NSCI 110 1st Edition Lecture 18 Outline of Last Lecture I. Biological responses to traumatic brain injuries depend on various physiological factorsa. Volume of central zone of impactb. Degree of inflammation and phagocytosisc. Extent of capillary proliferation and astrocytic scarringII. Secondary sources of injury may also harm the person suffering from a brain injurya. Intracranial hemorrhaging and pressureb. Ischemia c. Edema d. Hydrocephalye. Diaschisisf. 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 apoptosisb. Excess of cytochrome c released by mitochondriaII. There is an initial period of biological recovery followed by more psychological responsesa. Premorbid state followed by glial cell assistanceb. Eventually learning and compensatory mechanisms take overIII. There are numerous cellular mechanisms that follow the recovery perioda. Astrocytic aid involved in nerve growth factors and restoration of nutrientsb. Denervation hypersensitivityc. Synaptogenesisd. Cortical reorganizationIV. Through neuropsychological assessment the extent of brain and cognitive damage may be assesseda. Cognitive statusb. Behavioral compensationCurrent Lecture- Necrosis: cell death due to direct damage to the cell and loss of cellular integrity - Apoptosis: programmed cell deatho Cellular stress may be induced by ischemia (hypoxia, decreased nutrients)- Glutamatergic overstimulation leads to excitotoxicityo 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 activityo Higher depolarization Increased release of glutamate Increase in extracellular glutamate Prolonged activation of postsynaptic synapseso 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 recoveryo Percent recovery vs. timeo 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 againo The first three months of recovery is due to biological responses in the body Astrocyte functiono 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 nutrientso Nerve growth factors and other molecular mechanisms by astrocytic aido Dissipation of diaschisis in spared tissue at primary and distal tissueso Denervation hypersensitivity Net effects on a cell body may receives stronger or weaker input because multiple axons are destroyedo Collateral axonal sprouting or rerouting of axonso Synaptogenesis: several variations of ideas Creation of new synapses Silent synapseso Cortical reorganization and vicariation- Wada involves injecting a short-lasting barbiturate into the left or right carotid arteryo Shuts down function of left or right hemisphere- Some psychological factors (through neuropsychological assessment)o Cognitive statuso Behavioral compensation Therapy and rehabilitation Motivation and mood Psychological and social support systemso Complicating factors Monetary Functional disturbances Medical complicationso Other variables such as age,
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