Abstract

The Pathophysiology of Ischemic Stroke Studied by Radionuclide Imaging

Highlights

  • The energy demands of the nervous tissue are very high and sufficient blood supply to the brain must be maintained consistently

  • Ischemic stroke is caused by interruption or significant impairment of blood supply to the brain, which leads to a cascade of metabolic and molecular alterations resulting in functional disturbance and morphological damage

  • The changes in regional cerebral blood flow and in regional metabolism can be assessed by radionuclide imaging, especially single photon emission tomography (SPECT) and positron emission tomography (PET)

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Summary

Introduction

The energy demands of the nervous tissue are very high and sufficient blood supply to the brain must be maintained consistently. 130 billion neurons (21.5 billion in the neocortex)[1] comprises only 2 % of total body mass, yet consumes at rest approximately 20 % of the body’s total basal oxygen consumption supplied by 16 % of the cardiac blood output. Energy metabolism by functional activation is due mostly to stimulation of the Na+K+-ATPase activity to restore the ionic gradients across the cell membrane and the membrane potentials that were degraded by the spike activity and is rather high compared to the demand of neuronal cell bodies[2]. Circulatory disturbances and insufficient blood supply trigger a complex deleterious cascade of biochemical and molecular events leading to ischemic cell death (review in Hossmann 20094). Radionuclide imaging detects the pathophysiological changes occurring in ischemic stroke and may help in treatment decisions and may guide the development of new therapeutic strategies

Detection of the ischemic lesion
The concept of the ischemic penumbra and identification by imaging
Detection of hypoxic tissue
PET as a surrogate marker for treatment efficiency
Microglia activation as an indicator of inflammation
Hemodynamic and Metabolic Reserve
Findings
Complex activation studies
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