. A palpably depressed carotid pulsation suggests carotid stenotic or occlusive disease, although this is often not detected due to preserved pulsation in the patent overlying external carotid. The presence of an ipsilateral carotid bruit (usually in early systole and high-pitched) not referred from aortic valvular disease is strong evidence of carotid stenosis; however, almost 75% of patients with radiologically proved carotid stenosis do not have a bruit audible at the bedside. Remember, complete occlusion of the carotid artery will not have a bruit. Also, be aware that approximately 10% of adults who have a carotid bruit on routine examination with no history of ischemic disease have normal carotids on angiographic investigation. Therefore, when a localized bruit is heard over the carotids, atherosclerotic disease is present in 90% of cases, although the clinical significance of this bruit is not predictable.
When is a carotid lesion significant? Before blood flow is hemodynamically disrupted to a significant degree, a carotid stenosis must be at least two-thirds complete; the diameter of the lumen as demonstrated angiographically is usually 1 mm or smaller. As mentioned, approximately 90% of the population can, because of collateral circulation through the circle of Willis, withstand complete occlusion of a single carotid or vertebral artery without ischemic symptoms, barring the presence of other occlusive disease beyond the circle of Willis. Rapid occlusion by trauma or thrombus in an otherwise normal carotid is more likely to be associated with cerebral symptoms because of lack of time for development of effective collateral circulation.
In patients with a borderline-significant stenosis, significant drops in mean arterial blood pressure may cause focal symptoms of transient ischemia. However, the fall in blood pressure would have to be quite large and this is a rare mechanism of TIA. A higher proportion of transient ischemic episodes are due to microemboli arising from atherosclerotic plaques (particularly those with ulcers) in the cervical vessels. The emboli from ulcerated plaques may consist of platelet aggregates, small thrombi or atherosclerotic ulcer debris. Emboli typically are broken up rapidly on meeting the small vessels of the retina and brain and then pass distally with subsequent alleviation of ischemic symptoms and signs. These small emboli can sometimes be viewed by transcranial doppler assessment providing evidence for this mechanism.
Transient ischemic symptoms referable to the posterior vascular systems are quite variable, which is consonant with the many functional systems packed into the relatively small structure of the brain stem and posterior portions of the hemispheres. Alone or in various combinations, vertigo, bilateral blurring or loss of vision, ataxia, diplopia, bilateral or unilateral (occasionally alternating) sensory and motor deficits, and syncope are common manifestations of vertebrobasilar insufficiency. Transient vertigo or ill-defined dizziness is a very common complaint in persons past age 60 and is not necessarily related to ischemia. Indeed the most common cause is benign positional vertigo, a disorder of aging related to otolith displacement into the posterior semicircular canals and occasionally cervical spondylosis (see Chapter 6). The associated symptoms noted earlier must therefore be present before a clinical diagnosis of transient vertebrobasilar ischemia can be entertained.
Evidences of vertebral insufficiency at the bedside are: (1) depression of blood pressure in either arm, suggesting the possibility of subclavian or brachiocephalic (innominate) artery occlusion with reverse flow in the ipsilateral vertebral artery; (2) bruits over the supraclavicular regions in the absence of aortic ejection murmur, suggesting either subclavian or vertebral narrowing; (3) bruits over the posterior triangle of the neck, which may be changed on turning the head, suggesting vertebral narrowing; and (4) production of vertebrobasilar ischemia symptoms and signs by flexing, extending, or rotating the neck, suggesting osteoarthritic compression of the vertebral artery in the transverse vertebral foramina.
Transient neurological symptoms in individuals >45 years old are most commonly due to cerebrovascular events (TIA). However, there are a several other possibilities that should be considered. Migraine equivalent, focal seizures, benign positional vertigo, Meniere's disease, and demyelinating disease are the most commonly encountered categories of disease that can be mistaken for TIAs. Historical information is usually sufficient to eliminate or implicate these possibilities. Cranial arteritis (temporal arteritis) must be considered in the patient over 50 who has transient amaurosis usually with but occasionally without temporal headache. Such persons almost invariably have an elevated sedimentation rate (usually higher than 55 mm/hour) and may also have an associated proximal limb condition called polymyalgia rheumatica (chronic aching in the proximal limbs and pelvic and shoulder girdles associated with malaise). These patients usually have a positive temporal artery biopsy, and respond dramatically to corticosteroid therapy. Occasionally persons with cranial arteritis have a stroke caused by inflammatory occlusion of major cervical (most often the vertebral artery) or cerebral vessels. Therefore, a test of sedimentation rate should be ordered routinely in all stroke patients over the age of 50. Hypoglycemia is also a consideration, although such patients usually show evidence of diffuse bilateral cerebral dysfunction. Occasionally the low blood glucose level presents as focal and lateralized difficulty. It is reasonable therefore to check the blood glucose level early in all apparent stroke patients (this should also be done due to the fact that stroke victims with elevated sugar have a poorer prognosis and may require acute therapy). Treatment with glucose of the rare patient with hypoglycemic "stroke" may give dramatic results. Some patients with focal lesions (tumors or AVMs) may present with transient symptoms (probably due to ischemia in adjacent brain tissue by poorly regulated shunting of blood into the lesion).
