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Patients who received decompressive craniectomy (DC) are usually not regarded to qualify for brain death (BD) as intracranial pressure (ICP) is not assumed to reach levels critical enough to cause cerebral perfusion failure. Here we investigated the incidence of BD after DC and analyzed the pathophysiological mechanisms.We searched our chart records of patients with DC for individuals who developed BD (2010–2016). We then analyzed the course of ICP and cerebral perfusion pressure (CPP) prior to BD and results from radiological tests that aim at demonstrating loss of cerebral perfusion in BD.BD was diagnosed in 12 of 164 (incidence 7.3%) patients (age = 16–70 years; male = 7; mean longitudinal diameter: 136.2 mm). Mean latency between DC and BD was 69.4 h. Immediately after DC, mean ICP was 30.0 mm Hg (standard deviation ± 24.7 mm Hg), CPP was 56.8 mm Hg (± 28.1). In the course to BD, ICP increased to 95.8 mm Hg (± 16.1), CPP decreased to − 9.9 mm Hg (± 11.2). In patients in whom radiological methods were performed (n = 5) loss of cerebral perfusion was demonstrated.Our study evidences that DC does not exclude BD. Even after DC, BD is preceded by a severely reduced CPP, supporting loss of cerebral perfusion as a critical step in BD pathophysiology.Our study evidences that decompressive craniectomy (DC) does not exclude brain death (BD) development.Incidence of BD after DC in our study was 7.3%.Even in patients with DC, BD is preceded by a severely reduced cerebral perfusion pressure (CPP).Similar to patients without DC, critical closing pressure may be within positive ranges of CPP.Pathophysiology of BD after DC seems to be equal to BD without DC after primary brain injury.