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Middle Cerebral Artery Stroke

  • Author: Daniel I Slater, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
 
Updated: Jun 10, 2016
 

Overview

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

The MCA is by far the largest cerebral artery and is the vessel most commonly affected by cerebrovascular accident. 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.

This article focuses more on the postacute care and rehabilitation of patients with MCA stroke. However, evidence-based practice of acute stroke care obviously needs to be carried over into the rehabilitation setting. This is particularly true since patients are ideally being admitted to such settings quite early after their event. The American Heart Association guidelines are an excellent resource for standards of stroke care. Certified centers for stroke care have proven to have better outcomes in terms of morbidity, mortality, and eventual functional outcome relative to those without such specialization.[1, 2]

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Rehabilitation Setting Selection and Indications

Knowing and using objective criteria in recommending a rehabilitation plan best suited for a patient is imperative. This effort to maximize functional outcome and independence and targeting expensive resources to patients who will benefit is a very important role for physiatrists and other rehabilitation specialists.

Acute, inpatient rehabilitation is the most intense and expensive rehabilitation setting in terms of hours of therapy provided each day. Comparison to subacute rehabilitation, typically provided in a skilled nursing facility, in terms of functional outcome, is discussed later in this article. However, the basic criteria for admission to acute rehabilitation are as follows:

  • Potential for significant functional improvement requiring at least 2 therapy disciplines in a reasonable period
  • Realistic and safe discharge plan with family support and housing that allows return to the community rather than to a skilled nursing facility or long-term care
  • Medical stability, willingness, and ability to participate in at least 3 hours of therapy/day

Inpatient, subacute rehabilitation is generally offered at a skilled nursing facility or long-term acute care hospital. Patients with more complex medical care such as mechanical ventilation or advanced wound care often undergo at least their initial rehabilitation at a long-term acute care hospital. Both skilled nursing facility and long-term acute care hospital therapy is generally, but not always, with fewer hours of therapy offered per week. Such facilities are not bound to a minimum hours of therapy per day.

Home health and outpatient therapy are provided to patients after they complete their inpatient therapy or for those who are less impaired after their stroke.

Contraindications

Frankly, there are very few indications for no therapy and evidence does suggest that earlier mobilization translates to better long-term patient outcome.

Ideally, rehabilitation should begin immediately after a patient is admitted for stroke, barring additional medical issues aside from the stroke itself.[3]

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Best Practices

The American Heart Association (AHA) guidelines have become a widely used standard of care for individuals with both ischemic and hemorrhagic stroke. Comprehensive review of these guidelines is outside of the postacute stroke focus of this article. However, certain elements are quite relevant to the rehabilitation setting.

Certified stroke center

Patients should be directed to medical centers designated and accredited for the interdisciplinary care of stroke patients. Improved outcome in terms of mortality, length of stay, return to home, patient function, and cost of care have all been shown to be superior in care centers consistent in AHA guideline–based practices.[4] These centers must track and document consistent interdisciplinary practices in the care of stroke patients that are shown to improve outcomes. This care includes but is not exclusive to the following:

  • Appropriate and expedient use of thrombolytic therapy*
  • Dysphagia screening
  • Venous thromboembolism prophylaxis
  • Discharged on antithrombotic therapy*
  • Anticoagulation therapy for atrial fibrillation/flutter*
  • Discharged on statin medication*
  • Discharged on antihypertensive medication or documentation stating why contraindicated
  • Stroke education
  • Smoking cessation education
  • Assessed for rehabilitation

*Denotes care for ischemic but not hemorrhagic stroke.

Pharmaceutical management

Thrombolytic therapy should be administered in a very orchestrated and consistent manner, relying on emergent imaging and screening to ensure only patients with ischemic stroke and no contraindications receive such therapy. After ischemic stroke, patients should be discharged from acute care on a statin, antihypertensive, and appropriate antithrombotic and/or anticoagulation medicines to prevent recurrent stroke. The selection of such medications is dependent on the presence of comorbidities, including atrial fibrillation, coronary artery disease, congestive heart failure, and diabetes.

Dysphagia management and prevention and significance of aspiration pneumonia

The importance of recognizing and proactively managing impaired swallowing should not be underestimated. Dysphagia is seen in 42-67% of patients within the first 72 hours post stroke.[5] Per stroke guidelines, a basic swallow screen should be performed by nursing staff before any initial food or drink is provided to a patient.[6] Patients with findings suggestive of dysphagia, including cough, voice changes, level of consciousness, prolonged mastication, should be further evaluated by a speech therapist. To be clear, the initial screening process is not equivalent to a thorough evaluation of swallowing impairment.

A modified barium swallow or videofluoroscopy is used to ascertain if any feeding is safe and, if so, what consistency of solids and liquids are appropriate. Aspiration is defined as the penetration of food or saliva beyond the vocal chords and is termed silent if the patient is without symptoms such as cough when this penetration occurs. Bedside evaluation for dysphagia is certainly limited by the fact that as many as 40% of patients who aspirate do so silently. Accordingly, modified barium swallow is likely needed in all but a few cases of patients with any suspicion for dysphagia.