Treatment of the patient after a TIA is dependent upon recognizing that this places them at higher risk for ischemic stroke and that many of the risks are modifiable. To some extent, the selection of therapy is based on recognition of the specific etiology of the TIA, while some other recommendations are generic and appropriate for all such patients. For example, modification of stroke risk factors (smoking, hypertension, obesity, hypercholesterolemia, poor glucose regulation) are generic recommendations. Also, platelet antagonists generically decrease stroke risk after TIA (assuming that these medications are tolerated). They appear to work by decreasing platelet aggregation and the initiation of intravascular coagulation, a step in the genesis of stroke of many types. Antiplatelet medications have been clearly shown to prevent cerebral infarction by a number of multiple-institution studies. In particular, persons with TIAs appear to have approximately 20-30% less chance of going on to have a completed stroke if they take acetylsalicylic acid than if they do not. More recently, statin drugs have been shown to decrease the risk of stroke in patients with cerebrovascular disease. Interestingly, it is not clear whether this effect is actually due to the lipid-lowering effects of the medication. In any event, these medications should be considered earlier in the management of patients with cerebrovascular disease than would be warranted on the basis of their lipid profile alone.
Although these generic recommendations may be all that can be done to decrease the potential for stroke in the patient with small vessel disease, there are two specific scenarios that would call for additional or different therapy. These scenarios include the patient with severe atherosclerotic disease of the large vessels and the patient with significant risk for cerebral embolization from cardiac sources. In the former case, surgical intervention may be necessary (see below) while, in the latter case, anticoagulation is often appropriate.
Persons with clinical evidence of embolization from sources other than the cervical vessels (e.g., atrial fibrillation, diseased or prosthetic cardiac valves, and infarcted cardiac walls or aorta) may benefit from anticoagulation. It has now been shown that patients with chronic and intermittent atrial fibrillation, whether caused by rheumatic disease or atherosclerosis, should be on long-term, low-level anticoagulation with warfarin (Coumadin) (INR between 2 and 3). Patients with mechanical heart valves require even higher levels of anticoagulation.
There are some special cases that should be discussed. Individuals who have atrial fibrillation (AF), are under the age of 65, and who have no other evident cardiac disease on echocardiography (i.e., idiopathic AF) may not need warfarin. The incidence of complicating hemorrhage from the anticoagulant is higher than the incidence of embolic stroke in these patients. They may be treated with platelet inhibitors (aspirin, others), which have a small but significant prophylactic effect and fewer hemorrhagic side effects. However, other patients with atrial fibrillation should be maintained on warfarin unless their risk of bleeding with the anticoagulant exceeds their risk of stroke. This may occur in the patient who is at very high risk of falling, for example. Aspirin, alone, may provide these patients some prophylaxis with minimal risk of life-threatening hemorrhage (assuming that they do not develop gastritis or bleeding ulcers).
Another special case relative to embolization is the individual with a right-to-left shunt (either through the heart or lungs). Although selection criteria are not entirely established, most patients who have had a documented stroke or TIA due to such a shunt should be considered for closure. These days, there are an increasing number of methods for minimally invasive closure of shunts.
Carotid stenosis on the side of transient symptoms is the clearest reason for vascular surgery today. When stenosis exceeds 70% and in some cases of lower level stenosis when the plaque shows signs of irregularity, surgical treatment should be considered. At lower levels of stenosis, surgical treatments are no better than medical (platelet antagonists) and, of course, with low-level stenosis (<50%) surgical treatment is not as good as medical. There is more controversy about what to do in the case of high-level asymptomatic stenosis. Probably, platelet antagonists are most appropriate until stenosis is very high (>90%). Future studies will be needed to clarify this issue.
