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Definition
| brain floating in skull so sudden ovement smacks it against skull |
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Term
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Definition
| whitem atter and grey matter are of different densities. As a resulst, shearing may occur , in which axons are sheared off when brain bounces off |
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Term
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Definition
| coup- primary impact, contrecoup- secondary impact, can be worse than primary (brain in the skull). Infalls contrecoup contusions are more frequent than coup contusion |
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Term
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Definition
| any kind of active dmage accident etc. |
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Term
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Definition
| confuison headache, vision, tiredness, ringing of ears , bad taste in motuh, fatigue , change insleep patterns, can resovle on their own |
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Term
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Definition
| hheadaches that get worse nad dont go away, repeated vomotiign or nausea, cnvulsions, seizures. inability to awken form sleep. Really b ad- coma and death. |
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Term
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Definition
| stroke- rapid blockage of cerebral artery or bursting of vesel. Third leading cause of death in america, no 1. cause of adult disability. Aneurysm (spaceoccupying). AVM- can expand adn burst. |
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Term
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Definition
| sudden. efect on CNS: cell death duet o lack of oxygen, excytoxoins, rfreer adicals (ischeia, trauma nd epilepsy. Large amounts of glutamate relased. Free radicalsp osiionsu to neruosn and survival. |
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Term
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Definition
| can develop cysts and form space ocupying lesions |
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Term
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Definition
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Term
| spinal cord injury inflammatory response |
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Definition
| microglia, neutrophils, monocytes,lymphocytes. There are systemic effects. |
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Term
| Spian lcord complcaitions |
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Definition
| systemic comlpications- whoel body disease |
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Term
| management of spinal cord injury inflammatory repsosne |
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Definition
| methylprednisolone, erythopoeitin, minocycline. |
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Term
| surgical advances in spinal care |
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Definition
| implanting croots ,stablizaion of spine, imuplatnign avulsed roots |
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Term
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Definition
| tissue drsiuption: priamry cell death ,breakign of ons etc. Injured spnal cords show progressive tissue loss. Centrl hemmorhage necrosis developign within hours. Hti matter bloow flow falls byfifty person within firs t fewh ours. Metabolsim is comrpomised with high lactic acids levels Calcium levels increase and intracellularswelling due to this. Also increased intracellualr clacium elvels = activation of proteases and lipases- Ca bindin to mitochondria producing free radicals= apoptosis |
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Term
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Definition
| occurs to neurons first, but also spinal cord injury is demylinetating, with oligodendrocytes apoptosis induced |
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Term
| sequalae of SCI: break down of BBB |
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Definition
| pro-inflammatory cyotkien resposne (il-1,6,tnfa). activation of microglia and macrophages, as well as reactive astorcytes andliosis andexpression of inhibitory molecules |
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Term
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Definition
| reactive astroycyte resposnet o injury as part of inflammatory process and gliosis |
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Term
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Definition
| anteograde degeneration , axons degenerate from site of lesion forward. |
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Term
| injury resposne scenarios spina lcord |
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Definition
| anterograde where from that aprt forward. oR can lose entier cell due to lackq of stimulation from target. OR can lose multiple cells from lesion of one cell |
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Term
| severed axons fail toregenreate |
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Definition
| they actively retract away from injury site, nad also a physical barrier forms in spinal cord that htey would have to bridge. |
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Term
| jinjury to axon, myelin is cleared, and inhibitory factors disrupt axone xtension |
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Definition
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Term
| neonate s. adlt cns injury resposne |
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Definition
| neonates regenerate ,adults dont (PNS DOES grow) |
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Term
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Definition
| schwan cell regenrate and leave pathwaybeidn for axonsto follow |
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Term
| sciatnic nerve grafts induce axonal regenratino (in cns) |
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Definition
| so it is not neurons that stop learning hwo to go , it is related to the environment |
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Term
| cant regenreate through glial scar , matrix moelcules in glial scar: |
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Definition
| condroid sulfate is inhbiitory, NogA , myelin asosciated glycoprotein and oligodendroy myelin glyocorporein are inhiityor,proteoglycans are inhibitory as well. |
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Term
| apprcahces to recent spinal injury |
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Definition
| biochemic al o overocme inhibitory factors, ceullar substrates for axonal regen or as cell replacement therapy. management of inflammatory respoe |
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Term
| NOGo and growth inhbition |
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Definition
| Nogo is foudn on oligodendoryctes and has receptos on neurons .when neurosn get injured they increase bindign to NOgo- however NOGO has no signal trandsduction capabilties on its own, so therei s ac orepceptor for p75NTR. thsi combiantion eladsto activation of RhoA(?). iNbhition of this process least o increased sprouting (i.e.antibodies)- funtional recovery. |
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Term
| cellular therapies for spianl injury |
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Definition
| to providesubstrate for axonal regneration or remyelination |
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Term
| Human embyryonic stemm cells transplants in to spinal cor dinjury |
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Definition
| differeitnate itno glial cels (oligodendroscyte precursors) and increase remyelination as compared to control, and increased locomotory recovery. Also olfactory ensehating celsl are antoehr possible therapy |
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Term
| central plasticity of SCI |
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Definition
| as a aresutl of the injury, if spinal cord is injured, the central nervous system (particularly in cortex), have ability to reorganize themselves to recover function. |
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Term
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Definition
| found in increased levels in nfl players nad pro boxers |
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Term
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Definition
| Alzheimers protein. ALso assocaited with diffsue axoal injur7 |
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Term
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Definition
| grwoth inhibitory molecule |
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Term
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Definition
| grwoth inhbiitory molecule |
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Term
| myelin associated glycoprotein |
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Definition
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Term
| Olidogendrocyte myelin glycoprotein |
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Definition
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