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38 Cards in this Set

  • Front
  • Back
Types of Memory
1)Sensory Store

2)Working Memory

3)Long-Term Memory
Sensory Store
1)Iconic Store
2)Echoic Store
3)Haptic Store

Working Memory
-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
Long-Term Memory
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
Theories of Forgetting
1)Decay Theory
2)Interference Theory
3)Context Theory
Decay Theory
-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
Interference Theory
1)Retroactive Interference - New memories interfere with old memories

2)Proactive Interference - Old memories interfere with new memories
Context Theory
1)Environmental context
2)State dependent context (mood & drugs)
3)Interpretation of context changes
Retrograde Amnesia
-Forget what you used to know
-Temporal gradient
-Intact implicit memory
Anterograde Amnesia
-Unable to form new memories
-more common
-'frozen in time'
-Intact implicit memory
Global Amnesia
-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
BioBasis of Memory
-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
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
Dementia: Cortical
-Alzheimer's Disease(50% of all)
-Lewy Body Dementia
Dementia: Subcortical
-Parkinson's Disease
-Huntington's Disease
-Wilsons Disease
Alzheimer's Disease
-Memory-Working & recent memory are disrupted
--intact remote & implicit

-Language-Anomia-1st sign-Word Finding problems
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-
-Delusions=capgras syndrome
-Depression-not precursor
AD: Neuropathology
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
AD: Epidemiology
-Gender biases
-Race-african american, white
-Lower SES
-Less education-verbal intell.
-diet, stress
Indirect Relationships
-hormone imbalance
-oxidative stress
-inflammatory processes
-1% at 65
-3-10% between 66-74
-20% between 75-84
->20% at 85+
Genetics-unknown-APOE gene?
Mild Cognitive Impairment
-Transitional stage between cognitive changes of normal aging & more serious problems caused by AD
-Aware of deficits
-1 cognitive domain
-doesn't interfere with social/occupational function
-MCI Amnestic
-MCI multiple cognitive domain
-MCI single non-memory domain

"Risk "State"
Other Forms of Dementia
1)Vascular Dementia
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)
Symptoms & Brain Structures
1)Memory Deficits
-Intact implicit memory
-Confabulations with familiar memories
-No spontaneous conversation
-Poor insight into deficits
-Atrophy of frontal lobes
Brain Structures
-Mammillary Bodies in Hypothalamus
-Dorsomedial Nucleus at Thalamus
-Axons to Prefrontal Cortex
Long-Term Potentiation
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
Lateralization of Functions
1)Lateral Symmetry
2)Contralateral Mediation
-Motor Functions
-Right hemisphere controls left side of body & vice versa
3)Commisural Fibers - connects hemispheres - corupus callosum
Corpus Callosum
-disconnect hemispheres
-disconnection syndrome - between perception, comprehension, & response
Cerebral Dominance
Left Hemisphere
-Analytical thought, logic, language, math & science - Intentional control of expression

Right Hemisphere
-Holistic thought, intuition, creativity, art & music - Emotional Arousal
Broca's Aphasia
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
Wernicke's Aphasia
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
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
ADHD - Genetics
-high heritability
-higher rate if mom smoked
3)Brain Trauma
4)Genetic Origin
5)Environmental Factors
ADHD types
4 Types
1.Focused Attention
2.Sustained Attention(vigilance)
3.Divided Attention
4.Alternating Attention(shifting)
ADHD - Bio Basis
95% of normal brain volume
-Smaller cerebellum
-Smaller prefrontal cortex
Delay of Reinforcemnt
-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
-Brain Abnormalities
1)Enlarged Ventricles
2)Smaller Prefrontal Cortices
-Less gray matter
-Hypofrontality-diminished executive skills
-Seasonality Effect - winter
-Viral Illness
-Famine Related:Thiamine deficiency, toxin build up
-Larger ventricles
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
-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
-Increased dopamine produces same effects as decreased glutamate
-Sleep patterns
-shallow sleep
-reduced stage 3 & 4
-Fragmented:Awaken frequently
-More REM sleep - enter within 45min & have more eye movements
-Sleep deprivation
Depression & Genes
-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