Schizophrenia is a complex syndrome comprising positive, negative, and cognitive symptoms. While all of these factors may be involved in the genesis of AVH, a key limitation is that most of these studies were conducted in patients with schizophrenia. It should, however, be noted that results are inconsistent. Previous studies showed that the propensity to hear voices may be associated with a number of factors including decreased left cerebral dominance for language ( Levitan et al., 1999 Sommer et al., 2001 Weiss et al., 2006 Hugdahl et al., 2007), dysfunctional connectivity of frontal and temporoparietal language regions ( Frith et al., 1995 Spence et al., 2000 Ford et al., 2007 Kühn and Gallinat, 2010), decreases in psychophysiological measures of effortful attention ( Havermans et al., 1999 Turetsky et al., 2000), and dopamine dysfunction. The latter can be provided by trait studies that focus on comparing brain activation between individuals with and without AVH. Although these studies provide a helpful start at understanding what happens in the brain during AVH, they do not provide information about brain mechanisms predisposing a person to experience AVH. The first group of studies investigated the neural signature of AVH and revealed that AVH-related brain activation can be observed in frontal and temporoparietal language areas as well as in the parahippocampal region ( Jardri et al., 2010 Kühn and Gallinat, 2010). “state” studies) on the one hand and “trait” investigations on the other hand ( Kühn and Gallinat, 2010). Most of these can be divided into “symptom-capture” (a.k.a. Over the last decades a considerable number of studies aimed at elucidating the neurobiological mechanism of AVH in schizophrenia patients. This is, at present, hampered by the fact that the pathophysiology of AVH remains largely unknown. These hallucinations do, however, not respond to pharmaceutical intervention in 25–30% of patients, stressing the need for development of new treatment options ( Shergill et al., 1998). At present, the primary treatment for AVH in psychiatric patients consists of antipsychotic medication which is frequently combined with cognitive behavioral therapy. While AVH are not associated with distress in non-psychotic individuals, they can seriously disrupt social functioning in psychotic patients ( Nayani and David, 1996 Daalman et al., 2011). AVH are, however, most common in schizophrenia, in which they occur with an average prevalence of 70% ( Sartorius et al., 1986). AVH are even more common during periods of partial wakefulness, i.e., when falling asleep (hypnagogic hallucinations) or during waking (hypnopompic hallucinations). Moreover, these hallucinations are observed in ∼10–15% of healthy, i.e., non-psychotic, individuals in the general population ( Tien, 1991 Sommer et al., 2008 Beavan et al., 2011). Indeed, AVH are frequently observed in individuals with a neurological, neurodegenerative, or psychiatric disorder ( Aleman and Laroi, 2008). In contemporary Western societies auditory verbal hallucinations (AVH) or “voices” are generally considered an aspect of disease ( al-Issa, 1995). Finally, specific aspects of AVH such as voluntary control may be related to the timing of the supplementary motor area and language areas in the experience of AVH. Furthermore, it was observed that decreased cerebral dominance for language and dopamine dysfunction, which are consistently found in schizophrenia, are most likely not specifically related to AVH as these abnormalities were absent in healthy voice hearers. Moreover, while effortful attention appears not to be related to AVH, individuals prone to hallucinate seem to have an enhanced attention bias to auditory stimuli which may stem from aberrant activation of the anterior cingulated regions. This is in concordance with investigations that observed prominent activation of these areas during the state of AVH. These studies showed that increased sensitivity of auditory areas to auditory stimulation and aberrant connectivity of language production and perception areas is associated with AVH. Indeed a number of studies used this approach and investigated brain structure and function in non-psychotic individuals with AVH. As these non-psychotic individuals experience AVH in the absence of other psychiatric symptoms and medication-use they provide an excellent model to study AVH in isolation.
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