eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Middle Cerebral Artery Stroke

Daniel I Slater, MD, Medical Director, Department of Physical Medicine and Rehabilitation, St. Mary's Hospital
Sarah A Curtin, MD, Staff Physician, Department of Family Practice, St Mary's Hospital; Jeffery S Johns, MD, Associate Hospital Medical Director, Medical Director of Spinal Cord Injury Program, Brooks Rehabilitation Hospital; Adjunct Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, University of North Carolina School of Medicine; Cindy Schmidt, MPT, Physical Therapist, Department of Physical Medicine and Rehabilitation, St Mary's Hospital; Rachael Newbury, OT, Occupational Therapist, Department of Rehabilitation, Saint Mary's Hospital

Updated: Oct 6, 2009

Introduction

Background

Middle cerebral artery stroke describes the sudden onset of focal neurologic deficit resulting from brain infarction or ischemia 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 presence of specific neurologic deficits after MCA stroke and on the correlation of these deficits to outcomes and prognosis. 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. (See images below and Images 1-3.)

Day 1 after left middle cerebral artery cerebrovascular accident, ischemic damage.

Day 3 after right middle cerebral artery cerebrovascular accident.

Day 5 after right middle cerebral artery cerebrovascular accident.

Pathophysiology

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.

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. (See images below and Images 4-5.)

Normal magnetic resonance angiogram demonstrating intracerebral vascular anatomy.

Normal magnetic resonance angiogram demonstrating intracerebral vascular anatomy.

Frequency

United States

The frequency of middle cerebral artery stroke (MCA stroke) 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.¹

International

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.² This review did not distinguish between middle cerebral artery strokes and other CVAs.

Mortality/Morbidity

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.

Race

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.³

Sex

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

Age

Risk of middle cerebral artery stroke (MCA stroke) increases with age. The highest incidence of MCA strokes is in the seventh and eighth decades of life. Stroke in younger persons (aged 18-45 y) is far less common than in elderly persons. 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. 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.

