Middle Cerebral Artery Stroke
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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]
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.
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]
The American Heart Association 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.
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 American Heart Association 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.
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]
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 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 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.
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]
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.
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.
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.
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.
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.
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-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.
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]
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.
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]
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]
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]
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]
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]
An important role for the physiatrist, as well as the 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, 98]
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]
A study by Elofuke et al indicated that following intravenous thrombolysis for ischemic stroke, disappearance of the hyperdense middle cerebral artery sign (HMCAS) predicts better outcomes, both clinically and radiologically, and that thrombus length alone independently predicts HMCAS disappearance. The median thrombus length in patients in whom the HMCAS disappeared was 11 mm, compared with 17 mm in those whose HMCAS did not disappear. [93]
A multicenter, randomized, open-label study by Albers et al found that although the current recommendation is for eligible patients with stroke to undergo thrombectomy within 6 hours of symptom onset, patients can be successfully treated with thrombectomy between 6 and 16 hours after they were last well. The study involved patients with proximal MCA or internal carotid artery occlusion whose initial infarct size was below 70 mL and in whom the ratio of the volume of ischemic tissue as seen on perfusion imaging to the infarct volume was 1.8 or above. Patients were treated 6-16 hours after they were last known to be well. Compared with patients who received just standard medical therapy, those who underwent thrombectomy plus standard medical therapy demonstrated better functional outcomes, as measured on the modified Rankin Scale at 90 days. Moreover, the 90-day mortality rate in patients who underwent thrombectomy was 14%, compared with 26% in the group that received standard medical therapy alone. [99]
Similar results were obtained in a study by Nogueira et al. The investigators found that in patients with intracranial internal carotid artery or proximal MCA occlusion in whom a mismatch existed between clinical deficit severity and infarct volume, those who underwent thrombectomy plus standard care 6-24 hours after they were last known to be well had better 90-day disability outcomes than did patients who underwent standard care alone in the same time frame. However, the 90-day mortality rate for the two groups did not significantly differ. [100] Based on this study and the one above it, 2018 guidelines from the American Heart Association/American Stroke Association recommend that eligible patients undergo thrombectomy up to 16 hours after a stroke and state that it is “reasonable” for eligible patients to be treated by thrombectomy 16-24 hours poststroke. [101]
A study by Sundseth et al indicated that in patients with swollen MCA infarction who undergo decompressive craniectomy, involvement of additional anterior and/or posterior cerebral artery territory predicts early in-hospital death, while age, sex, time between stroke onset and decompressive craniectomy, National Institutes of Health Stroke Scale score on admission, pineal gland displacement, postsurgical pineal gland displacement reduction, and size of the craniectomy do not. [94]
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). [95] 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. [96, 97]
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.
Overview
What is middle cerebral artery stroke?
What is the middle cerebral artery (MCA)?
What has been the focus of research on middle cerebral artery (MCA) stroke?
How should a rehabilitation plan be formulated for middle cerebral artery (MCA) stroke?
What are the contraindications for rehabilitation for middle cerebral artery (MCA) stroke?
What is included in standard of care following middle cerebral artery (MCA) stroke?
What is thrombolytic therapy for middle cerebral artery (MCA) stroke?
How is hypertension managed following middle cerebral artery (MCA) stroke?
What information about middle cerebral artery (MCA) stroke should patients receive?
What is the role of music in the rehabilitation following middle cerebral artery (MCA) stroke?
What is the focus of rehabilitation following middle cerebral artery (MCA) stroke?
How are neuroplastic changes used in the rehabilitation of middle cerebral artery (MCA) stroke?
How is spasticity defined in middle cerebral artery (MCA) stroke and what can it lead to?
How is spasticity managed in middle cerebral artery (MCA) stroke?
What causes pain in middle cerebral artery (MCA) stroke?
How prevalent is centrally mediated pain following middle cerebral artery (MCA) stroke?
How can pain be prevented following middle cerebral artery (MCA) stroke?
What is the shoulder subluxation following middle cerebral artery (MCA) stroke?
What indicates the severity of shoulder subluxation following middle cerebral artery (MCA) stroke?
How is a shoulder subluxation prevented following middle cerebral artery (MCA) stroke?
How is depression prevented following middle cerebral artery (MCA) stroke?
What are treatment options for urinary incontinence following middle cerebral artery (MCA) stroke?
How does urinary tract infection affect the prognosis middle cerebral artery (MCA) stroke?
