Leaning Pitstop 1

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FlashCards sobre Leaning Pitstop 1, criado por kayle sands em 10-04-2018.
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FlashCards por kayle sands, atualizado more than 1 year ago
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Questão Responda
How 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
What 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
Not 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
What 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
What 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.
What 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
What 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
How 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)
What 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
What 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
What 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
What 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
What 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
What 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
What 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.
What 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
What 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
What 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])
Strengths 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?
What is the Attributional theory of H/D (Bentall, 1990; Slade & Bentall, 1988)? Three main pieces of evidence? *Limitations Hallucinations 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
How 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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