Aantekeningen Cognitieve Neuropsychologie
Lecture 1: Introduction
Before neuroimaging
- Measuring the size of the skull
- Systematic patient descriptions
- Application in psychiatry: development of theories on brain-behaviour relationships and
“organicity”: is there a hole in the brain? What part of the brain misses?
- Developing theories: hypothesis, testing theories about cognitive functioning.
During neuroimaging:
- “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.”
After neuroimaging:
- Has become highly relevant in modern-day healthcare.
- There is an increase in people with brain damage or dysfunction.
o Decrease in mortality rates because of improvements in medical care
o Aging
o Interest in quality of life
ICF model WHO
It is used to describe the consequences of a disease or disorder. It enables us to split out the
difference levels that a patient has.
ICF is useful in clinical neuropsychology
- Description of consequences of brain disease / disorder at three different levels: impairment,
limitation, restriction (‘handicap’).
- Identifying moderating factors
- Relevant for understanding subjective complains and problems in daily life
- Identifying target for treatment or optimalisation
➔ It is important to know at with levels the problems are, because you can target the right
problem. E.g. not improve the whole memory, but only help someone with how to write an
email.
The clinical neuropsychologists toolbox
- Assessment/diagnosis: tests, questionnaires, observation scales, interview techniques
- Treatment/intervention: psychotherapeutic techniques, cognitive training and rehabilitation
➔ Both are equally important
Testing hypothesis
- Multi-informed
o Patient
o Significant others
- Multi-method
o Tests
o Questionnaires
o Clinical interview
o Observation
- Multi-conceptual
o Neuropsychological
o Personality
o Contextual environment
Voor een Voorbeeld van een case: zie 43:00 in Lecture 1.
,Lecture 2: Memory disorders
Memory = the ability to encode information, store it and retrieve it.
The Atkinson-Shiffrin memory model (1968)
The Squire memory model (1994)
Neuroanatomical structures involved in memory processes
- Prefrontal cerebral cortex
- Parietal cortex
- Hippocampus
The Baddeley model of working memory (1974)
- the working memory has a limited (but no
fixed) duration (seconds).
- Limited capacity (visuospatial sketchpad and
phonological loop).
- Active processing (CE) of information in STM.
- Linked to long-term memory (two-way
communication).
,The dorsolateral prefrontal lobe
- Working memory: maintenance of information (short-term memory) plus
- Central executive: active processing of information
Characteristics of working memory
- Temporary
- Limited capacity (7+/-2 chunks)
Episodic memory formation – transition from Working Memory to Long Term Memory
- How is the transition from working memory (prefrontal) to long-term memory achieved?
- Information must be permanently stores -> episodic formation
- Binding: associative working memory
o Episodic buffer: involved in LTM encoding
o Also involved in the retrieval of previously encoded knowledge
Adjustment of working memory model by Baddeley (2000)
Diencephalon and medial temporal lobe (MTL) – Mammillary bodies and hippocampus
, Episodic memory formation – consolidation
After memories have been bound, consolidation (LTS) takes place
There are two major consolidation theories:
1. Standard consolidation model (Squire & Alvarez, 1995)
- After encoding, information retained in hippocampus and neocortex.
- Information recall strengthens the cortico-cortical connections.
- Making the memory hippocampus independent -> permanently stores 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 (already taken place in short-term tasks)
- Contextual information -> formation of episodes in the memory (time, place, etc.)
- ‘binding device’: linking item memory to source memory (what, where and when)
- Consolidation: long-term storage
- Disorder: antegrade amnesia (amnesic syndrome)
Amnestic syndrome
Two forms:
1. Hippocampal temporal variant – Only able to remember in the here and now.
- Deficit in forming long term memories.
2. Diencephalic variant – Korsakoff’s syndrome.
Hippocampal temporal amnesia
- Impaired encoding/consolidation of facts
- No confabulation or memory-monitoring problems
- Intact working/short-term memory
- Content gets lost rather than the context
- Can arise after encephalitis, hippocampectomy or traumatic brain injury.
Example: Patient H.M.
Korsakoff’s syndrome
- Sudden onset after Wernicke-Korsakoff psychosis (gait ataxia, eye movement disorder and
confusional state).
- Frontal and diencephalic damage (mammillary bodies and thalamus) as a result of chronic
thiamine deficiency (vitamin B1).
- Often caused by chronic alcohol abuse in combination with poor nutrition.
- Vitamin deficiency can result by other means, such as anorexia, pregnancy.
Diencephalic amnesia
Characteristics
- Personality changes with irritability or apathy
- Confabulation and lack of insight
- Executive dysfunction
- Amnestic syndrome characterised by:
o Anterograde amnesia
o Retrograde amnesia with temporal gradient in autobiographical memory
o Retrieval problems
o Contextual memory: problems with placing memories in time
Lecture 1: Introduction
Before neuroimaging
- Measuring the size of the skull
- Systematic patient descriptions
- Application in psychiatry: development of theories on brain-behaviour relationships and
“organicity”: is there a hole in the brain? What part of the brain misses?
