Middle Cerebral Artery Stroke Overview of Middle Cerebral Artery Stroke

Middle cerebral artery stroke describes the sudden onset of focal neurologic deficit resulting from brain infarction or ischemia (see the images below) in the territory supplied by the middle cerebral artery (MCA).

The MCA is by far the largest cerebral artery and is the vessel most commonly affected by cerebrovascular accident (CVA). The MCA supplies most of the outer convex brain surface, nearly all the basal ganglia, and the posterior and anterior internal capsules. Infarcts that occur within the vast distribution of this vessel lead to diverse neurologic sequelae. Understanding these neurologic deficits and their correlation to specific MCA territories has long been researched.

Research has also focused on the correlation between specific neurologic deficits after MCA stroke and differing outcomes and prognoses. Such efforts are important in ascertaining who may benefit from emergent antithrombotic therapies. Furthermore, these research efforts may later allow physiatrists to target rehabilitative efforts more effectively in appropriately selected patients who may derive benefit.

The medical management of acute stroke is not discussed in detail in this article. For more information on stroke, see Hemorrhagic Stroke and Ischemic Stroke.

Two approaches are used to describe middle cerebral artery (MCA) anatomy. The functional branching approach follows the MCA trunk from the source to the end branches. The segmental approach analyzes branches of the MCA in relation to brain landmarks, dividing the artery into 4 main segments. In the segmental approach, M1 is the portion most proximal to the origin of the vessel, and M4 includes the terminal MCA branches at the brain surface. (Normal intracerebral vascular anatomy is shown in the images below.)

The segmental approach is applied most often for angiographic purposes and relates segments of the MCA to specific cerebral landmarks. The first of 4 segments, M1, describes the artery from its origin to the limen insulae, most of which is the portion from which the lenticulostriate arteries arise. The second portion of M1 describes the 3 branches that result from the bifurcation of the MCA and enter the sylvian sulcus.

M2 is the segment that runs along the insula, and M3 follows the operculum superior to the insula. Finally, M4 describes branches of the MCA that perfuse nearly the entire convex surface of the cerebral hemispheres, aside from the frontal pole and posterior rim.

Using the functional branching approach to anatomy, the MCA generally arises as a single trunk 18-26 mm long with a diameter of approximately 3 mm. The first branches consist of 15-17 small lenticulostriate arteries that supply the putamen and pallidum or the lentiform nucleus, internal capsule, and caudate nucleus of the basal ganglia. Occasionally, a few of the smaller lenticulostriate arteries arise from the internal carotid arteries.

After the lenticulostriate branches, the MCA generally bifurcates, forming superior and inferior divisions. The superior branch supplies the prefrontal and orbitofrontal cortex, and the inferior branch supplies the anterior, middle, and polar temporal regions.

The main causes of stroke include ischemia, cardioembolism, hypercoagulable states, hemorrhage, hypertension, and amyloid or arteriovenous malformation.

Embolism

Estimates suggest that 15-30% of all strokes are thought to be of embolic etiology. The remaining cases have either an undetermined or a combined etiology or else are caused by dissection.^[1] Most of the sources in the literature support embolism as the primary etiology of middle cerebral artery (MCA) strokes.

Specifically, in a study by Moulin and coauthors, cardioembolism accounted for approximately 50% of total MCA strokes, 34% of deep MCA strokes, and 41% of cortical strokes.^[2] This same study, with a relatively large cohort, suggests that cardioembolism may be greatly underdiagnosed and may play a more common role in posterior and anterior cerebral strokes than previously thought.

The study also revealed paroxysmal atrial fibrillation in 65% of all stroke patients studied. This cardiac abnormality may be a common poststroke sequela, but its frequent occurrence certainly supports the need for cardiac monitoring and a high index of suspicion for cardioembolism in formulating a complete differential diagnosis.

Additionally, embolic strokes can occur through the atheromatous plaques of carotid disease. All of these data support widely accepted diagnostic studies, including carotid Doppler studies, transesophageal echocardiography studies, and telemetry to elucidate and treat pathology and prevent future embolic events.

The location of MCA stroke depends largely on the size of the embolic mass. Occlusion at the stem is rare and requires embolic matter of at least 3-5 mm. Emboli can arise because of intravascular, rigid foreign matter (eg, shotgun pellets, catheter tips, large thrombi combined with bacteria) or as a result of large calcific plaques formed through direct internal carotid trauma or puncture.

The etiology of occlusion of smaller and surface branches obviously is more diverse and most commonly involves cardiogenic emboli or material from an ipsilateral site of carotid atherosclerosis. Other sources of emboli include spontaneous dissection of a carotid artery, material from breast metastasis, a marantic embolus, fungal endocarditis, and paradoxical emboli due to a patent foramen ovale.

Embolization occurs with equal frequency in the right and the left MCA. Angiography reveals that these occlusions are usually found in the first 24 hours, but the vessels are generally patent within 48 hours. A persistent occlusion has a less favorable prognosis. The size of the infarct also depends on the collateral circulation, which is highly variable as a result of congenital vascular patterns and collateral vascular development secondary to long-standing atherosclerosis.

Indirect ischemia

Distal territories of the MCA are quite vulnerable to ischemia because of failure of perfusion due to arrhythmia and other causes of hypotension. Such compromise in circulation is especially significant in patients with carotid artery stenosis. The prevalence of strokes of this type is uncertain, but they are not thought to be uncommon, given the high correlation of carotid stenosis with distal territory stroke.

Atherosclerosis

Primary atherosclerosis of the MCA and branches accounts for only 7-8% of symptomatic MCA disease. Furthermore, many of these cases probably represent recanalized embolism and not true atherosclerosis.

Thrombosis

Although thrombotic occlusion of small and large vessels is still widely accepted as the primary etiology of strokes in general, causing approximately 51% of all strokes in the anterior, middle, and posterior cerebral vasculature combined, it is a relatively rare cause of MCA strokes. Only about 2-7% of ischemic events in the MCA territory are due to thrombotic occlusion. The diagnosis can be excluded using repeat angiography, but this is of questionable utility.

Other causes

Amyloid angiopathy is a rare etiology for lobar cortical strokes in elderly patients. Dissection and stenosis of the MCA are rarely documented as causes of MCA stroke.^[1]

Etiology in younger persons

Hemorrhagic stroke is the most common etiology in younger persons (aged 18-45 y), with intracranial hemorrhage accounting for 41% and subarachnoid hemorrhage accounting for 17% of strokes in persons in the younger age group. The remaining 42% of strokes due to ischemia generally require a more exhaustive workup to elucidate an etiology. Consider carotid or vertebral dissection, collagen-vascular disease, and coagulopathies.

Studies reveal that dissection is an underrecognized cause of stroke in younger populations. Still, even with advances in diagnostic options, 20% of strokes in younger persons continue to be of unknown etiology.

