Of 564 consecutive patients with transient ischemic attack, 350 (62%) had cranial computed tomography performed. Except for date of admission and smoking history, there were few differences between the patients evaluated with computed tomography and the 214 who were not Cerebral infarcts were found in 59 (17%) of the 350 tomographic evaluations. Previous clinically diagnosed stroke, older age, and male sex were all significantly associated with the occurrence of tomographically verified infarcts (/><0.05). After controlling for stroke history and other important covariates, patients with tomographically verified infarcts had significantly shorter survival times than did patients without evidence of infarction on computed tomography (p=0.035). Thus, cranial computed tomography findings appear to have important prognostic value for estimating survival following transient ischemic attack. (Stroke 1991^2:431-436)
We evaluated survival following stroke for patients from a five-county area of rural North Carolina enrolled in either of two community hospital-based stroke survey programs. In this area, the first program enrolled 843 stroke patients between 1970 and 1973 and the second program enrolled 786 stroke patients between 1979 and 1980. One-year survival increased from 49% in the first program to 62% in the second for all stroke patients, from 54% to 68% for patients with cerebral infarction, and from 18% to 55% for patients with cerebral hemorrhage. While other reports have attributed declining stroke mortality to a decline in the incidence of stroke, our study suggests that increased survival after stroke may account for a large portion of the decrease in stroke mortality. (Stroke 1989;20:345-350) T here has been a well documented and dramatic decline in stroke mortality 1 -5 since 1914 as well as much speculation regarding its cause(s). Declining stroke mortality must result from lowered stroke incidence and/or improved survival following stroke. Whisnant 4 demonstrated a decrease in stroke incidence in Rochester, Minnesota, that he attributed to advances in antihypertensive therapy. In reviewing Whisnant's report, Hachinski 6 agreed that the decline in mortality could be explained by a decrease in incidence but questioned whether more effective and widespread treatment of hypertension was the singular cause of the decline.The extent to which incidence studies conducted in "special" communities such as Rochester, Minnesota, or Framingham, Massachusetts, are representative of the US population may be debated. For example, Whisnant 4 noted that "antihypertensive Received April 27, 1988; accepted September 7, 1988. treatment was used rather frequently in Rochester after 1955. . .", a situation that clearly did not reflect practices in average health care. Dyken 7 noted that the relatively small improvement in acute stroke survival in Rochester (from 80% in 1945-1949 to 82% in 1970-1974) may indicate a higher quality of medical care earlier. Because a high standard of health care has been the norm in these special communities, improvements in their case fatality rates may not be representative of the situation for the nation as a whole. Nationwide, survival after stroke has also apparently been improving in both acute and long-term studies.7 Despite problems of comparing studies performed in different geographic/medical settings, Dyken 7 has observed that in studies completed before 1965 acute survival (38-63%) was much lower than in studies completed after that date (70-81%); he also noted similar improvements in long-term survival. Increased survival may be more important to declining stroke mortality nationwide than is apparent in either Rochester or Framingham.Expected survival after stroke has profound implications, not only for the patient and his or her care, but also for planners of health care systems. Previous studies of survival following stroke 8 -12 have identified numerous factors related to surviv...
Cranial computed tomography of 284 patients with transient ischemic attacks (TIAs) and without previous stroke was evaluated. The sample population included patients with carotid and/or vertebrobasilar TIAs. Computed tomography revealed cerebral infarction in 34 patients, including 5 with multiple infarctions. The lesion location was consistent with TIA symptoms in 16 patients. In another 16 patients, however, the lesion location did not correspond to the TIA symptoms; these lesions were attributed to previous silent infarctions. Two patients with multiple infarctions had both symptomatic and asymptomatic lesions. Age and carotid stenosis were each significantly related to an increased chance of detecting cerebral infarction (either symptomatic or asymptomatic). No significant relationship between race, gender, hypertension, diabetes, cardiac disease, or smoking and the incidence of infarction was found by either univariate or multivariate analyses.
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