However, to date, laboratory examinations have not been routinely and widely applied to check the effects of APA. To recover the platelet functions inhibited by APA, supplying platelets with normal function in the form of platelet transfusion might seem efficacious. Although several reports have described the effects of a PLT on survival of ICH patients who are taking APA, nevertheless the effect of a PLT on the outcome of ICH still remains unclear. For example, Creutzfeldt et al reported there was no clear benefit in terms of survival in the administration of a PLT to ICH patients taking APA and Ducruet et al reported that a PLT did not reduce the frequency of hematoma expansion in ICH patients receiving APA. In contrast, Naidech et al showed that, in ICH patients, the early use of a PLT improved platelet activity assay results and was associated ultimately with a smaller hemorrhage size and greater independence at 3 months. However, these results were only analyzed using a 2-sample test for equality of proportions, without multivariate regressions methods. We conducted this present study to clarify the impact of a PLT on survival of patients with ICH after taking APA. Unfortunately, we could not check the actual timing of PLT administration, although it appeared to be more than 6 hours after arrival. The median elapsed time from onset was 2 hours. After arrival at our hospital, checking neurological symptoms, eliciting the patient’s medical and drug histories from the family, laboratory examinations, and a CT examination were performed simultaneously. As a result, in our hospital, at least 6 hours may have elapsed before considering and ordering PLT. Secondly, to address the question of which patients truly need a PLT after developing an ICH while taking APAs. The negative impact of unnecessary administration of PLT includes overcoagulation and effects of the cytokines associated with the PLT will be concerned. After ICH onset, decreased blood flow to the area surrounding the clot causes local neuronal ischemia, leading to further cytotoxic edema and the toxic release of excitatory amino acids and inflammatory mediators. On diffusionweighted imaging, a significant number of ICH patients show acute ischemic lesions that are not contiguous with the hematoma. A PLT may induce unnecessary thrombus in and around the ischemic area, resulting in enlargement of the ischemic lesion and worsening of the brain injuries. The ICH area shows thrombin-induced activation of the inflammatory cascade and overexpression of matrix metalloproteinase, representing additional mechanisms contributing to breakdown of the blood-brain barrier, brain edema growth and neuronal death, all of which are recognized as secondary brain injuries after the onset of ICH. Platelets are the major supplier of MMPs, and therefore brain injury may be worsened by a PLT, as it will provide an inflammatory stimulus to the injured brain.