Clinical

Physical

Patients with middle cerebral artery stroke syndrome (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 (see Left-hemisphere (dominant) infarction, below).
• 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's 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.⁴
• Specific neurologic sequelae
  • Loss of consciousness - Initially this is rare after MCA stroke, but it occurs slightly more often than in vertebrobasilar strokes (8.4% vs 5.7%).⁵ Loss of consciousness most often is attributable to seizures, but it may result from secondary edema and subsequent brainstem herniation.
  • Hemiparesis and hemiplegia
    • 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.⁶ 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.^7,8 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
    • 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
    • Neglect in 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.⁹ 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
    • Autonomic disturbance 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.¹⁰
• Left-hemisphere (dominant) 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.¹¹ Other studies reveal bilateral speech representation in as many as 15% of left-handed patients.
  • Aphasia
    • 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's 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.¹²
      • The infarct responsible for Broca's 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.
      • Dyspraxia describes the impaired cooperation of the oropharyngeal and respiratory elements necessary for speech. Individuals with dyspraxia have a hesitant and somewhat telegraphic verbal response.
      • Agrammatism describes the shortened speech patients use to communicate. These individuals sometimes utter only individual words to communicate an idea.
    • Wernicke's 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. Patients with Wernicke's aphasia vocalize smoothly and with expression, but they demonstrate paraphasias or speech with distorted phonetic structure, word substitution, and additional prefixes and suffixes. The speech is fluent but can be without understandable words.
      • The infarct responsible for a classic Wernicke's aphasia includes the dominant posterior temporal, inferior parietal, and lateral temporo-occipital regions.
      • Contrary to the manifestation of motor aphasia, speech is rich in words but is missing key words and ideas and may be perseverative. The 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.¹³ 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's 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.
  • Apraxia
    • Apraxia refers to the inability to perform a previously learned task despite preserved strength, vision, and coordination. The condition is due to an insult to the dominant hemisphere.
    • When referring to apraxia, Mohr states, "Motor engrams (programs) that guide skilled acts have either been lost or cannot be accessed."^12,6 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.
    • 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.
    • Callosal apraxia is similar to ideomotor apraxia but only involves the nondominant arm.
    • 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.¹⁴ Often these movements are performed spontaneously. This condition coexists with Broca's aphasia in 90% of patients; however, the 2 disorders often exist independently.
• Right-hemisphere (nondominant) infarction - Motor deficits following infarction of the nondominant hemisphere parallel those described previously for dominant-hemisphere lesions. 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 impersistence and neglect.
  • Extinction - This describes inattention to one stimulus when 2 stimuli are presented simultaneously. Generally, the ignored stimulus is on the left side.
  • Neglect - According to Schwartz and colleagues, neglect is "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."¹⁵ Such unilateral neglect occurred in 29% of patients with right-sided brain damage versus 12% of patients with left-sided brain damage among a stroke population studied by Battersby and coauthors.¹⁶ 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.¹⁷ More sizable infarcts lead to anosognosia or imperception of field neglect and imply a much less favorable prognosis.
  • Impersistence - This term is used to describe an inability to persist in performing motor tasks; it is often accompanied with visuomotor and visuospatial deficits.¹⁸ This impairment places the patient at risk for an unfavorable rehabilitation outcome.
  • Dressing apraxia - This finding is much more common in cases of right-hemisphere infarcts and is attributable to difficulty distinguishing right from left and up from down. The patient is unable to dress without assistance despite having no apparent hemiplegia that would prevent the performance of this function.
  • Topographic memory deficit - This term is used when individuals become lost in familiar surroundings. The finding often follows right-hemisphere insults.
  • General confusion and delirium¹⁹ - These findings often are more commonly appreciated in patients with damage to the nondominant hemisphere. 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 - This 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.
  • Constructional apraxia - This defines 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.²⁰ In this group, 25 had left-sided damage and 42 had damage to the right hemisphere. The apraxia of the patients with a dominant-hemisphere infarct often is described as decreased attention to detail. The apraxia with right-sides damage is consistent with neglect, in which features to the left of midline are ignored.
  • Allesthesia - This term describes sensory referral. For example, a patient touched on the left side feels the touch on the right.
  • Aprosody, lack of intonation in speech, and affective agnosia - These terms refer to the inability to perceive or comprehend emotional intonation of speech. The 2 deficits often coexist and correlate with lesions in the right temporoparietal region.

Causes

The main causes of stroke include ischemia, cardioembolism, hypercoagulable states, hemorrhage, hypertension, and amyloid or arteriovenous malformation. 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; however, it is a relatively rare cause of middle cerebral artery strokes (MCA strokes). 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.²¹

• Embolism
  • Most of the sources in the literature support embolism as the primary etiology of MCA strokes. Specifically, cardioembolism accounted for approximately 50% of total MCA strokes, 34% of deep MCA strokes, and 41% of cortical strokes in a study by Moulin and coauthors.²² 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 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 such strokes 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 - Approximately 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.
• Amyloid angiopathy - This is a rare etiology for lobar cortical strokes in elderly patients.
• Other - Dissection and stenosis of the MCA are rarely documented as causes of MCA stroke.²¹
• Etiology based on age - 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.

Differential Diagnoses

Conversion Disorder
Hypoglycemia
Migraine Headache
Subdural Hematoma

Other Problems to Be Considered

Focal seizure
Tumor
Common neurologic deficits after stroke

Workup

Laboratory Studies

• Acute studies - 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
  • Chest radiography
  • Oxygen saturation and blood gas determination
  • Urinalysis and blood culture if fever is present
  • Blood studies
    • 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)
  • Specific studies for younger patients - May include protein C and protein S values, antithrombin III deficiency testing, and mutational analysis for the factor V Leiden gene
• Studies for subacute complications - These are needed to assess for associated conditions, such as deep venous thrombosis (DVT), pulmonary embolism, dysphagia, and urinary dysfunction.
  • Doppler ultrasonography - Generally, this 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 (see Medication, below).
  • Spiral computed tomography (CT) scanning - This 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.
  • Swallow studies - 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 endoscopic evaluation - This technique 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.
  • 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.

