Progression of distal symmetric polyneuropathy during diabetes mellitus: clinical, neurophysiological, haemorheological changes and self-rating scales of patients.
The complex interrelationships between progression of distal symmetric polyneuropathy (DSP) induced by diabetes mellitus and haemorheological alterations in correlation with the patients' self-rating scales about the progression of DSP were investigated. The study included 42 patients suffering from diabetes mellitus for 15 +/- 10 years. Clinical, neurophysiological and haemorheological follow-ups (platelet reactivity, erythrocyte aggregation, viscosity) were performed initially (A) and repeated 42 +/- 10 months later (B). At point B, clinical signs of DSP were found in 90.2% in the lower extremities, and 41.5% of the patients exhibited for the first time new symptoms and signs of DSP in the upper extremities. Besides conventional neurophysiological investigations (conduction velocity, amplitude) in the sural nerve, paired stimulation (LPSS) was applied. In peroneal nerve, conduction velocity, distal latency and F wave were estimated. These results confirmed the clinical progression of DSP (LPSS; p < 0.05). Platelet reactivity was statistically improved (p < 0.05) at point B predominantly as an effect of 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 self-rating scales showed that only 27% of the patients realized their progression of DSP. In conclusion, the results prove the clinical and neurophysiological progression of DSP and highlight that haemorheological changes may play a part in the conjectural pathogenesis of DSP. As patients to not realize the dramatic progression of DSP, information of the patients about the correlation between hyperglycaemia and progressive DSP should be reinforced.
Husstedt
I W
IW
Klinik und Poliklinik für Neurologie, Westfälischen Wilhelms-Universität, Münster, Germany.
Grotemeyer
K H
KH
Evers
S
S
Staschewski
F
F
Wertelewski
R
R
D000293:Adolescent; D000328:Adult; D000368:Aged; D001241:Aspirin / Q000008:administration & dosage; D001786:Blood Glucose / Q000378:metabolism; D001809:Blood Viscosity / Q000187:drug effects / Q000502:physiology*; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D004224:Diterpenes; D004903:Erythrocyte Aggregation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage; D005500:Follow-Up Studies; D007839:Functional Laterality / Q000187:drug effects / Q000502:physiology; D046934:Ginkgolides; D006801:Humans; D007783:Lactones / Q000008:administration & dosage; D007866:Leg / Q000098:blood supply / Q000294:innervation; D008297:Male; D008875:Middle Aged; D010543:Peroneal Nerve / Q000187:drug effects / Q000503:physiopathology; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology*; D011446:Prospective Studies; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D012212:Rheology; D013497:Sural Nerve / Q000187:drug effects / Q000503:physiopathology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D001786:Blood Glucose; D004224:Diterpenes; D005343:Fibrinolytic Agents; D046934:Ginkgolides; D007783:Lactones; C045856:ginkgolide B; D001241:Aspirin