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Flashcards in Learning & Memory Deck (46):

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



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



Process by which retrieval cues interact with stored info during the reconstruction of info into memory



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