The frequency of middle cerebral artery (MCA) stroke in the United States is reported to be more than 80 cases per 100,000 people. According to Barnett and colleagues, most strokes occur in the MCA territory of cerebral circulation.^[3]

A systematic review of stroke incidence worldwide found that between 1970 and 2008, stroke incidence decreased 42% in high-income countries and increased more than 100% in low- to middle-income nations; between 2000 and 2008, the overall stroke incidence in low- to middle-income countries was 20% higher than that in high-income countries.^[4] This review did not distinguish between MCA strokes and other cerebrovascular accidents (CVAs).

The risk of MCA stroke increases with age. The highest incidence of MCA strokes is in the seventh and eighth decades of life; the incidence in younger persons (aged 18-45 y) is far lower. Hemorrhagic stroke is the most common etiology, with intracranial hemorrhage accounting for 41% and subarachnoid hemorrhage accounting for 17% of strokes in persons in the younger age group.

Males are affected by MCA strokes more often than are females, with a male-to-female ratio of 3:1.

Ethnic minorities, specifically African and Mexican Americans, are at a significantly higher risk for ischemic stroke. One study revealed the total prevalence to be 191 strokes per 100,000 people surveyed in the black population, 149 strokes per 100,000 people surveyed in the Hispanic population, and 88 strokes per 100,000 people surveyed in the white population.^[5]

Basic physical findings

Patients with middle cerebral artery (MCA) stroke syndrome may have some basic physical findings, as follows.

Main trunk occlusion of either side yields contralateral hemiplegia, eye deviation toward the side of the MCA infarct, contralateral hemianopia, and contralateral hemianesthesia. Eye and head deviation toward the side of the lesion is probably due to damage of the lateral gaze center (Brodmann area 8), or it can represent classic neglect, particularly when the right MCA is involved.

Trunk occlusion involving the dominant hemisphere causes global aphasia, whereas involvement of the nondominant hemisphere causes impaired perception of deficits (anosognosia) resulting from the stroke and more qualitative deficits of speech.

Superior division infarcts lead to contralateral deficits with significant involvement of the upper extremity and face and partial sparing of the contralateral leg and foot.

Inferior division infarcts of the dominant hemisphere lead to Wernicke aphasia. Such infarcts on either side yield a superior quadrantanopsia or homonymous hemianopia, depending on the extent of infarction. Right inferior branch infarcts also may lead to a left visual neglect. Finally, resultant temporal lobe damage can lead to an agitated and confused state.^[6]

Specific neurologic sequelae

Loss of consciousness may occur. Initially this is rare after MCA stroke, but it occurs slightly more often than in vertebrobasilar strokes (8.4% vs 5.7%).^[7] Loss of consciousness most often is attributable to seizures, but it may result from secondary edema and subsequent brainstem herniation.

Motor deficits (hemiparesis and hemiplegia) may become apparent. Surprisingly, assigning clear-cut syndromes of weakness to specific territories of MCA infarct has posed a significant challenge. The prognosis of such motor deficit also has not completely been elucidated, with case reports of remarkable recovery from dense limb involvement.

Partial hemiparesis patterns have been mapped more readily to certain MCA territory infarcts. The National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) data bank project gathered pilot data from 488 patients with unilateral hemisphere strokes.^[8] The following conclusions arose from the analysis of the project data:

• Equivalent weakness of the hip, foot, shoulder, and hand was the most common finding among the patients in the NINCDS project, accounting for 71.2% of cases.
• Hemiparesis with distal predominance describes another 23.5% of cases, with weakness of the lower face, lower legs, toes, fingers, and forearm and sparing of the forehead and proximal muscles of the upper and lower extremities. The resultant deficit is believed to be due to the large representation of the affected muscles in the homunculus.

Faciobrachial paresis describes weakness of the lower face, jaw, tongue, oropharynx, and ipsilateral upper extremity. The weakness of the upper extremity is often more pronounced in the distal musculature of the hand and forearm.^{[9, 10]} These deficits result from ischemic insult of the insula and operculum.

Although uncommon, movement disorders such as athetosis, chorea, and dystonia have been described as sequelae of MCA territory stroke.

Visual deficits are common. Hemianopia has long been known to accompany the syndrome following a large MCA infarct; yet, only the superior portion of the optic radiation is supplied by the MCA. The resultant hemianopia is probably due to a massive infarct with subsequent edema affecting adjacent structures. Quadrantanopsia can be attributed to a parietal infarct affecting the deep fibers of the upper optic radiation; however, this condition is rare.

Neglect, in its classic form, has been attributed to parietal insult, but data from positron emission tomography (PET) scanning reveal that frontal lesions can cause similar but more transient sequelae.

At times, visual neglect is difficult to distinguish from hemianopia. Subtle signs (eg, a patient who responds to a stimulus from the left by turning right and also fails to blink upon threatening stimuli to the affected side) can aid in diagnosing neglect. Patients with visual neglect often have difficulty naming objects presented on the affected side.

Motor neglect with underuse of the side contralateral to the cerebral insult appears much like a hemiparesis. Special efforts must be made by the examiner to encourage the patient to demonstrate strength and dexterity.^[11] Typically, the patient has delayed withdrawal to noxious stimuli, fails to place the affected hand in the lap when seated, and falls heavily to the affected side with no apparent effort to minimize impact.

Autonomic dysfunction after MCA stroke often can be evidenced by contralateral edema of the hand and foot arising within hours of the infarct and lasting up to 2 weeks. This edema is in contrast to the dependent edema that develops subacutely in the distal aspect of a plegic extremity. Excessive sweating contralateral to the territory of an MCA stroke can be indicative of a larger lesion, affecting deep and superficial branches.^[12]

Manifestations of left (dominant) hemisphere infarction

The left cerebral hemisphere is dominant for speech and language in more than 95% of right-handed individuals. Defining cerebral dominance for left-handed individuals is more difficult, but most left-handed patients also appear to have a dominant left hemisphere. One study analyzing left-handed patients with aphasia showed that 60% had lesions confined to the left hemisphere.^[13] Other studies reveal bilateral speech representation in as many as 15% of left-handed patients.

The specific manifestations of left hemisphere infarction largely fall under the heading of either aphasia (or dysphasia) or apraxia (dyspraxia).

Ischemic injury to the sylvian fissure of the dominant hemisphere is the lesion most likely to lead to dysphasia. Describing deficits in speech may be easier if pathologies are categorized as fluent versus nonfluent. In this context, fluent does not describe correct use of language or grammar but simply the ability to produce sounds readily. Nonfluent dysphasia describes a deficit in which a difficulty in producing words or sounds is appreciated.

Surprisingly, studies have revealed patients with only mild speech deficits, despite localized infarcts in cerebral areas thought to be essential for speech and language. Such studies suggest a major role of deeper structures, particularly the thalamus, in this function.

