The positive symptoms of schizophrenia present one striking and debilitating aspect of the disorder and include delusions of control (where subjects take actions they perform to be done by others), thought insertion (where subjects have thoughts that they attribute as belonging to others), and auditory verbal hallucinations (AVH), where subjects hear the voices of others. A central question is how to explain why these symptoms occur. A central model is one that appeals to self- or source-monitoring. The general interest of this model is that it makes use of predictions, something of recent general interest and relevant to discussing the visual stream hypothesis and consciousness (a few posts from now).
Irwin Feinberg first suggested the application of self-modeling to schizophrenia, but Christopher Frith (and coworkers) is perhaps the first to come to mind when philosophers think of these models in schizophrenia. Judith Ford has done a lot of recent interesting empirical work to test the model. The basic idea is attributed to Helmholtz who raised it to explain spatial constancy in vision (why the world appears stable despite eye movement), and modern formulations of the model draw on the notions of efference copy or, as I prefer, corollary discharge. Put poetically, the proposed mechanism involves a signal (I’ll call it the corollary discharge) that allows a system to distinguish self from other. Given how I characterized the positive symptoms above, you can see a potential resonance in talk of an “other”. Yet while self-monitoring, as a family of models, is plausibly the received view in explanations of the positive symptoms, I do not think it can explain AVH.
Here’s a simple recounting of application of self-monitoring in the case of visual spatial constancy (my take on this phenomenon was first given here). When the eye moves, the projection of the world on the retina (the retinal image) also moves. When a projection of an object moves on the retina (while our eyes are still) we experience the motion of the object. So, why don’t we experience motion when we move our eyes. The Helmholtzian idea is that when our eyes move, our brains know that our eyes move, and with that information about the self, can tag moving retinal images as generated by movement of the self rather than the other (the external world). The signal of self-movement is carried in the corollary discharge, a copy or correlated signal generated by the motor system. Obviously, there’s more to the explanation than that, and indeed it gets quite complicated. Bruce Bridgeman, by the way, has done a lot of interesting work on this, and perhaps the best empirical evidence for a corollary discharge circuit in cortical control of eye movement comes from work by a former CNBC professor, Marc Sommer (see review here). The point is that spatial constancy is determined by a kind of self-monitoring based on corollary discharge, and the use of corollary discharge is quite prevalent in forward models of movement control. But how do we extend these ideas to AVH, and auditory phenomenon?
We can think of AVH as the result of failure of self-monitoring. First, a common view is that the substrate of AVH is inner speech, where the subject generates inner speech, but given failure of self-monitoring, loses track of that speech as self-generated. The application of self-monitoring is easiest here if we think of inner speech itself as involving a motoric component and so we can again call upon a corollary discharge signal. But say one loses track of the speech as self-generated by failure to process the corollary discharge signal. One then experiences that speech, but it is not tagged as one’s own speech (cf. the changes in retinal image not tagged as self-changed). So, the speech is experienced as “other” and this leads to AVH. This gets at the basic outline of the proposed explanation. I should emphasize that we have good empirical evidence that such self-monitoring mechanisms seem to be altered in patients with schizophrenia.
I think theorists of schizophrenia reach for this model in part because at a metaphorical level, it makes sense. This talk of the “other” and of “self-tagging” slots easily in our attempts to understand AVH. But it doesn’t make much sense once you start thinking about it in more purely mechanistic terms. Let me just raise two points:
- It is not clear how to understand the idea of a “self tag” such that it explains the sense of “otherness” in positive symptoms. Mechanistically, it is the corollary discharge signal, but that signal is used in a variety of domains where no “sense of self” is involved. This is where the poetic aspects of the model don’t have good correlates with plausible mechanisms.
- Self-monitoring models have lost track of the phenomenology: It seems that the substrate of AVH is not inner speech, or at least not in central cases. The reason is that AVH is auditory whereas inner speech often is not (many patients will attest to this difference when you ask them). Further, there are cases where patients respond to their AVH with inner speech which is problematic for the model since the self-monitoring has to go on and off in time with the inner dialogue, namely off with AVH, on with inner speech. This doesn’t seem very plausible.
Against this, I want to draw on the concept of automaticity in my last post to suggest another model that is much simpler. Notice that we can see the self-monitoring model as postulating AVH as the result of a failure in a control mechanism. Alternatively, AVH is just the spontaneous (automatic) activation of auditory representations of another person’s speech. As the surgeon Wilder Penfield showed when he directly stimulated auditory cortex in his patients, many then experienced auditory hallucinations. The Spontaneous Activity model holds that AVH is the result of overactivity in auditory cortex. Two things to note about this model:
- We know that such hallucinations can arise from within spontaneous activity of the auditory system.
- It is simpler in its explanation of “otherness” since the voice that is auditorily experienced is precisely another person’s voice. It’s built into the representation, and we do not need a convoluted explanation of how “otherness” arises due to failure of corollary discharge mechanisms.
These reflections don’t settle what I take to be an empirical question: what causes AVH? Self-monitoring models could be right, though I think that they are surprisingly undeveloped as explanations of AVH. Further, both models face a challenge in explaining why AVH has the properties that it does: voices are often heard as located within the head, are of specific voices, and almost always negative in semantic content.
Still, I think the Spontaneous Activity model should be the default view. What the Spontaneous Activity account gives you is a simple explanation of two phenomenal aspects of AVH: the sense of otherness and the involuntariness. You get otherness by virtue of the auditory representations literally representing the voice as of another and you get involuntariness precisely because AVH is automatic and, as I defined in the last post, against one’s intentions.
What of the other positive symptoms? I actually think something like the self-monitoring account will work for delusions of control since (a) I noted there is evidence of defective self-monitoring and (b) this model is best elaborated for the motor domain. I’m less sure about thought insertion, but that’s a difficult symptom to precisely pin down given different forms of thought. I’m more inclined to the spontaneous activity account for explaining why AVH arises, but it is in the end an empirical question.
A more detailed discussion of AVH is given my recent paper, and I am currently working with Raymond Cho (University of Pittsburgh Psychiatry) on thinking about how to test the model and perhaps actually testing it!