The Physiological Changes That Take Place Following Stroke - Essay Example

? The physiological changes that take place following stroke and how it affects recovery University Date Stroke, also sometimes called a brain attack or a cerebrovascular accident (CVA), occurs when blood flow is interrupted to part of the brain (Adams, 2007). Lack of blood in the brain translates in lack of oxygen and nutrient supply, as well as limitations in waste removal, whose consequences are the rapid death of brain cells. However, based on the afflicted side of the brain, stroke may lead to paralysis, impairment in oral speaking abilities, distortion of memory, and its loss and other cognitive abilities, coma, or cessation of life. There are two types of stroke ischemic and hemorrhagic, which can affect recovery as severity of stroke can greatly influence the recovery. As ischemic stroke have much better chance for recovery than hemorrhagic stroke (Aguilar, 2009). Stroke is fatal for about a quarter of the white male population, half of the black males population, quarter of the white female population and a roughly two fifths of the black female population. Survivors of strokes are usually left with significant impairments to their abilities, which require emergency treatment and comprehensive rehabilitation. This is in order to improve significantly both survival and recovery, as the effects are usually severe except in mild cases of stroke. Studies conducted in 2003 showed strong indications that treating stroke victims with certain antidepressant medications, despite their lack of depression improved their chances of living longer. People who received antidepressant treatment had an increased chance of survival in relation to cardiovascular events than those who did not receive antidepressant drugs (U.S. Department of Health and Human Services, 2008). Post stroke changes in blood pressure are crucial, as there is an occurrence of impairment in cerebral auto regulation, which under conventional conditions, serves to uphold constant cerebral blood flow in spite of changes in systemic BP. Both the systolic and diastolic BP rates are elevated following a stroke attack, where it seems to rise sharply at the time of stroke, and the blood pressure then declines within a week (Dawson, 2000). On the other hand, body temperatures rise by about 0.2°C over the first 24-36 h after stroke, and then begin to fall. Following this elevation, temperatures then seem decline within the first five days following the stroke, despite the lack of extensive studies into the rate of normalization (Dippel, 2003). Consequently, glucose levels appear to increase post stroke, in which case, hyperglycemia appears to have an affiliation with more severe stroke. Hyperglycemia after stroke is a phenomenon occurring often; with almost half of the victims having blood, glucose levels beyond 7.0 mmol/L. Regions affected by stroke may be crucial especially in relation with infarctions of the insular cortex, which is involved in the autonomic control of the neuroendocrine stress response. The control is believed to be affiliated with hyperglycemia, but this connection has been disagreed upon (Morfis, 1997). Transient hypoxia has been encounters in common interactions such as MRI scanning, where hypoxia is often experienced after stroke, but the frequency depends on the definition used. In stroke cases, hypoxia is usually affiliated with co-morbidities such as infections of the respiratory tract and failure of the cardiac system, where vascular dementia is also a frequent post-stroke problem described by the loss of cognitive role or thinking capabilities (Wong, 2007). It occurs when brain tissue is damaged following lower levels of blood flow to the brain in the event of a stroke of following multiple strokes. As a result, the damaged brain tissue inhibits the abilities of the victim in relation to information processing, and the consequences are loss of memory, confusion, reduced concentration span and problems handling everyday tasks. A stroke may affect a person's ability to perform abstract cognitive tasks, where the victims find it profoundly difficult to organize events and ideas, as well as solve unfamiliar problems or form judgments (Sugimori, 1995). In relation to communication, stroke leads to victims having challenges in expression and processing language, a condition termed as aphasia. A large percentage of the human populations do not appreciate its ability to communicate and swallow, but a sudden loss of these abilities can be devastating. Patients with these problems are referred to professionals, known as speech therapists. The role of speech therapists is the evaluation of the patient's communication and swallowing skills, and identification of any problems. Speech therapists also design an individual therapy program to help the patient improve his skills to the maximum potential (Adams, 2007). Many stroke patient experiences a feeling of anger, anxiety, sadness and fear, which lead to emotional disorders and depression. Depression manifests itself through sadness, tearfulness, lack of interest in daily activities, eight gain or loss, sleep and appetite loss, as well as fatigue; feelings of worthlessness or guilt. In addition, it also manifests itself through difficulty in thinking and poor concentration, as well as thoughts of death and suicide. Depression conventionally disappears after stroke as the victim recovers, in which case, family, friends and rehabilitation professionals can help in improving the situation. However, if signs of depression prolong, it is important to seek help from a specialized primary care medical doctor, psychotherapy physician, doctor of psychiatry or psychologist (Latchaw, 2003). Other than these, additional physio-cognitive disorders affecting the emotional abilities of a person may arise such as dysphagia, which occurs following stroke due to paralysis of throat muscles. In addition, Pseudo bulbar occurs characterized by uncontrolled and sudden attack of crying or laughing which called emotional liability. These emotional liabilities can cause perceptual problems