The surgical treatment of choice has been carotid endarterectomy, a procedure in which the carotid artery is opened and the diseased tissue is removed from the inside before the artery is closed up again. This procedure is associated with some stroke risk, but this perioperative stroke risk should be below 3% within the first month (with an overall complication rate of <5%, otherwise, it should not be performed due to superiority of medical management.). Completely occluded carotids are rarely operated on now because of the high risk of hemorrhagic complications and surgical failure as well as temporarily heightened stroke risk.
There are recent attempts to determine whether endovascular procedures might yield better results. One difficulty with angioplasty or stent placement is that the procedure may result in distal embolization due to disrupted plaque. Therefore, the most recent procedures have deployed a protective device downstream of the procedure. Although there have been some promising results, this remains under investigation. It should be noted that this procedure does have the potential for treating athersclerosis at other levels of the cerebral circulation (endarterectomy is only possible in a limited area of the extracranial carotid artery system).
Vertebrobasilar ischemic disease is rarely surgically approachable. The exceptions might include proximal subclavian or brachiocephalic stenosis, proximal vertebral stenosis, and vertebral impingement in the transverse cervical foramina by osteoarthritic spurs, and a variety of procedures have proved successful. In some cases of osteoarthritis, moderate immobilization of the neck with a soft orthopedic collar is often adequate to enable the person to avoid surgery.
In all patients going to surgery in most institutions, especially those with carotid disease, antiplatelet anticoagulation (where not medically contraindicated) is begun prior to surgery to decrease the incidence of operative embolization and is continued indefinitely after surgery.
Approximately 20% of persons who progress to cerebral infarction and approximately 10% of those who suffer a cerebral hemorrhage have a history of evolution of deficit over several hours to several days (and, rarely, longer). Anticoagulation with heparin has been commonly used and many consider it worthwhile, however, it is unproven therapy for patients with ischemic infarction-in-evolution. Of course, patient selection must be made with care because anticoagulation is contraindicated for persons with cerebral hemorrhage and also for those with severe hypertension. In Table 27-1 are listed some useful points to distinguish hemorrhage from ischemic infarction. However, there are many cases that cannot be clinically differentiated. The CT scan is considered the "gold standard" in this determination (since recently extravasated blood is very white on scans). Clearly this technique, which is rapid and noninvasive (and therefore not subject to the potential complications of invasive tests like lumbar puncture and arteriography), has revolutionized the emergency diagnosis of intracranial catastrophe (see Chapter 11).
In patients with clear-cut and substantial neurologic symptoms of very recent onset (less than 3 hours), urgent consideration should be given to possible thrombolysis (with tissue plasminogen activator - TPA). It is critical to know the precise moment at which the stroke began. Otherwise, it must be assumed that the stroke began immediately after the patient was last known to be well. The reason that this treatment should not be initiated after 3 hours from the onset of symptoms is that TPA performed later than this significantly increases the risk of bleeding as the injured brain tissue is reperfused. This treatment should only be initiated after a CT scan is performed, demonstrating that the stroke does not have a hemorrhagic component. Also, it should not be given in a patient with extremely high blood pressure (due to potential for hemorrhage). There have been ongoing studies to determine whether some more focused thrombolysis (through an endovascular catheter) might be beneficial when performed after this 3-hour window (without producing intolerably high bleeding complications). Additionally, a recently approved device (the Merci retrieval system) has been approved for human use, for the mechanical extraction of emboli in cerebral vessels. It must be remembered, however, that approval of a device does not mean that adequate investigation has been done in order to prove its utility, which remains under investigation.
While systemic thrombolysis (with TPA) represents an important intervention, the technique is applicable to a limited subset of the stroke patient population. The need for rigorous demonstration of a focal clinical deficit, for a precise time of onset of symptoms (<3 hours from treatment), and for a CT scan free from intraparenchymal hemorrhage prior to treatment, can only be met in a small group of the larger stroke population. Because of the severe time limits for intervention, a public education campaign has been launched throughout the country to establish stroke as a "911" emergency in hopes that patients will go to the hospital soon enough to make some of these acute therapies practical. Because of limitations in this approach we are looking for other ways to improve outcomes in the immediate post-stroke period.
Other modes of therapy, which have some rationale, but are unproved in efficacy, aim at relatively or absolutely increasing the collateral blood supply or the amount of tissue oxygen to regions of progressing ischemia. Oxygenation of an ischemic brain can be increased in the hyperbaric chamber and stroke dysfunction can be alleviated in some cases by this means. Unfortunately the deficits return when the patient is removed from the chamber. Standard means of oxygenation (e.g., nasal mask or catheter) have not proved useful unless they alleviate a systemic respiratory hypoxia. Hyperbaric oxygen has not, to date, been shown to improve long-term outcomes.
