Post-
stroke recrudescence (PSR) usually occurs in the setting of
infection,
hypotension,
hyponatremia,
insomnia or stress, and
benzodiazepine use. Animal studies have suggested an
infection-related immunologic mechanism for PSR. This retrospective study was designed to assess whether
infection-triggered PSR is related to a prior
infection during the index
stroke. We identified 95 patients admitted to Massachusetts General Hospital from 2000 to 2015 with post-
stroke recrudescence who had adequate medical record information concerning the index
stroke. The frequency of
infections, as well as other triggers such as
hypotension,
hyponatremia,
insomnia/stress, and
benzodiazepine use, was compared between the index
stroke and the PSR episode. Independent predictors of
infection-related PSR were identified using a logistic regression model. The mean age was 66 ± 17 years (53% female); 29 (31%) had
infections during the index
stroke as compared to 40 (42%) during the PSR episode. The frequency of PSR triggered by
infection was higher in patients with
infections during the index
stroke (65% vs 32%, p = 0.003). The same relationship occurred with
benzodiazepine-triggered PSR (41% vs 12%, p = 0.008). The frequencies of other triggers such as
hypotension,
hyponatremia and
insomnia/stress were not significantly different between the index
stroke and the PSR episode. In a logistic regression model,
infection during the index
stroke was an independent predictor of
infection-triggered PSR (odds ratio 4.85, 95% C.I. 1.7, 13.7). The association between
infection during index
stroke and
infection-triggered PSR supports the immunologic mechanism postulated in animal models.