in relation to their internal and external emotion expressions, where victims feel left out. Sensation is usually challenged, but it does not depart from the hemiplegic side, as the type and extent of deficit is related to the location and extent of the lesion. Detailed, restricted areas of dysfunction are usual with lesions in the cortex, although scattered presence in whole regions depicts deep lesions afflicted on the thalamus and adjacent structures. The symptoms of crossed anes­thesia (ipsilateral facial injuries with contralateral trunk and limb shortfalls) characterize brainstem injury, whereby proprioceptive losses are common and have a remarkable effect on mortal capabilities. Moreover, there is loss of superficial touch, pain, and temperature are also frequent whereby stroke may lead to many vision troubles for example vision loss and vision perception troubles (Morgenstern, 2010). Stroke patient have many vision problems called visual disturbances that are based on the region affected by the stroke in the brain, where survivors face balance and posture problems and disorientation. Other common problems following stroke is sleep disturbance as sleep more during day than at night and insomnia, where insomnia denotes not being able to fall or stay asleep. Sleep disorders in stroke are caused by abnormal breathing patterns that frequently disrupt sleep throughout the night. Seizures, which are brought about by sudden episodes of abnormal electrical activity of the brain, also occur following the onset of stroke (Christensen and Boysen, 2002). As such, stroke is one of the most common causes of seizures, which are can be characterized by spasm or convulsions. In addition to effects of stroke on sensation, damage to the brain due to stroke can sometimes cause tactile perception to be painful. In addition, sometimes tightness leads to pain in joints due to spasticity and stretch of the capsule on weight bearing joints. Post stroke fatigue is one of chronic symptoms and rest does not improve tactile perception in relation to joint pains. Urinary problems may also occur in stroke patient due to touch perception and the effect of stroke on sphincter muscles. Urinary incontinence may require temporary use of a catheter but generally, this problem improves quickly, and early removal of a catheter is desirable to prevent the development of infection. Abnormal posture as in the abnormal alignment of the head, trunk and limbs follow in the following ways, such that the head appears slightly extended, bending towards the affected side and rotating towards the non-affected side. Trunk experiences flexion towards the affected side due to spasticity and shortening of lattismus dorsi and rotation to this side. In relation to Upper limbs the shoulder (depression, retraction, adduction and internal rotation), elbow (flexion), radioulnar (pronation), wrist and fingers (flexion and ulnar deviation) and thumb (flexion and adduction). In addition, lower limbs: pelvic (elevated and retracted), hip (extension, adduction and internal rotation), knee (extension) and ankle (planter flexion and inversion of foot). However, functional impairments subsequent to stroke differ from one patient to the other, which generally include considerable problems in walking, rolling, standing and sitting for both moderate and serious acute stroke patients, which hampers their daily life as it affect their vital activities such as dressing and feeding. The above occurs following loss of fractionation, which is inability to make specific movement at single joint without moving other joints. This is in addition to, loss of balance reaction due to alteration of tone so postural adjustments are impaired. Ultimately, reflex sympathetic dystrophy (shoulder-hand syndrome) occurs in approximately a quarter the cases, where the patient experiences inflammation and tender­ness of hands and fingers alongside with pain in the shoulder. In addition, there are sympathetic vasomotor signs such as the occurrence of a glossy skin and atrophic changes, whereby patient experience difficulties in movement, immobilization that culminates to contracture, atrophy of skin, bone, and muscle and heightened stiffness. References Dawson SL, Blake MJ, Panerai RB, Potter JF. (2000). Dynamic but not static cerebral autoregulation is impaired in acute ischemic stroke. Cerebrovasc Dis.; 10:126–32. Sugimori H, Ibayashi S, Fujii K, Yao H, Sadoshima S, Fujishima M. (1995). Brain infarction developed in hypertensive and normotensive patients during hospitalization--hemodynamic factors. Angiology.; 46:473–80. Morfis L, Schwartz RS, Poulos R, Howes LG. (1997). Blood pressure changes in acute cerebral infarction and hemorrhage. Stroke.;28:1401–5. Christensen H and Boysen G. (2002). Blood glucose increases early after stroke onset: A study on serial measurements of blood glucose in acute stroke. Eur J Neurol.;9:297–301. Dippel DW, van Breda EJ, van der Worp HB, van Gemert HM, Kappelle LJ, Algra A, et al. (2003). Timing of the effect of acetaminophen on body temperature in patients with acute ischemic stroke. Neurology.;61:677–9. Wong AA, Davis JP, Schluter PJ, Henderson RD, O'Sullivan DJ, Read SJ. (2007). The time course and determinants of temperature within the first 48h after ischemic stroke. Cerebrovasc Dis.;24:104–10. Adams HP Jr, et al. (2007). Guidelines for the early management of adults with ischemic: Stroke, 38(5): 1655-1711 Aguilar MI, Hart R, Pearce LA. (2007). Oral anticoagulants versus antiplatelet therapy for preventing stroke in patients with non-valvular atrial fibrillation and no history of stroke or transient ischemic attacks. Cochrane Database Syst Rev. 18;(3):CD006186. Latchaw RE, et al. (2003). Guidelines and recommendations for perfusion imaging in cerebral ischemia. Stroke, 34(4): 1084-1104. U.S. Department of Health and Human Services. 2008 Physical Activity Guidelines for Americans (ODPHP Publication No. U0036). Retrieved from http://www.health.gov/paguidelines/pdf/paguide.pdf. Morgenstern LB, et al. (2010). Guidelines for the management of spontaneous intracerebral hemorrhage. Stroke, 41(9): 2108-2129. Read More