Broca aphasia, also termed expressive or motor aphasia, describes the ability to comprehend written and spoken language, with nonfluent or impaired expression of either spoken or written language.^[14] The infarct responsible for Broca aphasia encompasses the insula and frontoparietal operculum.

Global aphasia can be assumed wrongly in these patients if the examiner does not use comprehension testing with simple questions. Initially, the patient’s profound impairment is difficult to differentiate from a global aphasia, and only later does a speech disturbance arise that is isolated to writing (agraphia) and speech production.

Wernicke aphasia, also termed receptive or sensory aphasia, is caused most often by occlusion of the lower division of the MCA bifurcation or one of its branches. The infarct responsible for a classic Wernicke aphasia includes the dominant posterior temporal, inferior parietal, and lateral temporo-occipital regions.

Unlike patients with motor aphasia, patients with Wernicke aphasia vocalize smoothly and with expression, but they demonstrate paraphasias or speech with distorted phonetic structure, word substitution, and additional prefixes and suffixes. Their speech is fluent but is often missing key words and ideas and may be perseverative. Patients demonstrate pure-word deafness, with the inability to repeat words, along with alexia, the inability to recognize or comprehend written language.

The classic cause of conductive aphasia is thought to be a disruption of neural pathways or of the arcuate fasciculus connecting the motor and sensory areas concerned with speech.^[15] The clinical features of conductive aphasia are not explained completely by this theory. Distinguishing a conductive aphasia is an especially difficult challenge for the clinician.

Patients with conductive aphasia have significant difficulty repeating unfamiliar phrases and words and demonstrate much better auditory and written comprehension than do individuals with Wernicke aphasia; however, patients with conductive aphasia are more likely to recognize the deficit and to make an effort to self-correct.

Anatomically, insult to the isolated arcuate fasciculus is believed to be responsible for the symptoms; however, scant case reports actually document such a correlation. In fact, patients with the described syndrome more frequently have more superficial infarcts involving 1 or 2 recently discovered tracts.

Agrammatism describes the shortened speech patients use to communicate. These individuals sometimes utter only individual words to communicate an idea.

Apraxia refers to the inability to perform a previously learned task despite preserved strength, vision, and coordination. When referring to apraxia, Mohr states, “Motor engrams (programs) that guide skilled acts have either been lost or cannot be accessed.”^{[14, 8]} Generally, the ability is impaired rather than eliminated; thus, the term dyspraxia is more appropriate.

The most common form of apraxia is ideomotor apraxia, in which a disconnection is thought to exist between the cortex containing plans for movement and the cortex responsible for execution. On verbal command, the patient is uncoordinated in or is unable to perform simple tasks, such as imitating the use of a hammer and nail. Often, the patient performs the actual task with much greater precision. Aphasia and apraxia occur independently, and the cortex responsible for motor planning is thought to be in the superior parietal lobe.

Callosal apraxia is similar to ideomotor apraxia but only involves the nondominant arm.

Ideational apraxia describes an impaired ability to complete more complex multistep tasks, such as obtaining a glass of water. Not all experts agree that ideational and ideomotor apraxias are distinct entities.

Limb-kinetic apraxia refers to an impaired clumsy manipulation of objects in such tasks as combing one’s hair. Limb-kinetic apraxia can be accompanied by ataxia, choreoathetosis, spasticity, and weakness. Even after repeated efforts, performance only slightly improves.

Oral-buccal-lingual apraxia describes an impaired ability to perform complex movements of the tongue and face upon command.^[16] Often these movements are performed spontaneously. This condition coexists with Broca aphasia in 90% of patients; however, the 2 disorders often exist independently.

In the context of speech disturbances, the term dyspraxia is used to describe impaired cooperation of the oropharyngeal and respiratory elements necessary for speech. Individuals with this condition have a hesitant and somewhat telegraphic verbal response.

Manifestations of right (nondominant) hemisphere infarction

Motor deficits following infarction of the nondominant hemisphere parallel those described after infarction of the dominant hemisphere. Additionally, lesions of the nondominant hemisphere can lead to a variety of behavioral abnormalities. These behavioral deficits correlate much less to location and extent of the infarction than do deficits following infarcts of the dominant hemisphere, and some are predictive of an unfavorable long-term outcome after rehabilitation. Insults of the nondominant hemisphere can affect attention, leading to neglect and impersistence.

The term extinction is used to describe inattention to one stimulus when 2 stimuli are presented simultaneously. Generally, the ignored stimulus is on the left side.

The term neglect is used to describe “a lack of responsivity to stimuli on one side of the body, in the absence of any sensory or motor deficit severe enough to account for the imperception.”^[17] In a stroke population studied by Battersby and coauthors, such unilateral neglect occurred in 29% of patients with right-sided brain damage versus 12% of patients with left-sided brain damage.^[18]

In severe cases, the patient often ignores tactile, visual, and auditory stimuli on the left side and is turned chronically to the right side. When asked to bisect lines, the patient often does this far to the right of center. Unilateral spatial neglect is a subtler deficit, in which the patient may fail to read words or recognize figures to the left of midline.^[19] More sizable infarcts lead to anosognosia or imperception of field neglect and imply a much less favorable prognosis.

The term impersistence is used to describe an inability to persist in performing motor tasks; it is often accompanied by visuomotor and visuospatial deficits.^{[20, 21]} This impairment places the patient at risk for an unfavorable rehabilitation outcome.

The term dressing apraxia applies to a condition in which the patient is unable to dress without assistance, despite having no apparent hemiplegia that would prevent the performance of this function. It is a much more common finding in cases of right-hemisphere infarcts and is attributable to difficulty distinguishing right from left and up from down.

The term topographic memory deficit is used when individuals become lost in familiar surroundings. The finding often follows right-hemisphere insults.

General confusion and delirium often are more commonly appreciated in patients with damage to the nondominant hemisphere than in those with injuries to the dominant hemisphere.^[22] The central role the right hemisphere plays in attention, vigilance, and distinguishing stimuli is probably responsible for this common presentation.

Confabulation or unintentional fabrication of information is largely due to an inability to recognize errors, disinhibition, and memory deficits. These deficits all are common with damage to the nondominant hemisphere and to the frontal lobe.

The term constructional apraxia describes a difficulty in manipulating objects in space. This type of apraxia can be appreciated by having affected patients copy designs or build 3-dimensional models. This tendency is more common with right-sided lesions than with left-sided lesions, as is evident in a population of 67 patients with constructional apraxia studied by Piercy and colleagues.^[23] In this group, 25 had left-sided damage and 42 had damage to the right hemisphere.

The apraxia of patients with a dominant-hemisphere infarct often is described as decreased attention to detail. The apraxia with right-side damage is consistent with neglect, in which features to the left of midline are ignored.

The term allesthesia describes sensory referral. For example, a patient touched on the left side feels the touch on the right.

