Deterioration in acute ischemic stroke as the target for neuroprotection.
The prevention and treatment of progressing stroke should be one of the main therapeutic targets of neuroprotective therapies. Despite the high prevalence of progressing stroke in acute stroke (25-35%) and its importance as a predictor of poor outcome, no treatment capable of preventing early neurological deterioration (END) or of reducing its impact has yet been developed. It is essential that our understanding of END's underlying mechanisms be improved as it is currently not possible to predict its occurrence accurately. Published studies to date have been unable to identify a clinical profile which reliably predicts those patients likely to suffer neurological deterioration in the very early acute phase of ischemic stroke. In the following pages, we will discuss the present situation with regard to neurological worsening in general, paying special attention to END given the prognostic and therapeutic implications of this common condition. Factors associated with neurological deterioration and the potential mechanisms, particularly excitotoxic theory, are discussed.
Serena
Joaquín
J
Department of Neurology, Hospital Universitari Doctor Josep Trueta, Girona, Spain. nrl.jserena@htrueta.scs.es
Rodríguez-Yáñez
Manuel
M
Castellanos
Mar
M
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D001786:Blood Glucose; D001794:Blood Pressure; D001831:Body Temperature; D001921:Brain / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D002986:Clinical Trials as Topic; D003097:Collateral Circulation; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D004660:Encephalitis / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D020521:Stroke / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*
D000893:Anti-Inflammatory Agents; D001786:Blood Glucose; D016207:Cytokines; D018696:Neuroprotective Agents; D018698:Glutamic Acid