How common is fecal incontinence following middle cerebral artery (MCA) stroke?
How does fecal incontinence affect the prognosis of middle cerebral artery (MCA) stroke?
What are the treatment options for fecal incontinence following middle cerebral artery (MCA) stroke?
What should be included in patient education following middle cerebral artery (MCA) stroke?
What are activities-of-daily-living aids for the treatment of middle cerebral artery (MCA) stroke?
How does level of impairment affect rehabilitation for middle cerebral artery (MCA) stroke?
Where do most malignant middle cerebral artery (MCA) stroke occur?
What are common impairments in middle cerebral artery (MCA) stroke?
Why is neglect more common in right hemisphere middle cerebral artery (MCA) stroke?
What are the treatment approaches middle for cerebral artery (MCA) stroke rehabilitation?
What is partial visual occlusion for the treatment of middle cerebral artery (MCA) stroke?
What are the therapeutic techniques for hemiparesis in middle cerebral artery (MCA) stroke?
What is the role of gait training in the treatment of middle cerebral artery (MCA) stroke?
How is poststroke weakness defined in middle cerebral artery (MCA) stroke?
Which antiplatelet agents are used for the treatment of middle cerebral artery (MCA) stroke?
What is the role of antihypertensives in the treatment of middle cerebral artery (MCA) stroke?
What is the role of in the treatment of middle cerebral artery (MCA) stroke?
What is the role of antispasmodics in the treatment of middle cerebral artery (MCA) stroke?
What prognostic predictors have been found for middle cerebral artery (MCA) stroke?
What are the benefits of acute inpatient rehabilitation for middle cerebral artery (MCA) stroke?
What influences the outcome after a middle cerebral artery (MCA) stroke?
[Guideline] Song S, Fonarow GC, Pan W, et al. Get With The Guidelines – Stroke Program Participation and Clinical Outcomes for Medicare Beneficiaries. American Heart Association. Available at http://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_452561.pdf. Accessed: September 11, 2013.
Wentworth DA, Atkinson RP. Implementation of an acute stroke program decreases hospitalization costs and length of stay. Stroke. 1996 Jun. 27(6):1040-3. [Medline].
Cumming TB, Thrift AG, Collier JM, Churilov L, Dewey HM, Donnan GA. Very early mobilization after stroke fast-tracks return to walking: further results from the phase II AVERT randomized controlled trial. Stroke. 2011 Jan. 42(1):153-8. [Medline].
Cauraugh JH, Kim SB. Stroke motor recovery: active neuromuscular stimulation and repetitive practice schedules. J Neurol Neurosurg Psychiatry. 2003 Nov. 74(11):1562-6. [Medline].
Perry L, Love CP. Screening for dysphagia and aspiration in acute stroke: a systematic review. Dysphagia. 2001. 16(1):7-18. [Medline].
Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk BM. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013 Mar. 44(3):870-947. [Medline].
Mann G, Hankey GJ, Cameron D. Swallowing function after stroke: prognosis and prognostic factors at 6 months. Stroke. 1999 Apr. 30(4):744-8. [Medline].
Mukhopadhyay S, Katzenstein AL. Pulmonary disease due to aspiration of food and other particulate matter: a clinicopathologic study of 59 cases diagnosed on biopsy or resection specimens. Am J Surg Pathol. 2007 May. 31(5):752-9. [Medline].
Indredavik B, Rohweder G, Naalsund E, Lydersen S. Medical complications in a comprehensive stroke unit and an early supported discharge service. Stroke. 2008 Feb. 39(2):414-20. [Medline].
Kappelle LJ. Preventing deep vein thrombosis after stroke: strategies and recommendations. Curr Treat Options Neurol. 2011 Dec. 13(6):629-35. [Medline]. [Full Text].
CLOTS (Clots in Legs Or sTockings after Stroke) Trial Collaboration. Thigh-length versus below-knee stockings for deep venous thrombosis prophylaxis after stroke: a randomized trial. Ann Intern Med. 2010 Nov 2. 153(9):553-62. [Medline].
Sandercock PA, Counsell C, Tseng MC. Low-molecular-weight heparins or heparinoids versus standard unfractionated heparin for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Jul 16. CD000119. [Medline].
Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Circulation. 2007 Oct 16. 116(16):e391-413. [Medline].
Anderson CS, Huang Y, Wang JG, Arima H, Neal B, Peng B. Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol. 2008 May. 7(5):391-9. [Medline].