There has been substantial interest in the potential for protection of ischemic neurons, "cytoprotection". This remains an ongoing area of active research since several approaches have shown promise in experimental models. Unfortunately, to date, none of these approaches have proven to be of clinical utility. The two fundamental approaches that have been investigated are to decrease metabolic need in the ischemic area, or to interfere with processes that occur in the ischemic brain tissue that result in sustained damage to cells. The cerebral need for oxygen can be decreased by hypothermia and some depressant drugs (e.g., barbiturates). Experimental evidence in animals with vascular occlusions supports the hypothesis that this might preserve some ischemic neurons from destruction while collateral circulation develops. Little clinical data are available to support or refute these findings. In recent years, some very promising approaches to the preservation of neuronal tissue from ischemic damage have evolved. Excitatory neurotransmitters such as glutamate have been shown to be released in pathologically high concentrations during ischemia and flood the ischemic zone causing excessive opening of calcium channels. This results in a calcium flood into the neuron, which is toxic to the mitochondria and causes death of the neuron. Glutamate receptor blockers and also calcium channel blockers have been shown to decrease the extent of ischemic damage in experimental animals and continue to be investigated in early clinical studies. The prevention of peroxide and free radical formation, which occurs in ischemic tissue especially when reflow occurs, has also been shown to be useful in decreasing the extent of experimental ischemic damage. From animal studies it is clear that any of these protective agents, if they are to be successful, be given within hours of the onset of ischemia and infarction, with the rule being "the sooner the better".
In most institutions surgery is not considered a useful approach to the occlusive stroke-in-evolution. However, just as with thrombolytic agents, if the patient is seen early enough (within one to two hours of onset of symptoms) and found to have an occluding internal carotid artery in the neck, endarterectomy could prove to be effective. Of course, if the stroke process stabilizes spontaneously or by conservative therapy and little neurologic deficit remains, the patient should be considered for evaluation for prophylactic cervical vessel surgery if significant stenosis is identified (see below).
The completed cerebral infarction is defined in two ways, temporal and anatomical. Temporal completion is a fixed, neurologic deficit lasting more than several days. Any recovery that occurs thereafter is related to dissipation of edema, vascular collateralization of surviving but functionally depressed tissue, and functional reorganization of surviving brain. The last, though formerly believed of great importance, has the least significance in recovery except in children. As time progresses, patients may develop compensatory strategies, and this can be encouraged through physical and occupational therapy. Restriction of use of the good limb (forcing use of the affected limb) appears to improve outcome, possibly by encouraging plasticity of central pathways. Alternative communication strategies may also be enhanced by speech therapy. Anatomical completion refers to infarction of the entire region of supply of a major cerebral vessel (e.g., the middle cerebral artery). In this sense, infarction in the distribution of one branch of the middle cerebral artery, producing for example an isolated expressive aphasia or monoparesis, is considered incomplete.
No proved therapy exists for reversing the temporally completed infarction, whether anatomically complete or not. One approach, however, aims at preventing or suppressing the significant cerebral edema, which almost invariably follows infarction and may be clinically significant from eight hours to seven days following the primary insult. This edema, by compressing contiguous vessels, may increase the area of destruction and also can cause secondary brain stem compression by the various routes of herniation of brain substance (e.g., tentorial and foramen magnum herniation; see Chapter 17 on stupor and coma). Herniation with brain stem compression is the most common cause of death occurring during the acute phase of infarction and hemorrhage.
Various measures have been tried to prevent or lessen the edema to decrease both morbidity (size of stroke) and mortality. Corticosteroids, are not effective in decreasing the edema of cerebral ischemia, termed "cytotoxic edema." It is a common misperception that steroids are useful due to the fact that they are useful in decreasing the cerebral edema caused by neoplasms and inflammatory lesions. Hyperosmotic agents (e.g., urea, mannitol, glycerol), which dehydrate normal brain tissue, probably do not affect the edema in an ischemic or infarcted area that does not have access to the agents. They have not been clearly shown to decrease the morbidity of infarction. A drawback of hyperosmotic dehydration is that it increases blood viscosity and, therefore, could decrease blood flow into areas already compromised. If a patient is dehydrated early in the course of a stroke, careful hydration may, in fact, increase blood flow to the brain ischemic zones. Craniectomy in patients who are showing signs of herniation may be a better way to decompress the swollen brain and is being studied.
