College 1 (H2)
Behavioural symptoms
variables objectively assessed through tests + subjectively overserved by patient and significant others
Organicity
former term for brain damage or dysfunction
- vroeger: “Is there a hole in the brain?”
Later: hypothesis → testing theories about cognitive functioning
- “It’s not about the hole, it’s about the doughnut!” → it’s not about the damage of the brain, it’s about
assessment, treatment and care of individuals with cognitive (dys)functions as a result of brain
disorders
Clinical neuropsychology
applied science that studies relationship between brain (dys)functions and behaviour in patients and
application in assessment and treatment
1. Brain (dys)functioning
2. Contextual factions
- psychosocial, developmental, somatic (pain), performance validity
3. Everyday functioning
- home, social, work / study, family...
Clinical neuropsychology
- has become highly relevant in modern-day (mental) health care
- increase in people with brain damage or dysfunction:
1. decrease in mortality because of improvements in medical care
2. aging
3. more interest in quality of life
→ clinical neuropsychologist is scientist practitioner whose focus lies on behavior and cognition
→ clinical neuropsychologist is not brain researcher
International Classification of Functioning (ICF)
- description of consequences of brain disease / disorder
at 3 different levels:
- impairment, limitation, restriction (‘handicap’)
- identifying moderating factors
- relevant for understanding subjective complaints and
problems in daily life (school, work, social functioning)
- identifying target treatment or optimalisation
Diagnostic cycle
- analysis of complaints →
- interview with patient and informant
- analysis of problems →
- tests
- diagnosis →
- indication for treatment →
Neuropsychological methode
Before
- referral question →
- medical file and history →
,Testing
- clinical interview patient →
- interview significant others →
- formulating hypothesis →
- test selection and administration →
- behavioural observations →
After
- interpretation all test data →
- reporting
Confounding factor
element that affects test performance but doesn’t fall within measurement objective of a test
- underperformance = patient’s performance is impaired compared with what they would be able to
achieve if they were to make a normal effort → notice when:
- inconsistencies within test profile (e.g. higher scores on harder tasks)
- striking discrepancy between behavioural observations and test performance
- most of patient’s complaints are not in relation to severity of disorder
College 2 (H18)
The Atkinson-Shiffrin Memory Model (1968)
Memory
- Working memory = short-term memory
- Long-term memory
- declarative memory (explicit; consciously accessible)
- episodic memory → what, where, when
- semantic memory → general knowledge
- non-declarative memory (implicit)
- priming
- procedural learning
- conditioning
- habituation
Neuroanatomical structure involved in memory processes
- prefrontal cerebral cortex → working memory
- hippocampus → long-term storage; consolidation
- parietal cortex → long-term storage
Baddeley’s model of working memory (1974)
Working memory is split up into three parts (1&2 = short-term memory):
1. phonological loop
2. visuo-spatial sketchpad
3. central executive
, - limited (but no fixed) duration (seconds)
- limited capacity (visuospatial sketchpad and phonological loop); approximately 7 units
- active processing (CE) of info in short-term memory
- working memory linked to long-term memory (two-way communication)
The dorsolateral prefrontal lobe
- working memory → maintenance of info (short-term memory) &
- central executive → active processing of info
Characteristics of working memory:
- temporary
- limited capacity (7 +/- 2 chunks = cluster of information)
Transition from working memory tot long-term memory
- how is transition from working memory (prefrontal) to long-term memory (LTM) achieved?
- info must be permanently stored → episode formation
- memory binding = associative working memory → recall an event as a whole, not all the individual
information streams
- episodic buffer: involved in LTM encoding
- also involved in retrieval of previously encoded knowledge
Episodic memory formation: consolidation
After memories have been bound, consolidation (= long-term storage) takes place → two major theories:
1. Standard consolidation model (Squire & Alvarez, 1995)
- after encoding → info retained in hippocampus and neocortex
- info recall strengthens the cortico-cortical connections
- making memory hippocampus independent → don’t need hippocampus anymore once
memories are permanently stored in neocortex
2. Multiple trace theory (Nadel & Moscovitch, 1997)
- based on distinction semantic and episodic memory
- hippocampus always involved in retrieval and storage of episodic memories (even for very old
autobiographical memories)
- semantic memories stored in neocortex
Medial temporal lobe including the hippocampus
- encoding new knowledge → long-term encoding (which can already take place during short-term tasks)
- contextual info → formation of ‘episodes’ in the memory (place, time, etc.)
- ‘binding device’ → linking item memory (the content) to source memory (the source): ‘what, where
and when’
- consolidation → long-term storage
- disorder: anterograde amnesia (amnesic syndrome) → no longer able to form long-term episodic
memories
Two forms of amnestic syndromes:
1. Hippocampal temporal amnesia
- impaired encoding / consolidation of facts
- no confabulation (= type of memory error in which gaps in memory are unconsciously filled with
fabricated, misinterpreted or distorted info) or memory-monitoring problems
- intact working / short-term memory
- content (all memories) gets lost rather than the context (what, where, when)
- can arise after encephalitis, hippocampectomy or traumatic brain injury
, 2. Diencephalic amnesia
- sudden onset after Wernicke-Korsakoff syndrome → Wernicke syndrome:
- gait ataxia +
- eye movement disorder +
- confusional state
- frontal + diencephalic damage (mammillary bodies and thalamus) as result of chronic thiamine
deficiency (vitamin B1)
- B1 deficiency often caused by chronic alcohol abuse in combination with poor nutrition
- vitamin deficiency can result by other means → anorexia, pregnancy
Characteristics:
- personality changes with irritability or apathy
- confabulation and lack of insight
- executive dysfunction → problems with high-order cognitive processes (planning, organizing …)
+
Amnestic syndrome characterised by:
- anterograde amnesia = onvermogen nieuwe herinneringen te vormen vanaf moment dat
geheugenverlies begint
- retrograde amnesia = geheugenverlies waarbij iemand geen toegang meer heeft tot herinneringen
van vóór geheugenverlies begon, with temporal gradient (= events occurred in recent years are
remembered most poorly & memories of events in distant past are relatively intact) in autobiographical
memory
- retrieval problems (executive as well)
- contextual memory → problems with placing memories in time; info is there, but details are lost
- increased sensitivity to interference (proactive and retroactive)
- proactive interference = old memories disturb new memories
- retroactive interference = recent memories disturb older memories
Korsakoff’s syndrome
alcohol-induced major neurocognitive disorder (amnestic-confabulatory type) which involves impairment of
ability to learn new info or to retrieve previously learned info
- significant impairments in social or professional functioning + significant decline in relation to previous
level of functioning
- memory deficits should not be result of delirium or dementia only + remain present for longer than
usual during intoxication or alcohol withdrawal
- indirect consequence of alcohol use: residual deficit of long-term thiamine (B1) deficiency as a result of
AUD
- severe B1 deficiency may cause Wernicke’s encephalopathy = acute neuropsychiatric
syndrome characterised by ataxia, nystagmus, ophthalmoplegia, confusion and apathy
Neuropathological abnormalities
- microbleeds mainly found in mammillary bodies, thalamus (particularly mediodorsal nucleus) and
various structures around 3rd and 4th ventricles
- Wernicke’s encephalopathy is reversible with timely intervention with B1 supplementation → but:
80-90% develop Korsakoff’s syndrome (not reversible)
Reminiscence bump
effect dat men meer persoonlijke gebeurtenissen herinnert uit de tienerjaren dan uit andere periodes in het
autobiografisch geheugen → verklaringen:
- ‘neural optimum’
- many life events to remember
- first encounters: ‘novelty effect’
