The main goal of stroke management is to reduce brain injury and improve maximum patient recovery. Quick detection and appropriate emergency medical care are essential to optimize health outcomes. When available, patients are treated in an acute stroke unit for treatment. These units specialize in providing medical and surgical treatments aimed at stabilizing the patient's medical status. Standard assessments are also undertaken to assist in the development of appropriate treatment plans. Current research suggests that stroke units may be effective in reducing hospital mortality and length of stay.
Once patients are medically stable, their recovery focus shifts to rehabilitation. Some patients are transferred to inpatient rehabilitation programs, while others may be referred to outpatient care or home care. Inpatient programs are usually facilitated by interdisciplinary teams that may include doctors, nurses, pharmacists, physical therapists, occupational therapists, speech pathologists and languages, psychologists, and recreational therapists. Patients and their families/caregivers also play an integral role in this team. Families/carers involved in patient care tend to be ready for parenting roles as patients move from rehabilitation centers. While at the rehabilitation center, interdisciplinary teams ensure that patients achieve their maximum functional potential after returning home. The main objectives of this sub-acute recovery phase are to prevent secondary health complications, minimize disruption, and achieve functional goals that encourage independence in daily life activities.
In the next phase of stroke recovery , patients are encouraged to participate in a secondary prevention program for stroke. Follow-up is usually facilitated by the primary care provider of the patient.
The initial severity of disorders and individual characteristics, such as motivation, social support, and learning ability, are key predictors of stroke recovery outcomes. The response to treatment and recovery of the overall function depends greatly on the individual. Current evidence suggests that the most significant recovery outcome will occur within the first 12 weeks after a stroke.
Video Stroke recovery
History of neuro-stroke rehabilitation
In 1620, Johann Jakob Wepfer, by studying the brain of pigs, developed the theory that stroke is caused by impaired blood flow to the brain. After that, the focus becomes a way of treating stroke patients.
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 prescribing therapeutic exercises for stroke patients with good results. At that time, good results are considered to reach a degree of independence in which the patient can move from bed to wheelchair unaided.
In the early 1950s, Twitchell began studying the pattern of recovery in stroke patients. He reported to 121 patients whom he observed. He found that by four weeks, if there was some hand-restoration function, there was a 70% chance of making a full or good recovery. He reported that most of the recovery occurred in the first three months, and only a small recovery occurred after six months. More recent research has shown that a significant increase can be done many years after a stroke.
Around the same time, Brunnstrom also described the recovery process, and divided the process into seven stages. As knowledge of the science of brain recovery increases, intervention strategies have evolved. Knowledge of stroke and recovery after stroke has grown significantly in the late 20th and early 21st centuries.
Maps Stroke recovery
Current perspectives and therapeutic path
Motor re-learning
"Neurocognitive Rehabilitation by the Carlo Perfetti concept", widespread in many countries, is the application of the original motor re-learning theory.
Movement therapy triggered by constraint
The idea for therapy induced by obstacles is at least 100 years old. Significant research was conducted by Robert Oden. He was able to simulate strokes in the monkey's brain, causing hemiplegia. He then tied the hands of the good monkey, and forced the monkey to use his bad arm, and observed what happened. After two weeks of this therapy, the monkeys can reuse their hemiplegic arm once more. This is because of neuroplasticity. He did the same experiment without tying his arm, and waited six months after their injury. Monkeys without intervention can not use the affected arm even six months later. In 1918, the study was published, but received little attention.
Finally, the researchers began applying the technique to stroke patients, and it was called constricted movement therapy induced. In particular, the initial study 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. Therapy requires the use of soft gloves in good hands for 90% of the wake hours, forcing the use of affected hands. The patients underwent one-on-one therapy for six to eight hours per day for two weeks.
Evidence supporting the use of induced gait therapy therapy has evolved since it was introduced as an alternative treatment method for motor deficits of the upper extremities found in stroke populations. Recently, induced gait therapy has proven to be an effective rehabilitation technique at various stages of stroke recovery to improve upper limb motor function and used during daily life activities. The biggest increase was seen among people with strokes that showed some extension of the wrist and finger on affected limbs. Transcranial magnetic stimulation and brain imaging studies have shown that the brain undergoes changes in function and plastic structure in patients undergoing limited induction motion. This change accompanies the advantages in motor function of the upper limb of paretic. However, there is no established causal relationship between observed changes in brain function and structure and motor advantages due to movement therapy induced by constraints.
