||This article includes a list of references, but its sources remain unclear because it has insufficient inline citations. (March 2013)|
The primary goals of stroke management are to reduce brain injury and promote maximum patient recovery. Rapid detection and appropriate emergency medical care are essential for optimizing health outcomes. When available, patients are admitted to an acute stroke unit for treatment. These units specialize in providing medical and surgical care aimed at stabilizing the patient’s medical status. Standardized assessments are also performed to aid in the development of an appropriate care plan. Current research suggests that stroke units may be effective in reducing in-hospital fatality rates and the length of hospital stays.
Once a patient is medically stable, the focus of their recovery shifts to rehabilitation. Some patients are transferred to in-patient rehabilitation programs, while others may be referred to out-patient services or home-based care. In-patient programs are usually facilitated by an interdisciplinary team that may include a physician, nurse, pharmacist, physical therapist, occupational therapist, speech and language pathologist, psychologist, and recreation therapist. The patient and their family/caregivers also play an integral role on this team. The primary goals of this sub-acute phase of recovery include preventing secondary health complications, minimizing impairments, and achieving functional goals that promote independence in activities of daily living.
In the later phases of stroke recovery, patients are encouraged to participate in secondary prevention programs for stroke. Follow-up is usually facilitated by the patient’s primary care provider.
The initial severity of impairments and individual characteristics, such as motivation, social support, and learning ability, are key predictors of stroke recovery outcomes. Responses to treatment and overall recovery of function are highly dependent on the individual. Current evidence indicates that most significant recovery gains will occur within the first 12 weeks following a stroke.
- 1 History of stroke neuro-rehabilitation
- 2 Current perspectives and therapeutic avenues
- 3 Stem cells therapies (in research)
- 4 Training of muscles affected by the Upper Motor Neuron Syndrome
- 5 Shoulder subluxation following stroke
- 6 Post-stroke pain syndromes
- 7 Apraxia
- 8 Lateral medullary syndrome
- 9 Post-stroke depression
- 10 External links
- 11 References
History of stroke neuro-rehabilitation
In 1620, Johann Jakob Wepfer, by studying the brain of a pig, developed the theory that stroke was caused by an interruption of the flow of blood to the brain. After that, the focus became how to treat patients with stroke.
For most of the last century, people were discouraged from being active after a stroke. Around the 1950s, this attitude changed, and health professionals began prescription of therapeutic exercises for stroke patient with good results. At that point, a good outcome was considered to be achieving a level of independence in which patients are able to transfer from the bed to the wheelchair without assistance.
In the early 1950s, Twitchell began studying the pattern of recovery in stroke patients. He reported on 121 patients whom he had observed. He found that by four weeks, if there is some recovery of hand function, there is a 70% chance of making a full or good recovery. He reported that most recovery happens in the first three months, and only minor recovery occurs after six months. More recent research has demonstrated that significant improvement can be made years after the stroke.
Around the same time, Brunnstrom also described the process of recovery, and divided the process into seven stages. As knowledge of the science of brain recovery improved, intervention strategies have evolved. Knowledge of strokes and the process of recovery after strokes has developed significantly in the late 20th century and early 21st century.
Current perspectives and therapeutic avenues
Constraint-induced movement therapy
The idea for constraint-induced therapy is at least 100 years old. Significant research was carried out by Robert Oden. He was able to simulate a stroke in a monkey's brain, causing hemiplegia. He then bound up the monkey's good arm, and forced the monkey to use his bad arm, and observed what happened. After two weeks of this therapy, the monkeys were able to use their once hemiplegic arms again. This is due to neuroplasticity. He did the same experiment without binding the arms, and waited six months past their injury. The monkeys without the intervention were not able to use the affected arm even six months later. In 1918, this study was published, but it received little attention.
Eventually, researchers began to apply his technique to stroke patients, and it came to be called constraint-induced movement therapy. Notably, the initial studies focused on chronic stroke patients who were more than 12 months past their stroke. This challenged the belief held at that time that no recovery would occur after one year. The therapy entails wearing a soft mitt on the good hand for 90% of the waking hours, forcing use of the affected hand. The patients undergo intense one-on-one therapy for six to eight hours per day for two weeks.
Evidence that supports the use of constraint induced movement therapy has been growing since its introduction as an alternative treatment method for upper limb motor deficits found in stroke populations. Recently, constraint induced movement therapy has been shown to be an effective rehabilitation technique at varying stages of stroke recovery to improve upper limb motor function and use during daily activities of living. The greatest gains are seen among persons with stroke who exhibit some wrist and finger extension in the effected limb. Transcranial magnetic stimulation and brain imaging studies have demonstrated that the brain undergoes plastic changes in function and structure in patients that perform constraint induced movement therapy. These changes accompany the gains in motor function of the paretic upper limb. However, there is no established causal link between observed changes in brain function/structure and the motor gains due to constraint induced movement therapy.
Constraint induced movement therapy has recently been modified to treat aphasia in patients post CVA as well. This treatment intervention is know as Constraint Induced Aphasia Therapy (CIAT). The same general principals apply, however in this case, the client is constricted from using compensatory strategies to communicate such as gestures, writing, drawing, and pointing, and are encouraged to use verbal communication. Therapy is typically carried out in groups and barriers are used so hands, and any compensatory strategies are not seen. <Cohen, A. (2014). Constraint Induced Aphasia Therapy. Retrieved from http://researchandhope.com/constraint-induced-aphasia-therapy>
Mental Practice/Mental Imagery
Mental practice of movements, has been shown in many studies to be effective in promoting recovery of both arm and leg function after a stroke. It is often used by physical or occupational therapists in the rehab or homehealth setting, but can also be used as part of a patient's independent home exercise program. Mental Movement Therapy is one product available for assisting patients with guided mental imagery.
Such work represents a paradigm shift in the approach towards rehabilitation of the stroke-injured brain away from pharmacologic flooding of neuronal receptors and instead, towards targeted physiologic stimulation. In layman's terms, this electrical stimulation mimics the action of healthy muscle to improve function and aid in retraining weak muscles and normal movement. Functional Electrical Stimulation (FES) is commonly used in ‘foot-drop’ following stroke, but it can be used to help retrain movement in the arms or legs.
