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Traumatic brain injury (TBI) constitutes a heterogeneous condition that affects the most complex organ of the human body. It is commonly classified by its location as focal injury (e.g. epidural hematoma) and diffuse injury (e.g. diffuse axonal shearing injury) as well as by primary and secondary tissue injury. Accordingly, direct mechanical force causes the primary insult. The tissue damage occurring afterwards is subsumed under the term secondary brain damage. Some of these processes are overlapping and include in the early phase local cerebral ischemia resulting in excitotoxicity, which together with the triggered neuroinflammatory cascade causes the formation of cerebral edema and ultimately increased intracranial pressure once the intracranial compliance is exhausted. In survivors the long-term sequelae of the late stage include seizures caused by synaptic reorganization (incidence depending on the severity of TBI), persistent neuroinflammation promoting further neurodegeneration and increased risk for Alzheimer's disease probably because of TBI-related protein misfolding (tauopathy). Acute phase biomarkers of TBI should ideally originate from the injured brain. They should help distinguish disease severity and predict morbidity and mortality; however, the most commonly used biomarkers (S-100β and neurone-specific enolase) show a low specificity. In theory their successors (i. e. GFAP, pNF-H) seem more specific; however, these "new kids on the block" still need to be thoroughly investigated in large scale studies.

This article describes the imaging tools for efficient diagnostic management of head trauma victims. The basic mechanisms of brain injuries are explained and the imaging features are described. Computed tomography remains the most important method for the initial screening and follow-up investigation. Though magnetic resonance imaging has a higher sensitivity to most traumatic lesions, it does not play an important role in the acute phase of head trauma patients. In the first part of this paper clinical classifications, imaging modalities, extra-axial injuries, and contusions are described. In the second part of this paper intra-axial and secondary injuries are discussed.

CT findings of 46 patients with operatively confirmed chronic subdural hematomas are reviewed. The analysis of the EMI scans resulted in three different types of CT findings. Type 1 is characterized by decreased attenuation of the hematoma contents compared to brain tissue. The hematoma is visualized as a lens-shaped low density area between the skull and the surface of the brain. Type 2 apart from low density areas contains zones of increased attenuation due to recent bleeding into a watery chronic subdural hematoma. In many cases sedimentation causes a well-defined horizontal borderline between the thin fluid parts in the anterior portion and the blood debris in the posterior portion of the hematoma sac. Type 3 shows the same average absorption values as normal brain tissue, a direct visualization is not possible. However , the presence of a midline displacement in combination with ventricular compression and absence of a circumscript lesion even after contrast enhancement, allows the diagnosis of a unilateral chronic subdural hematoma in these cases too. Bilateral chronic subdural hematomas may cause considerable diagnostic difficulties if only one or none of the hematomas is visualized. A relatively small midline displacement points to a second bleeding on the opposite side. Most frequent were hematomas of type 1 (37%), type 2 and 3 could be observed in 30,5% resp. 32,5% of cases respectively.