Stroke

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[edit] Stroke

William Pryse-Phillips

T. Jock Murray

A stroke is a focal neurologic disorder that develops acutely because of a pathologic process affecting the blood vessels that results in ischemic damage to cells. Strokes are the third most common cause of death in our population (10.6% of deaths), with an annual incidence of about 200 cases per 100,000 population. Death caused by stroke is only one aspect of the problem, however, as a disturbing number of stroke patients survive but are severely disabled. These are people who were frequently quite well until the moment they were stricken. About 20% of them have their first stroke between the ages of 45 and 65 years.

[edit] CEREBROVASCULAR FLOW DYNAMICS

There are a few basic concepts important in understanding the dynamics of cerebrovascular disease. We stress the term dynamics because the older idea that the brain is supplied by a number of end-arteries is incorrect. Three factors that must be considered in understanding cerebral blood supply are the anatomy of the cerebral circulation, cerebral blood flow, and collateral blood supply.

[edit] Anatomy of the Cerebral Circulation

Two systems supply the brain—the carotid and the verte brobasilar—connected by the circle of Willis. The textbook picture of this anastomotic circle is unusual because congenital variations are seen in perhaps 85% of people. The circle may not be complete, or some of its major vessels may be absent or extremely small. The normal anatomy will not be considered here, but the major arteries are shown in Fig. 164-1.

Figure 164-1 Location of major arteries as seen from the base of the brain. The illustration also demonstrates the most common location of congenital aneurysms.

[edit] Collateral Supply

Many collateral vessels connect the major arteries (anterior, middle, and posterior cerebral and vertebrobasilar system) supplying the cerebrum and brainstem (Fig. 164-2). The circle of Willis acts as a collateral connection between the carotid and vertebrobasilar systems and the other collaterals connect the extracranial with the intracranial vessels.

Figure 164-2 Major vascular supply to brain. (From Barsan WG, Kothari R: Stroke. In Rosen P, et al: Emergency medicine: concepts and clinical practice, ed 4, St. Louis, 1998, Mosby.)

The branches of the major intracerebral vessels form an extensive collateral bed. Thus despite occlusion of a middle cerebral (MCA) and the posterior cerebral (PCA) arteries, blood supply to much of their territories may yet be maintained through their collateral connections. As a result, most infarctions do not exactly demarcate the anatomic distribution of a vessel involved. Occasionally this anastomotic area between two cerebral arteries (the “watershed”) is the site of infarction when both vessels are partially occluded and this border zone becomes ischemic.

An occlusion of a major intracerebral artery may be compensated for by redirection of the blood flow within the circle of Willis. For example, one anterior cerebral artery can be supplied from the other side through the anterior communicating artery.

Extracranial anastomoses can also supply intracranial structures. Carotid occlusion seldom causes blindness on that side because of the collateral connections between the external carotid and the ophthalmic arteries. The meningeal, occipital, thyrocervical, costocervical, and caroticotympanic arteries can reverse their flow and dilate, thus supplying the brain if an appropriate vessel obstruction has occurred.

This potentially extensive collateral system can come into play almost immediately, which explains many peculiarities about strokes, such as why they do not occur in some situations. The efficiency of the collaterals depends on the following:

• Their anatomy. Some congenital anomalies remove potential collateral patterns. Thus agenesis of the posterior communicating artery will make infarction of the occipital lobe on that side more likely if there is an occlusion of the vertebrobasilar system. If the posterior communicating artery is not functioning, the carotid system cannot deliver blood back to that side.
  
• The cross-sectional area of the lumina of the collateral supply. If the total area is equal to that of the occluded vessel, then the anastomoses will probably be adequate.
  
• The location of the collateral vessels. If the site of anastomosis is nearer to the heart and proximal to the occlusion, it tends to be more efficient. This of course depends on the number of anastomotic channels.
  
• The general state of the vascular system. Atherosclerotic lesions, for example, will impair the potential for the opening of collaterals.
  
• Timing. A sudden occlusion will allow little time for the collateral circulation to adapt to the altered flow patterns, whereas gradual occlusions can be compensated for by an efficient collateral circulation, with perhaps little or no neurologic deficit developing.
  

[edit] Cerebral Blood Flow

The cerebral vessels differ from those in the periphery. The sympathetic fibers anatomically present appear to have little functional significance except perhaps to regulate blood pressure effects in the larger vessels around the circle of Willis. The control of cerebral blood flow depends mainly on autoregulation, an intrinsic mechanism regulating vessel diameter, to keep cerebral blood flow constant in spite of a variety of anatomic and metabolic variations. Thus if blood pressure is reduced, dilation of the cerebral vessels occurs to maintain blood flow at a constant rate. Conversely, as in hypertension, cerebrovascular constriction keeps flow constant. Only in extreme situations do the vessels fail to compensate, allowing cerebral blood flow to fall.

Cerebral blood flow is, however, dramatically changed by altering the arterial CO₂ content, CO₂ being the most powerful cerebral vasodilator known. An increase in arterial oxygen tension causes vasoconstriction, as does alkalosis, but these factors and blood pressure are both weak in comparison to the effect of carbon dioxide. Drugs have little effect on cerebral blood flow. Intracranial pressure, sleep, the pH level of cerebrospinal fluid (CSF), and body temperature also have little effect in comparison.

Ischemia inhibits the process of cerebral autoregulation, and the presence of collaterals cannot compensate. Autoregulation may also be lost if there is a fall in diastolic blood pressure below 50 mm Hg or a rise above 150 mm Hg in the area of a cerebral infarction, or when there is severe vascular disease, such as widespread atherosclerosis or intracranial arteritis. When autoregulation fails, the cerebral blood flow has a linear relationship to the blood pressure. Elderly patients tend to lose some of this autoregulatory compensation and so are abnormally prone to the effects of hypotension and hypertension.

[edit] CLASSIFICATION OF STROKE

When considering the pathologic basis for strokes, the first essential differentiation to be made is between ischemic infarction and hemorrhage. (Sometimes, however, these occur together, as when spasm of cerebral vessels occurs distal to the site of a ruptured aneurysm that has produced hemorrhage; the spasm itself may produce ischemia and perhaps infarction.) The following four classes of ischemic stroke are defined according to their time-line and severity:

• Transient ischemic attack (TIA). Brief ischemia, most often caused by an embolus, producing focal symptoms and signs lasting (quite arbitrarily) less than 24 hours (and usually less than 6 minutes)
  
• Reversible ischemic neurologic deficit (RIND). The same as TIA, except that the signs persist for longer than 24 hours but less than 7 days before full clinical recovery occurs
  
• Evolving stroke. The term used for ischemic or hemorrhagic stroke that worsens under clinical scrutiny, usually in a step-wise fashion
  
• Completed stroke. An ischemic or a hemorrhagic stroke that has caused a maximal deficit and that may now start to show improvement
  

The lesion causing cerebral ischemia may be within the vessel (embolus), in the wall (e.g., spasm, arteritis, or ath erosclerosis), or entirely extracranial (hypoxemia or reduced cardiac output). Anoxia may produce relatively minor, transient symptoms and signs, or it may lead to infarction, an irreversible state of ischemic damage from which the brain cells cannot completely recover.

Intracranial hemorrhage may occur because of rupture of either of the smallest vessels deep in the substance of the brain or of an aneurysm, which is usually situated at the base of the brain and close to the circle of Willis. Less common causes of hemorrhage are bleeding from an arteriovenous malformation (AVM) or hemorrhagic infarction resulting from an embolus. These are intracerebral, but extracerebral bleeding can also occur (e.g., subdural or extradural hemorrhages).