Aspiration pneumonia, resultant from penetration of food, saliva, and gastric acid, has very serious ramifications, including high mortality, increased length of hospital stay, and poor functional outcome.[7] Early recognition and treatment of the condition with antibiotics and pulmonary toilet are vital to improving survival. Organisms responsible are often anaerobic and thus require differing antibiotic coverage than typical community-acquired pneumonia. The exact pathophysiology is still somewhat debated, as bronchial inflammation resultant from exposure to gastric acid, as well as bacterial infection, both likely contribute.[8]

Deep venous thrombosis and pulmonary embolism

Pulmonary embolism (PE) accounts for 10-25 % of mortality of patients after stroke. In addition, symptomatic deep venous thrombosis (DVT) and postphlebitis syndrome impede recovery and function for patients after stroke.[9] Prevention of DVT and PE is achieved either by patient mobilization or pharmaceutical intervention. Dehydration, hemorrhagic stroke, severity of paralysis, and age are all additional risk factors associated with increased likelihood of DVT.[10]

Recent evidence has shown that graded compression stockings are of no benefit in preventing DVT and increase incidence of skin breakdown.[11] Research on the benefit of pneumatic compression devices is so far inconclusive.

Daily, low-dose, low molecular weight heparin administered subcutaneously has been shown to reduce the incidence of DVT compared with unfractionated heparin. The rate of intracranial and major extracranial hemorrhage, 1%, was equal with low molecular weight heparin and unfractionated heparin. Expense of adverse drug events per patient associated with low molecular weight heparin is also significantly lower than unfractionated heparin in patients with ischemic stroke.[12]

Consideration of DVT prevention in patients with hemorrhagic stroke is challenging owing to the significantly higher rate of DVT and risk of rebleeding. Anticoagulation, using either low molecular weight heparin or unfractionated heparin has only shown a small and nonsignificant reduction in both DVT and mortality. Class IV evidence indicates it is most likely safe to start low molecular weight heparin in patients with nonexpanding hemorrhage 3-4 days post hemorrhagic stroke.

Ongoing research is examining the impact of early mobilization of stroke patients in terms of DVT prevention and other benefits. No clear data exist to indicate adequate mobility in deciding when to stop chemoprophylaxis.[13]

Hypertension management

More passive blood pressure management is pursued in acute care for ischemic stroke owing to concern for endangering the penumbra or area immediately adjacent to infarcted brain tissue. The target blood pressure for acute ischemic stroke within the first 24-72 hours is below 220/120 mm Hg. In the case of hemorrhagic stroke, pressure management is much more critical and remains important long term. Generally, the target is below 160/90 mm Hg, although new research shows benefit of lowering blood pressure even more aggressively.[14]

Again, the focus of this article is postacute stroke treatments. After 72 hours, it is prudent and safe to begin normalizing blood pressure, except in the rare case that the stroke is thought to have been caused by hemodynamic instability. Target blood pressures are below 140/90 mm Hg, except in patients with nephropathy or diabetes, for which the target is below 130/80 mm Hg.[15]

Smoking cessation

The patient should receive ongoing efforts and education to achieve and encourage discontinuation of tobacco use.

Stroke education

Patients should receive education regarding the causes of stroke to promote behaviors that will help prevent recurrence. This education also potentially serves to promote better community awareness of the signs and symptoms of stroke, with the hope of leading to earlier recognition and treatment.

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New Frontiers and the Place for Plasticity in the Rehabilitation Continuum

Rehabilitation after stroke is often focused on compensatory strategies to restore function rather than improve impairment.[16] An example is learning to dress with one arm rather than focus on retraining use of a patient’s hemiparetic upper extremity. Such emphasis on compensatory strategies has increased with cost reduction measures that have resulted in shorter acute rehabilitation lengths of stay.[17] These decreased days in inpatient rehabilitation settings have been shown to result in worse discharge outcomes.[18] In addition, focus on compensatory techniques to complete functional tasks at the expense of therapy directed toward remediating impairment could facilitate “learned nonuse” of a paretic extremity.

Neural plasticity has been defined as “any change in neuron structure or functions that is observed either directly from measures of individual neurons or inferred from measures taken across populations of neurons.”[19] A rapidly expanding body of evidence using both animal and human models has shown specific motor stimulation or movement can induce changes in the motor cortex both on a cellular level, as well as in the representative cortex devoted to limb or finger movement.[20, 21, 22] The profound implication of these basic research findings has inspired application towards recovery efforts for patients with various neurologic pathology, including stroke.

Neuroplastic changes have been fostered through traditional therapy, pharmaceutical therapy, and modality-based interventions. The changes are then observed with methods showing new synaptogenesis, as well as alterations in genetic expression, functional imaging, and evoked potential activity. Individualized therapy may someday rely on careful observation of impairment and functional disability, as well as on information derived from these sophisticated means of directly observing cortical activity and change. Currently, such endeavors are cost prohibitive, and use of basic science is largely reserved for academic research centers. However, these applications show potential to help even those with chronic impairment, well beyond what was formerly thought feasible in functional recovery.[4, 23]

Therapy-based interventions for hemiparesis have included robotic stimulation, manual stimulation, electrical stimulation, and constraint-induced movement and/or use of an effected extremity. These all would obviously seem contrary to rehabilitation that is solely devoted to compensatory techniques to complete functional tasks. However, newer therapeutic approaches appear to have potential in linking task-based challenges that also promote recovery of motor and cognitive function in stroke survivors.[24] These efforts are practical for allowing patients to be more independent and may also better motivate patients to stay engaged and motivated for their therapy. Ongoing efforts to link and practically exploit the growing understanding of neuroplasticity and translate this to improved stroke recovery make an exciting future in the field of rehabilitation.

