Evidence map›Paper›PMID 38844531›Full record

ReviewMolecular psychiatry2024

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

Matteo Martino, Paola Magioncalda

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Trial
  2. Polarisation of brain dynamics in mania and depression.Dialogues in clinical neuroscience · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Regional White Matter Lesion Load in Elderly Patients With Somatic vs. Non-Somatic Delusional Disorder.Psychogeriatrics : the official journal of the Japanese Psychogeriatric Society · 2025
    Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Matteo Martino *Graduate Institute of Mind Brain and Consciousness, Taipei Medical University, Taipei, Taiwan. matteomartino9@gmail.com.ORCID 0000-0002-3783-707X
Paola Magioncalda *International Master/Ph.D. Program in Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. paola.magioncalda@gmail.com.ORCID 0000-0003-4985-4819

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

BrainDelusionsHallucinationsPsychotic DisordersBrain MappingDefault Mode NetworkHumansImaginationMagnetic Resonance ImagingModels, NeurologicalNerve NetSchizophrenia

Identifiers

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.