Aiyagari V, Gorelick PB. Management of blood pressure for acute and recurrent stroke. Stroke. 2009 Jun. 40(6):2251-6. [Medline].
Zafonte R. Neural plasticity, potential novel therapies that may enhance neural plasticity in the future, and the role these treatments may have in persons with neurologic injuries. Introduction. PM R. 2010 Dec. 2(12 Suppl 2):S207. [Medline].
Fasoli SE, Krebs HI, Ferraro M, Hogan N, Volpe BT. Does shorter rehabilitation limit potential recovery poststroke?. Neurorehabil Neural Repair. 2004 Jun. 18(2):88-94. [Medline].
O’Brien SR, Xue Y, Ingersoll G, Kelly A. Shorter Length of Stay Is Associated With Worse Functional Outcomes for Medicare Beneficiaries With Stroke. Phys Ther. 2013 Jul 25. [Medline].
Warraich Z, Kleim JA. Neural plasticity: the biological substrate for neurorehabilitation. PM R. 2010 Dec. 2(12 Suppl 2):S208-19. [Medline].
Greenough WT, Larson JR, Withers GS. Effects of unilateral and bilateral training in a reaching task on dendritic branching of neurons in the rat motor-sensory forelimb cortex. Behav Neural Biol. 1985 Sep. 44(2):301-14. [Medline].
Kleim JA, Barbay S, Nudo RJ. Functional reorganization of the rat motor cortex following motor skill learning. J Neurophysiol. 1998 Dec. 80(6):3321-5. [Medline].
Perez MA, Lungholt BK, Nyborg K, Nielsen JB. Motor skill training induces changes in the excitability of the leg cortical area in healthy humans. Exp Brain Res. 2004 Nov. 159(2):197-205. [Medline].
Marcotte K, Adrover-Roig D, Damien B, de Preaumont M, Genereux S, Hubert M. Therapy-induced neuroplasticity in chronic aphasia. Neuropsychologia. 2012 Jul. 50(8):1776-86. [Medline].
Gillen G, Sabari J. Stroke Rehabilitation: A Function-Based Approach. 3rd ed. St. Louis, Mo: Mosby Elsevier; 2011.
Särkämö T, Ripollés P, Vepsäläinen H, et al. Structural changes induced by daily music listening in the recovering brain after middle cerebral artery stroke: a voxel-based morphometry study. Front Hum Neurosci. 2014. 8:245. [Medline]. [Full Text].
Braddom R et al. Physical Medicine and Rehabilitation. 3rd ed. Philadelphia, Pa: WB Saunders; 2007. 651-65.
Francisco GE, Boake C. Improvement in walking speed in poststroke spastic hemiplegia after intrathecal baclofen therapy: a preliminary study. Arch Phys Med Rehabil. 2003 Aug. 84(8):1194-9. [Medline].
Roy CW, Sands LD. Shoulder pain in acutely admitted hemiplegics. Clin Rehabil. 1994. 8(34):334-5.
Van Ouwenaller C, Laplace PM, Chantraine A. Painful shoulder in hemiplegia. Arch Phys Med Rehabil. 1986 Jan. 67(1):23-6. [Medline].
Middleton S, McElduff P, Ward J, et al. Implementation of evidence-based treatment protocols to manage fever, hyperglycaemia, and swallowing dysfunction in acute stroke (QASC): a cluster randomised controlled trial. Lancet. 2011 Nov 12. 378(9804):1699-706. [Medline].
Ada L, Foongchomcheay A, Canning C. Supportive devices for preventing and treating subluxation of the shoulder after stroke. Cochrane Database Syst Rev. 2005 Jan 25. CD003863. [Medline].
Williams LS. Depression and stroke: cause or consequence?. Semin Neurol. 2005 Dec. 25(4):396-409. [Medline].
Starkstein SE, Mizrahi R, Power BD. Antidepressant therapy in post-stroke depression. Expert Opin Pharmacother. 2008 Jun. 9(8):1291-8. [Medline].
Kucukalic A, Bravo-Mehmedbasic A, Kulenovic AD, Suljic-Mehmedika E. Venlafaxine efficacy and tolerability in the treatment of post-stroke depression. Psychiatr Danub. 2007 Jun. 19(1-2):56-60. [Medline].
Chollet F, Tardy J, Albucher JF, Thalamas C, Berard E, Lamy C. Fluoxetine for motor recovery after acute ischaemic stroke (FLAME): a randomised placebo-controlled trial. Lancet Neurol. 2011 Feb. 10(2):123-30. [Medline].
