Effects of Brain Damage and Brain Stimulation as a Window Into the Brain Flashcards
1
Q
PROBLEM OF CAUSALITY
A
- 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?”
2
Q
NON-ESSENTIAL ACTIVATIONS
A
- 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)
3
Q
DETERMINING CAUSALITY
A
- 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
4
Q
NEUROPSYCHOLOGY
A
- 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
5
Q
CLINICAL NEUROPSYCHOLOGY
A
- 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
6
Q
LANGUAGE AREAS
A
- Broca’s/Wernicke’s area
- Motor/auditory/primary visual cortex
- Angular gyrus
7
Q
BROCA’S AREA & SPEECH
A
- 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
8
Q
WERNICKE’S APHASIA
A
- ability to comprehend word meaning/reading/writing = highly impaired
- often use sentences BUT w/wrong/non-existent words
9
Q
CORPUS CALLOSUM
A
- 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)
10
Q
WADA TEST
A
- 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
11
Q
HM
A
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
12
Q
HIPPOCAMPAL FORMATION
A
- alveus
- dentate gyrus
- collateral sulcus
- entorhinal cortex
- subiculum
- fimbria
13
Q
TEMPORAL LOBE AMNESIA
A
- 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)
14
Q
HEMISPATIAL NEGLECT
A
- 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
15
Q
HEMISPATIAL NEGLECT SYMPTOMS
A
- 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
16
Q
WE DON’T KNOW WHAT’S HAPPENING IN NEGLECT
A
- 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
17
Q
NEUROIMAGING
A
- 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
18
Q
NEUROPSYCHOLOGY KEY APPROACHES
A
- 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
19
Q
LOGIC OF DISSOCIATIONS
A
- 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
20
Q
SINGLE DISSOCIATION
A
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
21
Q
DOUBLE DISSOCIATION
A
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
22
Q
NEUROPSYCHOLOGY LIMITS & POSITIVES
A
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
23
Q
TMS (TRANSCRANIAL MAGNETIC STIMULATION)
A
- 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
24
Q
TMS REACTIONS
A
- 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
25
TMS EFFECTS ON PERFORMANCE
- TMS pulse gen induces brief chaotic neural activity increase oft followed w/^ sustained excitability reduction resulting in neural activity disorganisation -> impaired performance
- SO effect similar to neuro lesion BUT mild/reversible/safe
- oft referred to as virtual lesion technique
26
TMS SPATIAL RESOLUTION
- 10-20mm; 5-10mm at best
| - influenced by distance from scalp, connectivity between target/adjacent regions
27
TMS TEMPORAL RESOLUTION
AMASSIAN et al (1989)
- pps presented w/sets of 3 letters; asked to report on each trial; TMS applied over visual cortex at slightly dif time
- TMS clearly capable of telling when targeted area involved in processing; single TMS pulse effects on beh = rather brief
- SO temporal resolution = high
28
TMS EFFECT INFERENCES
FUNCTIONAL ANATOMICAL INFERENCE
- cortical area x (connected network) essential for performing task
CHRONOMETRIC/TEMPORAL INFERENCE
- at what t (time) does stimulation effect performance replying on hypothetical psych process x?
PROCESS INTERACTION INFERENCE
- if disrupting process x ^ effectiveness of process y, they normally compete
29
TMS SUITABLE CONTROL CONDITION
- need to control for somatosensory/auditory TMS effects; no TM is enough as control as at least some effect due to elicited noise/sensation
- sham TMS = noise BUT no stimulation; doesn't control somatosensory component (scalp sensation, muscle twitches, discomfort)
- control site = better (over area unlikely as involved in task)
- sometimes difficult to ensure control site has equivalent somatosensory/auditory effects to test site
30
TMS LIMITS
- effects limited to cortex; can't reach deeper cortical/subcortical regions/structures (ie. hippocampus/thalamus)
- effects on beh/performance = ^ subtle so harder to detect than neuro damage effects in patients
- though safe associated w/small seizure risk; low stimulation minimises this; pps carefully screened
