Cognitive Neuropsychology
History
Concept of localisation
Phrenologists
Gall: Bumps /shape of skull hint to character
Abilities localized in the brain
Brain is Modular: Processes have locations: Fundamental for CNP
Identifying those locations important objective
Localizationists
Noted patterns of behaviour related to certain lesions
diagramm (process) makers: Lichteim
modelling cog. processes
Fell out of favour
Beavourism: we cannot know what is going on
Inconsistencies with localization
Case of phineas gage
CASE of Phineas Gage
Iron shot through frontal lobes altered social skills
Harlow (1868): Disrupted G. ability to plan and maintain acceptable behaviour
Paul Broca:
Patient: TAN TAN TAN: unterstand but not speak
Brocas Area: Imp. for coordinating speech musculature
Wernecke:
Pationent could speak but not understand speech
Wernickes Area: Imp. for storing sound patterns (phonemes)
Modern Cog. Neuropsychology
Provided Language of representatinos and processes
Away from localizatino to modeling(like diagramm makers)
Only input and output seems localized/ not higher functions
Important to guide Surgery (destroy language center)
Relevance Today through Technical Developements: fMRI
Validity of CNP
General Problems
Deficits are because of lesion
There might have been deficits before
Similiar damage=similiar deficits
But brains and lesions differ
Subtractivity: The brain is modular
Fodor says only for input and output - not i.e. problem solving
Patients develope compensatory strategies
Brain is plastic and can repair
Functions can move
Single case enough - there should be no martian
deep dislexia brain may not form normally/ genetic issues
We have comparable brains - no should be no martian among us
Problems with single case
Is he representative
Split brains may develop different
Hard to find double dissotiatian in one case
No correlations possilbe (size of area and ability)
Abilities vary over time? (test different times)
Select a single patient because he confirms theory
Problems with group
Are individuals (lesions) comparable?
Same symptoms but other behavioural differenes might be overlooked
Goals of CNP
Understanding lesions deficits
Localization/where
Methods
Neuroimaging
Wisconsin Card Sorting Task: -sort cards to constanly new rules--> Difficulty =Frontal lobes?
Post Mortem brain examination (TAN)
Assessment of deficit/What
Methods
Inteviews
Brain Imaging:
Damasio: difficulity in recognition: tools (a glove: "appears to have 5 outpoutchings ...") / animals/ people: reduction in brain areas
Subtopic
Problem: Images will not show the "how"
Images: Determine the level of when sth. is coloured
Standardised Tests
Wechsler Memory
Wechsler Intelligence
Birmingham Object Recognition
Normal -Cog. Metods
Memory tasks: Amnesics show recency effect/ not primacy
Coltheart: Model IAC Modil based on errors shown by dyslexics
Comp. data from other patients
Providing Treatments /How
Helping amnesics
Train procedural memory (JC ran own business)
Neuropage: implicitly learn to check the messenger to be reminded of...
HMs mirror drwaing improved (implicit learing)
Create / Support models
Former:Localization of Function: Now Understanding Processes
Data from other patients
Methods
Is model consistent with behaviour?
How to build models
Infer normal funcions from damaged systems
Split Brain
Sperry & Gazzaniga: Patients Left brain saw nothing: language / Right Spatial can draw object
Left analytical, right emotional
Ramachandran: Higher order lang. mean. trasf. cortically
Agnosia: (Object recog)
Humphreys & Riddoch: Recog. happening in stages
HJA: object: percept - doesn't look familiar
JF: semantics clear but cannot name
maybe more diffiuclt not different subsystems
single dissotiations
Goodale
Patient DFDorsal/ Ventral
Explicit No! Could not recognize even simple shapes
Implicit OK: grasping diretion or hand size
Face Regocnition
Capgras Delusion
Looks like wife but is imposter
Prosopagnosia
Not recognizing familiar persons
Double Dissotiation (different subsystems?)
Where
Recognition
Face Reogniton vs. Emotional Expression Recogntion
Speech
Broca / Wernecke
Memory
Amnesia
KF has defective STM but intact LTM
HM has deficient LTM but intact STM
Blindsight
Double Dis. in one Pateint: Differnt deficits blindsight vs. of intact vision
Why
Single disotiations: A but not B: --> A harder B?
Amisics loose A declarative but have B procedural
Problems with Double Dissot.
differnt stimuli (tests) might lead to errors
Living / non living in two labs
It is therefore important to ensure that a patient is tested in a variety of ways to ensure that seemingly normal performance is being produced in a normal fashion
Normal functioning
How much degradation is impairment
What is normal performance?
not both below normal: otherwise perhaps one impaird function
Could the patient use a compensatory strategy?(not really function on one task)
damaged connnectionist models (single system) behaves like doulbe dissoti.
Cognitive Modelling: If lesioned do react the same?
Success of CNP
Colthearts Model of dyslexia by testing lesioned brains (surface dyslexia= damage to lexical route)
vs Developemental dysl: difficulties learning
Models of face recognition vs. emotinal express
Treatment / rehab of amnesics (JS)
But problems with central systems (problem solving)