Update of Neuropathology and Neurological Recovery After Traumatic Brain Injury

Abstract

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.

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

“…Whereas initiated by immediate biomechanical forces, as describe above, much of the pathology of acute concussion is believed to be transient biochemical induced neurotransmitter disruptions initiated within 25-50 msec of impact. Tensil forces also disrupt the cytoskeletal status of the axon and its ability to function, including disrupted axonal permeability and transport (Povlishock & Katz, 2005). Disrupted cytoskeletal architecture, renders cells less functional and may have widespread effects on the injured brain , albeit transient in concussion.…”

Should anterior pituitary function be tested during follow-up of all patients presenting at the emergency department because of traumatic brain injury?

“…Head trauma can cause damage to any region in the brain (3). Involvement of the posterior pituitary gland during the acute phase after severe head trauma has been acknowledged for years, but trauma-induced anterior pituitary dysfunction was considered rare (4).…”

Modelos experimentales de traumatismo craneoencefálico

“…Respecto a las lesiones difusas, su presencia puede inferirse o sospecharse ante la ausencia de hallazgos patológicos en las imágenes de TC en pacientes con deterioro neurológico inicial o progresivo. Las lesiones difusas incluyen la lesión axonal difusa (LAD) y el edema cerebral difuso (swelling cerebral) 91 . La complejidad y heterogeneidad del TCE en humanos ha conducido al diseño de una gran variedad de modelos experimentales animales, cada uno de los cuáles reproduce un aspecto concreto del daño observado en la clínica 67 .…”