Evidence map›Paper›PMID 21811475›Full record

ArticleFrontiers in psychiatry2011

Hodological resonance, hodological variance, psychosis, and schizophrenia: a hypothetical model.

Paul Brian Lawrie Birkett

Open access · goldAbstract read
In one paragraph

Article in Frontiers in psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 82% of its field
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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

1 author at 1 institution in 3 countries.

Paul Brian Lawrie BirkettAcademic Clinical Psychiatry, Department of Neuroscience, University of Sheffield Sheffield, UK.
Harvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a disorder with a large number of clinical, neurobiological, and cognitive manifestations, none of which is invariably present. However it appears to be a single nosological entity. This article considers the likely characteristics of a pathology capable of such diverse consequences. It is argued that both deficit and psychotic symptoms can be manifestations of a single pathology. A general model of psychosis is proposed in which the informational sensitivity or responsivity of a network ("hodological resonance") becomes so high that it activates spontaneously, to produce a hallucination, if it is in sensory cortex, or another psychotic symptom if it is elsewhere. It is argued that this can come about because of high levels of modulation such as those assumed present in affective psychosis, or because of high levels of baseline resonance, such as those expected in deafferentation syndromes associated with hallucinations, for example, Charles Bonnet. It is further proposed that schizophrenia results from a process (probably neurodevelopmental) causing widespread increases of variance in baseline resonance; consequently some networks possess high baseline resonance and become susceptible to spontaneous activation. Deficit symptoms might result from the presence of networks with increased activation thresholds. This hodological variance model is explored in terms of schizo-affective disorder, transient psychotic symptoms, diathesis-stress models, mechanisms of antipsychotic pharmacotherapy and persistence of genes predisposing to schizophrenia. Predictions and implications of the model are discussed. In particular it suggests a need for more research into psychotic states and for more single case-based studies in schizophrenia.

Indexed as

connectivitydisease-modelhallucinationhodologypleiotropyprimingpsychosisschizophrenia

Identifiers

PMID21811475
PMCPMC3144467
OpenAlexW2159070467

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.