Trauma
Sam Mehta, Andrew Hindmarsh, Leila Rees in Handbook of General Surgical Emergencies, 2018
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.
Children's Brain Trauma
Rolland S. Parker in Concussive Brain Trauma, 2016
Contributors to behavioral and cognitive sequelae in children include severity of the trauma; bilateral characteristic of the lesion; localization (laterality; cortical vs. subcortical); secondary complications such as seizures and subdural hematoma; level of intelligence at the time of trauma; history of psychiatric disturbance; family adversity; family reaction to the trauma; and parental mental disorder (Birmaher & Williams, 1994). Diffuse brain injury appears to cause a reduction of mental speed, efficiency, and integration, with deficits of information processing, attention, and reaction time among the most prominent effects of head injury of any severity (Beers, 1992). Reaction speed of TBI children is slow to the point that bicycling in traffic is discouraged. Children with poor reaction time and equilibrium are at greater risk of falling. The need for assistance in school 2 years postinjury was predicted by injury severity detectable in neuropsychological dysfunctions at 3 months (Kinsella et al., 1997). The discriminating profile was impairment of verbal learning, memory, and slowing in speed of information processing. This pattern still existed 2 years postinjury. Some criteria for academic impairment are change in academic rank (standardized scores), placement in special education programs, need for additional tutoring, and grade repetition. Balancing such criteria of the outcome of TBI are teacher reluctance to identify low academic achievement after TBI, lack of available educational information, community attitudes, parent coping strategies, and material resources (Kinsella et al., 1997).
Examination of the Nervous System
Julian L Burton, Guy Rutty in The Hospital Autopsy, 2010
In many cases the post-mortem does not discover anything beyond what had been established clinically and using imaging in life. In other instances detailed assessment is required, especially where evidence of the existence or absence of secondary patterns of damage is required to link to suggestions of inappropriate clinical management. In such cases examination in the fresh state with limited histology may not be adequate to give a full explanation of the cause of death. As has been noted, particular difficulty may be encountered in the ascertainment of diffuse brain injury and traumatic axonal damage, where macroscopic evaluation is unreliable and limited histological examination is inadequate (Smith et al., 2003)
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).
Long-term cognitive disability after traumatic brain injury: Contribution of the DEX relative questionnaires
Published in Neuropsychological Rehabilitation, 2020
Blandine Lesimple, Elsa Caron, Muriel Lefort, Clara Debarle, Mélanie Pélégrini-Issac, Didier Cassereau, Sébastien Delphine, Grégory Torkomian, Valentine Battisti, Pierrette Bossale, Damien Galanaud, Louis Puybasset, Pascale Pradat-Diehl, Vincent Perlbarg
As far as anosognosia is concerned, results are heterogeneous from one study to another in the literature concerning the brain network involved in self-awareness. For example, according to Morton and Barker (2010), this complex process may imply prefrontal, inferior parietal and anterior temporal lobes, angular gyrus and supramarginal gyrus and, more generally, involve the anterior cingulate cortex, the anterior insula and fronto-parietal areas (Craig, 2009), which could be affected by a diffuse brain injury rather than a focal lesion (Morton & Barker, 2010). Anosognosia could be a dysfunctional result of a more extensive and distinct cerebral network (Morton & Barker, 2010). In this context, mean diffusivity is a measure that allows one to evaluate microstructural white matter integrity. After a mild TBI, Kinnunen et al. (2011) and Messé et al. (2011) have shown that an increased MD value could discriminate patients with poor outcome from those with a good outcome and from controls, three months after injury. Haberg et al. (2015) reported a correlation between the mean of MD measures and GOSE in TBI patients. Our results showed a link between global white matter alteration (in terms of MD value) and anosognosia, suggesting that anosognosia, even at long term after TBI, could be a consequence of brain damages.
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].
Related Knowledge Centers
- Brain Damage
- Injury
- Acquired Brain Injury
- Stroke
- Primary & Secondary Brain Injury
- Traffic Collision
- Penetrating Head Injury
- Gunshot Wound
- Broca'S Area
- Cerebral Contusion