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Comparement of Nerve Excitability among Diabetics with or without Polyneuropathy with Same Hba1c Levels and Diabetes Duration

Commentary Open Access
Cagdas Erdogan*
Pamukkale University School of Medicine, Depatment of Neurology, Denizli, Turkey
*Corresponding authors: Cagdas Erdogan
Pamukkale University School of Medicine
Department of Neurology, Denizli, Turkey
Tel: +90-4440728-5678
E-mail: drcagdaserdogan@gmail.com
 
Received September 19, 2011; Published August 31, 2012
 
Citation: Erdogan C (2012) Comparement of Nerve Excitability among Diabetics with or without Polyneuropathy with Same Hba1c Levels and Diabetes Duration. 1:287. doi:10.4172/scientificreports.287
 
Copyright: © 2012 Erdogan C. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
Abstract
 
Introduction: Recent studies have demonstrated that hyperglicemia played an important role in the development of diabetic neuropathy. However some patients may develop neuropathy while some with the same serum HbA1c levels do not. There seem to be some additional factors in the development of neuropathy. Strength duration properties indirectly reflect the function of some sodium channels and may give an idea about the nerve excitability. It may both demonstrate a hyperexcitable state or rather a hypoexcitability due to the prominent pathological process. In this study we compared the excitability properties of diabetic patients with or without polyneuropathy with the same HbA1c levels. We aimed to demonstrate a possible difference in the group’s response to hyperglicemia, if exists.
 
Matherials and methods: With this purpose, the excitability properties of 3 groups: type 2 diabetes with or without polyneuropathy and the control groups, were studied. To demonstrate a possible difference in their response to hyperglicemia, two diabetic groups were chosen to have serum HbA1c levels.
 
Results: The mean strength duration time constant was higher in the neuropathic group than the other two groups, suggesting a hyperexcitable state. Although the two diabetic groups had similar glucose levels and duration of diabetes, there were significant differences between two groups excitability properties. This result may suggest that hyperglicemia may not be enough for the development of neuropathy. The patients’ personal responses to hyperglicemia and ion channel functions may also play roles in the developing polyneuropathy.
 
Keywords
 
Diabetic neuropathy; Hyperglicemia; Nerve excitability properties
 
Introduction
 
Neuropathy is one of the major complications of diabetes and affects the patient’s quality of life, but clinical features may not be compatible with conventional nerve conduction studies [1].
 
It is well known that the severity and the duration of hyperglycemia play an important role in the pathogenesis of diabetic polyneuropathy. However, in clinical practice, some diabetic patients experience neuropathic pain or develop neuropathy while some others with the same HbAc levels and diabetes durations do not. This supports the idea that hyperglycemia may not be enough for the development of neuropathic process.
 
Some recent studies had demonstrated that there is variability among the excitability poperties of patients who had similar hyperglycemia levels and duration of diabetes [2]. The ones experiencing neuropathic pain had altered excitability properties while the ones without pain did not. They also reported that nerve excitability properties may be affected even before there is any electrophsiological evidence of developed polyneuropathy [2,3]. There are also some studies which aimed to show the excitability properties of the developed neuropathy [4]. Some of these studies found hyperexcitability [3,4] while some found a reduction in the excitability [5,6].
 
Strength Duration Time Constant (SDTC) may reflect the properties of sodium (Na) channels and may give an idea about the nerve excitability. Recently it was used to demostrate the excitability properties of the developed diabethic polyneuropathy [4]. It also was useful in the early clinical states [7].
 
In this study we aimed to demonstrate a possible difference in diabetic patients response to hyperglicemia. With this purpose we compared the excitability properties of diabetic patients with or without polyneuropathy who had similar HbA1c levels.
 