Imaging Studies

• CT scanning is the preferred study, being accessible, fast, and highly sensitive for excluding or confirming hemorrhage.²³  However, it is less sensitive than is magnetic resonance imaging (MRI) for the diagnosis of stroke within the first few hours of symptoms.
• CT angiography provides an image of the perfusion status of the brain parenchyma.²³ 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 but is limited by access and cost. (See image below and Image 6.) 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.²⁴
  • Perfusion-weighted imaging shows the actual zone of ischemic injury.

Magnetic resonance angiogram revealing right middle cerebral artery stroke.

• 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.
  • 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.²⁵
• 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.
• 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.

Other Tests

• 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).

Histologic Findings

The histologic character of the middle cerebral artery and its branches differs from 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.

Treatment

Rehabilitation Program

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, strength, physical conditioning, and mobility and to help them return to independent living.

The emphasis in rehabilitation for patients who have suffered a middle cerebral artery stroke 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. 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.

In order to achieve the goal of enabling the patient to become as independent as possible, several different treatment techniques are used by the physical therapist. Some of 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 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.

Rehabilitation after a stroke is very team oriented, with the physical therapist as an integral part. However, 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.

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. An occupational therapist's 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.⁷

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 therapy²⁶ ); 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 cerebrovascular accident (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 the recreational therapist 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.

Medical Issues/Complications

See Prognosis.

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.²⁷

Guidelines for carotid endarterectomy are available but are not addressed in this article. The American Heart Association/American Stroke Association Council published guidelines for the prevention of stroke in patients with ischemic stroke or transient ischemic attack (TIA) in 2006,²⁸  and updated these guidelines in 2008.²⁹  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.

Consultations

• Neuropsychologist - 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 cerebrovascular accident (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.
• Social worker - 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.

Medication

As previously mentioned, the American Heart Association/American Stroke Association Council formulated guidelines for the prevention of stroke in patients with ischemic stroke or TIA.²⁸ 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.³⁰ Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

The medical management of acute stroke is not discussed in this article.

Antiplatelet agents

These inhibit the cyclooxygenase (COX) system, decreasing levels of thromboxane A₂, which is a potent platelet activator.

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

Works by permanently inactivating COX-1 and COX-2 enzymes, thus inducing a defect in thromboxane-2 dependent platelet function.
A study in the United Kingdom demonstrated an effect at doses as low as 30 mg, much lower than the dose of aspirin required for an analgesic effect. This study compared regimens of 30 mg/d versus 283 mg/d and found no significant difference in incidence of stroke in 3131 at-risk patients; however, no evidence seems to suggest a dose-dependent benefit.

Dosing

Adult

325 mg PO qd

Pediatric

Not established

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; due to association of aspirin with Reye's syndrome, do not use in children (<16 y) with flu

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Salicylate toxicity occurs more often in children and can result in complications that include delirium, convulsions, coma, metabolic acidosis, and death from respiratory failure; children taking aspirin during a viral infection are prone to developing Reye's syndrome; GI effects of aspirin include epigastric distress, nausea, vomiting, and bleeding; aspirin hypersensitivity affects 15% of patients, with symptoms that include urticaria, bronchoconstriction, and angioneurotic edema

Clopidogrel (Plavix)

Selectively inhibits adenosine diphosphate–induced platelet aggregation. This effect occurs only in vivo, suggesting hepatic conversion to an active metabolite. The side effect profile of clopidogrel is favorable when compared with that of aspirin; there is a slightly higher frequency of rash and diarrhea with clopidogrel, but a slightly lower frequency of gastric upset or gastrointestinal bleeding. Clopidogrel is still more effective than aspirin alone in preventing stroke. Ongoing studies are investigating the additive antithrombotic effects of combination therapy with low-dose aspirin and clopidogrel.

Dosing

Adult

75 mg PO qd

Pediatric

Not established

Interactions

Coadministration with naproxen associated with increased occult GI blood loss; prolongs bleeding times; safety of coadministration with warfarin not established

Contraindications

Documented hypersensitivity; active pathologic bleeding (eg, peptic ulcer, intracranial hemorrhage)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients at increased risk of bleeding from trauma, surgery, or other pathologic conditions; caution in patients with lesions with propensity to bleed (eg, ulcers)

Ticlopidine (Ticlid)

Used in at-risk patients who are unable to tolerate aspirin. Ticlopidine has been found to have significantly greater efficacy in preventing stroke than does aspirin alone. Unfortunately, ticlopidine has serious adverse effects, including neutropenia, thrombocytopenia, and aplastic anemia. The high price of the medication and the drug's adverse effects have led to the decreased use of ticlopidine.