Nakayama H, Jorgensen HS, Pedersen PM, Raaschou HO, Olsen TS. Prevalence and risk factors of incontinence after stroke. The Copenhagen Stroke Study. Stroke. 1997 Jan. 28(1):58-62. [Medline].
van Kuijk AA, van der Linde H, van Limbeek J. Urinary incontinence in stroke patients after admission to a postacute inpatient rehabilitation program. Arch Phys Med Rehabil. 2001 Oct. 82(10):1407-11. [Medline].
Kolominsky-Rabas PL, Hilz MJ, Neundoerfer B, Heuschmann PU. Impact of urinary incontinence after stroke: results from a prospective population-based stroke register. Neurourol Urodyn. 2003. 22(4):322-7. [Medline].
Patel M, Coshall C, Rudd AG, Wolfe CD. Natural history and effects on 2-year outcomes of urinary incontinence after stroke. Stroke. 2001 Jan. 32(1):122-7. [Medline].
Brittain KR, Peet SM, Potter JF, Castleden CM. Prevalence and management of urinary incontinence in stroke survivors. Age Ageing. 1999 Oct. 28(6):509-11. [Medline].
Turhan N, Atalay A, Atabek HK. Impact of stroke etiology, lesion location and aging on post-stroke urinary incontinence as a predictor of functional recovery. Int J Rehabil Res. 2006 Dec. 29(4):335-8. [Medline].
Ween JE, Alexander MP, D’Esposito M, Roberts M. Incontinence after stroke in a rehabilitation setting: outcome associations and predictive factors. Neurology. 1996 Sep. 47(3):659-63. [Medline].
Brittain KR, Peet SM, Potter JF, Castleden CM. Prevalence and management of urinary incontinence in stroke survivors. Age Ageing. 1999 Oct. 28(6):509-11. [Medline].
Rigby H, Gubitz G, Eskes G, et al. Caring for stroke survivors: baseline and 1-year determinants of caregiver burden. Int J Stroke. 2009 Jun. 4(3):152-8. [Medline].
Divani AA, Vazquez G, Barrett AM, Asadollahi M, Luft AR. Risk factors associated with injury attributable to falling among elderly population with history of stroke. Stroke. 2009 Oct. 40(10):3286-92. [Medline].
Kuptniratsaikul V, Kovindha A, Suethanapornkul S, Manimmanakorn N, Archongka Y. Complications during the rehabilitation period in Thai patients with stroke: a multicenter prospective study. Am J Phys Med Rehabil. 2009 Feb. 88(2):92-9. [Medline].
Thomas LH, Cross S, Barrett J, French B, Leathley M, Sutton CJ. Treatment of urinary incontinence after stroke in adults. Cochrane Database Syst Rev. 2008. (1):CD004462. [Medline].
Dumoulin C, Korner-Bitensky N, Tannenbaum C. Urinary incontinence after stroke: identification, assessment, and intervention by rehabilitation professionals in Canada. Stroke. 2007 Oct. 38(10):2745-51. [Medline].
Cardenas DD, Monahan DM. Management of Bladder Dysfunction. Braddom, R ed. Physical Medicine & Rehabilitation. 3rd ed. Saunders: 2007. 617-635.
Abrams P, Andersson KE, Birder L, Brubaker L, Cardozo L, Chapple C. Fourth International Consultation on Incontinence Recommendations of the International Scientific Committee: Evaluation and treatment of urinary incontinence, pelvic organ prolapse, and fecal incontinence. Neurourol Urodyn. 2010. 29(1):213-40. [Medline].
Poisson SN, Johnston SC, Josephson SA. Urinary tract infections complicating stroke: mechanisms, consequences, and possible solutions. Stroke. 2010 Apr. 41(4):e180-4. [Medline].
Aslanyan S, Weir CJ, Diener HC, Kaste M, Lees KR. Pneumonia and urinary tract infection after acute ischaemic stroke: a tertiary analysis of the GAIN International trial. Eur J Neurol. 2004 Jan. 11(1):49-53. [Medline].
Ifejika-Jones NL, Peng H, Noser EA, Francisco GE, Grotta JC. Hospital-acquired symptomatic urinary tract infection in patients admitted to an academic stroke center affects discharge disposition. PM R. 2013 Jan. 5(1):9-15. [Medline].
Lusardi G, Lipp A, Shaw C. Antibiotic prophylaxis for short-term catheter bladder drainage in adults. Cochrane Database Syst Rev. 2013 Jul 3. 7:CD005428. [Medline].
