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A stroke is a cerebrovascular event resulting in rapid functional cell death in local tissue. Strokes, also known as cerebrovascular accidents (CVA) are a major cause of disability globally (Doyle, Simon, & Stenzel-Poore, 2008) and occur due to a disturbance in the blood supply to the brain. This disturbance in cerebral blood flow commonly results in a period of ischemia, an interruption to the delivery of oxygen to the brain tissue. Focal ischemia due to occlusion of brain artery is the cause of more than 80 % of all strokes (Flynn, MacWalter, & Doney, 2008). The other major cause of stroke is a hemorrhage, a rupture in a cerebral artery, although a number of hemorrhagic strokes are also caused by ischemic episodes (Donnan, Fisher, Macleod, & Davis, 2008).
A transient ischemic attack (TIA) as the name suggests, is also the result of an ischemic episode, but differs in longevity from a CVA. TIAs resolve within 24 hours and are therefore sometimes referred to as “mini-strokes”. TIAs share symptoms with other conditions such as disturbances of consciousness, mental health and balance as well as strokes and are therefore regularly misdiagnosed by medical professionals (Ferro et al., 1996).
Although TIAs share many symptoms with stroke, such as contralateral paralysis, numbness, motor weaknesses, impairments to the visual system, slurred speech and language comprehension and expression difficulties (aphasia), the primary difference between TIAs and CVAs is that these symptoms resolve within 24hrs (Easton et al., 2009). However, brain injury may still occur, even if the TIA lasts only a few minutes.
There are a number of documented warning signs or signals aiding early recognition of CVAs. The three key diagnostic signs are abnormal speech, sudden-onset facial weakness and a simple motor impairment known as arm drift when one arm involuntarily drifts downwards when a patient is asked to raise both arms (Goldstein & Simel, 2005). The presence of all three of these symptoms significantly increases the chance of stroke. Likewise, the absence of these face, arm and speech indicators greatly reduces the likelihood of stroke in the patient.
As well as these early recognition signs there are a number of risk factors for CVAs, which can also be taken into account when considering prevention, treatment and diagnosis of stroke. Many of the risk factors for stroke can be modified by implementing lifestyle changes. The risk factors include high blood pressure (Whisnant, 1996), atrial fibrillation (Wolf, Abbott, & Kannel, 1987), high blood cholesterol levels ("Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration," 1995), diabetes (Dormandy et al., 2005). Other lifestyle factors such as smoking, obesity, heavy alcohol consumption and sedentary behavior may also have a role in stroke susceptibility although the effectiveness of interventions involving lifestyle changes for prevention of CVAs, is unclear (Ezekowitz, Straus, Majumdar, & McAlister, 2003).
Initial treatment of ischemic stroke is aimed at removing the blockage (blood clot) as quickly as possible either mechanically (thrombectomy) or by breaking the clot down (thrombolysis). Rapid restoration of cerebral blood flow is crucial in order to limit cell death (Saver, 2006).
Treatment of hemorrhagic stroke requires a more complex neurological evaluation since the cause of the hemorrhage must first be established. Compared to ischemic stroke, the injury, resulting impairment and outcome in the case of hemorrhagic stroke is generally more severe and treatment will also depend on whether the hemorrhage is intracerebral or subrachnoid as the recommended treatment options differ depending on the anatomy of the injury and complicating factors (Barrett, Meschia, & Kramer, 2013).
Barrett, K., Meschia, J., & Kramer, A. (2013). Treatment of Hemorrhagic Stroke. In K. M. B. a. J. F. Meschia (Ed.), Stroke. Oxford: John Wiley & Sons.
Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration. (1995). Lancet, 346(8991-8992), 1647-1653.
Donnan, G. A., Fisher, M., Macleod, M., & Davis, S. M. (2008). Stroke. Lancet, 371(9624), 1612-1623. doi: 10.1016/S0140-6736(08)60694-7
Dormandy, J. A., Charbonnel, B., Eckland, D. J., Erdmann, E., Massi-Benedetti, M., Moules, I. K., . . . investigators, P. (2005). Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial. Lancet, 366(9493), 1279-1289. doi: 10.1016/S0140-6736(05)67528-9
Doyle, K. P., Simon, R. P., & Stenzel-Poore, M. P. (2008). Mechanisms of ischemic brain damage. Neuropharmacology, 55(3), 310-318. doi: 10.1016/j.neuropharm.2008.01.005
Easton, J. D., Saver, J. L., Albers, G. W., Alberts, M. J., Chaturvedi, S., Feldmann, E., . . . Disease, I. C. o. P. V. (2009). Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke, 40(6), 2276-2293. doi: 10.1161/STROKEAHA.108.192218
Ezekowitz, J. A., Straus, S. E., Majumdar, S. R., & McAlister, F. A. (2003). Stroke: strategies for primary prevention. Am Fam Physician, 68(12), 2379-2386.
Ferro, J. M., Falcão, I., Rodrigues, G., Canhão, P., Melo, T. P., Oliveira, V., . . . Salgado, A. V. (1996). Diagnosis of transient ischemic attack by the nonneurologist. A validation study. Stroke, 27(12), 2225-2229.
Flynn, R. W., MacWalter, R. S., & Doney, A. S. (2008). The cost of cerebral ischaemia. Neuropharmacology, 55(3), 250-256. doi: 10.1016/j.neuropharm.2008.05.031
Goldstein, L. B., & Simel, D. L. (2005). Is this patient having a stroke? JAMA, 293(19), 2391-2402. doi: 10.1001/jama.293.19.2391
Saver, J. L. (2006). Time is brain--quantified. Stroke, 37(1), 263-266. doi: 10.1161/01.STR.0000196957.55928.ab
Whisnant, J. P. (1996). Effectiveness versus efficacy of treatment of hypertension for stroke prevention. Neurology, 46(2), 301-307.
Wolf, P. A., Abbott, R. D., & Kannel, W. B. (1987). Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study. Arch Intern Med, 147(9), 1561-1564.
Free Evaluation Of The Causes Of Stroke Report Sample
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