Electrophysiological Evidence of Demyelination in Patients with Diabetic Neuropathy.
- Author:
Seok Beom KWON
1
;
Ki Han KWON
;
San JUNG
;
Mi Sun OH
;
Sung Hee HWANG
Author Information
1. Department of Neurology, Hallym University College of Medicine, Seoul, Korea. neurokkh@medigate.net
- Publication Type:Original Article
- Keywords:
Demyelination;
Conduction block;
Diabetes mellitus;
Polyneuropathy;
Chronic inflammatory demyelinating polyneuropathy
- MeSH:
Axons;
Demyelinating Diseases*;
Diabetes Mellitus;
Diabetic Neuropathies*;
Humans;
Immunoglobulins, Intravenous;
Neural Conduction;
Pathology;
Polyneuropathies;
Prevalence
- From:Journal of the Korean Neurological Association
2004;22(3):240-248
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Diabetic neuropathy is one of the most common neuropathies. Although pathologic studies show both segmental demyelination and axonal loss in diabetic neuropathy, the relative importance of segmental demyelination is debated. Conduction block (CB) is a physiologic hallmark of segmental demyelination. If segmental demyelination were a main pathology of diabetic neuropathy, CB should be common. We undertook this study to determine the prevalence of CB in diabetic patients. METHODS: Fifty-two consecutive diabetic patients (M=30, F=22) were referred to EMG laboratory and underwent routine nerve conduction studies (NCS). CB was defined by two methods. One was > 20% drop in peak-to-peak amplitude and < 15% change in negative-peak duration between proximal and distal stimulation sites. The other was > 50% drop in the amplitude and area. Clinical findings, electrophysiological data, and effectiveness of immunomodulating therapy for some patients with CB were reviewed. RESULTS: A total 326 nerves were studied. The criteria for 20% and 50% CB were met in 35 nerves in 19 patients and 7 nerves in 6 patients, respectively (prevalence=10.7%, 2.1%, respectively). Some patients with CB were treated with IVIG or steroid and had a good response. CONCLUSIONS: CB in diabetic neuropathy is not a common finding. The rarity of CB in diabetic neuropathy suggests that segmental demyelination is not a prominent part of the underlying pathology. The presence of CB and good responsiveness to immunomodulating therapy in diabetic neuropathy also suggest alternative or additional causes for neuropathy, such as chronic inflammatory demyelinating polyneuropathy.
