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Traumatic brain injury (TBI) constitutes a public health problem worldwide, because of its high incidence, morbidity and mortality. TBI is a leading cause of death and disability in the young, otherwise healthy, employed population that does not only mean a personal, or family-wise disaster, but a social burden as well. TBI is a very heterogeneous disease and affects the most complex organ of the body. The underlying pathomechanisms are still poorly understood. The present diagnostic tools might only reveal the “tip of the iceberg”, the proper therapeutic methods are equivocal and the protocols largely differ among the TBI centers. Hippocrates is said to have remarked in 400 BC that “No head injury is too severe to despair of, nor too trivial to ignore”. This statement briefly underscores the difficulties regarding the diagnosis and prognosis of TBI. Unfortunately, his words are relevant even today. Diffuse axonal injury (DAI) is one of the most important pathological components of TBI, as a result of traumatic acceleration/deceleration or rotational shear-strain forces leading to axonal/myelin stretching or disruption. Previously, DAI has been considered a primary-type injury, with the damage occurring at the time of the accident. Research has shown that the delayed mechanisms (secondary components of DAI) are generally more important. Originally DAI was suggested upon an inferential basis, in any patient who demonstrated clinical symptoms disproportionate to his or her CT-scan findings. This category was generally restricted for comatose patients, whose vast majority (>90%) remained in a persistent vegetative state. Recently, however the term DAI (or the synonym traumatic axonal injury) has been more widely used, applying to the entire severity range of TBI, including a spectrum of axonal damage from a subtle, reversible functional disorder to the true disconnection. The extent and severity of DAI is highly related to the clinical severity and outcome. However, clinical diagnostic tools including conventional imaging (clinical CT, MRI) fail to detect DAI due to its microscopic range. The role of the present routine imaging in TBI is limited to the recognition of pathologies that require surgical intervention (e.g. intracranial bleeding, fractures). In contrast, advanced imaging, due to high sensitivity may provide an insight into the microstructural and functional pathomechanisms of TBI. These methods may also aid the evaluation and prognosis assessment of TBI