Clinical Neuropsychology L7

partial or complete memory loss

- Surgery to relieve epilepsy in 1953 (27-y-o)- Bilateral medial-temporal lobe resection- Less frequent seizures, but severe amnesia- Unable to acquire new memories- Impaired spatial and topographic learning- Sparse learning of new words, events, people- Able to learn new motor skills

Long term moemory:

Explicit

Implicit

Emotional

Short term memory

Anterograde amnesia

Retrograde amnesia

Symptom of clinical conditions (e.g. Alzheimer disease, Korsakoff disease)

Traumatic Brain Injury (TBI)

Childhood Amnesia

Fugue state

Specific amnesias

• Problems with storage of new information in LTM ("consolidation")• Important role of medial temporal lobe (hippocampus and adjacentlimbic cortex)

• Problems with retrieving information from existing LTM• Important role of posterior parts of association cortex (temporal, parietal, occipital): storage of memory representations

– Time-dependent retrograde amnesia– Impairment prospective memory (e.g. keeping an appointment = anterograde amnesia)– Destination memory (past interactions: e.g. to whom we have told our a story)

– Inability to remember events from ~<4 years, few events 7-11 years– Role hippocampal neurogenesis? (Form new memories, disrupt already acquired circuits)

– Memory loss of personal history, sudden and usually transient– Korsakoff syndrome similar: confabulations

– E.g. only forget nouns (and not verbs), or only forget fruits (and not e.g. animals)

Episodic (autobiographic) memory

Semantic memory

time- and place-locked– Depends on ability to mentally displace oneself in time– Important role of medial temporal lobe (including hippocampus),ventral prefrontal cortex, and connection between these areas

specific facts (e.g., persons, events) and general knowledge (e.g., language, arithmetic)– Important role of temporal, posterior parietal, and occipital cortex

• Motor and cognitive skills (e.g., grammar rules, categorizing)• Daily habits• Classically conditioned responses• Priming (faster recognition of stimuli following earlierpresentation; relies on activation of immediate (i.e., short-term)memory within sensory cortical areas)

like implicit memory acts "bottom-up": emotional associations are automatically elicited by a stimulus or memory item ("cue")

Both types of memory function are relatively independent of each other, as apparent from studies in patients

Learning is a property of brain functions in general and may thus occur everywhere in the brainThere are thus many types of learning and memory

Lesions causing amnesia may have wide range of causes: a.o. traumata, infections, intoxications, degeneration (dementia)

Consolidation is necessary to store information as an explicit memory

Hippocampus

Paralimbic cortex (perirhinal, entorhinal, parahippocampal)

Amygdala

Prefrontal cortex

Medial thalamus

Important for consolidation of types of explicit memory, (spatial context is particularly important for episodic memory!)

Consolidation more severely affected by hippocampaldamage than retrieval  relate this to anterograde/retrograde amnesia!

Episodic (autobiographical) memory more affected thansemantic memory; ‘time travel’ (to past and future) isdiminished

“Interface” hippocampus - neocortex

Important for consolidation of episodic and semanticmemory information

crucial for emotional memory. It is responsible for emotional ‘coloring’ of new stimuli or events that are stored in memory

involved in encoding and retrieval of episodic and semantic memory

- Left PFC involved in encoding > retrieving semantic and episodic info- Retrieving episodic info right PFC > left PFC

important for consolidation in general. Increased connectivity with PFC and hippocampus during consolidation ->  Wernicke-Korsakoff syndrome

There is evidence that consolidation is not always permanent:– Information retrieved from LTM may be influenced by newexperiences– And may in a modified form be stored again in LTM (reconsolidation), sometimes in other locations

• R-sided lesions: on average more problems with nonverbal material (like faces, objects, spatial locations, maze learning tasks, geometrical figures, tones/melodies)• L-sided lesions: on average more problems with verbal material (like stories, words, numbers)

topographic amnesia (memory loss for spatial locations of objects and their relationships;)

- Acetylcholine (Ach) systems: cholinergic projections from nuclei in the basal forebrain (also see CH 5)- Serotonin (SE) and noradrenalin (NA) systems: projections from nuclei in the brainstem

often loss of neurons in cholinergic, serotonergic and/or noradrenergic systems (CH 5). E.g., Alzheimer’s disease

Degenerative form of dementia with progressive loss of cells/synaptic connections; cause lies within CNS

prominent damage to: (medial) temporal lobe

association areas are primarily affected

- Posterior parietal; spatial memory, spatial orientation, apraxia- Inferior temporal; object and face recognition as well as memory-> Limbic cortex (especially entorhinal); STM and LTM (mainly episodic)- Primary sensory and motor areas are spared for a relatively long time.

Initial loss of explicit memory, but later on, also loss of implicit memory (all kinds of daily life skills).

1. Anterograde amnesia in the earlier stages: initial degeneration of the medial temporal lobe (entorhinal cortex, hippocampus)2. Retrograde amnesia due to inevitable degeneration of the lateral temporal cortex, other parts of the posterior association cortex and frontal cortex in the later stages of the disease.

produces serious retrograde amnesia (effects on lateral temporal cortex and insula) and anterograde amnesia (effects on medial temporal lobe: hippocampus and paralimbic cortex)

- Established musician- 30-second episodic memory (‘just awoke’)

produces serious retrograde amnesia (effects on lateral temporal cortex and insula) and anterograde amnesia (effects on medial temporal lobe: hippocampus and paralimbic cortex)

(due to chronic alcoholism): complete anterograde amnesia and increasing retrograde amnesia

Characterized by confabulation, apathy, and indifference

Damage in medial thalamic nucleus (/mamillo-thalamic tract) together with general cerebral atrophy (particularly frontal) due to vitamin B1 (thiamine) deficiency

 Classical conditioning of– Motor responses: role of cerebellum– Emotional responses: role of amygdala Priming: role of primary and secondary sensory cortex

- Subject remembers practicing, but does not get better at the task- In contrast with case H.M. (anterograde amnesia), who would not remember practicing but would get better at the task.

amnestic subjects (explicit) perform on a similar level as control subjects.

Can have explicit and implicit properties!Evoking negative emotions in fear conditioning -> relies on different parts of the brain than non-emotional (e.g. motor) conditioning (both Pavlovian)

Amygdala damage abolishes emotional memory, but not implicit orexplicit memory

– Temporal or parietal association areasDependent on type of damage, problems may be modality-specific(for example, auditory or visual) or may be related to verbal or non-verbal material– Different regions of prefrontal cortex, having specific effects onworking memory (working memory is important type of STM)

Prefrontal cortex is involved in working memory for (a) identity ofobjects, (b) their spatial location, and (c) the order of presentation