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Cited by 140Schizophrenia research and treatmentMental Health and PsychiatryHallucinations in medical conditions

Schizophrenia, myelination, and delayed corollary discharges: a hypothesis

Open access
Whitford, T. J., Ford, J. M., Mathalon, D. H., Kubicki, M., Shenton, M. E.·2012·Schizophrenia Bulletin
DOI 10.1093/schbul/sbq105PMC PMC3329979
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Abstract

Any etiological theory of schizophrenia must account for at least 3 distinctive features of the disorder, namely its excessive dopamine neurotransmission, its frequent periadolescent onset, and its bizarre, pathognomonic symptoms. In this article, we theorize that each of these features could arise from a single underlying cause--namely abnormal myelination of late-developing frontal white matter fasciculi. Specifically, we suggest that abnormalities in frontal myelination result in conduction delays in the efference copies initiated by willed actions. These conduction delays cause the resulting corollary discharges to be generated too late to suppress the sensory consequences of the willed actions. The resulting ambiguity as to the origins of these actions represents a phenomenologically and neurophysiologically significant prediction error. On a phenomenological level, the perception of salience in a self-generated action leads to confusion as to its origins and, consequently, passivity experiences and auditory hallucinations. On a neurophysiological level, this prediction error leads to the increased activity of dopaminergic neurons in the midbrain. This dopaminergic activity causes previously insignificant events to be perceived as salient, which exacerbates the budding hallucinations and passivity experiences and triggers additional first-rank symptoms such as delusions of reference. The article concludes with a discussion of the implications of the theory and some testable predictions which may form a worthwhile basis for future research.

AI snapshot

Written from the paper’s full text.

TL;DR

The paper proposes that abnormal periadolescent myelination of late-developing frontal white matter fasciculi causes conduction delays in efference copies, leading to mistimed corollary discharges and prediction errors. These prediction errors are hypothesized to produce passivity experiences and auditory hallucinations directly and to drive excessive phasic midbrain dopamine activity, thereby generating additional psychotic symptoms.

Key findings

  • The theory aims to explain three features of schizophrenia from one underlying cause: excessive dopamine neurotransmission, periadolescent onset (majority of cases between ages 16 and 30 years), and pathognomonic symptoms such as passivity experiences, auditory hallucinations, and delusions of reference.
  • Frontal fasciculi are highlighted as consistently abnormal in schizophrenia and among the last to mature, with myelination continuing through adolescence and into early adulthood; myelin-specific abnormalities reported include reduced oligodendrocytes, irregular myelin microstructure, and subnormal myelin-related gene expression.
  • The proposed mechanism is that dysmyelination delays efference copies, so corollary discharges arrive too late to suppress sensory consequences of self-generated actions/cognitions, causing agency confusion and prediction errors; these prediction errors are proposed to increase phasic dopaminergic neuron activity and aberrant salience.
  • Testable predictions include that disrupting periadolescent myelination in vivo will increase phasic dopamine activity and dopamine release, that delaying sensory feedback by the conduction delay may rectify N1 suppression abnormalities (preliminary evidence cited with a 50-ms delay), and that remyelinating medications used in multiple sclerosis might treat some cases.

Methods

  • Design: theoretical hypothesis article, not an empirical study; it integrates prior neuroimaging, neuropathological, electrophysiological, and animal literature to propose a mechanistic model.
  • Data or sample: no new sample or primary data are reported; the paper cites prior findings, including multiple sclerosis optic nerve conduction delays of around 20 ms in the P1 visual-evoked potential and a study in which a subsecond delay made self-generated tactile sensations as ticklish as externally generated ones.
  • Main analysis: narrative synthesis and generation of five empirical predictions for future research.