Conversion-induced movement therapy has recently been modified to treat aphasia in post-CVA patients as well. This treatment intervention is known as Constraint Induced Aphasia Therapy (CIAT). The same general principles apply, but in this case, the client is limited from the use of compensation strategies to communicate such as gestures, writing, drawing and pointing, and is encouraged to use verbal communication. Therapy is usually done in groups and obstacles are used so that the hands, and any compensation strategies are not visible.
Mental/mental imagery training
Mental exercise exercises, have been shown in many studies to be effective in promoting the recovery of arm and leg function after a stroke. These are often used by physical or occupational therapists in a rehab or homehealth setting, but can also be used as part of a patient self-care home program. Mental Movement Therapy is one of the products available to help patients with guided mental imagery.
Brain repair
Electrical stimulation
The work represents a paradigm shift in approach to brain rehabilitation of stroke injuries away from pharmacologic flooding of neural receptors and vice versa, to targeted physiological stimuli. In layman's terms, this electrical stimulation mimics healthy muscle action to improve function and helps retrain weak muscles and normal movement. Functional Electrical Stimulation (FES) is usually used on 'foot-drop' after a stroke, but can be used to help retrain movement in the arms or legs.
Bobath (NDT)
In patients undergoing rehabilitation with stroke or central nervous system (cerebral palsy, etc.), Bobath, also known as Neurodevelopmental Treatment (NDT), is often the preferred treatment in North America. Bobath concept is best seen as a framework for interpretation and problem solving from individual patient presentations, along with their potential for improvement. The specifically emphasized motor control components are the integration of postural control and task performance, selective movement control for the production of coordinated sequences of movement and the contribution of sensory inputs to motor control and motor learning. Practical work is a component of a broad approach to treatment that includes an in-depth assessment of the movement strategies used by the patient to perform the task, and the identification of specific deficits of neurological and neuromuscular function. Numerous studies have been conducted comparing NDT with other treatment techniques such as neuromuscular proprioceptive facilitation (PNF stretching), as well as conventional treatment approaches (utilizing traditional exercises and functional activities), etc. Although widely used, based on the literature, NDT has failed to demonstrate any superiority over other available treatment techniques. In fact, the techniques compared with NDT in this study often yield similar results in terms of treatment effectiveness. Studies have shown significant findings for all of these treatment approaches when compared to control subjects and show that overall, rehabilitation is effective. It is important to note, however, that the NDT philosophy of "doing what is best" has caused heterogeneity in the literature in terms of what is an NDT technique, thus making it difficult to directly compare with other techniques.
Mirror Therapy
Mirror therapy (MT) has been used with some success in treating stroke patients. Clinical studies that combine mirror therapy with conventional rehabilitation have achieved the most positive results. However, there is no clear consensus about its effectiveness. In a recent survey of published research, Rothgangel concluded it
In stroke patients, we found moderate evidence quality that MT as adjunctive therapy improved arm restoration after stroke. The evidence quality on MT effects on recovery of lower limb function is still low, with only one effect of study reporting. In patients with CRPS and PLP, the quality of evidence was also low.
Stem cell therapy (in research)
The use of bone marrow-derived mesenchymal stem cells (MSC) in the treatment of ischemic stroke
Terminal differentiation of some somatic stem cells has recently been questioned after transplanted haematopoietic stem cell studies have demonstrated the development of myoblasts, endothelium, epithelial and neuroectodermal cells, suggesting pluripotency. These findings have led to the MSC being considered for the treatment of ischemic stroke, in particular directly enhancing neuroprotection and neurorestorative neurogenesis processes, angiogenesis and synaptic plasticity.
Possible mechanisms of neurorestoration and neuroprotection by MSCs after stroke
The transdiferensiasi MSC into neuron-like cells has been shown to be possible in vitro and these cells respond to central nervous system neurotransmitters. However, it is unlikely that this level of transdifferentiation occurs in vivo and that & lt; 1% of injected MSCs become completely differentiated and integrate in damaged areas. This suggests that MSC transdiferensiation into neurons or cells similar to neurons is not the main mechanism by which MSCs cause neurorestoration.
