Steven’s Handbook of Experimental Psychology. Memory and Cognitive Processes
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Signal detection and threshold modeling of confidence-rating ROCs: A critical test with minimal assumptions. Psychological Review, , Klauer, K. Journal of Mathematical Psychology, 67 , Journal of Mathematical Psychology, 64 , Modeling Source Memory Overdistribution. Castela, M. The impact of subjective recognition experiences on recognition heuristic use: A multinomial processing tree approach.
Singmann, H. Frontiers in Psychology. Dittrich, K. Analyzing distributional properties of interference effects across modalities: Chances and challenges. Psychological Research, 78 , Memory, 20 , Pachur, T. Knauff, M. Until about 15 years ago, the domains of cognition with which cognitive neuropsychologists were concerned were basic, well-understood and extensively-investigated aspects of cognition such as perception, attention, learning, memory, and the processing of spoken and written language.
But cognitive psychology has also been interested in more complex and less well-understood aspects of cognition too, such as thinking, reasoning and belief formation; and there are people who suffer from acquired or developmental disorders of cognition in these higher domains. Why not, then, use studies of such people to try to learn more about these higher-level domains of cognition?
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One might learn more about how beliefs are normally acquired by studying people with delusions; one might learn more about what underpins empathy by studying people who seem to lack a Theory of Mind. As disorders in these higher-level domains are typically labelled as psychiatric disorders this new kind of cognitive neuropsychology is known as cognitive neuropsychiatry Ellis, ; Coltheart, But it is crucial to appreciate that just as cognitive neuropsychology, despite its name, is not a kind of neuropsychology but a subfield of cognitive psychology, so it is important to appreciate that cognitive neuropsychiatry, despite its name, is not a kind of psychiatry but another subfield of cognitive psychology.
A very recent development in cognitive neuropsychology is computational cognitive neuropsychology see e. Coltheart, b. This is based on computational modelling of cognition.
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A computational model of cognition is a computer program which is capable of carrying out some particular cognitive activity such as reading aloud or spelling to dictation or recognizing objects AND which does so by the same processes which, according to some cognitive-psychological theory, are those that human cognizers use when performing this cognitive activity. So the program is an instantiation of the theory, the claim being that a formal description of how the program does the job for example, a description couched in box-and-arrow notation, or in the notation of production systems is also the correct formal description of how the mind does the job.
Computational cognitive neuropsychology involves damaging the program in various ways and studying whether there are any informative similarities between the impaired performance of the damaged program and the impaired performance of people with acquired disorders of the relevant domain of cognition. This is a rather rigorous way of testing the original cognitive theory. To obtain evidence relevant to the theory, one first has to implement the theory explicitly as a computer program; and then one has to determine whether the symptoms seen in various patients with relevantly disordered cognition can also be exhibited in the behaviour of the program when that program has been damaged.
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Cognitive neuropsychology shares with the rest of cognitive psychology the aim of discovering what the processing modules of some cognitive system are and what pathways of communication between them exist. That requires cognitive neuropsychology to make the assumption of subtractivity: the assumption that brain damage can subtract modules, or pathways of communication between modules, from the normal system, but cannot add new modules or new pathways.
Unless the assumption of subtractivity holds, one cannot make inferences about the functional architecture of the normal system from evidence concerning the functional architecture of a damaged system. One reason that cognitive-neuropsychological research is perennially exciting is that it continually reveals disorders of remarkable selectivity and specificity.
Patient KT McCarthy and Warrington, was normal at reading aloud pronounceable nonwords even though he would never have seen these before , but very impaired at reading aloud real words which he would have seen before, when these words disobeyed the spelling-sound rules of English irregular or exception words. Patient AC Coltheart.
Surely such results allow us to infer in a justified manner important things about the functional architectures of the cognitive systems involved in reading, object recognition and comprehension? Suppose, for example, we came across a stroke patient whose recognition of stimuli in all sensory modalities bar vision was intact; and he was not blind because he could describe well the visual properties of any stimulus he was looking at; yet he could not recognize objects, faces or printed words.
No matter how familiar such stimuli were, all looked completely unfamiliar to him. But there is an alternative and entirely reasonable inference: that there are three separate visual recognition modules, one for each of these classes of stimuli, and that they are located close together in the brain in a region with a single blood supply which the stroke had affected.
