Traumatic brain injury (TBI) is defined as a result of a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. This trauma can lead to temporary or permanent impairments of cognitive, physical and psychosocial functions, and an associated diminished or altered state of consciousness 1).
Head impact direction has been identified as an influential risk factor in the risk of traumatic brain injury (TBI) from animal and anatomic research.
Increased risk of incurring a subdural hematoma exists from impacts to the frontal or occipital regions, and parenchymal contusions from impacts to the side of the head. There was no definitive link between impact direction and subarachnoid hemorrhage. In addition, the results indicate that there is a continuum of stresses and strain magnitudes between lesion types when impact location is isolated, with subdural hematoma occurring at lower magnitudes for frontal and occipital region impacts, and contusions lower for impacts to the side.
This hospital data set suggests that there is an effect that impact direction has on TBI depending on the anatomy involved for each particular lesion 2).
After TBI, cerebral vascular endothelial cells play a crucial role in the pathogenesis of inflammation.
Following TBI, various mediators are released which enhance vasogenic and/or cytotoxic brain edema. These include glutamate, lactate, H(+), K(+), Ca(2+), nitric oxide, arachidonic acid and its metabolites, free oxygen radicals, histamine, and kinins. Thus, avoiding cerebral anaerobic metabolism and acidosis is beneficial to control lactate and H(+), but no compound inhibiting mediators/mediator channels showed beneficial results in conducted clinical trials, despite successful experimental studies.
White matter injury is an important contributor to long term motor and cognitive dysfunction after traumatic brain injury. During brain trauma, acceleration, deceleration, torsion, and compression forces often cause direct damage to the axon tracts, and pathways that are triggered by the initial injury can trigger molecular events that result in secondary axon degeneration. White matter injury is often associated with altered mental status, memory deficits, motor or autonomic dysfunction, and contribute to the development of chronic neurodegenerative diseases. The presence and proper functioning of oligodendrocyte precursor cells offer the potential for repair and recovery of injured white matter. The process of the proliferation, maturation of oligodendrocyte precursor cells and their migration to the site of injury to replace injured or lost oligodendrocytes is known as oligodendrogenesis 3).
The neuropathology of traumatic brain injury (TBI) from various causes in humans is not as yet fully understood.
Penetrating head injury and closed head injury (CHI) that are moderate to severe are more likely than mild TBI (mTBI) to cause gross disruption of the cerebral vasculature. Axonal injury is classically exhibited as diffuse axonal injury (DAI) in severe to moderate CHI. Diffuse axonal injury is also prevalent in penetrating head injury (PHI). It is less so in mTBI. There may be a unique pattern of periventricular axonal injury in explosive blast mTBI. Neuronal injury is more prevalent in PHI and moderate to severe CHI than mTBI. Astrocyte and microglial activation and proliferation are found in all forms of animal TBI models and in severe to moderate TBI in humans. Their activation in mTBI in the human brain has not yet been studied 4).
Due to the marked heterogeneity of human traumatic brain injury (TBI), none of the available animal model can reproduce the entire spectrum of TBI, especially mild focal TBI.
A stereotaxic coupled weight drop device was designed. Principle arm of device carries up to 500g weights which their force was conveyed to animal skull through a thin nail like metal tip. To determine the optimal configuration of the device to induce mild TBI, six different trials were designed. The optimal configuration of the instrument was used for evaluation of behavioral, histopathological and molecular changes of mild TBI.
Neurologic and motor coordination deficits observed sharply within 24h post injury period. Histological studies revealed a remarkable increase in the number of dark neurons in trauma site. TBI increased the expression of apoptotic proteins, Bax, BCl2 and cleaved caspase-3 in the hippocampus.
This device is capable to produce variable severity of TBI from mild to severe. The main advantage of the new TBI model is induction of mild local unilateral brain injury instead of traumatization of the whole brain. This model does not require craniotomy for induction of brain injury.
This novel animal TBI model mimics human mild focal brain injury. This model is suitable for evaluation of pathophysiology as well as screening of new therapies for mild TBI 5).