- Developing theories: hypothesis, testing theories about cognitive functioning.
During neuroimaging:
- “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.”
After neuroimaging:
- Has become highly relevant in modern-day healthcare.
- There is an increase in people with brain damage or dysfunction.
o Decrease in mortality rates because of improvements in medical care
o Aging
o Interest in quality of life
ICF model WHO
It is used to describe the consequences of a disease or disorder. It enables us to split out the
difference levels that a patient has.
ICF is useful in clinical neuropsychology
- Description of consequences of brain disease / disorder at three different levels: impairment,
limitation, restriction (‘handicap’).
- Identifying moderating factors
- Relevant for understanding subjective complains and problems in daily life
- Identifying target for treatment or optimalisation
➔ It is important to know at with levels the problems are, because you can target the right
problem. E.g. not improve the whole memory, but only help someone with how to write an
email.
The clinical neuropsychologists toolbox
- Assessment/diagnosis: tests, questionnaires, observation scales, interview techniques
- Treatment/intervention: psychotherapeutic techniques, cognitive training and rehabilitation
➔ Both are equally important
Testing hypothesis
- Multi-informed
o Patient
o Significant others
- Multi-method
o Tests
o Questionnaires
o Clinical interview
o Observation
- Multi-conceptual
o Neuropsychological
o Personality
o Contextual environment
Voor een Voorbeeld van een case: zie 43:00 in Lecture 1.
,Lecture 2: Memory disorders
Memory = the ability to encode information, store it and retrieve it.
The Atkinson-Shiffrin memory model (1968)
The Squire memory model (1994)
Neuroanatomical structures involved in memory processes
- Prefrontal cerebral cortex
- Parietal cortex
- Hippocampus
The Baddeley model of working memory (1974)
- the working memory has a limited (but no
fixed) duration (seconds).
- Limited capacity (visuospatial sketchpad and
phonological loop).
- Active processing (CE) of information in STM.
- Linked to long-term memory (two-way
communication).
,The dorsolateral prefrontal lobe
- Working memory: maintenance of information (short-term memory) plus
- Central executive: active processing of information
Characteristics of working memory
- Temporary
- Limited capacity (7+/-2 chunks)
Episodic memory formation – transition from Working Memory to Long Term Memory
- How is the transition from working memory (prefrontal) to long-term memory achieved?
- Information must be permanently stores -> episodic formation
- Binding: associative working memory
o Episodic buffer: involved in LTM encoding
o Also involved in the retrieval of previously encoded knowledge
Adjustment of working memory model by Baddeley (2000)
Diencephalon and medial temporal lobe (MTL) – Mammillary bodies and hippocampus
, Episodic memory formation – consolidation
After memories have been bound, consolidation (LTS) takes place
There are two major consolidation theories:
1. Standard consolidation model (Squire & Alvarez, 1995)
- After encoding, information retained in hippocampus and neocortex.
- Information recall strengthens the cortico-cortical connections.
- Making the memory hippocampus independent -> permanently stores 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 (already taken place in short-term tasks)
- Contextual information -> formation of episodes in the memory (time, place, etc.)
- ‘binding device’: linking item memory to source memory (what, where and when)
- Consolidation: long-term storage
- Disorder: antegrade amnesia (amnesic syndrome)
Amnestic syndrome
Two forms:
1. Hippocampal temporal variant – Only able to remember in the here and now.
- Deficit in forming long term memories.
2. Diencephalic variant – Korsakoff’s syndrome.
Hippocampal temporal amnesia
- Impaired encoding/consolidation of facts
- No confabulation or memory-monitoring problems
- Intact working/short-term memory
- Content gets lost rather than the context
- Can arise after encephalitis, hippocampectomy or traumatic brain injury.
Example: Patient H.M.
Korsakoff’s syndrome
- Sudden onset after Wernicke-Korsakoff psychosis (gait ataxia, eye movement disorder and
confusional state).
- Frontal and diencephalic damage (mammillary bodies and thalamus) as a result of chronic
thiamine deficiency (vitamin B1).
- Often caused by chronic alcohol abuse in combination with poor nutrition.
- Vitamin deficiency can result by other means, such as anorexia, pregnancy.
Diencephalic amnesia
Characteristics
- Personality changes with irritability or apathy
- Confabulation and lack of insight
- Executive dysfunction
- Amnestic syndrome characterised by:
o Anterograde amnesia
o Retrograde amnesia with temporal gradient in autobiographical memory
o Retrieval problems
o Contextual memory: problems with placing memories in time
