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Patients were consequently allocated into a FLAIR-positive and FLAIR-negative group.
Remarkably, hemorrhage was present in only 12 of 72 FLAIR-negative patients (16.7%).
To test for possible influencing factors, baseline characteristics were analyzed between the FLAIR-positive and FLAIR-negative group (Table 1).
FLAIR-positive lesions were associated with a bleeding rate of 80.0% compared with 16.7% in FLAIR-negative patients (P < 0.001; odds ratio 20.0, positive predictive value 0.8).
In contrast, FLAIR-positive lesions in diffusion-restricted areas were detected in only 25 patients (25.8%), while the remaining 72 patients (74.2%) were FLAIR-negative.
The rate of severe bleedings (PH-2) was not higher in patients with FLAIR-positive lesions than in FLAIR-negative patients (P = 0.144, Fisher's exact test).
17 found an odds ratio of 13.64 of symptomatic ICH in FLAIR-positive patients compared with FLAIR-negative patients treated with intravenous and/or intra-arterial thrombolysis up to 6 h after symptom onset.
However, in patients with FLAIR-positive lesions intracranial hemorrhage was not more frequently associated with clinical deterioration (six of 20 patients with bleeding complications, 30.0%) when compared with FLAIR-negative patients (five of 12 patients with bleeding complications, 41.6%; P = 0.703, Fisher's exact test).
Likewise, no significant differences between FLAIR-positive and FLAIR-negative patients were found for history of previous stroke, preexisting disability as indexed by mRS, time from symptom onset to tPA administration, history of drugs influencing the coagulation system and stroke severity as indicated by the NIHSS.
As a separate finding, our data provide circumstantial evidence to suggest that the time of stroke onset cannot be easily and confidently inferred from a combination of FLAIR-negative and DWI-positive stroke lesion, a finding at variance from previous claims 5– 7, 9, 15.
Many had become weary of the manager's tactics which were regarded as negative and lacking in flair.
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