Neurogenesis induction (development of new neurons) is another possible mechanism of neurorestoration; But the correlation with functional improvement after stroke is not established. The induced cell probably originates from the ventricular zone, subventricular zone and choroidal plexus, and migrates to areas in each of the damaged hemispheres. In contrast to induction of neurogenesis, induction of angiogenesis (development of new blood vessels) by MSCs has been associated with increased brain function after ischemic stroke and is associated with increased neuronal recruitment. In addition, synaptogenesis (the formation of new synapses between neurons) has been shown to increase after MSC treatment; This combination of increased neurogenesis, angiogenesis and synaptogenesis may lead to a more significant functional improvement in the damaged area as a result of MSC treatment.
MSC treatment has also been shown to have multiple neuroprotective effects, including a reduction in apoptosis, inflammation and demyelination, as well as an increase in astrocytic continuity. MSC treatment also appears to improve control of cerebral blood flow and blood-brain barrier permeability, as well as what is currently considered the most important mechanism of MSC treatment after stroke, endogenous activation of neuroprotection and reforestation pathways with cytokine release and trophic factors.
Although endogenous protective neuronal activation and neurorestoration may have a major part in improving brain function after stroke, it is likely that functional improvements as a result of MSC treatment are due to joint action via cellular and molecular mechanisms to influence neurorestoration and neuroprotection, not just a single mechanism. These effects are also modulated by key variables, including the number and type of MSC used, relative treatment times when patient stroke occurs, MSC delivery route, as well as patient variables (eg age, underlying conditions).
What this means for stroke patients and limitations or concerns with MSC as potential treatment
If MSC treatment is available for stroke patients, the current mortality and morbidity rates may increase substantially because of the direct increase of neuroprotection and neurorestoration mechanisms rather than only indirect facilitation or prevention of further damage, eg. decompression operation. However, for MSC treatment to be used effectively and safely in a clinical setting, further research needs to be done, especially in the field of determining the relative influence of key variables (especially patient variables) on patient outcomes as well as measuring potential risks, eg. tumor formation. Although ethical concerns are largely confined to the use of embryonic stem cells, it may also be important to address any possible ethical (but unlikely) problem over the use of somatic stem cells.
Muscle training influenced by top motor neuron syndrome
Muscles that are affected by upper motor neuron syndrome have many potential features of performance changes including: weakness, decreased motor control, clonus (a series of rapidly unconscious muscle contractions), excessive tendon reflexes, flexibility and decreased endurance. The term "flexibility" is often wrongly used interchangeably with upper motor neuron syndrome, and it is not uncommon to see patients labeled as convulsions indicating a series of UMN findings.
It is estimated that about 65% of individuals experience seizures after a stroke, and studies have revealed that about 40% of stroke survivors may still have spasticity at 12 months post stroke. Muscle tone changes may result from changes in the input balance of the reticulocyte and other descending pathways to the motor and internal 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 movements.
A variety of ways are available for the treatment of upper motor neurone syndrome. These include: exercise to improve strength, control and endurance, nonpharmacological therapy, oral drug therapy, intrathecal drug therapy, injections, and surgery. While Landau suggests that researchers do not believe that treating flexibility is valuable, many scholars and doctors continue to strive to manage/treat it.
Another group of researchers concluded that while spasticity may contribute to motor impairment and significant post-stroke activity, the role of flexibility has been over-emphasized in stroke rehabilitation. In a survey conducted by the National Stroke Association, while 58 percent of survivors in the survey experienced flexibility, only 51 percent of those receiving care for the condition.
Nonpharmacological Therapy
Care should be based on an assessment by a relevant health professional. For muscles with mild to moderate disturbances, exercise should be a mainstay of management, and may need to be prescribed by physiotherapists.
Muscles with severe disorders tend to be more limited in their ability to exercise and may require assistance to do this. They may require additional intervention, to manage larger neurological disorders as well as larger secondary complications. These interventions may include serial casting, flexibility exercises such as continuous positioning programs, and patients may require equipment, such as using a stand frame to maintain a standing position. Applying custom made Lycra suits may also be useful.