Limitations

  • The paper explicitly states the theory is “clearly highly speculative and would benefit from substantially more supporting evidence.”
  • The paper clarifies that it does not claim all patients with schizophrenia or psychosis have white matter fasciculi or corollary discharge abnormalities, and it notes that gray matter abnormalities are likely causal in many, if not most, cases; the relationship between gray and white matter abnormalities is “manifestly unclear.”
  • Evident from the text: the central mechanism is not directly tested in this article, and several predictions require new or unavailable methods, such as measuring phasic dopamine in vivo in real time.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1093/schbul/sbq105

Cites

93 of 93 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 86 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Patients with schizophrenia exhibit structural abnormalities in the cerebral white matter.

    “After more than 2 decades of neuroimaging research, it is now well established that patients with schizophrenia exhibit structural abnormalities in the cerebral white matter.”
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  • Premisecitation

    Patients with schizophrenia exhibit abnormally high levels of neural activity to self-generated sensory stimuli.

    “Evidence for this theory has been provided by studies showing that patients with schizophrenia exhibit abnormally high levels of neural activity to self-generated sensory stimuli.[56][57][58][59]”
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  • Premisecitation

    Multiple sclerosis patients with damage to the myelin of the optic nerve typically exhibit conduction delays of around 20 ms in the latency of the P1 component of the visual-evoked potential.

    “For example, multiple sclerosis patients with damage to the myelin of the optic nerve typically exhibit conduction delays of around 20 ms in the latency of the P1 component of the visual-evoked potential.[46][47][48]”
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  • Interpretationreasoning

    Schizophrenia may be underpinned by irregularities in normative periadolescent myelination, particularly in late-developing frontal fasciculi.

    “there is reason to believe that schizophrenia may be underpinned by irregularities in the normative processes of periadolescent myelination, 13 particularly in the latedeveloping frontal fasciculi.”
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  • Premisecitation

    Efference copies play a role in tagging self-generated actions as self-generated, enabling a distinction between sensations from self-generated movements and sensations from changes in the external world.

    “there is evidence to suggest that they also play a role in ''tagging'' self-generated actions as being self-generated, thereby enabling a distinction to be made between sensations resulting from self-generated movements and sensations resulting from changes in the external world.[53][54][55]”
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  • May combine two claims. 17
  • Classified as probably not a substantial claim. 11

  • May combine two claims.

    Premisecitation

    In schizophrenia, primary sensorimotor fasciculi appear comparatively unaffected, while structural abnormalities are consistently reported in frontal fasciculi connecting the frontal lobe with the rest of the brain, including the uncinate, arcuate, superior longitudinal, and cingulum bundle.

    “Specifically, while the primary sensorimotor fasciculi appear to be comparatively unaffected in patients in schizophrenia, structural abnormalities have consistently been reported in the fasciculi connecting the frontal lobe with the rest of the brain, such as the uncinate fasciculus, 25,26 arcuate fasciculus, 27,28 superior longitudinal fasciculus, 29,30 and cingulum bundle.31,32”
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  • Classified as probably not a substantial claim.

    Interpretationreasoning

    Abnormal myelination of late-developing frontal white matter fasciculi during periadolescent neurodevelopment could be a single underlying cause accounting for excessive dopamine neurotransmission, periadolescent onset, and bizarre pathognomonic symptoms of schizophrenia.

    “In this article, we theorize that each of these features could arise from a single underlying cause-namely abnormal myelination of late-developing frontal white matter fasciculi.”
    • Also stated in: § Abstract · hedged
      “The purpose of this article is to offer a theory as to how these 3 distinctive features could all potentially arise from a single underlying cause-namely, abnormal myelination of the frontally projecting white matter fasciculi during periadolescent neurodevelopment.”
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  • Classified as probably not a substantial claim.

    Premisecitation

    Schizophrenia involves bizarre pathognomonic clinical symptoms such as passivity experiences, auditory hallucinations, and delusions of reference.

