Delusions of Reference

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Delusions of reference has been defined as when neutral events are felt to refer to the self (Menon 2011). They in essence mean that environmental occurrences are taken to have a special meaning for individuals and only for them and not others. It has occurred via the television or the radio for example. It also seems that delusions of reference can be divided into two groups; delusions of observation and delusions of communication (Startup 2009; Bucci 2008; Bucci 2008b) with delusions of observations possibly being related to delusions of paranoia. 

 

The original study that found this division, used scores on the Scale for the Assessment of Positive Symptoms (with the reference question being replaced by several questions concerning this phenomena). After a factor analysis, there were high loadings for verbal, non-verbal, public media and inanimate which was taken to represent aspects of communication, while the second was loaded with gossip and being watched and was taken to represent being observed (Startup 2005). There are scales that have been developed to measure levels of ideas and delusions of reference. One of these is the Referential Thinking Scale which may tell apart patients with delusions of reference from health controls and patients without delusions of reference (Startup 2010).

 

An indication of the prevalence of ideas / delusions of reference comes from a study looking at a Hong Kong Chinese group of patients, with a point prevalence of 31.4% and prevalence of 65.7%. it was associated with auditory hallucinations, persecutory delusions, circumstantiality, impersistence, being unable to feel close to others and depression. Some complaints were being followed, or looked at, etc. and was also found in those in clinical remission (Wong 2008). 

 

In delusions of communication, the communication relates to the self but the patient attributes origin to some external agency. Hence, it might be that there are abnormalities in self-monitoring of non-verbal aspects of the self, e.g., they may be more likely to misinterpret incidental movements as gestures. To investigate this in more detail psychotic patients were compared to normal controls and they were asked to view clips of people on a computer screen and to determine whether movements made by the people in the clips were deliberate or incidental. Those with delusions of communication tended to make more errors than those without such delusions. They also were more likely to view gestures as signs of rejection, to view incidental movements as gestures (Bucci 2008) and more likely to detect gestures (Bucci 2008b).

 

Now the dominant theoretical framework for delusions of reference so far is that of Frith’s theory of mind model, but deficits here cannot account for delusions of reference, especially when we consider that delusions of persecution tend to be related to delusions of observation, rather than communication. A relatively new theory describes the genesis of delusions of reference as follows (Startup 2009).

1. Inappropriate attention is attached to irrelevant stimuli.

2. Non-verbal systems are activated.

3. Non-verbal signals are detected.

4. There is a search for meaning.

5. Formation of delusion.

6. Previous non-verbal communication is remembered.

 

Patients with social anxiety may have more ideas of reference (Wong 2008b). In terms of psychological styles, there may also be a link with internal attribution (Auckenthaler 2008). Also bringing in prediction error and the abnormal attribution of salience to environmental stimuli, those with delusions of reference may be more susceptible to having a higher signal to noise ratio, i.e., more likely to detect spurious signals that controls (Wong 2012). Such patients may also display a greater ability to detect their names spoken out aloud, presented with other distracting stimuli (Lawson 2016). 

 

Now when it comes to cognitive biases, we have evidence that there might be what is called a jumping to conclusions style in those with delusions. But most of these studies were done on the paranoid and there is evidence that such a deficit may not be found in those with delusions of reference. When 18 patients with schizophrenia all with prominent delusions of reference were compared to healthy controls on a jumping to conclusions task, a theory of mind task and attribution task, there was NO difference between the groups, i.e., there was no difference in the information required to come to a conclusion, there was no evidence of a personalising bias, but patients might have shown less externalising bias (Menon 2013). 

 

In studies done on the neurological substrates of referential activities, it seems that cortical midline structures (e.g., ventro / dorsomedial prefrontal cortex, anterior / posterior cingulate and precuneus) are involve. A ventral pathway (ventromedial prefrontal – ACC – subcortex) might be involved in attaching salience to stimuli, while a dorsal (dorsomedial prefrontal – cortical – subcortical pathway) may be involved in introspective activities and can interact with the more reflexive ventral pathway. This was looked at in patients with delusions of reference and compared with controls in terms of deciding on whether a sentence was about them or not. Those with delusions of reference were more likely to feel that the sentences were about them, especially sentences that did not refer to them in some way and they took longer to respond to stimuli that were not about felt to be self-referent. Again, there seemed to be activity in the central midline structures, with activity in the insula and ventral striatum being positively correlated with intensity of delusions of reference (Menon 2011).

 

Emotional / salience networks might in involved (Girard 2017). When schizophrenics with or without delusions of reference were compared to controls in terms of whether statements referred to them or not, found a posterior cortical midline structure was deactivated in controls, and an anterior cortical midline network that was hyperactive in delusional patients [the medial prefrontal].