The relative frequency of ischemic strokes (thrombotic or embolic) and of the various types of cerebral hemorrhage is in some dispute. For many years, thrombosis was considered to be by far the most common cause; for instance, the middle cerebral artery syndrome was thought to be due to occlusion of the MCA, until it was shown that almost half of these patients had a significant thrombotic lesion in a large vessel in the neck, usually in the internal carotid artery. We now recognize that emboli from these sites rather than decreased blood flow because of arterial narrowing or occlusion are the commonest cause of TIAs and strokes. The heart is also important in the pathogenesis of stroke, either because an arrhythmia reduces flow or as a result of cardiac emboli, as has been made plain by long-term cardiac monitoring and telemetry. In many cases of cerebral infarction in which no significant arterial disease is found at autopsy, there is evidence of a cardiac origin of an embolism unsuspected in life; this probably accounts for the strokes that previously had been ascribed to arterial spasm or hypotension. It seems that “atherosclerotic occlusive thrombosis,” a time-honored diagnosis in clinical neurology, might actually be quite unusual.

Although the syndrome of MCA infarction is the most common clinical stroke pattern, only 4% of cases can be shown at autopsy to have an actual occlusion of that vessel, embolism from the internal carotid artery or from cardiac lesions being much more common. Interest in the pathogenesis of stroke has therefore shifted outside of the head to the large vessels in the neck and to the cardiovascular system.

[edit] PATHOGENESIS OF STROKES

[edit] Thrombosis and Embolism

Atheromatous occlusion of the great vessels in the neck is more common at sites of bifurcation or change in course of the vessels (Fig. 164-3). Thus the origins of the innominate, carotid, subclavian, and vertebral arteries; the bifurcations of the carotid arteries; and the more tortuous portions of the cerebral and carotid arteries are the major sites of ath erosclerotic plaques, ulcers, and stenosis. Exposed collagen at these sites causes platelets to adhere to the wall because of a difference in electrical charge. These platelets release ADP, which results in their aggregation and the formation of a friable platelet thrombus that may either increase in size, ultimately occluding the vessel, or may break up to form emboli.

Figure 164-3 Common sites of atheromatous stenosis or ulceration in the neck vessels. (From Pryse-Phillips W, Murray TJ: Essential neurology: a concise textbook, ed 4, New York, 1992, Medical Examination Publishing.)

Cerebral emboli are usually composed of platelets, fibrin, cholesterol, and atheromatous material from ulcerated plaques if they arise from extracranial vessels. Emboli arising from the other sites listed in Box 164-1 are rare, in comparison. Except for infective emboli, which may produce a mycotic aneurysm, the clinical features of all emboli are more or less similar. These will be discussed in the next section.

Emboli may cause either transient ischemia in an area of brain, or infarction. If the blood supply is reinstituted by the opening of collateral vessels, or if the emboli break up, allowing blood to flow again, then the ischemia is transient and function is restored; in many instances emboli are completely asymptomatic.

Atherosclerosis is primarily a disorder of larger arteries. It is unusual to find typical changes of the condition more distal than the major branches of the arteries arising from the circle of Willis. This is in contrast with the vascular changes typical of hypertension, which are primarily found in arterioles.

[edit] Risk Factors.

The risk factors that predispose to the development of atherosclerosis in the cerebrovascular system are essentially the same as those for coronary and peripheral vascular disease (see Boxes 164-2 and 164-3). Virtually all can be treated. The most important include hypertension (both systolic and diastolic), hyperlipidemia, and diabetes. Obesity, ischemic heart disease, peripheral vascular disease, and (in younger people) oral contraceptives, migraine, cardiac lesions, and aneurysms are also important. Smoking and hyperlipidemia seem to pre dispose to ischemic heart disease. In the case of cerebral emboli, atrial fibrillation (from any cause), cardiomyopathy, valve prostheses, recent myocardial infarcts, and prolapsed mitral valve are the major risk factors.

TIAs are usually embolic, but other mechanisms can also produce brief ischemia. These include vascular spasm in migraine and severe hypertension and severe generalized reduction in cerebral blood flow caused by cardiac ar rhythmias or hypotension. Ischemia is particularly likely to occur if there is any preexisting obstruction in the cerebral vessels. Ischemia may also occur when an obstruction causes blood flow to be “stolen” from another area. A classic example of this is the subclavian steal syndrome. To com pensate for stenosis or occlusion of the first part of a subclavian artery, blood is diverted from one vertebral artery down the other one so it supplies the occluded subclavian at a point distal to the obstruction and prevents the normal flow of blood from the healthy vertebral artery into the basilar artery. Ischemia can also result from polycythemia because of slowed circulation or occlusion caused by the sludging effect of high-viscosity blood, or from marked anemia or vasculitis.

[edit] Intracranial Hemorrhage

Hypertension has been mentioned as a risk factor in the development of atherosclerosis and of thrombotic or embolic cerebrovascular disease, but it also predisposes to the development of intracranial hemorrhage. In a large majority of cases, one of two pathologic lesions is present. In the first, fibrinoid necrosis of arterioles deep in the white matter causes weakening of the arteriolar wall, with the production of tiny aneurysms bound by glial tissue (Charcot-Bouchard aneurysms). With continuing arteriolar damage and disruption of its muscular coat, further weakening of the wall may lead to hemorrhage that cannot be prevented by arteriolar constriction. The severity of a hemorrhage is widely variable. On the one hand, there may be no more than a few milliliters of blood released, splitting local white-matter fibers and producing a smaller area of local damage. Later, a small cavity may result called a lacune. If the hemorrhage is more severe it will act as a quickly expanding mass lesion, producing compressive brain destruction (Fig. 164-4). The blood will track further afield and often enters the CSF or the ventricles. The sudden hemorrhagic mass lesion pro duces widespread pressure increase that may compress the brainstem structures, causing hemorrhages in the pons (Duret hemorrhages). Most intracranial hemorrhages occur in the deep white matter of the brain, both they and the small lacunae being found in the putamen, the internal capsule, the corona radiata, and in the pons and deep white matter of the cerebellum.

Figure 164-4 Usual sites of lacunar infarcts in the deep white matter. A, Internal capsule/putamen; B, Thalamus, C, Mesencephalon; D, Pons. (From Pryse-Phillips W, Murray TJ: Essential neurology: a concise textbook, ed 4, New York, 1992, Medical Examination Publishing.)

The second major disorder causing intracerebral hemorrhage is a ruptured aneurysm. An aneurysm is a dilation of an artery, varying from a few millimeters to 2 or 3 cm in diameter. They occur at the bifurcation of a vessel where the media is weakest. In the presence of hypertension, raised pressure produces dilation at these sites, and in time ruptures the aneurysm, with bleeding into the subarachnoid space and often into the brain itself. Local vascular spasm caused both by vessel rupture and the presence of blood in the subarachnoid space results in further widespread vasospasm, increasing the risk of brain damage from ischemia. Thus, although the bleeding may remain within the subarachnoid space, a pale infarct in the distribution of the vessel intracerebrally may also be caused (Fig. 164-5).

Figure 164-5 Common sites of aneurysm formation at base of the brain. All but mycotic aneurysms tend to occur on the vessels of the circle of Willis or before the second branch of the vessels arising from it. (From Pryse-Phillips W, Murray TJ: Essential neurology: a concise textbook, ed 4, New York, 1992, Medical Examination Publishing.)

The other causes of intracranial hemorrhage listed in Box 164-3 are comparatively rare. About 90% of subarachnoid hemorrhages are due to ruptured berry aneurysms. For more complete lists of causes see Boxes 164-1, 164-2, and 164-4. Only the more common among these pathologies will be described here.

[edit] CLINICAL ISCHEMIC STROKE SYNDROMES

[edit] Transient Ischemic Attacks

TIAs are brief, transient, focal disturbances of neurologic function that clear without significant residual deficit within 24 hours. We have not been as strict in this definition as some authors (who regard any mild residual deficit after 24 hours as representing a cerebral infarction rather than a TIA), because our management of the patients with minimal deficit is the same as that for those with TIAs.

TIAs used to be referred to as “little strokes,” but they are harbingers of more serious ones. A careful history in stroke patients will elicit evidence of previous transient disturbances of function in about half of the cases. If a group of patients who have had TIAs is followed long term, 5% to 10% each year will have a major infarction or die; the greatest risk is in the 3 months after the first TIA. Overall, a patient has about a 40% chance of a major cerebral infarction within 5 years.✢✢Actually, the major cause of death is not a stroke but a myocardial infarction (MI), which affects 20% of patients with TIA within 5 years. In fact, a TIA is a better predictor of MI than is angina.