In patients undergoing rehabilitation with a stroke population or other central nervous system disorders (cerebral palsy,etc.), Bobath, also known as Neurodevelopmental Treatment (NDT), is often the treatment of choice in North America. The Bobath concept is best viewed as a framework for interpretation and problem solving of the individual patient’s presentation, along with their potential for improvement. Components of motor control that are specifically emphasized, are the integration of postural control and task performance, the control of selective movement for the production of coordinated sequences of movement and the contribution of sensory inputs to motor control and motor learning. Task practice is a component of a broad approach to treatment that includes in-depth assessment of the movement strategies utilized by the patient to perform tasks, and identification of specific deficits of neurological and neuromuscular functions. Many studies have been conducted comparing NDT with other treatment techniques such as proprioceptive neuromuscular facilitation (PNF stretching), as well as conventional treatment approaches (utilizing traditional exercises and functional activities), etc. Despite being widely used, based on the literature, NDT has failed to demonstrate any superiority over other treatment techniques available. In fact, the techniques compared with NDT in these studies often produce similar results in terms of treatment effectiveness. Research has demonstrated significant findings for all these treatment approaches when compared with control subjects and indicate that overall, rehabilitation is effective. It is important to note, however, that the NDT philosophy of “do what works best” has led to heterogeneity in the literature in terms of what constitutes an NDT technique, thus making it difficult to directly compare to other techniques.
Mirror therapy (MT) has been employed with some success in treating stroke patients. Clinical studies that have combined mirror therapy with conventional rehabilitation have achieved the most positive outcomes. However, there is no clear consensus as to its effectiveness. In a recent survey of the published research, Rothgangel concluded that
In stroke patients, we found a moderate quality of evidence that MT as an additional therapy improves recovery of arm function after stroke. The quality of evidence regarding the effects of MT on the recovery of lower limb functions is still low, with only one study reporting effects. In patients with CRPS and PLP, the quality of evidence is also low.
Stem cells therapies (in research)
Use of bone-marrow derived mesenchymal stem cells (MSCs) in the treatment of ischemic stroke
The terminal differentiation of some somatic stem cells has recently been called into question  after studies of transplanted haematopoietic stem cells showed the development of myoblasts, endothelium, epithelium  and neuroectodermal cells, suggesting pluripotency. These findings have led to MSCs being considered for treatment of ischemic stroke, specifically in directly enhancing neuroprotection and the neurorestorative processes of neurogenesis, angiogenesis and synaptic plasticity.
Possible mechanisms of neurorestoration and neuroprotection by MSCs after stroke
Transdifferentiation of MSCs into excitable neuron-like cells has been shown to be possible in vitro  and these cells respond to common central nervous system neurotransmitters. However, it is unlikely that this degree of transdifferentiation occurs in vivo and that <1% of injected MSCs become truly differentiated and integrate in the damaged area. This suggests that transdifferentiation of MSCs into neurons or neuron-like cells is not a major mechanism by which MSCs cause neurorestoration.
Induction of neurogenesis (development of new neurons) is another possible mechanism of neurorestoration; however its correlation with functional improvement after stroke is not well established. The inducted cells likely originate from the ventricular zone, subventricular zone and choroid plexus, and migrate to the areas in their respective hemispheres which are damaged. Unlike the induction of neurogenesis, the induction of angiogenesis (development of new blood vessels) by MSCs has been associated with improvements in brain function after ischemic strokes  and is linked to improved neuronal recruitment. In addition, synaptogenesis (formation of new synapses between neurons) has been shown to increase after MSC treatment; this combination of improved neurogenesis, angiogenesis and synaptogenesis may lead to a more significant functional improvement in damaged areas as a result of MSC treatment.
MSC treatment also has shown to have various neuroprotective effects, including reductions in apoptosis, inflammation and demyelination, as well as increased astrocyte survival rates. MSC treatment also appears to improve the control of cerebral blood flow and blood–brain barrier permeability, as well as what is currently thought to be the most important mechanism of MSC treatment after stroke, the activation of endogenous neuroprotection and neurorestoration pathways by the release of cytokines and trophic factors.
Although activation of endogenous neuroprotection and neurorestoration probably has a major part in the improvement of brain function after stroke, it is likely that the functional improvements as a result of MSC treatment are due to combined action via multiple cellular and molecular mechanisms to affect neurorestoration and neuroprotection, rather than just a single mechanism. These effects are also modulated by key variables, including the number of and type of MSCs used, timing of treatment relative to when the patient’s stroke occurred, route of delivery of the MSCs, as well as patient variables (e.g. age, underlying conditions).
What this means for stroke patients and the limitations or concerns with MSCs as a potential treatment
If MSC treatment becomes available for stroke patients, it is possible that current mortality and morbidity rates could substantially improve due to the direct enhancement of neuroprotection and neurorestoration mechanisms rather than only indirect facilitation or prevention of further damage, e.g. decompressive surgery. However, for MSC treatment to be used effectively and safely in a clinical setting, more research needs to be conducted, specifically in the areas of determining the relative influences of key variables (especially patient variables) on patient outcomes as well quantifying potential risks, e.g. tumour formation. Although ethical concerns are mostly limited to the use of embryonic stem cells, it may also be important to address any possible ethical concerns (however unlikely) over the use of somatic stem cells.
Training of muscles affected by the Upper Motor Neuron Syndrome
Muscles affected by the Upper Motor Neuron Syndrome have many potential features of altered performance including: weakness, decreased motor control, clonus (a series of involuntary rapid muscle contractions), exaggerated deep tendon reflexes, spasticity and decreased endurance. The term "spasticity" is often erroneously used interchangeably with Upper Motor Neuron Syndrome, and it is not unusual to see patients labeled as spastic who demonstrate an array of UMN findings.
It has been estimated that approximately 65% of individuals develop spasticity following stroke, and studies have revealed that approximately 40% of stroke victims may still have spasticity at 12 months post-stroke. The changes in muscle tone probably result from alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord, and the absence of an intact corticospinal system. In other words, there is damage to the part of the brain or spinal cord that controls voluntary movement.
Various means are available for the treatment of the effects of the Upper Motor Neuron Syndrome. These include: exercises to improve strength, control and endurance, nonpharmacologic therapies, oral drug therapy, intrathecal drug therapy, injections, and surgery. While Landau suggests that researchers do not believe that treating spasticity is worthwhile, many scholars and clinicians continue to attempt to manage/treat it.
Another group of researchers concluded that while spasticity may contribute to significant motor and activity impairments post-stroke, the role of spasticity has been overemphasized in stroke rehabilitation. In a survey done by the National Stroke Association, while 58 percent of survivors in the survey experienced spasticity, only 51 percent of those had received treatment for the condition.
Treatment should be based on assessment by the relevant health professionals. For muscles with mild-to-moderate impairment, exercise should be the mainstay of management, and is likely to need to be prescribed by a physiotherapist.
