To know about Acute Stroke

Back ground

Stroke is the clinical term for acute loss of perfusion to vascular territory of the brain, resulting in ischemia and a corresponding loss of neurologic function. Classified as either hemorrhagic or ischemic, strokes typically manifest with the sudden onset of focal neurologic deficits, such as weakness, sensory deficit, or difficulties with language. Ischemic strokes have a heterogeneous group of causes, including thrombosis, embolism, and hypoperfusion, whereas hemorrhagic strokes can be either intraparenchymal or subarachnoid.   

Only in recent years have advances been made that enable physicians to significantly improve the outcome of this devastating disease. A new era in acute stroke care began in 1995, when the National Institute of Neurologic Disorders and Stroke (NINDS) tissue plasminogen activator (t-PA) Stroke Study Group first presented data indicating that early administration of t-PA benefited a carefully selected patient group with acute ischemic stroke (AIS). Currently, t-PA is the only approved therapy for AIS, and despite proven efficacy, utilization rates of rt-PA remain low. 

Pathophysiology

The brain is the most metabolically active organ in the body. While representing only 2% of the body's mass, it requires 15-20% of the total resting cardiac output to provide the necessary glucose and oxygen for its metabolism. Ischemic strokes result from events that limit or stop blood flow, such as embolism, thrombosis in situ, or relative hypoperfusion. As blood flow decreases, neurons cease functioning, and irreversible neuronal ischemia and injury begin at blood flow rates of less than 18 mL/100 mg/min.  

Ischemic cascade 

The processes involved in stroke injury at the cellular level are referred to as the ischemic cascade. Many factors are thought to result in cell death and dysfunction, and others are being discovered at a rapid rate. Within seconds to minutes of the loss of glucose and oxygen delivery to neurons, the cellular ischemic cascade begins. This is a complex process that begins with cessation of the normal electrophysiologic function of the cells. The resultant neuronal and glial injury produces edema in the ensuing hours to days after stroke, causing further injury to the surrounding tissues. 

Ischemic penumbra 

An acute vascular occlusion produces heterogeneous regions of ischemia in the dependent vascular territory. The quantity of local blood flow is comprised of any residual flow in the major arterial source and the collateral supply, if any. Regions of the brain without significant flow are referred to collectively as the core, and these cells are presumed to die within minutes of stroke onset. Zones of decreased or marginal perfusion are collectively called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours because of marginal tissue perfusion, and currently studied pharmacologic interventions for preservation of neuronal tissue target this penumbra. 

Administration of t-PA to the patient with an acute stroke attempts to establish revascularization so that cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigate the effects of ischemia only if performed quickly. Neuroprotective strategies are intended to preserve the penumbral tissues and extend the time window for revascularization techniques. While none to date have shown broad benefit in clinical trials, several trials are underway. 

Mechanisms of stroke 

Embolic strokes 

Emboli may either be of cardiac or arterial origin. Cardiac sources include atrial fibrillation, recent myocardial infarction, prosthetic valves, native valvular disease, endocarditis, mural thrombi, dilated cardiomyopathy, or patent foramen ovale allowing passage of venous circulation emboli. Arterial sources are atherothrombolic or cholesterol emboli that develop in the arch of the aorta and in the extracranial arteries (ie, carotid and vertebral arteries). Embolic strokes tend to have a sudden onset, and neuroimaging may demonstrate previous infarcts in several vascular territories or calcific emboli. 

Thrombotic strokes 

Thrombotic strokes include large-vessel strokes and small-vessel or lacunar strokes. They are due to in situ occlusions on atherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches. Thrombogenic factors may include injury to and loss of endothelial cells exposing the subendothelium and platelet activation by the subendothelium, activation of the clotting cascade, inhibition of fibrinolysis, and blood stasis. Thrombotic strokes are generally thought to originate on ruptured atherosclerotic plaques. Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis. In other patients, especially younger patients, other causes should be considered, including hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein S deficiency), sickle cell disease, fibromuscular dysplasia, arterial dissections, and vasoconstriction associated with substance abuse. 

Lacunar stroke 

Lacunar strokes represent 20% of all ischemic strokes. They occur when the penetrating branches of the middle cerebral artery (MCA), the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery become occluded. Causes of lacunar infarcts include microatheroma, lipohyalinosis, fibrinoid necrosis secondary to hypertension or vasculitis, hyaline arteriosclerosis, and amyloid angiopathy. The great majority are related to hypertension. 

Watershed infarcts 

These infarcts, also known as border zone infarcts, develop from relative hypoperfusion in the most distal arterial territories and can produce bilateral symptoms. Frequently, these occur perioperatively or in situations of prolonged hypotension. 

Frequency

  United States

Approximately 705,000 strokes occur each year, including both new and recurrent cases. Of these strokes, approximately 625,000 are ischemic strokes. By the year 2025, the annual number of strokes is expected to reach 1 million. Currently, more than 4.4 million people in the United States are stroke survivors. 

International

As in the United States, stroke is the third leading cause of death in the industrialized countries of Europe and the leading cause of adult disability. The global incidence of stroke will only increase, since the population older than 65 years will rise from 390 million now to 800 million by 2025, representing 10% of the total population. 

Mortality/Morbidity

Stroke is the third leading cause of death in the United States (60.2 per 100,000), following cardiac and cancer-related deaths. Approximately 29% of patients die within 1 year following a stroke; this percentage rises in patients older than 65 years. Worldwide in 1990, more than 4.3 million people died of cerebrovascular disorders.  

 Stroke is the leading cause of disability in the United States; 31% of stroke survivors assistance with daily living, 20% need some type of assistance for walking, and 16% require admission to a long-term care facility. Furthermore, at least one third of stroke survivors have depression as well as many of their care providers.  

 The direct costs (ie, treatment) and indirect costs (ie, lost productivity) of stroke in the United States are approximately $43 billion/year.  

Race

In the United States, stroke has a higher incidence in the black population than in the white population. 

In black males, the incidence is approximately 93 per 100,000, with a death rate of approximately 51%. In black females, incidence is 79 per 100,000 with a death rate of 39.2%. Young blacks have a 2-5 times greater risk of ischemic stroke than the white population of the same age, and they are 2.5 times more likely to die of stroke. Blacks have an age-adjusted risk of death from stroke that is 1.49 times that of whites.  

White males have a stroke incidence of 62.8 per 100,000, with death being the final outcome in 26.3% of cases, compared with women who have a stroke incidence of 59 per 100,000 and a death rate of 39.2%.  

Hispanics have a lower overall incidence of stroke than whites and blacks but more frequent lacunar strokes and stroke at an earlier age.  

Sex

In patients younger than 60 years, the incidence of stroke is greater in males (3:2 ratio). 

Age

Stroke can occur in patients of all ages, including children.  

Risk of stroke increases with age, especially in patients older than 64 years, in whom 75% of all strokes occur.