Stroke

Both the occlusion of a blood vessel supplying the brain and the rupture of a cerebral vessel occur suddenly and mostly unexpectedly. Neurons are unable to tolerate oxygen and glucose deficiency for prolonged periods of time and neuronal death ensues shortly afterwards. Thus, symptom onset in stroke patients is acute. In general, a cerebrovascular accident may cause any type of neurological deficits, ranging from motor and sensory loss to cognitive impairment and decreased levels of consciousness. The type of deficits to be observed in an individual case largely depends on the location and the extent of the infarction. To some extent, on the basis of clinical symptoms, neurologists may deduce which part of the patient's brain is affected. Commonly observed neurological deficits include:

• Unilateral motor deficits, e.g., face drooping, hemiparesis/hemiplegia, inability to lift ipsilateral arm or abnormal gait
• Contralateral sensory loss
• Contralateral homonymous hemianopia
• Dysphasia
• Dysphagia
• Disturbance of consciousness
• Confusion
• Headache
• Nausea and vomiting

Space-occupying brain edema is a serious and potentially fatal complication of cerebrovascular accidents. It usually occurs between the second and fourth day after the onset of stroke symptoms [6] and possibly involves an exacerbation of neurological deficits. Brain edema is accompanied by an increase of intracranial pressure and thus, edema-mediated brain damage is not necessarily restricted to those brain regions originally affected by the cerebrovascular accident. Decreased levels of consciousness, hypertension, bradycardia and anisocoria may indicate a pathological rise of intracranial pressure due to cerebral edema.

Another possible source of delayed aggravation is reperfusion injury. Despite the fact that stroke therapy aims at recanalization and restoration of blood flow to affected brain regions, it can't currently be excluded that tissue reperfusion contributes to neuroinflammation and neuronal death. Although molecular and cellular events following tissue reperfusion are well described, evidence regarding possibly detrimental effects of reperfusion in stroke patients is still scarce [7].

Brain imaging is the single most important tool to assess cerebrovascular accidents. Both computed tomography scans and magnetic resonance imaging are employed to this end, and specific approaches include computed tomography or magnetic resonance angiography, diffusion- and perfusion-weighted imaging as well as fluid-attenuated inversion recovery [8] [9]:

• In most cases, initial computed tomography scans will be conducted without contrast agents to exclude intracranial hemorrhages as a possible cause of neurological deficits. This technique is widely available and results can be obtained within short periods of time.
• Subsequently, contrast-enhanced computed tomography angiograms may be recorded. They provide detailed information regarding the cause and location of the interruption of blood flow and are thus highly valuable in guiding treatment decisions.
• However, even greater sensitivity of stroke detection is attributed to diffusion-weighted magnetic resonance imaging. Major disadvantages of this technique are limited availability and high costs.

The aforementioned imaging methods are also very helpful to reveal the cause of the ischemic or hemorrhagic cerebral infarction, but should be complemented with blood analyses and cardiac examination.

Treatment for stroke includes acute stroke management and surgical management [10]. Acute stroke management includes restoration of homeostasis done by oxygen therapy, blood sugar control with optimal insulin therapy and antihypertensive treatment for hypertensive encephalopathy, hypertensive nephropathy, hypertensive cardiac failure, aortic dissection, preeclampsia and intracerebral hemorrhage. People with acute stroke have to be provided with aspirin, thrombolytic treatment, anticoagulants and tranquilizers. Surgery is necessary for supratentorial hemorrhage or cerebellar hematoma. Carotid endarterectomy is performed for carotid artery stenosis. Surgical decompressive hemicraniectomy is performed for middle cerebral artery infarction, which has to be finished within 48 hours [11].

Prognosis of stroke was observed in 77 patients in a 7 year follow-up study. The study revealed that 31 patients had normal cranial blood flow and the remaining 46 had subnormal cranial blood flow. During the follow-up study, 7 patients died, 3 from stroke and 4 from other causes. Out of 24 patients of subnormal cranial blood flow group, 13 died from stroke and 11 from various diseases. The survival rate was lower consistently in the subnormal cranial blood flow group than in the normal one. The difference in the survival rate was found significant during the 5 and 7 years of follow-up [5].

Etiologies of around 60 patients in the age range of 15 to 40 years with cerebral infarction in a research study by Grindal A.B. et. al. were monitored. Some of the causes for this disease were broadly identified as cardiac, hematologic, inflammatory, occlusive extra cranial vascular disease, postpartum and trauma. Cardiac causes are further divided into rheumatic heart disease with or without atrial fibrillation, sub-acute bacterial endocarditis, atrial fibrillation without rheumatic heart disease and myocardial infarction.

Hematologic causes are divided into polycythemia, sickle cell disease, thrombocytosis and disseminated intravascular coagulation. Inflammatory cause is subdivided into systemic lupus erythematosus, polyarteritis nodosa and syphilis. Other vascular causes of cerebral infarction are atherosclerosis-atherothrombosis, arterial dissection, cardio embolism, vasculitis, meningitis and fungal vasculitis, hypercoagulability, inherited metabolic disorders, and fibromuscular dysplasia and other angiopathies [2].

In a research sturdy conducted in 1994, hospital and population statistics show that cerebral infarction indicates about 80 percent of all strokes. A decrease in mortality associated stroke and cerebral infarction in particular was observed in many countries in the recent period. Research studies have explained that treatment of severe or moderate hypertension reduces the stroke incidence. Annual risk of cerebral infarction is found to be related to asymptomatic carotid artery stenosis, which is estimated to be between 1 and 2 percent [3].