Muscles with severe impairment are likely to be more limited in their ability to exercise and may require help to do this. They may require additional interventions, to manage the greater neurological impairment and also the greater secondary complications. These interventions may include serial casting, flexibility exercise such as sustained positioning programs, and patients may require equipment, such as using a standing frame to sustain a standing position. Applying specially made Lycra garments may also be beneficial.
Physiotherapy is beneficial in this area as it helps post-stroke individuals to progress through the stages of motor recovery. These stages were originally described by Twitchell and Brunnstrom, and may be known as the Brunnstrom Approach. Initially, post-stroke individuals suffer from flaccid paralysis. As recovery begins, and progresses, basic movement synergies will develop into more complex and difficult movement combinations. Concurrently, spasticity may develop and become quite severe before it begins to decline (if it does at all). Although an overall pattern of motor recovery exists, there is much variability between each individual’s recovery. As previously described, the role of spasticity in stroke rehabilitation is controversial. However, physiotherapy can help to improve motor performance, in part, through the management of spasticity.
Unaddressed spasticity will result in the maintenance of abnormal resting limb postures which can lead to contracture formation. In the arm, this may interfere with hand hygiene and dressing, whereas in the leg, abnormal resting postures may result in difficulty transferring. In order to help manage spasticity, physiotherapy interventions should focus on modifying or reducing muscle tone. Strategies include mobilizations of the affected limbs early in rehabilitation, along with elongation of the spastic muscle and sustained stretching. In addition, the passive manual technique of rhythmic rotation can help to increase initial range. Activating the antagonist (muscle) in a slow and controlled movement is a beneficial training strategy that can be used by post-stroke individuals. Splinting, to maintain muscle stretch and provide tone inhibition, and cold (i.e. in the form of ice packs), to decrease neural firing, are other strategies that can be used to temporarily decrease the extent of spasticity. The focus of physiotherapy for post-stroke individuals is to improve motor performance, in part, through the manipulation of muscle tone.
Oral drug therapies
Oral medications used for the treatment of spasticity include: diazepam (Valium), dantrolene sodium, baclofen, tizanidine, clonidine, gabapentin, and even cannabinoid-like compounds.³ The exact mechanism of these medications is not fully understood, but they are thought to act on neurotransmitters or neuromodulators within the central nervous system (CNS) or muscle itself, or to decrease the stretch reflexes. The problem with these medications is their potential side effects and the fact that, other than lessening painful or disruptive spasms and dystonic postures, drugs in general have not been shown to decrease impairments or lessen disabilities.
Intrathecal drug therapy
Intrathecal administration of drugs involves the implantation of a pump that delivers medication directly to the CNS. The benefit of this is that the drug remains in the spinal cord, without traveling in the bloodstream, and there are often fewer side effects. The most commonly used medication for this is baclofen but morphine sulfate and Fentanyl have been used as well, mainly for severe pain as a result of the spasticity.
Injections are focal treatments administered directly into the spastic muscle. Drugs used include: Botulinum toxin (BTX), phenol, alcohol, and lidocaine. Phenol and alcohol cause local muscle damage by denaturing protein, and thus relaxing the muscle. Botulinum toxin is a neurotoxin and it relaxes the muscle by preventing the release of a neurotransmitter (acetylcholine). Many studies have shown the benefits of BTX and it has also been demonstrated that repeat injections of BTX show unchanged effectiveness.
Surgical treatment for spasticity includes lengthening or releasing of muscle and tendons, procedures involving bones, and also selective dorsal rhizotomy. Rhizotomy, usually reserved for severe spasticity, involves cutting selective sensory nerve roots, as they probably play a role in generating spasticity.
Shoulder subluxation following stroke
Glenohumeral (or shoulder) subluxation is defined as a partial or incomplete dislocation of the shoulder joint that typically results from changes in the mechanical integrity of the joint. Subluxation is a common problem with hemiplegia, or weakness of the musculature of the upper limb. Traditionally this has been thought to be a significant cause of post-stroke shoulder pain, although a few recent studies have failed to show a direct correlation between shoulder subluxation and pain.
The exact etiology of subluxation in post-stroke patients is unclear but appears to be caused by weakness of the musculature supporting the shoulder joint. The shoulder is one of the most mobile joints in the body. To provide a high level of mobility the shoulder sacrifices ligamentous stability and as a result relies on the surrounding musculature (i.e., rotator cuff muscles, latissimus dorsi, and deltoid) for much of its support. This is in contrast to other less mobile joints such as the knee and hip, which have a significant amount of support from the joint capsule and surrounding ligaments. If a stroke damages the upper motor neurons controlling muscles of the upper limb, weakness and paralysis, followed by spasticity occurs in a somewhat predictable pattern. The muscles supporting the shoulder joint, particularly the supraspinatus and posterior deltoid become flaccid and can no longer offer adequate support leading to a downward and outward movement of arm at the shoulder joint causing tension on the relatively weak joint capsule. Other factors have also been cited as contributing to subluxation such as pulling on the hemiplegic arm and improper positioning.
Diagnosis can usually be made by palpation or by feeling the joint and surrounding tissues, although there is controversy as to whether or not the degree of subluxation can be measured clinically. If shoulder subluxation occurs, it can become a barrier to the rehabilitation process. Treatment involves measures to support the subluxed joint such as taping the joint, using a lapboard or armboard. A shoulder sling may be used, but is controversial and a few studies have shown no appreciable difference in range-of-motion, degree of subluxation, or pain when using a sling. A sling may also contribute to contractures and increased flexor tone if used for extended periods of time as it places the arm close to the body in adduction, internal rotation and elbow flexion. Use of a sling can also contribute to learned nonuse by preventing the functional and spontaneous use of the affected upper extremity. That said, a sling may be necessary for some therapy activities. Slings may be considered appropriate during therapy for initial transfer and gait training, but overall use should be limited. As the patient begins to recover, spasticity and voluntary movement of the shoulder will occur as well as reduction in the shoulder subluxation. Slings are of no value at this point.
Functional electrical stimulation (FES) has also shown promising results in treatment of subluxation, and reduction of pain, although some studies have shown a return of pain after discontinuation of FES. More recent research has failed to show any reduction of pain with the use of FES.
Logical treatment consists of preventive measures such as early range of motion, proper positioning, passive support of soft tissue structures and possibly early re-activation of shoulder musculature using functional electrical stimulation. Aggressive exercises such as overhead pulleys should be avoided with this population.
1. Teasell RW: "The Painful Hemiplegic Shoulder". Physical Medicine and Rehabilitation: State of the Art Reviews 1998; 12 (3): 489-500.
