View Comments By:Judith Ford
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:
Ford JM, Morris SE, Hoffman RE, Sommer I, Waters F, McCarthy-Jones S, Thoma RJ, Turner JA, Keedy SK, Badcock JC, Cuthbert BN. Studying Hallucinations Within the NIMH RDoC Framework. Schizophr Bull. 2014 May 21. Abstract
SRF held a webinar on Wednesday, May 28, on the application of the Research Domain Criteria (RDoC) to hallucinations, one of the core symptoms of schizophrenia. Our panel included Bruce Cuthbert of the NIMH, Ralph Hoffman of Yale University, Sarah Keedy of the University of Chicago, Iris Sommer of University Medical Center, Utrecht, and Jessica Turner of Georgia State University.
Listen to the Webinar
Bruce Cuthbert's Presentation
Ralph Hoffman's Presentation
Sarah Keedy's Presentation
Iris Sommer's Presentation
— Posted 20 May 2014Rich Lewine
— Posted 6 July 2014Ralph Hoffman
— Posted 8 July 2014
by Hakon Heimer
The Research Domain Criteria (RDoC) represent the efforts of the US National Institute of Mental Health to move beyond the categories of the Diagnostic and Statistical Manual of Mental Disorders (DSM) in research on mental illnesses. The criteria were developed out of the limelight for several years under the stewardship of Bruce Cuthbert at NIMH, but then burst onto the public scene in a very dramatic way last year (see The New York Times article and the NIMH/APA statement).
The goal of RDoC, which is "classifying psychopathology based on dimensions of observable behavior and neurobiological measures," seems like an arduous enough task for most psychiatric disorders, but how would one study the cardinal symptoms of schizophrenia—hallucinations and delusions—using the current limited access to human brain function? (And, of course, the question that follows every animal modeler: whether mice can hear squeaks that are not there.)
The RDoC work groups zeroed in on auditory hallucinations—specifically verbal hallucinations—as the lowest of these high-hanging fruit. The phenomenon occurs not only in schizophrenia or in other psychiatric disorders such as borderline personality disorder and post-traumatic stress disorder, but also in epilepsy, traumatic brain injury, acquired deafness, and other non-psychiatric disorders. Moreover, a growing body of research has proposed that people without psychiatric symptoms who report hearing voices might be on a continuum with people who hear voices in the company of other symptoms of schizophrenia.
Cuthbert and the RDoC work group believe that current technologies will allow the exploration of many different aspects of how hallucinations, and the experience of them, might be processed differently in the brain from the hearing of external speech. This webinar provided the researchers working on this project an opportunity to explain how they arrived at their conclusions and how hallucinations can fit into the RDoC Matrix, but more importantly, gave the research community a chance to offer any additional insights.
Comments on Online Discussion
Comment by: Judith Ford
Submitted 20 May 2014
Posted 20 May 2014
Agency: The ability to recognize one’s self as the agent of one’s actions and thoughts, including the recognition of one’s own body/body parts.
One core feature of auditory hallucinations (AHs) is that they are experienced as somewhat separate from one’s own mental processes. This lack of subjective experience of self, accompanied by false beliefs that they arise from an external agency, has traditionally been thought to reflect deficits in the sense of agency or self-monitoring. Feinberg (Feinberg, 1978) suggested that a basic neural mechanism (efference copy/corollary discharge) might underpin these deficits and ultimately result in AHs. During self-produced actions, corollary discharge signals alert the sensory cortex about the expected sensations. Feinberg further suggested that thoughts may conserve the mechanisms that evolved for motor actions, such that thoughts are associated with efference copy and corollary discharge signals. If these fail to be effectively transmitted to speech perception regions, thoughts may fail to be tagged as "self" and seem “non-self” to the person who experiences AH. Studies have now found evidence for impaired corollary signals during self-produced speech associated with AHs (Heinks-Maldonado et al., 2007). In addition, related approaches such as feed-forward models (Frith et al., 2000) and apparent mental causation (Wegner and Wheatley, 1999) have been applied to AHs (see Jones and Fernyhough, 2007), as have other fruitful ways forward (Wible, 2012). Indeed, clinical and non-clinical groups with AHs have difficulties in identifying their own actions and thoughts, and commonly misattribute self-generated behaviors to an external source (Waters et al., 2012).
