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Achilles tendinopathy: A prospective study on the effect of active rehabilitation and steroid inject

Discussion in 'Biomechanics, Sports and Foot orthoses' started by NewsBot, Nov 5, 2014.

  1. Mart

    Mart Well-Known Member

    That's an interesting idea. I would like to explore it further if you would like to. What do you think the mechanism for radicular retrocalcaneal pain looks like?
     
  2. gingerphysio

    gingerphysio Member

    Irritated nerves give rise to nociception. The brain eventually decides to provide levels of pain appropriate for that feature, depending on a raft of variables. Safety, locus of irritation, state of health , local and systemic metabolic activity, etc etc.. The very same mechanism then that gives rise to pain from local sources, applies to referred sources. Thus the pain and other effects, are the same. The experience of ( subjective) will also be identical.
    Attempts at differential diagnosis with, for instance, over pressure, stretch, palpation, injection, will also fail for the same reason. Every pain event is a nerve event.
    There are some features however, of a referred event that may be indicators.
    A high state of variability of the pain, of location, of timing, of severity, is common for referred pain, where the proximal spinal cause will also undergo states of variable tone.
     
  3. Mart

    Mart Well-Known Member

    Agreed except that it would seem highly improbable that the majority of people presenting with isolated retrocalcaneal pain would have L4-S3 injury which did not cause some other signs or symptoms. I have never seen that in hundreds of cases. If I see someone with suspicion for radicular symptoms they present quite differently than someone with sonographically visible tendocalcaneus tendonopathy. That is what bothers me most about your initial posting. Cheers Martin
     
  4. gingerphysio

    gingerphysio Member

    Every inflammatory event requires neurological support, distal inflammatory events are mediated by the same nerves as may be irritated by proximal spinal protective behaviour.
    You say L4-S3 injury, I say L5 protective behaviour, big difference. One is a pathological entity, related to either trauma or disease break down, the other is a reversible condition brought about as an instinctive muscular control feature of a healthy spine. Both can and often do cause referred events, the latter is much more common.
    Sonographic evidence of localised changes to tendons and surrounding soft tissues are not evidence of a stand alone local only condition, may be present without pain and are commonly caused by neurogenic means.
     
  5. Mart

    Mart Well-Known Member

    Thanks I think I understand your reasoning.

    Sonography can unequivocally demonstrate abnormal collagen structure in connective tissue and by virtue of Doppler imaging infer presence of neovascularisation. I agree that sonographic evidence of changes to collagen structure in tendon do not necessarily correlate with pain (but may); it is unclear why this is but plausible that tendon heals, not necessarily by reorganizing damaged tissue but by adding new elements to strengthen it. If that is true then the correlation of pain with dimensional and qualitative change may be phasic - in my experience that is what I see.

    Do you believe that tendonosis is caused by radiculogenic inflammation as opposed to mechanically mediated stress?

    Cheers Martin
     
  6. gingerphysio

    gingerphysio Member

    I don't see support( in my practical problem solving world )for tendinosis as a stand along entity. I do see situations emerge as explained above. My take is that the term is often misleading and used improperly to describe apparent tendon injury , when tendon pain may be the better and more accurate term. Tendon( and paratenon ) swelling and painful changes are commonly neurogenic in origin.
    I prefer to attempt to prove that a distal pain site is not referred, by attempts at proximal attention, than to prove ( wrong word but will do for now) it is referred. Ie I assume it will be a referred event unless the evidence for it to be so is absent.
    At no point should anyone infer from this description that I mean that ALL distal pain/swelling events are necessarily neurogenic. Certainly mechanical stressors do contribute to pain in structures. The point I attempt in all this is, that assuming a local event is not neurogenic in part or whole is often wrong and must be investigated as if it is so first, before a realistic interpretation is possible.
    It's friday afternoon and I may be rambling .

    Cheers
     
  7. Mart

    Mart Well-Known Member

    I appreciate your effort, this subject interests me. I am comfortable with talking about a tendon pain phenomena because it is unclear what causes it. I'm not sure though if I understood properly.

    are you saying that

    Tendonosis is independent of pain, the pain which I might associate with tendonosis occurs because the neurones which happen to terminate within the zone of tendonosis are coincidentally being impinged at L5?

    And / or

    If there's mechanical impingement at L5 this can set up signaling only via those specific fibres within the sciatic then tibial and/or sural nerve bundle which start and/or terminate in a specific tendocalcaneus region. This intern attracts inflammatory mediators into that zone. This inflammation then causes catabolic effect resulting in tendon degeneration?