Harari D, Coshall C, Rudd AG, Wolfe CD. New-onset fecal incontinence after stroke: prevalence, natural history, risk factors, and impact. Stroke. 2003 Jan. 34(1):144-50. [Medline].
Rastogi V, Lamb DG, Williamson JB, et al. Hemispheric differences in malignant middle cerebral artery stroke. J Neurol Sci. 2015 Jun 15. 353 (1-2):20-27. [Medline].
Heilman KM, Valenstein E. Mechanisms underlying hemispatial neglect. Ann Neurol. 1979 Feb. 5(2):166-70. [Medline].
Robertson IH, Tegner R, Tham K, Lo A, Nimmo-Smith I. Sustained attention training for unilateral neglect: theoretical and rehabilitation implications. J Clin Exp Neuropsychol. 1995 May. 17(3):416-30. [Medline].
Di Pellegrino G. Clock-drawing in a case of left visuo-spatial neglect: a deficit of disengagement?. Neuropsychologia. 1995 Mar. 33(3):353-8. [Medline].
Kinsbourne M. Mechanisms of unilateral neglect. Jennerod M, ed. Neurophysiological and Neurophsychological Aspects of Spatial Neglect. Amsterdam: Elsevier Science; 1987. 69-86.
Freeman E. Unilateral spatial neglect: new treatment approaches with potential application to occupational therapy. Am J Occup Ther. 2001 Jul-Aug. 55(4):401-8. [Medline].
Wolf SL, Lecraw DE, Barton LA, Jann BB. Forced use of hemiplegic upper extremities to reverse the effect of learned nonuse among chronic stroke and head-injured patients. Exp Neurol. 1989 May. 104(2):125-32. [Medline].
Robertson IH, North N. Spatio-motor cueing in unilateral left neglect: the role of hemispace, hand and motor activation. Neuropsychologia. 1992 Jun. 30(6):553-63. [Medline].
Robertson IH, North N. Active and passive activation of left limbs: influence on visual and sensory neglect. Neuropsychologia. 1993 Mar. 31(3):293-300. [Medline].
Arai T, Ohi H, Sasaki H, Nobuto H, Tanaka K. Hemispatial sunglasses: effect on unilateral spatial neglect. Arch Phys Med Rehabil. 1997 Feb. 78(2):230-2. [Medline].
Al-Aboudi W. Introduction to the Neuro-Integrative Functional Rehabilitation and Habilitation (Neuro-IFRAH) Approach in the Treatment and Management of Adults with Hemiplegia from a Stroke or Brain Injury. La Jolla: Neuro-IFRAH P. 2004.
Barbeau H, Visintin M. Optimal outcomes obtained with body-weight support combined with treadmill training in stroke subjects. Arch Phys Med Rehabil. 2003 Oct. 84(10):1458-65. [Medline].
Patten C, Lexell J, Brown HE. Weakness and strength training in persons with poststroke hemiplegia: rationale, method, and efficacy. J Rehabil Res Dev. 2004 May. 41(3A):293-312. [Medline].
Kirsteins AE, Black-Schaffer RM, Harvey RL. Stroke rehabilitation. 3. Rehabilitation management. Arch Phys Med Rehabil. 1999 May. 80(5 Suppl 1):S17-20. [Medline].
Prescribing information for Effient [package insert]. Indianapolis, Ind: Eli Lilly and Company. 2009.
Prescribing information for Brilinta [package insert]. Wilmington, Del: AstraZeneca. 2011.
Prescribing information for Aggrenox [package insert]. Ridgefield, Conn: Boehringer Ingelheim Pharmaceuticals. 2012.
Prescribing information for Plavix [package insert]. Bridgewater, NJ: Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership. 2011.
U.S. Food and Drug Administration. Information for healthcare professionals: update to the labeling of clopidogrel bisulfate (marketed as Plavix) to alert healthcare professionals about a drug interaction with omeprazole (marketed as Prilosec and Prilosec OTC). November 17, 2009.
Prescribing information for Eliquis [package insert]. Montreal, Queb: Bristol-Myers Squibb Canada. 2012.
Prescribing information for Pradaxa [package insert]. Ridgefield, Conn: Boehringer Ingelheim Pharmaceuticals. 2012.
Prescribing information for Xarelto [package insert]. Toronto, Canada: Bayer. 2012.
Prescribing information for Coumadin [package insert]. Princeton, NJ: Bristol-Myers Squibb. 2011.
Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000 Jan 20. 342(3):145-53. [Medline].
Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet. 2001 Sep 29. 358(9287):1033-41. [Medline].
Dahlof B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet. 2002 Mar 23. 359(9311):995-1003. [Medline].
Carlberg B, Samuelsson O, Lindholm LH. Atenolol in hypertension: is it a wise choice?. Lancet. 2004 Nov 6-12. 364(9446):1684-9. [Medline].
Milionis HJ, Giannopoulos S, Kosmidou M, et al. Statin therapy after first stroke reduces 10-year stroke recurrence and improves survival. Neurology. 2009 May 26. 72(21):1816-22. [Medline].
PL Detail-Document, Characteristics of the Various Statins. Pharmacist’s Letter/Prescriber’s Letter. May 2012.
Prescribing information for Lioresal [package insert]. East Hanover, NJ: Novartis Pharmaceuticals. 1988.
Prescribing information for Dantrium [package insert]. Rochester, Mich: JHP Pharmaceuticals. 2008.
Prescribing information for Zanaflex [package insert]. Hawthorne, NY: Acorda Therapeutics. 2006.
Lee M. Alfuzosin hydrochloride for the treatment of benign prostatic hyperplasia. Am J Health Syst Pharm. 2003 Jul 15. 60(14):1426-39. [Medline].
Barkin J. Overactive bladder. Can J Urol. 2011 Apr. 18 Suppl:8-13. [Medline].
Deutsch A, Granger CV, Heinemann AW, et al. Poststroke rehabilitation: outcomes and reimbursement of inpatient rehabilitation facilities and subacute rehabilitation programs. Stroke. 2006 Jun. 37(6):1477-82. [Medline].
Topcuoglu MA, Arsava EM, Akpinar E. Clot characteristics on computed tomography and response to thrombolysis in acute middle cerebral artery stroke. J Stroke Cerebrovasc Dis. 2015 Jun. 24 (6):1363-72. [Medline].
Xu Y, Qian G, Wei L, et al. Predictive Factors for the Spontaneous Recanalization of Large and Middle Cerebral Arteries after Acute Occlusion. J Stroke Cerebrovasc Dis. 2016 May 10. [Medline].
Elofuke P, Reid JM, Rana A, Macleod MJ. Disappearance of the hyperdense MCA sign after stroke thrombolysis: implications for prognosis and early patient selection for clot retrieval. J R Coll Physicians Edinb. 2016 Jun. 46 (2):81-86. [Medline].
Sundseth J, Sundseth A, Jacobsen EA, et al. Predictors of early in-hospital death after decompressive craniectomy in swollen middle cerebral artery infarction. Acta Neurochir (Wien). 2017 Feb. 159 (2):301-306. [Medline].
Harvey RL. Inpatient Rehab Facilities Benefit Post-stroke Care. Managed Care. Available at http://www.managedcaremag.com/archives/1001/1001.stroke.html. Accessed: September 11, 2013.
Retchin SM, Brown RS, Yeh SC, Chu D, Moreno L. Outcomes of stroke patients in Medicare fee for service and managed care. JAMA. 1997 Jul 9. 278(2):119-24. [Medline].
Duncan PW, Horner RD, Reker DM, et al. Adherence to postacute rehabilitation guidelines is associated with functional recovery in stroke. Stroke. 2002 Jan. 33(1):167-77. [Medline].
Walcott BP, Miller JC, Kwon CS, et al. Outcomes in severe middle cerebral artery ischemic stroke. Neurocrit Care. 2014 Aug. 21 (1):20-6. [Medline]. [Full Text].
Albers GW, Marks MP, Kemp S, et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med. 2018 Jan 24. [Medline]. [Full Text].
Nogueira RG, Jadhav AP, Haussen DC, et al. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct. N Engl J Med. 2018 Jan 4. 378 (1):11-21. [Medline].
[Guideline] Anderson P. New Stroke Guidelines Extend Thrombectomy to 24 Hours. Medscape Medical News. 2018 Jan 25. [Full Text].
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]
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]
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.
Kristen L Burnham, DPT Physical Therapist, Acute Care and Inpatient Rehabilitation, St Mary’s Hospital and Regional Medical Center
Disclosure: Nothing to disclose.
Tonya Marie Cook, PharmD Clinical Pharmacy Specialist, St Mary’s Hospital
Disclosure: Nothing to disclose.
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.
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.
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.
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.
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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