Influence of oxygen demand on electroencephalographic correlates to cerebral blood flow and oxygen metabolism in ischemic stroke patients

This chapter focuses on the primary causes and preventions of stroke. Ischemic stroke occurs when a localized area in the nervous system is deprived of glucose and oxygen because of inadequate cerebral blood flow. The severity of injury is a function of how much the blood flow has been reduced and for how long. In most cases, strokes can be diagnosed purely on the basis of the history and examination. After a stroke occurs, it will continue to manifest as a region of impeded diffusion (also referred to as “restricted diffusion”) on MRI for about two weeks, but MRI scans are unnecessary when the history and examination provide compelling evidence of a stroke and the mechanism of stroke is apparent. Some studies have shown that early rehabilitation allows stroke patients to recover more quickly and perhaps to a higher level of function. Stroke prevention will continue to be the cornerstone of stroke management. Primary prevention is directed toward the early recognition and treatment of risk factors that predispose to the development of cerebrovascular disease.

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Blood pressure reduction in hypertensive acute ischemic stroke patients does not affect cerebral blood flow

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x18774708 ◽

2018 ◽

Vol 39 (9) ◽

pp. 1878-1887 ◽

Cited By ~ 1

Author(s):

Mahesh Kate ◽

Negar Asdaghi ◽

Laura C Gioia ◽

Brian Buck ◽

Sumit R Majumdar ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Ischemic Stroke ◽

Acute Ischemic Stroke ◽

Antihypertensive Drugs ◽

Controlled Trial ◽

Blood Pressure Reduction ◽

Stroke Patients ◽

Before And After

The effect of blood pressure (BP) reduction on cerebral blood flow (CBF) in acute ischemic stroke is unknown. We measured regional CBF with perfusion-weighted MRI before and after BP treatment in a three-armed non-randomized prospective controlled trial. Treatment arm assignment was based on acute mean arterial pressure (MAP). Patients with (MAP) >120 mmHg ( n = 14) were treated with intravenous labetalol and sublingual (SL) nitroglycerin (labetalol group). Those with MAP 100–120 mmHg ( n = 17) were treated with SL nitroglycerin (0.3 mg) (‘NTG Group’) and those with baseline MAP<100 mmHg ( n = 18) were not treated with antihypertensive drugs (untreated group). Forty-nine patients (18 female, mean age 65.3 ± 12.9 years) were serially imaged. Labetalol reduced MAP by 12.5 (5.7–17.7) mmHg, p = 0.0002. MAP remained stable in the NTG (6.0 (0.4–16, p = 0.3) mmHg and untreated groups (−0.3 (−2.3–7.0, p = 0.2) mmHg. The volume of total hypoperfused tissue (CBF<18 ml/100 g/min) did not increase after labetalol (−1.1 ((−6.5)–(−0.2)) ml, p = 0.1), NTG (0 ((−1.5)–4.5) ml, p = 0.72), or no treatment 0.25 ((−10.1)–4.5) ml, p = 0.87). Antihypertensive therapy, based on presenting BP, in acute stroke patients was not associated with an increased volume of total hypoperfused tissue.

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