    “Third, the theory must account for the mechanism that gives rise to such bizarre yet pathognomonic clinical symptoms as passivity experiences, auditory hallucinations, and delusions of reference.”
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    Interpretationcitation

    Abnormalities in frontal myelination cause conduction delays in efference copies involved in predicting the neural consequences of self-generated actions.

    “we will argue that abnormalities in frontal myelination cause conduction delays in the efference copies that are involved in predicting the neural consequences of self-generated actions.”
    • Also stated in: § Abstract · hedged
      “Specifically, we suggest that structural abnormalities in the fasciculi connecting the motor-initiation areas of the frontal lobe with the temporal and parietal cortices cause conduction delays in the efference copies initiated by self-generated actions and arguably self-generated cognitions more generally.8”
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  • May combine two claims.

    Interpretationreasoning

    These conduction delays lead to prediction errors that cause certain psychotic symptoms directly and ultimately underpin the excessive phasic dopamine neurotransmission associated with psychotic symptoms of schizophrenia.

    “These conduction delays lead to prediction errors which, in addition to causing certain psychotic symptoms directly, ultimately also underpin the excessive phasic dopamine neurotransmission that has been associated with the psychotic symptoms of schizophrenia.6,7”
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    Premisecitation

    Schizophrenia symptoms commonly first present in late adolescence and early adulthood, with the majority of cases occurring between ages 16 and 30 years.

    “Second, the theory must account for why the symptoms of schizophrenia so commonly first present in late adolescence and early adulthood, with the majority of cases occurring between the ages of 16 and 30 years.5”
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  • May combine two claims.

    Premisecitation

    Schizophrenia is associated with excessive dopamine neurotransmission, consistent with increased phasic activity of midbrain dopaminergic neurons.

    “First, it must account for the excessive dopamine neurotransmission that has been associated with the psychotic symptoms of schizophrenia.”
    • Also stated in: § Abstract · boosted
      “Evidence for this hyperdopaminergia, which is consistent with increases in the phasic activity of midbrain dopaminergic neurons, 1 is provided by the fact that the vast majority of antipsychotic medications act as dopamine antagonists, 2”
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    Premisecitation

    Myelinated axons typically have higher conduction velocities than unmyelinated axons of the same caliber, and damage to myelin can result in conduction delays in neural discharges.

    “It is well established that myelinated axons typically have higher conduction velocities than unmyelinated axons of the same caliber 45 and that damage to the myelin can result in conduction delays in neural discharges.”
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    Premisecitation

    Frontal fasciculi are among the last fasciculi to structurally mature in the developing human brain, with myelination continuing through adolescence and into early adulthood.

    “Second, these frontal fasciculi are among the last fasciculi to structurally mature in the developing human brain, with myelination thought to continue through adolescence and into early adulthood, [40][41][42][43]”
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    Premisecitation

    Feinberg and Frith first developed the idea that passivity experiences and certain auditory hallucinations could be explained by efference copy/corollary discharge abnormalities disrupting patients' ability to distinguish between internally and externally generated events.

    “Feinberg 8 and Frith 9 first developed the idea that many of the most distinctive symptoms of schizophrenia-most notably the passivity experiences and certain types of auditory hallucinations-could be explained by efference copy/corollary discharge abnormalities disrupting patients' ability to distinguish between internally and externally generated events.”
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    Premisecitation

    Schizophrenia patients exhibit myelin-specific abnormalities including reduced numbers of oligodendrocytes, irregular myelin microstructure, and subnormal expression of myelin-related genes.

    “When combined with the fact that schizophrenia patients exhibit a range of myelin-specific abnormalities-including reduced numbers of oligodendrocytes, 19 irregular myelin microstructure, 20 and subnormal expression of myelin-related genes 44”
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    Premisecitation

    Corollary discharges are compared with or subtracted from actual sensory input; when well matched, this suppresses or dampens sensory stimulation produced by self-generated movements.