Hyperthermia is not uncommonly present in patients admitted with ischemic stroke because of infection, dehydration, or central hypothalamic thermal dysregulation. It is associated with increased ischemic damage because of increased metabolic demand of hyperthermic brain tissue or for other reasons. It should be treated quickly with temperature-lowering agents or procedures. Hyperglycemia is also a frequent temporary manifestation of stroke. Adrenalin outpouring and also increased cortisol production in the stressful circumstance of acute stroke (in an elderly patient with poor insulin reserve) is the likely etiology. Hyperglycemia likely reflects inadequate cellular glucose supply and should be remedied by careful lowering of blood glucose with insulin in the acute period. Hyperglycemia within the first 24 hours of stroke onset has been associated with increased stroke size.
Carotid surgical therapy in persons with an anatomically incomplete infarction is considered useful prophylaxis against complete infarction for those with milder deficits who have approachable ipsilateral cervical carotid stenotic disease which is 70% or greater in degree. Presently, most centers wait four to six weeks before carrying out the surgery in order to avoid possible hemorrhage into the necrotic infarcted zone when normal flow and pressure are re-established.
Of course, a major indication of high risk for stroke is the history of stroke. Therefore, careful consideration of modification of the various risk factors for stroke (see above) is critical.
Arteritis is an unusual cause of cerebrovascular occlusive or hemorrhagic disease and probably accounts for less than 1% of strokes in adults. The two major causes of inflammation and occlusion of the cerebral arteries are diffuse or focal autoimmune arteritis (e.g., polyarteritis nodosum, lupus erythematosus, giant cell and other cranial arthritides, and Takayasu's giant cell arteritis of the aortic arch vessels) and septic or infectious arteritis, which may be associated with purulent meningitis or direct involvement of arterial walls by fungi (mucormycosis and aspergillosis in debilitated, immune deficient, or diabetic individuals) or bacteria seeded to arteries from septic emboli of cardiac origin. Meningovascular syphilis is a rare cause of stroke today. Thrombotic occlusion of or intracranial hemorrhage from diseased and weakened arterial walls may occur with either autoimmune or septic arteritis. Hemorrhage is most commonly seen with fungal and bacterial involvement where the arterial walls may be weakened and balloon out to form aneurysms, which are prone to rupture. Treatment of arteritic stroke is aimed at the primary process (i.e., corticosteroids for autoimmune disease, antibiotics for infectious disease, surgery where possible for aneurysms) and supportive care. Occlusive strokes in children may follow viral illness and are therefore presumed by many to be caused by focal autoimmune inflammatory processes or direct viral involvement.
Migraine may rarely be associated with ischemic stroke, presumably on the basis of prolonged vasospasm or arterial edema. Women taking birth control medications are slightly more susceptible to cerebral arterial occlusion, and this susceptibility is increased if there is a history of migraine and if they smoke.
Carotid or vertebral artery dissection is an unusual but increasingly recognized cause of ischemic infarction. Blood enters the wall of the blood vessel and accumulates between the intimal (endothelial) and media of the carotid or vertebral vessels. This may occur due to disruption of the endothelium, with a flap forming, or due to rupture of a small blood vessel in the wall of the artery (the vasa vasorum). This is often traumatic, although the trauma may be trivial (such as turning or extending the head). Recently, it has been found that many patients with dissection have abnormally weakened connective tissue, sometimes associated with very clear connective tissue disorders (such as Marfan's syndrome or Ehrlers-Danlos' syndrome) and sometimes only observable at the ultrastructural or biochemical level. The blood in the artery wall enlarges the wall, narrowing or occluding the main flow. If adequate collateral circulation is not available, symptomatic ischemia may lead to infarction and permanent deficits. Further, clots may form above the constriction and release emboli upstream to cause ischemic lesions. Clot may be released from the subintimal column of relatively static blood if the dissection reenters the vessel lumen upstream and the thickened wall may obstruct arterial branches. Dissection is usually associated with acute pain in carotid and vertebral referral areas: the lateral aspect of the neck and the ears and mastoid region, and behind the eye for the carotid, and the posterior lateral neck and occipital region for the vertebral. Involvement of the carotid sympathetic plexus frequently results in an ipsilateral Homer's syndrome, a distinct diagnostic marker. Diagnosis is clinical and by imaging with invasive angiography, CT angiography or less sensitive magnetic resonance angiography. Treatment is controversial but the use of anticoagulation with heparin and then warfarin (to avoid embolic complications) is espoused by some. Surgery is not considered useful at this time. The prognosis tends to be good with or without therapy with spontaneous resolution of the dissection over weeks to months. Most asymptomatic dissections are probably misdiagnosed as atypical headaches.