Dosing

Adult

500 mg PO qd

Pediatric

Not established

Interactions

Effects may decrease with coadministration of corticosteroids and antacids; toxicity increases when taken concurrently with theophylline, cimetidine, aspirin, and NSAIDs

Contraindications

Documented hypersensitivity; neutropenia or thrombocytopenia, liver damage, and active bleeding disorders

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue if absolute neutrophil count decreases to <1200/µL or if platelet count falls to <80,000/µL

Anticoagulants

Anticoagulant medication is used to prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation.

Warfarin (Coumadin)

In the acute setting, focus should be on performing imaging studies to rule out cerebral hemorrhage and on other studies to help demonstrate a clear indication for this therapy. Middle cerebral artery strokes most often are caused by emboli, and thus, special attention should be paid to this important medication.
Warfarin inhibits vitamin K – dependent attachment of carboxyglutamyl residues to clotting factors II, VII, IX, and X, rendering them inactive. The effects can be reversed with vitamin K, but regeneration of active factors takes approximately 24 h.

Dosing

Adult

1-15 mg/d PO to achieve target INR between 2-3, possibly higher if patient has prosthetic cardiac valve

Pediatric

Not established

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Risk of major bleed after ischemic stroke significantly increased with warfarin use (A reversible ischemia trial studied 1316 patients with transient ischemic attack or minor stroke randomized to aspirin 30 mg/d or warfarin to achieve INR of 3-4.5; 53 major bleeds occurred in the group treated with warfarin, whereas only 6 patients had such complications with aspirin; the limitations of the study were that the aspirin dose was lower than the commonly used dose and the target INR was much higher than the one that currently is generally pursued; however, the study also demonstrated that the incidence of bleeding increases by a factor of 1.4 for each half-unit INR increase)

Follow-up

Further Inpatient Care

• 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.
• Serum glucose level management
  • 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 guidelines recommend treating hyperglycemia with fluids and insulin to achieve a level of less than 300 mg/dL.
• Blood pressure (BP) management
  • Hypertension is a major risk factor for cerebrovascular accident (CVA). However, acute reduction of 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 American Stroke Association 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.³¹ 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.³²
  • 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.
• 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 (95% confidence interval, 1.4-3.5; P <.002).
  • 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.³³
• 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). 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/American Stroke Association (AHA/ASA) published a science advisory recommending that the time window for tPA administration be increased to 4.5 hours after a stroke, although this change has not been approved by the FDA.³⁴ Research indicates that tPA is effective in patients even when administered within the 3- to 4.5-hour window,^35,36,37 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,³⁸ 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,³⁹ 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. See the eMedicine article Medical Treatment of Stroke for more details on thrombolytic treatments and eligibility.
• Anticoagulation (heparin and low–molecular weight heparin)
  • Anticoagulants 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 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.⁴⁰
  • The American Stroke Association's recommendations and guidelines on antithrombotic therapy issued in 2008, by the Eighth American College of Chest Physicians Consensus Conference (ACCP), do not recommend full-dose anticoagulation treatment for acute stroke patients (except in very specific patient populations).⁴¹

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.
• 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, suggests a population-based study by Dhamoon et al.⁴² 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 = 0.003) but did not occur in those with Medicare or private insurance (OR, 0.99; P = 0.92).

Inpatient & Outpatient Medications

• 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.
• A 2008 addendum to the AHA/ASA recommendations advises that aspirin (50 to 325 mg/d) monotherapy, the use of a combination of aspirin and extended-release dipyridamole, and clopidogrel monotherapy are acceptable options for initial therapy in patients with noncardioembolic ischemic stroke or TIA.²⁹ 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.⁴³
  
  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.²⁹

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.

