Diabetes mellitus (DM) is a widespread metabolic disorder characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. One of the most debilitating complications associated with long-standing diabetes is diabetic neuropathy, which affects nearly 50% of diabetic individuals during their lifetime (1). Peripheral neuropathy, particularly distal symmetric polyneuropathy, is the most common type and primarily manifests as a progressive loss of nerve function, impacting both sensory and motor fibers (2).

The underlying mechanisms of diabetic neuropathy are multifactorial, involving metabolic disturbances such as increased polyol pathway flux, oxidative stress, advanced glycation end-products (AGEs) formation, and microvascular insufficiency (3,4). These processes lead to structural and functional changes in peripheral nerves, resulting in reduced nerve conduction velocities (NCVs), which serve as reliable markers of nerve dysfunction (5).

Numerous studies have highlighted that the duration of diabetes is a critical risk factor for the development and progression of neuropathy (6,7). Prolonged exposure to hyperglycemia induces cumulative neural damage, which is detectable through nerve conduction studies (NCS) even in asymptomatic patients (8). NCVs tend to decline progressively with increasing disease duration, suggesting that early diagnosis and glycemic control may play a vital role in preserving nerve function (9).

Despite the known association between diabetes duration and nerve dysfunction, there remains a need for comparative data evaluating the specific impact on both sensory and motor components of peripheral nerves. This study was designed to assess and compare the changes in nerve conduction velocities among patients with short-term versus long-term diabetes to better understand the temporal progression of diabetic neuropathy.

A total of 60 participants with type 2 diabetes mellitus were enrolled and categorized into two groups based on the duration of their disease. Group A included 30 individuals with diabetes duration of less than 5 years, while Group B consisted of 30 individuals with diabetes duration exceeding 10 years.

Inclusion Criteria:

Participants aged between 40 and 65 years with a confirmed diagnosis of type 2 diabetes mellitus were included. All subjects had stable glycemic control, and none were on insulin therapy.

Exclusion Criteria:

Individuals with a history of alcohol abuse, smoking, thyroid dysfunction, vitamin B12 deficiency, renal impairment, or other known causes of neuropathy were excluded. Additionally, those with prior neurologic or musculoskeletal disorders affecting nerve function were not considered.

Nerve Conduction Study (NCS):

Nerve conduction testing was performed using a standard EMG-NCV machine under controlled room temperature (22–25°C). The median and ulnar nerves were assessed for motor conduction in the upper limbs, while the peroneal nerve was evaluated in the lower limb. Sensory conduction studies were conducted for the sural and median nerves. Surface electrodes were used following standard anatomical landmarks for stimulation and recording.

Motor nerve conduction velocity (MNCV) was measured by stimulating the nerve at two points and recording the muscle response, while sensory nerve conduction velocity (SNCV) was calculated based on the latency and distance between the stimulating and recording electrodes. All procedures followed the recommendations of the American Association of Neuromuscular & Electrodiagnostic Medicine.

Statistical Analysis:

Data were recorded and analyzed using SPSS version 25.0. Continuous variables were expressed as mean ± standard deviation. The comparison between the two groups was performed using the independent samples t-test. A p-value less than 0.05 was considered statistically significant.

A total of 60 participants were evaluated, with 30 in Group A (diabetes duration <5 years) and 30 in Group B (diabetes duration >10 years). The mean age of subjects in Group A was 51.2 ± 5.6 years, while that in Group B was 56.8 ± 6.2 years. The male-to-female ratio was similar in both groups.

Motor and sensory nerve conduction velocities were measured for the median, ulnar, peroneal, and sural nerves. A consistent decline in conduction velocities was observed in Group B compared to Group A across all nerves tested.

As shown in Table 1, the motor nerve conduction velocity (MNCV) of the median nerve in Group A was 52.3 ± 3.1 m/s, while in Group B it was reduced to 43.6 ± 4.7 m/s. Similarly, the ulnar nerve MNCV showed a decline from 53.7 ± 2.8 m/s in Group A to 45.1 ± 3.9 m/s in Group B. In the lower limbs, the peroneal nerve MNCV decreased from 47.9 ± 3.5 m/s in Group A to 39.2 ± 4.1 m/s in Group B.

Table 2 presents the sensory nerve conduction velocity (SNCV) values. The median nerve SNCV was 49.1 ± 3.2 m/s in Group A and 40.4 ± 4.3 m/s in Group B. The sural nerve SNCV declined from 47.8 ± 2.4 m/s in Group A to 38.9 ± 3.2 m/s in Group B. All differences between the groups were statistically significant (p < 0.01).

These findings indicate a marked reduction in both motor and sensory conduction velocities in individuals with longer duration of diabetes, suggesting progressive neuropathic changes.

Table 1: Comparison of Motor Nerve Conduction Velocities (MNCV) Between Groups

Table 2: Comparison of Sensory Nerve Conduction Velocities (SNCV) Between Groups

This study demonstrates a significant decline in both sensory and motor nerve conduction velocities (NCVs) in patients with longer durations of type 2 diabetes mellitus. The findings are consistent with previous literature indicating that the chronicity of hyperglycemia plays a crucial role in the development and progression of diabetic peripheral neuropathy (1,2).

Peripheral nerve dysfunction in diabetes is believed to arise from a combination of metabolic and vascular mechanisms. Chronic hyperglycemia initiates a cascade of pathophysiological changes, including the activation of the polyol pathway, accumulation of advanced glycation end-products (AGEs), and oxidative stress, which collectively damage the structure and function of peripheral nerves (3–5). These mechanisms contribute to demyelination, axonal degeneration, and microvascular changes, all of which are reflected in decreased NCVs (6,7).

The present study revealed that the median and ulnar nerves in the upper limbs and the peroneal and sural nerves in the lower limbs showed marked reductions in conduction velocities in patients with more than 10 years of diabetes, compared to those with less than 5 years. Similar results were reported by Dyck et al., who found that diabetic neuropathy progresses with time, particularly affecting distal nerve segments first due to their length-dependent vulnerability (8).

Motor nerves, especially in the lower extremities, are known to be affected earlier and more severely due to higher metabolic demands and longer axonal lengths (9,10). The significantly reduced motor NCVs in the peroneal nerve in our study support this hypothesis. Comparable findings have been documented in other cross-sectional studies assessing diabetic neuropathy across various populations (11,12).

Furthermore, sensory nerves, such as the sural and median nerves, also showed substantial slowing of conduction velocities. This is consistent with the fact that sensory fibers, being smaller and less myelinated, are more susceptible to ischemic and metabolic insults (13). Previous electrophysiological studies have emphasized that sensory NCV reduction often precedes clinical symptoms, highlighting the value of NCS in early detection (14,15).

In summary, this study reinforces the evidence that duration of diabetes mellitus is a key factor influencing the progression of peripheral neuropathy, as reflected in nerve conduction abnormalities. Early detection through routine nerve conduction studies and stringent glycemic control remains essential in mitigating long-term neurological complications in diabetic individuals.

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