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Exam summaries for Advanced Neuropsychology - Utrecht University €6,49   In winkelwagen

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Exam summaries for Advanced Neuropsychology - Utrecht University

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Exam summaries for Advanced Neuropsychology, including a chapter by chapter breakdown. Neuropsychology topics covered include: Intro to neuropsychology, perception, memory, attention, executive functions, social cognition, language.

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  • 21 februari 2024
  • 9
  • 2022/2023
  • College aantekeningen
  • Chris dijkerman
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 Introduction
-Neuropsychology = multidiscipline
-Aspects of Patient Relation  considerations for current behavior & Test performance
-Current behaviour = SES + current functioning + personality + social context + brain damage
-Hypothesis process:  theoretical framework  literature review  research question
-test considerations: reliable, valid, feasible, theoretically sound, ethical
Ethics: rules/regulations + values + moral principles + ethical practices + rules of conduct
NeuroRights: mental privacy + personal identity + free will + fair access + protection from bias
IMRAD: Intro, Method, Results, Analysis, Discussion
 Perception
(1) Vision: guide action + perceive face/objects + danger + appreciate + recognize + navigate
-Visual System = from eyes  optic chasm  opposite primary visual cortex  L/R visual fields
Visual perceptual deficits = damage between pathway from eye to visual cortex  location = defects
1.Akinetopsia = snapshots (Bilateral damage in V5/MT)  Patient MP
2.Achromatopsia = processing color (V4)  1 hemisphere or both
3.Visual Form Agnosia = shapes carbon monoxide Effron LOC in occipital lobes = face perception
Visual system pathways: 40% of brain area –beyond occipital lobes
- Ventral pathway = visual perception (e.g. what am I looking at?)
- Dorsal pathway = visual guidance (e.g. how am I doing it)
Higher-order perceptual disorders:
1.Visual Agnosia: selective deficit in object recognition (objects/faces)
1.1 Apperceptive agnosia = all features of object together to form coherence
1.2 Associative visual agnosia = can copy/draw but cannot link with identify
-Theories of Object Recognition: from basic visual representations  to more complex representations  to linking with
existing knowledge
Face Perception: separate system for faces  Model Bruce & Young – Parallel Systems = all happen in parallel (independent)
- Structural encoding  Face recognition unit  Facial speech analysis  Expression analysis
Prosopagnosia: unable to recognize faces
(2)Visuomotor Control: visual input guide action: (1) reaching = location (2) hand opening = size (3) hand orientation = object
orientation
-Optic Ataxia = using visual info about position/orientation of objects to guide actions (Posterior parietal lobe)
Separate visuomotor channels: primary visual cortex to premotor areas  reaching vs grasping
Obstacle Avoidance in optic ataxia: avoid dangerous objects or knocking things over
-(3)Body Perception: Rubber Hand Illusion: Requirements: (1) Multisensory synchronized info (2) temporal & spatial
integration (3) foreign part resemble own body (4) anatomically plausible orientation Proprioceptive Drift (locate hand)
-Enfacement illusion: take on characteristics of the other person (fear or compassion)
Use in Practice: (1) lesions cause body perception issues (e.g. phantom limbs) (2) body perception disturbances occur in
disorders (3) illusions simulate disorders & provide insight (4) additional info into disorders (5) provides treatment
Body Representations (Head & Holmes): multiple body representations linked to different functions
- (1) Body Schema (unconscious) standard against which changes in posture are measured
- (2) Superficial Schema (unconscious) central mapping of body surface from tactile info
- (3) Body Image (conscious) internal representation of experiencing self
Body matrix = network model of body perception = flexibility in different aspects of body  tactile, postural, spatial localization,
localization of touch, metric properties, tactile object recognition
Body perception disorders:
- (1) Structural Deficits: Finger Agnosia  Left-right orientation Gerstmann’s syndrome = 2 + dyscalculia + dysgraphia
- (2) Body Size (Metric) Deficits:Macrosomatognosia/Microsomatognosia = medial parietal cortex
- (3) Body Awareness Deficits: Anosognosia = deny  Anosodiaphoria = minimize
o Asomatognosia = reject ownership of limb  Somatoparaphrenia = attribute own arm to someone else
-Proprioception (Kinesthesia) = sense that lets us perceive location, movement, action of body parts
haptic exploration purposive action that encodes properties of objects) + targets on our own body
-Visual-cortical processing = 2 visual streams model  ventral (perception & recognition) & dorsal (guiding action)
Somatosensory systems of brain: processes input from different sub modalities (touch, proprioception, hot/cold, pain, itch) 
linked to receptors on skin, muscles, joints, tendons  primary somatosensory cortex (anterior parietal lobe) PSC contains
somatotopic map of the contralateral half of the body  parts with higher receptor density = more cortical surface
-Damage to primary somatosensory cortex = loss tactile and proprioceptive perception for contralateral half of the body
(hemianesthesia)
-Damage to insular cortex = loss of affective touch, pain & temperature  contralaterally
-Secondary Somatosensory cortex =higher-order somatosensory processing (more distributed system)  e.g extracting
features and recognizing stimuli, conscious bodily experience, spatial/structural aspects of body
numbsense = correctly respond to somatosensory stimuli at a higher chance, but cannot perceive
-Weber’s illusion: perceived distance between touches on a single skin surface is larger on regions of high tactile sensitivity
-Body Space: multimodal process to detect tactile stimuli  localize body parts with each other and in external space

