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Head Trauma
Published in Kenneth D Boffard, Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
Focal brain injuries: Impact forces acting directly on the head, create a wide range of focal lesions including contusion, brain laceration, epidural or subdural haematoma, subarachnoid or intracerebral haemorrhage. Contrecoup injury occurs when the brain impacts the opposite side of the skull to the impact. Fast acquisition of brain imaging promotes early diagnosis and prompt intervention that may critically affect patient outcome. However, most patients with TBI do not have a lesion suitable for neurosurgical intervention.
Back and central nervous system
Published in Aida Lai, Essential Concepts in Anatomy and Pathology for Undergraduate Revision, 2018
Head contusions Coup injury (contusion in parts of brain underlying site of trauma)Contrecoup injury (contusion in parts of brain directly opposite site of trauma)
Biomechanics and Tissue Injuries
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
Shear strain can be a reasonable predictor of DAI. In the human model, but not the porcine one, there were high shear stresses at the coup site and the brainstem. On the surface of both hemispheres, as well as on the surface of the corpus callosum, large shear strains were observed, which can stretch the axon and cause diffuse DAI. Pressure was distributed uniformly side to side across the brain except at the partition between hemisphere and cerebellum, with compression at the impact point and tension at a point opposite to the impact. Negative pressure (tensile strain) at the contrecoup site can cause brain contusion. Thus, it can be a mechanism for contrecoup injury. Maximum tensile strain was also generated at the dorsolateral part of the rostral brainstem. Although diffuse brain injury is characteristic for concussive level trauma, with the frontal and temporal tips most vulnerable, the effect upon the brainstem, which is bent, compressed, and rotated, is often underestimated.
Nanoparticle-based drug delivery for the treatment of traumatic brain injury
Published in Expert Opinion on Drug Delivery, 2023
Farrah S. Mohammed, Sacit Bulent Omay, Kevin N. Sheth, Jiangbing Zhou
Similar to humans with injury-induced epilepsy, rodents with CCI-induced TBIs may experience post-traumatic seizure activity [111]. Furthermore, the CCI model may inflict cytotoxic and vasogenic brain edema, often seen in the clinical human pathophysiology of TBI [46,104]. Dependent upon the severity, the neuropathology of rodent CCIs often includes a cortical contusion proximal to the impact site, subdural hematoma, BBB disruption, hypoperfusion, cavitation, and neurodegeneration. Upregulated inflammatory cascades lead to excitotoxicity, neuronal cell death, astrogliosis, microglial activation, axonal damage, and cortical spreading depressions [95,106]. Weaknesses of this model include the lack of brainstem deformation resulting in minimal mortality, as well as the lack of post-injury neuroscoring though, implementation of an NSS could improve this. Other focal injury models such as cryogenic injury models [112–114] and penetrating injury models, the only one in use today is the balloon inflation technique [115], can mimic some aspects of human TBI pathology but their clinical relevance is limited. For instance, in the cryogenic models, the focal traumas often lack the contrecoup injury and DAI often associated with human cerebral injuries.
Management of migrating intracranial bullet fragments in a 13-year-old female after firearm brain injury: technical and surgical nuances
Published in Brain Injury, 2022
John K. Yue, Diana Chang, Kasey J. Han, Albert S. Wang, Taemin Oh, Peter P. Sun
Primary (e.g. direct) injury to the skull and brain parenchyma is further exacerbated by missile fragmentation, increased missile velocity, ricochet/deviations from a straight path, and coup/contrecoup injury (12). Secondary injuries occur due to sequelae from elevated intracranial pressure (ICP), intracranial hemorrhage (ICH), and cerebral edema similar to blunt TBI, as well as migration. Late complications include bullet migration, seizures, traumatic aneurysms, and infection (13). Pediatric patients are especially vulnerable to missile injuries due to thinner bones of the skull and overlying soft tissue compared to adults (14).
Depressed skull fracture compressing eloquent cortex causing focal neurologic deficits
Published in Brain Injury, 2023
Alexander In, Brittany M. Stopa, Joshua A. Cuoco, Adeolu L. Olasunkanmi, John J. Entwistle
A 40-year-old man presented to the emergency department as a gold alert after falling 12 feet off of a ladder and striking his head. Glasgow Coma Scale was 15 on presentation. Neurologic examination demonstrated a left central facial nerve palsy, left hemiplegia, left hemianesthesia, and fixed right gaze deviation. The patient reported that such symptomatology developed immediately following the fall. There was no evidence of seizure activity witnessed in the field, in transport, or in the trauma bay. The initial CT head demonstrated a right parietal depressed skull fracture with compression of the right precentral gyrus and postcentral gyrus as well as right frontoparietal traumatic subarachnoid hemorrhage and a small right parietal intraparenchymal contusion (Figure 1). Completion films and vascular imaging, including CT angiography of the head and neck, were unrevealing. Anatomically, the neurologic deficits observed were thought to be due to a combination of blunt force trauma to the head (i.e., coup-contrecoup injury) and the depressed fracture fragment compressing the underlying eloquent cortex. Specifically, the left central facial nerve palsy and left hemiplegia were attributed to the depressed fracture fragment compressing the right precentral gyrus. The left hemianesthesia was attributed to the fracture compressing the right postcentral gyrus. The fixed right gaze deviation was difficult to explain based solely on fracture compression, given the topographical location of the frontal eye fields. Additional explanations considered included a coup-contrecoup injury to the right frontal eye field from the initial traumatic event or diffuse axonal injury. Nevertheless, the majority of the observed symptomatology could be plausibly explained by the fracture compressing the underlying eloquent cortex. As such, he was taken emergently to the operating room for right cranioplasty with elevation of the fracture fragment. Postoperative imaging demonstrated fracture reduction without evidence of complications (Figure 2). Immediately post-op, the facial nerve palsy and gaze deviation resolved; however, the hemiplegia and hemianesthesia persisted, prompting extensive physical therapy and inpatient rehabilitation. At his 2-month follow-up, he regained strength on the left with Medical Research Council (MRC) grade 4/5 power throughout and some persistent left hemianesthesia. At 6-month follow-up, he had regained full neurologic function without any residual deficits.