Särkämö et al found evidence that in patients with MCA stroke, listening to music during their recovery period can aid parts of the brain relating to verbal memory, attention, and language. In the study, the investigators examined magnetic resonance imaging (MRI) scans performed during the acute stage in 49 patients with MCA stroke and 6 months poststroke, including in 16 patients who listened to their favorite music during recovery, 18 patients who listened to audio books, and 15 patients who received no listening materials during their recovery.[25]

Patients in each of the three groups were found by 6-month follow-up to have undergone significant increases in the volume of gray matter in their brains. However, in patients with left hemisphere damage, those who listened to music showed greater volume increases in parts of the frontal lobe, specifically the left and right superior frontal gyrus and the right medial superior frontal gyrus, as well as in the limbic region, specifically the left ventral/subgenual anterior cingulate cortex and the right ventral striatum, than did those in the other two groups. According to the authors, a correlation existed between the changes in the above-listed regions of the frontal lobe and enhanced improvement in the patients’ language skills, verbal memory, and ability to focus attention, with a correlation also being observed between changes in the subgenual anterior cingulate cortex and mood improvement.[25]

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Complication Prevention

Spasticity

Spasticity is defined generally as the velocity dependent resistance of a muscle to passive range of motion. It is a common finding after middle cerebral artery (MCA) stroke and, if not proactively managed, can lead to serious complications, including contracture, pain, and skin breakdown. Contracture describes a fixed loss of range of motion of a joint and can occur from joint pathology, skin contracture after major burns, or, in the case of untreated spasticity, permanently shortened muscle.

Movement, in terms of both passive and active range of motion, is the most important measure to prevent loss of range of motion due to spasticity. Appropriate wheelchair positioning is also effective in decreasing spasticity. Bracing, especially at night, allows continuous passive range to tight, spastic muscle. This includes serial casting, which allows gradual increase in range over weeks.[26]

Oral medications also are often used for spasticity management, including tizanidine, baclofen, dantrolene, and benzodiazepines. . The functional benefit of these drugs is not well demonstrated despite their common use. These medications often have at least some sedating effect on patients, which should be weighed carefully in patients already with cognitive impairment and poststroke fatigue.

Several botulinum toxins are now widely used to treat more focal spasticity with injections. Studies regarding the benefits of such injections have not been conclusive in supporting the intervention. This may be due to errant needle placement, which is far more common than once appreciated, even in large muscles such as the gastrocnemius. The increased use of musculoskeletal ultrasound to guide needle placement may improve outcomes, and studies are underway.

Finally, the surgical implantation of an intrathecal baclofen pump has been shown to benefit those with particularly severe spasticity.[27]

Pain

Pain is not unusual and results from a variety of etiologies. The most common is shoulder pain of the effected side and is seen in 70-84% of patients with hemiplegia.[28] Shoulder pain appears to be far more correlative with spasticity than subluxation.[29] The anatomy and management of subluxation is therefore briefly covered in a later section. Treatments for spasticity as described previously are therefore more challenging depending on related shoulder pain. The use of analgesics and spasticity medications again needs to be weighed carefully against possibly compromising patient function and cognition.

Lack of sufficient shoulder joint range of motion can result in frozen shoulder, in which the patient has lost movement in various planes. This late and generally avoidable complication is often permanent and markedly limiting to long-term patient function. Conversely, aggressive range of motion can also be problematic owing to altered scapulohumeral rhythm seen in many stroke patients.

The interdisciplinary team should therefore focus on appropriate glenohumeral range of motion, with particular focus on external rotation and maintaining scapular mobility. Family and other caregivers should be made aware of injury potential of an unstable shoulder and should be educated on how to assist the patient in avoiding potentially harmful movements. Specifically, movements that can cause traction to the joint, as when the arm dangles or impingement seen in overhead activity and stretching, should be avoided.[30]

Centrally mediated pain is also seen in 12-25% of patients with hemiplegia. This is formally described as complex regional pain syndrome type I or reflex sympathetic dystrophy.[28] The most common presentation is shoulder-hand syndrome, which manifests as pain in both the hand and shoulder, usually sparing the elbow and forearm. The phenomenon follows stages of development, with initial and often severe allodynia, followed by skin and muscle atrophy and decreased range of motion, and, finally atrophy and deformity, over several months. Clinical examination reveals pain with metacarpal flexion and passive range of the shoulder that is often rapid.

The most important preventive treatments are appropriate range of motion and desensitization.[28] However, if these continue to become less tolerable and effective, further diagnostic workup, including triple-phase bone scanning, may be needed.

