China
Africa
Explore chapters and articles related to this topic
Traumatic axonal injury
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
Sampling protocols also have to comprehensively assess pathology associated with secondary hypoxic-ischaemic injury, including herniation-related injury given the confounding effects both may have on recognising TAI and tissue-tear lesions (see below). A sampling protocol covering all types of diffuse brain injury in a case of head injury is provided in Chapter 5.
Special Patient Situations
Published in Kenneth D Boffard, Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
Head injury remains the leading cause of traumatic death in children. CT is the most accurate imaging modality to evaluate paediatric patients with a suspected head injury. Diffuse brain injury occurs commonly in children. Techniques to improve cerebral monitoring have evolved considerably but their clinical application remains difficult. Decompressive craniectomy should be considered in patients who display evidence of sustained, refractory intracranial hypertension in the absence of signs of a dismal prognosis.
Trauma
Published in Sam Mehta, Andrew Hindmarsh, Leila Rees, Handbook of General Surgical Emergencies, 2018
Sam Mehta, Andrew Hindmarsh, Leila Rees
Diffuse brain injury occurs due to acceleration/deceleration injury, and varies in severity from mild concussion to diffuse axonal injury. Mild concussion: to make a diagnosis of mild concussion there must be no reduction in consciousness level, with temporary and mild symptoms only, including confusion, disorientation and retrograde/antegrade amnesia.Classical concussion: there may be a short period of loss of consciousness, with post-traumatic amnesia, the length of which indicates the severity of injury. A post-concussion syndrome may occur. This includes lethargy, memory problems, dizziness, nausea and depression. Up to one-third of patients with a mild head injury have some symptoms of memory, sleep or sexual disturbance.Diffuse axonal injury: post-traumatic coma which is not due to haematoma or ischaemia, although it may occur in combination with ischaemic damage.
Pharmacotherapy to prevent the onset of depression following traumatic brain injury
Published in Expert Opinion on Pharmacotherapy, 2022
Michele Fornaro, Assunta Trinchillo, Francesco Saccà, Felice Iasevoli, Maria Nolano, Andrea de Bartolomeis
Concussion, traumatic cerebral edema, diffuse brain injury, focal brain injury, epidural hemorrhage, traumatic subdural hemorrhage, intracranial injury with prolonged coma, other intracranial injuries, and crushing injury of the head occur all acutely after TBI, within a minutes or hours [7]. Very rarely, their onset can occur late, or after a further head injury occurs. Depressive symptoms and other neurobehavioral sequelae may likewise occur (or recur) after TBI, with different timing and severity [9]. Overall, the incidence of post-TBI depression ranges between 16–60%, [10,11]. Depressive symptoms may overlap with neurological ones – e.g. cognitive impairment or apathy, either in the acute- or the long-term setting, prompting for proactive pharmacological and non-pharmacological interventions aimed at minimizing the risk for the development of treatment-resistance phenomena upon careful appraised of potential benefits and harms [12].
The cortical and subcortical substrates of quality of life through substrates of self-awareness and executive functions, in chronic moderate-to-severe TBI
Published in Brain Injury, 2022
Eva Pettemeridou, Fofi Constantinidou
Traumatic brain injury (TBI) is a major cause of hospitalization, death, and chronic disability, globally (1,2). TBI is accompanied by long-term and progressive disabilities, such as significant neuropsychological impairment (2–6), including executive dysfunction (7,8), and deficits in self-awareness (SA; 2,8,9). Neuropsychological impairment has been associated with chronic and progressive brain volume loss (5,7,10,11), as TBI can result in a pathophysiologic sequelae. This pathophysiologic sequelae is analogous to the location and severity of the damage, diffuse effects, and secondary mechanisms of injury, leading to focal and diffuse brain injury. Contusions can directly disrupt function in both cortical and sub-cortical regions, with areas such as frontal and anterior temporal, and the hippocampus, respectively, being more vulnerable to the trauma due to their position within the skull (12–14).
An update on the pharmacological management and prevention of cerebral edema: current therapeutic strategies
Published in Expert Opinion on Pharmacotherapy, 2021
Melissa Pergakis, Neeraj Badjatia, J. Marc Simard
DECRA assessed the efficacy of bifronto-temporo-parietal decompressive craniectomy versus standard care in TBI patients with diffuse brain injury after failure of first tier therapies. Functional outcome at 6 months was worse in the patients who had craniectomy in comparison to those that had standard of care alone. Craniectomy, however, resulted in reduced ICP, fewer interventions for ICP, shorter duration of mechanical ventilation, and shorter duration of ICU stay. RESCUEicp assessed decompressive craniectomy (either hemicraniectomy or bifrontal craniectomy) when first-tier (head elevation, hypocapnia, analgesia, paralysis) and second-tier (mannitol, hypertonic saline, loop diuretics, hypothermia) therapies had failed. Patients who underwent decompressive craniectomy were less likely to die but were more likely to be severely disabled or in a vegetative state at 6 months. At 12 months, favorable outcome, based on the Glasgow Outcome Scale, was more common in patients who underwent decompression.