2. Boyd EA, Goudreau L, O'Riain MD, et al.: A radiological measure of shoulder subluxation in hemiplegia: its reliability and validity. Arch Phys Med Rehabil 1993 Feb; 74(2): 188-93
3. Brandstater ME: Stroke rehabilitation. In: DeLisa JA, et al., eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia: Lippincott-Raven; 1998:1165-1189.
4. Chae J, Yu DT, Walker ME, et al.: Intramuscular electrical stimulation for hemiplegic shoulder pain: a 12-month follow-up of a multiple-center, randomized clinical trial. Am J Phys Med Rehabil. 2005 Nov; 84(11): 832-42
5. Chantraine A, Baribeault A, Uebelhart D, Gremion G: Shoulder pain and dysfunction in hemiplegia: effects of functional electrical stimulation. Arch Phys Med Rehabil 1999 Mar; 80(3): 328-31
Post-stroke pain syndromes
Central Post-stroke Pain (CPSP) is neuropathic pain which is caused by damage to the neurons in the brain (central nervous system), as the result of a vascular injury. One study found that up to 8% of people who have had a stroke will develop Central Post-stroke Pain, and that the pain will be moderate to severe in 5% of those affected. The condition was formerly called “thalamic pain”, because of the high incidence among those with damage to the thalamus or thalamic nuclei. Now known as CPSP, it is characterized by perceived pain from non-painful stimuli, such as temperature and light touch. This altered perception of stimuli, or allodynia, can be difficult to assess due to the fact that the pain can change daily in description and location, and can appear anywhere from months to years after the stroke. CPSP can also lead to a heightened central response to painful sensations, or hyperpathia. Affected persons may describe the pain as cramping, burning, crushing, shooting, pins and needles, and even bloating or urinary urgency. Both the variation and mechanism of pain in CPSP have made it difficult to treat. Several strategies have been employed by physicians, including intravenous lidocaine, opioids/narcotics, anti-depressants, anti-epileptic medications and neurosurgical procedures with varying success. Higher rates of successful pain control in persons with CPSP can be achieved by treating other sequelae of stroke, such as depression and spasticity. As the age of the population increases, the diagnosis and management of CPSP will become increasingly important to improve the quality of life of an increasing number of stroke survivors.
An uncommon, less understood result of stroke is a condition called apraxia. This condition was initially recognized as: ‘Disorders of the execution of learned movements which cannot be accounted for by either weakness, incoordination, or sensory loss, nor by incomprehension of, or inattention to commands.’ Several forms of apraxia are recognized. Limb-kinetic apraxia is the inability to make precise or exact movements with a finger, an arm or a leg. idiomotor apraxia is the inability to carry out a command from the brain to mimic limb or head movements performed or suggested by others. Conceptual apraxia is similar to idiomotor apraxia, but infers a more profound malfunctioning in which the function of tools or objects is no longer understood. Ideational apraxia is the inability to create a plan for a specific movement. Buccofacial apraxia, or facial-oral apraxia, is the inability to coordinate and carry out facial and lip movements such as whistling, winking, coughing, etc. on command. Constructional apraxia affects the person’s ability to draw or copy simple diagrams, or to construct simple figures. Oculomotor apraxia is a condition in which the patient finds it difficult to move his/her eyes. Many believe that the most common form of apraxia is ideamotor apraxia, in which a disconnection between the area of the brain containing plans for a movement and the area of the brain that is responsible for executing that movement occurs.[full citation needed]
Unlike many effects of stroke, where the clinician is able to judge the particular area of the brain that a stroke has injured by certain signs or symptoms, the causation of apraxia is less clear. A common theory is that the part of the brain that contains information for previously learned skilled motor activities has been either lost or cannot be accessed. The condition is usually due to an insult to the dominant hemisphere of the brain. More often this is located in the frontal lobe of the left hemisphere of the brain. Treatment of acquired apraxia due to stroke usually consists of physical, occupational, and speech therapy. The Copenhagen Stroke Study, which is a large important study published in 2001, showed that out of 618 stroke patients, manual apraxia was found in 7% and oral apraxia was found in 6%. Both manual and oral apraxia were related to increasing severity of stroke. Oral apraxia was related with an increase in age at the time of the stroke. There was no difference in incidence among gender. It was also found that the finding of apraxia has no negative influence on ability to function after rehabilitation is completed. The National Institute of Neurological Disorders and Stroke (NINDS) is currently sponsoring a clinical trial to gain an understanding of how the brain operates while carrying out and controlling voluntary motor movements in normal subjects. The objective is to determine what goes wrong with these processes in the course of acquired apraxia due to stroke or brain injury.
Lateral medullary syndrome
Lateral medullary syndrome, also known as Wallenberg’s Syndrome, is caused by blockage of the posterior inferior cerebellar artery (PICA) or the vertebral arteries. Signs and symptoms include decreased pain and temperature on the same side of the face and opposite side of the body compared to the lesion, ataxia on the same side of the lesion, and Horner's syndrome on the same side of the face.
Treatment in the acute setting is mostly focused on symptomatic management. After initial treatment in the hospital, some patients will need short-term placement in a nursing home or rehabilitation facility before going home. In hospital settings the doctors work with speech pathologists in issues like these. Typically, a commonly used tool to assess the degree of severity of dysphagia and speech issues is the Barnes Jewish Hospital Stroke Dysphagia Screen, which offers a validated guide to assessing plan of action (solid food diet, all liquid diet, IV hydration, etc) for the patient while in the hospital and the proper course of action in the outpatient setting. Rehabilitation in Wallenberg’s Syndrome focuses on improving balance, coordination, working on activities of daily living, and improving speech and swallowing function. Severe nausea and vertigo can be present and limit progress in rehabilitation and recovery. Symptomatic treatment with anti-emetics and medications for the hiccups are important. Commonly used anti-emetics include ondansetron, metoclopramide, prochlorperazine, and promethazine. These medications are also used to treat hiccups, along with chlorpromazine. There are case reports of other medications useful in treating hiccups in Wallenberg’s Syndrome including baclofen and anti-epileptic medications. The prognosis for someone with lateral medullary syndrome depends upon the size and location of damaged area of the brain stem. Some individuals recover quickly while others may have significant neurological disabilities for months to years after the initial injury.
1. Hiccups Associated with Lateral Medullary Syndrome: A Case Report. American Journal of Physical Medicine & Rehabilitation. 76(2):144-146, March/April 1997. Nickerson, Robert B. MD 2; Atchison, James W. DO 3; Van Hoose, James D. MD; Hayes, Don BS.