Physiotherapy
Physiotherapy is beneficial in this area as it helps individuals post-stroke to progress through the motor recovery phase. These stages were originally described by Twitchell and Brunnstrom, and can be known as the Brunnstrom Approach. Initially, individuals post-stroke experience flaccid paralysis. When recovery begins, and develops, the basic movements of synergy will develop into a combination of more complex and difficult movements. Simultaneously, flexibility may develop and become very severe before it begins to decline (if any). Although the overall pattern of motor recovery exists, there is a great deal of variability between the recovery of each individual. As explained earlier, the role of spasticity in stroke rehabilitation remains controversial. However, physiotherapy can help improve motor performance, in part, through the management of flexibility.
Untrained spasticity will result in abnormal lower abdominal posture care which can lead to the formation of contractures. In the arm, this can interfere with hand hygiene and clothing, whereas in the legs, abnormal rest postures can cause transfer difficulties. To help manage flexibility, physiotherapy interventions should focus on modifying or reducing muscle tone. Strategies include mobilization of affected limbs early in rehabilitation, along with muscle extension of seizures and sustained stretching. In addition, rhythmic passive rotation manual techniques can help improve initial range. Enabling antagonists (muscles) in slow and controlled motion is a useful training strategy that individuals can use after a stroke. Splinting, to maintain muscle stretching and provide tone inhibition, and cold (ie in the form of ice packs), to reduce nerve shooting, is another strategy that can be used to temporarily reduce the degree of flexibility. The focus of physiotherapy for post-stroke individuals is to improve motor performance, in part, through the manipulation of muscle tone.
Oral drug therapy
Oral medications used for the treatment of spasticity include: diazepam (Valium), dantrolene sodium, baclofen, tizanidine, clonidine, gabapentin, and even canabinoid-like compounds. The exact mechanisms of these drugs are not fully understood, but they are thought to act on neurotransmitters or neuromodulators in the central nervous system (CNS) or muscle itself, or to reduce stretching reflexes. The problem with these drugs is their potential side effects and the fact that, in addition to reducing painful or disruptive spasms and dystonic postures, medications are generally not proven to reduce disturbance or reduce defects.
Intrathecal drug therapy
Intrathecal drug administration involves implantation of a pump that provides the drug directly to the CNS. The benefit of this is that the drug stays in the spinal cord, without traveling in the bloodstream, and there are often fewer side effects. The most common drug used for this is baclofen but morphine sulfate and Fentanyl have been used as well, especially for severe pain as a result of such flexibility.
Injection
Injections are a focus treatment that is given directly to the muscle spasms. Drugs used include: Botulinum toxin (BTX), phenol, alcohol, and lidocaine. Phenols and alcohols cause local muscle damage by denaturing proteins, thereby relaxing the muscles. Botulinum toxin is neurotoxin and relaxes muscles by preventing the release of neurotransmitters (acetylcholine). Many studies have demonstrated the benefits of BTX and have also shown that repeated BTX injections show unchanged effectiveness.
Surgery
Surgical treatment for spasticity includes elongation or release of muscles and tendons, procedures involving bone, as well as selective dorsal rhizotomy. Rhizotomy, usually reserved for severe flexibility, involves cutting selective sensory nerve roots, as they may play a role in generating spasticity.
Subluxation of shoulder after stroke
Subluxation of Glenohumeral (or shoulder) is defined as a partial or incomplete dislocation of the shoulder joint which usually results from changes in the mechanical integrity of the joint. Subluxation is a common problem with hemiplegia, or weakness of the upper limb muscles. Traditionally this has been considered a significant cause of post-stroke shoulder pain, although some new 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 due to muscle weakness supporting the shoulder joint. The shoulder is one of the most moving joints in the body. To provide a high degree of mobility, the shoulders sacrifice ligament stability and as a result depend on the surrounding muscles (ie rotator cuff, latissimus dorsi, and deltoid) for most support. This is different from other less mobile joints such as knees and hips, which have a large amount of support from the joint capsule and the surrounding ligaments. If a stroke damages the upper motor neuron that controls upper limb muscles, weakness and paralysis, followed by spasticity occurs in a somewhat predictable pattern. The muscles that support the shoulder joints, especially the delrasid and deluded posterior supraspinatus and can no longer offer sufficient support leads to downward and downward arm movement in the shoulder joint causing tension in the relatively weak joint capsule. Other factors have also been cited as contributing to subluxation such as pulling on the hemiplegia arm and inappropriately positioned.
