A working model of neural activity and phenomenal experience in psychosis.

Psychosis, involving hallucinations and delusions, arises from a combination of sensory system deficits and overactivity in brain networks linked to internal thought, such as the default-mode network. Hallucinations are tied to transient activation in sensory cortices (e.g., superior temporal gyrus) and increased connectivity in associative areas like the temporoparietal junction. Delusions are linked to hyperactivity in the medial prefrontal cortex. These changes cause internally generated imagery to become as vivid as real perceptions, impairing the ability to distinguish reality from imagination, leading to a loss of contact with the environment.

Study at a glance

Abstract

According to classical phenomenology, phenomenal experience is composed of perceptions (related to environmental stimuli) and imagery/ideas (unrelated to environmental stimuli). Intensity/vividness is supposed to represent the key phenomenal difference between perceptions and ideas, higher in perceptions than ideas, and thus the core subjective criterion to distinguish reality from imagination. At a neural level, phenomenal experience is related to brain activity in the sensory areas, driven by receptor stimulation (underlying perception) or associative areas (underlying imagery/ideas). An alteration of the phenomenal experience that leads to a loss of contact with reality characterizes psychosis, which mainly consists of hallucinations (false perceptions) and delusions (fixed ideas). According to the current data on their neural correlates across subclinical conditions and different neuropsychiatric disorders (such as schizophrenia), hallucinations are mainly associated with: transient (modality-specific) activations of sensory cortices (primarily superior temporal gyrus, occipito-temporal cortex, postcentral gyrus, and insula) during the hallucinatory experience; increased intrinsic activity/connectivity of associative/default-mode network (DMN) areas (primarily temporoparietal junction, posterior cingulate cortex, and medial prefrontal cortex); and deficits in the sensory systems. Analogously, delusions are mainly associated with increased intrinsic activity/connectivity of associative/DMN areas (primarily medial prefrontal cortex). Integrating these data into our three-dimensional model of neural activity and phenomenal-behavioral patterns, we propose the following model of psychosis. A functional/structural deficit in the sensory systems complemented by a functional reconfiguration of intrinsic brain activity favoring hyperactivity of associative/DMN areas may drive neuronal activations in the sensory (auditory/visual/somatosensory) areas and insular (interoceptive) areas with spatiotemporal configurations maximally independent from environmental stimuli and predominantly related to associative processing. This manifests in perception deficit and imagery/ideas composed of exteroceptive-like and interoceptive/affective-like elements that show a phenomenal intensity indistinguishable from perceptions, impairing the reality monitoring, along with minimal changeability by environmental stimuli, ultimately resulting in dissociation of the phenomenal experience from the environment, i.e., psychosis.