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Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It is multidisciplinary in the fact that it involves a team with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy and usually a physician trained in rehabiliation medicine. Some teams may also include psychologists and social workers and pharmacists.

For most stroke patients, the rehabilitation process includes occupational therapy (OT), physical therapy (PT), and speech therapy (SLP). OT involves exercise and training to help the stroke patient relearn everyday activities sometimes called the Activities of daily living (ADLs) such as eating and drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients who have problems understanding speech or written words, or problems forming speech. Speech Therapists also assess a persons ability to safely swallow after a stroke.

The team have regular meetings at which the patient and family may be present to discuss the current situation and to set goals and to ensure effective communication. In most cases the desired goal is to enable the patient to return home to independent living though this is not always possible.

Stroke rehabilitation can last anything from a few days up to several months. Most return of function is seen in the first few days and weeks and then falls off. It is unusual that there is complete recovery but not impossible. Most patients will improve to some extent.

After a stroke, control signals from the brain often cannot reach some muscles, typically in the hand or foot. Without these signals, the level of electrical activity in these muscles is too low for them to contract adequately on their own. This causes them to become increasingly weaker.

Knowledge of stroke and the process of recovery after stroke is in its relative infancy. It wasn’t until the year 1620 that Johan Wepfer, by studying the brain of a pig, came up with the theory that stroke was actually caused by an interruption of the flow of blood to the brain.¹ This was an important breakthrough, but now that we knew what strokes were caused by, the question was, how to treat patients with stroke.

For most of the last century, people were actually discouraged from being active after a stroke. Around the 1950’s, this attitude changed, and doctors began prescription 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 by without assistance.² This was still was 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 4 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 3 months, and only minor recovery occurs after 6 months.³

About that same time, Brunnstrom also described the process of recovery, and he divided the process up into 7 stages. As knowledge of the science of brain recovery improves, methods of intervening has evolved. There will be a continued fundamental shift in the processes used to facilitate stroke recovery.

Fundamental to neuro-rehabilitation is an understanding of how motor learning occurs. The term "motor learning" is used to describe a set of processes associated with practice or experience leading to "relatively" permanent changes in the capability for movement. The process of motor learning (or motor re-learning after a stroke) employs unassisted, goal-directed practice. This is the way that children, Olympic athletes, and stroke patients learn a motor skill. A new technique called constraint-induced therapy is a good example of motor re-learning.

The idea for constraint-induced therapy is actually about 100 years old. A significant research study occurred in about 1920 by a man named 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. 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. Of note, the initial studies focused on chronic stroke patients who were more than 12 months after their stroke. This challenged the prior held beliefs that no recovery will occur after one year. The therapy entails wearing a soft mitt on the good hand for 90 percent of the waking hours, forcing use of the affected hand. The patients undergo intense one-on-one therapy for 6 to 8 hours per day for two weeks.⁴

Because of dosage requirements and the need to deliver thousands of movements in a cost effective manner, automated computer programs and robotic assisted therapy systems are emerging.

In addition, cyclic electrical neuromuscular stimulation has been found in some studies to enhance motor recovery after stroke, with claims that it can reduce spasticity, strengthen muscles, and increase the range of movement of joints with prevention or correction of contractures.

The goal stroke neuro-rehabilitation is functional recovery for improved quality of life.

References: 1. S Licht. Stroke and its Rehabilitation. Wavely Press, Inc. Baltimore, MD. 1975. 2. S Licht. Stroke and its Rehabilitation. Wavely Press, Inc. Baltimore, MD. 1975. 3. TE Twitchell. The restoration of motor function following hemiplegia in man. Brain. 1951;74:443–480 4. Wolf, S. L. et al. Constraint induced movement therapy. JAMA 2006;296:2095-2104.

