Evidence map›Paper›PMID 10219752›Full record

ReviewBrain pathology (Zurich, Switzerland)1999

Diabetic neuropathies: features and mechanisms.

D W Zochodne

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  12. Role of advanced glycation endproducts and glyoxalase I in diabetic peripheral sensory neuropathy.Translational research : the journal of laboratory and clinical medicine · 2012
    Review
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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

1 author at 1 institution in 1 country.

D W ZochodneDepartment of Clinical Neurosciences, University of Calgary, Alberta. dzochodn@acs.ucalgary.ca
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic neuropathies include both focal neuropathies and diffuse polyneuropathy. Polyneuropathy, the most common of the diabetic neuropathies excluding focal entrapment, has not yet been explained by a single disease mechanism despite intensive investigation. A number of abnormalities appear to cascade into a 'vicious cycle' of progressive microvascular disease associated with motor, sensory and autonomic fiber loss. These abnormalities include excessive polyol (sugar alcohol) flux through the aldose reductase pathway, functional and structural alterations of nerve microvessels, nerve and ganglia hypoxia, oxidative stress, nonspecific glycosylation of axon and microvessel proteins, and impairment in the elaboration of trophic factors critical for peripheral nerves and their ganglia. While an initiating role for nerve ischemia in the development of polyneuropathy has been proposed, the evidence for it can be questioned. The role of sensory and autonomic ganglia in the development of polyneuropathy has had relatively less attention despite the possibility that they may be vulnerable to a variety of insults, particularly neurotrophin deficiency. Superimposed on the deficits of polyneuropathy is the failure of diabetic nerves to regenerate as effectively as nondiabetics. Polyneuropathy has not yet yielded to specific forms of treatment but a variety of new trials addressing plausible hypotheses have been initiated. This review will summarize some of the clinical, pathological and experimental work applied toward understanding human diabetic neuropathy and will emphasize ideas on pathogenesis.

Indexed as

AnimalsAutonomic Nervous SystemAutonomic Nervous System DiseasesDiabetic NeuropathiesHumansModels, NeurologicalPeripheral Nervous System Diseases

Identifiers

PMID10219752
PMCPMC8098200
OpenAlexW1986184217

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.