Stroke recovery

Stroke rehabilitation, or, in more optimistic terms, stroke recovery, 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 rehabilitation medicine. Some teams may also include psychologists and social workers and pharmacists. Patients may demand access to state of the art treatment with the help of their own doctor.

For most stroke patients, the rehabilitation process includes nursing, occupational therapy (OT), physical therapy (PT), and speech therapy (or speech language 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, if only traditional OT, PT and SLP are used. In contrast, brain repair, neurogenesis, and neural rewiring can eventually be enhanced significantly medically long after this short therapeutic window.

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.

Additional recommended knowledge

Daily Sensitivity Test

Essential Laboratory Skills Guide

Daily Visual Balance Check

History of Stroke Neuro-Rehabilitation

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 1950s, 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.

Current perspectives and therapeutic avenues

Motor re-learning

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.

• Constraint-induced movement therapy

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

• Robot-assisted movement therapy

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.

• Cyclic electrical neuromuscular stimulation

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.

Brain repair

• Stem cells

Stem cell transplantation is intended to replace dead brain cells. This therapy is promising, but many question are unanswered:

Basic and clinical research in stroke neurotransplantation remains in a nascent stage. Much more work is needed to further characterize the biology of different implant sources both in vitro and in vivo. Initial clinical data suggests that transplantation is technically feasible and can be performed safely, but the data are too preliminary and insufficient to assess efficacy.^[1]

• Growth factors

Growth factors in the brain promote neural repair, neurogenesis, and adaptative rewiring. When administered to the patient, they easily enter the brain. The enhancement of the trophic input in the brain is a promising strategy for stroke recovery.^[2]

• Monoamines and antidepressant therapies

Monoamines (noradrenaline, dopamine, and serotonin) are not only involved in mood (and in post-stroke depression) but they also enhance stroke recovery.^[3]

• Treatment of stroke-associated nutrient deficiencies

Folate deficiency and hyperhomocysteinemia are prevalent in elderly post-stroke victims and are "strongly and independedtly" associated with the development of cerebral atrophy.^[4]

• Inhibition of brain protein-degrading enzymes

Matrix metalloproteinases (MMPs) are elevated after stroke and are inversely correlated with functional recovery. MMPs also appear to reduce the levels of growth factors^[5] (also see Growth factors, supra). MMPs are attractive targets in other conditions where the conjunctive tissue is under proteolytic degradation, such as infectious diseases and malignancies.

• Inhibition of microglial activation

Following a brain insult, specialized brain cells called microglia as well as other glial cells (astrocytes) surround the site of the lesion and create a glial scar. Although this scar is likely the result of an adaptative mechanism, its volume is inversely correlated with recovery.^[6] In addition, post-stroke depression might be related to levels of inflammatory cytokines in the brain.^[7] Stroke recovery should thus involve the normalization of the immune activation surrounding the lesion.

• Electrical stimulation

Although direct electrical stimulation is not as fashionable as pharmacologic treatments, it is effective.

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.^[8]

• Acoustic electrical stimulation (rhythmic auditory stimulation)

The listening of rhythmic music enhances motor activity and encourages motion in stroke patients. Rhythmic auditory stimulation (RAS) was shown to be superior to Bobath-based training.^[9]

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.

Treatment of post-stroke spasticity

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, September 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.

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.

Dx 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 or tightening of the joint if used for extended periods of time. That said, a sling may be necessary for some therapy activities. 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. As with most conditions, the best 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.

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; Christopher Manley; 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 cortical 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.

References