Treatments, aside from the therapy described, include high-dose steroids, with a relatively slow taper over 2 weeks. A successful, pain-relieving, stellate ganglion block is therapeutic and is considered the criterion standard in the diagnosis of complex regional pain syndrome type I. Other medications used for this pain include gabapentin, tricyclic antidepressants, NSAIDS, carbamazepine, and nifedipine.[26]

Shoulder subluxation

Shoulder subluxation has long been used to describe lack of alignment of the humeral head in the glenoid fossa. While inferior subluxation is perhaps the most overt presentation, potential causes are multiple, as are other types of malalignment.

Measurement of inferior subluxation is not consistently indicative of the severity of subluxation.[28] The position and motion of the scapula must be carefully evaluated and monitored to achieve effective therapy. In addition, spinal alignment after stroke toward the side of paresis can also alter the angle of the glenoid fossa relative to the humerus.

Bracing and wheelchair positioning for shoulder subluxation is still a longstanding topic of debate. These interventions still show no benefit in terms of pain or function but also have not been shown to cause adverse shoulder contracture according to a recent literature review.[31] A lap tray or forearm gutter splint in wheelchair-bound patients is commonly used. Bobath, kinesiotape, and other slings are frequently used for patients during gait and standing activity.

Depression

The negative long- and short-term impact of poststroke depression is difficult to overstate. In short, poststroke depression increases mortality and healthcare usage and worsens both short- and long-term functional recovery. In addition, depression has been linked to subsequent loss of regained function, and this loss is often permanent, even after depression remits. Nonetheless, studies in the United States and abroad show that depression is more prevalent after stroke and is undertreated. Multiple screening tools have been shown to be reliable in the stroke population.[32]

Sertraline, citalopram, venlafaxine, and nortriptyline have all been shown to effectively treat depression after stroke.[33, 34] Whether this treatment improves mortality is still to be elucidated. Recent studies using fluoxetine have been less focused on depression and more focused on motor recovery. A few, including a relatively small but double-blinded, placebo-controlled study, have shown a significant improvement in motor recovery relative to an untreated cohort. Theoretically, this is thought to be due to modulation of cerebral plasticity.[35]

Urinary incontinence

Optimal management of poststroke urinary incontinence should be a high priority for the interdisciplinary rehabilitation team. Urinary incontinence is observed in approximately 44-69% of patient’s after stroke.[36, 37, 38] Numerous studies have demonstrated that poststroke urinary incontinence is associated with increased mortality and disability in the acute, postacute, and chronic phase of stroke recovery.[39, 40, 41] The presence of urinary incontinence in this population is also a major factor that determines a patient’s discharge disposition.[42] Poststroke urinary incontinence is associated with increased incidence of depression,[43] caregiver burden,[44] risk of falling,[45] and decline in self-reported quality of life.[46]

As the cause of urinary incontinence in stroke survivors is multifactorial, management strategies must be tailored to the individual needs of the patient. Significant consideration should be given to the possible mechanisms for urinary incontinence, including the assessment of premorbid incontinence. Currently, no evidence supports a single optimal treatment regimen for the management of poststroke urinary incontinence.[47] Bladder management methods that are successful in the nonstroke population are often used in the management of stroke patients. Currently, poststroke urinary incontinence is managed with behavioral, pharmacological, and surgical interventions.[48, 49]

Behavioral management techniques include timed voiding, Valsalva and Credé maneuvers, and pelvic floor exercises. Urinary collection devices, intermittent catheterization, and protective garments are used to manage the collection and disposal of urine.[37] The Fourth International Consultation on Incontinence Recommendations published in 2009 outline the most recent guidelines for the management of urinary incontinence and specialized management of neurogenic urinary incontinence, including pharmacological and surgical interventions.[50]

In the rehabilitation setting, urinary incontinence is traditionally managed by physicians and nurses. A few studies have examined the role of the interdisciplinary rehabilitation team in the treatment of poststroke urinary incontinence.

Urinary tract infection

Because acute stroke patients are entering rehabilitation programs earlier than ever before, it is important to understand the impact of urinary tract infections on this specific population. Patients with a diagnosis of acute stroke are more than twice as likely to develop urinary tract infections as other hospitalized patients, regardless of the use of urinary catheters.[51]

Urinary tract infections in poststroke patients also independently predict poor outcomes, including death, prolonged hospitalization, and poorer neurological outcomes.[52] Acute stroke patients with hospital-acquired symptomatic urinary tract infections are less likely to be discharged home.[53] Additionally, acute stroke patients with symptomatic urinary tract infections are more likely to perform at a lower functional level while participating in an acute inpatient rehabilitation program.

A Cochrane summary completed in 2013 found some evidence, albeit limited, for the benefit of prophylactic antibiotics in nonsurgical patients who undergo bladder drainage.[54] More research is clearly needed to evaluate the potential benefit to stroke patients with urinary incontinence and/or neurogenic retention in the acute and postacute setting.

