Online research in philosophy

Before a general cognitive model for recurrent complex visual hallucinations (RCVH) is accepted, there must be more research into the neuropsychological and cognitive characteristics of the various disorders in which they occur. Currently available data are insufficient to distinguish whether the similar phenomenology of RCVH across different disorders is in fact produced by a single or by multiple cognitive mechanisms.

There is little to refute in Collerton et al.'s argument that recurrent complex visual hallucinations involve multiple physiological mechanisms, and the target article's proposed PAD model implicitly incorporates this concept, advancing the field. The novel concept in this model is the intrusion of hallucinatory proto-objects into relatively preserved scenes. The weakness of the model is the lack of physiological detail for this mechanism.

Commentators agree that the Perception and Attention Deficit (PAD) model is a promising model for accounting for recurrent complex visual hallucinations (RCVH) across several disorders, though with varying detailed criticisms. Its central tenets are not modified, but further consideration of generative models of visual processing and the relationship of proto-objects and memory systems allows the PAD model to deal with variations in phenomenology. The commentaries suggest new ways to generate evidence that will test the model.

The Perception and Attention Deficit (PAD) model of visual hallucinations is as limited in generality as other models. It does, however, raise an interesting hypothesis on the role of attentional biases among proto-objects. The prediction that neither impaired attention nor impaired sensory activation alone will produce hallucinations should be addressed in future studies by analysing partial correlations between putative causes and hallucinatory effects.

Recent neural models clarify many properties of mental imagery as part of the process whereby bottom-up visual information is influenced by top-down expectations, and how these expectations control visual attention. Volitional signals can transform modulatory top-down signals into supra-threshold imagery. Visual hallucinations can occur when the normal control of these volitional signals is lost.

Applying Behrendt & Young's (B&Y's) model of thalamocortical synchrony to complex visual hallucinations in neurodegenerative disorders, such as dementia with Lewy bodies and progressive supranuclear palsy, leads us to propose that the primary pathology may be cortical rather than thalamic. Additionally, the extinction of active hallucinations by eye closure challenges their conception of the role of reduced sensory input.

A “multifactorial” model should accommodate a psychological perspective, aiming to relate the phenomenology of complex visual hallucinations not only to neurobiological findings but also an understanding of the patient's psychological problems and situation in life. Greater attention needs to be paid to the role of the “lack of insight” patients may have into their hallucinations and its relationship to cognitive impairment.

The dual-deficit model of visual hallucinations (Collerton et al. target article) is compared with the dual-deficit model of auditory hallucinations (Waters et al., in press). Differences in cognitive mechanisms described may be superficial. Similarities between these models may provide the basis for a general model of complex hallucinations extended across disorders and modalities, involving shared (overlapping) cognitive processes.

We tested Collerton et al.'s model of visual hallucinations by re-examining a data set for correlations between visual hallucinations and measures of attentional function in schizophrenia patients. These data did not support their model. We suggest that cortical hyperexcitability plays an important role in hallucinations, and propose an alternative model that links evidence for cortical hyperexcitability with abnormal neural dynamics.