Evidence map›Paper›PMID 41676131›Full record

ArticleFrontiers in systems neuroscience2025

The NERD model: reflex circuit dysfunction as a systems-level driver of persistent post-concussion symptoms.

Matthew M Antonucci, Kenneth Jay

Abstract read
In one paragraph

Article in Frontiers in systems neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
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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.

Matthew M AntonucciDepartment of Functional Neurology, Carrick Institute, Cape Canaveral, FL, United States.
Kenneth JayDepartment of Functional Neurology, Carrick Institute, Cape Canaveral, FL, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent post-concussive symptoms are often attributed to diffuse cortical dysfunction, yet this perspective may overlook key systems-level mechanisms. We propose a conceptual framework in which dysfunction arises from the dynamic interplay among five functional nodes: the sensory interface, reflex-brain stem hub, cerebellar module, basal ganglia-thalamic modulator, and cerebral cortex. Grounded in clinical observation and systems-level dynamic modeling, this framework treats the brain as a time-evolving control network that processes inputs, integrates them across hierarchical nodes, and generates adaptive or maladaptive outputs. Subcortical reflex circuits serve as critical nodes in the sensorimotor network, coordinating posture, orientation, and autonomic tone, and are modulated by cortical and thalamic systems. Injury to any of these nodes - or to the connections between them - can disrupt reflex control, distort afferent-efferent signaling, and compromise thalamocortical integration. The cerebellum calibrates predictive timing and coordination, while the basal ganglia-thalamic complex regulates gain and context-dependent gating. The cerebral cortex integrates intention, perception, and prediction to shape voluntary behavior and modulate reflex sensitivity. Reafferent feedback continuously updates the system, creating a dynamic loop of adaptation or maladaptation. Though this model has been applied clinically to guide early intervention, it remains a theoretical framework, untested by formal mathematical modeling or rigorous experimental validation. We offer it as a systems-level model that reframes post-concussive dysfunction as a network-level disorder, with reflex disintegration as a central, actionable mechanism.

Indexed as

cortical entrapmentfunctional neurologygain modulationnetwork rigidityneurorehabilitationpost-concussion symptomsreflex circuitssensorimotor integration

Identifiers

PMID41676131
PMCPMC12888038

What OpenQuestion holds

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Registered trials

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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.