    “These corollary discharges are then compared with, or ''subtracted from,'' the actual sensory input (ie, ''sensory reafference'') associated with executing the movement.”
    • Also stated in: § Abstract · plain
      “When Schizophrenia, Myelination, and Delayed Corollary Discharges the corollary discharge and sensory reafference are well matched, the subtractive comparison results in suppression or dampening of the sensory stimulation produced by self-generated movements.52”
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    Premisecitation

    Arnfred et al. argued that increased latencies of early proprioception-evoked potentials in schizophrenia patients could best be explained by instabilities in corollary discharge signals involved in preparing sensory cortices for feedback.

    “The basic idea that mistimed corollary discharges could underpin schizophrenia patients' abnormal perception of selfgenerated actions is also consistent with the suggestion of Arnfred and colleagues, 61 who argued that the increased latencies of early proprioception-evoked potentials exhibited by schizophrenia patients could best be explained by instabilities in the corollary discharge signals in”
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  • Classified as probably not a substantial claim.

    Interpretationreasoning

    If dysmyelination-induced delays in efference copies cause a discrepancy between sensory feedback predicted by the forward model and observed sensory feedback, this represents a prediction error that is both phenomenologically and neurophysiologically salient.

    “We suggest that if dysmyelination-induced delays in the efference copies initiated by self-generated actions cause a discrepancy between the sensory feedback predicted by the forward model (ie, the corollary discharge) and the observed sensory feedback, then this represents a prediction error, which is both a phenomenologically and neurophysiologically salient event.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    On a phenomenological level, perception of salience in a self-generated action could lead to confusion as to origins and hence passivity experiences for willed motor actions and auditory hallucinations for willed cognitions.

    “On a phenomenological level, the perception of salience in a self-generated action could lead to confusion as to the origins of the action and hence, as discussed above, passivity experiences in the case of willed motor actions and auditory hallucinations in the case of willed cognitions.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    This delayed suppression results in confusion as to the origins of actions, hence passivity experiences for willed motor actions and auditory hallucinations for willed cognitions.

    “This, in turn, results in confusion as to the origins of these actions and hence passivity experiences in the case of willed motor actions and auditory hallucinations in the case of willed cognitions.8,9”
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  • May combine two claims.

    Premisecitation

    Blakemore et al. reported that healthy participants rated self-generated tactile sensations as less ticklish than externally generated sensations when both were generated indirectly with a robotic arm, but rated them equally ticklish if a subsecond delay was imposed between instruction and execution.

    “Blakemore and colleagues 60 reported that while healthy participants rated self-generated tactile sensations as less ticklish than externally generated sensations when both were generated indirectly with a robotic arm, they rated the sensations as equally ticklish if a subsecond delay was imposed between when participants instructed the arm to tickle and when it actually executed the instruction.”
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  • May combine two claims.

    Interpretationreasoning

    These conduction delays result in delayed generation of corollary discharge signals in sensory regions, which occur too late to suppress the sensory activation associated with self-generated actions.

    “These conduction delays result in the delayed generation of corollary discharge signals in sensory regions, which consequently occur ''too late'' to suppress the sensory activation associated with the selfgenerated actions.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationcitation

    This could worsen budding passivity experiences and auditory hallucinations and cause previously insignificant external events to be perceived as salient and of special significance, thereby causing delusions of reference.

    “This could worsen the budding passivity experiences and auditory hallucinations and also cause previously insignificant events in the external world to be perceived as salient and of special significance to the patient, thereby causing other first-rank psychotic symptoms, such as delusions of reference.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationcitation

    Structural abnormalities in fasciculi connecting motor-initiation areas of the frontal lobe with the temporal and parietal cortices cause conduction delays in efference copies initiated by self-generated actions and cognitions.