Fecal incontinence

Although common after stroke, fecal incontinence is poorly studied in this population. Up to 40% of stroke survivors experience fecal incontinence in the acute phase of recovery, and up to 19% still experience fecal incontinence at 6 months.[34, 36]

Like urinary incontinence, fecal incontinence is a predictor of increased mortality.[31, 55] Urinary and fecal incontinence coexist in 80-90% of acute poststroke patients, and these 2 conditions remain strongly associated in the postacute period.[34] Fecal incontinence may also predict the likelihood of discharge to an extended care facility or necessitate home-health nursing services.

Bowel management methods that are successful in patients with other neurologic pathology are often used in the management of stroke patients in the rehabilitation setting. Treatment programs should be individualized and implemented by the interdisciplinary team. Interventions are directed at preventing unplanned bowel movements, preventing constipation, and promoting efficient and effective bowel care. As in other settings, fecal incontinence is often managed with protective garments and appropriate skin care to prevent incontinence-related skin breakdown. Scheduled bowel programs may be used for patients with neurogenic bowel. Physical and occupational therapy interventions are directed at solving functional toileting problems. Although anal sphincter and pelvic muscle strengthening exercises may be used to treat fecal incontinence, their efficacy is poorly studied in this population.

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Periprocedural Care

Patient education and consent

Informing patients and family members of the rigors of rehabilitation is essential so that they are empowered to make informed decisions. Family and patient education is imperative to rehabilitation and assures successful return home and to the community. Training of caregivers by therapists and nurses is an essential component of a good rehabilitation program.

Patient instructions

Instructions for patients need to take into consideration both educational level as well as cognitive impairments resulting from the stroke. Paraphrasing, repeating, and presenting instruction verbally, physically, and in writing may be necessary and determined based on the individual needs of the patient.

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Equipment

Mobility and gait-assistive devices

Gait-assistive devices progress from providing a greater amount of stability to providing only slight cues for balance. Front-wheel walkers have a large base of support and are very stable, providing significant stability. A patient with significant upper extremity paresis can use a large base hemiwalker as an alternative and can progress to a quad cane. A 4-wheel walker provides some balance assistance. However, with increased pressure on the walker and dependence for balance, the 4-wheel walker becomes less stable. It is recommended for patients who use an assistive device primarily to assist with endurance. A single-point cane provides the least stability of the assistive gait devices. It provides proprioceptive information for balance only.

Activities-of-daily-living aids

Activities-of-daily-livingaids are designed to maximize functional independence with basic daily tasks such as feeding, dressing, and grooming. Basic devices for assistance with meals are built-up silverware handles to assist with grip and plate guards to assist with loading food onto the utensil. A patient with poor proximal shoulder strength can be set up in a deltoid aide apparatus to assist with self-feeding. Multiple assistive aides are available for dressing including, sock aides, button aides, reachers, long-handle shoe horns, and elasticized shoe laces, to name a few.

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Treatment Considerations

With any approach to stroke rehabilitation, treatment considerations are primarily focused on the impairment level. Impairments vary in complexity and severity in relation to the location and extent of the infarct. The patient’s premorbid functional level can significantly influence mobility and independence during recovery.

A literature review by Rastogi et al suggested that malignant MCA strokes occur more frequently in the right hemisphere and that such right-sided strokes are associated with a higher morbidity rate than are those in the left hemisphere. Of 2673 patients with malignant MCA stroke for whom laterality information was available, 1687 of them (63%) had a right-hemispheric stroke, and while mortality rates between left- and right-hemispheric strokes were similar, the rate of sequelae was significantly greater for strokes in the right hemisphere.[56]

Common impairments seen with middle cerebral artery (MCA) stroke include, but are not limited to, neglect, hemiparesis, ataxia, perceptual deficits, cognitive deficits, speech deficits, and visual disorders. Hemiparesis, sensory deficits, and ataxia can occur with either a right or left hemisphere lesion and typically affect the contralateral side. Speech impairments and aphasias are more typical with a left hemisphere lesion, while perceptual deficits are more commonly associated with a right hemisphere lesion.

Issues with neglect are commonly seen with a right hemisphere infarct. Patients with neglect have significant impairment in functional mobility. Multiple theories have been advanced on the neurophysiological basis of neglect. These theories include the attention-arousal theory,[57] hemispheric specialization,[58] disengagement theory[59] , and interhemispheric interaction and inhibition.[60]

Two treatment approaches, constraint-induced therapy and partial visual occlusion, involve decreasing the amount of sensory input to the less involved side.[61]

With constraint-induced therapy, the less-affected limb, typically the upper extremity, is restricted by either an arm sling or a hand mitt. There is extensive research on the efficacy of constraint-induced therapy for treatment of hemiparesis. Wolf et al completed the first major study on forced-use therapy.[62] They defined forced use as, “directing patient effort and attention toward the affected hemiparetic upper extremity to the exclusion of the uninvolved, contralateral limb.” Constraint-induced therapy also has excellent potential for increasing spatial awareness in patients with neglect. Further research has found that active movement of the affected upper extremity could reduce the symptoms of visuospatial neglect.[63, 64]

Partial visual occlusion also helps to decrease sensory input to the less affected side. This is accomplished by patching or partially occluding a patient’s glasses in the nonneglected hemifield. This encourages head turning and visual scanning to the neglected visual field.[65]

