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There is considerable support nowadays for a continuum model of psychosis, whereby symptoms associated with psychosis also occur in psychiatrically healthy populations (e.g. van Os et al., 2009; although see e.g. David, 2010, for a recent sceptical view). A new article by Dutch researchers (Diederen et al., in press) reports on an fMRI study designed to test whether neural activation associated with ‘healthy’ voice-hearing experiences differs from that observed in psychiatric patients. To our knowledge, this is only the second neuroimaging study to include a non-psychiatric voice-hearing group (the first was Linden et al., 2010).
To see how the 21 healthy voice-hearers were recruited, we need to go back to an earlier report from this group. In an article published last year in Schizophrenia Bulletin (Sommer et al., 2010) scores from around 4,000 respondents to a website questionnaire (a version of the Launay-Slade Hallucination Scale) led to the identification of a group of 103 people who had genuine voice-hearing experiences but no psychopathology. The 42 people who were scanned in the new study were selected from this larger sample, and matched to data from an existing fMRI dataset from psychiatric patients with a range of disorders (including schizophrenia, schizoaffective disorder and psychosis Not Otherwise Specified).
The researchers used quite stringent criteria for including participants’ scan data in their analyses. To be included, participants had to have had at least four AVH experiences during the 8-minute scan period, with a minimum total duration of fifty seconds. Participants indicated when they were hearing a voice by squeezing a balloon and releasing it when the voice stopped.
Half of the 42 subjects met these criteria, giving a sample of 21 nonclinical voice-hearers whose data could be matched with those from psychosis patients. Although the team was interested in differences in activation across the brain, they constrained their analyses by focusing in on regions known to be involved in AVHs, such as the bilateral inferior frontal gyri (including Broca’s area), insula, superior and middle temporal gyri, cerebellum and parahippocampal gyrus. They made no specific hypotheses, however, about particular regions of difference in activation. To determine whether the groups differed in activation, they compared data from the two samples first in their specific region of interest and then (in an exploratory fashion) across the whole brain.
The results of these analyses were rather simple. In both groups, the areas that were expected to activate mostly did activate. There were no differences in activation between the groups, however, leading the researchers to conclude that nonclinical and clinical AVHs do not differ in terms of their underlying neural activation.
Do these findings support the continuum hypothesis of psychosis? The continuum model would hold that voice-hearing experiences, no matter to whom they are occurring, will result from the same underlying neurophysiological processes. The researchers conclude, however, that their results cannot be used either to support or refute the continuum hypothesis, as the common patterns of activation they reported might have arisen through different mechanisms. The authors also point out that it would be interesting (although impossible in this study because of limitations on sample size) to compare patients with different diagnoses, such as schizophrenia and psychosis Not Otherwise Specified.
A number of further interesting questions arise from this report. One possible criticism is that the study did not gather any information about the content of the voice-hearing experiences, such as information about what the voices were saying, or other qualitative details. As voice-hearing experiences are highly heterogeneous, this would seem to be an important issue for future research.
A second point is that, as you would expect, the psychosis group presented with other symptoms such as delusions. This makes the lack of differences in activation even more striking. If neural activations between deluded psychosis patients and non-deluded healthy controls are so similar, what does that tell us about the neural basis of these other psychotic symptoms? Although the nonclinical group did not have clinical delusions, they did score more highly (relative to controls) on a schizotypy measure, which may well indicate relatively high levels of delusionality. That might point to the conclusion that the two groups were not actually all that different in terms of symptomatology, and that a more salient difference between them might be their levels of social functioning.
David, A. S. (2010). Why we need more debate on whether psychotic symptoms lie on a continuum with normality. Psychological Medicine, 40, 1935-1942.
Diederen, K. M. J., Daalman, K., de Weijer, A. D., Neggers, S. F. W., van Gastel, W., Blom, J. D., Kahn, R. S., & Sommer, I. E. C. (in press). Auditory hallucinations elicit similar brain activation in psychotic and nonpsychotic individuals. Schizophrenia Bulletin.
Linden, D. E. J., Thornton, K., Kuswanto, C. N., Johnston, S. J., van de Ven, V., & Jackson, M. C. (2010). The brain’s voices: Comparing nonclinical auditory hallucinations and imagery. Cerebral Cortex, 21, 330-337.
Sommer, I. E. C., Daalman, K., Rietkerk, T., Diederen, K. M., Bakker, S., Wijkstra, J., & Boks, M. P. M. (2010). Healthy individuals with auditory verbal hallucinations: Who are they? Psychiatric assessments of a selected sample of 103 subjects. Schizophrenia Bulletin, 36, 633-641.
van Os, J., Linscott, R. J., Myin-Germeys, I., Delespaul, P., & Krabbendam, L. (2009). A systematic review and meta-analysis of the psychosis continuum: Evidence for a psychosis proneness-persistence-impairment model of psychotic disorder. Psychological Medicine, 39, 179-195.
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