Journal List > Korean J Clin Neurophysiol > v.16(1) > 1084144

Lee, Han, and Kim: Peripheral Nerve Abnormalities in Patients with Newly Diagnosed Type I and II Diabetes Mellitus

Abstract

Background:

Early detection of neuropathy may prevent further progression of this complication in the diabetic patients. The purpose of this study was to evaluate the prevalence of early neuropathic complication in patients with newly diagnosed type 1 and type 2 diabetes.

Methods:

Nerve conduction studies (median, ulnar, posterior tibial, peroneal, and sural nerves) were performed for 49 type 1 (27 males, mean 14.1±7.5 years) and 40 type 2 (27 males, 42.0±14.1 years) diabetic patients at onset of diabetes. Children with age at onset under 4 years and adults over 55 years were excluded to eliminate the aging effect and the influence of obstructive arteriosclerosis. Neuropathy was defined as abnormal nerve conduction findings in two or more nerves including the sural nerve.

Results:

Mean HbA1c level was 12.6±3.3% for type 1 and 10.5±2.9% for type 2 diabetes. The prevalence of neuropathy was 12.2% for type 1, and 35.0% for type 2 diabetes, respectively. There were significant trends in the prevalence of neuropathy with increasing age (p<0.05). The effect of the mean level of glycosylated hemoglobin on the prevalence of polyneuropathy at onset of diabetes was borderline (p=0.0532). Neither sex of the patients nor the type of diabetes affected the neurophysiologic abnormalities at the diagnosis.

Conclusions:

Even in a population with diabetes at the diagnosis, the prevalence of subclinical neuropathy was not low. Neuropathy has been significantly associated with increasing age indicating the possibility of longer duration of undetected diabetes among them, especially in type 2 diabetes. (Korean J Clin Neurophysiol 2014;16:8-14)

REFERENCES

1.Meltzer S., Leite L., Daneman D., Gerstein HC., Lau D., Ludwig S, et al. Clinical practice guidelines of the management of diabetes in Canada. Canadian Diabetes Association. CMAJ. 1998. 159(Suppl 8):): S1-S29.
2.Dyck PJ., Bushek W., Spring EM., Karnes JL., Litchy WJ., O'Brien PC, et al. Vibratory and cooling detection thresholds compared with other testsin diagnosing and staging diabetic neuropathy. Diabetes Care. 1987. 10:432–440.
3.Ficicloglu C., Aydina A., Haktan M., Kiziltan M. Peripheral neuropathy in children with insulin-dependent diabetes mellitus. Turk J Pediatr. 1994. 36:97–104.
4.Solders G., Thalme B., Aguirre-Aquino M., Brandt L., Berg U., Persson A. Nerve conduction and autonomic nerve function in diabetic children. A 10-year follow-up study. Acta Paediatr. 1997. 86:361–366.
crossref
5.Dyck PJ. Detection, characterization, and staging of polyneuropathy: asessed in diabetics. Muscle Nerve. 1988. 11:21–32.
6.Oh SJ. Clinical Electromyography: Nerve Conduction Studies. 3rd ed.Philadelphia, Baltimore: Williams & Wilkins;2003. p. 37–135.
7.Lee S., Han H., Kim H. A 5-yr follow-up nerve conduction study for the detection of subclinical diabetic neuropathy in children with newly diagnosed insulin-dependent diabetes mellitus. Pediatric Diabetes. 2010. 11:521–528.
crossref
8.England JD., Gronseth GS., Franklin G., Miller RG., Asbury AK., Carter GT, et al. Distal symmetric polyneuropathy: a definition for clinical research. Report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2005. 64:199–207.
crossref
9.Comi G., Canal N., Lozza L., Beccaria L., Meschi F., Vanini R, et al. Peripheral nerve abnormalities in newly-diagnosed diabetic children. Acta Diabetol Lat. 1986. 23:69–75.
crossref
10.Lehtinen JM., Uusitupa M., Siitonen O., Pyörälä K. Prevalence of neuropathy in newly diagnosed NIDDM and nondiabetic control subjects. Diabetes. 1989. 38:1307–1313.
crossref
11.Partanen J., Niskanen L., Lehtinen J., Mervaala E., Siitonen O., Uusitupa M. Natural history of peripheral neuropathy in patients with non-insulin-dependent diabetes mellitus. N Engl J Med. 1995. 333:89–94.
crossref
12.Rota E., Quadri R., Fanti E., Poglio F., Paolasso I., Ciaramitaro P, et al. Clinical and electrophysiological correlations in type 2 diabetes mellitus at diagnosis. Diabetes Res Clin Pract. 2007. 76:152–154.
crossref
13.Karmakar RN., Khandakar MR., Gangopadhyay PK., Ghosh K., Babu AS. Albuminuria and neuropathy in newly detected diabetics: profile and correlation. J Indian Med Assoc. 2011. 109:396–399.
14.Daube JR. Electrophysiologic testing in diabetic neuropathy. Dyck PJ, Thomas PK, editors. Diabetic neuropathy. 2nd ed.Philadelphia: WB Saunders;1999. p. 222–238.
15.Sima AA., Kamiya H. Diabetic neuropathy differs in type 1 and type 2 diabetes. Ann NY Acad Sci. 2006. 1084:235–249.
crossref
16.Kempler P., Tesfaye S., Chaturvedi N., Stevens LK., Webb DJ., Eaton S, et al. Autonomic neuropathy is associated with increased cardiovascular risk factors: the EURODIABIDDM Complications Study. Diabet Med. 2002. 19:900–909.