Hemiparesis of the contralateral extremities is frequently seen in varying degrees of severity. In addition to limb involvement, impairment in postural stability that affects the patient’s static and dynamic balance is common. Therapeutic handling techniques are based on the concepts of facilitating wanted movements, inhibiting unwanted movements, and using key points of control on the patient’s body to achieve the desired effect. The Neuro-Developmental technique (NDT), formerly termed Bobath, and Neuro-IFRAH (neuro-integrative functional rehabilitation and habilitation) are the primary handling techniques developed for hemiparetic adults. The Neuro-IFRAH technique was developed by Waleed Al-Oboudi after many years as a clinical instructor and lecturer both nationally and internationally for the NDT Association. Both techniques are similar in their emphasis on postural control, quality of movement, and whole body use/function.

Therapeutic progressions begin with static seated balance, emphasizing appropriate midline orientation, and progress to dynamic sitting balance with the ability to incorporate reach into any sitting activity. Reach is in any direction, not defined by distance or extremity. Balance involves the use of the entire body with internal and/or external support.[66] Various other tools assist in achieving balance; manual facilitation to trunk postural muscles and extremities, facilitation range of motion, and use of mirrors for visual feedback are examples. Achieving postural alignment is key to achieving successful and efficient weight shifts.

Once achieved, the progression moves to dynamic stability with transitional movements. These are movements from one posture to another or movements within a posture, providing a change in location and/or orientation in space; an is example is a transfer from one surface to another.[52]

Once postural stability is functional in sitting, a similar progression can be followed in standing. Standing static balance, weight acceptance, and weight shift are all prerequisites for successful gait training. Assisted balance work in quadruped, half, and tall kneeling on a therapy mat table are effective in challenging balance through transitional movements and increasing supported weightbearing on hemiparetic limbs for increased facilitation. Half and tall kneeling are valuable tools to assist in the progression to standing balance and weight shifting because of their shorter lever arms against gravity. These are also positions in which patients have greater surface area for external base of support, which helps to increase patient confidence and decrease fear of falling.

Gait training typically begins with pregait activities while standing at a hemirail or parallel bars. Pregait training involves the initial skills of lateral weight shift and weight acceptance on and off the hemiparetic limb. Progression is then to forward and retro weight shifts in a staggered-stance position. Strength and motor coordination/control in the trunk and hemiparetic lower limb determines the amount of physical assist provided by the therapist. Once effective weight shifts have been achieved, the progression continues to reciprocal steps. Functional weight shifting is of primary importance throughout initial gait-training activities in order to prevent dependence on a fixed assistive device for balance.

Body weight support treadmill training (BSWTT) is an available tool to assist with gait training. Patents are suspended in a harness that can support a percentage of their body weight. BSWTT allows therapists to manually facilitate leg advancement and knee control with walking. Partial body weight support allows patients to walk at a higher cadence and to maintain their walking effort for a longer duration. BSWTT positively affects over-ground walking speed, and more severely impaired patients often see greater improvements in gait and balance dysfunction.[67]

Poststroke weakness presents a significant barrier to patient safety and functional mobility. Poststroke weakness can be broadly defined as decreased magnitude of force production, slowness to produce force, rapid onset of fatigue, excessive sense of effort, and difficulty with force production in a functional task.[68] Therapeutic exercise interventions are frequently based in functional activities such as activities of daily living and mobility tasks. Incorporated into functional tasks are techniques of repetitive motion training consistent with a traditional therapeutic exercise program. Repetition of tasks, in addition to building strength, improves motor coordination, motor control, and sensation of the movement.[69]

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Pharmacotherapy

Multiple medications are often used to manage complications of a middle cerebral artery (MCA) stroke and to decrease the risk of a recurrent stroke. Within each class of medication used, multiple agents may be selected, allowing for tailored therapy.

Hematologic agents

Medication selection is based on the etiology of the MCA stroke, comorbidities, and past medical history. Commonly used antiplatelet agents include aspirin, dipyridamole/aspirin, and clopidogrel. An increased bleeding risk is common to all of the medications within this class. Of note, prasugrel is contraindicated in patients with a history of stroke[70] and ticagrelor is only approved for use in patients with acute coronary syndrome.[71] While warfarin remains a common oral anticoagulant, newer agents include apixaban, dabigatran, and rivaroxaban.

