PROGRESSION OF DISTAL SYMMETRICAL POLYNEUROPATHY DURING DIABETES-MELLITUS - CLINICAL, NEUROPHYSIOLOGICAL, HEMORHEOLOGICAL CHANGES AND SELF-RATING SCALES OF PATIENTS

Citation
Iw. Husstedt et al., PROGRESSION OF DISTAL SYMMETRICAL POLYNEUROPATHY DURING DIABETES-MELLITUS - CLINICAL, NEUROPHYSIOLOGICAL, HEMORHEOLOGICAL CHANGES AND SELF-RATING SCALES OF PATIENTS, European neurology, 37(2), 1997, pp. 90-94
Citations number
20
Categorie Soggetti
Clinical Neurology",Neurosciences
Journal title
ISSN journal
00143022
Volume
37
Issue
2
Year of publication
1997
Pages
90 - 94
Database
ISI
SICI code
0014-3022(1997)37:2<90:PODSPD>2.0.ZU;2-H
Abstract
The complex interrelationships between progression of distal symmetric polyneuropathy (DSP) induced by diabetes mellitus and haemorheologica l alterations in correlation with the patients' self-rating scales abo ut the progression of DSP were investigated. The study included 42 pat ients suffering from diabetes mellitus for 15 +/- 10 years. Clinical, neurophysiological and haemorheological follow-ups (platelet reactivit y, erythrocyte aggregation, viscosity) were performed initially (A) an d repeated 42 +/- 10 months later (B), At point B, clinical signs of D SP were found in 90.2% in the lower extremities, and 41.5% of the pati ents exhibited for the first time new symptoms and signs of DSP in the upper extremities, Besides conventional neurophysiological investigat ions (conduction velocity, amplitude) in the sural nerve, paired stimu lation (LPSS) was applied, In peroneal nerve, conduction velocity, dis tal latency and F wave were estimated. These results confirmed the cli nical progression of DSP (LPSS; p < 0.05). Platelet reactivity was sta tistically improved (p < 0.05) at point B predominantly as an effect o f treatment (acetylsalicylic acid, Ginkgo biloba), whereas erythrocyte aggregation was increased at point B with and without treatment (p < 0.05). Blood glucose levels were abnormal at both points, Analogue sel f-rating scales showed that only 27% of the patients realized their pr ogression of DSP. In conclusion, the results prove the clinical and ne urophysiological progression of DSP and highlight that haemorheologica l changes may play a part in the conjectural pathogenesis of DSP. As p atients to not realize the dramatic progression of DSP, information of the patients about the correlation between hyperglycaemia and progres sive DSP should be reinforced.