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Stroke recovery

From Wikipedia, the free encyclopedia

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.[1] 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.[2] Standardized assessments are also performed to aid in the development of an appropriate care plan.[3] Current research suggests that stroke units may be effective in reducing in-hospital fatality rates and the length of hospital stays.[4]

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, physical therapist, occupational therapist, speech and language pathologist, psychologist, and recreation therapist.[3] 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.[2]

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.[2]

The initial severity of impairments and individual characteristics, such as motivation, social support, and learning ability, are key predictors of stroke recovery outcomes.[5] 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.[5]

History of stroke neuro-rehabilitation

Knowledge of stroke and the process of recovery after stroke has developed enormously in the late 20th century and early 21st century. It was not until the year 1620 that Johan Wepfer, by studying the brain of a pig, came up with the theory that stroke was caused by an interruption of the flow of blood to the brain.[6] This was an important breakthrough, but once the cause of strokes was known, the question became how to treat patients with stroke.

For most of the last century, people were actually 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. Still, 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. This was still a fairly bleak outlook, but the situation was improving.

In the early 1950s, Twitchell began studying the pattern of recovery in stroke patients. He reported on 121 patients 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.[7] 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 improves, methods of intervening have evolved. There will be a continued fundamental shift in the processes used to facilitate stroke recovery.

Current perspectives and therapeutic avenues

Motor re-learning

"Neurocognitive Rehabilitation by Carlo Perfetti concept", widespread in many countries, is an original motor re-learning theories application.[8]

Constraint-induced movement therapy

The idea for constraint-induced therapy is actually 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.[9]

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 will 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.[10]

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.[11] 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.[12] 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.[11][13]

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.[14] 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.[15]

Brain repair

Electrical stimulation

Such work represents a paradigm shift in the approach towards rehabilitation of the stroke-injured brain away from pharmacologic flooding of neuronal receptors, instead towards targeted physiologic stimulation.[16]

Acoustic electrical stimulation (rhythmic auditory stimulation)

Rhythmic auditory stimulation (RAS) was shown to be superior to Bobath-based training.[17]

Bobath (NDT))

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. Many studies have been conducted comparing NDT with other treatment techniques such as Proprioceptive Neuromuscular Facilitation (PNF), as well as conventional treatment approaches (utilizing traditional exercises and functional activities), etc.[18][19][20] Despite being so widely used, based on the literature, NDT has failed to demonstrate any superiority over other treatment techniques available.[18][19][20] In fact, the techniques compared with NDT in these studies often produce similar results in terms of treatment effectiveness.[18][19][20] Research has demonstrated significant findings for all these treatment approaches when compared with control subjects and indicate that overall, rehabilitation is effective.[18][19][20] It is important to note, however, that the NDT philosophy of “do what works best” has led to a lot of heterogeneity in the literature in terms of what constitutes as a NDT technique, thus making it difficult to directly compare to other techniques.[18][19][20] [21]

Mirror Therapy

Mirror therapy (MT) was first introduced by Vilayanur S. Ramachandran and colleagues, and employed in “mirror box” treatment for phantom pain in arm amputees. The individual is presented with the mirror image of his or her unaffected arm by placing a mirror in front of the individual. Movements are performed with the unaffected arm, with the affected arm out of view, while the person watches the mirror image. The unaffected arm is perceived by the person as the affected arm, inducing an illusory effect, and leading to increased activation of the affected hemisphere of the brain.[22]

Mirror therapy has been employed with stroke patients with successful results.[23] Improvements in a variety of functional actions have been noted, including reach and grasp movements, as well as improvement in neglect score and light touch sensation of the affected limb.[22] Positive effects of mirror therapy have been described in several studies focused on upper-extremity motor recovery, as well as in one examining the lower-extremity.[23]

The evidence supports the application of MT in stroke rehabilitation, as it might accelerate recovery of function.[23] It is suggested that MT may be most effective when applied within the first 3 months after stroke, when recovery is generally the greatest.[22]

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 Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page). after studies of transplanted haematopoietic stem cells showed the development of myoblasts Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page)., endothelium Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page)., epithelium Cite error: The <ref> tag has too many names (see the help page). and neuroectodermal cells Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page)., suggesting pluripotency. These findings have led to MSCs being considered for treatment of ischemic stroke [24], 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 Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page). and these cells respond to common central nervous system neurotransmitters Cite error: The <ref> tag has too many names (see the help page).. 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 Cite error: The <ref> tag has too many names (see the help page).. 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 [25]. The inducted cells probably originate from the ventricular zone, subventricular zone and choroid plexus, and migrate to the areas in their respective hemispheres which are damaged Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).. 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 Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page). and is linked to improved neuronal recruitment Cite error: The <ref> tag has too many names (see the help page).. In addition, synaptogenesis (formation of new synapses between neurons) has been shown to increase after MSC treatment [26]Cite error: The <ref> tag has too many names (see the help page).; 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 Cite error: The <ref> tag has too many names (see the help page)., including reductions in apoptosis Cite error: The <ref> tag has too many names (see the help page)., inflammation and demyelination, as well as increased astrocyte survival rates Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).. MSC treatment also appears to improve the control of cerebral blood flow and blood-brain barrier permeability Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page)., 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 Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page).Cite error: The <ref> tag has too many names (see the help page)..

