Stroke has been traditionally regarded as a catastrophic event in which maximal damage to brain tissue occurs almost immediately. Recently, clinical and animal research has revealed that the ultimate degree of tissue damage in a stroke is not determined in the first few minutes but instead evolves over a period of hours to days. Amplification of excitotoxic neurotransmitter release, progressive intracellular calcium accumulation, blood-brain barrier compromise, and regional inflammation all may play a role in delayed neuronal death. In conjunction with monitoring physiologic variables, including blood pressure and oxygen saturation, careful observation of clinical neurologic progression may provide an understanding of the """"""""window of opportunity"""""""" for acute interventional therapy. In meeting the primary objective of this study 75 consecutive stroke patients were admitted to the National Naval Medical Center (NNMC) within 24 hr of the onset of cerebral ischemic symptoms . A record was kept of the progression of clinical deficits over the first 48 hr. A standardized examination (the NIH Stroke Scale) was performed on admission and every 8 hr for 48 hr. The patients were monitored in the neurology ICU with a continuous recording of blood pressure, heart rate, and oxygen saturation obtained over this same period. The goal of analysis was to identify the percent of NNMC patients who would develop significant progression in the acute postischemic period. Subgroup analysis showed that patients with initial NIH stroke scores of greater than or equal to 10 were more likely to show progression (P=0.001) than those with scores of < 10. Additionally, the presence of atrial fibrillation and a higher minimal arterial blood pressure were also associated with a higher risk of progression (P=0.007 & P=0.042 respectively.)
