Related Experiment Video
Updated: May 23, 2026
06:40
Screening of Axonal Degeneration in Carpal Tunnel Syndrome Using Ultrasonography and Nerve Conduction Studies
Published on: January 11, 2019
Time-course changes in nerve conduction velocity (NCV) in type 2 diabetes.
Jiro Morimoto1, Yutaka Suzuki, Ai Tada
1Saitama Social Insurance Hospital the Department of Internal Medicine, Saitama, Japan. jiromt2@kxb.biglobe.ne.jp
Journal of Diabetes and Its Complications
|April 17, 2012
Summary
Nerve conduction velocity (NCV) reduction in type 2 diabetes patients strongly correlates with retinopathy progression. While blood glucose control may slow NCV decline, it cannot completely prevent diabetic sensorimotor polyneuropathy (DSPN) progression.
Area of Science:
- Diabetology
- Neurology
- Ophthalmology
Background:
- Diabetic sensorimotor polyneuropathy (DSPN) is a common complication of type 2 diabetes.
- Nerve conduction velocity (NCV) is a key indicator of peripheral nerve function.
- Understanding the temporal relationship between NCV, retinopathy, and glycemic control is crucial for managing DSPN.
Purpose of the Study:
- To investigate the 10-year time-course relationship between NCV and retinopathy stage in type 2 diabetes patients.
- To clarify the association between NCV and glycated hemoglobin (HbA1c) levels over time.
- To discuss the natural progression of DSPN based on these findings.
Main Methods:
- Annual NCV measurements (MCV and SCV) over 10 years in 474 type 2 diabetes patients.
- Grouping patients based on retinopathy stage and HbA1c levels.
- Analyzing time-course relationships between NCV, retinopathy, and HbA1c.
Main Results:
- NCV reduction strongly correlated with retinopathy progression; NCV decreased as retinopathy worsened.
- Continuous NCV reduction was observed with advancing retinopathy stages.
- While HbA1c control moderately reduced NCV decline, it did not prevent morbid reduction.
Conclusions:
- NCV reduction is closely linked to retinopathy progression, preceding its clinical manifestation by over a decade.
- Blood glucose control can attenuate NCV reduction but not prevent it entirely.
- DSPN is a progressive complication that develops early in diabetes and worsens alongside retinopathy, posing challenges for complete prevention.
Related Concept Videos
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
01:24Type II Diabetes II: Pathophysiology
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
01:22Diabetic Neuropathy
DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
01:19Type I Diabetes III: Clinical Manifestations
Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
01:25Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis
Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...
01:26Type II Diabetes I: Introduction
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...