    “Specifically, we suggest that structural abnormalities in the fasciculi connecting the motor-initiation areas of the frontal lobe with the temporal and parietal cortices cause conduction delays in the efference copies initiated by self-generated actions and arguably self-generated cognitions more generally.8”
    Quote in the paperNot a substantial claim0 of 1 sources checked
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  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Garver et al. suggested that patients may have experienced compromised myelin integrity during psychosis with repair during remission, given marked increases in mean diffusivity with DTI when floridly psychotic versus medication-induced remission.

    “A similar idea has previously been proposed by Garver and colleagues 76 who suggested that the patients in their study may have expe-rienced ''compromised myelin integrity during psychosis with repair during remission'' (p.49), given that they showed marked increases in mean diffusivity with Diffusion Tensor Imaging when floridly psychotic as opposed to when experiencing a medication-induced”
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  • May combine two claims.

    Interpretationreasoning

    Not all patients diagnosed with schizophrenia, and far fewer all patients diagnosed with psychosis, necessarily have abnormalities in either their white matter fasciculi or corollary discharge mechanisms.

    “we do not mean to suggest that all patients diagnosed with schizophrenia, far less all patients diagnosed with psychosis, necessarily have abnormalities in either their white matter fasciculi or corollary discharge mechanisms.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    Some recent studies have inferred changes in the activity of dopaminergic neurons from variations in the blood oxygen level-dependent signal in midbrain nuclei.

    “some recent studies have inferred changes in the activity of dopaminergic neurons on the basis of variations in the blood oxygen level-dependent signal in midbrain nuclei, 82,83”
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  • Probably not a substantial claim: may not pass S1 (asserted). May combine two claims.

    Interpretationreasoning

    If schizophrenia patients experience dysmyelination in frontal fasciculi, variable conduction velocities of corollary discharges could lead to variation in suppression of sensory targets, variability in prediction errors, variability in dopaminergic neuron activities, and ultimately the dynamic profile of psychotic symptoms.

    “If, as discussed previously, schizophrenia patients experience dysmyelination in their frontal fasciculi, then the consequently variable conduction velocities of corollary discharges traveling along these fasciculi could lead to variation in the extent to which they suppress their sensory targets.This, we suggest, could give rise to variability in the magnitude of the associated prediction errors,”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationcitation

    Increased phasic activity of dopaminergic neurons could drown out dopaminergic activity associated with reinforcing or motivationally salient stimuli, leading to negative symptoms such as anhedonia, avolition, and apathy.

    “With respect to the etiology of negative symptoms, it is possible that the increased phasic activity of these dopaminergic neurons could ''drown out'' the dopaminergic activity typically associated with reinforcing or motivationally salient stimuli, as per the suggestion of Roiser et al. 69 The consequently reduced valence of typically reinforcing stimuli could underlie such negative symptoms of”
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  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Schultz et al. found that positive prediction errors were associated with increased firing rates in dopaminergic neurons, while negative prediction errors were associated with decreased firing rates.

    “Schultz et al 62 used a reward-conditioning procedure and found that while ''positive'' prediction errors (ie, prediction errors for which the actual outcome was more rewarding than the predicted outcome) were associated with increased firing rates in dopaminergic neurons, ''negative'' prediction errors (ie, for which the actual outcome was less rewarding than the predicted outcome) were”
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26 of 26

  • The authors state this as an assumption.

    Schizophrenia patients experience conduction delays in neural discharges traveling along frontal fasciculi.

    “Given the frontal white matter abnormalities exhibited by patients with schizophrenia, it seems reasonable to assume that they would also experience conduction delays in neural discharges traveling along these frontal fasciculi.”
1 of 1

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In the much larger human brain, myelin regulation of cortico-cortical long-range axons such as transcallosal cortical projections is also crucial, and is necessary for cognition and learning.

    “In the much larger human brain, myelin regulation of cortico‐cortical long‐range axons such as transcallosal cortical projections is also crucial (Nave, 2010 ), and is necessary for cognition and learning (Nave & Ehrenreich, 2014 ; Whitford, Ford, Mathalon, Kubicki, & Shenton, 2012 ).”

