How is it that many schizophrenics identify certain instances of verbal imagery as hallucinatory? Most investigators have assumed that alterations in sensory features of imagery explain this. This approach, however, has not yielded a definitive picture of the nature of verbal hallucinations. An alternative perspective suggests itself if one allows the possibility that the nonself quality of hallucinations is inferred on the basis of the experience of unintendedness that accompanies imagery production. Information-processing models of “intentional” cognitive processes call for abstract (...) planning representations that are linked to goals and beliefs. Unintended actions - and imagery - can reflect planning disruptions whereby cognitive products do not cohere with concurrent goals. A model of schizophrenic speech disorganization is presented that postulates a disturbance of discourse planning. Insofar as verbal imagery can be viewed as inwardly directed speech, a consequence of such planning disturbances could be the production of unintended imagery. This link between the outward disorganization of schizophrenic speech and unintended verbal imagery is statistically supported by comparing the speech behavior of hallucinating and nonhallucinating schizophrenics. Studies of “borderline” hallucinations during normal, “goal-less” relaxation and drowsiness suggest that experiential unintendedness leads to a nonpathological variant of hallucinatory otherness that is correctable upon emerging from such passive cognitive states. This contrasts with the schizophrenic case, where nonconcordance with cognitive goals reinforces the unintendedness of verbal images and sustains the conviction of an external source. This model compares favorably with earlier models of verbal hallucinations and provides further evidence for a language production disorder in many schizophrenics.Short Abstract: How is it that many schizophrenics identify certain instances of verbal imagery as hallucinatory? This paper proposes that the critical feature identifying hallucinations is the experience of unintendedness. This experience is nonpathological during passive conscious states but pathological if occurring during goal-directed cognitive processing. A model of schizophrenic speech disorganization is presented that postulates a disturbance of discourse planning that specifies communicative intentions. These alterations could generate unintended verbal imagery as well. Statistical data are offered to support the model, and relevant empirical studies are reviewed. (shrink)
The present study examined the effects of thought suppression on sleep-onset mentation. It was hypothesized that the decrease of attentional control in the transition to sleep would lead to a rebound of a suppressed thought in hypnagogic mentation. Twenty-four young adults spent two consecutive nights in a sleep laboratory. Half of the participants were instructed to suppress a target thought, whereas the other half freely thought of anything at all. To assess target thought frequency, three different measures were used in (...) the wake state and mentation reports were repeatedly prompted by a computer at sleep onset. In support of the hypothesis, results revealed a reversal of target thought frequency at sleep onset: Participants instructed to suppress reported fewer target thoughts than did controls before falling asleep, but more target thoughts afterwards. (shrink)
The terms 'reference', 'representation', and 'perception', have not been univocally used. This thesis provides a new theory which explains reference, representation and perception by showing that each has primary and derived forms, related more-or-less recursively. -/- The primary forms are located in a simple model which is based on the structure of a computer. The structure presented is a 'minimal' model, that is, the smallest structure in which the simplest kinds of reference, representation, and perception occur. -/- An analogical relation (...) constructed between the simple model and a person in the world provides an account of the simplest forms of, and an explanation for the derived forms of each. The relation presented sheds light on our corresponding ordinary notions and shows that they can all be explained or accounted for entirely within the cause-effect paradigm. -/- In effect, this thesis presents the 'essence' of each of reference, representation, and perception. (shrink)
Multidisciplinary studies indicate that auditory hallucinations may arise from speech perception neurocircuitry without disrupted theory of mind capacities. Computer simulations of excessive pruning in speech perception neural networks provide a model for these hallucinations and demonstrate that connectivity reductions just below a “psychotogenic threshold” enhance information processing. These data suggest a process whereby vulnerability to schizophrenia is maintained in the human population despite reproductive disadvantages of this illness.
We propose that the primary cause of schizophrenia is a pathological extension of synaptic pruning involving local connectivity that unfolds ordinarily during adolescence. Computer simulations suggest that this pathology provides reasonable accounts of a range of symptoms in schizophrenia, and is consistent with recent postmortem and genetic studies. NMDA-receptors play a regulatory role in maintaining and/or eliminating cortical synapses, and therefore may play a pathophysiological role.
Transcranial magnetic stimulation, EEG, and behavioral studies by our group implicate spurious activation of speech perception neurocircuitry in the genesis of auditory hallucinations in schizophrenia. The neurobiological basis of these abnormalities remains uncertain, however. We review our ongoing studies, which suggest that altered cortical coupling underlies speech processing in schizophrenia and is expressed via disrupted gamma resonances and impaired corollary discharge function of self-generated verbal thought.
Further tests of Amit's model are indicated. One strategy is to use the apparent coding sparseness of the model to make predictions about coding sparseness in Miyashita's network. A second approach is to use memory overload to induce false positive responses in modules and biological systems. In closing, the importance of temporal coding and timing requirements in developing biologically plausible attractor networks is mentioned.
In order to reach a better understanding of brain function, conceptual synergies linking empirical neurobiological studies and neurocomputational studies should be pursued. I describe an example of a potential synergy based on studies of neural network pruning. Simulations demonstrate that selective elimination of connections enhances the computational capacity of networks capable of temporal processing. These findings may shed light on the functional significance of postnatal neuro-developmental pruning of cortical connections that occurs in mammals.
Although Freud's merits may be readily acknowledged in the year of his 150th birthday, recent findings on repression-related phenomena cannot be accommodated by his classic conception, on which Erdelyi's theory is built. This point is illustrated by discussing the role of inhibitory processes. The unified theory of repression should be elaborated to generate falsifiable predictions on the reported phenomena.