Vasospasm occurs in a significant number of persons with subarachnoid hemorrhage and can be severe enough to cause ischemia and infarction. The spasm is thought to be related to release of vasoactive substances (e.g., serotonin) into the subarachnoid space from extravasated platelets and possibly also basophils. Prophylactic treatment with centrally active calcium channel blockers, which may either decrease vasospasm or ischemic damage, or both, has shown some promise.
Hyperviscosity and hypercoagulable states predispose to arterial occlusive disease, and the risk is greatly amplified if arteriosclerotic vessel changes are already present. Hyperviscosity that causes a sluggish blood flow and a predisposition to coagulation is associated with dehydration, hyperproteinemias, and dysproteinemias (e.g., macroglobulinemias, cold agglutinins), polycythemia, leukemia, and sickle cell disease. Thrombocythemia (excessive platelets), thrombotic thrombocytopenia purpura (abnormal platelets), and rare cancer-associated coagulopathies are examples of excessive clotting capacity that predisposes to arterial occlusion. Antiphospholipid antibodies are a cause of vascular occlusive disease being given more attention. Some individuals who have had stroke have been shown to have high titers of antiphospholipid antibodies, in particular, some patients with malignancy or connective tissue diseases; and some medications have also been implicated. These antibodies (e.g., anticardiolipin antibody and lupus anticoagulant) are associated with thrombotic disease and a number of other conditions such as spontaneous abortions and presently are not well understood. Prophylactic therapy with antiplatelet agents and/or antithrombin agents is being used empirically.
Symptomatic cerebral vein or venous sinus occlusion is rare. This may be explained in part by the rich interconnections in the cerebral venous system and the lack of valves in the major sinuses. Both contribute to create a collateral circulation safety factor when focal portions of the venous system are obstructed.
When major channels are occluded, such as the posterior portions of the sagittal sinus, a lateral sinus, or the internal cerebral veins, collateral circulation is frequently inadequate and edema and hemorrhagic infarction may occur and cause a stroke-like picture with headache, focal and diffuse deficits and focal and generalized seizures. Edema may appear rapidly and massively and lead to rostrocaudal deterioration (herniation) and death (see Chapter 17).
Some predisposing elements in venous occlusion are severe dehydration (causing hyperviscosity of blood flow and increased coagulability), other causes of hypercoagulable states (discussed earlier), and infection of the meninges or neighboring structures involving vein and sinus walls (purulent meningitis, chronic otitis media, and chronic sinusitis). The risk of cerebral sinus thrombosis is higher during the postpartum period either because of dehydration or for other reasons.
Therapy is aimed at treating the primary process when possible, decreasing edema and suppressing seizures. If the patient survives the acute period, recanalization of the veins often occurs and considerable function may return to the involved cerebral tissue, which has not lost its arterial supply.
Intracranial hemorrhage falls into two major categories: (1) spontaneous hemorrhage (associated with hypertension and with congenital or other arterial aneurysms and arteriovenous malformations); and (2) traumatic hemorrhages into the epidural, subdural, and subarachnoid spaces or parenchyma of the central nervous system. Traumatic hemorrhage is discussed in Chapter 29.
Spontaneous intracranial hemorrhage accounts for approximately 20% of all strokes. The primary hemorrhage may be into the parenchyma of the central nervous system or into the subarachnoid space. Parenchymal hemorrhages often rupture into the ventricular system or into the subarachnoid space, whereas primary subarachnoid hemorrhages frequently dissect into the cerebral parenchyma.
Intraparenchymal hemorrhages are almost invariably associated with hypertension and are presumed by many to be the result of weakening of arterial walls by the trauma of an excessive pulse pressure. The most common sites of involvement are: (1) the region of the putamen-external capsule in the distribution of the lenticulostriate branches of the middle cerebral artery (50%); (2) the thalamus in the distribution of the small penetrating vessels from the posterior cerebral and posterior communicating arteries (10%); (3) the cerebellum in the distribution of the deep penetrating branches of the superior cerebellar artery (10%); and (4) the pons in the distribution of the paramedian branches of the basilar artery (10%). The remaining 20% occur into the white matter of various lobes of the cerebral hemispheres. Another etiology for the lobar hemorrhage has recently been described. In aging individuals, and especially in those with Alzheimer's Disease, amyloid deposition may occur in the penetrating cortical vessels, making the vessels more friable and subject to hemorrhage. Typically, the hemorrhage is lobar (i.e., immediately subcortical) and the likelihood that amyloid angiopathy is the etiology of the hemorrhage is increased if there is no past history of hypertension.
