Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury
Diffuse axonal injury is a serious neurological condition that results in cognitive, physical, and behavioral changes. It compromises the patient's ability to reintegrate into society, return to work, and lead a normal life. The condition usually persists long after the traumatic event, requiring continued treatment to prevent permanent damage. Diffuse axonal injury leaves brain tissue functionally compromised but gradually regains normal function due to its plasticity.
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Postoperative care is aimed at reducing ICP and improving cerebral blood flow. Patients with severe DAI should expect prolonged rehabilitative therapy, including physical, occupational, and speech therapy. Patients with a severe DAI may be left with a permanent disability. A neurosurgeon will prescribe a treatment plan based on the severity of the patient's symptoms. While a cure for DAI is not possible, it is possible to slow down its progression and reduce symptoms.
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The exact cause of DAI remains unknown, but shearing forces in white-matter fiber tracts are thought to be the primary contributor. It is most often a result of high-impact injuries. Patients who develop this injury usually experience prolonged periods of unconsciousness or coma, regaining movement only after several weeks or months. Patients may initially appear restless or have autonomic symptoms. The symptoms of diffuse axonal injury can range from a mild coma to a full blown coma.
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Diffuse axonal injury (DAI) is a common pathologic consequence of traumatic brain injury. Axons are highly organized in white matter tracts and are supple under normal conditions. Rapid deformation associated with brain trauma causes axons to become brittle. It damages the axonal cytoskeleton and leads to swelling in discrete bulb formations and elongated varicosities. Calcium entry into damaged axons is believed to initiate further damage by activating proteases.
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Diffuse axonal injury occurs when the brain shifts rapidly inside the skull, tearing long fibers in the brain. These damaged fibers are responsible for communication between nerves in the brain, resulting in a coma or other physical and cognitive impairment. Diffuse axonal injury can be difficult to detect with MRI or CT scans, making it one of the most devastating types of traumatic brain injury.
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Diffuse axonal injury is associated with traumatic brain injury and should be investigated by a neuropsychologist. MRI and cranial computed tomography may also be used to confirm the diagnosis. Neuropsychological tests may be required to determine whether the patient has any cognitive impairment. Symptoms of diffuse axonal injury may range from a mild headache to a comatose state.
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Secondary factors cause a cascade of biochemical events in the brain following TBI. The influx of calcium results in high intracellular sodium levels and activation of calcium-dependent neutral cysteine proteases, which hydrolyze proteins. This leads to increased cellular necrosis, which is associated with the development of apoptosis. In addition, high levels of intracellular calcium stimulate activation of caspase-3 and calpain, which are involved in necrotic cell death.
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In a prospective cohort study, axonal injury in the brain can affect the outcome of a patient's life. Diffuse axonal injury (DAI) is associated with a poorer outcome in patients than with less serious injuries. Most patients will be in a coma or persistent vegetative state if DAI is severe. But for milder forms, rehabilitation may be possible. But, in severe cases, reversal of the injury is not possible.
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In the acute phase, DAI is difficult to detect. However, a combination of clinical signs and imaging may suggest a diagnosis, but confirmation is usually only possible after postmortem. Imaging after traumatic axonal injury can be helpful in diagnosing DAI, and CTs are routinely used in trauma centers. However, their low resolution makes them inconclusive for DAI diagnosis. Also, CTs can be inconvenient to use in unstable patients.