Contributions of emotional prosody comprehension deficits to the formation of auditory verbal hallucinations in schizophrenia

Roskamp Laboratory of Brain Development, Modulation and Repair. Department of Psychiatry and Neurosciences, Morsani College of Medicine, University of South Florida, FL, USA.
Clinical psychology review (Impact Factor: 7.18). 02/2012; 32(4):244-50. DOI: 10.1016/j.cpr.2012.02.003
Source: PubMed

ABSTRACT Deficits in emotional processing have been widely described in schizophrenia. Associations of positive symptoms with poor emotional prosody comprehension (EPC) have been reported at the phenomenological, behavioral, and neural levels. This review focuses on the relation between emotional processing deficits and auditory verbal hallucinations (AVH). We explore the possibility that the relation between AVH and EPC in schizophrenia might be mediated by the disruption of a common mechanism intrinsic to auditory processing, and that, moreover, prosodic feature processing deficits play a pivotal role in the formation of AVH. The review concludes with proposing a mechanism by which AVH are constituted and showing how different aspects of our neuropsychological model can explain the constellation of subjective experiences which occur in relation to AVH.

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    ABSTRACT: MOSELEY, P., Fernyhough, C. and Ellison, A. Auditory verbal hallucinations as atypical inner speech monitoring, and the potential of neurostimulation as a treatment option. NEUROSCI BIOBEHAV REV 37(X) XXX-XXX,2013.- Auditory verbal hallucinations (AVHs) are the experience of hearing voices in the absence of any speaker, often associated with a schizophrenia diagnosis. Prominent cognitive models of AVHs suggest they may be the result of inner speech being misattributed to an external or non-self source, due to atypical self- or reality monitoring. These arguments are supported by studies showing that people experiencing AVHs often show an externalising bias during monitoring tasks, and neuroimaging evidence which implicates superior temporal brain regions, both during AVHs and during tasks that measure verbal self-monitoring performance. Recently, efficacy of noninvasive neurostimulation techniques as a treatment option for AVHs has been tested. Meta-analyses show a moderate effect size in reduction of AVH frequency, but there has been little attempt to explain the therapeutic effect of neurostimulation in relation to existing cognitive models. This article reviews inner speech models of AVHs, and argues that a possible explanation for reduction in frequency following treatment may be modulation of activity in the brain regions involving the monitoring of inner speech.
    Neuroscience & Biobehavioral Reviews 10/2013; 37(10). DOI:10.1016/j.neubiorev.2013.10.001 · 10.28 Impact Factor
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    ABSTRACT: Introduction Auditory hallucinations occur in schizophrenia and also in the general population. However, evidence points to differences in the nature and the mechanisms of clinical and non-clinical hallucinations, challenging the dominant assumption that they represent the same phenomenon. The current study extended this evidence by examining voice identity perception in hallucination-prone individuals. In schizophrenia, deficiencies discriminating between real (external) voices have been linked to basic acoustic cues, but voice discrimination has not yet been investigated in non-clinical hallucinations. Methods Using a task identical to that employed in patients, multidimensional scaling of voice dissimilarity judgements was used to examine how healthy individuals differing in hallucination-proneness (30 high and 30 low hallucination-prone individuals) distinguish pairs of unfamiliar voices. The resulting dimensions were interpreted with reference to acoustic measures relevant to voice identity. Results A two-dimensional "voice space", defined by fundamental frequency (F0) and formant dispersion (Df), was derived for high and low hallucination-prone groups. There were no significant differences in speaker discrimination for high versus low hallucination-prone individuals on the basis of either F0 or Df. Conclusions These findings suggest voice identity perception is not impaired in healthy individuals predisposed to hallucinations, adding a further challenge to the continuum model of psychotic symptoms.
    Cognitive Neuropsychiatry 12/2013; DOI:10.1080/13546805.2013.865512 · 2.18 Impact Factor
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    ABSTRACT: Auditory verbal hallucinations (AVH) are one of the most common and most distressing symptoms of schizophrenia. Despite fundamental research, the underlying neurocognitive and neurobiological mechanisms are still a matter of debate. Previous studies suggested that "hearing voices" is associated with a number of factors including local deficits in the left auditory cortex and a disturbed connectivity of frontal and temporoparietal language-related areas. In addition, it is hypothesized that the interhemispheric pathways connecting right and left auditory cortices might be involved in the pathogenesis of AVH. Findings based on Diffusion-Tensor-Imaging (DTI) measurements revealed a remarkable interindividual variability in size and shape of the interhemispheric auditory pathways. Interestingly, schizophrenia patients suffering from AVH exhibited increased fractional anisotropy (FA) in the interhemispheric fibers than non-hallucinating patients. Thus, higher FA-values indicate an increased severity of AVH. Moreover, a dichotic listening (DL) task showed that the interindividual variability in the interhemispheric auditory pathways was reflected in the behavioral outcome: stronger pathways supported a better information transfer and consequently improved speech perception. This detection indicates a specific structure-function relationship, which seems to be interindividually variable. This review focuses on recent findings concerning the structure-function relationship of the interhemispheric pathways in controls, hallucinating and non-hallucinating schizophrenia patients and concludes that changes in the structural and functional connectivity of auditory areas are involved in the pathophysiology of AVH.
    Frontiers in Human Neuroscience 02/2014; 8:55. DOI:10.3389/fnhum.2014.00055 · 2.90 Impact Factor


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Jun 1, 2014