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38 Cards in this Set
- Front
- Back
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Types of Memory
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1)Sensory Store
2)Working Memory 3)Long-Term Memory |
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Sensory Store
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1)Iconic Store
2)Echoic Store 3)Haptic Store 250-500msec |
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Working Memory
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-Holds 7+-2
1)Central Executive: directs attention toward 1 stimulus or another & determines which items will be stored in memory 2)Phonological Loop: stores auditory info & words 3)Visuospatial Sketchpad: stores visual info |
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Long-Term Memory
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1)Explicit-conscious & intentional remembering
-1.Semantic-recall of general facts -2.Episodic-recall of an event or episode 2)Implicit-unconscious & unintentional remembering -priming, emotional response, muscular skeletal, procedural memory 3)Declarative-recall of factual info 4)Nondeclarative-recall of procedures |
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Theories of Forgetting
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1)Decay Theory
2)Interference Theory 3)Context Theory |
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Decay Theory
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-Predicts that older memories will always be more decayed than newer memories
-All memories decay at the same rate --some start out stronger than others -Problem:Time is a poor explanation |
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Interference Theory
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1)Retroactive Interference - New memories interfere with old memories
2)Proactive Interference - Old memories interfere with new memories |
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Context Theory
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1)Environmental context
2)State dependent context (mood & drugs) 3)Interpretation of context changes |
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Retrograde Amnesia
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-Forget what you used to know
-Temporal gradient -Intact implicit memory |
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Anterograde Amnesia
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-Unable to form new memories
-more common -'frozen in time' -Intact implicit memory |
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Global Amnesia
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-case of H.M.
-Damaged hippocampus, amygdala, entorhinal cortex -Intact working memory & intact implicit memory -Disrupted long-term memory -Memory isn't unitary construct -poor explicit memory except childhood memories -Memory is independent of other higher order functions --no overall loss of cognitive functioning -Trouble with new long term declarative memories - learning new facts -Can form new procedural memories |
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BioBasis of Memory
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Hippocampus
-Anterograde Amnesia --Gateway to permanency-- consolidation of memories -Damage impairs recent learning, more than older ones -Reverberating circuit - self-exciting loop of neurons -Emotionally charged memories consolidate quick (role of amygdala) -Basal forebrain--Acetylcholine -Thalamus-Retrograde Amnesia |
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Dementia
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Impairment of memory & at least 2 other areas of cognitive domains which should be severe enough to interfere with ADL's & not due to physical effects of stroke
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Dementia: Cortical
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Degenerative
-Alzheimer's Disease(50% of all) -Lewy Body Dementia |
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Dementia: Subcortical
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Degenerative
-Parkinson's Disease -Huntington's Disease -Wilsons Disease |
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Alzheimer's Disease
Deficits |
-Memory-Working & recent memory are disrupted
--intact remote & implicit -Language-Anomia-1st sign-Word Finding problems |
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Alzheimer's Disease
Other Deficits |
1.Agnosia-visual spatial problems
2.Executive Functioning-problem solving, abstract thinking, comprehenision 3.Apraxia-motor signs are rare but progressive 4.Behavioral Disturbances- -Early=Apathy -Late=Irritability -Delusions=capgras syndrome -Depression-not precursor |
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AD: Neuropathology
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1)Plaques-formed from degenerating axons & dendrites - accumulates in space between neurons - produced by Amyloid
2)Neurofibrillary Tangles- Formed from degenerating structures within neuronal cell bodyes - Produced by Tau 3)Neuronal Loss- -Curcumin-(in yellow die & curries) Reduced Amyloid levels & Plaques Brain Structures:Hippocampus, Basal Forebrain & frontal, temporal, parietal lobes Neurotransmitters: Acetylcholine & norepinephrine & serotonin |
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AD: Epidemiology
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Relationships
-Gender biases -Race-african american, white -Lower SES -Less education-verbal intell. -lifestyle -diet, stress Indirect Relationships -aluminum -hormone imbalance -estrogen -oxidative stress -inflammatory processes -viruses AGe -1% at 65 -3-10% between 66-74 -20% between 75-84 ->20% at 85+ Genetics-unknown-APOE gene? |
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Mild Cognitive Impairment
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-Transitional stage between cognitive changes of normal aging & more serious problems caused by AD
Characteristics -Aware of deficits -1 cognitive domain -doesn't interfere with social/occupational function Types -MCI Amnestic -MCI multiple cognitive domain -MCI single non-memory domain "Risk "State" |
