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CLINICAL AND ELECTROPHYSIOLOGICAL EVALUATION OF DIABETIC
NEUROPATHY
¹Nimatov Ziyodullo,
²Begimova Sabina
³Khakimova Sokhiba Ziyadulloevna
¹'²1st-year Residents, Department of Neurology,
Samarkand State Medical University
³Head of the Department of Neurology, Samarkand State Medical University
Affiliation: Department of Neurology,
Samarkand State Medical University, Uzbekistan.
https://doi.org/10.5281/zenodo.15511317
Research Objective
: To evaluate the clinical presentations and electrophysiological
patterns of diabetic peripheral neuropathy (DPN) and investigate their correlations with disease
duration, glycemic control, and patient-reported outcomes.
Introduction
: Diabetic neuropathy is one of the most common chronic complications of
diabetes mellitus, affecting approximately 50% of diabetic patients during the course of the disease.
The most prevalent type is diabetic peripheral neuropathy, which is characterized by
symmetrical, length-dependent sensorimotor polyneuropathy.
This complication is responsible for significant morbidity, including chronic pain, sensory
deficits, motor dysfunction, and increased risk of foot ulcers and amputations. Despite its
prevalence, DPN remains underdiagnosed, especially in early stages, due to its gradual onset and
variability in symptom presentation.
Electrophysiological studies, particularly nerve conduction studies (NCS), are essential for
early detection and grading of neuropathy severity. These objective tools complement clinical
assessments and help differentiate between axonal and demyelinating pathologies. Moreover,
correlation with glycemic control (measured via HbA1c) offers insights into disease progression
and response to treatment.
Materials and Methods
: This prospective cross-sectional study was conducted at the
Neurology Department of Samarkand State Medical University over 24 months. A total of 112
patients with type 2 diabetes mellitus (T2DM) were enrolled.
Inclusion criteria
:
a.
Diagnosis of T2DM confirmed for at least 5 years
b.
Age range: 35–75 years
c.
Clinical symptoms of peripheral neuropathy
d.
Willingness to participate and sign informed consent
Exclusion criteria
:
a.
History of alcohol abuse, vitamin B12 deficiency, or uremia
b.
Coexisting neurological disorders (e.g., CIDP, radiculopathy)
c.
Amputated limbs preventing proper NCS
Assessment Tools:
1. Detailed clinical neurological examination
2. Michigan Neuropathy Screening Instrument (MNSI)
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3. Visual Analog Scale (VAS) for pain evaluation
4. HbA1c measurement
5. Nerve conduction studies using standardized protocols (motor and sensory nerves:
peroneal, tibial, median, ulnar, sural)
6. Grading neuropathy using the Dyck criteria
Results
: Of the 112 patients, 58 (51.8%) were female and 54 (48.2%) were male. The mean
age was 59.2 ± 9.1 years, and the mean duration of diabetes was 9.8 ± 4.6 years. Elevated HbA1c
levels (>8.0%) were found in 72% of the cohort.
Clinical Findings
:
a.
81% of patients had symptoms of burning, numbness, or tingling in the feet
b.
63% demonstrated decreased vibration perception (128 Hz tuning fork)
c.
42% showed reduced ankle reflexes
d.
Pain was reported as moderate to severe in 66% of cases (VAS > 5)
Electrophysiological Findings
:
a.
Sensory nerve action potentials (SNAPs) were reduced in the sural nerve in 84% of patients
b.
Motor nerve conduction velocity (MNCV) was decreased in the tibial and peroneal nerves
in 78%
c.
Mixed sensorimotor neuropathy patterns were predominant (72%)
d.
Predominantly axonal degeneration was seen in 69% of cases; 18% showed demyelinating
features
Correlation Analysis
:
a.
A strong correlation (r = -0.71, p < 0.001) between higher HbA1c levels and lower
conduction velocities
b.
Longer diabetes duration (>10 years) associated with severe NCS abnormalities (p = 0.002)
c.
Pain severity (VAS) was moderately correlated with reduced SNAPs in the sural nerve (r
= -0.54)
Conclusion
: Diabetic peripheral neuropathy is a common and debilitating complication of
long-standing diabetes. The results of this study emphasize the critical role of early clinical
screening and electrophysiological testing in identifying neuropathy, even in subclinical stages.
Clinical manifestations such as burning pain, paresthesia, and reduced vibratory sensation
are often the first indicators of nerve dysfunction. However, these symptoms alone may not capture
the extent of neural damage. Therefore, electrophysiological studies serve as a valuable diagnostic
adjunct to clinical evaluation, particularly in detecting asymptomatic neuropathy.
The predominance of axonal degeneration patterns suggests chronic metabolic insult to
peripheral nerves, primarily due to poor glycemic control. The significant correlation between
elevated HbA1c levels and slowed nerve conduction underscores the need for strict metabolic
regulation.
Patients with longer diabetes duration are more prone to advanced neuropathic changes,
highlighting the importance of routine nerve conduction screening in diabetic care protocols.
Furthermore, patient-reported outcomes such as pain severity should be integrated into clinical
decision-making for comprehensive management.
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Overall, the study supports that a combination of symptomatology, standardized clinical
scoring systems, and electrophysiological data provides a robust framework for diagnosing,
staging, and monitoring diabetic neuropathy. Proactive identification and intervention can reduce
the risk of severe complications such as foot ulcers, infections, and amputations, ultimately
improving patient quality of life and reducing healthcare burden.
Future efforts should focus on developing individualized treatment plans combining
pharmacologic and non-pharmacologic strategies, including lifestyle interventions, physical
therapy, and glycemic optimization. Such an integrated approach can effectively delay progression
and improve outcomes in patients suffering from diabetic neuropathy.
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