2. Physical Medicine and Rehabilitation Board Review (Paperback). Sara J. Cuccurullo
4. Dysphagia in Lateral Medullary Infarction (Wallenberg’s Syndrome) . An Acute Disconnection Syndrome in Premotor Neurons Related to Swallowing Activity? Stroke. 2001;32:2081. Ibrahim Aydogdu, MD; Cumhur Ertekin, MD; Sultan Tarlaci, MD; Bulent Turman, MD, PhD; Nefati Kiylioglu, MD Yaprak Secil, MD
5. Edmiaston J, Connor LT, Loehr L, Nassief A. Validation of a dysphagia screening tool in acute stroke patients. Am J Crit Care. 2010 Jul;19(4):357-64. doi: 10.4037/ajcc2009961. Epub 2009 Oct 29.
Depression is a commonly reported consequence of stroke and is seen in anywhere from 25-50% of patients. The Diagnostic and Statistical Manual (DSM-IV-TR) defines post-stroke depression as “a mood disorder due to a general medical condition (i.e. stroke) that is judged to be due to the direct physiological effects of [that] condition.” Post-stroke depression may involve depressed mood and decreased interest and pleasure that impairs social and occupational functioning, but does not necessarily need to meet the full criteria of a major depressive disorder.
The first studies to look for an association between specific stroke lesions and the occurrence of depression reported a correlation between left frontal lesions and major depression. Damage to the frontal noradrenergic, dopaminergic, and serotonergic projections were thought to cause a depletion of catecholamines, leading to depression. However, more recent studies have demonstrated that the anatomic aspects of a lesion do not necessarily correlate with the occurrence of depression. Other psychological factors can lead to the development of depression including personal and social losses related to the physical disabilities often caused by a stroke.
The incidence of post-stroke depression peaks at 3–6 months and usually resolves within 1–2 years after the stroke, although a minority of patients can go on to develop chronic depression. The diagnosis of post-stroke depression is complicated by other consequences of stroke such as fatigue and psychomotor retardation – which do not necessarily indicate the presence of depression. Loss of interest in activities and relationships should prompt an evaluation for depression.
Traditionally, tricyclic antidepressants (TCAs), such as nortriptyline, have been used in the treatment of post-stroke depression. More recently, the selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and citalopram, have become the pharmacologic therapy of choice due to the lower incidence of side effects. Also, psychologic treatment such as cognitive behavioral therapy, group therapy, and family therapy are reported to be useful adjuncts to treatment.
Overall, the development of post-stroke depression can play a significant role in a patient’s recovery from a stroke. For instance, the severity of post-stroke depression has been associated with severity of impairment in activities of daily living (ADLs). By effectively treating depression, patients experience a greater recovery of basic ADLs such as dressing, eating and ambulating, as well as instrumental ADLs, such as the ability to take care of financial and household matters. In essence, recognition and treatment of post-stroke depression leads to greater functional ability for the patient over time.
1. Berg A, Palomaki, H, et al.: Poststroke Depression: An 18-Month Follow-UP. Stroke 2003; 34: 138.
2. Brandstater ME: Stroke Rehabilitation. In : DeLisa JA, et al., eds. Rehabilitation Medicine: Principles and Practices. 3rd ed. Philadelphia: Lippincott-Raven; 1998:1165-1189.
3. Grasso MG, Pantano P, et al.: Mesial temporal cortex hypoperfusion is associated with depression in subcortical stroke. Stroke. 1994 May; 25(5): 980 - 85.
4. Mayberg HS, Robinson, RG, et al.: PET imaging of cortic al S2 serotonin receptors after stroke: lateralized changes and relationship to depression. Am J Psychiatry 1998; 145(8): 937-43.
5. Robinson RG "Poststroke depression: prevalence, diagnosis, treatment and disease progression. Biological Psychiatry 2003 Aug; 54(3): 376-87. 6. 7. Dohle, C., Pullen, J., Nakaten, A., Kust, J., Rietz, C. & Karbe, H. Mirror therapy promotes recovery from severe hemiparesis: A randomized controlled trial. Neurorehabilitation and Neural Repair 2009; 23(3): 209-217.
- National Stroke Association: Stroke Recovery - How do I recover from a stroke?
- Post Stroke Dysphagia Screen
- Common Depression score for post-stroke patients
- Jauch, E., Cucchiara, B., Adeoya, O., Meurer, W., Brice, J., Chan, Y., Gentile, N., & Hazinski, M., E. C.; Cucchiara, B.; Adeoye, O.; Meurer, W.; Brice, J.; Chan, Y.; Gentile, N.; Hazinski, M. F. (2010). "Part II: Adult Stroke: 2010 American Heart Association Guidelines for CardioPulmonary Resuscitation and Emergency Cardiovascular Care". Circulation 122 (suppl 3): S818–S828. doi:10.1161/CIRCULATIONAHA.110.971044. Retrieved 13 May 2011.
- Duncan, P., Zorowitz, R., Bates, B., Choi, J., Glasberg, J., Graham, G., Katz, R., Lamberty, K., & Reker, D., P. W.; Zorowitz, R.; Bates, B.; Choi, J. Y.; Glasberg, J. J.; Graham, G. D.; Katz, R. C.; Lamberty, K.; Reker, D. (2005). "Management of Adult Stroke Rehabilitation Care: A Clinical Practice Guideline". Stroke 36 (9): e100–e143. doi:10.1161/01.STR.0000180861.54180.FF. PMID 16120836. Retrieved 13 May 2011.
- Lindsay MP, Gubitz G, Bayley M, Hill MD, Davies-Schinkel C, Singh S, and Phillips S. Canadian Best Practice Recommendations for Stroke Care (Update 2010). On behalf of the Canadian Stroke Strategy Best Practices and Standards Writing Group. 2010; Ottawa, Ontario Canada: Canadian Stroke Network.
- Feng Zhu, H., Newcommon, N., Cooper, E., Green, T., Seal, B., Klein, G., Weir, N., Coutts, S., Watson, T., Barber, P., Demchuk, A., & Hill., M., H. F.; Newcommon, N. N.; Cooper, M. E.; Green, T. L.; Seal, B.; Klein, G.; Weir, N. U.; Coutts, S. B.; et al. (2009). "Impact of a Stroke Unit on Length of Hospital Stay and In-Hospital Case Fatality". Stroke 40 (1): 18–23. doi:10.1161/STROKEAHA.108.527606. PMID 19008467. Retrieved 13 May 2011.
- Teasell, R.; Bayona, N.; Bitensky, J. (2011). "Background Concepts in Stroke Rehabiliitation" (PDF). Evidence Based Review of Stroke Rehabilitation (Version 13): 1–44. Retrieved 13 May 2011.
