Evidence map›Paper›PMID 26989220›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2016

Physiology in Medicine: neuromuscular consequences of diabetic neuropathy.

Matti D Allen, Timothy J Doherty, Charles L Rice, Kurt Kimpinski

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 5 pooled it
2.9field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 5 syntheses or guidelines pooled it, 61 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Matti D AllenSchool of Medicine, Queen's University, Kingston, Ontario, Canada; School of Kinesiology and Health Studies, Faculty of Health Sciences, Queen's University, Kingston, Ontario, Canada; School of Kinesiology, Faculty of Health Sciences, University of Western Ontario, London, Ontario, Canada; kkimpin@uwo.ca.ORCID 0000-0002-0755-3164
Timothy J DohertySchool of Kinesiology, Faculty of Health Sciences, University of Western Ontario, London, Ontario, Canada; Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada; Department of Physical Medicine and Rehabilitation, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada; and.
Charles L RiceSchool of Kinesiology, Faculty of Health Sciences, University of Western Ontario, London, Ontario, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
Kurt KimpinskiDepartment of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada;
Western University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic polyneuropathy (DPN) refers to peripheral nerve dysfunction as a complication of diabetes mellitus. This condition is relatively common and is likely a result of vascular and/or metabolic disturbances related to diabetes. In the early or less severe stages of DPN it typically results in sensory impairments but can eventually lead to major dysfunction of the neuromuscular system. Some of these impairments may include muscle atrophy and weakness, slowing of muscle contraction, and loss of power and endurance. Combined with sensory deficits these changes in the motor system can contribute to decreased functional capacity, impaired mobility, altered gait, and increased fall risk. There is no pharmacological disease-modifying therapy available for DPN and the mainstay of treatment is linked to treating the diabetes itself and revolves around strict glycemic control. Exercise therapy (including aerobic, strength, or balance training-based exercise) appears to be a promising preventative and treatment strategy for patients with DPN and those at risk. The goal of this Physiology in Medicine article is to highlight important and overlooked dysfunction of the neuromuscular system as a result of DPN with an emphasis on the physiologic basis for that dysfunction. Additionally, we sought to provide information that clinicians can use when following patients with diabetes or DPN including support for the inclusion of exercise-based therapy as an effective, accessible, and inexpensive form of treatment.

Indexed as

Diabetic NeuropathiesExercise TherapyHumansMuscle ContractionMuscle, SkeletalNeuromuscular Diseasesdiabetesexercisefatiguemuscleweakness

Identifiers

PMID26989220
PMCPMC4967246
OpenAlexW2307714472

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.