Transient Ischemic Attacks Before Ischemic Stroke: Preconditioning the Human Brain?

Abstract

Background and Purpose-We investigated whether transient ischemic attacks (TIAs) before stroke can induce tolerance by raising the threshold of tissue vulnerability in the human brain. Methods-Sixty-five patients with first-ever ischemic territorial stroke received diffusion-and perfusion-weighted MRI within 12 hours of symptom onset. Epidemiological and clinical data, lesion volumes in T2, apparent diffusion coefficient (ADC) maps and perfusion maps, and cerebral blood flow and cerebral blood volume values were compared between patients with and without a prodromal TIA. Results-Despite similar size and severity of the perfusion deficit, initial diffusion lesions tended to be smaller and final infarct volumes were significantly reduced (final T2: 9.

Spectacular Shrinking Deficit: Insights from Multimodal Magnetic Resonance Imaging after Embolic Middle Cerebral Artery Occlusion in Sprague—Dawley Rats

“…This seems to be of special interest given the contradicting significance attributed to brief cerebral ischemia. Whereas some studies found that transient cerebral ischemia may improve stroke outcome by serving as a preconditioning stimulus that triggers neuroprotective pathways in the brain (Castillo et al, 2003;Wegener et al, 2004), others demonstrated secondary deterioration on MRI (Fujioka et al, 1999a) or neurological function (Johnston et al, 2003;Smith et al, 2005) similar to the herein observed pathology. Hence, withholding treatment in these patients should be reconsidered and more aggressive interventions may be indicated in patients with rapidly improving symptoms, who currently are often treated with little urgency or concern (Johnston et al, 2003;Smith et al, 2005).…”

Induction of Ischemic Tolerance Protects the Retina From Diabetic Retinopathy

“…11 Moreover, clinical studies support the effectiveness of IPC in the brain of humans with transient ischemic attacks. 14 Although IPC confers robust neuroprotection in different models of ischemia, its clinical utilization is mostly limited because the onset of retinal ischemia is largely unpredictable, in contrast to the onset of reperfusion that could be more predictable. In this vein, another endogenous form of ischemic protection, in which a short series of repetitive cycles of brief ischemia/reperfusion are applied immediately at the onset of reperfusion, termed postconditioning, has been reported in several tissues.…”

3-Nitropropionic Acid-Induced Ischemia Tolerance in the Rat Brain is Mediated by Reduced Metabolic Activity and Cerebral Blood Flow

“…The sum of all areas with loss of NeuN staining was multiplied by the distance between slices, deriving lesion volume in mm 3 .…”

“…The interest in ischemia tolerance was fueled by clinical observations that a brief episode of ischemia such as a transient ischemic attack of the brain or preinfarction angina of the heart, might protect against subsequent stroke or heart attack, similar to experimental preconditioning. [2][3][4] To study mechanisms involved in ischemia tolerance, several experimental preconditioning strategies have been described in vivo and in vitro, such as hypoxia, brief episodes of ischemia, or oxygen-glucose deprivation. [5][6][7][8] Some of the mechanisms identified include attenuation of excitatory damage through reduced glutamate release and downregulation of NMDA receptors, changes in gene expression patterns favoring neuroprotection, as well as neurorestorative responses such as the induction of neural progenitor cells.…”