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Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury


Diffuse axonal injury is a type of brain damage characterized by disconnection of the axons of neurons. It affects multiple regions of the brain, including the temporal and frontal lobes, corpus callosum, and brainstem. Patients often show deficits on bilateral neurological examinations. The disease is classified based on pathophysiological lesions in white matter tracts and clinical presentations. Diffuse axonal injury causes mechanical disruption of the cytoskeleton of neurons, causing swelling, proteolysis, and microscopic changes in neuronal structure.

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The preferred diagnostic modality for diffuse axonal damage is MRI, which is sensitive to blood-borne paramagnetic components. An MRI can also show susceptibility artefacts at the grey-white matter junction, corpus callosum, and brain stem. While MRIs can be a reliable tool for diagnosing diffuse axonal injury, they can also produce false negatives. Other methods of assessing the damage to the brain include EEG (electroencephalography), which measures electrical activity in the brain.

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Diffuse axonal injury has three stages, which are characterized by varying degrees of severity. Depending on the severity, various treatment options are available. Although it is difficult to cure diffuse axonal injury, treatment options can alleviate its symptoms and prevent it from advancing. Once diagnosed, your doctor can suggest a treatment regimen. Once you've determined your symptoms, it's essential to consult with a neurosurgeon or neuropsychologist.

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Physical therapy is another treatment for DAI. Physical therapy can help you regain control of affected body parts. It can also help the brain recover neuroplasticity. The goal of physical therapy is to improve cerebral blood flow and reduce the ICP. Rehabilitative therapy may include occupational therapy, speech therapy, and physical rehabilitation. It will take months to recover fully from diffuse axonal injury, so it is important to seek treatment as soon as possible.

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Diffuse axonal injury affects white matter tracts in the brain. Patients may experience a wide spectrum of neurological dysfunction, from a clinically insignificant coma to a comatose state. Most patients will have symptoms of multiple sclerosis, including headaches, seizures, and dizziness. Eventually, these symptoms may lead to a permanent coma. This condition is usually the result of an accident, such as a car crash.

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Diffuse axonal injury is a form of traumatic brain injury in which the brain shifts rapidly inside the skull. When this happens, the brain fibers are torn, disrupting the communication between different parts of the brain. Diffuse axonal injury can result in a coma or physical and cognitive impairment. Affected people may also experience elevated intracranial pressure and cerebral edema. Treatment is focused on reducing swelling and restoring normal brain function.

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DAI is associated with a number of secondary factors that push injured cells toward cell death. Among these are high intracellular sodium levels, which are a consequence of voltage-gated sodium channels. These high levels of intracellular sodium stimulate calcium-dependent neutral cysteine proteases (caspases-3), which hydrolyze proteins. These processes result in an increased incidence of apoptosis. In addition to these effects, ATP and Ca2+ are required for cellular survival.

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Another mechanism of DAI is asymmetric deformation. In contrast to contusive mechanisms, axons undergo complex stress fields that result in deformation of intracellular organelles. The energy that is delivered over a millisecond span of time is also less pronounced and produces a less severe degree of deformation of the substance of the brain away from the point of impact. In addition, the shear stress is not transmitted through the brain's surface to the predominately involved areas. The brainstem and cerebellum are the most likely regions involved in DAI.

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Generalized ventricular enlargement has been associated with problems with information processing. The delayed ventricular dilation in patients with DAI has a stronger impact on neuropsychological tests, which is consistent with the effects of DAI. Additionally, there have been several studies indicating a link between DTI measurements and long-term functional outcomes in patients with CC. The results of these studies have been awaited for a long time.

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DTT is an excellent tool for detecting DAI early, which is potentially treatable. The DTT technique allows a physician to visualize the extent of damage in the white matter fiber tract of the brain. However, because the number of deaths and dependence events in the patients with DAI is relatively small, confidence intervals of the model are disproportionately large. The results are inconsistent and warrant further research. Therefore, it is important to consult with a neurologist to confirm the diagnosis of DAI in the first 72 hours.

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