[edit] Clinical Features.

Symptoms associated with TIA may involve either the carotid or the vertebrobasilar system. Typical symptoms in the carotid territory include amaurosis fugax, a monocular visual disturbance consisting of abrupt, painless loss of function, “like a curtain being drawn” over part of the visual field, reaching maximum deficit within minutes or less, and clearing progressively over minutes or hours. During this period a pale embolus may be visible in a retinal arteriole.

Other classic symptoms of TIA include the following:

• Monoparesis, hemiparesis, or clumsiness of one limb
  
• Numbness, loss of sensation, or paresthesias involving one or both limbs on one side
  
• Dysphasia
  
• Homonymous hemianopia
  
• Ipsilateral blurring of vision
  

Vertebrobasilar TIAs usually present with multiple symp toms; it is unwise to diagnose vertebrobasilar disease when only one is present. Vertebrobasilar symptoms include the following:

• Numbness, loss of sensation, or weakness involving one or both sides of the face, arm, or leg
  
• Complete or partial loss of vision in both eyes, often with vertigo or dizziness
  
• Homonymous hemianopia
  
• Diplopia
  
• Ataxia, imbalance, or staggering
  
• Drop attacks (sudden collapse with loss of muscle tone but without prolonged loss of consciousness, though brief unconsciousness can occur)
  
• Transient amnesic attacks
  
• Alternating hemiplegia (involvement of the face on one side and the arm and leg on the other)
  

Although in perhaps 40% of cases the attacks stop spontaneously, the chances of stroke are still high and an aggressive attitude toward therapy is warranted. The various causes of TIAs are shown in Box 164-4. All of the pathologies that may lead to TIAs should be considered, as should the conditions that may masquerade as them, before a diagnosis of TIA caused by platelet embolism is made (Box 164-5).

An atherosclerotic basis is suspected if there is evidence of vascular disease elsewhere, such as intermittent claudication, angina, or a history of myocardial infarction. The physician should also look for atherosclerotic changes in the fundi, an absence of peripheral pulses, and hypertension. The presence of a number of the risk factors mentioned earlier should also point in this direction. A bruit may be heard, localized to the carotid bifurcation in the neck, but this is an overrated sign of carotid vascular disease; many patients with carotid stenosis do not have a bruit, because occluded carotid vessels are silent, and because people can have bruits of no significance.

[edit] Embolic and Thrombotic Infarction

Embolic and thrombotic infarctions are together known as atherothrombotic brain infarcts and are classed together here, first because a clinical differentiation is often impossible, second because both are often operational in a patient, and last because thrombotic strokes are uncommon compared with embolic strokes (Box 164-6).

[edit] Clinical Features.

In acute infarction the onset may be sudden, progressive over a short period of hours, or step-wise over a day or more. A history of TIAs can be elicited in half of the cases.

Most patients are over 55 years old, but strokes can occur at any age. There is frequently evidence of atherosclerotic disease in the peripheral or cardiac vessels by history or examination, and risk factors may be expected.

Many of these patients do not lose consciousness unless the brainstem reticular activating system is involved, but drowsiness, confusion, or stupor is common if strokes involve large areas or cause a rise in intracranial pressure. Typically the patient suffers the event during the night and awakes with the deficit, whereas intracerebral hemorrhages tend to occur during the day.

The focal abnormalities that result from a stroke depend entirely on which area of the brain has suffered ischemic damage. Some common syndromes are described here but there are many variations on these patterns, and partial syndromes are very common. Remember that an infarction in the distribution of a vessel does not necessarily mean that there is any pathologic process in that vessel itself. The problem is often in the neck vessels or heart, or the ischemia may be due to hemodynamic change from hypotension, cardiac arrhythmia, anemia, or polycythemia.

[edit] Carotid Syndromes

[edit] Middle Cerebral Territory Infarction.

The most common pattern of stroke is a middle cerebral territory infarction. Signs include homonymous hemianopia indicating involvement of the optic radiation. Typically the eyes are deviated toward the infarcted hemisphere✢✢The pattern is the other way around with brainstem strokes, in which the eyes are deviated away from the side of the infarct (when it is unilateral).and there is lower quadrant facial weakness and a spastic hemiparesis on the opposite side, the arm being involved more than the leg. Tone in the affected limbs may initially be decreased, but spasticity develops over days or weeks. Sometimes the leg has neither significant sensory nor motor involvement and the face and arm are involved in isolation. Hemisensory loss in the face and arm is common on the side opposite the infarction, but the trunk and leg tend to be much less involved. If the dominant hemisphere is involved, an expressive and/or receptive dysphasia may occur, whereas nondominant hemisphere lesions cause a parietal lobe syndrome that includes complex sensory find ings and sensory perceptual difficulties. Right hemisphere lesions often induce a confusional state, and those on the left cause a depressive syndrome in the later stages.

Brain swelling may cause coning and occlusion of one or both PCAs, producing hemianopia or cortical blindness. MCA infarct is illustrated in Fig. 164-6.

Figure 164-6 MCA territory infarction. Scan taken shortly after the onset of patient's symptoms demonstrates the following structures are hypodense because of infarction: basal ganglia, insula (loss of insular stripe), and temporal lobe. (From Cwinn AA, Grahovac SZ: Emergency CT scans of the head: a practical atlas, St. Louis, 1998, Mosby.)

With occlusion of the internal carotid artery (ICA) in the neck, the anterior cerebral artery usually gets enough blood from the opposite side through the anterior communicating artery, which prevents infarction in the frontal and medial portions of the hemisphere; the PCA should get an ade quate supply from the vertebrobasilar system. Thus carotid occlusion often manifests as an infarction in the territory of the MCA but not in the entire carotid distribution.

Although the presence of a localized bruit over the bifurcation of the carotid may indicate a stenotic lesion, palpation of the vessel is of dubious value because the presence of the external carotid artery (ECA) may allow one to feel a normal pulse in that area. If there is a marked difference in the carotid pulses on the two sides, however, this may indicate common carotid artery occlusion on the side of the reduced pulse. Occlusion of the ICA may be suggested by relatively increased pulses in the facial or superficial temporal vessels on that side because these are branches of the ECA, which is now receiving all the carotid blood supply. This is a difficult judgment to make, however. Orbital bruits may suggest ICA stenosis.

[edit] Anterior Cerebral Territory Infarction.

Infarction in the anterior cerebral territory is a much less common type of stroke and is characterized by more marked weakness of the leg than of the arm. The face is usually spared, but the patient's head and eyes are deviated toward the infarcted hemisphere. Sensory changes in the leg are minimal or absent. Urinary incontinence and personality changes may develop. If the dominant hemisphere is involved, an expres sive dysphasia is common, whereas with the nondominant hemisphere apraxia of the opposite limbs or of all limbs may be found. Occasionally a syndrome suggesting cerebellar disease results from disruption of fibers connecting the frontal lobes to the cerebellum. Incoordination and ataxia on the side opposite the infarction are the chief signs; nystagmus and speech abnormalities are less common than with true cerebellar lesions. Another clue to the frontal localization is the finding of unilateral cerebellar signs on the same side as pyramidal changes.

[edit] Cerebral Hypoperfusion.

Generalized cerebral hypoperfusion syndromes occur in patients with severe extracranial arterial disease affecting more than one vessel, especially when there is an abrupt reduction in cardiac output and thus of cerebral perfusion pressure. Patients most often complain of light-headedness, imbalance, and weakness of the limbs, and examination reveals such nonspecific findings as poverty of speech, mild dementia, and impaired memory. There is no orthostatic hypotension, but the symptoms improve with recumbency and naturally with restoration of cardiac output. In more severe cases, watershed infarcts occur. These comprise 10% of all infarcts and usually are due to an abrupt and severe fall in cerebral perfusion pressure or to ICA occlusion; they lead to ischemia of those parts of the brain situated between the territories of supply of the middle and anterior or middle and posterior cerebral arteries and the subcortical white matter. The most characteristic syndromes include transcortical dysphasia, hemianopia, and sensory or motor deficits.

