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This review focuses on the potential for traumatic brain injury to evoke both focal and diffuse changes within the brain parenchyma, while considering the cellular constituents involved and the subcellular perturbations that contribute to their dysfunction. New insight is provided on the pathobiology of traumatically induced cell body injury and diffuse axonal damage. The consequences of axonal damage in terms of subsequent deafferentation and any potential retrograde cell death and atrophy are addressed. The regional and global metabolic sequelae are also considered. This detailed presentation of the neuropathological consequences of traumatic brain injury is used to set the stage for better appreciating the neurological recovery occurring after traumatic injury. Although the pathological and clinical effects of focal and diffuse damage are usually intermingled, the different clinical manifestations of recovery patterns associated with focal versus diffuse injuries are presented. The recognizable patterns of recovery, involving unconsciousness, posttraumatic confusion/amnesia, and postconfusional restoration, that typically occur across the full spectrum of diffuse injury are described, recognizing that the patient's long-term recovery may involve more idiosyncratic combinations of dysfunction. The review highlights the relationship of focal lesions to localizing syndromes that may be embedded in the evolving natural history of diffuse pathology. It is noted that injuries with primarily focal pathology do not necessarily follow a comparable pattern of recovery with distinct phases. Potential linkages of these recovery patterns to the known neuropathological sequelae of injury and various reparative mechanisms are considered and it is proposed that potential biological markers and newer imaging technologies will better define these linkages.