Conduction Slowing in Painful versus Painless Diabetic Neuropathy.
- Author:
Jong Seok BAE
1
;
Ji Youn KIM
;
Seok Min GO
;
Sung Sik PARK
;
Jin Young AHN
;
Min Ky KIM
;
Byoung Joon KIM
Author Information
1. Department of Neurology, Seoul Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Diabetic neuropathies;
Neural conduction;
Pain;
Electrophysiology
- MeSH:
Action Potentials;
Amyotrophic Lateral Sclerosis;
Axons;
Diabetic Neuropathies*;
Electrophysiology;
Humans;
Inflammation;
Lower Extremity;
Neural Conduction;
Polyneuropathies
- From:Journal of the Korean Neurological Association
2005;23(4):471-477
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Motor conduction slowing in diabetic distal symmetrical polyneuropathy (DSP) generally exceeds that in distal axonal polyneuropathy. Additional mechanisms secondary to axonal injury may contribute towards this slowing. However, clinical and pathophysiological significances of motor conduction slowing have been rarely discussed. The purpose of this study is to evaluate the clinical and pathophysiological significance of conduction slowing in DSP. METHODS: We analyzed motor conduction studies of 39 patients with symptomatic painful DSP and 24 patients with asymptomatic painless DSP. Motor conduction studies of 39 patients with amyotrophic lateral sclerosis (ALS) were used as controls for the amplitude-dependent slowing of conduction. Percentages of normal limits were calculated for the compound muscle action potential amplitude (CMAP), distal motor latency (DL), and conduction velocity (CV), and converted to a square root (SQRT) form. The changes of SQRT-DL or SQRT-CV according to SQRT-CMAP changes were plotted and analyzed. RESULTS: Regression analysis showed that DL and CV were amplitude-dependent in both painless DSP and ALS. The changes of DL and CV in painful DSP did not show amplitude-dependency except DL in the lower extremities. CONCLUSIONS: This data supports the hypothesis that the mechanism of slowing is similar in both painless DSP and ALS and results from the loss of large, fast-conducting fibers. Lack of amplitude-dependency of conduction slowing in painful DSP may reflect the combined axonal and demyelinating changes, possibly due to inflammation.