Table 1. Hematologic Agents Mechanisms of Action and Considerations (Open Table in a new window)

Drug Mechanism of Action Consideration
Antiplatelets
Aspirin Inhibits cyclo-oxygenase May also be used to treat mild to moderate pain and headaches
Dipyridamole/aspirin Inhibits platelet adenosine uptake and cyclo-oxygenase[72] Twice daily dosing



Headaches are a common adverse effect, which may limit tolerability of therapy[73]



Clopidogrel Blocks platelet adenosine diphosphate (ADP) P2Y12 receptor[74] Avoidance of omeprazole and esomeprazole with clopidogrel was recommended in the 2009 FDA release warning about reduced efficacy[75]
Anticoagulants
Apixaban Direct factor Xa inhibitor[76] Not recommended for use in patients with CrCl < 15 mL/min or severe liver impairment
Dabigatran Direct thrombin inhibitor[77] Dosage adjustment needed for CrCl 50 mL/min or less
Rivaroxaban Direct factor Xa inhibitor[78] Dosage adjustment needed for CrCl 50 mL/min or less



Underweight patients have a slightly increased level/response[78]



Warfarin Inhibits formation of vitamin-K dependent clotting factors[79] Dosing based on international normalized ratio



Multiple food and drug interactions[79]



Antihypertensives

Hypertension is a risk factor for recurrent strokes and is often managed with thiazide diuretics, calcium-channel blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors), and angiotensin receptor blockers (ARBs). A number of studies, including the Heart Outcomes Prevention Evaluation (HOPE) study and the Perindopril Protection Against Recurrent Stroke Study (PROGRESS), support the use of ACE inhibitors with or without the combination of a thiazide diuretic to reduce the reduce the risk of stroke recurrence.[80, 81] The Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study supports the use of ARBs to reduce the risk of stroke recurrence.[82]

Beta-blockers are generally considered second-line agents but are often used for rate control. Of note, a meta-analysis has suggested higher mortality with atenolol compared with other antihypertensives when used as initial monotherapy for hypertension.[83]

Statins

HMG-CoA reductase inhibitors, or statins, have been shown to decrease the 10-year risk for recurrent stroke.[84] The individual agent should be selected based on potency needed, drug-statin interactions, and tolerability. Statin potency from lowest to highest based on the maximum dose is fluvastatin, pravastatin, lovastatin, simvastatin, atorvastatin, and rosuvastatin.[85]

Antispasmodics

Consider the use of an oral muscle relaxant if spasticity is resulting in pain or is impeding rehabilitation. CNS depression such as drowsiness and dizziness is a common adverse effect of all muscle relaxants.

Table 2. Antispasmodics Mechanisms of Action, Significant Adverse Effects, and Considerations. (Open Table in a new window)

Drug Mechanism of Action Significant Adverse Effect Consideration
Baclofen Inhibits spinal reflexes[86] Withdrawal syndrome may include hallucinations and seizures[86] Dose reduction may be needed with renal impairment[86]
Dantrolene Interferes with the release of calcium from the sarcoplasmic reticulum[87] Both diarrhea and hepatotoxicity are dose dependent and may limit use[87] Baseline and periodic liver function tests recommended[61]
Tizanidine Alpha2-adrenergic agonist that decreases excitatory input to alpha motor neurons[88] Hypotension and hepatotoxicity



Withdrawal syndrome may include tachycardia and hypertonia[88]



Effect is generally only 3-6 hours, necessitating doses being reserved for times relief is needed most



Baseline and periodic liver function tests recommended



Dose reduction may be needed with renal impairment[88]



 

Alpha-adrenergic blockers and anticholinergics

Treatment of uninhibited bladder resultant from stroke may include the use of alpha-adrenergic blockers or anticholinergics. Of the alpha-adrenergic blockers, tamsulosin is associated with less orthostatic hypotension than terazosin, doxazosin, prazosin, and alfuzosin.[89] Anticholinergics such as oxybutynin and tolterodine may also be used. The newer longer-acting antimuscarinic agents have fewer adverse effects and may promote better adherence.[90]

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Outcomes

An important role for the physiatrist and, as well as neurologist, in the postacute care of stroke patients is to discern prognosis based on predictors available. Such assessment is vital in planning and selecting appropriate rehabilitation and in preparing the patient and family for adjustments and adaptations needed to accommodate resultant disability. Early predictors include stroke severity in terms of extent on radiologic studies, National Institutes of Health Stroke scores in the acute setting, age, and other medical comorbidities. Later predictors include social support, bowel and bladder continence, trunk stability, presence of visuospatial disorders such as neglect, and flaccid paralysis.[26]

A study by Topcuoglu et al indicated that the National Institutes of Health Stroke Scale and a computed tomography angiography (CTA)-based modified clot burden score can serve as independent negative predictors for early dramatic recovery and favorable third-month prognosis in acute MCA stroke. The study included 131 patients with acute MCA stroke who underwent intravenous thrombolysis and/or interventional thrombolysis/thrombectomy.[91]

A study by Xu et al suggested that in cases of acute ischemic stroke due to occlusion of the large or middle cerebral arteries, spontaneous recanalization of the arteries is less likely in patients with atrial fibrillation and more likely in those with stage 3 hypertension. The study included 139 patients, with evaluation made of the MCA, carotid artery, and vertebral and basilar arteries. In the 23 who underwent spontaneous recanalization, the prevalence of atrial fibrillation was 0% (versus 29.31% in the other patients), while the prevalence of stage 3 hypertension was 60.87% (versus 32.76% in the other patients).[92]

In this period of increasing financial scrutiny and increased use of evidence-based medicine, comparison of postacute rehabilitation settings is growing more robust. Acute, inpatient rehabilitation facilities generally deliver more hours of and greater interdisciplinary care for stroke patients. However, the cost of rehabilitation delivered per patient from these facilities has been found to be around twice as expensive ($12,320) when compared with subacute or skilled nursing facilities ($6215).[93] Highly complex and prolonged stroke care, such as mechanical ventilation, is often achieved in long-term acute care facilities and obviously is more expensive.

