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Stress can cause acute and chronic changes in certain brain areas which can cause long-term damage. [4] Over-secretion of stress hormones most frequently impairs long-term delayed recall memory, but can enhance short-term, immediate recall memory. This enhancement is particularly relative in emotional memory.
Many now believe stress to be the most significant factor for the onset of depression. As discussed above, hippocampal cells are sensitive to stress which can lead to decreased neurogenesis. This area is being considered more frequently when examining the causes and treatments of depression.
According to Shonkoff, extreme, long-lasting stress in the absence of supportive relationships to buffer the effects of a heightened stress response can produce damage and weakening of bodily and brain systems, which can lead to diminished physical and mental health throughout a person's lifetime. Extreme exposure to such toxic stress can ...
Short-term stress can actually shrink the size of you brain, learn the science and how to stop the damage
Even a mild incident can have long-term effects or cause symptoms to appear years later. [5] Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. Wernicke's aphasia is associated with anomia, unknowingly making up words , and problems with comprehension.
Brain injuries can also be the result of a stroke as the resulting lack of oxygen can cause damage to the location of the cerebrovascular accident (CVA). The effects of a CVA in the left and right hemispheres of the brain include short-term memory impairment, and difficulty acquiring and retaining new information.
[1] [2] Microinfarcts can be found in 25-50% of all elderly deceased persons. Microinfarcts may be the second most important cause of dementia, after Alzheimer's disease. [3] [4] Microinfarcts are microscopic lesions, of cellular death or tissue necrosis, which are a result of pathologies involving small vessels.
Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. [5] Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. [6]