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39 Cards in this Set
- Front
- Back
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How many assumptions does cognitive neuropsychology need according to lecture?
What are they? |
6
1. functional isomorphism 2. fractionation 3. transparency 4. functional continuity 5. faith in functional categories 6. faith in induction |
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What is Functional isomorphism? and why is it necessary to cognitive neuropsychology?
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Functional isomorphism means that impaired performance has the SAME RELATION to the impaired cognitive system as normal performance had to the unimpaired system.
If not, we have no ground. Our subjects may be a different type of thing than we are; and Neuropsychology and experimental psychology would be split. |
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What is the term for this assumption of cognitive neuropsychology:
Functional computations are LOCAL such that brain damage selectively impairs some functions but leaves others intact. |
Fractionation
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What is the term for this assumption of cognitive neuropsychology:
A lesion affects the region/function damaged, but not other regions/functions. (Under this assumption (and perhaps only under it?), changes to the system due to damage will be comprehensible within an accepted theoretical framework) |
Transparency
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What is diaschisis?
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A loss of functional activity in a region of the nervous system, resulting from injury to some OTHER connected region of the system.
[contradicts assumption of transparency?] |
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What is meant by an assumption of "functional continuity"? Why would non-continuity of function be a problem?
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No NEW processing structures are PRODUCED by damage.
If the structure under study changes with damage, no inferences to normal processing will be possible. Note that dynamic process views may dispute this seemingly obvious assumption. |
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What is meant by a "faith in functional categories"?
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In order to avoid strategic compensation for deficits, there must be identification of the proper [low level] function.
However, one of the strengths of cognitive neuropsychology is that is can provide ‘existence proofs’ of unsuspected functionality. |
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What is meant by a "faith in induction"?
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because there is no experimental control of their main source of data, neuropsychologists must rely on inductive probability
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Which assumption does Westbury say is really a ‘high level’ meta-assumption with respect to many of the other assumptions?
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functional isomorphism
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If any of the assumptions do not hold, what is the implication for cognitive neuropsychology?
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It will be difficult or IMPOSSIBLE. OR, they will have to rely more on data from other disciplines.
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When, and by whom, was alien hand syndrome first reported? What was shown to be the neuro-basis of the syndrome?
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Goldstein 1908
(although one suspects that earlier reports might have been reported as supernatural events) Neuro-basis: lesions throughout the right hemisphere, including the corpus callosum |
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What is diagonistic apraxia?
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the name of alien hand syndrome when it was first reported
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Are all patients with alien hand syndrome quite disturbed?
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No. Some patients have found their own alien hand to be ‘acceptable and positive’, while others have denied that the rogue arm was even their own.
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Do leg movements or arm movements require more cooperative behavior between hemispheres?
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the legs require more...
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What is the role of the SMA?
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The SMA plays a role in PLANNING COMPLEX movements.
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During a simple finger flexion, is the motor cortex or the somatic sensory cortex active?
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Both.
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If carrying out a finger movement sequence, which areas are active?
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motor cortex,
somatic sensory cortex, AND supplementary cortex |
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What areas are active during the mental rehearsal of a finger movement sequence?
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ONLY supplementary cortex.
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What is the ratio of right hemisphere to left hemisphere lesions involved in Alien Hand Syndrome?
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L:R :: 9:2
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What are the two possible lesion locations that result in AHS?
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lesion is either medio-frontal, or callosal, or possibly both
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If lesions are in the LEFT hemisphere, what regions MUST be damaged in order to result in AHS? (three main areas)
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All LH lesions are medial frontal, and involve medial premotor area including the supplementary motor area, anterior cingulate, and anterior corpus callosum
With lesion confined to the CC and often involving bilateral medial frontal lobes, patients have had AHS in non-dominant limb, usually in intermanual conflic (e.g., activated by dominant hand) |
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How does damage to the frontal lobes (especially in the right hemisphere) cause AHS? What type of damage is NECESSARY for AHS? What does this suggest?
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Damage in the frontal lobes (esp. in RH) impairs avoidance/inhibition responses, thereby releasing positive exploratory behaviors.
Anterior CC damage is necessary, suggesting contralateral (non-dominant, usually right) side input plays a role in inhibiting the behaviors which emerge in AHS . |
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What two symptoms can function to bring primary motor cortex under control? Which is internally dependent and which is externally contingent?
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Medial premotor area (SMA): internally dependent, predictive, projectional
A more lateral ‘arcuate premotor area’ (APA): Externally contingent and object oriented Unilateral lesions in SMA + in the anterior CC release ispilateral motor cortex from inhibition, allowing the second externally-driven system to take over control |
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Why are left lesions predominant in AHS?
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B/c the left prefrontal cortex controls much of the positive exploratory behaviors associated with AHS. Lesioning of the left releases inhibition from the RH [I think he meant LH], allowing AHS behaviors to be released, appearing in the contralateral (usually right) side.
...however, additional complications suggest that this story is a bit simplistic. |
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Which neuropsychological assumption does the case of AHS seem to undermine?
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the assumption of functional continuity (that no new processing structures are produced by damage).