    From Motor learning requires myelination to reduce asynchrony and spontaneity in neural activity (2020) · cites this paper as Whitford, Ford, Mathalon, Kubicki, & Shenton, 2012

    The paper’s Abstract describes myelinated white-matter tracts as infrastructure for long-distance neural communication and suggests that disrupted timing could impair the binding of cognitive features. It does not establish that myelin regulation is necessary for cognition and learning; learning is not addressed in the relevant passages. The transcallosal example is attached to a different citation in the citing sentence. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • The dampened N1 finding could reflect the failure of an efference copy to successfully dampen activity in sensory areas after self-produced speech, perhaps due to a delayed corollary discharge.

    “This finding could reflect the failure of an efference copy to successfully dampen activity in sensory areas after self-produced speech, perhaps due to a delayed corollary discharge (Whitford et al., 2012).”

    From Auditory verbal hallucinations as atypical inner speech monitoring, and the potential of neurostimulation as a treatment option (2013) · cites this paper as Whitford et al., 2012

  • Some models specify that the efference copy will dampen activity in the appropriate sensory area, to label the percept as self-generated.

    “Some models specify that the efference copy will dampen activity in the appropriate sensory area, to label the percept as self-generated (Ford and Mathalon, 2005; Whitford et al., 2012).”

    From Auditory verbal hallucinations as atypical inner speech monitoring, and the potential of neurostimulation as a treatment option (2013) · cites this paper as Whitford et al., 2012

Cites

Flagged first, then by citations

Research works printed but not linked: 5

  1. 1991, 41, 1
  2. 2007, 44, 522
  3. 2000, 96, 651
  4. 1988, 24, 19
  5. 2007, The British Journal of Psychiatry, 51, s13

Cited by

Sorted by citations

Related

Authors
Whitford, T. J., Ford, J. M., Mathalon, D. H., Kubicki, M., & Shenton, M. E.
Affiliations
  • Brigham and Women's Hospital (US)
  • San Francisco VA Medical Center (US)
Corresponding author
Whitford, T. J.
ORCID
Venue
Schizophrenia Bulletin
Publisher
Oxford University Press (OUP)
Published
2010-09-20
Volume
38
Issue
3
Pages
486-494
ISSN
  • 0586-7614 (ISSN-L)
  • 1745-1701
DOI
10.1093/schbul/sbq105
PMC
PMC3329979
OpenAlex
W2096194883
Semantic Scholar
7895955d3b719aae5e18be032ce1e36b1a1b09f9
Cited by
140
References
93
Citations by year
2026: 5 · 2025: 9 · 2024: 13 · 2023: 4 · 2022: 4 · 2021: 6 · 2020: 3 · 2019: 20 · 2018: 8 · 2017: 6 · 2016: 7 · 2015: 14 · 2014: 12 · 2013: 11 · 2012: 8
FWCI
6.34
Type
journal article
Language
en
Open access
Locations
  • Schizophrenia Bulletin (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Minerva Access (University of Melbourne) (submittedVersion)
Funders
  • U.S. Department of Veterans Affairs
  • National Institutes of Health (R01 MH 50747, 5r01mh058262-17, 520627, MH076989)
  • Medical Research Council
  • National Health and Medical Research Council (R01 MH 50747, R03 MH068464-0, 520627, K05 MH 070047, P50 MH 080272)
  • National Institute of Mental Health (K02MH067967, P50MH080272, K05MH070047, R01MH-058262, R01MH050740, R01MH076989, R03MH068464, R03 MH068464-0, R01MH 50747)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
  • Social Sciences › Arts and Humanities › Philosophy › Mental Health and Psychiatry
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Hallucinations in medical conditions
Keywords
etiology of schizophrenia, myelination
MeSH terms
Dopamine, Frontal Lobe, Humans, Myelin Sheath, Psychological Theory, Schizophrenia

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