Diagnosis can usually be done by palpation or by feeling of joint tissue and surroundings, although there is controversy as to whether or not the degree of subluxation can be measured clinically. In case of shoulder subluxation, this may be a hindrance to the rehabilitation process. Treatment involves actions to support the subluxial joint such as gluing the joints, using a lapboard or armboard. A shoulder sash can be used, but it is controversial and some studies show no difference in range of motion, subluxation level, or pain when using a sling. A sling may also contribute to contracture and increase flexor tone if used for a long time as it places the arm close to the body in adduction, internal rotation and elbow flexion. The use of slings can also contribute to non-active learning by preventing the functional and spontaneous use of the affected upper extremities. It is said that a sling may be necessary for some therapeutic activities. Sling can be considered appropriate during therapy for initial transfer and gait training, but overall use should be limited. As the patient begins to recover, voluntary shoulder spasticity and movement will occur as well as subtraction of shoulder subluxation. Sling has no value at this point.
Functional electrical stimulation (FES) also showed promising results in the treatment of subluxation, and pain reduction, although some studies indicate the return of pain after the discontinuation of FES. More recent research has failed to show a reduction in pain with the use of FES.
Logical treatments consist of precautions such as initial range of motion, precise positioning, passive support of soft tissue structures and the possibility of re-activation of shoulder muscles using functional electrical stimulation. Aggressive exercises such as overhead pulleys should be avoided with this population.
References
- Teasell RW: "Poor Hemiplegia Shoulders". Physical Treatment and Rehabilitation: State of the Art Reviews 1998; 12 (3): 489-500.
- Boyd EA, Goudreau L, O'Riain MD, et al.: Radiological size of shoulder subluxation in hemiplegia: reliability and validity. Arch Phys Med Rehabil 1993 Feb; 74 (2): 188-93
- Brandstater ME: Rehabilitation of stroke. In: DeLisa JA, et al., Eds. Rehabilitation Treatment: Principles and Practice. 3rd edition. Philadelphia: Lippincott-Raven; 1998: 1165-1189.
- Chae J, Yu DT, Walker ME, et al. Intramuscular electric stimulation for hemiplegic shoulder pain: 12 months of follow-up from multi-center randomized clinical trials. Am J Med Med Rehabilitation. 2005 Nov; 84 (11): 832-42
- Chantraine A, Baribeault A, Uebelhart D, Gremion G: Shoulder pain and dysfunction in hemiplegia: the effect of functional electrical stimulation. Arch Phys Med Rehabil 1999 March; 80 (3): 328-31
Post-stroke pain syndrome
Central post stroke pain (CPSP) is a neuropathic pain caused by damage to neurons in the brain (the central nervous system), as a result of vascular injury. One study found that up to 8% of people who had a stroke would develop post-stroke central pain, and that the pain would be moderate to severe in 5% of those affected. This condition was previously called "thalamic pain", because of the high incidence among those who suffered damage to the thalamus or nucleus of the thalamus. Now known as the CPSP, it is characterized by the pain felt from non-painful stimuli, such as temperature and light touch. This perception of altered stimuli, or allodynia, can be difficult to assess due to the fact that pain can change daily in the description and location, and can appear anywhere from month to year after a stroke. CPSP can also cause an increased central response to painful sensation, or hyperpathia. The affected person can describe pain such as cramps, burning, crushing, firing, pinch and needle, and even bloating or urinary urgency. Both variations and the pain mechanism in CPSP have made it difficult to treat. Several strategies have been used by doctors, including intravenous lidocaine, opioids/narcotics, anti-depressants, anti-epileptic drugs and neurosurgical procedures with varying success. Higher levels of pain control in people with CPSP can be achieved by treating other sequelae, such as depression and spasticity. As people age, diagnosis and management of CPSP will become increasingly important to improve the quality of life of more stroke patients.
