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Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury

Diffuse axonal injury (DAI) is a lesion in the brain that causes a variety of physical, cognitive, and behavioral changes. DAI significantly compromises the patient's social reintegration, return to productivity, and quality of life. This condition is typically chronic, lasting well beyond the acute phase of treatment. Although the brain tissue is essentially destroyed, its function gradually returns once the clinical condition stabilizes. Neuroplasticity, which allows the brain to rebuild damaged neural connections, promotes recovery and promotes functional improvement.

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Different severity levels result in varying degrees of DAI. A mild DAI is thought to be comparable to a concussion. While most people recover from a mild DAI, the majority of survivors do not regain consciousness. The few who regain consciousness typically suffer significant impairment. In severe cases, however, the brain is severely damaged. This injury may be life-threatening. In addition, it is difficult to predict the full recovery of an individual.

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Patients with severe diffuse axonal injury may suffer prolonged periods of unconsciousness. The swelling may occur due to shearing and cause further damage. Treatment includes medications to control swelling in the brain. Other interventions may include counseling, occupational therapy, and physical therapy. The patient will continue to require monitoring throughout the treatment process. The goal of a multidisciplinary rehabilitation plan is to restore the patient to the same level of functioning as they were before their injury.

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Diffuse axonal injury is characterized by varying degrees of neurodegeneration. Acute DAI can result in secondary axotomy due to biochemical factors. This condition is characterized by histologic changes that correspond to a Wallerian-type axotomy. Axonal bulbs, axoplasm, and small clusters of microglia are characteristic features of DAI. The latter is often fatal, resulting in complete degeneration of the distal segment.

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The extent of DAI is based on the severity of the injury. Axons are the pathways through which nerve impulses travel. In severe cases, axons are literally sheared. Lesions usually occur in the white matter, where axons are the most susceptible to the damage. In the early stages, DAI lesions are located primarily in the subcortical and deep white matter of the cerebrum, and eventually in the brainstem.

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In severe cases, Diffuse axonal injury may be so severe that patients may require hospitalization. In severe cases, the patient may experience neurological dysfunction ranging from clinically insignificant to comatose. Most patients have a GCS of eight or less. The severity of symptoms will determine the type of impairment a patient has. If the injury is severe enough, the patient may have permanent cognitive and physical disabilities.

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Although Diffuse axonal injury is a distinct type of primary traumatic brain injury, the association between it and a poor outcome has not been conclusive. Several studies have challenged this view. One study revealed that subjects with predominant DAI did recover from their injuries faster than those with focal lesions. Another study indicated that fewer patients with DAI had impaired cognitive function than those with focal lesions. Further, a recent study found a significant correlation between DAI and postmortem neuropsychological impairments.

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While initial noncontrast CT is generally normal in patients with DAI, later imaging results are not as clear. In nonhemorrhagic DAI, the patient's image may show multiple hypodense foci at sites of shear injury and possibly associated hemorrhage. These lesions are usually ovoid in shape and have a long axis parallel to the axonal direction. These lesions tend to become more prominent over time, but the clinical findings should be consistent with the diagnosis.

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The best available marker of head injury is the brain volume, but some models are more challenging to apply than others. DAI is characterized by widespread axonal damage, as well as disruption in the axonal cytoskeleton. The damage is often diffuse and progressive, and secondary physiological alterations include disrupted axonal transport and increased levels of tau and amyloid precursor proteins. These damage-causing agents are associated with a range of secondary outcomes, including delayed axonal disconnection.

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In recent years, the method of DTI tractography has been widely used for detecting DAI. This technique enables early detection and is associated with therapeutic interventions. It has limitations, however, including an increased rate of fiber regrowth after a DAI than standard measures. In addition, fiber tracking relies on a DTI algorithm with relatively poor gradient-encoding directions. Further studies are needed to assess the effect of fiber tracking in a clinical setting.

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