- S Licht. Stroke and its Rehabilitation. Wavely Press, Inc. Baltimore, MD. 1975.
- Twitchell TE (1951). "The restoration of motor function following hemiplegia in man". Brain 74 (4): 443–480. doi:10.1093/brain/74.4.443. PMID 14895765.
- Carlo Perfetti (1979), La rieducazione motoria dell’emiplegico. Ghedini, Milano.
- Oden, Robert (1918-03-23). "SYSTEMATIC THERAPEUTIC EXERCISES IN THE MANAGEMENT OF THE PARALYSES IN HEMIPLEGIA". Journal of the American Medical Association 70 (12): 828–833. doi:10.1001/jama.1918.02600120008003.
- Wolf S. L., et al. (2006). "Effect of constraint-induced movement therapy on upper extremity function 3 to 9 months after stroke: the EXCITE randomized clinical trial". JAMA 296 (17): 2095–2104. doi:10.1001/jama.296.17.2095. PMID 17077374.
- Hakkennes, S; Keating, J. (2005). nes.pdf "Constraint-induced movement therapy following stroke: a systematic review of randomised controlled trials" Check
value (help) (PDF). Australian Journal of physiotherapy 51 (2): 221–231. doi:10.1016/S0004-9514(05)70003-9. Retrieved 13 May 2011.
- Siebers, A.; Oberg, U.; Skargren, E. (October 2010). "The Effect of Modified Constraint-Induced Movement Therapy on Spasticity and Motor Function of the Affected Arm in Patients with Chronic Stroke". Physiotherapy Canada 62 (4): 388–396. doi:10.3138/physio.62.4.388. PMC 2958081. PMID 21886380. Retrieved 12 May 2011.
- Wittenberg, G; Schaechter, J. (2009). "The neural basis of constraint-induced movement therapy". Current Opinion in Neurology 22 (6): 582–588. doi:10.1097/WCO.0b013e3283320229. PMID 19741529. Retrieved 12 May 2011.
- Dickstein R and Deutsch JE. Motor Imagery in physical therapist practice. Phys Ther 2007;(87)7:942-953.
- "Mental Movement Therapy". Stroke Rehab Product.
- Brown JA (2006). "Recovery of motor function after stroke". Prog. Brain Res. Progress in Brain Research 157: 223–8. doi:10.1016/S0079-6123(06)57015-3. ISBN 978-0-444-51602-2. PMID 17046674.
- Brock, Kim; Haase, Gerlinde. Rothacher, Gerhard. and Cotton, Susan (October 2011). "Does physiotherapy based on the Bobath concept, in conjunction with a task practice, achieve greater improvement in walking ability in people with stroke compared to physiotherapy focused on structured task practice alone? A pilot randomized controlled trial". Clinical Rehabilitation 25 (10): 903–912. doi:10.1177/0269215511406557. PMID 21788266.
- Dickstein R., Hocherman S., Shaham R.; Hocherman; Pillar; Shaham (1986). "Stroke Rehabilitation. Three Exercise Therapy Approaches". Physical Therapy 66 (8): 1233–1238. PMID 3737695.
- Martin L., Baker R., Harvey A.; Baker; Harvey (2010). "A Systematic Review of Common Physiotherapy Interventions in School-Aged Children with Cerebral Palsy". Physical & Occupational Therapy in Pediatrics 30 (4): 294–312. doi:10.3109/01942638.2010.500581.
- Kollen, B., Lennon, S., Lyons, B. et al. The Effectiveness of the Bobath Concept in Stroke Rehabilitation: What is the Evidence?. 'Stroke. 2009; 40(4) e89-e97.
- Kollen, B. J.; Lennon, S.; Lyons, B.; Wheatley-Smith, L.; Scheper, M.; Buurke, J. H.; Halfens, J.; Geurts, A. C. H.; Kwakkel, G. (2009). "The Effectiveness of the Bobath Concept in Stroke Rehabilitation: What is the Evidence?" (PDF). Stroke. pp. e89–e97. doi:10.1161/STROKEAHA.108.533828. Retrieved 4 May 2012.
- /Subeyaz,S, Yavuzer,G, Sezer,N, Koseoglu,F, Mirror Therapy Enhances Lower-Extemity Motor Recovery and Motor Functioning After Stroke: A Randomized Controlled Trial, Archives Physical Medicine and Rehabilitation, Vol 88, May 2007 
- Rothgangel,S, Braun,S, Beurskens,A, Seitz,R, Wade,D, The clinical aspects of mirror therapy in rehabilitation: a systematic review of the literature, Journal of Rehabilitation Research, 34:1-13,2011 
- Pittenger MF Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, Moorman MA, Simonetti DW, Craig S, Marshak DR; MacKay; Beck; Jaiswal; Douglas; Mosca; Moorman; Simonetti; et al. (1999). "Multilineage potential of adult human mesenchymal stem cells". Science 284 (5411): 143–147. Bibcode:1999Sci...284..143P. doi:10.1126/science.284.5411.143. PMID 10102814.
- Jiang Y, Jahagirdar BN, Reinhardt RL, Schwartz RE, Keene CD, Ortiz-Gonzalez XR, Reyes M, Lenvik T, Lund T; et al. (2002). "Pluripotency of mesenchymal stem cells derived from adult marrow". Nature 418 (6893): 41–49. doi:10.1038/nature00870. PMID 12077603.
- Ferrari G, Cusella G, Angelis D, Coletta M, Paolucci E, Stornaiuolo A, Cossu G, Mavilio F; et al. (1998). "Muscle regeneration by bone marrow-derived myogenic progenitors". Science 279 (5356): 528–530. Bibcode:1998Sci...279.1528F. doi:10.1126/science.279.5356.1528.
- Jackson KA, Majka SM, Wang H, Pocius J, Hartley CJ, Majesky MW, Entman ML, Michael LH, Hirschi KK; et al. (2001). "Regeneration of ischemic cardiac muscle and vascular endothelium by adult stem cells". Journal of Clinical Investigation 107 (11): 1395–1402. doi:10.1172/JCI12150. PMC 209322. PMID 11390421.
- Orlic D, Kajstura J, Chimenti S, Jakoniuk I, Anderson SM, Li B, Pickel J, McKay R, Nadal-Ginard B; Kajstura; Chimenti; Jakoniuk; Anderson; Li; Pickel; McKay; et al. (2001). "Bone marrow cells regenerate infarcted myocardium". Nature 410 (6829): 701–705. Bibcode:2001Natur.410..701O. doi:10.1038/35070587. PMID 11287958.