[edit] Vertebrobasilar Syndromes

[edit] Posterior Cerebral Territory Infarction.

The clinical picture of posterior cerebral territory infarction is variable, depending on whether the infarction occurs in the distal or more proximal distribution of the artery (Fig. 164-7). With a distal infarct, a homonymous hemianopia results. If the artery is occluded proximally near its origin, then branches to the thalamus and brainstem may be involved, producing a mild hemiparesis and a thalamic syndrome of contralateral sensory loss and pain. In other cases, cerebellar ataxia, receptive dysphasia (if the infarction is on the dominant side), and transient confusion and memory loss are the main features. If ischemia occurs in the territory of both posterior cerebral arteries, as from hypotension or basilar artery occlusion, the patients often develop cortical blindness, sometimes with denial (Anton's syndrome) and agitated delirium. Variable visual field defects can be documented as the patient progressively improves.

Figure 164-7 Occipital lobe infarct (posterior cerebral artery territory). Note the large right occipital hypodensity with mass effect caused by infarction. (From Cwinn AA, Grahovac SZ: Emergency CT scans of the head: a practical atlas, St. Louis, 1998, Mosby.)

[edit] Brainstem Infarction.

The vertebral arteries give rise to the posterior inferior cerebellar arteries, which supply the lateral medulla and inferior cerebellum. Occlusion or ischemia in this area will give rise to a classic lateral medullary syndrome. In this syndrome, damage to the inferior cerebellar peduncle produces a homolateral cerebellar ataxia; damage to the nucleus ambiguus causes dysarthria and dysphonia, and involvement of the descending sympathetic fibers causes Horner's syndrome on the same side. The descending nucleus and tract of the V nerve will be involved, producing loss of pinprick and temperature sensation on the same side of the face, whereas involvement of the adjacent ascending lateral spinothalamic tract produces similar findings in the arm, trunk, and leg on the opposite side of the body. Vertigo, caused by ischemia of the vestibular nuclei, and hiccup are also frequent symptoms. Because the pyramidal tracts and the medial lemniscus are centrally placed and are supplied by paramedian branches of the vertebral and basilar arteries, they are not affected in this condition.

Other brainstem ischemic syndromes probably will cause alternating hemiplegia and signs indicating damage to, for example, the reticular activating system (RAS), cerebellum, and sensory tracts, with marked changes in blood pressure, pulse and respiratory rates, and possibly homonymous hemianopia due to PCA occlusion.

Occlusion of the basilar artery is often fatal. Because so many ascending and descending tracts and cranial nerve nuclei are closely applied in a small volume of the brainstem, symptoms and signs will be severe, extensive, and bilateral (although not necessarily symmetric). Involvement of any of the cranial nerves from III to XI, of the cerebellum, of corticospinal and corticobulbar tracts, and of the reticular system is the result. These patients are usually admitted to the hospital in coma and seldom survive.

[edit] Vertebrobasilar Insufficiency.

The term vertebrobasilar insufficiency (VBI) is used for the syndrome of brainstem ischemia caused by generalized decreased perfusion, hypertension or hypotension, atherosclerosis, or steal syndromes. (Cardiac emboli usually land in the carotid territory.) Cervical spondylosis predisposes to VBI by compressing the vertebral arteries as they run through the bony canals of the cervi cal vertebrae. Symptoms sometimes can be produced by extending or rotating the head and neck to one side or the other; turning the head occludes one vertebral artery even in normal people.

[edit] Clinical features.

Symptoms of VBI resemble those of TIAs in that territory (see p. 1539). They include nausea and vomiting, vertigo, transient paresthesias in the face or limbs, tinnitus, diplopia, blurring of vision, hemianopia or even total blindness, ataxia, limb weakness, and occipital headache. Transient reduction in consciousness, deafness, and unilateral or bilateral limb weakness are other possible complaints. Typical signs include nystagmus and various other signs of cranial nerve involvement, patchy pyramidal tract signs, and cerebellar incoordination. There may be a subclavian bruit or differences between the systolic blood pressures in the arms of 20 mm Hg or more. In the event of cerebellar infarction, the same symptoms are accompanied by signs of a mass lesion compressing the brainstem and raising intracranial pressure.

The prognosis with small infarctions in the vertebrobasilar territory is better than with those in the carotid territory, and recovery from a mild vertebrobasilar infarction is usually excellent. Angiography is seldom warranted in patients with VBI because surgery in this area is less well developed than in the carotid system and a specific lesion is less often found in this territory; therefore management is seldom altered by the angiographic findings. However, brainstem and cerebellar infarcts are well shown by computed tomography (CT) scans, and surgery may be lifesaving if a swollen, infarcted cerebellum is causing compression of the brainstem.

[edit] Spinal Cord Infarction.

Thrombosis of the anterior spinal artery is rare and is usually secondary to trauma or cervical spondylosis. Infarctions of the spinal cord are usually caused by global decrease in perfusion pressure, and they usually occur in thoracic regions. Occlusion of a radicular artery by an atherosclerotic plaque, a ruptured intervertebral disk, direct trauma, or (more commonly) by atheroma or aortic aneurysm blocking the supplying arteries as they leave the aorta can cause infarcts at other sites, and infarction can also occur during aortic surgery.

[edit] Clinical features.

The clinical features of spinal cord infarction indicate involvement of the anterior two thirds of the spinal cord in the distribution of the anterior spinal artery, because the posterior third of the cord is supplied by the two posterior spinal arteries, which have more extensive anastomoses. Damage to the corticospinal tracts produces paraplegia and a spastic bladder. Spinothalamic involvement gives rise to loss of pain and temperature sensation up to the level of the infarction, and damage to the anterior horn cells produces a lower motor neuron lesion with fasciculations at the level of the lesion. Pain is usually not a feature because the posterior sensory roots are supplied by the posterior spinal arteries.

Venous infarcts of the cord occur in patients already predisposed to venous embolism (e.g., in cases involving pregnancy, thrombophlebitis, or polycythemia); spinal pain with sensory and motor long tract signs are characteristic features.

[edit] Cerebral Venous Infarction.

The major cerebral venous sinuses and veins can become thrombosed, usually due to infection; hemorrhage and edema result from the obstruction to venous outflow from the brain. Cavernous sinus obstruction may cause a distinctive syndrome of chemosis, proptosis, and painful ophthalmoplegia, which can be unilateral or bilateral. With obstruction to other venous sinuses the features may be less specific and the patient may show focal deficits, headache, decreasing consciousness, seizures, and papilledema, and may progress to death. The headache of cerebral venous thrombosis (CVT) is a common feature but varies from a moderate pressure sensation to a severe pain and is usually sensitive to aggravation by coughing or bending. The onset can be sudden or slow over weeks. Suspicion should be raised when the headache is constant and increasing, the patient's condition is worsening, and focal neurologic signs appear. CVT can also present initially with an encephalopathic picture, especially in children and in the elderly and cachectic.

On CT images, the changes may be minimal or non specific, but if contrast is used 20% will have features that suggest the diagnosis, such as the “empty delta sign” in the posterior sagittal sinus caused by contrast in the collateral veins in the sinus wall but lack of contrast in the sinus because of clotting. Magnetic resonance imaging (MRI) is more helpful because it will show the thrombus in the sinus and can be used to follow the progress of the condition.

A search for the underlying cause should be made as soon as the diagnosis is made, looking for local infection, trauma, general infection, dehydration, malignancy, and hematologic disorders such as polycythemia, sickle cell disease, and coagulation disorders. The disorder is frequently associated with pregnancy or the use of oral contraceptives. In about 20% of cases no cause will be found.

