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Related Concept Videos

Diabetic Neuropathy01:22

Diabetic Neuropathy

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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...
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Diabetic Foot Ulcer01:31

Diabetic Foot Ulcer

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Definition A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.Pathophysiology • The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing. • Neuropathy is the most common factor. Sensory...
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Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

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The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
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Multiple Sclerosis l: Introduction01:19

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Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
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Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
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Related Experiment Video

Updated: Apr 20, 2026

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
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Motor neuropathy.

Henning Andersen1

  • 1Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.

Handbook of Clinical Neurology
|November 21, 2014
PubMed
Summary
This summary is machine-generated.

Diabetic patients with distal symmetric sensorimotor polyneuropathy (DSPN) experience significant muscle weakness and atrophy in their legs. This neuromuscular impairment accelerates over time, increasing fall and foot ulcer risks.

Keywords:
dynamometryexercisemuscle qualitymuscular atrophyweakness, motor dysfunction

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Area of Science:

  • Neurology
  • Diabetology
  • Musculoskeletal Research

Background:

  • Distal symmetric sensorimotor polyneuropathy (DSPN) in diabetes typically affects sensory and motor nerves.
  • Motor system involvement, specifically muscle weakness, is often overlooked in diabetic DSPN.
  • Diabetes itself may compromise muscle quality independent of neuropathy.

Purpose of the Study:

  • To investigate the prevalence and characteristics of muscle weakness in diabetic patients with DSPN.
  • To assess the relationship between muscle weakness, DSPN severity, and disease progression.
  • To examine the impact of diabetes and DSPN on muscle structure and quality.

Main Methods:

  • Utilized dynamometry to quantify muscle strength at the ankle and knee.
  • Employed MRI to evaluate muscle atrophy in the lower legs and feet.
  • Conducted long-term follow-up studies to track changes in muscle strength and atrophy.

Main Results:

  • Substantial muscle weakness at the ankle and knee was observed in both type 1 and type 2 diabetic patients with DSPN.
  • Muscle weakness correlated significantly with DSPN signs and severity.
  • Longitudinal studies revealed accelerated muscle strength loss and atrophy in neuropathic patients compared to controls.
  • Diabetes was associated with lower muscle quality, indicating reduced strength per muscle unit.

Conclusions:

  • Muscle weakness and atrophy are significant, often underappreciated, complications of diabetic DSPN.
  • These neuromuscular deficits contribute to impaired mobility, increased fall risk, and foot ulcer development.
  • Further research is needed to explore the efficacy of interventions like training in managing DSPN-related muscle dysfunction.