Cases and figures Epidemiology The patients at risk of diffuse axonal injury belong to the same cohort as those who suffer traumatic brain injury and as such young men are very much over-represented. Clinical presentation Typically, patients who are shown to have diffuse axonal injury have loss of consciousness at the time of the accident. Post-traumatic coma may last a considerable time and is often attributed to coexistent more visible injury e. As such the diagnosis is often not suspected until later when patients fail to recover neurologically as expected. Pathology Diffuse axonal injury is the result of shearing forces, typically from rotational acceleration most often a deceleration.
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Cases and figures Epidemiology The patients at risk of diffuse axonal injury belong to the same cohort as those who suffer traumatic brain injury and as such young men are very much over-represented.
Clinical presentation Typically, patients who are shown to have diffuse axonal injury have loss of consciousness at the time of the accident. Post-traumatic coma may last a considerable time and is often attributed to coexistent more visible injury e. As such the diagnosis is often not suspected until later when patients fail to recover neurologically as expected.
Pathology Diffuse axonal injury is the result of shearing forces, typically from rotational acceleration most often a deceleration. In the majority of cases, these forces result in damage to the cells and result in edema. Actual complete tearing of the axons is only seen in severe cases. CT Non-contrast CT of the brain is routine in patients presenting with head injuries. Unfortunately, it is not sensitive to subtle diffuse axonal injury and as such, some patients with relatively normal CT scans may have significant unexplained neurological deficit 4,5.
The appearance depends on whether or not the lesions are overtly hemorrhagic. Hemorrhagic lesions will be hyperdense and range in size from a few millimeters to a few centimeters in diameter. Non-hemorrhagic lesions are hypodense. They typically become more evident over the first few days as edema develops around them. They may be associated with significant and disproportionate cerebral swelling. When lesions are hemorrhagic, and especially when they are large, then CT is quite sensitive.
As such, it is usually a safe assumption that if a couple of small hemorrhagic lesions are visible on CT, the degree of damage is much greater. MRI MRI is the modality of choice for assessing suspected diffuse axonal injury even in patients with entirely normal CT of the brain 5,6.
MRI, especially SWI or GRE sequences, exquisitely sensitive to paramagnetic blood products may demonstrate small regions of susceptibility artefact at the grey-white matter junction, in the corpus callosum or the brain stem. Some lesions may be entirely non-hemorrhagic even using high field strength SWI sequences. Over the first few days, the degree of surrounding edema will typically increase, although by 3-months post-injury FLAIR changes will have largely resolved 7.
In contrast, SWI changes will usually take longer to resolve, although by months post-injury there will have been substantial resolution 7. This is to be expected as edema is faster to resolve than hemorrhage. Importantly, it should be noted, that even with high field strength modern scanners, the absence of findings does not categorically exclude the presence of axonal injury.
MR spectroscopy MRS can be of benefit in identifying patients with grade I injury which may be inapparent on other sequences. Features typically demonstrate elevation of choline peak and reduction of NAA 3. Treatment and prognosis Unfortunately little can be done for patients with diffuse axonal injury other than trying to minimize secondary damage caused by cerebral edema, hypoxia, etc.
The amount of axonal injury in the brainstem is predictive of long-term vegetative state, whereas supratentorial injury can result in focal neurological or neuropsychiatric deficits 1. Differential diagnosis c ortical contusions the main differential in patients with head injuries typically located superficially, involving the cortex rather than at the grey-white matter junction and are usually associated with variable amounts of extra-axial blood subarachnoid and subdural.
LESION AXONAL DIFUSA CLASIFICACION PDF
Faezil Magnetic resonance textural evaluation is an useful tool for determining differences among various tissues, including tissues that appear apparently normal on visual analysis. Disability and Rehabilitation ; Hyperprolactinemia and male reproductive functions. Immun Ageing, 6pp. Homogeneity characterization of ethylene-co-vinyl acetate copolymer EVA and hydrophobic silica nanocomposite by low field NMR; Caracterizacao da homogeneidade de nanocomposito do copolimero etileno acetato de vinila EVA e silica hidrofobica atraves de ressonancia magnetica nuclear de baixo campo. A high interobserver agreement was observed as the four sequences were analyzed. Prediction axoal length of hospital stay following stroke. There was a problem providing the content you requested All except one subject had bilateral piercings.
TRAUMATISMO CRANEOENCEFÁLICO: LESIÓN AXONAL DIFUSA
Kasho En las degeneraciones parenquimatosas se distinguen dos tipos que son: Si continua navegando, consideramos que acepta su uso. Mordisquean y lamen sus heridas. Mammosomatotroph adenoma of the pituitary associated with gigantism and hyperprolactinemia. La escala es gratuita, pero se debe solicitar al autor. Se usan sus hojas machacadas para aliviar las cefaleas. Morphology and edges were properly evaluated up toa 1: Stroke, 21pp. SD and hyperprolactinemia were not correlated.
Lesión axonal difusa: Síntomas, signos y diagnóstico
Lesión axonal difusa