Brain Vol. 127 No. 12 © Guarantors of Brain 2004; all rights reserved
Letter to the Editor |
Skin denervation in type 2 diabetes: correlations with diabetic duration and functional impairments—a comment
1 Institute of Neurology, Catholic University, 2 Don C. Gnocchi Foundation, Rome, Italy and 3 Department of Clinical Neurophysiology, Uppsala, Sweden
Correspondence to: Irene Aprile, Institute of Neurology, Università Cattolica, L.go F. Vito 1, 00168, Rome, Italy E-mail: i.aprile{at}rm.unicatt.it
Received June 21, 2004. Accepted September 23, 2004.
Sir,
We read with great interest the article by Shun et al. (2004)
recently published in your journal. The authors report on a significant skin denervation and its correlations with diabetes duration and functional impairments. On nerve conduction studies, they observed abnormal findings in only 
50% of diabetic patients. It is well known that conventional nerve conduction tests fail to detect function of the most distal part of sensory nerve fibres or receptors.
Recently we reported on a neurophysiological pattern providing data on the most extreme segments of peripheral sensory nerves (Aprile et al., 2003). During conventional orthodromic sensory conduction studies using submaximal stimulus intensity, a sensory response characterized by a morphology with two peaks (double peak potential) is observed; the second peak disappears with increasing stimulation strength, and a typical compound sensory action potential (CSAP) with higher amplitude is seen (Fig. 1). Our previous experiments provided evidence according to which the second peak is due to anodal submaximal stimulation of fibres other than those stimulated by the cathode. Several experiments and finally a study with repeated topical applications of capsaicin to human skin definitely demonstrated that the cathode directly stimulates the sensory nerve while the anode stimulates receptors or skin nerve endings (Aprile et al., 2003, 2004).
|
Hence, with this test, we assess the function of what the authors measured anatomopathologically using skin biopsy. It is interesting to compare the results reported by Shun and colleagues with the results we obtained in a preliminary study on the anodal submaximal stimulation in 24 patients with type 2 diabetes (18 males and four females, mean age 54 years, range 41–65, mean duration of diabetes 5 years). We also performed an assessment on a control group matched by gender and age with the group of diabetic patients. In all patients, clinical history was appraised and clinical examination was performed. With regard to neurophysiological evaluation, the conventional nerve conduction study included sural, peroneal, median (motor and sensory) and ulnar (motor and sensory) nerves. Moreover, the sensory threshold and features of anodal submaximal stimulation at the median nerve (III digit–wrist segment) were evaluated in all of the cases. All diabetic patients were referred to our EMG laboratory for paraesthesia and disaesthesia of the feet or distal leg without abnormal signs at clinical examination. Conventional nerve conduction tests showed abnormal findings in 33% patients (in four patients slowing of at least one sensory nerve conduction velocity, in no patients slowing of at least one motor conduction velocity, in no patients reduction of at least one sensory amplitude response, in two patients reduction of at least one motor amplitude response, and in two patients more than one abnormal finding). The anodal stimulation results showed abnormal findings (the stimulus intensity needed to obtain the second peak was higher than in the control group) in 67% of patients. Moreover, statistical analysis showed significant differences between the diabetic patients group and the control group in the sensory thresholds (P < 0.009) and in the submaximal stimulus intensity necessary to obtain the double peak picture (P < 0.005) (see Fig. 2). These results strongly suggest a functional impairment of receptors or skin nerve endings.
|
Our results, obtained with a different test, seem to agree with those observed by Shun and colleagues and confirm skin denervation in diabetic neuropathy. Moreover, both their results and ours suggest the importance of evaluating skin denervation at least at an early stage of diabetic neuropathy.
References
Aprile I, Stalberg E, Tonali P, Padua L. Double peak sensory responses at submaximal stimulation. Clin Neurophysiol 2003; 114: 256–62.[CrossRef][Web of Science][Medline]
Aprile I, Stalberg E, Caliandro P, Pazzaglia C, Tonali P, Foshini M, Trotta E, et al. New neurophysiological findings on skin receptors or intradermal nerve endings after repetitive capsaicin application. J Periph Nerv Syst 2004; 9: 109–10.
Shun CT, Chang YC, Wu HP, Hsieh SC, Lin WM, Lin YH, et al. Skin denervation in type 2 diabetes: correlations with diabetic duration and functional impairments. Brain 2004; 127: 1593–605.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||