pathology: insertional tendinopathy

yogabook / pathologie / insertional tendinopathy

insertional tendinopathy (enthesiopathy, myotendinosis, tendoperiostosis, tendoperiostitis. )

Definition of

Painful conditions at the transition of the tendons to their insertion (origin/attachment), these arise almost exclusively due to incorrect loading/overloading, in practice usually as overuse syndrome. Other causes are local ischaemia, extreme hypothermia of the tissue, hypertonicity of the related muscle, local trauma, locally reduced vascularisation and some predisposing diseases, especially metabolic and endocrinological diseases, but also IBD, and predisposing medications.
The following disorders are known:

  1. Achillodynia: Triceps surae
  2. Epicondylitis humeri radialis (golfer’s elbow): Extensor carpi radialis longus, extensor carpi radialis brevis, extensor carpi ulnaris, extensor carpi digitorum
  3. Epicondylitis humeri ulnaris (tennis elbow): Flexor carpi ulnaris, flexor carpi radialis, pronator teres, flexor digitorum superficialis, palmaris longus
  4. Gracilis syndrome proximal (attributed to the footballer’s groin) or distal (a possible form of pes anserinus syndrome)
  5. Patellar tendinopathy: quadriceps
  6. ITBS (tractus iliotibialis syndrome)
  7. Supraspinatus tendon syndrome
  8. Styloiditis radii
  9. Ulnar styloiditis
  10. Biceps brachii origin irritation of the long head with subluxated humeral head (a tendinopathy rather than an insertional tendinopathy)
  11. Subscapularis: powerful, sudden endorotation movements, e.g. when throwing, can trigger
  12. Hip adductors: Misalignments of the hip joint change the lever arms and can therefore lead to overloading. Shortening is also often the cause
  13. PHT (Proximal Hamstring Tendinopathy: Ischiocrural group, various sporting and non-sporting triggers)
  14. Rectus femoris: especially in the case of shortening, especially when moving from prolonged hip flexion to extension
  15. Iliopsoas: especially with shortening, especially when moving from prolonged hip flexion to extension
  16. Pes anserinus syndrome: Gracilis or internal hamstrings
  17. Posterior tibialis: medial-plantar stabilizer of the longitudinal arch of the foot. Supination trauma can render its distal joint partners dysfunctional
  18. Coracobrachialis insertional tendinopathy
  19. Bench Presser’s Shoulder

In principle, tendinopathies change behavior and can lead to tendinopathies of the antagonists through avoidance behavior. The triggering factor does not necessarily have to be the amount of load, it can also be the mode of loading, especially if it is of a swinging nature and frequently puts undue strain on the tendon elasticity. The most important pillars of therapy are avoiding the triggering strain as strictly as possible or modifying the strain and training the affected muscles appropriately. In the exercise therapy of various insertional tendopathies, the long-promoted isolated eccentric training has been shown to be superior to isolated concentric training, however, it has not been shown that omitting concentric exercise has an advantage. A study comparing cortisone therapy against eccentric squat training and heavy slow resistance training only showed good results in the long term for those actively training. The HSR team performed better. In a study on mid-level achillodynia, eccentric training and HSR showed good results, but subjective satisfaction was greater in the HSR group.

Insertional tendopathy (enthesiopathy or enthesopathy) must not be confused with primary inflammatory enthesitis, which is a concomitant disease in spondyloarthritis, ankylosing spondylitis (Bechterew’s desease), reactive arthritis (Reiter’s disease), psoriatic arthritis, Whipple’s disease, juvenile oligoarthritis type 1 or IBD.

Cause

  1. Overuse
  2. traumatic overload
  3. Taking fluoroquinolones (special antibiotics, levofloxacin is considered to be particularly harmful)

Predisposing

– Musculoskeletal system

  1. Muscular imbalances, especially hypertonus and restricted flexibility of the antagonists, but also hypertonus and shortening of the affected muscles themselves
  2. untrained condition
  3. Deviations from the norm in physique
  4. Misalignment of joints(subluxation)
  5. Joint dysfunctions such as SI joint blockage
  6. Misalignment of joints
  7. Axial misalignments
  8. Joint instabilities
  9. Pelvic obliquity
  10. in lower extremity: leg length discrepancies

– Behavior

  1. Overuse
  2. Exertion that is not adapted to the level of training, especially for those who are untrained or under-trained.
  3. physical conditions: Cold, wet, hard floors during training
  4. Technical defects
  5. Chronic overloading in one joint due to hypomobility in a neighboring joint
  6. Permanent or frequent pressure loading, for example of the supraspinatus tendonin the case of a cranialized humeral headdue to imbalances
  7. one-sided loads
  8. Prolonged static loads lead to supply deficiencies and degeneration
  9. Too few regeneration phases

– Dispositional diseases

  1. Ankylosing spondylitis, RA

Diagnosis

  1. Pain provocation tests to confirm and differentiate from bursitis, joint disorders, bottleneck syndromes and others
  2. Oedematous deposits with fatty degeneration.
  3. Fibrous roughening, possibly with partial ruptures
  4. Exostoses, bone spurs

