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Diffuse Axonal Injury Rehabilitation - Oren Zarif - Diffuse Axonal Injury

Diffuse axonal injury is a devastating condition in which axons are torn from neurons and swell. The brain is already under a great deal of pressure and increased pressure may cause even more damage. Additionally, shearing may release chemicals that further contribute to the brain injury. The main symptom of diffuse axonal injury is a lack of consciousness, which can last for six hours. However, a patient can also experience other symptoms of brain damage.

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Diffuse axonal injury has three distinct stages. Depending on the level of the injury, various treatment options are available. Although the injury cannot be cured, treatment aims to alleviate symptoms and prevent the brain damage from worsening. There is no definite cure for diffuse axonal injury. Rehabilitation therapy involves restoring function to affected parts of the brain and helping the brain heal. Here are some of the main treatment options for diffuse axonal injury:

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The axon is a vital component of a nerve cell. Its function is to transmit messages from the brain to the body. In cases of diffuse axonal injury, the axon is disrupted by the rapid movements of the brain in the skull. This results in severe compression and local swelling. Further, the axons can die. In such cases, the patient can go into a vegetative state.

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Although the precise cause of diffuse axonal injury is unknown, researchers believe that it is caused by the shearing forces of the white-matter fiber tracts. Most commonly, the disorder occurs after a high-impact accident, such as a traumatic brain injury. Diffuse axonal injury patients have periods of unresponsiveness and coma, but are capable of recovering their movement. Patients may initially appear restless, but they may also experience autonomic symptoms.

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If the symptoms of diffuse axonal injury are ambiguous, MRI is the preferred modality. It is sensitive to paramagnetic blood products, and can also show susceptibility artefacts in the corpus callosum, brainstem, and parasagittal white matter. Non-hemorrhagic lesions may appear as high FLAIR signals. The study found that MRI was an effective method of diagnosing diffuse axonal injury in this way.

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When the GCS is less than eight for over six hours, a patient has been diagnosed with diffuse axonal injury. Patients with diffuse axonal injury may experience a spectrum of neurological symptoms, ranging from minor headaches and dizziness to comatose states. In severe cases, the patient may lose consciousness and remain in a vegetative state for months or even years. And, in most cases, the symptoms are so severe that the patient may require a long hospital stay.

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In vitro models of DAI produce a calcium influx, but not immediately after the trauma. Nevertheless, the activity of Ca-ATPase is not affected until 15 minutes and four hours after the injury. The increased calcium concentration results in the compaction of neurofilaments, collapse of sidearms, and loss of axonal microtubules. The presence of excessive calcium causes abnormal receptor activation in the brain, altering intracellular signal transduction pathways and altering cell function. This results in the production of arachidonic acid, which activates ion channel activity and leads to inflammatory eicosanoids and the production of strong oxidants.

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Although an in vivo model of DAI is necessary to evaluate the effects of trauma on the brain, no available experimental DAI models can simulate moderate or mild DAI. In vitro experiments, researchers can stretch the optic nerves to mimic a moderate or severe case. Other models involve a plastic disk attached to the skull and the effects of a blow to the head. Although the latter two models are ideal for studying DAI, they are not entirely accurate.

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Diffuse axonal injury (DAI) results in swelling within the brain. While steroids can help reduce the swelling, there are no surgical options for this condition. If the condition is severe, the patient may not recover from the trauma, and the injury will cause the patient to remain in a vegetative state or even worse. But even if DAI is mild, it may be possible to undergo rehabilitation after the trauma.

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DTT has the potential to detect DAI early, when treatment is still possible. It has also been shown to have a positive correlation with long-term outcome in patients with chronic TBI. However, these methods are relatively new and have their limitations. For example, the fibers can migrate onto another tract or fail to terminate at an early stage. In addition, there are very few directions that are gradient-encoding. Nevertheless, DTI-based measurements of WM hyperintensity volume are more sensitive than the latter and may provide information about early DAI.

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