The terms aprosody, lack of intonation in speech, and affective agnosia refer to the inability to perceive or comprehend emotional intonation of speech. These deficits often coexist and correlate with lesions in the right temporoparietal region.

Complications

Spasticity (ie, velocity-dependent resistance to passive range of motion) is often seen as a result of stroke. This can lead to several complications, including loss of function, pain, skin breakdown, and heterotopic ossification.

Initially, the treatment of noxious stimulation, such as infection, skin breakdown, and pain, should be pursued. Further management generally involves a combination of therapy, bracing, and medication, sometimes combined with focal neuromuscular blockade with botulinum toxin or, more rarely, with neurolysis with phenol.

Surgical intervention, such as tenotomy, is generally reserved for the most severe cases in which function can be gained or severe pain relieved.

The differential diagnosis for middle cerebral artery stroke includes the following:

• Conversion Disorder
• Hypoglycemia
• Migraine Headache
• Subdural Hematoma

Other problems to be considered are as follows:

• Focal seizure
• Tumor
• Common neurologic deficits after stroke

The acute medical management of stroke starts with the basics of airway and breathing and moves on to the performance of tests and studies, such as the following, to obtain pertinent information and laboratory values:

• Electrocardiography - Electrocardiography is essential in all stroke patients in the acute phase of care in order to evaluate for arrhythmias that would predispose a patient to embolic events (eg, atrial fibrillation).
• Chest radiography
• Oxygen saturation and blood gas determination
• Urinalysis and blood culture if fever is present

Blood studies include the following:

• Complete blood count (CBC)
• Erythrocyte sedimentation rate
• Cardiac enzyme levels
• Electrolyte values
• Serum glucose values
• Creatinine and blood urea nitrogen (BUN) levels
• Liver function testing
• Coagulation profile (ie, prothrombin time and international normalized ratio, activated partial thromboplastin time)
• Toxicology screen
• Human chorionic gonadotropin level (if appropriate)

In younger patients, tests may include protein C and protein S values, antithrombin III deficiency testing, and mutational analysis for the factor V Leiden gene. Additional tests may also be indicated to assess for associated conditions, such as deep venous thrombosis (DVT), pulmonary embolism, dysphagia, and urinary dysfunction.

Transcranial Doppler ultrasonography uses low-frequency pulsed sound waves to detect intracranial vessels. It is used primarily in major stroke centers and neurologic intensive care units as a noninvasive technique to evaluate the patency of intracranial vessels.

Middle cerebral artery (MCA) patency has prognostic significance. A meta-analysis of transcranial ultrasonographic studies in acute stroke found that MCA occlusion was associated with a significantly increased risk for death, whereas MCA patency was associated with an increased likelihood of clinical improvement within 4 days. A significant association was also found between full recanalization within 6 hours after symptom onset and clinical improvement within 48 hours.^[24]

Carotid duplex ultrasonography is useful to establish the source of embolic strokes once the patient is stabilized. Carotid ultrasonography or Doppler is also useful in defining carotid artery stenosis.

Generally, Doppler ultrasonography is the study of choice to evaluate for DVT. Detection of DVT is vital because such thromboses can lead pulmonary embolism, which is the most common cause of death in the 2-4 weeks following a stroke. The risk from subsequent anticoagulant use is much lower than that from untreated DVT).

Computed tomography (CT) scanning is the preferred study, being accessible, fast, and highly sensitive for excluding or confirming hemorrhage.^[25] However, it is less sensitive than is magnetic resonance imaging (MRI) for the diagnosis of stroke within the first few hours of symptoms.

Spiral CT scanning is the study of choice to evaluate for pulmonary embolism in stroke patients with dyspnea, pleuritic chest pain, tachypnea, tachycardia, or hypoxemia. Blood gas measurement or oxygen saturation determination is often an unreliable measure to assess for this serious disorder.

CT angiography provides an image of the perfusion status of the brain parenchyma.^{[25, 26]} It can be performed immediately after an initial CT scan and requires only an additional 5 minutes of imaging time. The combination of CT scanning and CT angiography greatly increases the diagnostic value of CT scanning in stroke patients.

MRI has excellent sensitivity for early diagnosis (see the image below) but is limited by access and cost. MRI provides 2 different types of images, diffusion-weighted and perfusion-weighted. Diffusion-weighted imaging can detect ischemic injury within 15-30 minutes of onset. It shows evidence of ischemic injury but not ischemia itself. One study found that diffusion-weighted MRI was significantly superior to CT scanning in the diagnosis of acute (< 6 h) stroke.^[27] Perfusion-weighted imaging shows the actual zone of ischemic injury.

Barium swallow

Aspiration due to dysphagia is a common sequela following MCA stroke. Modified barium swallow is still the most commonly used means to document and assess the severity of dysphagia.

Fiberoptic endoscopy

Fiberoptic endoscopic evaluation provides real-time images similar to those from videofluoroscopy, with additional advantages. The procedure can be performed at the bedside, uses food rather than contrast, can be repeated often, without radiation exposure, and is tolerable for longer periods.

Echocardiography

Transthoracic and transesophageal echocardiography are also recommended to evaluate for a cardiac or aortic source in embolic strokes. If no thrombus is seen with transthoracic echocardiography but cardioembolic stroke is suspected, transesophageal echocardiography is performed.

Voiding analysis

Urinary dysfunction is not uncommon after stroke and can lead to infection and more serious consequences, such as urosepsis, hydronephrosis, and renal failure. Generally after a stroke, patients have disinhibited bladder function with recurrent detrusor spasticity and incontinence. This problem can often be addressed with frequent, scheduled voiding times. However, sometimes urinary retention can occur and must be detected early to prevent serious complications.

Portable bladder scanners are an important tool to assess bladder volume before and after voiding. Straight catheterization also serves this function but, obviously, is more invasive.

The histologic character of the middle cerebral artery (MCA) and its branches differs from that of extracranial vessels, with a thinner adventitia and media, thicker internal elastic lamina, and no vasa vasorum. These characteristics may reflect less stretch to the vessel and its branches than is common in arteries perfusing other tissues. The thicker lamina may serve to decrease or dampen wide pulse pressure.

Initial and postacute management of stroke

Most patients who have experienced a stroke have other comorbid diseases and are at an increased risk of an adverse cardiac event during the immediate poststroke phase.

Meticulous management of hypertension, diabetes, atrial fibrillation, congestive heart failure, and pulmonary diseases (eg, sleep apnea, chronic obstructive pulmonary disease) is essential in assuring maximal functional outcome from rehabilitation. Additionally, cardiac parameters and precautions must be monitored and used throughout the course of the patient’s acute and rehabilitative course of care.

