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Cognitive Neuropsychiatry Full Exam Notes - Utrecht University €6,49   In winkelwagen

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Cognitive Neuropsychiatry Full Exam Notes - Utrecht University

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Cognitive Neuropsychiatry Exam notes covering all topics: Body perception in Anorexia, Dissociative Disorders, Borderline Personality Disorder, Post Traumatic Stress Disorder, Schizophrenia Spectrum Disorder, Hallucinations, Psychosis, Aggression, Psychopathy, Social Hierarchy, Aggression, Morality...

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  • 27 februari 2024
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  • 2023/2024
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BID in ANOREXIA
- AN diagnosis: (A) limited food intake (B) Fear gaining weight (C) Disturbed perception/experience of body
- Body perception: see/feel/think about own body  current treatment CBT (cognition/affect)  not perception
(know/feel)
- AN = multisensory disorder  more severe than assumed
- Body representation: abstract collection of body perceptionsintegratesuses sensory inputblueprint of
body/size conscious & unconscious main function to use & move body + protect from harm not an image
o Body cognitions: emotions/attitudes/semantics
o Body perception: visual/tactile/feeling
o Body action: planning/execute motor action
- Homunculus: somatosensory/motor representation on brain rescaled using body representation
- Body awareness: body in spacelocation/coordination based on size
- AN: disturbed body size stored in brain’s body representation affects multiple senses & modalities
o Tactile Size perception: caliper overestimated in AN different receptor density and sensitivity more
sensitive but less specificimpact tactile processing receptors relay info to brain size model of object is
projected onto size in distorted body representation feel bigger
o Body Scaled Action: move body through door/crowds rotate at 40%  brain uses overestimated body size
representation (which is larger) experience self as larger
- Treatment: use perceptual distortions to improve/treat AN (RHI) synchronous = ownership  estimate hand width
pre/post RHI  change occurs in both conditions  entire VR body overestimation normalizes and remains at FU 
altered perception in body size is flexible and remains stable over time even emotional body parts & asynchronous
 not linked to body ownership  not treatment
- Intervention: hoop training choose fits body coach through size smaller over time direct evidence forced to
actually experience body size (think/talk/see/move/feel) = multisensory visual size estimation + tactile size estimation
+ action planning
Study 01: study full scope of body representation in 4 domains of BID (attitudes/visual/tactile/affordance perception) 
visual size estimation (VSE); Tactile Size Estimation (TSE); Hoop Task (HT)  HC, AN, Remitted
- Incorrect notion of body size = body image disturbance  develop/maintain ED + complicates recovery remitted
- No standard treatment targeting BID in AN  bodily experience persists after treatment possible trait factor (stable
pattern thoughts/emotions over long period)
- AN: stronger negative attitudes VSE: difference across groups AN/Remitted/HC TET: no difference across groups
(unclear)  HT: AN overestimated more than Remitted
- Confirms BID in remitted AN in visual perception and affordance perception but not in body attitudes
- Multiple sensory domains in BID can improve efficiency of conventional treatments
Study 02: full body illusion (FBI) for emotional body parts  AN showed less overestimation after FBI for circumference on
emotional/non-emotional parts also asynchronous & at FU disturbed body size experience in AN is flexible and can be
changed
- AN treatment does not target multisensory disturbance body representation: experience body & size incl. body
image (perceptual representation) + body schema (motor action)
- Overestimate tactile/haptic perception/integration of visual & proprioceptive info/ body scaled action/ interoceptive
awareness, sensitivity  cross-modal integration of sensory signals is disturbed
- Seeing touch on fake body while being touched on actual body = integrates 2 separate streams
- Initial overestimation in RHI normalizes after multisensory body illusion make size estimation on most recent visual
input  discrepancy between knowing & feeling their size (e.g, body experience) unaffected structural body
- Pre-FBI: AN misestimated width/circumference Post-FBI: decreased misestimation FU: size estimates normalized
change from pre-to-FU was largest in AN FBI alters body size perception positively affects persistent body size
disturbance in AN possible to change embodiment does not result in fake body being added to body
representation
- AN have weaker central coherence to HC (poor global processing) more detailed focused to specific body parts 
visual processing bias (overestimates body size) by blocking visual input: body estimates normalize (shift to other
senses) illusion is not related to improved body size but experimental setting is NB.
Aetiologias of Dissociative Disorders (DID)
- Dissociation: outer body/unreality/memory lapse  amnesia (forget) / absorption (focus) / derealization or
depersonalization (word/self not real)  frequency & intensity = clinical threshold
- Dissociative Amnesia: cannot recall info during trauma
- Dissociative Fugue: unplanned trips  cannot recall past  new characteristics  cannot recall the fugue state
- Reason for dissociation: sleep deprivation/trauma protection/coping high emotion intensity escape  depends on
severity & duration of abuse  more affected in critical periods
- Dissociative Identity Disorder (DID): how valid is identity fragmentation  vulnerabilities: suggestibility/ fantasy-
proneness  treatment lengthy & ineffective