[edit] DIFFERENTIAL DIAGNOSIS OF STROKES

In assessing any acute cerebral catastrophe we must consider the differential diagnosis of ischemic and hemorrhagic strokes from other common nonvascular pathologies that may also cause the sudden appearance of neurologic signs. Epileptic seizures with Todd's paralysis are sometimes indistinguishable from strokes when first seen, particularly because emboli and hemorrhages may sometimes present with seizures. Tumors, cerebral abscesses, and extradural or subdural hematomas can all mimic stroke, and one should never assume without question that an elderly patient with the sudden onset of a grave neurologic disorder is necessarily suffering from a stroke. In younger patients, diseases of the arterial wall that are not atherosclerotic (but caused by, for example, infection, diabetes, dissection of the arterial wall or collagen-vascular disease) also have to be considered.

[edit] CLINICAL FEATURES OF HEMORRHAGIC STROKE SYNDROMES

Intracerebral hemorrhages may be small (producing a small lacune) or large (producing a sudden increase in intracranial pressure caused by the enlarging clot, as well as signs of focal brain destruction). Both of these types of hemorrhage are associated with hypertension, which can produce strokes in a number of ways. In malignant hypertension, intracranial arteriospasm and cerebral edema sometimes produce reversible focal and general ischemic damage characterized by decreasing consciousness, seizures, fundal hemorrhages, and papilledema (hypertensive encephalopathy). Congenital berry aneurysms bleed when the blood pressure is elevated. Hypertension also accelerates the development of atherosclerosis.

[edit] Lacunar Strokes

Lacunar strokes may be the most common vascular lesions occurring in the brain. These small, cystic spaces resulting from healed ischemic infarcts can be found in many routine autopsies, particularly in patients who have had hypertension. They are most commonly located in the thalamus, striatum, internal capsule, and pons and occasionally in the cerebellum and corona radiata. A large majority are asymptomatic, but in about 20% of cases a stroke syndrome occurs. Representative syndromes (from about 20 defined) include the following:

• Apure motor hemiplegia. Here the lesion is in the internal capsule or in the base of the pons.
  
• Apure hemisensory syndrome. The lesion is in the ventrolateral nucleus of the thalamus.
  
• Cerebellar and pyramidal signs occurring together in the same leg (and less obviously in the arm). The lesion involves the superior cerebellar peduncle fibers after they have crossed and the corticospinal fibers at the level of the midbrain.
  
• A syndrome of slurred speech, facial weakness, and clumsy hand(dysarthria-clumsy hand syndrome) caused by a lacune in the base of the pons. Involvement of the face and tongue accounts for the dysarthria, while the clumsy hand is a manifestation of a pyramidal lesion or of a mild cerebellar syndrome.
  
• Unilateral third nerve palsy with contralateral hemiplegia(Weber syndrome).
  
• Cerebellar ataxia and crossed third nerve palsy(Claude syndrome).
  
• Hemiballismus from a lesion in the subthalamic nucleus.
  
• A “locked in syndrome” caused by bilateral lesions of the ventral pons.
  
• A “top of the basilar syndrome” with unilateral or bilateral third nerve palsies, paralysis of downward gaze, and drowsiness caused by infarction in the territory of a penetrating arteriole arising from the distal part of the artery.
  

These syndromes are relatively mild and often transient; they have a good prognosis, particularly if the patient's blood pressure is controlled in the future. If they are recognized, these syndromes usually do not require extensive investigation because the angiogram is usually normal. CT scans show a small area of infarction in 25% of cases and evidence of bleeding in a few.

[edit] Parenchymal Hemorrhage

In contrast to the relatively benign lacunar syndromes, primary hypertensive intracerebral hemorrhage is frequently fatal. In this situation a Charcot-Bouchard aneurysm or a small artery ruptures, causing a fiber-splitting hemorrhage that can be small but is more usually moderate or massive. The intracerebral bleeding stops only when the blood pressure falls, pressure within the clot rises, or vasospasm in the artery prevents further bleeding.

Parenchymal hemorrhage occurs in hypertensive patients in the same sites that lacunar strokes develop (putamen 55%, thalamus 25%, cerebellum 10%, subcortical 10%, pons 7%). The most common area is that supplied by the deep penetrating vessels branching from the MCA around the internal capsule.

[edit] Clinical Features.

Symptoms of parenchymal hemorrhage are usually severe, with a sudden onset, most often during the day. The deficit is maximal within minutes of the onset of hemorrhage, and the patient often loses consciousness after complaining of a severe headache with nausea and vomiting. This is one of the most common causes of sudden death.

A grand mal seizure may occur, with or without a focal onset. Such a combination of headache and vomiting strongly suggests an intracerebral or a subarachnoid hemorrhage. In those patients who do not immediately lose consciousness, confusion, headache, oculomotor pareses, and hemiparesis are common, as are signs of raised intracranial pressure eventually.

The focal signs that might allow one to localize the lesion are at times clouded by the presence of coma, meningism, or raised intracranial pressure. With hemorrhage into the putamen, both eyes deviate conjugately to the side of the cerebral lesion and away from the hemiparesis, whereas with thalamic hemorrhage, the eyes are deviated downward, the pupils are small and sluggish to reaction, and there may be aphasia and sensorimotor deficit. If the patient is conscious, unilateral sensory loss is likely to be detected.

With pontine hemorrhage the patient is usually comatose, with Cheyne-Stokes or neurogenic hyperventilation, pinpoint pupils, hyperpyrexia, facial weakness, and flaccid quadriplegia. Decerebrate rigidity is typical. With cerebellar hemorrhage there may be conjugate deviation of the eyes (toward the other side) or a VI nerve palsy without pupillary signs; often there is no hemiparesis either. These patients may have only a transient period of unconsciousness, after which they awaken with vomiting and severe occipital headache. When they can cooperate, facial weakness, cerebellar signs, and meningism will usually be present.

There is a particular danger of tonsillar herniation caused by raised intracranial pressure; however, if the syndrome is recognized, immediate neurosurgical intervention may allow excellent recovery. Although angiography can demonstrate the mass effect of a hemorrhage in the cerebellum, it is best shown by a CT scan that is angled to see the cerebellum and brainstem.

The differentiation of bleeding at other sites is probably less important, but the recognition and removal of any large intracerebral clot can result in excellent improvement if there is no evidence of brainstem compression.

Hemorrhages sometimes occur from AVMs, in bleeding diatheses, after trauma, or because of disease of the vessel wall such as cerebral amyloid angiopathy. In many of these conditions, the CT scan shows that the bleed is in or just beneath the cortex—a very atypical site for primary intracerebral hemorrhage.

[edit] Subarachnoid Hemorrhage

Most patients with subarachnoid hemorrhage (SAH) bleed from a ruptured berry aneurysm. Such intracranial aneurysms are usually found on the vessels around the circle of Willis or on the arteries directly leading from it (Fig. 164-8) at sites of bifurcation, where the muscular medial coat is deficient and the elastica and intima may be damaged by hypertension.✢✢The sites of bleeding aneurysms are quite easy to remember; about one third occur on the MCA, one fourth on the anterior cerebral artery/anterior communicating artery, one fifth on the internal carotid artery/posterior communicating artery, and one sixth on the basilar artery or its branches. One in five patients will have multiple aneurysms.

Figure 164-8 Enhanced CT scan of a berry aneurysm demonstrates an 8-mm left ophthalmic artery aneurysm (arrow). (From Little N, Eelkema EA: Headache. In Rosen P, et al: Diagnostic radiology in emergency medicine, St. Louis, 1992, Mosby.)

Under these circumstances the intima is unable to withstand the increased intraluminal pressure and bulges out. Because the intracranial vessels are not covered by adventitia, the aneurysm expands, and those over 10 mm in diameter often rupture. Before doing so, they may compress local structures, such as the III nerves. The risk of SAH is also much increased in smokers and in women taking oral contraceptives.

[edit] Clinical Features.

When an aneurysm ruptures into the subarachnoid space it produces sudden, severe, explosive headache, with transient or prolonged loss of consciousness in about half of the patients (Fig. 164-9). Occasionally a grand mal seizure occurs. If the patient is awake, severe headache and meningism are the major complaints. Examination shows meningism, confusion, preretinal (subhyaloid) hemorrhages on funduscopy, Babinski's signs, and other focal neurologic deficits.

