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Ed psych Chapter 13

by: Caoimhe Notetaker

Ed psych Chapter 13 Psyc3200

Marketplace > Tulane University > Psychlogy > Psyc3200 > Ed psych Chapter 13
Caoimhe Notetaker
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Chapter 13 notes
Educational psychology
Sarah Grey
Class Notes
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This 10 page Class Notes was uploaded by Caoimhe Notetaker on Tuesday November 17, 2015. The Class Notes belongs to Psyc3200 at Tulane University taught by Sarah Grey in Summer 2015. Since its upload, it has received 15 views. For similar materials see Educational psychology in Psychlogy at Tulane University.


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Date Created: 11/17/15
Chapter 10: brain damage and neuroplasticity 11/17/2015 ▯ Causes of brain damage: ▯ Brain tumors  Tumors= mass of cells that grows independently of the rest of the body  20% meningioma’s (grow between meninges) are encapsulated tumors and almost always benign  Most brain tumors are infiltrating tumors (grow diffusely through surrounding tissue) usually malignant (difficult to remove and any remaining tissue continues to grow)  Gliomas (brain tumors that developed from glial cells) are infiltrating, rapidly growing, and common  Metastic tumors- grow from infiltrating cells that are carried to the brain o Many originate as lung cancer ▯ Cerebrovascular disorders: STROKES  Strokes= sudden onset of cerebrovascular disorders that cause brain damage  3 leading cause of death in US  Symptoms dependent on area of brain effected  But common consequences include o Amnesia o Aphasia o Paralysis o Coma  Infarct: area of dead of dying tissue produced by stroke  Penumbra: surrounding infract, dysfunctional area of brain  Two major types of strokes 1. Results from cerebral hemorrhage (bleeding in brain) o Occurs when cerebral blood vessels ruptures and blood seeps to surrounding neural tissue o Bursting aneurysm  Aneurysm can be congenital (present at birth) or can result from exposure to vascular poisons and infections 2. Results from Cerebral Ischemia o Disruption of blood supply to an area of brain o Main causes= thrombosis, embolism, arteriosclerosis o Takes a while to develop brain damage o Does not occur equally in all parts of brain (hippocampus is highly susceptible) o Glutamate plays a certain role in stroke induced brain damage  When blood vessel is blocked, blood deprived neurons become overactive and release excessive quantities of Glutamate which over activates glutamate receptors in membrane of post synaptic neurons (Most NMDA) which results in large numbers of Na+ and Ca2+ ions to enter post synaptic neurons which…  Triggers release of excessive glutamate (perpetuate cycle)  Trigger internal reactions that ultimately kill post- synaptic neurons  Possibility of preventing stroke-related brain damage by blocking glutamataminergic cascade ▯ Closed Head Injuries  Contusion- involves damage to the cerebral circulatory system o Produces hemorrhaging and results in a hematoma o Skull hardness is a major factor in development of contusions o Often occurs on side opposite to blow- contrecoup injuries  Concussion- disturbance of consciousness but no evidence of contusion o Punch- drunk syndrome= dementia and cerebral scarring observed in those with repeated concussions ▯ Infections of the brain  Encephalitis- inflammation resulting from brain infection  Bacterial infection o Lead to formation of cerebral abscesses, meningitis o Syphilis- dormant for several years before coming virulent and attacking many parts of body, including brain. Results in General paresis (insanity and dementia)  Viral infections o Rabies- particular affinity for nervous system  Lethal effects on brain but doesn’t usually attack brain for at least 1 month o Mumps/herpes- can attack nervous system but don’t have to.  Doesn’t always (or often) attack brain ▯ Neurotoxins  Nervous system can be damaged by exposure to any one of a variety of toxic chemicals toxic psychosis  Tardive dyskinesia (TD) motor disorder, symptom of drug used in 1950s to treat neurological disorders ▯ Genetic factors  Caused by abnormal recessive genes  Or genetic accident (down syndrome) o Accident occurs during ovulation, more likely in older mothers ▯ Programmed cells death  All types of brain damage produce neural damage by activating apoptotic programs of self destruction  Semi-damaged cells may attempt to commit suicide  A lot of neuron death following brain damage is necrotic  Apoptotic is better- gradual process, no inflammation and not likely to damage near by cells ▯ Neurological Disorders ▯ Epilepsy  Primary symptom= seizure; repeatedly generated by their own chronic brain dysfunction  1% of population  Types of seizures 1. Convulsions (motor seizures)  Involve tremors (clonus) and rigidity (tonus) and loss of balance and consciousness *Not all seizures take this form. Many involves subtle changes of thought mood or behavior that is not easily distinguishable from normal ongoing behavior  All previously mentioned causes of brain damage can lead to epilepsy  Over 70 faulty genes have been linked to epilepsy  Faults in inhibiting synapses  Diagnosis rest heavily of EEG- high amp EEG spikes  Epileptic auras- psychological changes right before attack o Nature of auras linked to location of epileptic focus o Warns individual of oncoming attack  Once diagnosed with epilepsy it is usual to assign to one of two general categories (partial or generalized) then to one of respective subcategories o Such different types lead many to believe it is better to think of epilepsy not as one single disease but as many related diseases  PARTIAL o Doesn’t involve entire brain o Behavioral symptoms depend on where discharges begin and where they spread o Not usually total loss of consciousness or equilibrium o Simple  Sensory and/or motor o Complex  Temporal lobes  Automatism  