Apraxia
An unusual and poorly understood stroke is a condition called apraxia. This condition was initially recognized as: 'The disruption of the execution of an educated movement that can not be accounted for either by weakness, incoordination, or sensory loss, nor by incomplete understanding, or lack of attention to command.' Some forms of apraxia are recognized. Apraxia gastric-kinetic is the inability to make proper or precise movements with fingers, arms or legs. idiomotor apraxia is the inability to perform orders from the brain to mimic the movement of a limb or head performed or suggested by another person. Apraxia is conceptually similar to the idiomotor apraxia, but concludes a deeper breakdown in which the function of the tool or object is no longer understood. Ideational apraxia is the inability to make plans for a particular movement. Buccofacial apraxia, or oral-facial apraxia, is the inability to coordinate and perform facial and lips movements such as whistling, winking, coughing, etc. on orders. Constructive apraxia affects a person's ability to draw or copy simple diagrams, or to build simple figures. Oculomotor apraxia is a condition in which the patient finds it difficult to move his eyes. Many believe that the most common form of apraxia is idiomotor apraxia, where a disconnection between the brain area containing the plan for the movement and the area of ​​the brain responsible for executing the movement occurs.
Unlike many stroke effects, where doctors are able to assess a specific area of ​​the brain whose stroke has been injured by certain signs or symptoms, the cause of apraxia is less clear. A general theory is that parts of the brain that contain information for previously learned motor activity have been lost or inaccessible. This condition is usually due to insult to the dominant brain hemisphere. More often this is located in the frontal lobe of the left brain of the brain. Treatment of apraxia acquired by stroke usually consists of physical therapy, occupation, and speech. The Copenhagen Stroke Study, an important study published in 2001, showed that of 618 stroke patients, manual apraxia was found in 7% and oral apraxia was found in 6%. Manual and oral apraxia is associated with increased stroke severity. Oral apraxia is associated with increased age at the time of stroke. There is no difference in incidence between the sexes. It was also found that apraxia findings did not have a negative effect on functional ability after rehabilitation was completed. The National Institute of Neurological Disorders and Stroke (NINDS) currently sponsors clinical trials to gain an understanding of how the brain operates while exercising and controlling voluntary motor movements on normal subjects. The goal is to determine what is wrong with these processes in the course of apraxia acquired due to a stroke or brain injury.
Lateral medullary syndrome
Lateral medullary syndrome, also known as Wallenberg syndrome, is caused by inferior posterior cerebral artery blockage (PICA) or vertebral artery. Signs and symptoms include decreased pain and temperature on the same side of the face and opposite side of the body compared to lesions, ataxia on the same side of the lesion, and Horner syndrome on the same side of the face.
Treatment in the acute setting is largely focused on symptomatic management. After initial treatment at the hospital, some patients will require short-term placement in nursing homes or rehabilitation facilities before returning home. At the hospital, doctors work with speech pathologists on issues like this. Typically, the usual tool used to assess the severity of dysphagia and speech problems is Barnes Jewish Hospital Stroke Dysphagia Screen, which offers validated guidelines for assessing action plans (solid food diets, all liquid diets, hydration IV, etc.) for patients at hospitals and appropriate measures in outpatient settings. Rehabilitation in Wallenberg's Syndrome focuses on improving balance, coordination, working on the activities of everyday life, and improving speech and swallowing. Severe nausea and vertigo may present and limit progress in rehabilitation and recovery. Symptomatic treatment with antiemetics and medications for important hiccups. Commonly used antiemetics include ondansetron, metoclopramide, prochlorperazine, and promethazine. These medications are also used to treat hiccups, along with chlorpromazine. There are reports of other drug cases that are useful in treating hiccups in Wallenberg's Syndrome including baclofen and anti-epileptic drugs. The prognosis for a person with lateral medullary syndrome depends on the size and location of the damaged area of ​​the brainstem. Some individuals recover quickly while others may have significant neurological disorders for months to years after the initial injury.
References
- Hiccup Related to Lateral Medullary Syndrome: Case Report. American Journal of Physical Medicine & amp; Rehabilitation. 76 (2): 144-146, March/April 1997. [3] Nickerson, Robert B. MD 2; Atchison, James W. DO 3; Van Hoose, James D. MD; Hayes, Don BS.