, Active touch & haptic object recognition: microgeometrical properties (texture, density, thermal properties) = input receptors
of skin  macrogeomectrical properties (size/shape) = input from tactile / proprioceptive receptors of muscle, tendon, joint
-Tactile apraxia: Deficits in exploratory hand movements: adjusting hand to character of object (superior posterior parietal)
Haptic Object Recognition: exploratory hand movements, recognizing objects by touch  multiple somatosensory signals
Tactile agnosia: deficit in building the object representation or accessing semantic properties
-Tactile associate agnosia: representation of object is achieved (e.g. can draw) BUT access to semantic knowledge is lost
Peripersonal Space: Area surrounding our body where objects are located (defense & social value)  Posterior parietal regions
+ dorsal premotor  receptive fields linked to head/hand/arm = Cross-modal attentional cueing
Visuomotor reaching/grasping: spatial info for goal-directed arm movements needs visual + somatosensory systems 
Reaching = Dependent on location  grasping = dependent on size
Optic ataxia = selective visuomotor deficit for grasping while reaching is intact
Obstacle Avoidance avoid objects when grasping potential target
requires visuomotor response (minimum distance) increases movement (slowing to improve accuracy) action specification
combined mode: target selection + action specification (parallel) position of non-target is more important: visual dorsal
Visuomotor Control: Reference Frames:
- visuomotor dorsal stream = egocentric coding of targets
- visuomotor ventral stream = allocentric coding of spatial representation
3 Aspects of bodily experience & sensory-guided action: Same underlying neural mechanism = fronto-parietal networks
- (1) Spatial aspects of somatosensory processing = external stimuli & own body
- (2) Representation of Space surrounding Body: peripersonal space
- (3) Visual/Non-visual sensory processes for reaching and grasping
 Memory
(1) Multiple Memory Systems: different systems guide actions in different ways (different circuitry)  HM
- Declarative = explicit/conscious (often impaired) vs Non-declarative = implicit/unconscious
- HM: removed hippocampus (declarative memory)  global anterograde amnesia (Episodic & semantic memory)
Theoretical Viewpoints:
- Tulving (2001): learning = perceptualsemanticepisodic system (semantic does not rely on episodic)
- Baddeley (1988): semantic learning is accumulated residue of multiple previous episodic memories
- Greenberg & Verfaille (2010): episodic memory is the binding of semantic info + context -episodic facilitates semantic
-Procedural learning & priming (non-declarative/ Implicit)  familiarity/recognition – without conscious recall
-Old Episodic Memories old episodic memory become a semantic fact
-Metamemory insight into own memory (e.g. self-reflection)
Surprising sparing: declarative spatial memories layout of house: Multiple exposures + multiple sensory inputs (
-Informed consent= (1) Full information (2) Voluntary participation (3) Capacity to make decisions
-Self-identity = current & long-term goals (working memory, future thinking) + life narrative + semantic & episodic memory
-Requirements of Informed consent: Full info + Declarative & WM + Consider of possible outcomes + Future thinking
Spatial learning: navigation strategies: Egocentric vs Allocentric
-Egocentric (personal viewpoint) = sequence of turns with own body (parietal & somatosensory areas)
-Allocentric (environment based) = landmarks & cognitive maps  hippocampus + PFC (allocentric map)
-Patient Case Jon: perinatal anoxia (oxygen)  developmental amnesia  3 Memory impairments: episodic, temporal, spatial
-Recall/remember = place, time, how, with whom (contextual) vs Recognise/Familiar/knowing = just feeling/sense
-King et al Experiment 2: VR courtyard, different views objects in different places from viewpoint
- (1) Same View: egocentric snapshot / egocentric motor vector / allocentric - (Jon is spared)
- (2) Shifted View: only allocentric – (Jon is impaired) - hippocampus
- (3) Altered Background: can only be solved by egocentric motor vector – (Jon is impaired) - hippocampus
-Eventscape: mental time travel, recollection & re-assembling of events  mentally unfold (using cognitive map)
-MTL structures (hippocampus) = long-term declarative memory (conscious recollection), + new semantic knowledge
-STM not dependent on MTL (e.g. encode new info)
Extrahippocampal sites: memory  visual recognition memory, spatial memory, semantic memory  different MTL structures
-2 kinds of recognition processes (with different neural substrates) (1) conscious recollection = hippocampus vs (2) Familiarity
judgements = perirhinal cortex (
Multiple-trace theory: dissociation within remote memory where autobiographical memory is the most severely affected by
MTL lesions, whereas for personal semantics, public events and famous people are less severely affected
Dual process model: familiarity is commonly impaired in amnesic patients, recollection is more disrupted
OR More general memory function: neither mutually exclusive e.g. hippocampus is involved in all forms of explicit or declarative
memory including familiarity based recognition and semantic memory
Jon had impaired Context-dependent memory (where he received the object or who he received it from)  spared recognition
of content of the event (which object)
-Spatial deficit to theories of hippocampal functioning:
-cognitive map theory = flexibility of hippocampal allocentric system to manipulate novel starting positions
extrahippocampal process of familiarity-based recognition

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