GENERALIZED o Involve entire brain, either simultaneously or spread to whole brain o Tonic Chronic seizure- loss of consciousness and equilibrium and tonic-clonic convulsions  Tongue biting, urinating, and cyanosis  Hypoxia (shortage of O2 to tissue) white itself can be damaging o Absence seizure: no convulsion, a cessation of ongoing behavior (a vacant look)  EEG- bilaterally symmetrical 3 per sec spike and wave discharge  Most common in children, tend to cease at puberty **No cure- frequency and severity can be decreased for some people with medication. Brain surgery in very serious cases ▯ Parkinson’s  Movement disorder of middle/old age  Affect 1%-2% of elderly population  More prevalent in men  Symptom can start mild (slight stiffness or tremor) but increase with age  Symptoms of full blown disease= tremor during inactivity, trouble initiating movement  Thought of as “thinking people trapped in bodies they cant control”  Associated with widespread degeneration but specifically substantia nigra (midbrain)  Results from a decrease in dopamine o L Dopa can delay symptoms but not long term solution o Deep brain stimulation= controversial short term treatment with serious side effects ▯ Huntington’s disease  Progressive motor disorder  1/10000  Simple genetic bases and always associated with dementia  1 signs = increased fidgeting and develops into jerky movements of entire limbs  Incapable of feeding themselves, controlling bowels, or recognizing children  No cure; death usually occurs about 15 years after 1 signs  Passed by single mutated dominant gene st  Continues to be passed on because 1 symptoms don’t appear until after child has been born  There IS a test to find out ▯ Multiple sclerosis  Attacks myelin of axons in CNS  Typically attacks young people about to begin adult life st  1 - microscopic areas of degeneration on myelin sheath, eventually axons become dysfunctional and degenerate  Autoimmune disorder  Nature and severity of disorder depend on number, size and position of sclerotic lesion  Can be periods of remission  Symptoms= visual disturbances, numbness, tremors, ataxia, cognitive deficits and emotional changes  Increased role of genetic factors (as compared to most diseases)  immuno-modulary drugs- widely used, slight benefits ▯ Alzheimer’s  # 1 cause of dementia  1-% of people over 65  Early stage= selective decline in attentions, personality changes  Intermediate stages= confusion, irritability, deterioration of speech  Late stages= difficulty swallowing and control of bladder  Cant get a definitive diagnosis till autopsy  Defining characteristics o Neurofibrillary tangles o Amyloid plaques o Micro bleeds *Not sure which is primary—currently think amyloid plaques  Part prevalent in medial temporal lobe (amygdala, hippocampus) – memory  And inferior temporal, posterior parietal, and prefrontal—mediate cognitive function  Major genetic component ▯ Animal models of human neurological disease  Even best animal models display only SOME of the features of the disease they are modeling  Kindling model of epilepsy  Transgenic mouse model of Alzheimer’s  MPTP model of Parkinson’s ▯ Responses to nervous system damage  Neural degeneration o Cutting axons result in  Anterograde degeneration: degeneration of distal segment  Occurs quickly after axotomy  Retrograde degeneration: degeneration of proximal segment  In 2-3 days changes become apparent o Early degeneration changes suggest death of neuron o Early regeneration indicates involvement in massive protein synthesis- replace axons o Transneural degeneration- degeneration spreads from damaged neurons to neurons  On which they synapse- anterograde  That synapse on them- retrograde  Neural regeneration o Regrowth of damaged neurons o Regeneration is virtually nonexistent in CNS of adult mammals- limited to PNS o Regrowthstsually beings 2-3 days after axonal damage  1 – if original Schwann cell myelin sheaths remain intact- regenerating peripheral axons grow through them  2nd if peripheral nerves is severed regenerating axon tips grow in incorrect sheaths which are guided to incorrect destinations  3 if cut ends becomes widely separated non meaningful regeneration- neurons dies  Something about PNS environment promotes regenerations  Schwann cells- release stimulating neurotrophin factors  Neural reorganization o In lab animals  Studied under 2 conditions  Damage to peripheral  Damage to cortical areas o In humans  Findings= consistent with hypothesis that there is continuous competition for cortical space by functional circuits  Without visual input there is an expansion of auditory/somatosensory cortex  Two mechanisms account for reorganization  A strengthening of existing connections  Rapid reorganization to quick for neural growth never change more than 2 mm of surface  Establishment of new connections by collateral sprouting  Magnitude of long term reorganization  Recovery of function o Poorly understood bc improvements tend to be modest and there are other compensatory changes that can be confused with it o Recovery is most likely when lesions are small and patient is young o Cognitive resolve is thought to play a roles  Also used to explain why educated people are less susceptible to age related brain deterioration ▯ Neuroplasticity and treatment of CNS damage  Early transplant test were successful but unfortunately patients experienced bad side effects after a year  Extremely active research area today  Principle that neurons are in a competitive situation emerged  Designed rehabilitation based on this principle- constraint-induced therapy  Shown that people who are cognitively and physically active are less likely to contract neurological disorders  Enriched environments have been shown to increase dendritic branching, size and number of dendritic spines, size of synapse, rate of adult neuronogeneisis and levels of neurotrophic factors ▯ ▯


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