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Leaning Pitstop 1

kayle sands Inglés 21 fichas

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  1. 1How does disinhibition relate to aura and hallucinatory experience?- Visual information overwhelms visual neurons, causing them to fire inappropriately, leading to disinhibition and (simple) hallucinations/aura
  2. 2What factors may predispose someone to experience neural disinhibition and aura?- Neuronal vulnerabilities (e.g. deficits in axonal transmission, Fail inhibit, aberrant connectivity, GABA deficit) can lead to hyperexcitable brains
    - Genetics
  3. 3Not all instances of disinhibition result in sensory hallucination – why?- Depends on where excitation occurs and its propagation
    - It is a necessary, but not sufficient condition for H. to occur
    -disinhibition can sometimes resolve itself e.g. microseizures
  4. 4What is stable processing and what can disrupt this?The effects of excitation and inhibition usually cancel each other out - excessive excitation or under inhibition can lead to neural disinhibition
  5. 5What are the two types of sensory hallucination as defined by Kluver (1966) and Siegal (1977) ?= Kluver's hallucinatory form constants (phosphenes, cobwebs, tunnels, spirals) - simple, occur across wide variety conditions
    = Siegal's 2-stage model:
    Stage 1 - geometric imagery, thought reflect disinhibition in early visual centres (V1)
    Stage 2 - complex imagery (faces, landscapes, objects), reflect activation/release internal images, memories ect.
  6. 6What is Cowan's computational model of form constants and what did it attempt to address? What are its strengths and limitations?- Address explanatory gap in early investigations which tell us what was experienced, but not how (only suggests disinhibition)
    - Based on structures in early centres brain, and properties neuronal propagation
    - Specific cells in the outer cortex are organised into columns which are function specific
    - Waves and patterns of activity in this architecture produce geometric hallucinations
    - Plausible account, good explanatory power as links structure and function
    - Doesn't explain some aspects of phenomenology
  7. 7What is the difference between sensations and perception?- Stimulus provides sensation (data) and perception is interpretation of the data.
    - Brain actively constructs and interpret world, some are fallacies based on corrupt data and problems interpreting e.g. inattentional blindness
  8. 8How does Emmert's Law (1881) show how perception goes beyond sensation in the context of afterimages?-Afterimages (continuing percept of image when no longer present) increase in size when projected to greater distance, despite statistical size being fixed on retina
    - EL = changes in physical size will depend on distance, despite unchanged retinal image size
    - perception based on internal hypotheses and not copies of world (sens)
  9. 9What is the difference between illusions, hallucinations and delusions?Illusions - Mistake of perception (misperceive visual stimuli)
    Delusions - A false belief based on icorrect inferences about external reality, sustained despite strongly opposing evidence
    Hallucinations - False sensory perception in absence of actual external stimuli
  10. 10What is the Spreading Cortical Depression Model? MRI evidence? What clinical cases studies are associated with this?Slow waves of hyper-excitation followed by suppression
    Hadjikhan et al. (2001) - MRI readings consistent progression of aura central/perihp visual field
    Migraine, Visual Stress, Seizures and CBS
  11. 11What evidence is there for less-inhibited brains in migraine?- VEP (Gawel et al. (1988) = inc VEP amplitudes in MA
    - Meta-contast masking (Palmer et al. 2000) = MA better, less inhib, GABA deficit
    - TMS Aurora et al. (1998) = reduced phosph threshold MA
    - fMRI (Datta et al. 2013) = inc ab resp in MA
  12. 12What is Pattern-Glare/Visual stress and how can it be treated?Certain visual patterns/stimuli can induce distortions which reflect CH
    Those neuronal vulnerabilities more susceptible e.g. migraine
    Wilkins & Evans (2001) P-G Test
    Colorimetry
  13. 13What are the different types of seizures? And what are the most seizure-prone brain areas?Simple Partial - Conscious, neocortex
    Complex Partial - Consciousness lost/impaired, predominantly subcortical (hippocampal formation) but can be cortical (TL) - assoc with complex hallucination
  14. 14What is the evidence for the association between complex seizures and high order hallucinations?- Penfield (1955) = artificial brain stimulation of TLE elicited 'engrams'
    *unlikely mem/wide-spread stim/same stim, diff image*
    -Halgreen (1978) = stereotaxic co-ord, strength stim had to be sufficient to evoke widespread potentials, compreh related disrupt
    *don't separate cort/sub-cort*
    -Gloor (1986) = ^did, sub-cort (limbic) crucial complex hallucination
    *low intensity, small regions stim
  15. 15What is Charles-Bonnet Syndrome and how do brain-imaging studies show that patients are 'truly seeing'?CBS are hallucinations of the blind which occur due to reduction sens. input to eye
    Ffytche et al. (1998) = MRI show inc activity in brain region corresponding to content of hallucination e.g. colour, faces. Visual H. failed to correlate with areas outside of visual areas.
  16. 16What are the two theories for CBS?Cortical release - visual centres become released by reduction in sensory input which leads to disinhibition
    Cortical irritability - focused clusters of minor lesions, disinhibition due to irritation
  17. 17What is the medical model view of hallucinations? What are the problems with this?MM views hallucinations as reflective of underlying psychopathologies - a diagnostic tool for disease and abnormality, need to be treated
    Hallucinations occur in the non-path population (Bentall, 1990) - undermining them as diagnostic
  18. 18What is the continuum view of hallucination? Examples of continuums?All people can be placed on a continuum of hallucinatory/delusion proneness. H/D are extreme ends of normal processing and not reflective of psychopathology. No distinction between patients/normal, all have capacity to hallucinate.
    H- Neural instability (Persinger, 2001), D- schizotypy (normal - severe [schizotype])
  19. 19Strengths and limitations of continuum view?- Multidimensional continuas
    -explains hallucinations in normal
    -navigates demarcation issues
    - What do continuums reflect? What factors predispose one to a higher place? Why do these factors occur in the first place?
    -How are experiences sustained/transient?
    - Veridical vs non-veridical
    - generic scoring
    *view has never contended to explain these*
    -Is it equally useful for explaining H+D in P+N? are experiences different?
  20. 20What is the Attributional theory of H/D (Bentall, 1990; Slade & Bentall, 1988)? Three main pieces of evidence? *LimitationsHallucinations reflect a failure in 'reality discrimination processes', where internal imagery is misattributed for external stimulation
    1) Mintz & Alpert = White Christmas Test
    2) Haddock et al. (1995) = Verbal transformation task (suggestibility)
    3) Slade & Bentall (1985) = SDT (percept sens + resp bias) - hallunication and prone more false alarms
    *Does it apply well to normals?
    *Why do clinical interventions work?
    *Vague, how is it discim and what parts fail?
    *why are H domain-specific
  21. 21How does source monitoring and reality monitoring link? What are two examples of failures in source monitoring?Errors in SM (misattribution sources) have implications for ability to discriminate reality.
    False memories
    Paired-associates design = highly recalled items guessed as being more frequent
    fMRI (Gonsalves et al. 2004) = uncertainity about memory leads recruitment other strategies e.g. vividness. False memories occured more than false alarms, activation of brain regions associated visual imagery (e.g. ACC)
    *demand characteristics?
    Auditory Hallucinations
    Gabbard et al. (1997) = EMG correlates of subvoclaization coincides begin H.
    McGuire et al. (1993) - SPECT- Aud H. activate Brocas area.
    Scechtman (1998) = PET - activation ACC heard and hallucinate (not imagined) - inappropriate activation may lead alienation inner speech. (but what is this region doing?)

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Fichas sobre Leaning Pitstop 1, creado por kayle sands el 10/04/2018.
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