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Minerva Medica 2000 January-February;91(1-2):1-6


language: Italian

Study of onset and progression of peripheral neuropathy and hypertension in NIDDM

Jarmuzewska E. A., Ghidoni A.


Background. Diabetic neuropathy is the most common pathology affecting the peripheral nervous system. In prognostic terms, it is the most devastating complication of diabetes. About 50% of diabetics suffer from neuropathy between 25-30 years after the diagnosis of diabetes, even if over the past few decades there has been a considerable improvement in the diagnostic methods and criteria used to classify peripheral neuropathies, many of which are related to the development of neurophysiology. However, we still do not know enough about the incidence, prevalence and natural history of peripheral neuropathy diagnosed using clinical and electrophysiological criteria in non-insulin dependent diabetic patients. Methods. The authors carried out a randomized study of the relationship between glucose intolerance, hyperglycemia, hyperinsulinemia, hypertension and early and manifest forms of peripheral neuropathy in 32 patients with NIDDM (aged 41-72 years old, duration of diabetes 1-27 years) over a 24-month period. In 11 patients diabetes was almost at onset (Group 1): 8 cases with diabetes for 1-2.5 years (4 hypertensives and 4 normotensives) and 3 cases with diabetes for 4 years (all normotensive). Twenty-one patients (Group 2) had had diabetes for longer (5-27 years): 5 were hypertensive and 16 normotensive. A full longitudinal neurophysiological study (EMG and ENG) was performed. In 11 NIDDM in Group 1, at basal conditions carpal tunnel syndrome (right CTS) was revealed in 1 case, right CTS with diffuse radiculopathy in 1 case, diffuse radiculopathy in 2 cases, lumbosacral radiculopathy in 1 case, and 1 right CTS with ''mixed'' symptoms. EMG-ENG were normal in 2 patients. Results. The following developments were noted during the follow-up: rapid deterioration due to the onset of motor sensitive polyneuropathy (MSPN) in 1 patient, 3 cases of chronic neurogenic disorder with active denervation, 2 cases of ''mixed'' type symptoms. The results were only comparable in 2 cases. In 3 NIDDM with diabetes for 4 years, 1 patient presented MSPN and 2 were affected by chronic neurogenic disorders; during the follow-up the conduction of MSPN and active denervation deteriorated into chronic neurogenic syndrome. Moreover, 6 initially normotensive NIDDM developed hypertension. In 21 NIDDM of Group 2, 7 of the 16 who were initially normotensive became hypertensive. Three new cases of polyneuropathy were also reported in this group, and 5 already had MSPN but showed a deterioration of conduction during the follow-up in 1 case. One patient presented active denervation in chronic neurogenic symptoms and chronic neurogenic symptom was comparable in 1 case. One patient presented a normal EMG-ENG at both the start and end of the study. ''Mixed'' type of symptoms were recorded at the basal level in 11 patients (defined as the presence on the EMG of muscular areas with multiphase potentials of brief duration and low amplitude, first recruited under slight voluntary effort, isolated or mixed with areas of neurogenic potentials). Over the course of 12-24 months, eight patients deteriorated with chronic neurogenic symptoms without active denervation in 5 and present in 2 cases. One case also showed a deterioration of carpal tunnel syndrome. Conclusions. These results show that 1) metabolic control and a complete neurophysiological examination are essential for preventing and identifying the onset and progress of neuromuscular damage; 2) the onset or deterioration of these two complications mainly had a less well known common cause which was less studied and described.

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