There are other, less common conditions that can result in primary intraparenchymal hemorrhage. For example, they can occur with bleeding diatheses such as thrombocytopenia, leukemia, and anticoagulant therapy. They are a feared complication of the use of TPA either for heart attack or stroke. Intraparenchymal hemorrhage can occur due to arteriovenous and capillary malformations and can also occur due to bleeding into a necrotic area of brain due to a large stroke (often called "hemorrhagic conversion). Massive hemorrhage may also occur into rapidly growing malignant neoplasms, which outstrip their blood supply and develop central necrosis.
It is frequently difficult to clinically differentiate the patient with intraparenchymal hemorrhage from one with massive ischemic infarction. Of course, a CT scan is the "gold standard" for this differentiation in the ED. However, there are certain aspects of the history and observations are suggestive of hemorrhage (see Table 27-1). A history of poorly controlled hypertension, acute headache, and vomiting at the onset of stroke are common in hemorrhage. Additionally, hemorrhage often produces signs of rapidly expanding unilateral intracranial mass (e.g., evidence of secondary compression of the brain stem leading to decreasing awareness and coma, progressive pupillary dilation, paralysis of eye movements, abnormal respiratory patterns of neurogenic origin [see Chapter 17], papilledema, and hemorrhages on ophthalmoscopic examination). It is critical to recognize cerebellar hemorrhage as early as possible. If nausea and vomiting with associated occipital headache and ataxia precede cranial nerve dysfunction and depression of consciousness in a hypertensive patient, it is important to consider cerebellar hemorrhage because it may be surgically remediable. Unfortunately, thalamic, pontine, and putamenal hemorrhages usually are not surgically approachable without producing intolerable surgical morbidity. If available, as mentioned earlier, computerized axial tomographic radiography (CT scanning) quickly determines the presence and location of intracranial hemorrhage (see Chapter 11 ).
Intraparenchymal hemorrhage causes death in almost two thirds of an unselected series of patients, with the exception of cerebellar hemorrhage, which, when treated by aspiration, may have a mortality of less than 50%. Lobar hemorrhage may have a mortality of less than 50% with or without surgical treatment. The comatose patient with intraparenchymal hemorrhage at any site rarely survives; the alert and stable patient has a much better prognosis.
CT scanning has recognized many small intraparenchymal self-limited hemorrhages that in the past were evident only as rapid-onset clinical deficits of a focal nature and presumed to be ischemic strokes. Adding these cases to the total population of persons with hemorrhage has progressively decreased the mortality statistics. Nevertheless, for the clinically catastrophic presentation, the prognosis for survival still remains very poor.
Ninety percent of primary subarachnoid hemorrhages arise from congenitally derived arterial outpouchings (berry aneurysms) that lie at bifurcations of the major components of the circle of Willis. The most common sites are the carotid-posterior communicating and the anterior cerebral-anterior communicating artery junctions. Defects in the elastic membrane and media of the arteries are considered the basis for berry aneurysm formation. It is possible that these defects are congenital, although it is clear that the actual aneurysmal outpouchings develop over the course of time. They rupture most often in early to late middle life, rarely in childhood, presumably after years of pulsatile trauma have caused them to balloon into a thin-walled sac. The presence of hypertension predisposes to earlier ruptures. Approximately 1-2% of the population has berry aneurysms as determined in general autopsy series. Much less than 1-2% of the population develops subarachnoid hemorrhage so the incidence of hemorrhage of an unruptured aneurysm must be small. Aneurysms 10 mm or larger in diameter are considered to be the most likely to rupture. Of those who have aneurysms, approximately 15% have more than one.
Rarely, aneurysms can develop from bacterial or fungal inflammation and necrosis of arterial walls (as described in the earlier section on occlusive disease). Aneurysms associated with bacteria occur most frequently in small arterial branches over the surface of the cerebral or cerebellar hemispheres. With fungal involvement, major arteries at the base of the brain are the most common target.
Approximately 10% of subarachnoid hemorrhages originate from congenital arteriovenous malformations, which reach the surface of the cerebral hemispheres or ventricular system.
