Trauma

Blumbergs, Peter; Reilly, Peter; Vink, Robert

doi:10.1201/b13319-12

Cited by 27 publications

(73 citation statements)

References 214 publications

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“…APP is the most sensitive, early immunohistochemical marker of early axonal injury, with immunopositive injury being detected as early as 1.75 to 3 hours after injury, the number and size of the axonal swellings (spheroids) increasing over the next 24 hours. 1 Although no axonal damage was detected during routine examination of HE-stained brain sections in any of the brains from the 4 groups of sheep, numerous APP-immunoreactive injured axons were found in some edematous areas near injured blood vessels in brains of sheep inoculated with the wild-type or etx-complemented strains. This axonal injury could have been the result of hypoxia-ischemia from an edema-associated reduction in cerebral perfusion or a direct cytotoxic effect of extravasated ETX.…”

Section: Discussionmentioning

confidence: 99%

Comparative Neuropathology of Ovine Enterotoxemia Produced by Clostridium perfringens Type D Wild-Type Strain CN1020 and Its Genetically Modified Derivatives

et al. 2014

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Clostridium perfringens type D causes enterotoxemia in sheep and goats. The disease is mediated by epsilon toxin (ETX), which affects the cerebrovascular endothelium, increasing vascular permeability and leading to cerebral edema. In the present study, we compared the distribution and severity of the cerebrovascular changes induced in lambs by C. perfringens type D strain CN1020, its isogenic etx null mutant, and the ETX-producing complemented mutant. We also applied histochemical and immunohistochemical markers to further characterize the brain lesions induced by ETX. Both ETX-producing strains induced extensive cerebrovascular damage that did not differ significantly between each other in nature, neuroanatomic distribution, or severity. By contrast, lambs inoculated with the etx mutant or sterile, nontoxic culture medium did not develop detectable brain lesions, confirming that the neuropathologic effects observed in these infections are dependent on ETX production. Lambs treated with the wild-type and complemented strains showed perivascular and mural vascular edema, as well as serum albumin extravasation, particularly severe in the cerebral white matter, midbrain, medulla oblongata, and cerebellum. Brains of animals inoculated with the ETX-producing strains showed decreased expression of glial fibrillary acidic protein and increased expression of aquaporin-4 in the end-feet processes of the astrocytes around blood vessels. Early axonal injury was demonstrated with anti-amyloid precursor protein immunohistochemistry. Perivascular accumulation of macrophages/microglia with intracytoplasmic albumin globules was also observed in these animals. This study demonstrates that ETX is responsible for the major cerebrovascular changes in C. perfringens type D-induced disease.

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Section: Discussionmentioning

confidence: 99%

Comparative Neuropathology of Ovine Enterotoxemia Produced by Clostridium perfringens Type D Wild-Type Strain CN1020 and Its Genetically Modified Derivatives

et al. 2014

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“…13,15,66,103 TBI has received relatively little attention in the veterinary literature, 39,83,118 and much of our understanding of TBI in animals is derived from neuropathologic studies of human neurotrauma cases. While most domestic animal species have a relatively large gyrencephalic brain resembling that of humans and although the general pattern of reaction of their brains to a traumatic insult appears to be similar, extrapolating human TBI findings to the veterinary sphere can sometimes be problematic.…”

Section: Classification Of Tbimentioning

confidence: 99%

“…This interplay between primary and secondary injury explains why an animal presenting initially with a mild brain injury may subsequently develop severe brain damage and, conversely, why one with a seemingly life-threatening condition substantially recovers. 2,13,15 The traumatic brain lesion develops through several phases, each with its own pathophysiology and outcome, which may or may not lead to the next phase, depending on the severity of the injury and the efficiency of repair. Pathologic processes in TBI occur not as separate events but as a cascading phenomenon, which is dynamic, unstereotypic, and inherently unpredictable.…”