If proceed with this assumption we might take the existence of AHS to be evidence of an Id-like unconscious seething just below our awareness, kept in check by inhibitory centers in pre-frontal cortex. (b/c we have to say that the new behaviors unleashed in AHS were already present in the brain). |
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What is the main significance of the Bisiach & Luzzatti study?
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That neglect patient's deficits are not due to sensory or memory impairments, but rather to deficit in ATTENTION.
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What was shown, in one study with 13 contralateral neglect patients, to be the greatest area of lesion overlap?
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most common lesion site is INFERIOR PARIETAL lobe
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Given that hemineglect patients' consciousness is hardly affected by their awareness and perception being limited to one side of the world [that is, they don't feel strange or any different than before.. or that something is off], what might we say about those who experience hallucinations and delusions?
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It makes us better able to understand how those with hallucinations and delusions can so easily accept their revised view of the world.
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What is anosagnosia?
what does nosos mean? what does gnosis mean? |
A more extreme version of hemi-neglect: a denial of paralysis by some people who have the left side of their bodies completely paralyzed due to RH stroke.
nosos: disease gnosis: knowledge |
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In a study by Ramachandran, when three anosagnosic patients were given a choice between two possibles tasks (one unimanual and one bimanual), which were patients more likely to choose? And what does this suggest?
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On 17/18 trials, patients chose the (impossible) bimanual task and exhibited no learning, nor any frustration when they failed.
This suggests that patients either have NO TACIT KNOWLEDGE of their paralysis, OR if they do, they CANNOT ACCESS this knowledge WHEN CHOOSING between a uni/bimanual task. |
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What is the Freudian view for anosagnosia? What evidence undermines it?
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The anosagnosis is a defense mechanism to protect the ego as the patient does not want to confront the unpleasantness of the paralysis.
However, anosagnosia only occurs when the lesion site is in a particular spot. |
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What is the neurological view of anosagnosia? What is some evidence in favor of it? (hint: it is a difference between RH and LH patients)
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denial = direct consequence of the neglect syndrome
Ramachandran has suggested that an "ANOMALY DETECTOR" exists in the RIGHT PARIETAL LOBE which generates a paradigm shift of consciousness anomalies/discrepancies are too large: if damaged, bad rationalizations go unchallenged. evidence: RH patients construct more elaborate [more discrepant?] rationalizations than LH patients. Since patients simply do not know that they are paralyzed, it is impossible for them to construct a story that includes this fact: so they easily construct a different story |
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What is akinetopsia? the cause (area of damage,etc.)? what is the main point of it/significance for psychopathology?
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a failure to see motion
(atopsia = failure to see) due to damage to V5, an area sensitive to motion (cells are directionally tuned). however, the problem may not lie in V5 per se, but in the failure of V1 to be able to synthesize the percept properly in the absence of input from V5... shows how our visual experience is constructed, rather than taken in as a whole. when we think of sensory/motor functions as been constructed from multiple pieces of independently-computed evidence, it is easy to extrapolate this to higher cognition such that social knowledge, intellectual functions, and emotional valence calculations are also being constructed from multiple quasi-independent subfunction calculations. (so that changes in any one of the contributing subfunctions might radically change the high-level interpretation of the whole experience) |
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What four things are detected in those with blindsight (cortical blindness), as listed in the lecture? (hint: for #4, explain when a sort of explicit processing can take place.)
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a) neuroendocrine responses
Melatonin suppression in response to bright light occurs even in retinally-blind subjects Mediated via retinal ganglion cells projecting to the hypothalamus However, there is no localizing possibility with this response b) reflexive responses (pupil changes, blink reflexes, and nystagmus) c)implicit (unconscious) processing -The subject is neither asked about nor aware of an unseen stimulus presented inside a field defect Presentation of a stimulus inside a field defect can alter processing of seen stimuli -RT effects, shape judgment effects, after-image effects, motion effects, lexical semantic effects d)explicit (but not really conscious) processing: using forced choice patients can detect stimuli vs no-stimuli; displacement; direction of displacement; wavelength; some shapes |
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What is the implications of the blindsight phenomenon for psychopathology? What is another example that relates?
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We cannot take our conscious experience to be a true model of the information our brains our actually processing.
Also, defects in processing information may lead to high-level defects in the quality of our subjective experience. Capgras syndrome is another example of this. |
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Name three causes that can result in Capgras. What is the area affected in capgras syndrome?
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Capgras syndrome (and related neurological ‘reduplicative delusions’) can occur in disorders such as stroke, brain tumor, and encephalitis
studies strongly support right frontotemporal involvement (it is believed that the syndrome results from the disconnection of limbic systems from cortical systems) |
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How does the intentional stance blur the difference between disorders of perception and disorders of belief? (That is, what does it suggest about the difference: is it for descriptive convenience or for explanatory precision?)
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it suggests that the difference is one of descriptive convenience, rather than of explanatory precision
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What are beliefs in Dennett's view?
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beliefs are a short-hand SUMMARY of a set of PSYCHIC FORCES that includes (among others) PERCEPTION, memory, emotion, desire, and need.
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how are aberrant beliefs continuous with normal beliefs?
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they are both the best short-hand description that we can accept of a complex set of psychological forces
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