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Diabetic Neuropathy

Diabetic 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...

Diabetic Nephropathy

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Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...

Action Potentials

Action Potentials

Action Potential

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...

Action Potential

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...

Action Potential: Phases of Stimulation

Action Potential: Phases of Stimulation

The action potential is a complex electrical event that occurs in excitable cells, such as neurons and muscle cells. It consists of several distinct phases, each with specific characteristics.
Resting Phase:
In this phase, the cell's membrane is at its resting potential, typically around -70 millivolts (mV) for neurons. Inside the cell, there is a higher concentration of potassium ions (K+) and a lower concentration of sodium ions (Na+). Voltage-gated sodium channels are closed, and...

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Recording Network Activity in Spinal Nociceptive Circuits Using Microelectrode Arrays

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Activity-dependent excitability changes suggest Na+/K+ pump dysfunction in diabetic neuropathy.

Arun V Krishnan¹, Cindy S-Y Lin, Matthew C Kiernan

¹Prince of Wales Medical Research Institute, Prince of Wales Clinical School, University of New South Wales, Randwick, Sydney, NSW, Australia.

Brain : a Journal of Neurology

|March 26, 2008

Summary

Na(+)/K(+) pump dysfunction contributes to diabetic neuropathy (DN) by impairing nerve excitability and axonal function. This dysfunction may lead to conduction failure, causing weakness and fatigue in DN patients.

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Area of Science:

Neuroscience
Diabetology
Ion Channel Physiology

Background:

Diabetic neuropathy (DN) is a common complication of diabetes mellitus.
The underlying mechanisms of DN, particularly the role of ion channel dysfunction, require further elucidation.

Purpose of the Study:

To investigate the role of sodium-potassium (Na(+)/K(+)) pump dysfunction in the development of diabetic neuropathy.
To assess nerve excitability changes in patients with and without diabetic neuropathy.

Main Methods:

Nerve excitability techniques were employed in 15 patients with established DN and 10 diabetic patients without neuropathy (DWN).
Excitability parameters were measured at baseline and after 1-minute maximal voluntary contraction (MVC) of the abductor pollicis brevis muscle.

Main Results:

DN patients exhibited reduced compound muscle action potential (CMAP) amplitude, decreased strength-duration time constant, and prolonged refractoriness, indicating reduced nodal Na(+) conductances.
Following MVC, DN patients showed a smaller increase in threshold and slower recovery compared to controls, suggesting impaired Na(+)/K(+) pump function.
Diabetic patients without neuropathy (DWN) did not show significant excitability alterations compared to controls.

Conclusions:

Na(+)/K(+) pump dysfunction, alongside reduced nodal Na(+) currents, likely contributes to conduction failure in diabetic neuropathy.
These alterations in nerve excitability are associated with clinical symptoms of weakness and fatigue in DN patients.