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)