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Approaches to Understanding Auditory Hallucinations

Posted on 12 Sep 2012
View full article Flavie Waters Paul Allen Judith Ford Iris Sommer

Thanks to the Maryland Psychiatric Research Center and Oxford University Press, publishers of Schizophrenia Bulletin, for providing open access to the introductory article for this Webinar.


Read a series of questions and panelists' answersPosted 22 October 2012

Click on the image to launch the recording.

The Participants' Presentation

Iris Sommer's Presentation

Judith Ford's Presentation


Auditory hallucinations are a hallmark of schizophrenia, but they afflict people without the disorder, too. Looking closer at this population may clarify how auditory hallucinations arise, as they occur outside of the complicated spectrum of other schizophrenia symptoms. On 13 September 2012, we hosted a 1.5-hour Webinar led by Flavie Waters of the University of Western Australia, with presentations by Paul Allen of the Institute of Psychiatry, Judith Ford of the University of California, San Francisco, and Iris Sommer of University Medical Center Utrecht.

The short slide presentations were based on a series of articles in the July issue of the Schizophrenia Bulletin, which in turn sprang from the first meeting of the International Consortium on Hallucination Research and Related Symptoms, held in London in September 2011. There, researchers laid out a framework to study auditory hallucinations in schizophrenia and in nonclinical populations with a variety of methods. The questions they raised, and which we discussed in the Webinar, included:

  • How do the basic features of auditory hallucinations, like voice characteristics, differ between schizophrenia and other people who experience auditory hallucinations?
  • What are the cognitive processes and brain regions involved?
  • Are there electrophysiological signatures that mark a brain prone to auditory hallucinations, and do these hold true for nonclinical people with hallucinations?
  • Finally, what treatment options are there?

Making headway in these questions in both schizophrenia and other groups will elucidate the origins of auditory hallucinations, and refine methods for treatment.

Waters F. Multidisciplinary approaches to understanding auditory hallucinations in schizophrenia and nonschizophrenia populations: the international consortium on hallucination research. Schizophr Bull. 2012 Jun ;38(4):693-4. Abstract

Questions and Panelists' Answers—Posted 22 October 2012

Q: Dr. Sommer, do you know of anyone who has looked at the differences between D2R long (postsynaptic) versus D2R short (presynaptic) in the treatment of AH?

A: Good point. In patients with psychosis, the main increase in the DA route is presynaptic, while all antipsychotic agents work on the postsynaptic part. It would make sense to try to reduce presynaptic DA (see Howes et al., 2012).

Q: What about anticholinergic medication for Charles Bonnet syndrome?

A: Pharmacological treatment of Bonnet syndrome is not straightforward. Anticholinergic therapeutics would not be effective, but perhaps you mean acetylcholinesterase inhibitors such as donepezil and rivastigmine. These have been tried and are sometimes effective.

Q: Have you ever thought that maybe "the voice" is the one that needs the therapy and not the patient in front of you?

A: I don't see voices as persons, but as a phenomenon/symptom. So no, the patient is always my focus.

Q: I believe that too many people are started on antipsychotics based on an improper understanding of hallucinations.

A: Thanks for sharing your thoughts. I'd like to know your arguments for that opinion.

Q: Are there any phenomenological characteristics of auditory hallucinations that characterize those occurring in non-clinical populations?

A: Quite clearly. Non-clinical populations usually experience voices with a neutral or even positive emotional content. In addition, age of onset is frequently lower.

Q: How would one manage a client for whom the content of "voices" is not bothersome, but for whom the volume creates problems, and has so far been refractory to several antipsychotics? Thanks.

A: It is important to know if this person also had delusions. If so, this may be a reason to continue medication, even when not effective for the voices. Has he/she already tried clozapine? It has rather severe side effects, but is the most effective medication in patients with resistant symptoms. If no medication is needed (no delusions), coping techniques to activate the language areas might be useful.

Q: What happens when language deteriorates with swearing and inappropriate sexual language with hallucinations on a consistent basis?

A: Hallucinations frequently consist of this type of language, especially in persons with a psychotic disorder. It may indicate involvement of the right hemisphere areas (see Sommer et al., 2008).

Q: Dr. Ford, what is the correlation of these EEG measures with trigger brain areas for AH?

A: The ERP studies show that the auditory cortex is either busy or preoccupied in anticipation of hearing voices in people who experience auditory verbal hallucinations (AVHs). We know from symptom-capture studies that the auditory cortex is a key region activated during the experience of AVHs.

Q: This is a question for Judith Ford. Has hyperconnectivity between different brain regions been found regarding positive content in auditory hallucinations, as some of the voices people hear may actually become comforting?

A: Only recently have we begun to focus on the symptoms of schizophrenia, and instead, the field spent decades trying to use EEG and ERP data to demonstrate that schizophrenia is a brain-based illness. This is by way of saying that the content of voices, while important and interesting in its own right, has not been addressed with these methods. I am now using fMRI data to address that question.

Q: How do you reconcile evidence for decreased frontotemporal connectivity with evidence of increased frontotemporal (striatal) connectivity in AVH sufferers? Are these differences between trait and state?

A: This is a difficult question for me, as I see decreased frontal-temporal connectivity using EEG data that has millisecond resolution, and increased connectivity among some of the language areas of the brain using fMRI data with a much slower resolution. The difference lies in the different resolution of the methods (fast vs. slow), the different tasks (talking vs. rest), or the different regions inspected. The talking (EEG) data could only reflect trait effects, as the patients were not hallucinating while talking. The rest (fMRI) data probably involve both trait and state aspects of voices.

Q: Why are the vast majority of auditory hallucinations in the psychotic and normal patients of human speech as opposed to other complex noise?

A: In my view, daydreams are the raw material of hallucinations. And although my daydreams may be different from those of others, I do not experience complex noise, although I may hear music. Music hallucinations are not uncommon, but are not a cardinal symptom of schizophrenia.

Q: Can any of the authors direct us to the most comprehensive account regarding the assessment of hallucinations?

A: Aleman, André; Larøi, Frank. Hallucinations: The Science of Idiosyncratic Perception. Washington, DC, US; and Massoud Stephane (2006) "The Assessment of Auditory Hallucinations." Chapter 6. In Neuroscience of Hallucinations. Renaud Jardri, Arnaud Cachia, Pierre Thomas Delphine.

Q: In understanding true and pseudo-auditory hallucinations, how does one differentiate?

A: Pseudo-hallucinations have often been thought to be isolated experiences that occur mainly inside the head. They are also thought to be closely related to vivid imagery, and to be associated with better insight. However, Aleman and Larøi, (2011) argue that it may be more helpful to see auditory hallucinations as having several dimensions (vividness, degree insight, inside/outside), each occurring on a continuum of severity.