Figure 164-9 Subarachnoid hemorrhage. Note blood in the basal cistern and interhemispheric fissure. (From Cwinn AA, Grahovac SZ: Emergency CT scans of the head: a practical atlas, St. Louis, 1998, Mosby.)

Monocular blindness and a severe confusional state may attend the rupture of an aneurysm on the anterior com municating artery, whereas a III nerve palsy is commonly found with an aneurysm on the posterior communicating artery. Apart from these, few signs exist to help one locate the site of the aneurysm clinically, although motor asymmetries may assist in lateralization. Minor bleeding may have occurred in the past, producing only a “sentinel headache,” nuchal rigidity, or evidence of transient mild central nervous system (CNS) dysfunction, symptoms that were ignored.

Metabolic changes associated with SAH frequently include diencephalic stimulation with alteration of sympathetic function. Both blood sugar levels and blood pressure tend to be elevated, and ECG abnormalities are common. The latter may be due to alteration in sympathetic tone and include bradycardia with a prolonged QT interval and large upright or deeply inverted T waves. The ECG changes often suggest a myocardial infarction, and appropriate treatment may therefore be withheld if it is not recognized that such changes are extremely common in SAH.

In patients who have had an acute onset with coma, the diagnosis from primary intracerebral hemorrhage can be difficult. In any case in which intracerebral bleeding is likely, CSF examination is potentially dangerous, but it is particularly so in the patient with an intracerebral clot. If the diagnosis of SAH can be made clinically, there is no point in performing a lumbar puncture, especially because the CT scan can determine the presence of blood in the brain, subarachnoid space, and basal cisterns. The absence of blood in the cisterns on the CT scan is a good prognostic sign. In patients with an acute severe headache that could have been caused by a small bleed—a warning leak—the CT may be negative and lumbar puncture will be required, but it may take at least 4 hours after the bleed for red cells in the CSF to reach the lumbar region.

[edit] Differential Diagnosis.

Other conditions may be confused with SAH or sentinel headache. Meningitis or encephalitis of sudden onset may mimic it, and if there is any doubt about the diagnosis and the question of meningitis has been raised, lumbar puncture is justifiable. Some red cells may be found in the CSF in cases of herpes simplex encephalitis and also with embolic infarction, because of migration of red cells from the damaged brain into the subarachnoid space. These conditions do not give rise to frank blood in the CSF, however. Patients taking monoamine oxidase inhibitors (MAOIs) and who eat foods containing tyramine may have symptoms and signs similar to SAH, with increased blood pressure and severe headache without any actual bleeding, although SAH has also complicated this situation. Severe migraine headaches (particularly in patients who have not had migraine before), coital cephalgia, and severe cluster headache may resemble SAH, but these patients will have clear CSF. Acute neck strain, pituitary infarction, hypertensive encephalopathy, and severe systemic infections may also cause difficulty in diagnosis.

About 1 in 10 cases of SAH are due to bleeding from an AVM (Fig. 164-10). Such patients may have a history of previous subarachnoid bleeding, and there is a history of recurrent seizures in 30%, recurrent vascular headaches in 10%, and focal neurologic findings in 50%. These patients are usually in a much younger age group than those with SAH caused by a ruptured aneurysm. Any premonitory features preceding the typical signs of a subarachnoid hemorrhage in a young person should make the physician consider the diagnosis of AVM. Patients with bleeding disorders and those on anticoagulants may rarely bleed into the CSF, but in these cases bleeding is seldom severe and the correct diagnosis is often suggested by the history, physical examination, and initial laboratory values.

Figure 164-10 A and B, Enhanced CT scans of bilateral arteriovenous malformations. With intravenous enhancement, the right (arrow 1) and left (arrow 2) arteriovenous malformations undergo dense enhancement. There is rim enhancement of the hematoma (arrow 3). (From Little N, Eelkema EA: Headache. In Rosen P, et al: Diagnostic radiology in emergency medicine, St. Louis, 1992, Mosby.)

Spinal subarachnoid hemorrhage is distinctly uncommon. The clinical features include sudden severe root pain with incapacitating backache and meningism. This triad is vir tually diagnostic and early transfer to a neurosurgical unit is mandatory.

[edit] Prognosis.

The prognosis for patients with SAH is not good. About half of the patients who have a bleed die within the first month; by the end of the first year well over half have died. The greatest mortality is within the first 10 days, but there is a further chance of rebleeding when the clot around the ruptured aneurysm lyses at the end of the second week. If the patient survives the first 3 months, the mortality rate for the next 5 years is only about 10%. Death in the first month is usually due to brain destruction or distortion, rebleeding, raised intracranial pressure, or brainstem compression.

Vasospasm is one cause of secondary deterioration of consciousness with increasing physical signs. It is usually treated with blood volume repletion and calcium channel blockers. Hyponatremia, hydrocephalus, infarcts, cardiac dysrhythmias, seizures, and rebleeding are the other leading causes of deterioration. Epsilon aminocaproic acid reduces rebleeding but may increase the risk of ischemic complications. The prognosis for patients with AVMs is much better, although they tend to bleed again.

[edit] Prognosis and Complications.

The management of SAH is considered below. Given successful surgical inter vention after a SAH and good control of blood pressure in the future, an additional SAH is not likely. However, the patient always has a slightly increased risk, particularly if there is another aneurysm present, which is why asymptomatic aneurysms are attacked surgically if possible. The long-term complications of blood in the CSF include both acute and normal pressure hydrocephalus, and the patient may be left with some deficit after the initial episode. However, these complications are not common. In about 25% of cases, no cause for the bleeding is ever diagnosed; these patients may have an even better prognosis than those who undergo surgery. It is possible that in many of these cases, the aneurysm was destroyed by the bleed, or arteriospasm prevented further loss of blood, and spontaneous healing occurred. Sometimes, a repeat angiogram after 2 weeks will show an aneurysm that was not seen during the first study, probably because of vasospasm.

[edit] MANAGEMENT OF STROKES

Some details of management have already been given but the following material provides a general outline for the acute, postacute, and long-term or chronic stages.

[edit] Acute Management

The initial history and findings are particularly important in determining those specific measures that must be taken for each individual patient. An assessment of the patient's general status (including pulse rate, blood pressure, respiratory rate and pattern, and hydration) and of neurologic signs (level of consciousness, speech, pupils and other brainstem reflexes, and limb movements) is essential. Observation for changing signs is far more useful than any single evaluation, however precise.

In all patients who are comatose, supportive measures must be provided, including the establishment of an airway and, if necessary, assisted ventilation. An intravenous (IV) line should be put in to maintain fluid and electrolyte balance, and all patients need intermittent catheterization.

Investigations in the acute stage need be but few. The purpose is to prove the diagnosis of stroke rather than, for example, tumor; to assess its extent; and to note any complications at this stage. ECG, radiographs of the chest, and routine hematologic and biochemical tests will be required, and an early CT scan will be of value, particularly in cases of diagnostic doubt, to rule out hemorrhage, to show cerebellar infarction or bleeding, or in cases of unexplained deterioration. Angiography may be useful in certain circumstances but this decision will be made by a neurologist. Cardiac monitoring may be indicated when there is clinical evidence of a dysrhythmia.

The use of anticoagulants is discussed later. Steroids are prescribed more to assuage the anxiety of the physician than to provide effective reduction in intracranial pressure, because in cases of cytotoxic cerebral edema (the type that occurs in stroke) they are ineffective.

In the acute stage the awake patient may be supported by reassurance and explanation of the nature of his disease; the patient's family should be told of the diagnostic possibilities and the likely prognosis, although prognoses given at an early stage are often embarrassingly wrong. The uncertainty of the situation, however, should be recognized by the family.

