NSCI 110 1st Edition Lecture 18 Outline of Last Lecture I Biological responses to traumatic brain injuries depend on various physiological factors a Volume of central zone of impact b Degree of inflammation and phagocytosis c Extent of capillary proliferation and astrocytic scarring II Secondary sources of injury may also harm the person suffering from a brain injury a Intracranial hemorrhaging and pressure b Ischemia c Edema d Hydrocephaly e Diaschisis f Seizures Outline of Current Lecture I Excessive amounts of glutamate overstimulates a neuron and may lead to excitotoxicity a Increased and prolonged depolarization of membrane results in apoptosis b Excess of cytochrome c released by mitochondria II There is an initial period of biological recovery followed by more psychological responses a Premorbid state followed by glial cell assistance b Eventually learning and compensatory mechanisms take over III There are numerous cellular mechanisms that follow the recovery period a Astrocytic aid involved in nerve growth factors and restoration of nutrients b Denervation hypersensitivity c Synaptogenesis d Cortical reorganization IV Through neuropsychological assessment the extent of brain and cognitive damage may be assessed a Cognitive status b Behavioral compensation Current Lecture Necrosis cell death due to direct damage to the cell and loss of cellular integrity Apoptosis programmed cell death o Cellular stress may be induced by ischemia hypoxia decreased nutrients Glutamatergic overstimulation leads to excitotoxicity o Ischemia induced because of lower energy levels less activity by mitochondria These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute o Sodium potassium pump decreases activity o Higher depolarization Increased release of glutamate Increase in extracellular glutamate Prolonged activation of postsynaptic synapses o Prolonged depolarization of a neuron Leads to Bcl 2 molecules being blocked so there is an excess of cytochrome c being released by the mitochondria More cleavage of caspase 3 activating this enzyme Fragmentation of DNA membrane disintegration chromosome condensation cytoskeletal damage Obligatory cell death Time course of recovery o Percent recovery vs time o Premorbid refers to the time before the injury Used as a comparison to measure the deficit the person is experiencing If unconscious premorbid ends when the person gains back consciousness so you can assess true cognitive damage After recovery the person may reach premorbid levels again o The first three months of recovery is due to biological responses in the body Astrocyte function o These biological processes eventually slow and there is a shift to more psychological responses Learning and compensatory mechanisms Some cellular mechanisms o Restoration of oxygen and nutrients o Nerve growth factors and other molecular mechanisms by astrocytic aid o Dissipation of diaschisis in spared tissue at primary and distal tissues o Denervation hypersensitivity Net effects on a cell body may receives stronger or weaker input because multiple axons are destroyed o Collateral axonal sprouting or rerouting of axons o Synaptogenesis several variations of ideas Creation of new synapses Silent synapses o Cortical reorganization and vicariation Wada involves injecting a short lasting barbiturate into the left or right carotid artery o Shuts down function of left or right hemisphere Some psychological factors through neuropsychological assessment o Cognitive status o Behavioral compensation Therapy and rehabilitation Motivation and mood Psychological and social support systems o Complicating factors Monetary Functional disturbances Medical complications o Other variables such as age drugs
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