INTRODUCTION
Peripheral neuropathy is a common disabling complication in patients with diabetes and this complication is related to the duration of the disease process. The prevalence of diabetic neuropathy appears to parallel with duration and severity of hyperglycemia in both type1 and type 2 diabetes, there may be a relationship between degree of hyperglycemia and impairment of nerve that intensified metabolic control can prevent or delay the development of diabetic neuropathy1.
Though people with diabetes can develop neurological problems at any time the relation between duration of diabetes and the development of the clinical complication is still in controversy. Hands and feet are the targets for several diabetes-related complications. Diabetic cheiroarthropathy, also known as diabetic stiff hand syndrome or limited joint mobility, is found in 8-50% of all people with type 1 diabetes and is also seen in those with type 2 diabetes.
The prevalence increases with duration of diabetes and this condition is associated with and predictive of other diabetic complications 2. One indication of the presence of this condition is known as the "prayer sign". This is patients' inability to press their palms together completely without a gap remaining between opposed palms and fingers 3.
Motor neuropathy causes atrophy of the muscles of the foot and ankle, resulting in instability in the flexion And extension of the foot and reduced ankle muscle strength. The combination of muscle weakness and loss of sensory information reception and integration lead to gait imbalance and high plantar pressures4.
Patients with diabetes mellitus are vulnerable to high plantar pressures and ulceration, and are thus more likely to develop bone deformities that affect ankle joint position and velocity; which are both important components of anteroposterior body movement. The combination of loss of sensation, limited ankle mobility, and muscle weakness are associated with increased incidence of falls, ulceration, and amputation in the population of those with diabetic peripheral neuropathy5.
Weakness in the ankle musculature may cause individuals with diabetic peripheral neuropathy to display decreased ankle mobility and power, the impairments associated with decreased ankle weakness cause persons with diabetic peripheral neuropathy to manifest a different foot loading pattern6. Moreover Giacomozzi et al. (2002) investigated that, center of pressure in the diabetic foot and observed that individuals with diabetic peripheral neuropathy lacked an appropriate loading response phase at heel strike. Instead, they exhibited a forward heel strike that produced a flat-foot gait pattern7.
The present study was designed to observe the effects of increasing duration of diabetes on electrophysiological study of peripheral nerves (motor) in patients having type 2 diabetes and also to find out a base line data in healthy subjects. The findings will be helpful as background information for better management of the patients suffering from diabetic neuropathy.
SUBJECTS AND METHODS
Sixty subjects of equal sexes were included in the study.
Patients: Group (A) Twenty (10 male 10 female) diabetic patients with duration of diabetes for 5-10 years, Group (B) Twenty (10 male 10 female) diabetic patients with duration of diabetes for 10-15 years. Patients within these 2 groups were matched regarding age and body mass index. Diabetic subjects were selected from the outpatient clinic of Neurology clinic and Neuro-rehabilitation clinics.
Control: Group (C) Twenty (13 male and 7 female) non-diabetic apparently healthy controls. Persons having history of diabetes up to second degree relations were excluded.
The diagnosis of diabetes was established according to Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (1997)8.
The patients were subjected to:
A. Thorough history taking, general examination to detect complication of diabetes and neurological assessment including the assessment of the motor power, muscle state, and reflexes. Also assessment of the sensory system both superficial and deep sensation.
B. Range of motion of wrist and ankle (flexion-extension) were measured by electronic goniometer [digital electronic geniometer IN 30921 USA]. The range is calculated in degrees.
C. Muscle power of wrist and ankle(flexors- extensors) were measured by Tensiometer [Lafayette 01163 USA].
D. Neurophysiological assessment of ulnar and peroneal nerves. Nerve conduction parameters included Motor nerve conduction velocities, action potential amplitude and latencies of ulnar and peroneal nerves [Cadwell Kd- 026A USA].
E. Informed consent was taken from each of the subjects.
Statistical Methods
All statistical analyses were performed using package for social science (SPSS) version 10 for windows. All parametric variables were expressed as mean±SD and median. One way ANOVA test was performed as the test of significance. The t-test was used to compare between medians, p values of less than 0.05 were considered as statistically significant.
RESULTS
Mean duration of the first group was 7.2±0.5 years and the mean duration of the second group was 12.3±0.6 years with a statistically significant difference.
Statistical differences in fasting serum glucose values between the diabetic groups were not significant (P value=0.3). On the other hand the 3 groups were matched regarding the age, sex and body mass index without statistically significant differences.
There was significant decrease in range of motion at ankle and wrist joints between control and patient groups. On the other hand there was statistically significant difference between the range of motion between patients with short and long duration of diabetes.
