Traumatic head injury increases effect of Alzheimer disease which disrupts activity of neurotransmitters and electrical charges travel within cells. Alzheimer disease is characterized by synaptic loss and neuronal death with gross brain atrophy. Falls are common in older population which lead to prolong hospital stay and serious medical complications such as traumatic brain injury.
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Traumatic head injury cause brain tissue to swell which prevent fluids from leaving brain and broken pieces of skull can rupture blood vessels in head. Effect of traumatic brain injury is crucial due to the association of cognitive impairment, decrease motor function, and neuroinflammation with Alzheimer’s disease, especially in women with the APOE genotype. Reducing the onset with preventative measures including diet modification, physical activities, and continuous intellectual stimulation constituting a medical management and care plan.
Neuroinflammation and cognitive impairment role on the brain is critical to traumatic brain injury with Alzheimer disease. Brains immune cells play an important role in healing process, removal of dead, and damaged neurons which doesn’t occur cause of the traumatic brain injury. Amnesia is memory loss and different types include retrograde amnesia and anterograde amnesia. Retrograde amnesia hinders ability to retrieve memories that were already stored in brain and limited to period before head injury or before Alzheimer disease develops. Anterograde amnesia lose capacity to make new memories and present for events that occur or information that is present after brain injury or Alzheimer disease. Aphasia is impaired communication and apraxia is deficit involuntary motor skills.
Neuroinflammation is cellular damage and loss of neuronal functions occurring when brain or spinal cord become inflamed cause by irritation and swelling of brain tissue or blood vessels. Brain swelling cause increased intracranial pressure (ICP) which prevent blood flow to brain and deprived it of oxygen need to function. Brain fog occurs due to decrease communication between neurons leading to damaged brain cells and brain decelerating. Inflammation cause deficits such as memory loss, decrease alertness, change in concentration and behavior, confusion, mood swings, and distortions in thought. Chronic cerebral inflammation associated with increased proinflammatory cytokines capable of mediating neural protection and regeneration. Traumatic brain injury follows by oxidative stress and hypoxia which stimulate microglia and astrocytes. Continuing neuroinflammation and oxidative stress occur in existence of brain damage and functional impairments (O’Brien, 2015).
Cognitive impairment is act of knowing, thinking, ability to choose, understand, remember information. Problems include attention and concentration, speech and language, learning and memory, problem-solving, decision-making, and judgment. First, unable to pay attention and concentration resulting in restless, distraction, difficulty working on more than one task at a time, problem carrying on long conversation or sitting still for long period of time. Second, problem with processing and understanding information slow down and result in taking longer to grasp what other say,
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