If the patient is seen within 3 hours after the stroke begins, therapy with tissue plasminogen activator (t-PA) may be considered. The patient must be assessed, a CT scan performed, and the therapy administered within 3 hours. Rapid management and decision making are mandatory for successful thrombolytic therapy. Patients cannot be considered if the onset is uncertain, such as when the patient awakens with a stroke. If there is a hemorrhage on the CT scan, t-PA is contraindicated. Patients are not considered for t-PA if they have minor symptoms or are clearly recovering, or if they have a history of recent trauma, neurosurgery, clotting disorder, seizure, hyperglycemia, or hypertension. There is a risk of cerebral hemorrhage from the therapy, but despite that, the treated patients have better outcomes in terms of mortality and major deficit, indicating that selected patients can have brain tissue preserved by the t-PA.

[edit] Postacute Stage

[edit] Transient Ischemic Attacks.

Because the symptoms and signs are transient, the patient experiencing a TIA requires explanation and reassurance about the nature of the problem to be convinced of the need for further investigations. These investigations are indeed necessary, both to assess the various risk factors and to determine the nature of the TIA that has occurred. We use as routine tests a complete blood count, including platelet estimation and ESR; BUN; syphilitic serology; uric acid; AC and 2-hour PC sugar; serum lipid profile and electrophoresis; chest radiograph and ECG; and we order a glucose tolerance test in some cases. The CT scan is negative in TIAs but positive within a day of a completed stroke. Doppler studies are used to determine whether carotid obstruction means surgery. One must also look for evidence of the conditions listed in Boxes 164-4 and 164-5.

The treatment of TIAs is evolving as studies more clearly define who will benefit from the therapeutic options. If severe (over 75%) localized atherosclerotic stenosis of a carotid (or subclavian) artery can be identified, surgical endarterectomy is appropriate treatment. However, the value of this procedure over “medical” forms of therapy in preventing a future stroke when the stenosis is less than 75% is less convincing. Operable lesions are more common in patients with prior TIAs, hypertension, claudication, and a carotid bruit. However, only half of the patients with TIAs actually have any demonstrable ipsilateral lesion at all.

Anticoagulant therapy diminishes or completely stops TIAs in 80% of cases but as yet there is no good evidence that anticoagulants significantly reduce the ultimate mortality rate, although they may prevent strokes in the most dangerous period, namely the 3 months after the first TIA. In assessing surgery and use of anticoagulants, we must recall that many patients with TIAs are not candidates for either option because other serious medical disease is present.

Because most TIAs appear to be due to platelet emboli, therapy with platelet-inhibiting agents such as clopidogrel or aspirin is used. Both have been shown to reduce strokes and deaths. Aspirin cannot be tolerated by about one third of patients because of gastric upset or ulceration. Although these side effects are less often a problem with clopidogrel, that drug is more expensive and thrombocytopenia has been described as a rare complication. Results with an aspirin and dipyridamole combination (Aggvenox) are the best to date. Therefore patients who present with transient episodes of neurologic dysfunction of sudden onset and brief duration should be referred for further investigation. If a localized area of arterial disease can be demonstrated on arteriography, then either surgical therapy or antiplatelet drugs should be considered.

[edit] Infarction.

Most patients with strokes should be admitted to the hospital. Many will have an altered state of consciousness, and continued attention to the airway, ven tilatory function, blood pressure, skin, bladder and bowel care, fluid and electrolyte balance, and calorie and vitamin intake will all be necessary. Patients do better in specialized stroke units. Investigations of value are the same as for TIAs but in all cases a CT scan is indicated, if only to determine the extent of the infarct and to rule out intracranial bleeding.

When the type and site of the lesion have been diagnosed and as soon as the patient is stable, conscious, and rational, he or she should be allowed initially to sit up in bed and later in a chair, and physiotherapy begun. Active physiotherapy should replace passive therapy as early as possible, and ambulation should be encouraged, with emphasis on gait training and use of the limbs. Hemiparesis also causes some diminution in ventilation, so chest physiotherapy may be required. As soon as it is practical, urinary catheterization should be stopped if it has been necessary at all. Antiepileptic drugs are not routinely given because seizures follow strokes in only about 10% of cases, usually as a late complication.

An isotope scan during the first 3 or 4 days after the stroke should be negative, but it becomes positive at about 6 days. If it is positive on the first day, the physician should suspect a cerebral tumor or AVM. If the diagnosis is in doubt, an angiogram may be performed, but it is otherwise not indicated in a completed infarct. A lumbar puncture is only indicated if meningeal infection is suspected. The required history, examination, and investigation for risk factors are the same as those performed for patients with TIAs.

The place of anticoagulants in therapy remains ill-defined. If the stroke is due to an embolism from a cardiac lesion, and if the infarct is not large and the blood pressure not grossly raised, then heparin may be given after 24 hours. We also give anticoagulants to patients whose stroke deficit is evolving under observation and whose CT scan shows no hemorrhage. In all other cases we advise against anticoagulant use in the acute or postacute stages, but may use them (with little experimental support) for a flurry of TIAs not prevented by antiplatelet agents. After a completed stroke, clopidogrel or aspirin and dipyridamole will likely reduce the likelihood of further infarcts, and one of these agents appears to be indicated in all such cases.

Bad prognostic factors are increased age, reduced con scious level, and severe hemiplegia, hemianopia, or higher cerebral dysfunction. Female patients and those with hyper tension or past myocardial infarcts also do less well.

[edit] Parenchymal Hemorrhage.

The management of patients with parenchymal hemorrhage is almost exactly the same as those with infarct. Greater attention must be paid, however, to reduction of blood pressure to normal levels, always attempting to keep the diastolic pressure below 100 mm Hg, and preferably lower than 90 mm Hg. A CT scan will be positive immediately. If there is any suggestion of cerebellar hemorrhage, lumbar puncture must be avoided and a neurosurgeon should be called immediately. Patients with lacunar strokes diagnosed by CT scan can be managed in the same way as those with TIAs, except that angiography is usually negative.

[edit] Subarachnoid Hemorrhage.

When patients with suspected SAH arrive in the emergency room, the physician should order urinalysis, ECG, routine hematology, biochemistry, and a coagulation profile, and arrange for an urgent CT scan. Patients who are awake and in pain should be sedated with phenothiazines or demerol. Hypertension above 100 mm Hg diastolic should be treated. Fluids should be restricted and the patient catheterized. The earlier an angiogram can be done and the aneurysm surgically attacked, the better.

The patient should be transferred to a neurosurgical unit when his or her condition is stable (signs are static or improving and the blood pressure is normal). In a neurosurgical unit, CT scanning and four-vessel angiography should be performed. In 20% of cases the patient has multiple aneurysms and it is important to note those angiographic changes indicating which aneurysm has bled. Aneurysms in most sites are susceptible to either direct or indirect surgical treatment, with the approaches varying from tying the carotid artery in the neck to a direct attack, clipping the aneurysm itself, wrapping it with muscle or plastic resins, or thrombosing it with foreign material. The chance of rebleeding may be lessened by a number of regimens, including the use of epsilon aminocaproic acid; therapy for arteriospasm (calcium channel blockers) and for raised intracranial pressure will also be required in a number of patients.

[edit] Long-term Management

There are three important aspects of late management that are often overlooked. The first is the availability of many rehabilitation services. Speech therapists may assist the patient's recovery to some degree of useful language com munication and may also provide a great psychologic boost to the patient who is continually frustrated by difficulties in communicating. Physiotherapists may aid in gait and arm retraining, and occupational therapists develop competency in the activities of daily living. Social services can greatly help the patient to realize those benefits to which he is entitled by his sickness, and they may arrange suitable placement. Home care and social and nursing services may also be called in to assist the patient in returning home, and they may provide follow-up assessments of his or her ability to function in the home and reliability in taking prescribed medication.

A second factor is the importance of continuing therapy for the prevention of further strokes. The use of anti-aggregants, proper treatment for hyperlipidemia, weight reduction, diets, and specific treatment for hypertension, diabetes, and other risk factors have a large part to play in the prophylaxis of further attacks. In cases where there may be familial risk factors such as hyperlipidemia, hypertension, or diabetes, other family members should be assessed to prevent vascular disease occurring in them as well. It has been well shown that the prognosis in patients after a stroke can be dramatically improved if all risk factors are continually monitored. In one study the 5-year mortality rate in those who were followed carefully by managing all risk factors was about 15%, compared with 65% in the patients who were not so treated.