The infarction on the first day appears as poorly demarcated area of softening. In the last stages of edema, the infarction appears hypodense and bright on T2 magnetic resonance imaging. The tissue of infarction will get demarcated sharply and will soften progressively. The tissue starts disintegrating from the second week and a cavity is created at that place. The anatomy of vascular territories indicates the size and location of the infarction. Microscopic evaluation during the first 24 to 48 hours discloses anoxic neurons, vacuolization of the white matter due to disentanglement of swellings of myelin and axon. Initially, there was inflammation around the blood vessels due to the release of arachidonic acid and other fatty acids. As the infarction degenerates, proliferation of peripheral region endothelial cells will continue and the capillaries will form a dead tissue [4].

Appropriate risk assessment tool is used for assessing cardiovascular risk. Lifestyle factors like dietary advice, physical activity, weight management, alcohol consumption, and cessation of smoking are performed to prevent the disease. Drug treatment for hypertension, anti-thrombosis, lipid lowering and aspirin are helpful in primary prevention. Secondary prevention is possible with the use of dipyridamole, clopidogrel and anti-lipid agents [12].

Cerebral infarction of the brain is associated with the tiny spheroidal necrosis of the nervous tissue in the ischemic area with the distribution of the arterial vessel. Ischemia precedes infarction and both are reversible. If infarction is permanent, then there will be irreversible damage to the nervous tissue. Necrosis of nervous tissue needs not occur in all the ischemic cases. Various cell types have different intensities of sensitivities to ischemia. Penumbra is the peripheral area of the ischemic region, where the cells survive for a few hours under risk, if the blood circulation is not established. When a vessel is occluded, the entire region that it is supplying does not become ischemic as collateral circulation occurs effectively and quickly.

Circle of Willis and anastomoses of carotid arteries are examples of effective collateral circulation. Main reasons for cerebral infarction include atherosclerotic obstruction of bigger vessels, embolic blocking of distal vessels, arterial spasm and vasculitis. Common symptoms include stroke accompanied by neurological syndromes [1].

• Definition: Tiny spheroidal necrosis of nervous tissue in the ischemic area with the arterial vessel distribution is called as cerebral infarction of the brain. If the damage due to infarction is permanent in the nervous tissue, then it is irreversible. 
• Cause: Some of the causes of cerebral infarction include atherosclerosis, vasculitis, cardio-embolism, systemic lupus erythematosus, vascular spasm, meningitis, sickle cell disease, hypercoagulability and inherited metabolic disorders.
• Symptoms: Some of the symptoms of cerebral infarction are contralateral hemiplegia that is initially flaccid and then become spastic, sensory loss, homonymous hemianopia and dysphasia. 
• Diagnosis: Initial diagnosis of cerebral infarction is done by blood tests, ventricular hypertrophy is evaluated by electrocardiogram, chest X-ray and echocardiography are utilized for assessing large left atrium and myocardial infarction. Brain imaging is performed for patients having undergone blood tests and those with severe headache.
• Treatment: Acute stroke management for cerebral infarction is done by oxygen therapy, antihypertensive treatment and optimal insulin therapy. Acute stroke is treated with anticoagulants, thrombolytic treatment, aspirin, and tranquilizers. Surgery is suggested for cerebellar hematoma. 

1. Amarenco P, Lavallée PC, Labreuche J, et al. Prevalence of coronary atherosclerosis in patients with cerebral infarction. Stroke 2011; 42:22.
2. Moncayo J, Devuyst G, Van Melle G, Bogousslavsky J. Coexisting causes of ischemic stroke. Arch Neurol 2000; 57:1139.
3. Caplan LR, Gorelick PB, Hier DB. Race, sex and occlusive cerebrovascular disease: a review. Stroke 1986; 17:648.
4. Caplan LR. Brain embolism. In: Practical Clinical Neurocardiology, Caplan LR, Chimowitz M, Hurst JW. (Eds), Marcel Dekker, New York 1999
5. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke 2001; 32:2426.
6. Bardutzky J, Schwab S. Antiedema therapy in ischemic stroke. Stroke. 2007; 38(11):3084-3094.
7. Nour M, Scalzo F, Liebeskind DS. Ischemia-reperfusion injury in stroke. Interv Neurol. 2013; 1(3-4):185-199.
8. Birenbaum D, Bancroft LW, Felsberg GJ. Imaging in acute stroke. West J Emerg Med. 2011; 12(1):67-76.
9. Wintermark M, Sanelli PC, Albers GW, et al. Imaging recommendations for acute stroke and transient ischemic attack patients: A joint statement by the American Society of Neuroradiology, the American College of Radiology, and the Society of NeuroInterventional Surgery. AJNR Am J Neuroradiol. 2013; 34(11):E117-127.
10. Goldstein LB, Samsa GP. Reliability of the National Institutes of Health Stroke Scale. Extension to non-neurologists in the context of a clinical trial. Stroke 1997; 28:307.
11. Bruno A, Durkalski VL, Hall CE, et al. The Stroke Hyperglycemia Insulin Network Effort (SHINE) trial protocol: a randomized, blinded, efficacy trial of standard vs. intensive hyperglycemia management in acute stroke. Int J Stroke 2014; 9:246.
12. Aiyagari V, Gorelick PB. Management of blood pressure for acute and recurrent stroke. Stroke 2009; 40:2251.

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