Spasticity is a condition that commonly affects muscles in people following upper motor neuron lesions, such as stroke. It has been estimated that approximately 65% of individuals develop spasticity following stroke ¹, and studies have revealed that approximately 40% of stroke victims may still have spasticity at 12 months post-stroke.² Spasticity has been described as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex”. ¹ It can also be described as a “wicked charley horse”, and once spasticity is established, the chronically shortened muscle may develop physical changes such as shortening and contracture that further contribute to muscle stiffness.³ These tight, stiff muscles can make movement, especially of the arms or legs, difficult or uncontrollable.⁴ The pathophysiologic basis of spasticity is incompletely understood. 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.³ In other words there is damage to the part of the brain or spinal cord that controls voluntary movement.

After stroke spasticity can occur in any muscle group, but it most commonly affects the arm, with typical posturing being a clenched fist, bent elbow, and arm pressed against the chest; ^5-7 this can significantly interfere with a stroke victim’s ability to perform daily activities such as dressing and eating.

Various means are available for the treatment of post-stroke spasticity. These include: nonpharmacologic therapies, oral drug therapy, intrathecal drug therapy, injections, and surgery.^1,3,8,9

Nonpharmacologic therapies

Nonpharmacologic therapies include stretching, splinting, serial casting, dynamic splinting, biofeedback, and electrical stimulation.^1,8,9 These therapies have been the traditional forms of treatment for spasticity and should be begun as early as possible. The aim of these therapies is to lengthen the overactive muscle, improve range of motion, prevent further contracture, and decrease the noxious stimuli that may affect the spinal circuit of spasticity. Applying contracture preventative positioning has been shown to slow down development of shoulder abduction contractures ¹⁰, and using Lycra garments for the upper extremity may also be beneficial.¹¹

Oral drug therapies

Oral medications used for the treatment of spasticity include: Diazepam(Valium), Dantrolene sodium, Baclofen, Tizanidine, Clonidine, Gabapentin,^1,3,8 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 effects1 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.¹²

Intrathecal drug therapy

Intrathecal administration of drugs involves the implantation of a pump that delivers medication directly to the CNS.^1,3 The benefit of this is that the drug remains in the spinal cord, without traveling in the bloodstream, and there are often less 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.^1,3,8 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 BTX¹ and it has also been demonstrated that repeat injections of BTX show unchanged effectiveness.¹³

Surgery

Surgical treatment for spasticity includes lengthening or releasing of muscle and tendons, procedures involving bones, and also selective dorsal rhizotomy.^3,8 Rhizotomy, usually reserved for severe spasticity, involves cutting selective sensory nerve roots, as they probably play a role in generating spasticity.

References:

1. J Gallichio. Pharmacologic management of spasticity following stroke. Phys Ther. 2004;84(10):973-981. 2. CL Watkins, et al. Prevalence of spasticity post stroke, Clinical Rehabilitation. 2002;16:515-522. 3. ZF Vanek. Spasticity. eMedicine article, May, 2005, http://www.emedicine.com/neuro/topic706.htm. 4. http://www.stroke.org. 5. http://www.excite.wustl.edu/newsletters/vol%20207%20spasticity.pdf. 6. http://strokeassociation.org. 7. AD Pandyan, et al. Contractures in the post-stroke wrist: a pilot study of its time course of development and its association with upper limb recovery. Clinical Rehabilitation. 2003;17:88-95. 8. N Mayer, et al. Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, We Move, Sept 2002. 9. BJ Young, et al., Physical Medicine and Rehabilitation Secrets, 2nd Edition, Hanley & Belfus, Inc. 2002, pp442-446. 10. LD de Jong, et al. Contracture preventive positioning of the hemiplegic arm in subacute stroke patients: a pilot randomized controlled trial. Clinical Rehabilitation. 2006;20(8):656-667. 11. JM Gracies, et al. Lycra garments designed for patients with upper limb spasticity: mechanical effects in normal subjects. Arch Phys Med Rehabil 1997; 78(10): 1066-71[Medline] 12. BH Dobkin. The Clinical Science of Neurologic Rehabilitation. New York, NY. Oxford University Press. 2003. 13. G Lagalla, et al. Post-stroke spasticity management with repeated botulinum toxin injections of the upper limb. Am J Phys Med Rehabil. 2000;79(4):377-84.

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, opiods/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.