Effects of Brain Damage and Brain Stimulation as a Window Into the Brain Flashcards
PROBLEM OF CAUSALITY
- brain imaging allows examination of brain substrates of psych processes
- BUT neuroimaging techniques (ie. fMRI/PET/other measurements) suffer from serious limit: causality
- if brain activity associated w/task/hypothetical psych process doesn’t mean activity causes observed beh/hypothesised psych process
- BUT ask: “how can activation of brain area (ie. BOLD fMRI signal change) systematically relate to psych process unless area involved in process generation?”
NON-ESSENTIAL ACTIVATIONS
- some brain regions may be involved in new task learning BUT may not be required once task = learned (ie. multiple demand system)
- some areas recruited as back-up in case processing requires extra resources/effort
- some process As essential for task may often co-occur w/process B that isn’t essential (ie. reading on laptop often hand-in-hand w/typing so reading may elicit activations related to typing BUT typing unlikely to link w/reading performance)
DETERMINING CAUSALITY
- only definitive solution = examination if beh/performance affected when brain activity disrupted in particular area
- lesions produced experimentally in animals
- for humans, one examines:
1. NEUROSURGERY - brain tissue removal for neuro/psych disorder treatment (often epilepsy)
2. STROKE - cerebrovascular accident resulting w/blood circulation disruption in brain OR haemorhage
3. BRAIN TRAUMA/INJURY
4. NEURODEGENERATION - brain tissue degeneration in dementia
5. INFECTION - affected brain tissue
NEUROPSYCHOLOGY
- psych area examining effects of brain damage on abilities/behaviour
- if particular brain region/structure damage systematically associated w/certain cog impairment, that region is necessary for cog process to function SO region must be (part of) anatomical substrate for given cog processes
- emerged in 19th century w/French neurologist Paul Broca identified post-mortem that inferior frontal cortex (Broca’s area) damage likely cause of severe language impairment in patient
CLINICAL NEUROPSYCHOLOGY
- applied clinical neuro-psych variant
- experts on beh/emotional BD consequences via patient assessment
- diagnose neural disorders; help patients/families adjust
- work in hospitals/care homes/rehab centres
LANGUAGE AREAS
- Broca’s/Wernicke’s area
- Motor/auditory/primary visual cortex
- Angular gyrus
BROCA’S AREA & SPEECH
- Broca studied patients brains w/aphasia (impaired speech)
- one (Mr Leborgne) nicknamed “Tan” via inability to utter anything else
- 1861; via post-mortem autopsy, Broca found Tan had lesion caused via syphilis in left inferior frontal lobe
- subsequent research confirmed that these area lesions indeed result in language impairments
WERNICKE’S APHASIA
- ability to comprehend word meaning/reading/writing = highly impaired
- often use sentences BUT w/wrong/non-existent words
CORPUS CALLOSUM
- white matter tracts (numerous axons) connecting hemispheres
SPERRY & GAZZANIGA - studied patients who underwent callosotomy (cutting/severing Corpus Callosum to limit epileptic activity spread from one hemisphere to next)
WADA TEST
- reversible numbing of left hemisphere via sodium amytal injection
- language localisation = heavily left biased
- split-brain/Wada test studies show that linguistic competence of right hemisphere = limited
HM
MILNER
- HM (most famous clinical human memory case)
- to treat severe epilepsy (27y) received bilateral medial temporal lobe resection
- after epilepsy = greatly improved BUT showed nearly total profound amnesia persisting for whole life
HIPPOCAMPAL FORMATION
- alveus
- dentate gyrus
- collateral sulcus
- entorhinal cortex
- subiculum
- fimbria
TEMPORAL LOBE AMNESIA
- HM = profound anterograde amnesia; formed almost no new episodic memories following surgery; years of memory testing exps BUT he remembered none
- HM = partial retrograde amnesia; recalled early childhood (memory retrieval spared) BUT not years immediately before surgery
- normal WM; 6 numbers remembered w/constant uninterrupted rehearsal
- normal procedural/lexical memory (ie. writing)
HEMISPATIAL NEGLECT
- inattention to parts of visual field
- affects 2/3 right hemispheric stroke patients
- differ from v mild -> complete
- strongly affect independence
- crucially different from (cortical) blindness
- parietal lobe damage SO seems crucially involved in attention to items regulation
HEMISPATIAL NEGLECT SYMPTOMS
- only attend items on right
- move in opposite direction from one if coming from neglected side
- problems reading
- ignoring objects in environment
- problems navigating space
- not using particular limbs
- lack of insight
WE DON’T KNOW WHAT’S HAPPENING IN NEGLECT
- neglect is caused by multitude of problems
- lateralisation of left visual field suggests to some indication that attention is inherently biased to right and some function bringing it left is impaired
- also possibility of something going wrong in internal space representation (some missing so not used)
- also possibility of initiation of motor system in certain directions is impaired
NEUROIMAGING
- may want to run imaging to see WHERE certain task/function is localised OR…
- may be interested in if certain task/condition has qualitatively different activation patterns from another regardless of precise localisation
- some say above is more useful for psychs as tells whether 2 experimental conditions rely on same processes or qualitatively dif ones
NEUROPSYCHOLOGY KEY APPROACHES
- same neuroimaging approaches distinguished in neuropsychology aka:
- classical neuropsychology = localisation focus
- cognitive neuropsychology = cog architecture via beh performance identification relying on qualitatively similar/dif processes regardless of localisation; relies on dissociation logic
LOGIC OF DISSOCIATIONS
- neuro-psych data used to test theories about architecture of psych processes even w/o knowing exact exact damage location
- one want to investigate psych processes in recognition/letter writing; key question of if vowel recognition relies on dif psych processes from consonants
- say BD impairs vowel processing BUT spares consonants; dissociation may indicate dif processing of letter classes
- NOTE: determining exact damage location ISN’T crucial for above inference
SINGLE DISSOCIATION
CUBELLI (1991)
- one patient left out vowels, the other consonants
- this single dissociation ISN’T sufficient for conclusion of qualitative dif in vowel/consonant representation
- possible for same mental computations in both BUT consonants may be easier visually than vowels
SO more resilient to BD but no clear dif
- BUT if true, one shouldn’t find patients w/impaired processing of consonants yet spared vowels
DOUBLE DISSOCIATION
KAY & HANLEY (1994)
- identified patient w/^ consonant errors than vowels
- existence of opposite patterns = double dissociation
- hard to explain as quantitative dif where one item (vowels/consonants) if more damage effect resilient
NEUROPSYCHOLOGY LIMITS & POSITIVES
POSITIVES
- over electrophysiology/neuroimaging enables causal inference
LIMIT
- trauma/neuro degeneration lesions rarely anatomically selective; usually affect multiple regions/structures
- BD associated w/gen cog/emo/personality changes whose cog performance effect is v considerable/difficult to separate from effects of damage to specific region/structure
TMS (TRANSCRANIAL MAGNETIC STIMULATION)
- non-invasive magnetic stimulation of human motor cortex
- large current briefly discharged into wire coil held on subject’s head; generates rapidly changing/^ magnetic field around wire; passes into brain
- in cortex, magnetic field generates electric/ionic current through neurons’ membranes
TMS REACTIONS
- primary motor cortex = muscle contraction induction resulting w/finger twitches
- primary/secondary visual cortex = flashing pattern (phosphenes) perception; shape/size depends on exact site/strength/duration/stimulation timing