According to the new (2009) definition, sudden, reversible, short-lasting and spontaneously resolving loss of consciousness associated with a transient, global decrease in cerebral blood flow occurs during syncope. Syncope-associated cerebral ischaemia lasts from a few to several seconds. Near infrared spectroscopy reveals decreased oxygenated haemoglobin and increased reduced haemoglobin levels. If cerebral ischaemia is due to stroke, blood–brain barrier damage and tau protein diffusion into the cerebrospinal fluid occur. Cerebrospinal fluid tau levels can be both, a useful biomarker in the assessment of ischaemic extent and a prognostic factor. The aim of the study was to evaluate whether there is an increase in serum tau protein levels during syncope, which could correspond to a stroke model of brain injury. Material and methods: The study group included 32 patients, and the control group included 38 patients (mean age for both groups was 15 years). Syncope was induced by tilt table testing. The test was performed according to the Westminster protocol. Three blood samples were collected (at baseline as well as 6 and 24 hours afterwards) to measure tau levels. Results: No differences in tau levels were demonstrated between the study group and controls (p > 0.05). Conclusions: The extent of brain injury in adolescents with syncope is insufficient to induce significantly increased serum tau levels. However, the study should be continued to assess the levels of this marker in different types of syncope.