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Incidence, causes and predictors of neurological deterioration occurring within 24 h following acute ischaemic stroke: a systematic review with pathophysiological implications
  1. Pierre Seners1,
  2. Guillaume Turc1,
  3. Catherine Oppenheim2,
  4. Jean-Claude Baron1
  1. 1Sorbonne Paris Cité, INSERM UMR S894, Service de Neurologie, Université Paris Descartes, Hôpital Sainte-Anne, Paris, France
  2. 2Sorbonne Paris Cité, INSERM UMR S894, Service de Neuroradiologie, Centre Hospitalier Sainte-Anne, Université Paris Descartes, Paris, France
  1. Correspondence to Professor Jean-Claude Baron, INSERM UMR S894, 2ter rue d'Alésia, Paris 75014, France; jean-claude.baron{at}inserm.fr

Abstract

Early neurological deterioration (END) following ischaemic stroke is a serious event with manageable causes in only a fraction of patients. The incidence, causes and predictors of END occurring within 24 h of acute ischaemic stroke (END24) have not been systematically reviewed. We systematically reviewed Medline and Embase from January 1990 to April 2013 for all studies on END24 following acute ischaemic stroke (<8 h from onset). We recorded the incidence and presumed causes of and factors associated with END24. Thirty-six studies were included. Depending on the definition used, the incidence of END24 markedly varied among studies. Using the most widely used change in National Institutes of Health Stroke Scale ≥4 definition, the pooled incidence was 13.8% following thrombolysis, ascribed to intracranial haemorrhage and malignant oedema each in ∼20% of these. As other mechanisms were rarely reported, in the majority no clear cause was identified. Few data on END24 occurring in non-thrombolysed patients were available. Across thrombolysed and non-thrombolysed samples, the strongest and most consistent admission predictors were hyperglycaemia, no prior aspirin use, prior transient ischaemic attacks, proximal arterial occlusion and presence of early CT changes, and the most consistent 24 h follow-up associated factors were no recanalisation/reocclusion, large infarcts and intracranial haemorrhage. Finally, END24 was strongly predictive of poor outcome. The above findings are discussed with emphasis on END without a clear mechanism. Data on incidence and predictors of the latter subtype is scarce, and future studies using systematic imaging protocols should address its underlying pathophysiology. This may in turn lead to rational preventative and therapeutic measures for this ominous event.

  • Stroke
  • Systematic Reviews
  • MRI

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