In a single-blind cluster, randomized, controlled trial, stroke patients in acute stroke units (ASUs) were evaluated 90 days after hospital admission. ASUs were randomly appointed to intervention (n=10) or control (n=9). Those patients who received a multidisciplinary intervention focusing on evidence-based management of fever, hyperglycemia, and swallowing dysfunction were much less likely to be dead or dependent at 90 days, despite the severity of the stroke, compared with the control ASU patients.^[28]

Control of serum glucose level

Managing hypoglycemia and hyperglycemia is important. Evidence supports the association of acute and significant hyperglycemia with poor outcomes, leading to conditions such as intracerebral hemorrhage and, ultimately, a dependent state.

Several points about glucose management in acute stroke have been noted. Hyperglycemia increases lactate production in the brain, and this facilitates the transition of hypoperfused, at-risk tissue into infarction. The American Stroke Association (ASA) guidelines recommend treating hyperglycemia with fluids and insulin to achieve a level of less than 300 mg/dL.

Control of blood pressure

Hypertension is a major risk factor for cerebrovascular accident (CVA). However, acute reduction of blood pressure (BP) in the event of a stroke does not necessarily benefit the patient. The initial rise in BP after a stroke is believed to act as a neuroprotective response to increase blood flow to the brain.

The data on BP management in acute stroke is very controversial and ambiguous. The consensus of the 2007 Scientific Statement from the Stroke Council of the ASA states that, pending further data, antihypertensive agents should not be used unless the diastolic BP is greater than 120 mm Hg or the systolic BP is greater than 220 mm Hg.^[29]

Encouraging data emerged in 2009 with the publication of a randomized, controlled, double-blind pilot trial that investigated lowering of BP in 179 patients with systolic BP greater than 160 mm Hg within 36 hours of symptom onset: in this trial, treatment with lisinopril or labetalol reduced 3-month mortality by half.^[30]

If treatment is necessary, agents such as labetalol are recommended because they can be titrated easily and because they minimally affect the cerebral blood vessels. Oral agents such as nicardipine and captopril are also recommended.

Patients who are candidates for thrombolytic agents must be specifically managed, and the physician must follow guidelines for BP control.

Normalization of body temperature

Fever appears to be related to stroke severity, infarct size, mortality, and outcome in persons with an acute CVA. For each 1°C increase in body temperature, the relative risk of poor outcome rose by 2.2.

A reasonable plan is to keep the patient normothermic with acetaminophen. However, a Cochrane review found no evidence from randomized trials to support routine use of pharmacologic or physical strategies to reduce temperature in patients with acute stroke.^[31]

Thrombolysis

Thrombolysis remains a controversial topic, and it is still undergoing much research to weigh the risks and benefits in acute stroke treatment.

The only therapy currently approved by the US Food and Drug Administration (FDA) for acute stroke is intravenous alteplase, a recombinant tissue-type plasminogen activator (tPA).^[32] This appears to improve functional outcome at 3 months if given within 3 hours of the onset of symptoms and the patient meets the rigorous criteria for treatment.

In 2009, however, the American Heart Association (AHA) and the ASA published a science advisory recommending that the time window for tPA administration be increased to 4.5 hours after a stroke, though this change has not been approved by the FDA.^[33]

Research indicates that tPA is effective in patients even when administered within the 3- to 4.5-hour window,^{[34, 35, 36]} but the AHA/ASA stated that, despite its recommendation, the effectiveness of tPA administration in comparison with other treatments for thrombosis, within that time period, is not yet known.

The eligibility criteria for treatment between 3 and 4.5 hours are similar to those employed for treatment prior to 3 hours, as established in the AHA/ASA’s 2007 guidelines,^[29] but with the exclusion criteria expanded to include any of the following patient characteristics:

• Age greater than 80 years
• Use of oral anticoagulants
• Baseline National Institutes of Health (NIH) Stroke Scale score >25
• A history of both stroke and diabetes

The major studies that have evaluated the use of alteplase are the National Institute of Neurological Disorders and Stroke (NINDS) trial, the Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS) trial,^[37] and the European Cooperative Acute Stroke Study (ECASS) trial, which together have included 2775 patients.

The practical use of thrombolytic agents is very limited because only approximately 22% of CVA patients present to an emergency department within 3 hours of the onset of symptoms, and only approximately 8% meet all the eligibility criteria. For more details on thrombolytic treatments and eligibility, see Medical Treatment of Stroke.

Anticoagulation

Anticoagulants (heparin and low-molecular-weight heparin) are often used in the acute stroke inpatient setting to prevent recurrent stroke and to improve the outcome for neurologic function. They are also used at lower, prophylactic doses to prevent deep vein thrombosis (DVT) and subsequent thromboembolism.

A Cochrane review looked at 24 trials involving 23,748 patients and concluded that anticoagulants did not reduce the patients’ odds of dying or of becoming dependent. Nine in 1000 fewer recurrent strokes occurred in treated patients; however, 9 in 1000 had an increase in intracranial hemorrhages. Fewer pulmonary emboli were reported, but this was offset by the number of major extracranial hemorrhages.^[38]

The ASA’s recommendations and guidelines on antithrombotic therapy issued in 2008, by the Eighth American College of Chest Physicians (ACCP) Consensus Conference, do not recommend full-dose anticoagulation treatment for acute stroke patients (except in very specific patient populations).^[39]

Efficacy of poststroke rehabilitation

Justification for rehabilitation can be challenging in this era of tight resource management; however, one randomized, prospective study noted a correlation between admission to rehabilitation units versus medical stroke units to shorter length of hospital stay, increased functional gains on discharge, and an actual decrease in the duration and amount of therapies provided. Surprisingly, this same study noted no difference in the rate of discharge to home.

Another study randomizing patients to stroke rehabilitation versus medical stroke units noted that stroke rehabilitation admission correlated with increased functional independence and decreased 6-week mortality. A meta-analysis of 8 studies and 1586 patients revealed that rehabilitation at stroke units also significantly reduced mortality at 3 months and 1 year after stroke.^[40]

Time delay before rehabilitation admission was an important factor in ideal outcomes. Specifically, admission within 72 hours after cerebrovascular accident (CVA) correlated with decreased length of stay and increased gains in activities of daily living and ambulation.

A retrospective, cohort study determined that 1 year after a stroke, the rate of patient survival differed based on postacute care rehabilitation services. Patients who received care from an inpatient rehabilitation hospital, either through home health or outpatient services, had better 1-year survival than those who were admitted to a skilled nursing facility. Variables such as age, sex, race or ethnicity, history of a previous stroke, comorbid conditions, and service area also were significantly linked with 1-year mortality.^[41]

A study compared the outcomes of poststroke patients in 9 different hospital units (ie, 6 stroke rehabilitation units and 3 general rehabilitation units).^{[42, 43]} A total of 1437 patients were studied; patients in an inpatient multidisciplinary rehabilitation setting had a statistically significant reduction in the odds of death, institutionalization, and dependency.