Materials and Methods
 
28 diabetic patients with polyneuropathy (DM+PNP), 28 diabetic patients without polyneuropathy(DM-PNP) and 26 healty controls were studied. Some recent studies reported a possible alteration of nerve excitability in patients experiencing neuropathic pain even in the lack of PNP [2,3], so DM-PNP group included patients who were not complaining of any symptoms suggesting neuropathic pain and whose conventional nerve conduction studies were within normal limits. Polyneuropathy was diagnosed with the evidence of involvement of at least 3 peripheric nerves. Diabetic patients were all type 2 DM, and were not receiving insulin. None of the individuals were using any drugs which may have an effect on the ion channels. HbA1c levels and the duration of diabetes were similar in both diabetic groups. SDTC and rheobase (Rhb) were recorded from extensor digitorum brevis(EDB) and peroneal nerve was stimulated from the ankle. Maximum amplitude values were recorded and 40 % of these values were calculated as the target values. The stimulation intensities needed to create these target values were recorded for each stimulation durations of 0.04,0.1,0.2,0.3,0.5,0.7 and 1 miliseconds (msn) [4]. SDTC and rheobase values were calculated for all individuals using the Weiss formula [7]. The milliseconds (0.04, 0.1, 0.2, 0.3, 0.5, 0.7, and 1 ) were replaced in the x axis and the miliampere values needed to create the target amplitude are placed in the y axis. SDTC is the value when y is zero( where the line crosses the x axis) Rheobase is the incline of this line. To avoid a possible difference which may be caused by sex or age [7], all groups were chosen to have similar age or sex specialities (all groups had age matched half male and half female individuals). Data were inserted to SPSS 17.0. One way ANOVA and Benferroni correction were used for the analyses among the groups.
 
Results
 
The mean age values were 48.9 ± 12.30 in DM+PNP group, 50.2 ± 11.84 in DM-PNP group and 47.4 ± 13.26 in control group.Both DM+PNP and DM-PNP groups had similar HbA1c levels and the duration of diabetes were also similar in both groups (Table 1). The SDTc values (Table 2) were significantly prolonged in the DM+PNP group than both the DM-PNP(p=0.025) and the control group(p=0.017). Though the SDTc values of DM-PNP group were higher than the control group (Table 2) the difference was not significant(p=0.452).The Rheobase values (Table 2) were significantly smaller in the DM+PNP group than the DM-PNP(p=0.038) and the control group (p=0.024). The difference between the control and the DM-PNP group was not significant (p=0.382).
 
Table 1: Mean glycosylated hemoglobine and duration of diabetes of the diabetic groups.
 
Table 2: Mean strength duration time constant and rheobase values of the groups.
 
Conclusion
 
Hyperglycemia plays an important role in the development of neuropathic process by causing structural and functional changes on the ion channels which affects metabolic transport [8].
 
Although both diabetic groups’ HbA1c levels and diabetes duration times were similar, the ones with polyneuropathy seemed to be more sensitive and were affected from the hyperglycemia. The polyneuropathy group had higher excitability properties than the group without polyneuropathy. This supports the possibility that the hyperglicemia may not be the only cause in neuropathic process.
 
The SDTC reflects the persistent Na+ channels and may give an idea about the excitability properties of a nerve [9]. Some recent studies have mentioned a hyper excitable state [2,3] while the others reported hypo excitability in diabetic polyneuropathy. This seems to be controversial but the predominance of different pathological processes may be the cause of different electrophysiological results. Prolonged SDTC means an increment in the excitability which may be caused by the increased number of Na channels. An axonal damage may trigger an expression of these Na channels in the damaged place [10]. Also axonal sprouting and new collaterals may provide an increment in the number of total Na channels [11]. Finally, the increased number of persistent Na+ channels may cause prolonged SDTC. On the other hand, if the axonal loss causing a reduction in the total amount of Na channels or the metabolic dysfunction of ion channels are prominent in the pathological process, this should also cause shortened SDTc levels reflecting a hypoexcitability. As a result, SDTc may reflect different results at different neuropathic states so may not be proper for evaulating a developed PNP. Both diabetic groups had similar HbA1c levels but their responses to hyperglicemia seem to be different, suggesting that there should be some additional conditions underlying the polyneuropathy process. There may a possibility that peripheric Na+ channels of the patients developing polyneuropathy should be more responsible to hyperglicemia. Also some patients may experience neuropathic pain while others with same HbA1c levels may not. The same enviromental factor may be causing different processes because of a probable structural variation in the ion channels. If this variation of ion channels should be well defined, perhaps it would be possible to predict the risk of neuropathy before the development of neuropathic process. Future studies should be designed to assess the ion channels of patients in earlier stages of diabetes and to follow up and demonstrate who will develop neuropathy.
 
 
References