Acute Ischemic Stroke Treatment

Acute Ischemic Stroke Treatment

Rafael H Llinas
Published: US Neurological Disease 2006 Issue II
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Introduction

The treatment of acute stroke has changed profoundly in the last 10 years. People with strokes are being treated more aggressively and in a more comprehensive manner than in the past. The change in attitude toward stroke began with visionaries such as C Miller Fisher, who began to formally categorize the subtypes and different causes of stroke. It was at this time that carotid stenosis was not only understood to be a cause of stroke, but also the first experiments for prevention of recurrent stroke with surgical procedures began. As time passed, once the etiology of stroke could be determined, strategies for prevention of recurrence of stroke were investigated.

Paradigm Shift in Acute Stroke Care

Probably the most important paradigm shift in acute stroke care was with the National Institute of Neurological Disorders and Stroke (NINDS) Tissue Plasminogen Activator (t-PA) trial. This study showed benefit with medication that can break apart the clots that cause acute strokes. This was not a new idea. Studies using thrombolytics to treat strokes go back as far as 1958, when Sussman et al.1 used fibrinolysin (Plasmin) to thrombolyse strokes, and the randomized placebo-controlled trial of intravenous streptokinase by Meyer et al. was performed in 1965.2 Unfortunately, these trials showed either no benefit over placebo, or benefit in some and hemorrhagic transformation of some of the strokes.

In 1995, the NINDS t-PA for acute ischemic stroke trial was published in the New England Journal of Medicine. It showed that, compared with placebo, a ‘clot busting agent’ could be infused intravenously into stroke patients safely, with benefit at 90 days. The NINDS t-PA trial was different to the other thrombolytic trials as it used t-PA instead of streptomycin or fibrolyse and had a very strict list of contraindications to use.3 These contraindications allowed for selection of patients who were most likely to benefit. Of the multiple contraindications, the most vital is the three-hour window. This t-PA was found beneficial if given within three hours of onset of the stroke. In fact, the greatest benefit is seen within the first 90 minutes from stroke onset.4

This evidence changed entirely how clinicians were dealing with stroke patients. With the NINDS trial, stroke became an emergency to be evaluated and treated quickly instead of a tragedy with little or no hope for improvement besides time and physical therapy.Another thing changed with the NINDS trials, which was the vital importance of a clinical neurologist as part of the acute evaluation of stroke patients.

Acute Evaluation of Stroke

Previously, stroke was almost universally thought of as a medical disease treated by internists because the causes of stroke (high blood pressure, arteriosclerosis, atrial fibrillation, and hypercoaguable states) were considered internal medicine disorders. However, the acute evaluation of stroke patients is required by a neurologist or clinicians trained by a neurologist, since the only objective test for stroke is clinical examination in the first three hours. A normal computed tomography (CT) scan, normal blood tests, and a careful history and neurological examination are the only ways to diagnose an acute stroke. There is no blood test or electrocardiogram (ECG) specific for stroke, and CT scans may be entirely normal for up to six hours after the acute onset of stroke. Thus, the neurologist became an irreplaceable member of the team to acutely evaluate stroke patients

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