Effects of TBI can include impaired thinking or memory, movement, sensation e.
Secondary Injury Secondary types of traumatic brain injury TBI are attributable to further cellular damage from the effects of primary injuries. Secondary injuries may develop over a period of hours or days following the initial traumatic assault.
Secondary brain injury is mediated through the following neurochemical mediators [ 18 ]: EAAs can cause an influx of chloride and sodium, leading to acute neuronal swelling.
EAAs can also cause an influx of calcium, which is linked to delayed damage.
Tamoxifen is a potent inhibitor of VRACs and potentially could be of therapeutic value. Endogenous opioid peptides These may contribute to the exacerbation of neurologic damage by modulating the presynaptic release of EAA neurotransmitters.
Activation of the muscarinic cholinergic systems in the rostral pons mediates behavioral suppression, which often is observed in TBI, as well as LOC. Heightened metabolism in the injured brain is stimulated by an increase in the circulating levels of catecholamines from TBI-induced stimulation of the sympathoadrenomedullary axis and serotonergic system with associated depression in glucose utilization [ 20 ]contributing to further brain injury.
Other biochemical processes leading to a greater severity of injury include an increase in extracellular potassium, leading to edema; an increase in cytokines, contributing to inflammation; and a decrease in intracellular magnesium, contributing to calcium influx.
Increased pressure also can lead to cerebral hypoxia, cerebral ischemia, cerebral edema, hydrocephalus, and brain herniation. Cerebral edema Edema may be caused by the effects of the above-mentioned neurochemical transmitters and by increased ICP.
Disruption of the blood-brain barrier, with impairment of vasomotor autoregulation leading to dilatation of cerebral blood vessels, also contributes.
Hydrocephalus The communicating type of hydrocephalus is more common in TBI than is the noncommunicating type. The communicating type frequently results from the presence of blood products that cause obstruction of the flow of the cerebral spinal fluid CSF in the subarachnoid space and the absorption of CSF through the arachnoid villi.
The noncommunicating type of hydrocephalus is often caused by blood clot obstruction of blood flow at the interventricular foramen, third ventricle, cerebral aqueduct, or fourth ventricle. Brain herniation Supratentorial herniation is attributable to direct mechanical compression by an accumulating mass or to increased intracranial pressure.
Subfalcine herniation - The cingulate gyrus of the frontal lobe is pushed beneath the falx cerebri when an expanding mass lesion causes a medial shift of the ipsilateral hemisphere.
This is the most common type of herniation. Central transtentorial herniation - This type of injury is characterized by the displacement of the basal nuclei and cerebral hemispheres downward while the diencephalon and adjacent midbrain are pushed through the tentorial notch.
Uncal herniation - This type of injury involves the displacement of the medial edge of the uncus and the hippocampal gyrus medially and over the ipsilateral edge of the tentorium cerebelli foramen, causing compression of the midbrain; the ipsilateral or contralateral third nerve may be stretched or compressed.
Cerebellar herniation - This injury is marked by an infratentorial herniation in which the tonsil of the cerebellum is pushed through the foramen magnum and compresses the medulla, leading to bradycardia and respiratory arrest.
Chronic traumatic encephalopathy Persons with a history of repetitive brain trauma, including boxers and football players, are at risk for developing chronic traumatic encephalopathy CTEa progressive degenerative disease. The condition is also characterized by ventricular dilatation and by fenestration of the cavum septum pellucidum, as well as the accumulation of phosphorylated tau in the brain, with deposits of the protein being found in the sulci and in perivascular areas of the cerebral cortex.
Symptoms of CTE include memory loss, confusion, impaired judgment, reduced impulse control, aggression, explosive anger, depression, and progressive dementia.
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Detection of blast-related traumatic brain injury in U. N Engl J Med. Diffuse axonal injury and traumatic coma in the primate.On February 4, , an autopsy report from Massachusetts confirmed discovered high Stage 3 chronic traumatic encephalopathy (CTE) in Ken Stabler's brain after his death.
 On March 14, , the top NFL official, Jeff Miller, publicly admitted that there is a link between football and CTE at the roundtable discussion on concussions. Traumatic brain injury (TBI) is a major cause of death and disability in the United States.
TBIs contribute to about 30% of all injury deaths. 1 Every day, people in the United States die from injuries that include TBI. 1 Those who survive a TBI can face effects that .
Sports-Related Traumatic Brain Injury. Nearly , sports-related traumatic brain injuries (TBIs) occur each year in the United States.
1 Athletes involved in sports such as football, hockey and boxing are at significant risk of TBI due to the high level of contact inherent in these sports.
Head injuries are also extremely common in sports such as . One goal of research on traumatic brain injury and chronic traumatic encephalopathy is to understand why acute traumatic brain injury involves Aβ accumulation, yet the neuropathology of chronic.
A concussion is the most common type of traumatic brain injury and results from forceful trauma like a football tackle, a car crash, a bad fall, or a bomb blast.
The link between football and traumatic brain injury continues to strengthen. Now, one of the largest studies on the subject to date finds that out of deceased NFL players had chronic.