Regardless, acute rehabilitation, compared with rehabilitation at a skilled nursing facility, does appear to result in lower mortality, decreased hospital re-admission, higher likelihood of return home in the short and longer term, and greater improvement in motor and cognitive function.[94, 95]

The Centers for Medicare and Medicaid Services do approve and fund admission for their covered patients to acute rehabilitation, so long as successful discharge home can be achieved in a reasonable period (approximately 2-3 wk).

Accordingly, a patient’s social support, in terms of a spouse or other caregiver, is often paramount in the physiatrist’s recommendation for a skilled nursing facility or acute rehabilitation. They often are trained in the physical care and supervision of patients with cognitive and physical disabilities resultant from stroke and are key players on the rehabilitation team.

In summary, outcome after stroke is definitely influenced by the rehabilitation setting, which often depends on the ability and availability of a patient’s family to provide care. Physiatrists need to weigh early and later prognostic indicators, as well as social support, before recommending the appropriate postacute rehabilitation setting.

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Contributor Information and Disclosures
Author

Daniel I Slater, MD Medical Director, Department of Rehabilitation, St Mary’s Hospital; Medical Director, Virginia NeuroCare; Co-founder, PosAbilities Unlimited

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)

Sharon Conrad Golden, RN, ANP-BC Nurse Practitioner, Department of Physical Medicine and Rehabilitation, Multicare Health System Allenmore Hospital

Sharon Conrad Golden, RN, ANP-BC is a member of the following medical societies: Association of Rehabilitation Nurses

Disclosure: Nothing to disclose.

Tonya Marie Cook, PharmD Clinical Pharmacy Specialist, St Mary’s Hospital

Disclosure: Nothing to disclose.

Kristen L Burnham, DPT Physical Therapist, Acute Care and Inpatient Rehabilitation, St Mary’s Hospital and Regional Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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 Association for Physician Leadership, American Medical Association, Academy of Spinal Cord Injury Professionals

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Patrick J Potter, MD, FRCSC Associate Professor, Department of Physical Medicine and Rehabilitation, University of Western Ontario School of Medicine; Consulting Staff, Department of Physical Medicine and Rehabilitation, St Joseph's Health Care Centre

Patrick J Potter, MD, FRCSC is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, College of Physicians and Surgeons of Ontario, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Acknowledgements

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

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, 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.

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Day 1 after left middle cerebral artery stroke, ischemic damage.
Day 3 after left middle cerebral artery stroke.
Day 5 after left middle cerebral artery stroke.
Normal magnetic resonance angiogram demonstrating intracerebral vascular anatomy.
Normal magnetic resonance angiogram demonstrating intracerebral vascular anatomy.
Magnetic resonance angiogram revealing right middle cerebral artery stroke.
Table 1. Hematologic Agents Mechanisms of Action and Considerations
Drug Mechanism of Action Consideration
Antiplatelets
Aspirin Inhibits cyclo-oxygenase May also be used to treat mild to moderate pain and headaches
Dipyridamole/aspirin Inhibits platelet adenosine uptake and cyclo-oxygenase[72] Twice daily dosing



Headaches are a common adverse effect, which may limit tolerability of therapy[73]



Clopidogrel Blocks platelet adenosine diphosphate (ADP) P2Y12 receptor[74] Avoidance of omeprazole and esomeprazole with clopidogrel was recommended in the 2009 FDA release warning about reduced efficacy[75]
Anticoagulants
Apixaban Direct factor Xa inhibitor[76] Not recommended for use in patients with CrCl < 15 mL/min or severe liver impairment
Dabigatran Direct thrombin inhibitor[77] Dosage adjustment needed for CrCl 50 mL/min or less
Rivaroxaban Direct factor Xa inhibitor[78] Dosage adjustment needed for CrCl 50 mL/min or less



Underweight patients have a slightly increased level/response[78]



Warfarin Inhibits formation of vitamin-K dependent clotting factors[79] Dosing based on international normalized ratio



Multiple food and drug interactions[79]



Table 2. Antispasmodics Mechanisms of Action, Significant Adverse Effects, and Considerations.
Drug Mechanism of Action Significant Adverse Effect Consideration
Baclofen Inhibits spinal reflexes[86] Withdrawal syndrome may include hallucinations and seizures[86] Dose reduction may be needed with renal impairment[86]
Dantrolene Interferes with the release of calcium from the sarcoplasmic reticulum[87] Both diarrhea and hepatotoxicity are dose dependent and may limit use[87] Baseline and periodic liver function tests recommended[61]
Tizanidine Alpha2-adrenergic agonist that decreases excitatory input to alpha motor neurons[88] Hypotension and hepatotoxicity



Withdrawal syndrome may include tachycardia and hypertonia[88]



Effect is generally only 3-6 hours, necessitating doses being reserved for times relief is needed most



Baseline and periodic liver function tests recommended



Dose reduction may be needed with renal impairment[88]



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