Prognosis

• More than 200 studies, dating from 1950-1998, were cited in a review article focusing on outcome after stroke.⁴⁴ 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 was 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 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 problems¹⁷
    • 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 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.⁴⁵
  • 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.

Miscellaneous

Medicolegal Pitfalls

• The 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.⁴⁶
  • 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.
  • 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.

Special Concerns

A study compared the outcomes of poststroke patients in 9 different hospital units (ie, 6 stroke rehabilitation units and 3 general rehabilitation units).^47,48 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.⁴⁹

Multimedia

Media file 1: Day 1 after left middle cerebral artery cerebrovascular accident, ischemic damage.

Media file 2: Day 3 after right middle cerebral artery cerebrovascular accident.

Media file 3: Day 5 after right middle cerebral artery cerebrovascular accident.

Media file 4: Normal magnetic resonance angiogram demonstrating intracerebral vascular anatomy.

Media file 5: Normal magnetic resonance angiogram demonstrating intracerebral vascular anatomy.

Media file 6: Magnetic resonance angiogram revealing right middle cerebral artery stroke.

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Keywords

middle cerebral artery stroke, cerebrovascular accident, CVA stroke symptoms, symptoms of stroke, stroke rehabilitation, MCA, MCA stroke, cerebral artery, middle cerebral artery, MCA, ischemic, transient ischemic attack, TIA, middle cerebral artery infarction, brain infarction, brain ischemia, hemorrhagic stroke, ischemic stroke, neurologic deficits

Contributor Information and Disclosures

Author

Daniel I Slater, MD, Medical Director, Department of Physical Medicine and Rehabilitation, St. Mary's Hospital
Daniel I Slater, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

Coauthor(s)

Sarah A Curtin, MD, Staff Physician, Department of Family Practice, St Mary's Hospital
Sarah A Curtin, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Jeffery S Johns, MD, Associate Hospital Medical Director, Medical Director of Spinal Cord Injury Program, Brooks Rehabilitation Hospital; Adjunct Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, University of North Carolina School of Medicine
Jeffery S Johns, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Paraplegia Society, American Spinal Injury Association, Association of Academic Physiatrists, and Florida Medical Association
Disclosure: Nothing to disclose.

Cindy Schmidt, MPT, Physical Therapist, Department of Physical Medicine and Rehabilitation, St Mary's Hospital
Disclosure: Nothing to disclose.

Rachael Newbury, OT, Occupational Therapist, Department of Rehabilitation, Saint Mary's Hospital
Disclosure: Nothing to disclose.

Medical Editor

Patrick J Potter, MD, FRCP(C), Associate Professor, Physical Medicine and Rehabilitation, The University of Western Ontario; Consulting Staff, Department of Physical Medicine and Rehabilitation, St Joseph's Health Care Centre
Patrick J Potter, MD, FRCP(C) is a member of the following medical societies: American Paraplegia Society, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard Salcido, MD, Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds Novaritis; Novaritis  Novaritis; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

We would like to acknowledge Jenny L Tipton, MA, SLP, Speech-Language Pathologist, Department of Rehabilitation, Saint Mary's Hospital, for her previous contribution to this article.

Related eMedicine topics:
Anterior Circulation Stroke
Medical Treatment of Stroke
Motor Recovery In Stroke
Stroke, Hemorrhagic
Stroke, Ischemic
Stroke Motor Impairment
Transient Ischemic Attack

Clinical guidelines:
Antithrombotic and thrombolytic therapy for ischemic stroke. American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). American College of Chest Physicians - Medical Specialty Society.  2001 Jan (revised 2008 Jun).  40 pages.  NGC:006668

Assessment: transcranial Doppler ultrasonography: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. American Academy of Neurology - Medical Specialty Society.  2004 May 11 .  14 pages .  NGC:003644

(1) Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack. (2) Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack. American Heart Association - Professional Association
American Stroke Association - Disease Specific Society.  2006 Feb (addendum released 2008 May).  Original guideline: 41 pages; Addendum: 6 pages.  NGC:006659

Clinical trials:
Carotid Occlusion Surgery Study (COSS)

Effects of Carotid Stent Design on Cerebral Embolization

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