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Description
Flashcards by kayle sands, updated more than 1 year ago
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Created by kayle sands
over 6 years ago
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| Question | Answer |
| 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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