Evidence map›Paper›PMID 10373711›Full record

Trial reportThe Journal of physiology1999

Changes in excitability indices of cutaneous afferents produced by ischaemia in human subjects.

J Grosskreutz, C Lin, I Mogyoros, D Burke

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Acute Foot Warming Enhances Plantar Tactile Sensitivity With Limited Postural Control Effects in Obese Older Adults.Physiotherapy research international : the journal for researchers and clinicians in physical therapy · 2026
    Article
  3. Article
  4. Axonal Excitability in Amyotrophic Lateral Sclerosis : Axonal Excitability in ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

4 authors at 2 institutions in 1 country.

J GrosskreutzDepartment of Neurology, The Prince Henry and Prince of Wales Hospitals, Prince of Wales Medical Research Institute, and University of New South Wales, Sydney, Australia.
C Lin
I Mogyoros
D Burke
UNSW Sydney · AUNeuroscience Research Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The present study was undertaken to determine whether mechanisms other than membrane depolarization contribute to the changes in excitability of cutaneous afferents of the median nerve under ischaemic conditions. 2. In six healthy subjects, axonal excitability was measured as the reciprocal of the threshold for a compound sensory action potential (CSAP) of 50% maximal amplitude. Refractoriness and supernormality were measured as threshold changes 2 and 7 ms, respectively, after supramaximal conditioning stimuli. The strength-duration time constant (tauSD) was calculated from the thresholds for unconditioned CSAPs using test stimuli of 0.1 and 1.0 ms duration. Changes in these indices were measured when subthreshold polarizing currents lasting 10 or 100 ms were applied, before, during and after ischaemia for 13 min. 3. At rest, the change in supernormality produced by polarizing currents was greater with the longer polarizing current, indicating that it took up to 100 ms to charge the internodal capacitance. 4. Refractoriness and its dependence on excitability increased more than expected during ischaemia. Supernormality was abolished during ischaemia, and reached a maximum after ischaemia but was then barely altered by polarizing current. tauSD had a similar relationship to excitability before, during and after ischaemia. 5. By contrast, during continuous depolarizing current for 8 min to mimic the depolarization produced by ischaemia, the relationship between excitability and refractoriness was the same during the depolarization as before it. 6. It is suggested that the large increase in refractoriness during ischaemia might be due to interference with the recovery from inactivation of transient sodium channels by an intra-axonal substrate of ischaemia. The post-ischaemic increase in supernormality and the lack of change with changes in axonal excitability can be explained by blockage of voltage-dependent potassium channels.

Indexed as

Action PotentialsAlgorithmsElectrophysiologyFemaleHumansIschemiaMaleMembrane PotentialsNeurons, AfferentPotassium ChannelsRefractory Period, ElectrophysiologicalRegional Blood FlowSkinPotassium Channels

Identifiers

PMID10373711
PMCPMC2269401
OpenAlexW2124532330

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.