The benefits of stroke units appear to extend beyond level I institutions. An Australian study that analyzed 17,659 admissions for ischemic stroke in 22 hospitals before and after the rollout of stroke units found that in smaller hospitals, the introduction of stroke units resulted in decreased deaths, increased discharges to home, and decreased discharges to nursing homes.^[44]

Determining the poststroke time frame in which therapies are no longer efficacious is also complex. One study examined a patient population at 1 year following stroke. These patients received 5 weeks of outpatient rehabilitation, undergoing daily 2-hour sessions of physical and occupational therapy. Significant gains in activities of daily living skills, balance, and weight shifting were noted.

Physical therapy

Rehabilitation can be explained as the planned withdrawal of support in order to enable the patient to become as independent as possible. This is achieved by an interdisciplinary team of professionals, one member of which is the physical therapist. Physical therapists work with patients to help them regain motor control,^[21] strength, physical conditioning, and mobility and to help them return to independent living.

In rehabilitation for patients who have suffered a middle cerebral artery (MCA) stroke, the emphasis is on patient and family/caregiver education, which includes involvement of the patient and the family in goal setting and in planning and implementing treatments. Within all disciplines, attention must also be given to psychological and social issues.

Rehabilitation after a stroke is very team oriented. All team members are involved in developing a comprehensive discharge plan, for which the goal is a smooth transition to the community. This includes promotion of social reintegration and resumption of roles in the home and family, as well as in the recreational and vocational domains.

Physical therapy in a rehabilitation facility begins with a comprehensive evaluation of motor function, mobility, balance, coordination, sensation, and proprioception. Tests used to measure these include, but are not limited to, manual muscle testing, postural evaluation, gait analysis, functional assessment, and the Berg balance scale test.

The team also evaluates family/caregiver support and the patient’s living environment, which aides in the discharge plan. Goals that are measurable and realistic are set by the patient, family, and rehabilitation team, and these goals are reevaluated at regular intervals.

Toward the goal of enabling the patient to become as independent as possible, several different treatment techniques are used by the physical therapist. These include neurodevelopmental technique (NDT), proprioceptive neuromuscular facilitation (PNF), balance training, manual therapy, neuromuscular electrical stimulation (NMES), biofeedback, aqua therapy, myofascial release, frequency-specific microcurrent, and cardiovascular training. For example, independent ambulation is often an important goal that requires several stages of recovery.

Initially, patients exhibit poor trunk control, are unable to bear weight on the affected extremity, and are unable to advance the leg during the swing phase of gait. Initial physical therapy therefore focuses on posture, trunk control, and weight transfer to the hemiparetic lower extremity.

Treatment often begins with NDT- or PNF-based mat exercises or with balance work on a Swiss ball to gain trunk control. Progression is to standing weight-bearing and weight-shift exercises, which lead to the patient taking his/her first steps in the parallel bars; this may be coupled with NMES to enhance muscle function.

Partial body weight–supported gait training may be performed on or off the treadmill, with the patient safely secured in a harness system that supports varying degrees of the patient’s body weight. This allows the therapist to assist the patient in achieving a more natural, sustained gait pattern earlier in the stages of recovery than would otherwise be possible. The final step is gait either with or without an assistive device, such as a walker or cane, depending on the patient’s level of function.

Many different types of adaptive devices and durable medical equipment are also available to assist the patient in becoming more independent. For example, many patients have weakness of ankle dorsiflexion and require an ankle-foot orthosis to prevent foot drop and maintain knee extension during weight bearing. Physical therapists also assist in proper fitting of a wheelchair for a patient to allow more immediate increased independence from a wheelchair level while continuing to work towards independence with walking.

Although the physical therapist is an integral part of the rehabilitation team, the most important part of that team is the patient, and his or her drive to succeed is imperative for a successful outcome.

Occupational therapy

Occupational therapists specialize in retraining patients to perform activities of daily living. They teach and develop strategies for the patient and rehabilitation team to enhance patient success in independence. This may include the use of adaptive equipment or compensatory strategies or the redevelopment of skills that were lost because of motor function, perception, and cognitive deficits.

A systematic review of 112 studies from 2003 through 2008 provides support for clinical recommendations and evidence-based protocols for cognitive rehabilitation for those with traumatic brain injury (TBI) and stroke. Interventions for attention, memory, social communication skills, executive function, and for comprehensive-holistic neuropsychologic rehabilitation are supported. Additionally, evidence supports visuospatial rehabilitation and interventions for aphasia and apraxia after right hemisphere stroke and left hemisphere stroke, respectively.^[45]

Initially, the focus is often basic self-care. This then progresses to higher-level activities in homemaking and eventually to training for a return to work. These skills frequently require the mobility and strength developed in physical therapy and the cognitive retraining acquired in speech therapy. Caregiver training and education is always part of a patient’s treatment; they are imperative aspects of the patient’s recovery.

The occupational therapist combines the skills developed from all the disciplines into an ability to perform functional tasks. The occupational therapist also may complete home evaluations to assist in discharge planning and to make home modifications and equipment recommendations.

The occupational therapist also assists in upper extremity rehabilitation. The therapist assesses the range of motion, muscle strength, and sensation of the upper extremities. These assessment skills are essential in helping the patient to regain optimal function and to prevent injury, such as increased subluxation, contractures, or loss of range of motion in the wrist and finger flexors. To prevent patient injury, a wrist-hand orthosis is often used to prevent excessive flexion and extension and to maintain a functional position.

Occupational therapists can be trained in multiple methods to reeducate a hemiparetic limb. Common treatment philosophies for remediating motor control, such as Bobath NDT, Brunnstrom movement therapy, and PNF, are often used in combination with activities of daily living to regain muscle function and skill. Other modalities used in therapy include electromyography, biofeedback, and electrical stimulation.^[9]

A controversial method of upper extremity rehabilitation is the application of constraint-induced movement therapy (CIMT). This involves the forced use of a paretic limb by restraining the nonaffected limb for a short time. A randomized, controlled trial in 52 patients undergoing inpatient stroke rehabilitation found that CIMT was no more effective than traditional therapy^[46] ); in addition, patients who received high-intensity CIMT showed significantly less improvement at day 90, indicating an inverse dose-response relationship.

The trend of decreasing length of stay in acute rehabilitation facilities has lessened the use of such modalities, with more emphasis on compensatory techniques using the nonaffected limb.

Occupational therapists strive to develop treatment plans that are client centered and purpose driven. They serve a unique place in the rehabilitation team, enhancing patient recovery by acting as the “glue” between therapies, medical clinicians, and families.

Speech therapy

The speech-language pathologist (SLP) specializes in the assessment and treatment of communication and swallowing disorders that can follow a CVA, including aphasia, apraxia of speech, dysarthria, and dysphagia. CVA-related cognitive deficits may also impact communication and swallowing secondary to decreased attention, memory, and problem solving.

