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Auditory/verbal hallucinations (AVHs) are comprised of spoken conversational speech seeming to arise from specific, nonself speakers. One hertz repetitive transcranial magnetic stimulation (rTMS) reduces excitability in the brain region stimulated. Studies utilizing 1-Hz rTMS delivered to the left temporoparietal cortex, a brain area critical to speech perception, have demonstrated statistically significant improvements in AVHs relative to sham simulation. A novel mechanism of AVHs is proposed whereby dramatic pre-psychotic social withdrawal prompts neuroplastic reorganization by the "social brain" to produce spurious social meaning via hallucinations of conversational speech. Preliminary evidence supporting this hypothesis includes a very high rate of social withdrawal emerging prior to the onset of frank psychosis in patients who develop schizophrenia and AVHs. Moreover, reduced AVHs elicited by temporoparietal 1-Hz rTMS are likely to reflect enhanced long-term depression. Some evidence suggests a loss of long-term depression following experimentally-induced deafferentation. Finally, abnormal cortico-cortical coupling is associated with AVHs and also is a common outcome of deafferentation. Auditory/verbal hallucinations (AVHs) of spoken speech or "voices" are reported by 60-80% of persons with schizophrenia at various times during the course of illness. AVHs are associated with high levels of distress, functional disability, and can lead to violent acts. Among patients with AVHs, these symptoms remain poorly or incompletely responsive to currently available treatments in approximately 25% of cases. For patients with AVHs who do respond to antipsychotic drugs, there is a very high likelihood that these experiences will recur in subsequent episodes. A more precise characterization of underlying pathophysiology may lead to more efficacious treatments.

Atendency to extract spurious, message-like meaning from meaningless noise was assessed as a risk factor leading to schizophrenia-spectrum disorders by assessing word length of speech illusions elicited by multispeaker babble in 43 people with prodromal symptoms. These individuals were randomised to olanzapine v. placebo groups during year 1 followed by no pharmacological treatment for those with no disorder conversion during year 2. A time-dependent Cox regression analysis of conversion to schizophrenia-spectrum disorder revealed a significant interaction between condition (olanzapine v. no drug) and length of speech illusion, with the latter strongly predicting subsequent conversion during medication-free intervals but not during olanzapine treatment.

A number of studies suggest that schizophrenia may arise from overzealous pruning of synapses that are an extension of normal developmental pruning during adolescence. Moreover, there has been a long history of studies suggesting that this disorder arises from alterations in the dopaminergic neuromodulatory systems. In order to further assess and compare these two hypotheses, a computer simulation of some aspects of speech perception was developed utilizing a recurrent, backpropagation model of working memory previously reported by Elman . This system was found to produce spontaneous percepts simulating hallucinated speech when the working memory component either was excessively pruned or when neuronal responses were modulated to simulatea hyperdopaminergic system. These hallucinogenic systems also demonstrated disruptions in processing input information when "phonetic information" was degraded. The perceptual performance of these systems were compared to that of actual hallucinating patients and normal controls while tracking (repeating while simultaneously listening to) speech that was phonetically degraded. We found that the neural network simulation producing the best match to speech tracking performance of human hallucinators was an overpruned system with compensatory hypodopaminergic adjustments. These data suggest that the primary pathophysiology of schizophrenia arises from curtailed connectivity in working memory systems and that dopaminergic alterations reflect secondary compensatory adjustments.

Objective: The authors tested a model of hallucinated "voices" based on a neural network computer simulation of disordered speech perception., Method: Twenty-four patients with schizophrenia spectrum disorders who reported hallucinated voices were compared with 21 patients with schizophrenia spectrum disorders who did not report voices and 26 normal subjects. Narrative speech perception was assessed through use of a masked speech tracking task with three levels of superimposed phonetic noise. A sentence repetition task was used to assess grammar-dependent verbal working memory, and an auditory continuous performance task was used to assess nonlanguage attention., Results: Masked speech tracking task and sentence repetition performance by hallucinating patients was impaired relative to both nonhallucinating patients and normal subjects. Although both hallucinating and nonhallucinating patients demonstrated auditory attention impairments when compared to normal subjects, the two patient groups did not differ with respect to these variables., Conclusions: Results support the hypothesis that hallucinated voices in schizophrenia arise from disrupted speech perception and verbal working memory systems rather than from nonlanguage cognitive or attentional deficits.

The mechanism of hallucinated speech or 'voices', a symptom commonly reported by schizophrenic patients, is poorly understood. We have undertaken two types of study to explore the hypothesis that this symptom arises from pathologically altered speech perception networks. The first consists of neural network computer simulations of narrative speech perception. We have shown that if these networks are partially disconnected or undergo a 'monamine' neuromodulatory disturbance, 'hallucinated speech' (speech percepts occurring in the absence of phonetic input) are simulated as well as specific speech perception impairments. The latter finding prompted us to conduct parallel studies of actual schizophrenic patients using a 'masked speech tracking' (MST) task. MST requires subjects to track narrative speech the phonetic clarity of which is reduced with superimposed multispeaker 'babble.' Hallucinators demonstrated speech perception impairments and experimentally induced perceptual 'illusions' which clearly differentiated them from non-hallucinators and normal controls. Our results support the hypothesis that 'voices' are spurious products of altered speech perception networks.

One of us has hypothesised that the 'voices' of schizophrenic patients reflect altered preconscious planning of discourse that can produce involuntary 'inner speech' as well as incoherent overt speech. Some schizophrenic patients reporting voices do not, however, have disorganised speech. We hypothesise that these 'counterexample' patients compensate for impairments of discourse planning by reducing language complexity and relying on highly rehearsed topics. A 'language therapy' designed to challenge and enhance novel discourse planning was administered to four such patients; three had significant albeit temporary reductions in the severity of their voices. These clinical findings provide further evidence that alterations of discourse planning may underlie hallucinated voices.

The etiology of schizophrenic hallucinations of 'voices' remains unknown. The following is a discussion of a hypothesis linking these hallucinatory phenomena to a disruption in discourse planning. The relationship between normal imagery and hallucination is discussed. The concept of 'alien intentionality' is introduced, and a theoretical argument is presented which links this phenomenon with the exteriorization of internal images. Statistical data linking discourse planning disruptions and schizophrenic data are reviewed, and a description of the treatment of a hallucinating schizophrenic via a novel type of speech therapy is described.