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Biological Psychology > Effects of Brain Damage and Brain Stimulation as a Window Into the Brain > Flashcards

Effects of Brain Damage and Brain Stimulation as a Window Into the Brain Flashcards

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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?”
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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)
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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
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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
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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
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6
Q

LANGUAGE AREAS

A
  • Broca’s/Wernicke’s area
  • Motor/auditory/primary visual cortex
  • Angular gyrus
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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
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8
Q

WERNICKE’S APHASIA

A
  • ability to comprehend word meaning/reading/writing = highly impaired
  • often use sentences BUT w/wrong/non-existent words
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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)
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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
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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
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12
Q

HIPPOCAMPAL FORMATION

A
  • alveus
  • dentate gyrus
  • collateral sulcus
  • entorhinal cortex
  • subiculum
  • fimbria
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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)
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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
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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
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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
Q

TMS EFFECTS ON PERFORMANCE

A
  • 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
Q

TMS SPATIAL RESOLUTION

A
  • 10-20mm; 5-10mm at best

- influenced by distance from scalp, connectivity between target/adjacent regions

27
Q

TMS TEMPORAL RESOLUTION

A

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
Q

TMS EFFECT INFERENCES

A

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
Q

TMS SUITABLE CONTROL CONDITION

A
  • 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
Q

TMS LIMITS

A
  • 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

Biological Psychology (21 decks)

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