medwireNews: Both small and large nerve fiber impairment can be detected among people with well-controlled recent-onset type 1 or type 2 diabetes, and may regress with time, shows German research presented at the virtual 57th EASD Annual Meeting.
Gidon Bönhof, from Heine University Düsseldorf, told delegates it has traditionally been suggested that “injury to small nerve fibers precedes large fiber impairment in the early development of DSPN [diabetic sensorimotor polyneuropathy].”
The current analysis, however, suggests that large and small fiber damage can occur in parallel and in fact “large fiber dysfunction seems more frequent than abnormal small fiber morphology in recent-onset diabetes,” Bönhof remarked.
He reported that, at baseline, DSPN, defined by the Toronto Consensus criteria, was present in 8.1% of 350 German Diabetes Study participants with type 1 diabetes and 13.3% of 570 participants with type 2 diabetes. All participants had a diabetes duration of less than 1 year, and a median glycated hemoglobin level of 6.3–6.4% (45–46 mmol/mol).
Nerve conduction studies and quantitative sensory testing revealed that, compared with age-matched controls, individuals with type 1 diabetes had impaired function in five large-fiber indices, namely ulnar and peroneal motor nerve conduction velocity, sural sensory nerve conduction velocity (SNCV) and action potential, and malleolar vibration perception threshold.
They also had significantly higher rates of intraepidermal nerve fiber density (IENFD) abnormalities, indicating small fiber dysfunction, versus controls, as well as a higher incidence of abnormal Neuropathy Symptom Scores (NSS) and Neuropathy Disability Scores (NDS).
The people with type 2 diabetes had impaired function relative to controls in the same five large fiber indices as the people with type 1 diabetes, along with worse median motor nerve conduction velocity, and worse median and ulnar sensory nerve action potential.
For the small-fiber measures, abnormal scores on IENFD as well as warm thermal detection thresholds were more common in the type 2 diabetes group versus controls, as were abnormal neuropathic symptoms, pain, and deficit scores.
Bönhof said that a subset of participants was followed up for 5 years (n=179 for type 1 and 291 for type 2 diabetes), and this analysis showed that abnormal nerve function can both progress and regress.
For example, sural SNCV remained abnormal in 3.4% of people with type 1 diabetes, regressed to normal in 5.1% and progressed to abnormal in 6.2%. The corresponding proportions among the participants with type 2 diabetes were 5.9%, 3.7%, and 8.4%.
In the people with type 2 diabetes, IENFD remained abnormal in 11.6% of 69 participants with follow-up data, regressed in 8.7% and progressed in 18.8%, which Bönhof pointed out was the biggest progression rate overall.
Finally, he showed that DSPN remained abnormal in 2.6% and 7.8% of people with type 1 (n=179) and type 2 (n=291) diabetes respectively, regressed to normal in a respective 10.3% and 6.5%, and progressed to abnormal in a corresponding 5.8% and 10.4%.
Bönhof concluded: “Regression of DSPN or individual nerve alteration is possible to a meaningful degree.”
The study findings are also published in Brain.
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EASD Annual Meeting; Sept 27–Oct 1, 2021
Brain 2021; doi: 10.1093/brain/awab330