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Diffuse Axonal Injury - Oren Zarif - Diffuse Axonal Injury

Diffuse axonal injury (DAI) is an extremely devastating neurological condition. Treatments for DAI focus on prevention and rehabilitation of secondary injuries, both of which increase mortality. Secondary injuries may include cerebral edema, hypoxia with coexisting hypotension, or elevated intracranial pressure. Therefore, it is important to provide prompt treatment to prevent cerebral edema and hypotension. In addition, proper management of DAI can help the patient recover from the disorder.

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The clinical diagnosis of DAI is based on the severity of the damage. Patients with a GCS of less than eight should be considered for evaluation. The severity of the diffuse axonal injury is related to the clinical presentation. Mild DAI typically presents with headache, dizziness, and fatigue, while severe DAI is accompanied by loss of consciousness and persistent vegetative state. Very few patients regain consciousness within the first year of their injury.

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The most common symptoms of DAI include cognitive and physical changes, as well as problems with social reintegration and productivity. The damage is long-lasting, resulting in compromised quality of life. The impact of the crash causes brain tissue to shift in the seat and the skull, compromising both the patient's ability to socially reintegrate. Once the clinical condition stabilizes, the brain tissue is slowly able to recover. The plasticity of neurons in the brain allows these connections to remodel, resulting in a more functional neuron.

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MRI is the imaging modality of choice in the diagnosis of DAI. It is sensitive to paramagnetic blood products and can detect susceptibility artefacts in the corpus callosum and brain stem. In some cases, axonal injury may not be hemorrhagic, but still present as a high-FLAIR signal. If these abnormalities are suspected, it is important to diagnose them as soon as possible.

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Although the impact of a head injury may be the most significant cause of DAI, biochemical cascades are responsible for most of the damage. The most common biochemical pathway involved in the axonal disconnect is a biochemical response to physical stress and stretching caused by the impact. In addition, biochemical cascades disrupt cytoskeleton and proteolytic metabolism. These processes are exacerbated by sodium channel opening, which opens up the axolemma.

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When these mechanisms fail, an increased calcium-sodium influx initiates a cascade of secondary biochemical events. Calcium enters the axon via the reverse operation of the Na+-Ca2+ exchange. It is not immediately apparent whether the influx is caused by a cellular reaction or by calcium-sodium overload. The latter results in an axonal stretch that causes cell death.

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Diffuse axonal injury can lead to widespread neurological damage, which is why it's a complication of brain trauma. Patients with DAI commonly experience neurological dysfunction ranging from clinically insignificant to comatose. The severity of the condition varies widely, but most patients have an overall GCS of 8 or less. In addition to neurological damage, DAI patients can have permanent disabilities. In addition to the neurological impairments caused by DAI, the severity and duration of recovery will depend on the affected nerves.

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Fortunately, a variety of experimental neurotrauma models are available to mimic the effects of DAI. Although no in-vivo model is ideal for mimicking the effects of moderate or severe DAI, it is possible to simulate DAI in animals with a cellular model. The use of an artificial lasso or a mechanical device to stretch optic nerves simulates a human-like shaking motion. Moreover, the animals are smaller than humans, which mimics the physical and biochemical processes that lead to DAI.

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The severity of DAI is a strong risk factor for axonal injury. This is because an initial traumatic impact causes a large amount of damage. The CT scan of a patient with DAI is shown in Figure 4.

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In clinical trials, the number of lesions identified on imaging has been associated with the outcome of patients with DAI. In a longitudinal study, the greater the number of lesions, the more severe the impairment of functionality at 12 months. The study also revealed that DAI is related to generalized ventricular enlargement, which has been associated with impaired information processing. In addition, DAI is related to hippocampal atrophy, which may have particular relevance to memory.

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