Aphasia assessment and treatment focus on expressive and receptive language skills. Expressive language treatment targets the ability to code thoughts and ideas into verbal expression, written language, and gestures. Treatment of receptive language addresses the ability to comprehend verbal and written expression and gestures.

Communication techniques for individuals with aphasia depend on the levels of expressive and receptive abilities indicated by the SLP through ongoing assessment. Techniques may include speaking slowly while using shorter, simpler sentences and environmental cues.

Speech therapy also manages communication deficits associated with apraxia of speech. After determining the range of deficits, treatment should focus on the systematic practice of sound production. Treatment should begin with simple sounds and then proceed to complex sound combinations, carefully moving the patient from automatic to spontaneous speech.

With severe apraxia of speech, a combined use of verbal expression, gestures, writing, and augmentative devices may be needed to communicate. To reduce the stress of communication, patients often require extra time to respond. Also, background noise and distractions should be minimized.

Following a CVA, dysarthria may result from impaired muscular control, due to problems such as weakness, incoordination, or paralysis of speech musculature. Areas that may be involved include respiration, phonation, articulation, prosody, and resonance. Each aspect of this speech system affects the overall intelligibility and normalcy of speech. The SLP works to strengthen and modify affected aspects by implementing exercise programs and the use of compensatory strategies to improve speech production.

Swallowing difficulties also may result from a CVA, occurring largely due to weakness, incoordination, and decreased sensation of the swallowing system. Dysphagia refers to impaired oral, pharyngeal, and esophageal phases of swallowing. Dysphagia may lead to poor nutrition or to complications from aspiration during oral intake. The SLP specializes in assessing dysphagia through different types of swallowing evaluations.

A bedside swallowing evaluation involves careful observation of swallowing behaviors with trials of food and liquid. Using instrumentation to observe the swallow may be indicated if swallowing safety and rehabilitation needs cannot be addressed through a bedside evaluation. Most commonly, videofluoroscopy or fiberoptic endoscopic evaluation of swallowing (FEES) provides objective assessment of swallowing function and airway protection.

Based on these assessments, the SLP may implement diet modifications, swallowing techniques and postures, strengthening programs, and assessments for improvements in response to treatment.

The SLP is also involved in the rehabilitation of cognitive deficits resulting from a CVA. The SLP is trained in providing treatment that addresses impairments in attention, memory, perception, organization, reasoning, and problem solving. After determining cognitive deficits, treatment consists of functional goals for increased independence.

The SLP can provide strategies for better communication with the individual. Such strategies may include decreasing external stimulation or distractions and providing verbal and written information. In addition, repetition of important information and tasks may improve the individual’s understanding and recall. The SLP reviews progress and makes further recommendations based on improvements.

Recreational therapy

The importance of recreational therapy in successful rehabilitation should not be understated. Reintroduction of leisure-time activity can provide a motivational and nonthreatening method to assess and treat deficits incurred by patients who have experienced a stroke. Recreational activity also can provide an outlet for patients. Furthermore, participation in activities inside and outside the hospital setting can be essential to rebuilding patient confidence and can help to facilitate successful community reintegration.

In a 2009 study, Särkämö et al concluded that following neural damage, patients can undergo long-term plastic changes in early sensory processing by listening to music and speech. They suggested that such changes may help to restore higher cognitive functions in these patients.^[47]

The study was designed to investigate whether listening daily to music or speech can improve auditory sensory memory in patients who have suffered neural damage. Fifty-four patients in the acute recovery phase following MCA stroke were divided into a music group, an audio book group, and a control group. In order to index the patients’ auditory sensory memory, magnetic mismatch negativity (MMNm) responses to variations in the frequency and duration of sound were measured over a 6-month follow-up period, using whole-head magnetoencephalography.

The authors found a significant increase in the frequency MMNm amplitude in the music and audio book patients over that of the controls. Moreover, the audio book group showed a greater increase in the duration MMNm amplitude than did the other 2 groups. The authors also found a correlation in the music group between frequency MMNm amplitude changes and improvements in verbal memory and focused attention.

Surgical intervention

In patients with space-occupying hemispheric infarction, surgical decompression within 48 hours of stroke onset has been shown to reduce patient mortality and improve functional outcome; however, there is no evidence that surgical decompression improves functional outcome if the procedure is delayed for up to 96 hours after stroke onset.^[48]

In a randomized trial, the risk for recurrent ipsilateral ischemic stroke at 2 years was not lowered for patients with symptomatic atherosclerotic internal carotid artery occlusion and hemodynamic cerebral ischemia who received extracranial-intracranial bypass surgery along with best medical therapy compared with those patients who only received best medical therapy.^[49]

Guidelines for carotid endarterectomy are available but are not addressed in this article. It is recommended to consult the AHA/ASA Council guidelines for the prevention of stroke in patients with ischemic stroke or transient ischemic attack (TIA), first published in 2006^[50] and updated in 2008.^[51]

Consultations

The neuropsychologist faces the challenging task of elucidating and treating the diverse array of cognitive and sensory deficits resulting from stroke. Furthermore, the role of the neuropsychologist extends to addressing issues such as depression, which is present in up to 50% of patients after a CVA. Adjustment issues faced by the patient and significant others in areas such as coping, dependency, and sexuality must be addressed to provide complete rehabilitation.

The social worker plays an essential role in stroke rehabilitation. Often, the patient, prior to his/her stroke, was the primary caregiver or supporter of a significant other. Facing new disability is overwhelming emotionally to family members and to patients. Unfortunately, the financial impact of such a catastrophe can also be daunting. The social worker plays the key role of educating the patient and family about available services and benefits and ensures safe, realistic, and adequate disposition after discharge.

Deterrence/prevention

As previously mentioned, the AHA/ASA Council has formulated guidelines for the prevention of stroke in patients with ischemic stroke or TIA.^{[50, 51]} The team of authors presents an evidence-based review of practice and offers guidelines in the acute and long-term treatment and prevention of ischemic stroke in numerous clinical scenarios.

With regard to pharmacologic stroke prophylaxis, widely used medications are aspirin, clopidogrel, and (to a lesser extent) ticlopidine. Warfarin also may be necessary for certain patient populations. Several oral anticoagulant medications, including ximelagatran, are in the final stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke.^[52] Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

The 2008 addendum to the AHA/ASA recommendations advises that aspirin (50 to 325 mg/d) monotherapy, combined aspirin and extended-release dipyridamole therapy, and clopidogrel monotherapy are acceptable options for initial therapy in patients with noncardioembolic ischemic stroke or TIA.^[51] A meta-analysis of 5 trials found the combination of aspirin and dipyridamole to be more effective than aspirin alone for the secondary prevention of stroke and other vascular events in patients with TIA or ischemic stroke of presumed arterial origin.^[53]

Because clopidogrel administered with aspirin increases hemorrhage risk, the use of these drugs in combination is not routinely recommended for patients with ischemic stroke or TIA, except in individuals with a specific indication for this treatment, such as a coronary stent or acute coronary syndrome. Clopidogrel is also a reasonable choice for patients who are allergic to aspirin.^[51]

Diet and nutrition can also play a part in the prevention of a stroke. Poor nutrition, including high salt or sodium intake, decreased potassium intake, and excess alcohol consumption, may lead to increased stroke risk. However, diets rich in fruits, vegetables, and low-fat dairy products may help lower blood pressure and lower the risk of stroke.