- Physical Treatment and Rehabilitation Board Review (Paperback). Sara J. Cuccurullo
- http://www.healthline.com/galecontent/wallenberg-syndrome
- Dysphagia in Lateral Medullary Initiation (Wallenberg syndrome). Acute Respiratory syndrome in Premotor Neurons Associated with Swallowing Activity? Blow. 2001; 32: 2081. Ibrahim Aydogdu, MD; Cumhur Ertekin, MD; Sultan Tarlaci, MD; Bulent Turman, MD, PhD; Nefati Kiylioglu, MD Yaprak Secil, MD
- Edmiaston J, Connor LT, Loehr L, Nassief A. Validation of dysphagia screening tool in acute stroke patients. Am J Crit Care. July 2010; 19 (4): 357-64. doi: 10.4037/ajcc2009961. Epub 2009 October 29th.
Post-stroke depression
Depression is a commonly reported consequence of stroke and is seen anywhere from 25-50% of patients. The Diagnostic and Statistical Statistics Manual (DSM-IV-TR) defines post-stroke depression as "a mood disorder due to a common medical condition (ie a stroke) assessed for direct physiological effects of the condition". Post-stroke depression may involve depressed mood and decreased interest and pleasure that impair social and occupational function, but it does not necessarily have to meet the complete criteria of major depressive disorder.
The first study to look for links between specific stroke lesions and the occurrence of depression reported a correlation between left frontal lesions and severe depression. Noradrenergic frontal damage, dopaminergic, and serotonergic projection are thought to cause catecholamine depletion, which causes depression. However, more recent studies have shown that the anatomical aspect of the lesions is not always correlated with the occurrence of depression. Other psychological factors can lead to the development of depression including personal and social losses associated with physical disabilities that are often caused by a stroke.
The incidence of post-stroke depression reaches 3-6 months and usually disappears within 1-2 years after a stroke, although a small percentage of patients may continue to experience chronic depression. The diagnosis of post-stroke depression is complicated by other consequences of stroke such as fatigue and psychomotor retardation - which does not necessarily indicate depression. Loss of interest in activities and relationships should encourage evaluation for depression.
Traditionally, tricyclic antidepressants (TCAs), such as nortriptyline, have been used in the treatment of post-stroke depression. Recently, selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and citalopram, have been the preferred pharmacological therapy due to a lower incidence of adverse events. Also, psychological treatments such as cognitive behavioral therapy, group therapy, and family therapy are reported to be useful adjuncts for treatment.
Overall, the development of post-stroke depression can play an important role in the recovery of patients from stroke. For example, the severity of post-stroke depression has been associated with the severity of disturbance in daily living activities (ADLs). By effectively treating depression, patients experience greater recovery from basic ADL such as dressing, eating and ambulation, as well as the instrumental ADL, such as the ability to take care of financial and household issues. In essence, the introduction and treatment of post-stroke depression leads to greater functional capability for patients over time.
References
- Berg A, Palomaki, H, et al.: Poststroke Depression: Follow-Up 18 Months. Stroke 2003; 34: 138.
- Brand Brand ME: Rehabilitation Stroke. In: DeLisa JA, et al., Eds. Rehabilitation Treatment: Principles and Practice. 3rd edition. Philadelphia: Lippincott-Raven; 1998: 1165-1189.
- Grasso MG, Pantano P, et al. Mesial temporal cortex hypoperfusion is associated with depression in subcortical stroke. Stroke. 1994 May; 25 (5): 980-85.
- Mayberg HS, Robinson, RG, et al.: PET serotonin S2 receptor cortical imaging after stroke: lateral changes and association with depression. Am J Psychiatry 1998; 145 (8): 937-43.
- Robinson RG "Post-stroke depression: prevalence, diagnosis, treatment, and progression of the disease. Biological Psychiatry 2003 August; 54 (3): 376-87.
- Dohle, C., Pullen, J., Nakaten, A., Kust, J., Rietz, C. & amp; Karbe, H. Mirror therapy promotes recovery from severe hemiparesis: A randomized controlled trial. Neurorehabilitation and Neural Repair 2009; 23 (3): 209-217.
References
External links
- National Stroke Association: Stroke Recovery - How to recover from a stroke?
- Post Dysphagia Stroke Screen
- General Depression Score for post-stroke patients
Source of the article : Wikipedia
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