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Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury


A diagnosis of diffuse axonal injury (DAI) requires prompt medical attention, and rehabilitative care must follow. Treatment should be directed towards prevention of secondary injuries, and facilitate functional recovery. Various secondary injuries can increase the risk of death, such as cerebral edema, hypotension, and elevated intracranial pressure. Prompt care should be given to avoid underlying conditions that may lead to these complications.

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Diffuse axonal injury affects the interconnection of neuronal fibers, resulting in the loss of the connections between them. It frequently affects a variety of functional areas of the brain, and patients often present with symptoms that are consistent with bilateral neurological examination deficits. This disorder commonly affects the frontal and temporal white matter, the corpus callosum, and the brainstem. The Adams classification of diffuse axonal injury is based on pathological lesions in the white matter tracts, as well as the clinical presentation of patients. In addition to the loss of interconnections, axonal portions of neurons are damaged mechanically, resulting in swelling, proteinase degradation, and microscopic changes in neuronal structure.

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The effects of diffuse axonal injury are often subtle and unrelated to the mechanism of impact. Diffuse axonal injury affects the central nervous system, resulting in ventricular dilatation and the loss of adjacent white matter. Diffuse axonal injury is distinct from other types of head trauma, which is why it is important to consider the mechanism of the injury when making a diagnosis of diffuse axonal injury.

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There is no one cause of DIA, but DAI occurs in many cases and can lead to death in up to 25% of cases. Some patients with TBI may not have a full diagnosis of DAI, but postmortem studies have indicated a high incidence of diffuse axonal injury. The effects of DAI can range from loss of memory to confusion. This condition requires immediate medical attention, as well as rehabilitative treatment.

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Diffuse axonal injury is a form of traumatic brain injury. It occurs when the brain decelerates quickly, causing damage to long nerve fibers. The result is widespread brain damage. Most patients suffer a coma and are left in a vegetative state. This form of brain damage can be difficult to detect, even with CT and MRI scans. The most severe cases are usually permanent and result in impairments that vary in severity.

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Diffuse axonal injury has two main causes. It affects neurons by damaging the axons throughout the brain. An impact causes some lesions, but the axons themselves are the most important cause of the injury. Impact triggers a series of biochemical cascades. This process results in axonal stretching and cell death. The process of axonal stretching begins one to six hours after the trauma and axonal transport stops.

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Diffuse axonal injury usually occurs in the dorsolateral quadrant of the rostral brainstem, near the superior cerebellar peduncles. It typically results in hemorrhagic lesions and eventually becomes a scarred area. Diffuse axonal injury does not occur exclusively in the rostral brainstem. It can affect any region in the midbrain.

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The inflammatory response in the brain is mediated by microglia. Microglia are immunohistochemically labeled and localize to the site of the trauma. They then become activated and isolate structures that have been damaged. This infiltration lasts for two to three weeks or more, depending on the severity of the axonal injury. As the inflammatory response in the brain continues, the brain is more susceptible to compression induced damage and death.

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Despite its seriousness, DAI is often the result of an accident that has caused brain damage. It causes extensive damage to neurons in the brain and can result in secondary axotomy or corticospinal lesions. Further, DAI can cause degeneration of the distal segments of the brain. As a result, patients with DAI may experience neurological problems months to years after the initial trauma.

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In animal models, DAI usually occurs at the periphery of a lesion, and involves different areas of the brain. Animals with DAI have smaller brain volumes than patients with DAI. In these animal models, the cellular morphology and biochemical cascade of DAI are mimicked, resulting in prolonged unconsciousness and impaired balance. Furthermore, the histological analysis revealed that the brain regions involved in human DAI are similar.

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The DTI technique has been used in the study. It measures the amount of water in the tissue and provides structural information. It is highly predictive of the eventual outcome and correlates well with the modified Rankin score. The results were similar in males and females. However, some patients have been studied with DTI. One patient died. The research is ongoing. However, more studies are needed to evaluate the role of DTI in DAI.

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