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Cerebral softening, also known as encephalomalacia, is a localized softening of the substance of the brain, due to bleeding or inflammation. Three varieties, distinguished by their color and representing different stages of the disease progress, are known respectively as red, yellow, and white softening.
Micrograph showing gliosis in the cerebellum. Reactive astrocytes on the left display severe proliferation and domain overlap. Reactive astrogliosis is the most common form of gliosis and involves the proliferation of astrocytes, a type of glial cell responsible for maintaining extracellular ion and neurotransmitter concentrations, modulating synapse function, and forming the blood–brain ...
A glial scar formation is a reactive cellular process involving astrogliosis that occurs after injury to the central nervous system.As with scarring in other organs and tissues, the glial scar is the body's mechanism to protect and begin the healing process in the nervous system.
Myelomalacia is a pathological term referring to the softening of the spinal cord. [1] Possible causes of myelomalacia include cervical myelopathy, hemorrhagic infarction, or acute injury, such as that caused by intervertebral disc extrusion.
It is important to differentiate PVL from the following major white matter lesions in the cerebral hemispheres: edematous hemorrhagic leukoencephalopathy (OGL), telentsefalny gliosis (TG), diffuse leukomalacia (DFL), subcortical leukomalacia (SL), periventricular hemorrhagic infarction (PHI), intracerebral hemorrhage ( ICH), multicystic ...
The histologic findings are diffuse, irregular loss of axons and myelin accompanied by widespread gliosis, tissue death due to an infarction or loss of blood supply to the brain, and changes in the plasticity of the arteries. The pathologic mechanism may be damage caused by severe atherosclerosis. The onset of this disease is typically between ...
Evidence from subcortical small infarcts suggests that motor fibers are somatotopically arranged in the human corona radiata. Following subtotal brain damage, localization of the corticofugal projection in the corona radiata and internal capsule can assist in evaluating a patient's residual motor capacity and predicting their potential for functional restitution.
These changes are associated with diffuse gliosis, moderate loss of axons and many axonal spheroids. [1] Activated or ameboid microglia and macrophages that contain myelin debris, lipid droplets and brown autofluorescent pigment granules are found in the areas with demyelination and axonal spheroids.