Section: Blunt Nonmissile Head Injurymentioning

confidence: 99%

Forensic Pathology of Traumatic Brain Injury

Finnie

2016

Vet Pathol

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Traumatic brain injury constitutes a significant proportion of cases requiring forensic examination, and it encompasses (1) blunt, nonmissile head injury, especially involving motor vehicle accidents, and (2) penetrating, missile injury produced by a range of highand lower-velocity projectiles. This review examines the complex pathophysiology and biomechanics of both types of neurotrauma and assesses the macroscopic and histologic features of component lesions, which may be used to determine the cause and manner of death resulting from an intentional assault or accident. Estimation of the survival time postinjury by pathologic examination is also important where malicious head injury is suspected, in an attempt to ascertain a time at which the traumatic event might have been committed, thereby evaluating the authenticity of statements made by the alleged perpetrator.Keywords traumatic brain injury, veterinary forensic neuropathology, artifacts, contusions, axonal injury, cerebral ischemia, brain edema, intracranial hemorrhage, ischemic-hypoxic encephalopathy, gunshot wounds, captive bolt stunning, age of lesions In human medicine, forensic pathology has evolved into a distinct subspecialty. While veterinary pathologists have traditionally been infrequently called on to adjudicate in forensic cases where intentional head trauma is suspected, such cases are becoming more common and require more in-depth forensic knowledge. When an animal presents with signs of external head trauma, such as scalp bruises and skin abrasions, abetted by a reliable history of a traumatic event, a diagnosis of traumatic brain injury (TBI) may be relatively straightforward. However, in the absence of visible evidence of trauma and a reliable history, the onset of neurologic signs may provide the only clue that a traumatic event has occurred, especially since grazing livestock and free-roaming companion animals are not closely scrutinized.In forensic pathology, the timing of tissue responses is often the primary medicolegal task, particularly as it may support or refute statements made by a suspected perpetrator of abuse. These pathologic determinations usually depend on an estimate of the time between a traumatic insult and death. This interval between a traumatic event and circulatory arrest is defined as the survival time and, as such, equates to duration of the brain circulation after injury, although the latter can vary among the brain regions. However, while an estimate of the survival time following head trauma is sometimes possible by the application of relevant histologic and immunohistochemical techniques, the ability to date/age an injury solely on this basis should not be overestimated. 66,75,103 It is not always possible to accurately date TBI lesions because (1) determinations are variously based on studies in humans, experimental animal models (usually laboratory rodents), or both and (2) it is not always stated from which species the data were derived and how these timings were calculated. 46 These assessments are...

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“…2 Of these, profound edema has been clearly associated with mortality following severe TBI, as well as in the development of significant morbidity in up to 50% of surviving TBI patients. 4 It is widely accepted that the development of edema has adverse consequences on outcome through effects on intracranial pressure (ICP).…”

Section: Introductionmentioning

confidence: 99%

“…Primary events are made up of the mechanical processes that occur at the time of the trauma, including tissue shearing, laceration, and stretching of nerve fibers. 2 Preventive measures such as helmets, airbags, and seatbelts are the only interventions that can prevent or attenuate these primary events. In contrast, secondary injury evolves over minutes to days and even months after the initial event and is made up of delayed biochemical and physiological factors that are initiated by the primary event.…”

Section: Introductionmentioning

confidence: 99%

Substance P Antagonists as a Therapeutic Approach to Improving Outcome Following Traumatic Brain Injury

Vink

Heuvel

2010

Neurotherapeutics

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Summary:Although a number of secondary injury factors are known to contribute to the development of morphological injury and functional deficits following traumatic brain injury, accumulating evidence has suggested that neuropeptides, and in particular substance P, may play a critical role. Substance P is released early following acute injury to the CNS as part of a neurogenic inflammatory response. In so doing, it facilitates an increase in the permeability of the bloodbrain barrier and the development of vasogenic edema. At the cellular level, substance P has been shown to directly result in neuronal cell death; functionally, substance P has been implicated in learning and memory, mood and anxiety, stress mechanisms, emotion-processing, migraine, emesis, pain, and seizures, all of which may be adversely affected after brain injury. Inhibition of post-traumatic substance P activity, either by preventing release or by antagonism of the neurokinin-1 receptor, has consistently resulted in a profound decrease in development of edema and marked improvements in functional outcome. This review summarizes the current evidence supporting a role for substance P in acute brain injury.

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Trauma

Cited by 27 publications

References 214 publications

Comparative Neuropathology of Ovine Enterotoxemia Produced by Clostridium perfringens Type D Wild-Type Strain CN1020 and Its Genetically Modified Derivatives

Comparative Neuropathology of Ovine Enterotoxemia Produced by Clostridium perfringens Type D Wild-Type Strain CN1020 and Its Genetically Modified Derivatives

Forensic Pathology of Traumatic Brain Injury

Substance P Antagonists as a Therapeutic Approach to Improving Outcome Following Traumatic Brain Injury

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