Importantly, there are several different forms of AHs (McCarthy-Jones et al., 2014); some people report “own thought” AHs, formerly termed "Gedanken Lautwerden." The neural mechanisms responsible for self and non-self AHs could be different (Sommer et al., 2010). For people who can distinguish between their voices and their responses to the voices, self-monitoring failure is a less parsimonious explanation.
Feinberg I. Efference copy and corollary discharge: implications for thinking and its disorders. Schizophr Bull . 1978 ; 4(4):636-40. Abstract
Frith CD, Blakemore S, Wolpert DM. Explaining the symptoms of schizophrenia: abnormalities in the awareness of action. Brain Res Brain Res Rev . 2000 Mar ; 31(2-3):357-63. Abstract
Heinks-Maldonado TH, Mathalon DH, Houde JF, Gray M, Faustman WO, Ford JM. Relationship of imprecise corollary discharge in schizophrenia to auditory hallucinations. Arch Gen Psychiatry . 2007 Mar ; 64(3):286-96. Abstract
Jones SR, Fernyhough C. Thought as action: inner speech, self-monitoring, and auditory verbal hallucinations. Conscious Cogn . 2007 Jun ; 16(2):391-9. Abstract
McCarthy-Jones S, Trauer T, Mackinnon A, Sims E, Thomas N, Copolov DL. A new phenomenological survey of auditory hallucinations: evidence for subtypes and implications for theory and practice. Schizophr Bull . 2014 Jan ; 40(1):231-5. Abstract
Sommer IE, Selten JP, Diederen KM, Blom JD. Dissecting auditory verbal hallucinations into two components: audibility (Gedankenlautwerden) and alienation (thought insertion). Psychopathology . 2010 ; 43(2):137-40. Abstract
Waters F, Woodward T, Allen P, Aleman A, Sommer I. Self-recognition deficits in schizophrenia patients with auditory hallucinations: a meta-analysis of the literature. Schizophr Bull . 2012 Jun ; 38(4):741-50. Abstract
Wegner DM, Wheatley T. Apparent mental causation. Sources of the experience of will. Am Psychol . 1999 Jul ; 54(7):480-92. Abstract
Wible CG. Schizophrenia as a disorder of social communication. Schizophr Res Treatment . 2012 ; 2012:920485. Abstract
View all comments by Judith FordComment by: Rich Lewine
Submitted 3 July 2014
Posted 6 July 2014
First, thank you, Dr. Hoffman, for a thought-provoking presentation. Second, a question: To what extent does the valence of the hallucinated voice determine whether it follows social isolation in your study. Put another way, if one is socially isolated (and carries the risk factors for psychosis), is one just as likely to hallucinate a negative, threatening, critical voice as a neutral or positive, supportive one?
View all comments by Rich LewineComment by: Ralph Hoffman
Submitted 8 July 2014
Posted 8 July 2014
Reply to Comment by R. Lewine
I am not sure of the answer, but in thinking back on representative patients, I suspect that the more social disconnection prior to hallucination onset, the more negative the content/emotional tone of the hallucinations when they emerge, as you suggest. I think the reason for this is that these individuals have higher levels of anxiety and fearfulness, and that their overall emotional state shapes the "hallucination anlage." My sense is that for people who go on to develop schizophrenia, just about everyone has some social disconnection prior to onset of AVHs due to wide-ranging circumstances, but there are varying degrees and durations of these social network disruptions.
I would suggest that a common illness progression may be as follows: In the face of more mild social disconnection sufficient to induce AVHs, there is further secondary and gradual social withdrawal due to preoccupation with the voice world (possibly over months to years), turning their voices secondarily from positive (or at least quasi-interesting and captivating) to negative. I suspect that for non-schizophrenic voice-hearers who don't get tagged with a major psychiatric diagnosis such as those studied by Iris Sommer, they are able to maintain their social world even while retreating periodically into their own voice world for brief periods. So the whole social connectivity/hallucination dynamic then stabilizes in a different place. Implicit in this view is the idea that maintaining a social network requires effort and work, and when neglected or lost, negative emotional states can arise that shape psychotic experience. Thanks for your excellent question! I would like to pursue it further now that you raise it.
View all comments by Ralph Hoffman