This illustrates why cognitive neuropsychology does not regard the observation of an association between impairments as offering a secure basis for making inferences about functional architecture. Suppose now, however, we came across a second stroke patient, one whose recognition of stimuli in all sensory modalities bar vision was intact; and he was not blind because he could describe well the visual properties of any stimulus he was looking at; and he could not recognize objects even though he could recognize faces or printed words.
Here we have, not an association, but a dissociation , of deficits: impaired object recognition with intact face and word recognition. Might we not infer from this dissociation that the functional architecture of the visual recognition system includes a module specialized just for object recognition and not used for recognizing faces or printed words? Such inferences from dissociations however are open to a straightforward objection too. Perhaps there is a single visual recognition module that is used for recognizing objects, faces and printed words, but objects are more difficult for it to recognize than are faces or printed words.
If that were so, and the module were partially impaired by brain damage, the module might still be able to accomplish easier tasks face and word recognition whilst producing imperfect performance in the task hardest for it object recognition. This argument makes the data from this patient compatible with two different proposals about the functional architecture of visual recognition.
What the cognitive neuropsychologist wants are data that can be reasonably argued to specifically favour one particular proposal about functional architecture at the expense of competing proposals. Such data cannot be provided by observations of associations or single dissociations, but they can be provided by observations of double dissociations. Suppose a third stroke patient is seen whose recognition of stimuli in all sensory modalities bar vision was intact; and he was not blind because he could describe well the visual properties of any stimulus he was looking at; and he could not recognize faces, even though he could recognize objects and printed words.
When this third patient is considered in conjunction with the second patient, just described, we have a double dissociation of deficits: impaired object recognition with intact face recognition in one patient, and the opposite pattern in another. One might infer from the data from these two patients that there is a module dedicated to object recognition and a distinct module dedicated to face recognition. This inference is not open to the objection that can be made to inference from association, and it is not open to the objection which can be made to the inference from single dissociations.
That is why cognitive neuropsychologists focus on the study of double dissociations when making inferences about the functional architecture of cognition from patient data.
Of course, no cognitive neuropsychologist would ever claim that it is indubitably the case, given this observed double dissociation, that there must be distinct object and face recognition modules. However, inferences from double dissociation have the virtue that they have no consistent intrinsic weaknesses unlike inferences from association or single dissociation ; so these are perfectly reasonable inferences to make.
And furthermore, if anyone wishes to dispute the particular functional architecture some theorist has inferred from some double dissociation, it is up to them to propose an alternative architecture which is also compatible with the observed double-dissociation data. At least as far as reading at the single word level is concerned, this is a model of how we recognize print and how we read aloud. Each of the boxes and arrows in the model is motivated, in the sense that if any one of them were deleted from the system, there would be some reading task that skilled readers can do which the system could not do.
It follows that if brain damage affected any module or any pathway in the system, some form of reading disorder - some kind of acquired dyslexia - would result. What the actual pattern of preserved and impaired reading abilities would be would vary as a function of which modules or pathways were preserved.
So there is no sense in grouping patients under syndrome labels, and studying syndromes. Each patient a cognitive neuropsychologist sees will thus almost certainly be different from every other, and that is why cognitive neuropsychology is the study of single cases, not data averaged across a group of patients.
How then can generalization, a sine qua non of science, be achieved? It is achieved because all the patients are assumed to be performing with some damaged version of the same cognitive system. Thus, for example, the cognitive-neuropsychological evaluation of the model of reading in Figure 1 proceeds by investigating whether that model can account for all the reading symptoms seen in every patient with acquired dyslexia who comes along. Cognitive neuropsychology first began to flourish in the second half of the Nineteenth Century, initially in relation to disorders in the comprehension and production of spoken language aphasia.
Continental neurologists such as Broca , Lichtheim and Wernicke studied patients with aphasia and inferred information-processing models of the normal language-processing system from the patterns of preserved and impaired language abilities they saw in their patients. They even expressed these models as box-and-arrow flowcharts of information processing, which is the universal notation in modern cognitive neuropsychology as in Figure 1. Cognitive neuropsychology was thus flourishing by the early Twentieth Century.
But then it rapidly lost favour. This happened for two reasons, one to do with psychology and the other to do with neurology. We have become so enmeshed in speculative questions concerning the elements of mind. All that should be studied by psychologists is what could be objectively observed: stimuli and an organism's responses to them. This doctrine is known as behaviourism.