While often considered to be solely a symptom of schizophrenia, “recent studies have identified that about 4%-5% of the general population experience “hearing voices” when excluding previous mental health problems, medication, drug use, and other potentially confounding factors in this group of individuals”. A recent study [1] found:
“…7.3% of the sample reported a life-time prevalence of AVH. Those with AVH were more likely to be single and unemployed, reported higher levels of depression and anxiety, and experienced a higher number of severe life events compared with those without AVH. Only 16% of those who experienced AVH in the general population sought professional help for these experiences. Compared to those who did not seek professional help, participants that had were more likely to experience AVH with a negative content, experience them on a daily basis, undergo negative reactions when experiencing AVH, and resist AVH. In conclusion, the prevalence of AVH was found to be relatively high. The results also revealed higher levels of reduced mental health for individuals who sought professional help, followed by those who did not, compared with those who had never experienced AVH”
Prevalence rates of AVHs are estimated at 11.3-62.8% in patients with bipolar disorder and 5.4-40.6% in patients with major depression [2] Hearing voices due to trauma is also common and “it has been suggested on the basis of the negative emotional content of AVHs that they may represent misinterpreted recall of strong emotional and traumatic memories that would act like intrusions, and that are mislabeled as coming from the outer world.” Other models include “a failure to adequately monitor and label verbal thoughts as coming from the inside rather than from the outside of the patient’s head, often called an “inner speech” model”
A recent article goes into more detail:
Auditory hallucinations: A review of the ERC “VOICE” project (2015)
In this invited review I provide a selective overview of recent research on brain mechanisms and cognitive processes involved in auditory hallucinations. The review is focused on research carried out in the “VOICE” ERC Advanced Grant Project, funded by the European Research Council, but I also review and discuss the literature in general. Auditory hallucinations are suggested to be perceptual phenomena, with a neuronal origin in the speech perception areas in the temporal lobe. The phenomenology of auditory hallucinations is conceptualized along three domains, or dimensions; a perceptual dimension, experienced as someone speaking to the patient; a cognitive dimension, experienced as an inability to inhibit, or ignore the voices, and an emotional dimension, experienced as the “voices” having primarily a negative, or sinister, emotional tone. I will review cognitive, imaging, and neurochemistry data related to these dimensions, primarily the first two. The reviewed data are summarized in a model that sees auditory hallucinations as initiated from temporal lobe neuronal hyper-activation that draws attentional focus inward, and which is not inhibited due to frontal lobe hypo-activation. It is further suggested that this is maintained through abnormal glutamate and possibly gamma-amino-butyric-acid transmitter mediation, which could point towards new pathways for pharmacological treatment. A final section discusses new methods of acquiring quantitative data on the phenomenology and subjective experience of auditory hallucination that goes beyond standard interview questionnaires, by suggesting an iPhone/iPod app.
“AVHs are the most characteristic symptom of schizophrenia and psychosis, and they “define” the disorder from a clinical and phenomenological point of view. Clinically, what drains the patient both cognitively, emotionally, and physically is the ongoing “dialogue” and typically negative comments and commands from the “voice”, which recruits almost all available cognitive resources, and with the resulting typical signs of reality disorientation, and inward attentional focus. From a phenomenological point of view, AVHs are characterized by a limited set of core features; the experience is auditory in nature, with a distinct perceptual quality of “hearing a voice”… The “voice” is typically localized outside of the head, although recent research has shown that hearing the “voice” as coming from the inside is more common than previously believed. The “voices” also typically have negative emotional valence, which is in addition experienced as controlling the patient, revealing a lack of executive cognitive power by the patient.”
Some interventions are mentioned:
“Failure of attention and executive control in AVH patients may also be the starting point for novel cognitive training attempts. Cognitive behavior therapy for schizophrenia and auditory hallucinations has long been directed towards giving the patient the skills necessary to voluntarily inhibit and shift attention away from the “voice”. Recent approaches to cognitive therapy have been more focused on specific training procedures, rather than inducing a therapeutic change of strategy. Thus, a distinction can be made between treatments which in the case of schizophrenia will mean abolishing symptoms, therapies inducing new strategies on how to cope with stressful situations, and training which is specifically aimed at handling a single event, or symptom. We have developed an iPod/iPhone app based on the dichotic listening paradigm, described above, as a tool to learn how to inhibit and ignore the “voice”, also to be used in social situations, like riding on a bus, or being in other social situations, which can be used “there-and-then” whenever the patient feels the urge to have help in withstanding the “voice”. Preliminary results from 15 patients show some promising effects that warrant further research on the use of app-technology for training and learning new mental skills in patients with schizophrenia.”
The neurochemistry of AVHs is ‘reviewed’:
“…We do not know what triggers an AVH at the cellular level, causing the subjective experience of perceiving a “voice” in the absence of an external stimulus…
Glutamate is suggested to have an effect on positive symptoms associated with schizophrenia through balancing sub-cortical dopamine release. The classic pathway for the involvement of glutamate in schizophrenia and in the regulation of positive symptoms is that reduced cortical glutamate levels, and/or dysfunctional N-methyl-D-aspartate (NMDA) receptors, hypo-activate GABA interneurons, which leaves striatal dopamine release uninhibited, resulting in dopamine excess in the schizophrenia brain. The finding of reduced glutamate levels in schizophrenia patients would fit with a number of other studies which show that when healthy individuals are given ketamin and phencyclidin (PCP), which are drugs that act as NMDA receptor antagonists, they show signs and symptoms of a psychosis. The possible relationship between glutamate reduction and dopamine was described by Carlsson et al such that prefrontal glutamate release will result in activation of GABA interneurons to balance too high levels of glutamate, which will also have an inhibitory effect on striatal dopamine release. When glutamate levels fall below critical levels or when GABA receptors are dysfunctional, GABA interneurons will consequently be hypo-activated and dopamine release will be correspondingly uninhibited. This will result in excess dopamine, and in particular dopamine D2-receptor activity, producing positive psychotic symptoms. It should be pointed out, however, that a more recent article concluded after reviewing the schizophrenia literature, with both decreases and increases of dopamine, particularly in frontal regions”
advancingschizophreniatherapeutics 