<p>Epicondylopathy is a degenerative disease of the tendon insertion at the lateral (radial) or medial (ulnar) epicondyle of the humerus, commonly referred to as “tennis elbow” or “golfer’s elbow.” It results from mechanical overuse or repetitive microtrauma, leading to angiofibroblastic hyperplasia and structural changes in the tendon. Strong Type I collagen fibers degenerate to less resistant Type III collagen fibers. Although neurogenic inflammatory responses occur, this is not a classic inflammation, making the term “-itis” misleading.</p><p>The incidence is 1–3%, typically affecting individuals aged 40–60, regardless of gender or athletic activity. Risk factors include age, smoking, obesity, repetitive movements and depressive disorders. The condition can be acute (&lt;6 months) or chronic (&gt;6 months).</p><p>Diagnosis is primarily clinical, based on history, inspection, palpation, and provocation tests, supplemented by imaging techniques such as ultrasound, X-ray, or MRI to differentiate and assess structural damage. Common comorbidities like instability, osteoarthritis, or nerve compression syndromes must be ruled out.</p><p>Treatment is usually conservative, combining load adjustment, physiotherapy, pain management, and, in some cases, injections (e.g. PRP). Surgery is rarely indicated in therapy-resistant cases. Despite a potentially prolonged healing process (6 months to 2 years), the prognosis with conservative therapy is favorable. Imaging findings do not necessarily correlate with clinical symptoms.</p>

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Konservative Therapie bei Epikondylopathie

  • Hannes Degenhardt,
  • Anja Hirschmüller

摘要

Epicondylopathy is a degenerative disease of the tendon insertion at the lateral (radial) or medial (ulnar) epicondyle of the humerus, commonly referred to as “tennis elbow” or “golfer’s elbow.” It results from mechanical overuse or repetitive microtrauma, leading to angiofibroblastic hyperplasia and structural changes in the tendon. Strong Type I collagen fibers degenerate to less resistant Type III collagen fibers. Although neurogenic inflammatory responses occur, this is not a classic inflammation, making the term “-itis” misleading.

The incidence is 1–3%, typically affecting individuals aged 40–60, regardless of gender or athletic activity. Risk factors include age, smoking, obesity, repetitive movements and depressive disorders. The condition can be acute (<6 months) or chronic (>6 months).

Diagnosis is primarily clinical, based on history, inspection, palpation, and provocation tests, supplemented by imaging techniques such as ultrasound, X-ray, or MRI to differentiate and assess structural damage. Common comorbidities like instability, osteoarthritis, or nerve compression syndromes must be ruled out.

Treatment is usually conservative, combining load adjustment, physiotherapy, pain management, and, in some cases, injections (e.g. PRP). Surgery is rarely indicated in therapy-resistant cases. Despite a potentially prolonged healing process (6 months to 2 years), the prognosis with conservative therapy is favorable. Imaging findings do not necessarily correlate with clinical symptoms.