Brain Injury Association of Tasmania http://www.biat.org.au
Brain Injury Network of South Australia http://www.binsa.org
Brain Injury Association of NSW http://www.biansw.org.au
Cicuendez et al. retrospectively analyzed 264 TBI patients to whom a MR had been performed in the first 60 days after trauma. All clinical variables related to prognosis were registered, as well as the data from the initial computed tomography. The MR imaging protocol consisted of a 3-plane localizer sequence T1-weighted and T2-weighted fast spin-echo, FLAIR and gradient-echo images (GRET2*). Traumatic axonal injury (TAI) lesions were classified according to Gentry and Firsching classifications. They calculated weighted kappa coefficients and the area under the ROC curve for each MR sequence. A multivariable analyses was performed to correlate MR findings in each sequence with the final outcome of the patients.
TAI lesions were adequately visualized on T2, FLAIR and GRET2* sequences in more than 80% of the studies. Subcortical TAI lesions were well on FLAIR and GRET2* sequences visualized hemorrhagic TAI lesions. We saw that these MR sequences had a high inter-rater agreement for TAI diagnosis (0.8). T2 sequence presented the highest value on ROC curve in Gentry (0.68, 95%CI: 0.61-0.76, p<0.001, Nagerlkerke-R2 0.26) and Firsching classifications (0.64, 95%CI 0.57-0.72, p<0.001, Nagerlkerke-R2 0.19), followed by FLAIR and GRET2* sequences. Both classifications determined by each of these sequences were associated with poor outcome after performing a multivariable analyses adjusted for prognostic factors (p<0.02).
They recommend to perform conventional MR study in subacute phase including T2, FLAIR and GRET2* sequences for visualize TAI lesions. These MR findings added prognostic information in TBI patients 7).
634 consecutive neurosurgical trauma patients, who presented with mild-to-severe traumatic brain injury (TBI) from January 2013 to April 2014 at a tertiary care center in rural Nepal. All pertinent medical records (including all available imaging studies) were reviewed by the neurosurgical consultant and the radiologist on call. Patients' worst CT image scores and their outcome at 30 days were assessed and recorded. They then assessed their independent performance in predicting the mortality and also tried to seek the individual variables that had significant interplay for determining the same.
Both imaging score Marshall CT classification and Rotterdam CT score can be used to reliably predict mortality in patients with acute TBI with high prognostic accuracy. Other specific CT characteristics that can be used to predict early mortality are traumatic subarachnoid hemorrhage, midline shift, and status of the peri-mesencephalic cisterns.
They demonstrated in this cohort that though the Marshall CT classification has the high predictive power to determine the mortality, better discrimination could be sought through the application of the Rotterdam CT score that encompasses various individual CT parameters. They thereby recommend the use of such comprehensive prognostic model so as to augment the predictive power for properly dichotomizing the prognosis of the patients with TBI. In the future, it will therefore be important to develop prognostic models that are applicable for the majority of patients in the world they live in, and not just a privileged few who can use resources not necessarily representative of their societal environment 8).
Of 66 patients with head injuries who had talked at some time after injury, 25% did not have intracranial hematoma at necropsy. Most of these had intracranial hypertension, and the commonest finding was local swelling related to contusions. Almost half of the non-haematoma cases had ischaemic or hypoxic brain damage, usually without contusions; 3 were children who had had status epilepticus. Fatality without raised I.C.P. was most often due to meningitis. In deteriorating patients without haematoma mortality and morbidity might be reduced by more diagnosis and treatment, particularly of raised ICP 9).
Manual of Traumatic Brain Injury: Assessment and Management
Management of Adults With Traumatic Brain Injury
Understanding Traumatic Brain Injury: Current Research and Future Directions
Textbook of Traumatic Brain Injury
Brain Injury Medicine, 2nd Edition: Principles and Practice
TRAUMATIC BRAIN INJURY, AN ISSUE OF NEUROSURGERY CLINICS OF NORTH AMERICA, 1E (THE CLINICS: SURGERY)