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In recent years, instances of neurotrauma in the elderly have been increasing. This article addresses the clinical characteristics, management strategy, and outcome in elderly patients with traumatic brain injury (TBI). Falls to the ground either from standing or from heights are the most common causes of TBI in the elderly, since both motor and physiological functions are degraded in the elderly. Subdural, contusional and intracerebral hematomas are more common in the elderly than the young as the acute traumatic intracranial lesion. High frequency of those lesions has been proposed to be associated with increased volume of the subdural space resulting from the atrophy of the brain in the elderly. The delayed aggravation of intracranial hematomas has been also explained by such anatomical and physiological changes present in the elderly. Delayed hyperemia/hyperperfusion may also be a characteristic of the elderly TBI, although its mechanisms are not fully understood. In addition, widely used pre-injury anticoagulant and antiplatelet therapies may be associated with delayed aggravation, making the management difficult for elderly TBI. It is an urgent issue to establish preventions and treatments for elderly TBI, since its outcome has been remained poor for more than 40 years.

Traumatic acute subdural hematoma (ASDH) is a major clinical entity in traumatic brain injury (TBI). It acts as a space occupying lesion to increase intracranial pressure, and is often complicated by co-existing lesions, and is modified by cerebral blood flow (CBF) changes, coagulopathy, and delayed hematomas. Because of its complicated pathophysiology, the mortality of ASDH is still remaining high. In this review article, its epidemiology, pathophyiology, surgical treatment, and salvage ability are described. With regard to epidemiology, as the population ages, growing number of elderly patients with ASDH, especially patients with prehospital anticoagulant and antiplatelets, increase. Concerning pathophysiology, in addition to well-known initial intracranial hypertension and subsequent ischemia, delayed hyperemia/hyperperfusion, or delayed hematoma is being recognized frequently in recent years. However, optimal treatments for these delayed phenomenons have not been established yet. With regard to surgical procedures, all of craniotomy, decompressive craniectomy, and initial trephination strategies seem to be effective, but superiority of each procedure have not been established yet. Since Glasgow Coma Scale (GCS) scores, age, papillary reaction, and computed tomographic findings are strongly correlated to outcome, each factor has been investigated as an indicator of salvage ability. None of them, however, has been defined as such one. In future studies, epidemiological changes as population ages, management of delayed pathophysiology, superiority of each surgical procedures, and salvage ability should be addressed.