Table 1.
Proportion of patients showing altered nerves in NCS at the diagnosis of diabetes mellitus
No. of nerves altered Type 1 DM (n=49, %) Type 2 DM (n=40, %)
1 13 (26.5) 6 (15.0)
2 8 (16.3) 14 (35.0)
3 9 (18.4) 7 (17.5)
4 2 (4.1) 7 (17.5)
5 1 (2.0) 2 (5.0)

DM; diabetes mellitus, NCS; nerve conduction study.

Table 2.
Percentage of patients showing each single nerve altered at the diagnosis of diabetes mellitus
Type 1 DM (n=49, %) Type 2 DM (n=40, %)
Motor nerves
Median 17 (34.7) 20 (50.0)
Ulnar 9 (18.4) 18 (45.0)
Tibial 4 (8.2) 8 (20.5)
Peroneal 22 (44.9) 23 (57.5)
Sensory nerves
Median 14 (28.6) 20 (50.0)
Ulnar 11 (22.4) 11 (27.5)
Sural 6 (12.2) 14 (35.0)

DM; diabetes mellitus.

Table 3.
Proportion of patients showing altered parameters of nerve conduction study at the diagnosis of diabetes mellitus
No. of parameters* altered Type 1 DM (n=49, %) Type 2 DM (n=40, %)
1 11 (22.4) 4 (10.0)
2 6 (12.2) 8 (20.0)
3 5 (10.2) 7 (17.5)
4 4 (8.2) 4 (15.0)
5 2 (4.1) 6 (15.0)
6 2 (4.1) 0
7 2 (4.1) 1 (2.5)
8 1 (2.0) 1 (2.5)
9 0 0
10 0 2 (5.0)
11 0 0
12 0 0
13 0 2 (5.0)

DM; diabetes mellitus, NCS; nerve conduction study.

* Parameters; Terminal latencies, conduction velocities, and amplitudes of compound action potentials of median, ulnar, posterior tibial and peroneal nerves, nerve conduction velocities and amplitudes of sensory nerve action potentials of median, ulnar, and sural nerves.

Table 4.
Relative number of patients with pathological values (mean±2.5 SD) at the diagnosis of diabetes mellitus. Normal limit is given in the parenthesis
Nerve Type 1 DM (n=49, %) Type 2 DM (n=40, %)
Median motor
TL (3.6 ms) 4 (8.2) 9 (22.5)
CV (50 m/s) 15 (30.6) 17 (42.5)
CMAP (5 mV) 3 (6.1) 2 (5.0)
Ulnar motor
TL (2.5 ms) 4 (8.2) 12 (30.0)
CV (50 m/s) 5 (10.2) 10 (25.0)
CMAP (5 mV) 0 0
Tibial motor
TL (5 ms) 3 (6.1) 7 (17.5)
CV (40 m/s) 1 (2.0) 3 (7.5)
CMAP (5 mV) 0 0
Peroneal motor
TL (4.6 ms) 4 (8.2) 7 (17.5)
CV (40 m/s) 6 (12.2) 9 (22.5)
CMAP (4 mV) 19 (38.8) 18 (45.0)
Median sensory
CV (41 m/s) 14 (28.6) 20 (50.0)
SNAP (10 µV) 1 (2.0) 3 (7.5)
Ulnar sensory
CV (40 m/s) 9 (18.4) 8 (20.0)
SNAP (8 µV) 2 (4.1) 4 (10.0)
Sural
CV (36 m/s) 6 (12.2) 13 (32.5)
SNAP (6 µV) 2 (4.1) 6 (15.0)

CMAP; compound muscle action potential, CV; conduction velocity, DM; diabetes mellitus, SNAP; sensory nerve action potential, TL; terminal latency.

TOOLS
Similar articles