Pathobiology of traumatically induced axonal injury in animals and man

Povlishock, John T.

doi:10.1016/s0196-0644(05)82738-6

Cited by 221 publications

(123 citation statements)

References 21 publications

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“…Subsequent swelling of the axon occurs in discrete bulb formations or in elongated variscosities that accumulate in organelles. Ultimately swollen axons may become disconnected (Povlishock, 1993) and contribute to additional neuropathologic changes in brain tissue (Fig. 2).…”

Section: Diffuse Injurymentioning

confidence: 99%

Animal models of traumatic brain injury: A critical evaluation

O’Connor

Smyth

Gilchrist

2011

Pharmacology & Therapeutics

142

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Section: Diffuse Injurymentioning

confidence: 99%

Animal models of traumatic brain injury: A critical evaluation

O’Connor

Smyth

Gilchrist

2011

Pharmacology & Therapeutics

142

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“…Our current understanding recognizes DAI to be a progressive process evoked by the tear/shearing forces of acceleration-deceleration injury. These forceps can cause axonal alterations leading to ultimate disconnection-either via the formation of swollen axon bulbs or swelling, vacuolization, and disruption of the injured axon-segment (Povlishock and Stone, 2001;Povlishock et al, 1983;Povlishock, 1993). In humans, such brain injuries evoke DAI in the corpus callosum, subcortical white matter, and the brainstem-typically resulting in a deeply altered level of consciousness.…”

Section: Introductionmentioning

confidence: 99%

Traumatic Axonal Injury in the Spinal Cord Evoked by Traumatic Brain Injury

Czeiter

Pál

Kövesdi

et al. 2008

Journal of Neurotrauma

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Although it is well known that traumatic brain injury (TBI) evokes traumatic axonal injury (TAI) within the brain, TBI-induced axonal damage in the spinal cord (SC) has been less extensively investigated. Detection of such axonal injury in the spinal cord would further the complexity of TBI while also challenging some functional neurobehavioral endpoints frequently used to assess recovery in various models of TBI. To assess TAI in the spinal cord associated with TBI, we analyzed the craniocervical junction (CCJ), cervico-thoracic (CT), and thoraco-lumber (ThL) spinal cord in a rodent model of impact acceleration of TBI of varying severities. Rats were transcardially fixed with aldehydes at 2, 6, and 24 h post-injury (n ‫؍‬ 36); each group included on sham-injured rodent. Semi-serial vibratome sections were reacted with antibodies targeting TAI via alteration in cytoskeletal integrity or impaired axonal transport. Consistent with previous observations in this model, the CCJ contained numerous injured axons. Immunoreactive, damaged axonal profiles were also detected as caudal, as the ThL spinal cord displayed morphological characteristics entirely consistent with those described in the brainstem and the CCJ. Quantitative analyses demonstrated that the occurrence and extent of TAI is positively associated with the impact/energy of injury and negatively with the distance from the brainstem. These observations show that TBI can evoke TAI in regions remote from the injury site, including the spinal cord itself. This finding is relevant to shaken baby syndrome as well as during the analysis of data in functional recovery in various models of TBI.

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“…4 Injury can be focal or diffuse: sudden deceleration or rotational acceleration injury, which generates shearing forces with consequent diffuse axonal injury within the brain, has been implicated as a significant etiology of post-TBI symptoms. 5 Cortical contusion can result in a loss of function served by a given brain area. White matter lesions can result in interruption of information being transmitted between cortical areas within the brain.…”

Section: Pathophysiologymentioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury

Riggio

Wong

2009

Mount Sinai J Medicine

106

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The neurobehavioral sequelae of traumatic brain injury consist of a spectrum of somatic and neuropsychiatric symptoms. The neuropsychiatric symptoms are divided into cognitive and behavioral presentations. In the literature, these neurobehavioral sequelae have been called postconcussive symptoms, postconcussive syndrome, and postconcussive disorder; however, the authors of this review do not use this terminology because the symptoms are not restricted to patients with concussion but instead can be found in all traumatic brain injury patients of all injury severities. The development of neurobehavioral sequelae after traumatic brain injury is a multifactorial process. The patient evaluation requires a multidisciplinary approach in order to delineate physiologic dysfunction and place deficits in the context of the patient's preinjury and postinjury psychiatric status. Consequently, the evaluation of the posttraumatic brain injury patient with neurobehavioral sequelae requires a carefully structured history and physical examination with an emphasis on neurological and psychiatric function. Adjunctive evaluations must be tailored to the patient with neuroimaging, neurophysiological, and neuropsychiatric testing. Maximized outcomes may be achieved by the performance of a careful and detailed assessment that places complaints within the context of the individual.

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Pathobiology of traumatically induced axonal injury in animals and man

Cited by 221 publications

References 21 publications

Animal models of traumatic brain injury: A critical evaluation

Animal models of traumatic brain injury: A critical evaluation

Traumatic Axonal Injury in the Spinal Cord Evoked by Traumatic Brain Injury

Neurobehavioral sequelae of traumatic brain injury

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