- Asahara T, Masuda H, Takahashi T, Kalka C, Pastore C, Silver M, Kearne M, Magner M, Isner JM; et al. (1999). "Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization". Circulation Research 85 (3): 221–228. doi:10.1161/01.res.85.3.221. PMID 10436164.
- Lin Y, Weisdorf DJ, Solovey A, Hebbel RP; et al. (2000). "Origins of circulating endothelial cells and endothelial outgrowth from blood". Journal of Clinical Investigation 105 (1): 71–77. doi:10.1172/JCI8071. PMC 382587. PMID 10619863.
- Krause DS, Theise ND, Collector MI, Henegariu O, Hwang S, Gardner R, Neutzel S, Sharkis SJ; et al. (2001). "Multi-organ, multi-lineage engraftment by a single bone marrow-derived stem cell". Cell 105 (3): 369–377. doi:10.1016/S0092-8674(01)00328-2. PMID 11348593.
- Kopen G, Prockop D, Phinney D; et al. (1999). "Marrow stromal cells migrate throughout forebrain and cerebellum, and they differentiate into astrocytes after injection into neonatal mouse brains". Proceedings of the National Academy of Sciences USA 96 (19): 10711–10716. Bibcode:1999PNAS...9610711K. doi:10.1073/pnas.96.19.10711.
- Brazelton TR, Rossi FMV, Keshet GI, Blau HE; et al. (2000). "From marrow to brain: expression of neuronal phenotypes in adult mice". Science 290 (5497): 1775–1779. Bibcode:2000Sci...290.1775B. doi:10.1126/science.290.5497.1775. PMID 11099418.
- Mezey E, Chandross KJ, Harta G, Maki RA, McKercher SR; et al. (2000). "Turning blood into brain: cells bearing neuronal antigens generated in vivo from bone marrow". Science 290 (5497): 1779–1782. Bibcode:2000Sci...290.1779M. doi:10.1126/science.290.5497.1779. PMID 11099419.
- Sanchez-Ramos J, Song S, Cardozo-Pelaez F, Hazzi C, Stedeford T, Willing A, Freeman TB, Saporta S, Janssen W; et al. (2000). "Adult bone marrow stromal cells differentiate into neural cells in vitro". Experimental Neurology 164 (2): 247–256. doi:10.1006/exnr.2000.7389. PMID 10915564.
- Dharmasaroja P (2008). "Bone marrow-derived mesenchymal stem cells for the treatment of ischemic stroke". Journal of Clinical Neuroscience 16 (1): 12–20. doi:10.1016/j.jocn.2008.05.006. PMID 19017556.
- Wislet-Gendebien S, Hans G, Leprince P, Rigo JM, Moonen G, Rogister B; et al. (2005). "Plasticity of cultured mesenchymal stem cells: switch from nestin-positive to excitable neuron-like phenotype". Stem Cells 23 (3): 392–402. doi:10.1634/stemcells.2004-0149. PMID 15749934.
- Chen X, Li Y, Wang L, Katakowski M, Zhang L, Chen J, Xu Y, Gautam SC, Chopp M; et al. (2002). "Ischemic rat brain extracts induce human marrow stromal cell growth factor production". Neuropathology 22 (4): 275–279. doi:10.1046/j.1440-1789.2002.00450.x. PMID 12564767.
- Li Y, Chen J, Chopp M; et al. (2002). "Cell proliferation and differentiation from ependymal, subependymal and choroid plexus cells in response to stroke in rats". Journal of the Neurological Sciences 193 (2): 137–146. doi:10.1016/S0022-510X(01)00657-8. PMID 11790394.
- Chen J, Li Y, Katakowski M, Chen X, Wang L, Lu D, Lu M, Gautam SC, Chopp M (2003) Intravenous bone marrow stromal cell therapy reduces apoptosis and promotes endogenous cell proliferation after stroke in female rat. Journal of Neuroscience Research 73:778–786.
- Lee J, Kuroda S, Shichinohe H, Ikeda J, Seki T, Hida K, Tada M, Sawada K, Iwasaki Y; et al. (2003). "Migration and differentiation of nuclear fluorescence-labeled bone marrow stromal cells after transplantation into cerebral infarct and spinal cord injury in mice". Neuropathology 23 (3): 169–180. doi:10.1046/j.1440-1789.2003.00496.x. PMID 14570283.
- Yano S, Kuroda S, Shichinohe H, Hida K, Iwasaki Y; et al. (2005). "Do bone marrow stromal cells proliferate after transplantation into mice cerebral infarct?–A double labelling study". Brain Research 1065 (1–2): 60–67. doi:10.1016/j.brainres.2005.10.031. PMID 16313889.
- Liu H, Honmou O, Harada K, Nakamura K, Houkin K, Hamada H, Kocsis JD; et al. (2006). "Neuroprotection by PlGF gene-modified human mesenchymal stem cells after cerebral ischaemia". Brain 129 (Pt 10): 2734–2745. doi:10.1093/brain/awl207. PMC 2605397. PMID 16901914.
- Shen LH, Li Y, Chen J, Zhang J, Vanguri P, Borneman J, Chopp M; et al. (2006). "Intracarotid transplantation of bone marrow stromal cells increases axon-myelin remodelling after stroke". Neuroscience 137 (2): 393–399. doi:10.1016/j.neuroscience.2005.08.092. PMID 16298076.
- Louissaint Jr A, Rao S, Leventhal C, Goldman SA; et al. (2002). "Coordinated interaction of neurogenesis and angiogenesis in the adult songbird brain". Neuron 34 (6): 945–960. doi:10.1016/S0896-6273(02)00722-5. PMID 12086642.
- Chen J, Chopp M (2006) Neurorestorative treatment of stroke: cell and pharmacological approaches. NeuroRX 3:466–473.
- Li Y, Chen J, Zhang CL, Zhang CL, Wang L, Lu D, Katakowski M, Gao Q, Shen LH, Zhang J, Lu M, Chopp M (2005) Gliosis and brain remodeling after treatment of stroke in rats with marrow stromal cells. Glia 49:407–417.
- Parr AM, Tator CH, Keating A (2007) Bone marrow-derived mesenchymal stromal cells for the repair of central nervous system injury. Bone Marrow Transplantation 40:609–619.
- Borlongan CV, Lind JG, Dillon-Carter O, Yu G, Hadman M, Cheng C, Carroll J, Hess DC; et al. (2004). "Intracerebral xenografts of mouse bone marrow cells in adult rats facilitate restoration of cerebral blood flow and blood–brain barrier". Brain Research 1009 (1–2): 26–33. doi:10.1016/j.brainres.2004.02.050. PMID 15120580.
