Learning & Memory Flashcards
Phonological loop (Baddeley)
Repository for verbally encoded items combined with rehearsal mechanism which recycles verbal material to refresh memory tract
Medial temporal lobe amnesia
Historically described as having preserved insight, increased rates of forgetting, limited RA, lack of confabulation Causes: axonia, limbic encephalitis, stroke, probably AD
Damage to what structure can lead to impaired implicit memory?
Basal ganglia
Dual code theory
Concrete words can be represented by an imaginal code & verbal code whereas abstract words give rise only to a verbal code
Lateral limbic circuit
Amygdala => dorsomedial nucleus of thalamus => orbitofrontal cortex => uncus => amygdala
Release from proactive interference
Improved memory performance for stimulus words following a shift in semantic category
Very poor encoding, delayed recall & recognition - this memory pattern is associated with
Impaired encoding & consolidation; B frontal lesions affecting orbitofrontal & medial frontal structures, medial diencephalic lesions, or B mesial temporal damage found in pts with severe TBIs or severe AD
Episodic buffer (Baddeley)
Temporary & limited capacity storage system that holds & integrates info of different modalities through linkage with LTM
Consolidation theory (Squire & Bayley)
Role of hippocampus is to consolidate new memories; newer memories are lost b/c they are still in the hippocampus, older memories have been consolidated
Transient global amnesia
Profound AA problems & variable profiles of RA, perhaps b/c of retrieval problems No obvious cause Assoc. w/ decreased perfusion to medial temporal or diencephalic regions
Organic amnesia
AA is severe; RA usu. temporally grade Causes include temporal lobe surgery, chronic alcohol abuse, brain injuries, anoxia/ischemia, encephalitis, epilepsy, tumor, CVA
Visuo-spatial sketchpad (Baddeley)
Retains visuospatial material in STM
How does the amygdala function in memory?
Believed to be involved in association a stimulus with a reward
Normal encoding, normal recall, impaired recognition - this memory pattern is associated with
Inattention/variable motivation, non-neurological memory impairment
Associative long-term potentiation
When weak & strong synapses to a single neuron are stimulated at approximately the same time, the weak synapses become strengthened
Anterograde amnesia
Impaired in conscious, deliberate recall of info initially learned after illness onset
Ribot’s law (of regression)
Vulnerability of memory loss to neurological insult is an inverse function of the age of the memories
According to Moscovitch, the following CNS structures mediate what aspects of memory performance? 1) Nonfrontal neocortical 2) Basal ganglia 3) Medial temporal/hippocampal 4) Central-system frontal lobe
1) perceptual & semantic modules maintaining performance on item-specific, implicit memory 2) performance on sensorimotor procedural tests 3) encoding, storage, retrieval on explicit episodic memory (things that are associative/cue dependent) 4) performance on strategic explicit & rule-based tests
Poor encoding, severe delayed recall impairment, & mildly impaired recognition - this memory pattern is associated with
Deficits of consolidation & rapid forgetting; initial stages of AD, B mesial temporal dysfx
Information-processing model of memory
1) Attention 2) Encoding 3) Storage 4) Consolidation (integrate new memories into cognitive/linguistic schema) 5) Retrieval
Multiple-trace theory (Nadel & Moscovitch)
3 kinds of memory: autobiographic memories, factual semantic memory, general somatic memory All are differentially susceptible to medial-temporal lobe injury Memories change w/ passage of time as they are recalled, reevaluated, & restored
Korsakoff’s syndrome
Severe anterograde amnesia, extensive impairment of remote memory, visuospatial & sensory processing deficits, lack of insight, apathy, intact incidental, semantic, or procedural memory B damage along the diencephalon midline, generalized cerebral atrophy
Elaboration
Memory process in which the products of initial encoding are enriched by further processing
3 patterns of retrograde amensia
Temporally limited: involves few yrs prior to onset of amnesia w/ relative sparing of more remote time periods Temporally-graded: affects all time periods, w/ greater impairment of memories in more recent past Nonspecific or pervasive: affects all time periods equally
3 components of Baddeley’s working memory model
Phonological loop, visualspatial sketchpad, central executive (and episodic buffer)
Normal encoding, poor recall, good recognition - this memory pattern is associated with
Deficits in retrieval; subcortical or vascular dementias
Poor initial encoding with appropriate improvement across repeated trials, variable recall, normal recognition - this memory pattern is associated with
Severe depression or anxiety
Implicit learning engages brain circuits involving
BG, prefrontal cortex, amygdala
Long-term potentiation
Strengthening of a synaptic connection that results when a synapse of one neuron repeatedly fires and excites another neuron, there is a permanent change in the recieving neuron, the excitatory neuron, or both
Bilateral diencephalic damage leads to
Global anterograde amnesia
Variable encoding, variable recall, good recognition - this memory pattern is associated with
Inefficient encoding w/ intact consolidation; dementias affecting the frontal lobes or etiologies affecting attention such as TBI
Diencephalic amnesia
Deficits in initial processing stages of memory; confabulation; sensitivity to proactive interference; lack of insight Causes: infarcts of the thalamic arteries, trauma, diencephalic tumors, Korsakoff’s
Explicit learning occurs largely in which structures?
Diencephalic, hippocampus & surrounding structures
Frontally-related amnesia
Attentional deficits, retrieval may be normal, unawareness of memory problems & tendency to confabulate are common
What is the role of the basal forebrain in memory
Nucleus basalis of Meynert sends fibers to various regions including the hippocampus, cerebral cortex; functions are disrupted in ACoA strokes & AD
Differences between temporal lobe amnesia & Korsakoff’s
TL: normal release from proactive interference Korsakoff’s: extensive loss of remote memory
Functional amnesia
Typically arises after psychological trauma AA does not usually occur, RA is extensive & frequently includes loss of personal identity
Encoding specificity principle
Retrieval of an event is a function of the overlap between the context of learning & that of the retrieval
Basic forms of learning
Perceptual, stimulus-response, motor, relational
Ecphory
Process by which retrieval cues interact with stored info during the reconstruction of info into memory
Equipotentiality
Lashley posits that memory impairment does not depend on localization of a lesion but on the amount of tissue damaged; any part of the cortex is equally able to perform tasks
Reconsolidation theory (Tronson & Taylor)
Proposes that memories will rarely consist of a single trace or neural substrate; each time a memory is used, it is reconsolidated
Central executive (Baddeley)
Acts as a supervisory system & controls flow of info from & to slave systems Capacity is limited, performance begins to break down as demands increase Proposed to be located in prefrontal cortex
Hebb Rule
If a synapse repeatedly becomes active at about the same time the postsynaptic neurons fires, changes will take place in the structure or chemistry of the synapse that will strengthen it. neurons that fire together wire together.
Atkinson & Shiffrin’s 3-stage model of declarative memory
1) sensory memory - holds memory for 1-2 sec 2) short-term memory - immediate memory, rehearsal, longer impermanent memories 3) long-term memory - relatively permanent storage of memory; requires alterations in neuron, synapse, elaboration of dendrite, etc.
Wernicke-Korsakoff syndrome
Classic triad of gait ataxia, oculomotor problems (nystagmus), confusion
