Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury

Diffuse axonal injury is a form of severe traumatic brain injury. Symptoms of this condition are broad and impact a person's physical, mental, and social status. They also impact their quality of life and their ability to return to work, school, or social life. Fortunately, the effects of diffuse axonal injury often last for a long time after the traumatic event. Because brain tissue is plastic, it can re-shape itself and re-form neural connections.

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Treatment of diffuse axonal injury focuses on preventing secondary injuries and facilitating rehabilitation. If left untreated, secondary injuries can cause increased mortality, such as cerebral edema and hypoxia with co-existing hypotension. Prompt care is essential to prevent the onset of cerebral edema and elevated intracranial pressure. While there is no specific cure for diffuse axonal injury, early recognition and treatment may lead to the most successful outcome.

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Diffuse axonal injury is a neurological condition that affects the white matter tracts in the brain. The symptoms of this disorder may be mild or severe and range from a headache to dizziness. In severe cases, an individual may be comatose or in a persistent vegetative state. The severity of the disorder determines the extent of the impairment. Approximately forty percent of people with DAI require hospitalization.

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Diffuse axonal injury has three stages. Treatment varies according to the stage of the disease. Once diagnosed, treatment may target specific symptoms and prevent the condition from worsening. This way, if it's detected in time, it may be possible to prevent serious consequences. The goal of treatment is to manage symptoms and prevent the damage to the brain from progressing further. You will most likely need to undergo an MRI to get a clearer picture of the condition.

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The biochemical response is the biggest impact on the axon. In the absence of ATP, the axon fails to maintain its Ca++, K+, and Na+ homeostasis. The abnormal activation of axonal receptors can alter intracellular signal transduction pathways. This, in turn, alters the function of the cell. In addition, axons cross the synapse, which is the area of brain tissue where nerve impulses travel.

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The severity of the disorder has a poor prognosis, but it does not mean the patient has no hope. Surgical intervention is often undertaken to reduce ICP and improve cerebral blood flow. Patients should expect long-term rehabilitative therapies, including physical, occupational, speech, and psychological therapies. Depending on the severity of the case, neurosurgery and neurology can guide the therapy. However, rehabilitative therapies may not be sufficient for the treatment of this condition.

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The effects of DAI depend on the location of the damage. The most common manifestations are enlarged ventricles and brain hemispheres. Patients with DAI also have abnormal muscle tone, and their Glasgow Coma Scale scores are higher in people with more diffuse axonal injury than those with focal lesions alone. The severity of the damage has been linked to the deposition of amyloid precursor protein.