There was significant decrease in motor power at ankle and wrist joints between control and patient groups. On the other hand there was no statistically significant difference between the motor power between patients with short and long duration of diabetes.
There was significant decrease in nerve conduction velocities in ulnar and peroneal nerves between patients and control. There was no statistically significant between patients with short and long duration of diabetes
Peroneal nerve conduction was slower than that of ulnar conduction velocities with a statistically significant difference.
DISCUSSION
This work aimed at assessment of the effect of duration of diabetes on the range of motion, muscle power at wrist and ankle joints beside assessment of nerve conduction of ulnar and peroneal nerves.
Selection of 2 groups of diabetic patients with no statistical significant difference regarding the known confounding factors such as age, sex variability, level of diabetic control and body mass index will help in delineating the effect of the disease duration. Moreover they were comparable to a matched healthy control.
The present study shows significant motor function deterioration in the diabetic groups with both shorter and longer duration of diabetes in comparison to non diabetic group. Male patients were more affected than female patients.
Data presented in this study showed that although there was a reduction in the distal motor power, range of motion and nerve conduction assessment there was no statistically significant difference between patients with short and long duration of diabetes. These findings goes with the previously reported data by Graham et al.9, who reported that motor defects are common in diabetes with neuropathy and increase in frequency with the duration of the disease. Though not significant, tendency for reduction in UNCV and PNCV and increase in Ulnar and Peroneal distal latency were observed in diabetic group with longer duration of the disease in comparison to non diabetic group. No significant changes were observed regarding these parameters between non diabetic and diabetic group having shorter duration of diabetes. On the other hand Gomez-Viera (2001) reported that the risk distal sensory motor neuropathy in diabetic patients increase with diabetes duration. The results of our study could be explained by the good control of blood sugar levels in both groups which throw light towards the fact that it is the degree of glycemic control is more effective at hand functions than the duration of the disease perse10.
The present study also showed significant reduction in amplitude and conduction velocity in motor nerves of diabetic group with shorter duration of diabetes which were more pronounced in peroneal nerves. This findings supports the observation of Greene et al.11. On the contrary, in diabetic group with relatively longer duration of diabetes CMAP amplitude and conduction velocity were found to be variably affected in motor nerves. Zochodne (2006) also observed the same12.
Maser et al. (2001) suggested that increasing muscle strength may increase forces on the forefoot and may contribute to increased ulceration risk via increased plantar pressure13. This was demonstrated through observations Ellis (2004) of positive correlation between muscle strength and stiffness in individuals with peripheral neuropathy as compared to aged-matched controls14. Their findings were important in determining that persons with limited muscle function may increase passive torque (stiffness) to increase muscle strength.
Since the generation of concentric plantar flexor peak torque is required to complete a task, lack of torque as a consequence of decreased muscle strength, results in the production of passive peak torque in order to complete the task. Increased passive torque can result in the increased risk of injury to the related tissues. Therefore, it has been suggested that by increasing plantar flexor muscle strength an increase in plantar pressure may lead to an increased risk of ulceration15.
In contrast, researches have suggested that dorsiflexion range of motion exercises may decrease high plantar pressures16. Berham and Tinder (2007) performed a randomized controlled study with 21 diabetic patients and after one month of range of motion therapy, that demonstrated an average decrease stage of 4.2% in peak planter pressures for each gait cycle stage. The statistically significant decrease in peak plantar pressures in the intervention occurred during the early (p=0.049) stages of the gait cycle. Additionally, the investigators suggested a trend in the treatment group toward a decrease in joint stiffness although it was not statistically significant17.
Our study agree with Fulk et al. (2010), who stated that, gait deficits such as decreased speed, stride length, ankle range of motion and postural instability seen in the diabetic peripheral neuropathy population are associated with fall risks18. Patients with diabetic peripheral neuropathy have decreased proprioceptive input that normally plays a role in adjusting irregularities in movements and maintaining balance. To compensate for the sensory loss, subjects with diabetic peripheral neuropathy require increased cognitive control while walking and decrease their walking speeds to improve stability19.
Also, our study is in accordance with the work of Franklin and colleagues (2009), whom stated that, the reduced of walking speed was attributed to diminished proprioception, ankle mobility and plantar flexor strength in patients with diabetic peripheral neuropathy20. Similarity, Mueller and colleagues (2004) attributed the differences in gait to decreased ankle strength and mobility in persons with diabetic peripheral neuropathy and s history of ulcers6. Pirart (2009) noted that inactivity of patients recovering from a neuropathic ulcer may contribute to the weakness in the ankle rather than complications associated with diabetic peripheral neuropathy1.
[Disclosure: Authors report no conflict of interest]
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