Evidence map›Paper›PMID 37986628›Full record

ArticleeLife2023

Against cortical reorganisation.

Tamar R Makin, John W Krakauer

Abstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing 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

68 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Excitatory and inhibitory networks diverge following early blindness.Cerebral cortex (New York, N.Y. : 1991) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. How deep is your recovery? Rethinking true motor recovery versus compensation in neurorehabilitation.International journal of rehabilitation research. Internationale Zeitschrift fur Rehabilitationsforschung. Revue internationale de recherches de readaptation · 2026
    Review
  9. Review
  10. Article
  11. Right hemisphere language network plasticity in aphasia.Brain : a journal of neurology · 2026
    Article
  12. Review
  13. Review
  14. The Emergence of Topography and Hemispheric Lateralization in High-Level Vision.Quarterly journal of experimental psychology (2006) · 2026
    Review
  15. Article
  16. Neurology of social graces in patients with language deficits.Journal of neurology, neurosurgery, and psychiatry · 2026
    Article
  17. Recovery of Retinal Terminal Fields after Traumatic Brain Injury: Evidence of Collateral Sprouting and Sexual Dimorphism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  18. A complex network perspective on brain disease.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  19. Review
  20. Review

8 more citing papers are in PubMed but not listed here.

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.

Tamar R MakinMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0002-5816-8979
John W KrakauerDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States.ORCID 0000-0002-4316-1846

Funding

Medical Research Council MC_UU_00030/10Wellcome TrustWellcome Trust 215575/Z/19/Z
6 · The paper itself

Abstract

Neurological insults, such as congenital blindness, deafness, amputation, and stroke, often result in surprising and impressive behavioural changes. Cortical reorganisation, which refers to preserved brain tissue taking on a new functional role, is often invoked to account for these behavioural changes. Here, we revisit many of the classical animal and patient cortical remapping studies that spawned this notion of reorganisation. We highlight empirical, methodological, and conceptual problems that call this notion into doubt. We argue that appeal to the idea of reorganisation is attributable in part to the way that cortical maps are empirically derived. Specifically, cortical maps are often defined based on oversimplified assumptions of 'winner-takes-all', which in turn leads to an erroneous interpretation of what it means when these maps appear to change. Conceptually, remapping is interpreted as a circuit receiving novel input and processing it in a way unrelated to its original function. This implies that neurons are either pluripotent enough to change what they are tuned to or that a circuit can change what it computes. Instead of reorganisation, we argue that remapping is more likely to occur due to potentiation of pre-existing architecture that already has the requisite representational and computational capacity pre-injury. This architecture can be facilitated via Hebbian and homeostatic plasticity mechanisms. Crucially, our revised framework proposes that opportunities for functional change are constrained throughout the lifespan by the underlying structural 'blueprint'. At no period, including early in development, does the cortex offer structural opportunities for functional pluripotency. We conclude that reorganisation as a distinct form of cortical plasticity, ubiquitously evoked with words such as 'take-over'' and 'rewiring', does not exist.

Indexed as

BrainStrokeAmputation, SurgicalAnimalsBrain MappingHumansNeuronal Plasticityamputationblindnessdeafnessdeprivationneuroscienceplasticityrehabilitationstroke

Identifiers

PMID37986628
PMCPMC10662956

What OpenQuestion holds

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LicenceCC BY
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.