, - Structural Dissociation Model (Trauma model): childhood abuse identity development dissociation don’t
develop coherent identity split to deal with trauma  Treatment: map identities  establish collaboration 
integrate into 1
- Socio-Cognitive Model (Vulnerability model): mood swings/lack behaviour control  social learning/culture factors
confused & want explanation highly suggestible play into fantasy treatment: focus on symptoms don’t
encourage separation
- Inter-Identity Amnesia: recurrent gaps in memory = inconsistent with normal forgetfulness implicit memory task
o Recall list A  Recall List B  objective transfer of information
o Use trauma related words  recollect more negative related words (same as HC)
o Evaluative conditioning: pair neutral image with negative/positive stimulus  learn words & connotations
o Affective priming: target stimuli is facilitated if prime + target have same affective valence  DID = primed
o No objective evidence for inter-identity amnesia
- New treatment: Schema Therapy: rapid shift in emotion/behaviour (like BPD) operationalized as modes in DID
express dysfunctional modes aim to develop more functional modes & replace maladaptive coping transdiagnostic
 focus on what function the identify shift is causing
- Trauma is not sufficient nor necessary to develop DID
- DSM-5: (1) inter-identity amnesia (unproven)  (2) separate identity states (difficult to prove)
- Neuroimaging: risk of cherry picking/post-hoc reasoning reverse inference (brain activity infer function)
Study 01: DID 2/more distinct personality states + discontinuity in self + recurrent memory gaps
- Psychodynamic therapy: (1) safety/stabilize (2) trauma confronted (3) identity integrated/rehab 
co-consciousness/communication/integrate need less stress, ego strength, social support
lengthy/dropout/delayed
- Schema therapy: DID experience compartmentalized identities no proof of inter-identity amnesia (intact memory
pathways) shifts in feelings/emotions/behaviour mimic BPD/PTSD/PD  role of therapeutic relation for corrective
experience  emphasize consequence of early neglect/abuse and explain drastic shifts  normalize identities 
reframe as modes  robust/low dropout  symptom reduction  adapt protocol for DID  identify identities
underlying needs  imagery to process trauma early (overcome cognitive avoidance)
Study 02: Trauma model: causal link between trauma & dissociation  Socio-cognitive model (fantasy-prone, suggestibility,
media, cognitive failure) strengths/limitations  link dissociation & sleep disturbance, hyper-associativity, set shifts,
deficits in meta consciousness, self-regulation  transtheoretical variables
- Transtheoretical/Transdiagnostic Framework: beyond TM/SCM advance etiology (metaconsciousness, cognitive
association, affective processes, emotion regulation, sleep)
- TM: dissociation = unconscious defense/coping  automatic  escape aversive event  difference in how trauma is
defined, correlation variable, no objective evidence of abuse, overlap with other disorders
- SCM: tendency to over-report/exaggerate  not objectively measured mixed findings
- Commonality: DID do not really experience multiple indwelling identities despite their subjective experience 
decreased connectivity/coherence in brain (less integrated mental functioning) disorder of self-understanding
- Meta consciousness: aware and comprehend own mental state and infer state of others (ToM)  link subjective
experience and behaviours, cognition, affect, situation antecedents  inability to reflect  fundamental attribution
error = attribute shifting cognitive-emotional-behavioural sets to multiple selves
- Self-control/self-regulation: poor executive control, self-regulation, cognitive inhibition  especially in emotional
contexts  poor parent-child attachments = cannot regulate emotions  negative emotions disrupt cognitions
- Hyper-associativity: activation & fluency of semantically & emotionally related concepts (associational threads) rapid
shift between overmodulated & under modulated emotional states automatic cognitive-behavioural-affective
association networks  associative identity disorder = integrative/associational processes
- Set switching: difficulty in sustained attention, integrating thoughts, coherent interpretations  inefficient memory
inhibition  forgetting  avoidance based set shifts = create distance/separation
- Sleep-Wakefulness: adverse events and negative emotions disrupt the sleep-wake cycle  non-trauma pathway to
dissociation  longer REM  poor sleep quality  affects daily neurocognitive activity (EFs and emotion regulation)
- Stress/Trauma: adverse events disrupt sleep  depersonalization  hyperassociation
- Dissociation in BPD: unstable self image  stress related paranoid ideation / dissociation / sleep problems
- Dissociation in Schizophrenia: sleep disturbance  unusual experiences  associational processes
- Biological etiology of dissociation: R dlPFC activated & ACC inhibited  damaged connections
- DID: hypo-aroused state (overmodulated emotion regulation) – EFs/Attention/memory/learning  hyper-aroused
state (under modulated emotion regulation) – failed prefrontal inhibition  overmodulated state to under modulated
state triggers hyper association
Body Plasticity in Borderline Personality Disorder
- BPD: (1) intense/unstable moods (2) impulsive (3) oversimplified BW thinking  unstable sense of self  radical life
changes  misinterpret actions of others  idealization/devaluation
- Functional impairments: relationship with self & others
- Treatment: CBT  symptoms studied in isolation  not managed as whole
- Main symptoms: (1) identity disturbance (2) dissociative disturbance (3) extreme mood (4) avoid abandonment

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