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Other Forms of Dementia
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1)Vascular Dementia
2)Lewy-Body 3)Kosakoff's Amnesia -STM may be normal -Progressive-Neurological Problems=Peripheral Neuropathy & Gait imbalance -Occurs from: Thiamine deficiency, alcohol abuse (5%) 4)Frontotemporal Dementia(Pick's Disease) |
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Korsakoff's
Symptoms & Brain Structures |
1)Memory Deficits
-Intact implicit memory -Confabulations with familiar memories -No spontaneous conversation -Apathy -Poor insight into deficits -Atrophy of frontal lobes Brain Structures -Mammillary Bodies in Hypothalamus -Dorsomedial Nucleus at Thalamus -Axons to Prefrontal Cortex |
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Long-Term Potentiation
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Plasticity
1)Synapses activated at high frequencies 2)Leave synapses more responsive to new input 3 Properties 1.Specificity-Only active cells become strengthened 2.Cooperativity-Simultaneous stimulation produces stronger long-term potentiation 3.Associativity-Pairing weak input with strong input enhances later responses to weak input -Prominent in hippocampus |
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Lateralization of Functions
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1)Lateral Symmetry
2)Contralateral Mediation -Motor Functions -Right hemisphere controls left side of body & vice versa 3)Commisural Fibers - connects hemispheres - corupus callosum |
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Corpus Callosum
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-Commissurotomy
-disconnect hemispheres -disconnection syndrome - between perception, comprehension, & response |
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Cerebral Dominance
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Left Hemisphere
-Analytical thought, logic, language, math & science - Intentional control of expression Right Hemisphere -Holistic thought, intuition, creativity, art & music - Emotional Arousal |
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Broca's Aphasia
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Language Production
-Nonfluent Aphasia -Inability to produce meaningful speech -Location of grammar -Loss of fluent speech - impaired use & understanding or prepositions, word endings, & other grammar -Difficulty speaking & writing & grammar -Also show comprehension deficits -<50% with lesions in area had Broca's Aphasia |
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Wernicke's Aphasia
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Language Comprehension
-Fluent Aphasia -Dissociation between words and meaning -location of meaning -poor language comprehension & difficulty remembering names of objects -trouble understanding speech & recalling names of objects -10% develop aphasia with lesions |
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Dyslexia
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Specific impairment of reading in a person with adequate skills in other academic areas
-Most common learning d/o in US Brain Structures: 1)Underactivation of Angular Gyrus & Wernicke's Area 2)Decreased volume in Broca's Area -activation in right hemisphere |
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ADHD - Genetics
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90%
-high heritability -higher rate if mom smoked 1)Neuroanatomical 2)Neurochemical 3)Brain Trauma 4)Genetic Origin 5)Environmental Factors |
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ADHD types
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1)Inattentive
2)Hyperactive 3)Combined 4 Types 1.Focused Attention 2.Sustained Attention(vigilance) 3.Divided Attention 4.Alternating Attention(shifting) |
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ADHD - Bio Basis
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95% of normal brain volume
-Smaller cerebellum -Smaller prefrontal cortex Neurochemical -Dopamine -Norepinephrine Delay of Reinforcemnt |
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Schizophrenia
-Neurodevelopment Hypothesis |
-Based on abnormalities in the prenatal or neonatal development of the nervous system, which lead to subtle abnormalities of brain anatomy & major abnormalities in behavior
-later stress may aggravate symptoms but don't cause them |
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Schizophrenia
-Brain Abnormalities -Neurodevelopment |
1)Enlarged Ventricles
2)Smaller Prefrontal Cortices -Less gray matter -Hypofrontality-diminished executive skills --Causes: -Seasonality Effect - winter -Viral Illness -Famine Related:Thiamine deficiency, toxin build up -Larger ventricles |
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Schizophrenia
Dopamine Hypothesis |
Too Much Dopamine
-Positive Symptoms -dopamine agonist & antagonist -More dopamine receptors -Results from excess dopamine at dopamine synapses in certain brain areas -Twice as many D2 receptors |
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Schizophrenia
Glutamate |
-Less than normal glutamate release (especially in prefrontal cortex)
-Stimulating NMDA receptors trigger insertion of dopamine receptors into membrane --Integration Theory -Prefrontal hypoactivity produces hyperactivity of dopamine in nucleus accumbens -Cure--Glycine? -Increased dopamine produces same effects as decreased glutamate |
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Depression
-Sleep patterns |
-shallow sleep
-reduced stage 3 & 4 -Fragmented:Awaken frequently -More REM sleep - enter within 45min & have more eye movements Treatment: -Sleep deprivation |
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Depression & Genes
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-Family has 10X increase in chance
-Twin = 70% -Two short alleles associated with increased likelihood of depression after stressful events (only found in 10%) -Two long Forms: --More likely to respond to antidepressants --More likely to respond to placebo --Better outcome |
