Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury
The treatment of diffuse axonal injury is focused on prevention of secondary injuries and rehabilitation. Secondary injuries can include cerebral edema, hypoxia with coexisting hypotension, or elevated intracranial pressure. The presence of any of these injuries should prompt immediate treatment, particularly if they are life threatening. In the early stages of this disorder, treatment should begin with appropriate anti-inflammatory and pain-relieving medications.
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Diffuse axonal injury results in a variety of physical, behavioral, and cognitive changes. These changes may impair social reintegration, return to productivity, and quality of life. The damage is persistent even after acute treatment has ended, and it may be years before a patient's condition stabilizes. Neuronal tissue is functionally impaired for the first two years after the traumatic event, but it gradually regains normal function. Due to its plasticity, brain cells are remodeled and their neural connections become more complex.
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Postoperative care for DAI includes several interventions to reduce ICP and improve cerebral blood flow. Patients with severe DAI are expected to undergo prolonged rehabilitation, including physical, occupational, and speech therapy. It is important to note that rehabilitative therapy is not a substitute for surgical treatment. Many patients rehabilitate completely with the right medications. Ultimately, axonal injury can result in a functional deterioration of brain function.
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Diffuse axonal injury is the result of shearing forces that have caused damage to the white matter tracts of the brain. Patients with DAI usually experience a prolonged period of unresponsiveness or coma, but eventually regain movement and consciousness. Some patients initially exhibit restlessness and autonomic symptoms, including nausea, vomiting, and gastrointestinal disorders. They may also develop elevated intracranial pressure and ventricular dilatation.
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Various forms of DAI cause different symptoms and outcomes. In severe cases, the brain may die due to a lack of blood flow or swelling. In the majority of cases, the axons are not fully severe, but they do experience a few small lesions. The majority of the damage is caused by biochemical pathways. In addition to physical stress, axonal damage is often characterized by disconnection and edema.
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Diffuse axonal injury is characterized by numerous focal lesions, most commonly located in the grey-white matter junction, corpus callosum, and brainstem. Patients with Diffuse axonal injury commonly experience mild to severe neurological impairment, with most patients exhibiting GCS of less than eight. In severe cases, patients may lose consciousness and remain in a vegetative state for many months or years.
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People with Diffuse axonal injury may experience a variety of secondary effects, but many recover the affected functions and improve their quality of life. The cause of Diffuse axonal injury is unknown, although the brain is injured rapidly during a jolt or collision. The sudden shift of the brain inside the skull causes the long connecting fibers to be torn. The resulting damage can result in devastating effects on a person's ability to perform everyday tasks.
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When the degree of DAI is suspected, MRIs may be used to confirm or rule out the diagnosis. MRIs can detect diffuse axonal injury early in the process, minimizing the risk of secondary damage due to cerebral edema, or by detecting the disorder early in the process. Although DTT has little diagnostic value, early detection of these neurosurgical complications can help patients avoid serious consequences. In addition to early recognition, MRI may detect underlying neurological conditions such as traumatic brain injury and stroke.
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The diagnosis of DAI is based on clinical findings. Patients with DAI are often in a coma and are likely to have subdural or epidural hematomas. It is the primary lesion in rotational acceleration-deceleration head injuries. DAI occurs in hemorrhagic foci of the brainstem and corpus callosum. There is no definitive treatment for DAI.