The third factor that always warrants careful attention is the presence of depression. A stroke is well named, for it often strikes down men and women in their years of greatest achievement and happiness, devastating their ambitions and chilling them with the fear of impending renewed disaster. Depression is not just a neurotic tilt at the windmill of an unkind world, nor is it purely an expression of chemical dysfunction in the limbic system. It is, in part, both of these; in addition, depression is a near-universal response of the mind to damage of its own substrate, the brain. When the stroke patient seems to perform well on formal examination but does not go to work, can climb the stairs to his bedroom but will not visit across the road, and writes his will but will not read a book, then the physician must search for other somatic and mental symptoms of depressive illness. When they are found, these symptoms should not be regarded as the inevitable and immutable consequences of brain damage, but rather a further challenge to the diagnostic and therapeutic skills that every physician can, and must, meet.

[edit] END OF LIFE CARE

The challenge to achieve the best quality of life for patients with advanced or major illnesses requires attention not only to the treatment of the disease and related symptoms, but also to factors that influence the quality of a person's life. A good place to start is to help patients retain their identity by reinforcing those aspects of their lives that have defined who they are and to not reinforce the relative anonymity often conveyed by seriously debilitating illness. Secondly, meaningful stimulation should be provided to help them keep going and to eliminate the boredom of empty hours dragging by. Finally it is important to remove causes of stress and to provide support that conveys caring and security.

Goals for a plan of management may be based on these factors and the many aspects of daily life outlined in Box 164-7. Guidelines for critical areas of end of life care were published by the project entitled Strengthening Nursing Education to Improve End of Life Care. Extensive website resources that address end of life care are listed below.

[edit] REFERENCES

[edit] ADDITIONAL READINGS

• HP AdamsJr: Treating ischemic stroke as an emergency. Arch Neuro 1998; 55:457 - 461.
• WM Clark, GW Albers: The ATLANTIS rt-PA (Alteplase) acute stroke trial: final results. Stroke 1999; 30:234.
• BR Ferrell, R Virani, N Grant: Analysis of end of life content in nursing textbooks. Oncol Nurs Forum 1999; 26:869 - 876.
• PA Wolf: Prevention of stroke. Lancet 1998; 352 (suppl III):15 - 18.

[edit] End of Life Care

• RM Carroll-Johnson LM Gorman NJ Bush Psychosocial nursing care. Pittsburgh: Oncology Nursing Press; 1998:editor
• DF Cella: Measuring quality of life in palliative care. Semin Oncol 1995; 22:73 - 81.
• D Cella: Quality of Life: the concept. J Palliat Care 1992; 8 (3):8 - 13.
• JJ Clinch, D Dudgeon, H Schipper: Quality of life assessment in palliative care. D Doyle GWC Hanks N McDonald Oxford textbook of palliative medicine. ed 2. Oxford, UK: Oxford Medical Publication; 1998:83 - 94.
• SR Cohen, BM Mount: Quality of life in terminal illness: defining and measuring subjective well-being in the dying. J Palliat Care 1992; 8 (3):40 - 45.
• SR Cohen, BM Mount, MG Strobel,et al.: The McGill quality of life questionnaire: a measure of quality of life appropriate for people with advanced disease. A preliminary study of validity and acceptability. Palliat Med 1995; 9:207 - 219.
• S Donnely, D Walsh: Quality of life assessment in advanced cancer. Palliat Med 1996; 10:275 - 283.
• CE Ferrans: Development of a quality of life index for patients with cancer. Oncol Nurs Forum 1990; 17:15 - 21.
• CE Ferrans, MJ Powers: Development of a quality of life index: development and psychometric properties. Adv Nurs Sci 1985; 8 (1):15 - 24.
• MJ Field, CK Cassel: Approaching death: improving care at the end of life Washington, DC: National Academy Press; 1997:
• J Lynn: An 88-year-old woman facing the end of life. J Am Med Assoc 1997; 277 (20):1633 - 1640.
• SC McMillan, M Mahon: Measuring quality of life in hospice patients using a newly developed hospice quality of life index. Qual Life Res 1994; 3:437 - 447.
• RT Skeel: Measurement of outcomes in supportive oncology: quality of life. AM Berger RK Portenoy DE Weissman Principles and practice of supportive oncology. Philadelphia: Lippincott-Raven; 1998:875 - 888.
• FW Smeenk, LP de Witte, JC van Haastregt,et al.: Transmural care of terminal cancer patients: effects on the quality of life of direct caregivers. Nurs Res 1998; 47 (3):129 - 136.

[edit] WEBSITES

• Agency for Health Care Policy and Research www.achpr.gov
• American Academy of Hospice and Palliative Medicine www.aahpm.org
• American Association for Therapeutic Humor www.aath.org
• American Board of Internal Medicine—Care for the Dying, Physician Narratives www.abim.org/pubs/narr001.html
• The American Geriatrics Society www.americangeriatrics.org
• American Massage Therapy Association www.amtamassage.org
• American Medical Association www.ama-assn.org:80/about.htm
• American Music Therapy Association www.namt.com
• American Pain Society www.ampainsoc.org
• American Society for the Advancement of Palliative Care www.asap-care.com
• American Society for Bioethics and Humanities www.asbh.org
• American Society of Law, Medicine, and Ethics www.aslme.org
• ABCD Americans for Better Care of the Dying www.abcd-caring.com
• Approaching Death: Improving Care at the End of Life www2.nas.edu/hcs/21da.html
• Association of Cancer Online Resources www.acor.org; www.medinfo.org
• Association of Death Education and Counseling www.adec.org
• Before I Die: Medical Care and Personal Choices www.wnet.org/archive/bid
• Bereavement and Hospice Support Netline www.ubalt.edu/www/bereavement
• Better Health www.BetterHealth.com
• Breast Cancer Information Clearinghouse www.nysernet.org/bcic
• Cancer Net Cancernet.nci.nih.gov/
• Caregiver Network www.caregiver.on.ca/index.html
• Caregiver Survival Resources www.caregiver911.com/
• Catholic Health Association of the United States www.chausa.org
• Center to Improve Care of the Dying www.gwu.edu/˜cicd
• Center for Medical Ethics and Mediation www.wh.com/cmem
• Choice in Dying www.echonyc.com/˜choice/
• The Compassionate Friends www.jjt.com
• Death, Dying and Grief Resources www.katsden.com/webster/index.html
• Death Net www.rights.org/deathnet/
• Department of Health and Human Services, Healthfinder www.healthfinder.gov
• Dying Well www.dyingwell.com/
• Elizabeth Kubler Ross, M.D., “On Death and Dying” www.doubleclickd.com/kubler.html
• Growth House www.growthhouse.org
• History of Body Donation www.com.uci.edu/˜anatomy/willed_body/wbpol.htm
• Hospice Foundation of America www.hospicefoundation.org
• Hospice Hands hospice-cares.com
• International Association for the Study of Pain www.halcyon.com/iasp
• The International Work Group on Death, Dying and Bereavement www.wwdc.com/death/iwg/iwg.html
• Last Acts www.lastacts.org
• Lindesmith www.lindesmith.org/about_tlc/pain.html
• Medical College of Wisconsin Bioethics www.mcw.edu/bioethics/
• Medical College of Wisconsin Palliative Care Programs www.mcw.edu/pallmed/
• Memorial Sloan Kettering Cancer Center www.mskcc.org
• The Nathan Cummings Foundation www.ncf.org/ncf/aboutncf/about.html
• National Association for Home Care www.nahc.org/
• National Center for Health Statistics www.cdc.gov/nchswww/about/about.htm
• National Conference of State Legislatures www.ncsl.org/programs/pubs/endoflife.htm
• National Family Caregivers Association www.nfcacares.org
• National Hospice Organization www.nho.org
• National Institute of Aging www.nih.gov/nia/