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Auditory verbal hallucinations (AVH) in schizophrenia spectrum disorders (SSDs) may arise from misattributed inner speech. However, it is unclear if inner speech frequency and phenomenology differ in schizophrenia-spectrum voice-hearers compared with healthy individuals, and how different inner speech varieties relate to AVH and affect. Using experience sampling methodology (ESM), this study examined the moment-to-moment dynamics between inner speech varieties, AVH, and affect.
Methods
Participants completed 6 days of ESM on an electronic device, responding to 10 daily prompts on inner speech varieties (i.e. dialogic, evaluative, other people, condensed, and positive), AVH, and affect. Responses from 32 individuals with SSDs with current AVH (‘SSD’) and 34 healthy controls (‘HC’) were analyzed using linear mixed modeling.
Results
SSD reported significantly more inner speech moments and higher momentary intensity of evaluative, other people, condensed, and positive inner speech compared with HC, but not for dialogic inner speech. Within SSD, higher momentary intensities of dialogic, evaluative, other people, and condensed inner speech were associated with higher AVH levels. Momentary negative affect (NA) moderated the association between evaluative inner speech and AVH, with a stronger association at higher NA levels.
Conclusions
SSDs with current AVH experience more frequent inner speech and exhibit a distinct phenomenological profile compared with healthy individuals. Several inner speech varieties are associated with AVH severity momentarily, supporting the hypothesis that inner speech contributes to AVH at the phenomenological level. This study highlights the emotional state as an important moderator of the inner speech–AVH relationship and as a potential therapeutic target.
By
Thomas J. Whitford, Department of Psychiatry Brigham and Women's Hospital Harvard School of Medicine Boston, MA, USA and Department of Psychiatry Melbourne Neuropsychiatry Centre University of Melbourne Melbourne, Australia,
Marek Kubicki, Department of Psychiatry VA Boston Healthcare System and Department of Psychiatry Brigham and Women's Hospital Harvard Medical School Boston, MA, USA,
Martha E. Shenton, VA Boston Healthcare System and Department of Psychiatry Brigham and Women's Hospital Harvard Medical School Boston, MA, USA
Emil Kraepelin, one of the founding fathers of the diagnostic concept of schizophrenia, argued that the disorder was underpinned by abnormalities in brain structure. In his 1899 textbook, Kraepelin wrote: “in dementia praecox [schizophrenia], partial damage to, or destruction of, cells of the cerebral cortex must probably occur” (Kraepelin,1907). Since that time, an enormous amount of research has been undertaken with an eye to determining whether or not Kraepelin was correct. Until recently, the question of whether patients with schizophrenia (SZ) exhibit abnormalities in brain structure was more or less synonymous with the question of whether they exhibit abnormalities in gray matter (GM). The GM, so-called because of its grayish appearance in post-mortem tissue sections, is thought to consist primarily of neuron bodies, dendrites, axon terminals and other synaptic infrastructure and certain classes of neuroglia. Until recently, the vast majority of research aimed at investigating the neuroanatomical underpinnings of SZ has focused on GM. This is perhaps understandable, given that GM comprises both the brain's fundamental units of information processing (neurons) and the sites-of-action for most psychotropic medications (synapses). In recent years, however, a growing proportion of contemporary research has begun to focus on the “other half of the brain” (as wryly denoted by Fields, 2004), i.e. the white matter. The white matter (WM) is primarily constituted of myelinated axon sheaths, which form the infrastructure for signal transmission between spatially discrete populations of neurons.
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