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) [27].

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. Though, 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 [28], 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.[29]

It has been estimated that approximately 65% of individuals develop spasticity following stroke,[30] and studies have revealed that approximately 40% of stroke victims may still have spasticity at 12 months post-stroke.[31] 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.[32] 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.[30][32][33][34] Researchers do not believe that treating spasticity is worthwhile. A letter to the editor of Stroke magazine. Spasticity After Stroke: Why Bother? William M. Landau, MD However, the perseverative preoccupation of professional neurologists and therapists with the purpose of overpowering the spasticity ogre seems to be an endemic, intractably-taught delusion that afflicts both scholars and clinicians.[35] Another group of researchers writing in Movement Disorder Virtual University Incidence and Consequences of Spasticity After Stroke

The authors conclude, “spasticity seems to contribute to motor impairments and activity limitations and may be a severe problem for some patients after stroke,” but, they note, “Our findings support the opinion…that the focus on spasticity in stroke rehabilitation is out of step with its clinical importance.[36] In a survey done by the National Stroke Association, however, while 58 percent of survivors in the survey experience spasticity, only 51 percent of those have received treatment for this condition.[37]

Nonpharmacologic therapies

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 or other health professional skilled in neurological rehabilitation.

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.[38]

Physiotherapy

Physiotherapy is beneficial in this area as it helps post-stroke individuals to progress through the stages of motor recovery.[39] These stages were originally described by Twitchell and Brunnstrom, and may be known as the Brunnstrom Approach.[40][41] Initially, post-stroke individuals suffer from flaccid paralysis.[42] As recovery begins, and progresses, basic movement synergies will develop into more complex and difficult movement combinations.[40][41] Concurrently, spasticity may develop and become quite severe before it begins to decline (if at all).[40][41] 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.[43]

Without its reduction, spasticity will result in the maintenance of abnormal resting limb postures which can lead to contracture formation.[43] 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.[39] Strategies include mobilizations of the affected limbs early in rehabilitation, along with elongation of the spastic muscle and sustained stretching.[39] In addition, the passive manual technique of rhythmic rotation can help to increase initial range.[39] Activating the antagonist (muscle) in a slow and controlled movement is a beneficial training strategy that can be used by post-stroke individuals.[43] 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 spasticity.[44] The focus of physiotherapy for post-stroke individuals is to improve motor performance, in part, through the manipulation of muscle tone.[43]

Oral drug therapies

Oral medications used for the treatment of spasticity include: diazepam (Valium), dantrolene sodium, baclofen, tizanidine, clonidine, gabapentin,[30][32][33] 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.[45]

Intrathecal drug therapy

Intrathecal administration of drugs involves the implantation of a pump that delivers medication directly to the CNS.[30][32] 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

Injections are focal treatments administered directly into the spastic muscle. Drugs used include: Botulinum toxin (BTX), Phenol, alcohol, and Lidocaine.[30][32][33] 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[30] and it has also been demonstrated that repeat injections of BTX show unchanged effectiveness.[46]

Surgery

Surgical treatment for spasticity includes lengthening or releasing of muscle and tendons, procedures involving bones, and also selective dorsal rhizotomy.[32][33] 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 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.[47]

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.[48]

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.[49]

References

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.1 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.² 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.

References

1. Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen TS. Incidence of central poststroke pain. Pain 1995; 61: 187-193. 2. Nicholson B. Evaluation and treatment of central pain syndromes. Neurology 2004; 62 (supp) S30-36.

Apraxia

A not too uncommon, but less understood result of stroke, as well as metabolic and traumatic insult to the brain, 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.’1 Several forms of apraxia are recognized³. Limb-kinetic apraxia is the inability to make precise or exact movements with a finger, an arm or a leg. Ideamotor 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 ideamotor 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.²

Whereas with many affects 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 case is not as clear with apraxia. A common theory as to why this condition results is that the part of the brain that contains information for previously learned skilled motor activities, such as using a spoon to scoop up soup and place it in your mouth, 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%.4 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. Their objective is to try to determine what goes wrong with these processes in the course of acquired apraxia due to stroke or brain injury.4

References

1. Rehabilitation and management of apraxia after stroke, Can Heugten CM. Reviews in Clinical Gerontology (2001), 11: 177-184 Cambridge University Press.
2. www.emedicine.com
3. www.cigna.com/healthinfo/nord766.html
4. Pedersen PM et al. Manual and Oral Apraxia in Acute Stroke, Frequency and Influence on Functional Outcome: The Copenhagen Stroke Study. American Journal of Physical Medicine and Rehabilitation 2001; 80(9):685-692.

Lateral medullary syndrome

Lateral medullary syndrome, also known as Wallenberg’s Syndrome, is caused by blockage of 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. 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 odansetron, metoclopromide, 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. 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.

References

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
3. http://www.healthline.com/galecontent/wallenberg-syndrome
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

Post-stroke depression

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 that lead 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.

References

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.[50] 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.

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