- Shen LH, Li Y, Chen J, Zacharek A, Gao Q, Kapke A, Lu M, Raginski K, Vanguri P, Smith A, Chopp M (2007) Therapeutic benefit of bone marrow stromal cells administered 1 month after stroke. Journal of Cerebral Blood Flow Metabolism 27:6–13.
- Zhang J, Li Y, Chen J, Yang M, Katakowski M, Lu M, Chopp M; et al. (2004). "Expression of insulin-like growth factor 1 and receptor in ischemic rats treated with human marrow stromal cells". Brain Research 1030 (1): 19–27. doi:10.1016/j.brainres.2004.09.061. PMID 15567334.
- Cui X, Chen J, Zacharek A, Roberts C, Kapke A, Savant-Bhonsale S, Chopp M; et al. (2007). "Nitric oxide donor upregulation of stromal cell-derived factor-1/chemokine (CXC motif) receptor 4 enhances bone marrow stromal cell migration into ischemic brain after stroke". Stem Cells 25 (11): 2777–2785. doi:10.1634/stemcells.2007-0169. PMC 2792206. PMID 17641243.
- Frankel MS (2000). "In search of stem cell policy". Science 298 (5457): 1397. doi:10.1126/science.287.5457.1397.
- Ivanhoe CB, Reistetter TA: "Spasticity: The misunderstood part of the upper motor neuron syndrome" Am J Phys Med Rehabil 2004;83(suppl):S3–S9.
- Gallichio J (2004). "Pharmacologic management of spasticity following stroke". Phys Ther 84 (10): 973–981. PMID 15449979.
- Watkins CL, et al. (2002). "Prevalence of spasticity post stroke". Clinical Rehabilitation 16 (5): 515–522. doi:10.1191/0269215502cr512oa. PMID 12194622.
- Vanek ZF Menkes JH (2005) "Spasticity" eMedicine article
- Mayer et al. (September 2002) "Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin" We Move
- Young BJ et al. (2002) Physical Medicine and Rehabilitation Secrets, 2nd Edition, Hanley & Belfus, Inc. , pp442–446
- Landau WM; Sommerfeld, D. K.; Eek, E.; Svensson, A.-K.; Holmqvist, L. W.; Von Arbin, M. H. (August 2004). "Spasticity after stroke: why bother?". Stroke 35 (8): 1787–8; author reply 1787–8. doi:10.1161/01.STR.0000136388.80433.eb. PMID 15232114.
- Sommerfeld DK, Eek EU, Svensson AK, Holmqvist LW, von Arbin MH; Eek; Svensson; Holmqvist; von Arbin (January 2004). "Spasticity after stroke: its occurrence and association with motor impairments and activity limitations". Stroke 35 (1): 134–9. doi:10.1161/01.STR.0000105386.05173.5E. PMID 14684785.
- "Recovery From A Stroke". Retrieved 24 Dec 2010.
- Gracies JM, et al. (1997). "Lycra garments designed for patients with upper limb spasticity: mechanical effects in normal subjects". Arch Phys Med Rehabil 78 (10): 1066–71. doi:10.1016/S0003-9993(97)90129-5. PMID 9339154.
- O'Sullivan, Susan. B (2007). "Stroke". In O'Sullivan, S.B., and Schmitz, T.J. Physical Rehabilitation 5. Philadelphia: F.A. Davis Company. p. 744.
- Twitchell, T (1951). "The restoration of motor function following hemiplegia in man". Brain 47 (4): 443–80. doi:10.1093/brain/74.4.443. PMID 14895765.
- Brunnstrom, S (1966). "Motor testing procedures in hemiplegia based on recovery stages". J Am Phys Ther Assoc 46: 357.
- O'Sullivan, Susan. B (2007). "Stroke". In O'Sullivan, S.B., and Schmitz, T.J. Physical Rehabilitation 5. Philadelphia: F.A. Davis Company. p. 719.
- Bhakta, Bipin B (2000). "Management of spasticity in stroke". British Medical Bulletin 56 (2): 476–485. doi:10.1258/0007142001903111. PMID 11092096.
- O'Sullivan, Susan. B (2007). "Stroke". In O'Sullivan, S.B., and Schmitz, T.J. Physical Rehabilitation 5. Philadelphia: F.A. Davis Company. pp. 744–5.
- Dobkin BH (2003) The Clinical Science of Neurologic Rehabilitation. New York, NY. Oxford University Press
- Lagalla G, et al. (2000). "Post-stroke spasticity management with repeated botulinum toxin injections of the upper limb". Am J Phys Med Rehabil 79 (4): 377–84. doi:10.1097/00002060-200007000-00010.
- O'Sullivan and Schmitz, eds. (2007). "Stroke". Physical Rehabilitation. Fifth Edition. Philadelphia, PA: F.A. Davis Company. pp. 753–754. ISBN 978-0-8036-1247-1.
- KOYUNCU, E.; NAKIPOGLU-YUZER, G., DOGAN, OZGIRGIN, N. A., & (2010). "The effectiveness of functional electrical stimulation for the treatment of shoulder subluxation and shoulder pain in hemiplegic patients: A randomized controlled trial". Disability and Rehabilitation 32 (7): 560–566. doi:10.3109/09638280903183811. PMID 20136474.
- Kumar, R.; Metter, E.; Mehta, A.; Chew, T. (August 1990). "Shoulder pain in hemiplegia: The role of exercise". American Journal of Physical Medicine & Rehabilitation 69 (4): 205–208. doi:10.1097/00002060-199008000-00007.
- Andersen G Vestergaard K Ingeman-Nielsen M Tensen TS; Vestergaard; Ingeman-Nielsen; Jensen (1995). "Incidence of Central Poststroke Pain". Pain 61 (2): 187–196. doi:10.1016/0304-3959(94)00144-4.
- Nicholson B (2004). "Evaluation and Treatment of Central Pain Syndromes". Neurology. 62(supp): S30–36. doi:10.1212/wnl.62.5_suppl_2.s30.
- Can Heugten CM (2001). "Rehabilitation and Management of Apraxia After Stroke". Reviews in Clinical Gerontology 11: 177–184.
- Pederson PM; et al. (2001). "Manual and Oral Apraxia in Acute Stroke, Frequency and Influence on Functional Outcome: The Copenhagen Stroke Study". American Journal of Physical Medicine 80 (9): 685–692.
- Flor H., Diers M.; Diers (2009). "Sensorimotor training and cortical reorganization". NeuroRehabilitation 25 (1): 19–27. doi:10.3233/NRE-2009-0496 (inactive 2015-02-01). PMID 19713616.