The clinical presentation of subarachnoid hemorrhage is classically associated with sudden onset of a severe headache occasionally initiated by a "popping" or "bursting" sensation. The breakdown products of blood cause a chemical meningitis within several hours following the hemorrhage, which is manifested as nuchal rigidity and frequently a low-grade fever. Platelet or basophil lysis or just the mechanical trauma of tearing of the aneurysm wall may cause some vasospasm and ischemia-infarction with focal or diffuse neurologic deficit. Large amounts of subarachnoid blood frequently block egress of cerebrospinal fluid (CSF) from the subarachnoid space by plugging the arachnoid villi or obstructing CSF flow from the basal cisternae over the hemispheres or by both processes. This results in an acute communicating hydrocephalus with diffuse cerebral dysfunction. With partial blocks or the development of a chronic inflammatory response to the presence of blood, a slowly progressive communicating hydrocephalus may develop and appear as progressive dementia with gait abnormality and incontinence (see Chapter 16). This may become manifest after the patient has been improving from the acute hemorrhagic event.
Focal signs may also be caused by dissection of the subarachnoid hemorrhage into the parenchyma of the brain. This occurs most commonly with anterior communicating aneurysms, which are tightly enclosed between the frontal lobes, and middle cerebral aneurysms, which are tightly enclosed between the operculum and the insula.
In the absence of focal signs, the CSF must be examined by lumbar puncture to determine whether subarachnoid hemorrhage is present. If there are focal signs the diagnostic procedures of choice are CT scanning to determine the presence or absence of hemorrhage and radiographic opacification of the cerebral arteries (angiography) to find the aneurysm or arteriovenous malformation if surgery is being considered. Lumbar puncture is somewhat risky because it may lead to further hemispheric shift and secondary brain stem compression if there is an expanding hemorrhagic mass (see Chapter 17). A negative CT scan in a patient suspected of subarachnoid hemorrhage does not rule out subarachnoid hemorrhage. Therefore, a subsequent lumbar puncture is necessary.
Aneurysm surgery in the hands of a skilled surgeon is successful in selected cases. Clipping the neck of the aneurysm is generally the procedure of choice.
Arteriovenous malformations may be suspected before hemorrhage occurs because they may give rise to unilateral vascular headaches, sometimes focal seizures, and/or sensorimotor deficits. Some have an audible bruit that can be heard by listening over the skull.
The mortality from untreated subarachnoid hemorrhage is approximately 50%, although this refers mainly to hemorrhage from aneurysm (coma in the early phase of subarachnoid hemorrhage being an indicator of very poor prognosis). Arteriovenous hemorrhages tend to occur in a lower pressure system and cause less tissue destruction. They are more likely to arrest spontaneously. The mortality from arteriovenous malformation hemorrhage is approximately 10%. Rebleeding from a ruptured aneurysm, which is likely to occur in the first two weeks after the initial hemorrhage, is the major cause of death after surviving the primary hemorrhage.
- Marshall, J.: The Management of Cerebrovascular Disease, Ed. 3. Oxford, Blackwell Scientific Publications, 1976.
- Caplan, L.R. and Stein, R.W.: Stroke. Butterworths, Boston, 1986.
- Millikin, C.H., McDowell, F., and Easton, J.D.: Stroke. Lea & Febiger, Philadelphia, 1987.
- Barnett HIM et al: Stroke: Pathophysiology, Diagnosis and Management, ed. 3. WB Saunders, 1998.
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.
27-1. How common is stroke (cerebrovascular accident - CVA)?
27-2. Approximately what percentage of strokes are ischemic?
27-3. What is the pathology of atherosclerotic-thrombotic strokes?
27-4. What are potential sites of emboli to the cerebral circulation?
27-5. What is vasculitis and what causes it?
27-6. What are the symptoms of stroke?
27-7. What is a transient ischemic attack (TIA)
27-8. What are risk factors for small vessel disease?
27-9. What is the treatment for small vessel ischemic disease?
27-10. What are risk factors for large vessel disease?
27-11. What is the treatment for large vessel cerebrovascular disease?
27-12. What are risk factors for embolic CVA?
27-13. What is the treatment for embolic strokes?
27-14. What are some causes of stroke due to increased viscosity of the blood?
27-15. List major risk factors for stroke.
27-16. What are the general preventative measures for stroke?
27-17. What is the treatment for a transient ischemic attack?
27-18. What major factors prevent the development of stroke with occlusion of cerebral blood vessels?
27-19. What are the potential causes of stroke in young individuals?
27-20. Outside of risk factor modification, what are the roles for the different treatment options for stroke prevention?
27-21. What are the therapeutic options for a stroke in progress?
27-22. How can ischemic stroke result in death?
27-23. What are the stages of recovery from stroke?
27-24. What are the types of intracranial hemorrhage?
27-25. What are some causes of intracranial hemorrhage?
27-26. What are the potential complications of subarachnoid hemorrhage?