Symptoms

  1. Pressure soreness
  2. slight pain on movement
  3. marked to bright pain on exertion, especially with eccentric contraction, usually also marked pain on stretching
  4. Painful restriction of movement
  5. Initially painful inhibition of muscle function, then hardening of the muscle, later atrophy and weakening due to rest
  6. General symptoms possible: sleep disorder, depression

Complications

  1. Contralateral overuse syndrome due to pain avoidance
  2. Torn tendon
  3. Limescale deposits
  4. Bone spur formation

Therapy

  1. Break from sport, temporary immobilization if necessary
  2. Heat/cold applications
  3. Electrotherapy
  4. Shock wave therapy
  5. PT
  6. Supports support proprioception
  7. Analgesics, anti-inflammatory drugs, local anesthetic infiltrations
  8. Surgery: severing of the tendon insertion
  9. Adapted strength training: angepasstes Kräftigungstraining: HSR (heavy slow repetitions); In rehabilitative training (in contrast to sport and everyday life), up to NRS-3 or even NRS-5 equivalent pain may be felt if the pain subsides within 24 hours and does not increase over the exercise sessions

NHK

  1. Acupuncture
  2. Neural therapy
  3. Osteopathy
  4. Manual therapy
  5. Phytotherapy
  6. Schüssler salts
  7. Taping

Asana practice and movement therapy

As insertional tendinopathies are generally neither congenital nor traumatically acquired and are usually not inflammatory either, but are primarily caused by overuse (note: overuse is always individual), the most important pillar of therapy is to protect the degenerated tendon tissue from further overuse and at the same time to strengthen it through targeted, moderate loading. Probably without exception, it must be recommended to conscientiously avoid triggering pain, both in everyday life and in sports. There is evidence that pain sensations of up to NRS 3 out of 10 are permissible in rehabilitative training under the conditions that a) the pain is reversible within 24 hours and b) the pain does not increase over the individual training sessions on subsequent days (irrespective of rest days). Of course, it must also be checked whether there are any predisposing factors (see above), which must then be eliminated as far as possible.

The pain-inducing movements must be identified and may only be undertaken up to the point where the pain is triggered, depending on the load and sarcomere length. A functional correlation between the load and the sarcomere length is often found in such a way that a higher load triggers pain even with a shorter sarcomere length than a lower load. Using the example of the PHT, this means that hip flexion movements can only be performed up to a certain flexion angle. If the torque in the hip joint and thus the tendon force to be applied by the hamstrings is increased, for example by holding dumbbells in the hands, pain is triggered even at smaller flexion angles. A promising rehabilitative approach is usually to strengthen the tendon tissue through a large number of repetitions in a still tolerable working range and to slowly increase the load up to just tolerable loads, accepting that the working range becomes smaller and smaller as the load increases.

In addition, rehabilitative training can also extend into the moderately painful range under the above-mentioned conditions, as strengthening the structures is the most important therapeutic approach alongside protection from further irritation. The tendon tissue tends to be significantly strengthened when there is sufficient tendon strength and hardly ever with many repetitions with low loads. Prolonged exposure of the affected tendons to pressure should also be avoided. In the case of PHT, for example, this means not sitting for too long every day and preferably only intermittently, whereby the pelvis must not tilt backwards as this would compress the tendons more. The use of a seat cushion that slopes forwards is a good aid here.

In principle, an insertion tendinopathy would heal in a similar time even without rehabilitative training through pure rest, but the recurrence rate is then much higher.


In principle, an insertion tendinopathy would heal in a similar time even without rehabilitative training through pure rest, but the recurrence rate is then much higher. Depending on the severity, the disorder may well take six months to heal. It is important to use the time until healing with rehabilitative and strengthening training so that the original demands and loads do not lead to the same disorder again immediately after healing. Otherwise, the result would be an indefinite reduction in resilience, the extent of which cannot be precisely defined. In cases such as golfer’s elbow, tennis elbow and pes anserinus syndrome, the insertion of at least one, possibly several (not necessarily functionally identical) muscles is affected. This or these muscles must be identified by means of functional testing (pain provocation test by stretching and loading) so that, on the one hand, the load can be specifically reduced just before the pain is triggered and, on the other hand, the muscle-tendon system can be specifically rehabilitatively trained. It is largely irrelevant whether it is a tendon of origin, as in the case of golfer’s elbow, tennis elbow and PHT, or a tendon of insertion, as in pes anserinus syndrome. Rehabilitative training should restore full resilience. Ideally, the affected person will eventually realize that they no longer need to spare the previously affected area in everyday activities. As there is a fundamental tendency for recurrence, a certain degree of preservation of the stretching ability of the muscles and strengthening of the muscles and their tendons is indicated in the long term.

In some cases, it may be important to also strengthen the synergists of the muscles so that the agonists are less challenged in corresponding situations, in other words, a weakness of the muscles themselves in the sense of reduced resilience, but also a weakness of the synergists predisposes to insertional tendopathy. An example of this is the gluteus maximus as synergist of the PHT affected by the hamstrings.