Hemodynamic Factors and Perfusion Abnormalities in Early Neurological Deterioration

• Published in: Stroke (1970) Vol. 40; no. 6; p. e443
• Main Authors: Alawneh, Josef A., Moustafa, Ramez Reda, Baron, Jean-Claude
• Format: Journal Article
• Language: English
• Published: United States 01.06.2009
• Subjects: Brain Ischemia - complications; Cerebrovascular Circulation - physiology; Cerebrovascular Disorders - etiology; Cerebrovascular Disorders - pathology; Cerebrovascular Disorders - physiopathology; Disease Progression; Hemodynamics - physiology; Humans; Infarction, Middle Cerebral Artery - complications; Infarction, Middle Cerebral Artery - pathology; Magnetic Resonance Imaging; Nerve Degeneration - etiology; Nerve Degeneration - physiopathology; Prognosis; Stroke - etiology; Stroke - pathology; Stroke - physiopathology; Tomography, X-Ray Computed
• ISSN: 0039-2499; 1524-4628; 1524-4628
• DOI: 10.1161/STROKEAHA.108.532465

Background and Purpose— Early neurological deterioration (END) is a relatively common unfavorable course after anterior circulation ischemic stroke that can lead to worse clinical outcome. None of the END predictors identified so far is sufficiently reliable to be used in clinical practice and the mechanisms underlying END are not fully understood. We review the evidence from the literature for a role of hemodynamic and perfusion abnormalities, more specifically infarction of the oligemia, in END. Summary of Review— After an overview of the neuroimaging, including perfusion imaging, predictors of END, we review the putative mechanisms of END with a special focus on hemodynamic factors. The evidence relating perfusion abnormalities to END is addressed and potential hemodynamic mechanisms are suggested. Conclusions— Hemodynamic factors and perfusion abnormalities are likely to play a critical role in END. Infarction of the oligemic tissue surrounding the penumbra could be the putative culprit leading to END as a result of perfusion, but also physiological and biochemical abnormalities. Further studies addressing the role of the oligemia in END and developing measures to protect its progression to infarction are now needed.