A study by Holmes et al tried to establish a correlation between homocysteine levels and strokes in randomized genetic trials. While the reduction of homocysteine levels using folate supplementation did not result in stroke reductions, this may be attributed to the studies being performed in regions with high-folate consumption. Further studies are required in regions with low-folate consumption.^[54]

Further outpatient care

Depression, reduced sex drive, poor adjustment, equipment and transportation needs, spasticity, and reflex sympathetic dystrophy can become more pronounced after hospital discharge. As many as 8% of patients develop a seizure disorder after stroke. The physiatrist plays an important role in understanding and addressing the ongoing needs of patients following discharge from inpatient stroke rehabilitation.

A population-based study by Dhamoon et al suggested that within a group of patients who have suffered ischemic stroke, there will be an annual decline for up to 5 years in the proportion of patients who are functionally independent that is unrelated to recurrent stroke and other risk factors.^[55] In the study, 525 patients aged 40 years or older (mean age, 68.6 y) with incident ischemic stroke were prospectively followed at 6 months and annually for 5 years.

During that time, the proportion of patients with a Barthel Index score of 95 or higher declined (odds ratio [OR], 0.91; 95% confidence interval, 0.84-0.99). The decline was independent of age, stroke severity, and other predictors of functional decline, occurring even in patients who did not suffer recurrent stroke or myocardial infarction. The authors also found that the decline occurred in patients who were receiving Medicaid or who had no health insurance (OR, 0.84; P = .003) but did not occur in those with Medicare or private insurance (OR, 0.99; P = .92).

Patients who have had a stroke often leave the inpatient setting with a complex set of medical problems that require multiple medications. A typical patient may require medicine for hypertension, anticoagulation, sleep, spasticity, and depression. The recognition of drug interactions and knowledge of the physical and cognitive adverse effects of medications is paramount for effective management.

Sleep medications are important in reestablishing a sleep schedule. Trazodone often is used in low doses (50-150 mg qhs). Medications that impair cognitive function (eg, benzodiazepines, diphenhydramine [Benadryl]) generally are avoided.

BP management is of obvious importance. Often, calcium-channel blocking agents are chosen in geriatric populations because of their lower drug-interaction profile. In the class of beta-blockers, atenolol is often selected over metoprolol, owing to its lower central-acting effects.

Mortality

A significant number of patients (15-30%) die from acute stroke within the first 30 days after the event. Survival after hemorrhagic stroke is less common, with only a 20% survival rate. Death in the first week after stroke is directly due to the stroke in 90% of cases. Pulmonary embolism is the most common cause of death within 2-4 weeks of stroke. Pneumonia is the most common cause of mortality within 2-3 months after the event. Thereafter, cardiac disease is the most common cause of death.

In a single-blind cluster, randomized, controlled trial, stroke patients in acute stroke units (ASUs) were evaluated 90 days after hospital admission. ASUs were randomly appointed to intervention (n=10) or control (n=9). Those patients who received a multidisciplinary intervention focusing on evidence-based management of fever, hyperglycemia, and swallowing dysfunction were much less likely to be dead or dependent at 90 days, despite the severity of the stroke, compared with the control ASU patients.^[28]

Factors predictive of outcome

More than 200 studies, dating from 1950-1998, were cited in a review article focusing on outcome after stroke.^[56] Among the studies, the most significant issue was the heterogeneity of factors assessed, such as functional status, living situation, morbidity and mortality, and quality of life. The varying study methodologies also were a significant issue. Hence, comparing and summarizing these data pose a significant challenge.

The ideal study, according to the review, is prospective, randomized, and blinded. The author asserts that cohort size, selection criteria, statistical analysis, functional assessment measures used, and appropriateness of conclusions also must be considered. Using this standard for rating articles, the following data regarding the predictive value of functional deficits and medical comorbidities were obtained from articles rated as good or excellent:

The following factors more consistently seemed to predict unfavorable outcomes in this review of studies:

• Incontinence of the bowel or bladder, with bowel incontinence conveying a less favorable prognosis (This finding was replicated in several studies.)
• Increased systolic blood pressure (BP) on acute admission
• Poor sitting balance
• Delay in rehabilitation admission
• Poor gait
• Low scores on formal cognitive tests (eg, Wechsler Performance IQ, Porteus Maze)
• Electrocardiographic abnormalities
• Elevated erythrocyte sedimentation rate
• Dysphasia
• Homonymous hemianopia
• Poor arm and leg power
• Apraxia
• Hemianesthesia
• Neglect
• Denial
• Spatial perception problems^[19]
• Initial unconsciousness
• Perceptual intellectual deficits
• Altered mentation
• Prior history of stroke
• Nystagmus

The following conditions were shown to increase short-term mortality:

• History of congestive heart failure
• Angina and myocardial infarction
• Delay in acute hospital admission
• Poor orientation
• Increased cranial nerve deficits
• Paralyzed conjugate gaze
• Increased white blood cell (WBC) count

The following were correlated with long-term mortality:

• ST elevation and disorientation upon hospital discharge
• Poor motor persistence
• Half-hour recall
• Left versus right hemiplegia
• Diabetes mellitus
• Poor upper extremity motor recovery and control
• Prolonged onset to rehabilitation

The following were correlated with increased mortality following stroke:

• Acute congestive heart failure
• Glucose level greater than 140 mg/dL
• Nonlacunar versus lacunar stroke

This study also noted a correlation of stroke recurrence with a history of alcohol abuse, hypertension, and elevated blood glucose levels in the first 48 hours after admission.

The following factors were described as predictive of good functional improvement in the upper extremity after stroke:

• Age younger than 65 years
• Smaller lesion on computed tomography (CT) scanning
• Orientation at admission
• Functional improvement correlates with higher scores on the Embedded Figures Test

Advanced age consistently correlated with nursing home placement and shorter inpatient stay for rehabilitation. More disagreement seems to exist in the literature as to whether advanced age is a predictor of functional outcome.

According to several studies, the patient’s sex does not appear to affect outcome after stroke.

Perhaps surprisingly, no correlation of outcomes with increased income and marital status was noted; however, in-house and out-of-house support correlated with improved 1-year function, mortality, discharge disposition, and life satisfaction.^[57]

Relatively few studies described how medical factors correlate with outcome after stroke, and functional presentations deemed to have no predictive value in functional outcome included lower limb function, expression of emotions, and 2-point discrimination.