Evidence map›Paper›PMID 23630492›Full record

ArticleFrontiers in computational neuroscience2013

Cortical information flow in Parkinson's disease: a composite network/field model.

Cliff C Kerr, Sacha J Van Albada, Samuel A Neymotin, George L Chadderdon, P A Robinson, William W Lytton

Abstract read
In one paragraph

Article in Frontiers in computational neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Computer modeling for pharmacological treatments for dystonia.Drug discovery today. Disease models · 2016
    Article
  13. Article
  14. Towards real-time communication betweenJournal of computational surgery · 2014
    Article
  15. Neural masses and fields: modeling the dynamics of brain activity.Frontiers in computational neuroscience · 2014
    Article
  16. Article
  17. Reaction-diffusion in the NEURON simulator.Frontiers in neuroinformatics · 2013
    Article
  18. 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

6 authors.

Cliff C KerrDepartment of Physiology and Pharmacology, State University of New York Downstate Medical Center Brooklyn, NY, USA ; School of Physics, University of Sydney NSW, Australia ; Brain Dynamics Centre, Westmead Millennium Institute Westmead, NSW, Australia.
Sacha J Van Albada
Samuel A Neymotin
George L Chadderdon
P A Robinson
William W Lytton

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The basal ganglia play a crucial role in the execution of movements, as demonstrated by the severe motor deficits that accompany Parkinson's disease (PD). Since motor commands originate in the cortex, an important question is how the basal ganglia influence cortical information flow, and how this influence becomes pathological in PD. To explore this, we developed a composite neuronal network/neural field model. The network model consisted of 4950 spiking neurons, divided into 15 excitatory and inhibitory cell populations in the thalamus and cortex. The field model consisted of the cortex, thalamus, striatum, subthalamic nucleus, and globus pallidus. Both models have been separately validated in previous work. Three field models were used: one with basal ganglia parameters based on data from healthy individuals, one based on data from individuals with PD, and one purely thalamocortical model. Spikes generated by these field models were then used to drive the network model. Compared to the network driven by the healthy model, the PD-driven network had lower firing rates, a shift in spectral power toward lower frequencies, and higher probability of bursting; each of these findings is consistent with empirical data on PD. In the healthy model, we found strong Granger causality between cortical layers in the beta and low gamma frequency bands, but this causality was largely absent in the PD model. In particular, the reduction in Granger causality from the main "input" layer of the cortex (layer 4) to the main "output" layer (layer 5) was pronounced. This may account for symptoms of PD that seem to reflect deficits in information flow, such as bradykinesia. In general, these results demonstrate that the brain's large-scale oscillatory environment, represented here by the field model, strongly influences the information processing that occurs within its subnetworks. Hence, it may be preferable to drive spiking network models with physiologically realistic inputs rather than pure white noise.

Indexed as

basal gangliacortexGranger causalityinterlaminar processingneural field modelParkinsons's diseasespiking neural networksthalamus

Identifiers

PMID23630492
PMCPMC3635017

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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.