Ephaptic crosstalk in Painful Diabetic Neuropathy: an electrodiagnostic study.
Ahmad Asmedi(1*), Samekto Wibowo(2), Lucas Meliala(3)
(1) Doctoral Student, Doctoral Programme, Department of Neurology, Dr. Sardjito General Hospital/Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta
(2) Department of Neurology, Dr. Sardjito General Hospital/Faculty of Medicine, Universitas Gadja Mada, Yogyakarta
(3) Department of Neurology, Dr. Sardjito General Hospital/Faculty of Medicine, Universitas Gadja Mada, Yogyakarta
(*) Corresponding Author
Abstract
Painful Diabetic Neuropathy (PDN) is a common complication of diabetes mellitus
(DM) which significantly causes pain and distress in patients. Release of factors from
degenerating fibers activating adjacent fibers to produce ephaptic crosstalk have been
proposed as one of the pain mechanism in PDN. Here we aim to detect ephaptic crosstalk
between small fibers and large fibers in PDN subjects by comparing the electrodiagnostic
result of patients with PDN and patients without PDN.
This study used cohort prospective design. Patients with type 2 DM or impaired
glucose tolerance (IGT) without PDN from several health facilities in Yogyakarta were
followed for 12 months for the occurrence of PDN. Demographic, clinical, laboratory and
electrodiagnostic data from all patients were collected and analyzed.
One hundred and forty-one subjects (58 men, 83 women) with an average age of 51
years (range, 40–61 years), were enrolled in this study. After 48 weeks of observation,
12 subjects were found to have PDN. The differences of distal latency between PDN
and non-PDN group were significant when measured in median sensory nerve (4.47 ms
±2.43 versus 3.39 ms ±1.79, p = 0.002), tibial motor nerve (6.96 ms ±3.07 versus
5.90 ms ±2.17, p = 0.041), and sural sensory nerve (6.02 ms ±3.56 versus 3.55
ms ±2.90, p <0.001). Among all parameters measured in this study, the H-reflex had
higher abnormality persentage compared to other electrodiagnostic variable (H latency =
30%, H amplitude = 71%, H/M Ratio = 88%, and H-M IPL = 15%).
Our result shows that small fiber neuropathy in PDN can be detected by electrodiagnostic
study which measures large fibers function. This indicates that ephaptic crosstalk
between small fiber and large fiber happens in PDN.
(DM) which significantly causes pain and distress in patients. Release of factors from
degenerating fibers activating adjacent fibers to produce ephaptic crosstalk have been
proposed as one of the pain mechanism in PDN. Here we aim to detect ephaptic crosstalk
between small fibers and large fibers in PDN subjects by comparing the electrodiagnostic
result of patients with PDN and patients without PDN.
This study used cohort prospective design. Patients with type 2 DM or impaired
glucose tolerance (IGT) without PDN from several health facilities in Yogyakarta were
followed for 12 months for the occurrence of PDN. Demographic, clinical, laboratory and
electrodiagnostic data from all patients were collected and analyzed.
One hundred and forty-one subjects (58 men, 83 women) with an average age of 51
years (range, 40–61 years), were enrolled in this study. After 48 weeks of observation,
12 subjects were found to have PDN. The differences of distal latency between PDN
and non-PDN group were significant when measured in median sensory nerve (4.47 ms
±2.43 versus 3.39 ms ±1.79, p = 0.002), tibial motor nerve (6.96 ms ±3.07 versus
5.90 ms ±2.17, p = 0.041), and sural sensory nerve (6.02 ms ±3.56 versus 3.55
ms ±2.90, p <0.001). Among all parameters measured in this study, the H-reflex had
higher abnormality persentage compared to other electrodiagnostic variable (H latency =
30%, H amplitude = 71%, H/M Ratio = 88%, and H-M IPL = 15%).
Our result shows that small fiber neuropathy in PDN can be detected by electrodiagnostic
study which measures large fibers function. This indicates that ephaptic crosstalk
between small fiber and large fiber happens in PDN.
Keywords
Painful diabetic neuropathy – NCS – ephaptic– Diabetes Mellitus
Full Text:
PDFDOI: https://doi.org/10.19106/JMedSci005002201806
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