    And/or

    If the tendocalcaneus becomes degenerated this may lead to postural changes to the spine which cause L5 impingement and this intern results in refered pain within the degenerated zone?

    Cheers Martin
     
  8. gingerphysio

    gingerphysio Member

    Morning Martin. I'm going to start with the last on your list.
    Interesting things happen at the spine when a person limps, protective behaviour (SPB)is my best attempt at wrapping those changes up into a comprehensive whole.
    Regardless of the reason for the limp in the first place, altered trunk and pelvic muscle tone, altered patterns of recruitment , fatigues associated with those changes will often set a lower back to protect itself. This then may become the source for proximal ( sciatic , for instance) irritation of large nerves, which may then result in referred events. Thus re creating , extending and possibly worsening any pain associated with the original distal injury.
    Post # rehab is a good case in point.
    An otherwise well healed # site, may remain niggly and difficult 12 months+ after full radiologicaly demonstrated healing has been achieved.
    Examination commonly reveals a tight, immobile, series of lumbar spinal joints, worse on the # side, that respond well to mobilisation. Thus returning a non protected state of mobility to that series of spinal joints, with the effect of returning similar positive effects immediately to adjacent nerves. The # area pain disappears and may only return if repeated episodes of SPB occur.
    The brain creates pathways for ease of operation, once established , the pain and feedback related pathways associated with limb #, will remain viable, long after the # heals. A proximal nerve irritant induces nociception in the same nerve associated with the body part of the original #. The brain does not need to create a new pathway when one already exists. The referred pain then appears to occur in the original site .

    Your second paragraph is a good short version of what kept me awake last night. Not me in pain , but the best quick way to describe neurophysiological cause and effect.
    I would also suggest that not every structure will have the same physiology, there fore not every structure will respond the same to similar neurogenic input.
    eg, the calf muscles will not generally erupt in a protracted disruption to it's ligentous fibres, have massive swelling events or tear itself apart under the effect of protein breakdown caused by the low back. Instead what we see is an unwillingness to relax. This may increase risk to itself under eccentric load and lead to failure and injury.
    The achilles paratenon however is a very different structure, endowed with stretch receptors, richly vascularised, tendinous rather than muscular, it's response to similar altered neural input is necessarily different.

    Tendinosis and any other local events as you know, may or may not be painful. Presuming that inflammatory changes are occurring is another common diagnostic error. Pain occurs in the brain and nowhere else, highly variable.
    Hope this helps Martin,
    Cheers
     
  9. Mart

    Mart Well-Known Member

    Thanks that was interesting stuff. I admit to some bias against what I regard as mindless chiropractic dogma and your initial post triggered that. I am ignorant of credible literature which explores your ideas and would be greatful if you could suggest a couple of papers for me to read. What you posted makes sense but I um unclear is this is empiric speculation on your part or if there is a body of evidence to support that.

    I'm skeptical but very interested in the idea

    "A proximal nerve irritant induces nociception in the same nerve associated with the body part of the original #. The brain does not need to create a new pathway when one already exists. The referred pain then appears to occur in the original site" if you can support that outside of an anecdotal claim I will be very greatful to you. Thanks for being sleepless with thought - We have that in common :) Cheers Martin
     
  10. gingerphysio

    gingerphysio Member

    I too am often torn when reading chiropractic dogma. Mostly because, even when they may be right,( it does occur) the purpose of chiropractic remains a short term only, management for life schtick, rather than realistic science based treatments to fully and permanently solve problems.
    I have given lectures where chiros are present, and had conversations after. They seem not to be able to comprehend that I would even attempt to fully solve a spinal problem, let alone achieve that aim. Their profit first mindset is comprehensive and lasting.
    I have no papers for you to read Martin.
    Cheers
     
  11. Mart

    Mart Well-Known Member

    I guess your hypothesis has not been researched or published?

    Ihave no problem accepting the idea of post traumatic nociceptor pathway sensitization, the research on preemptive pain management for surgery seems convincing. What is new to me is the notion that proximal nerve impingement can selectively trigger that pathway, clearly if that is true and as common as you believe it is important. I am trying to unravel the diagnostic conundrum from a podiatrists perspective.

    The vast majority of people I see with retrocalcaneal pain attributed to tendonosis do not have allodynia or peripheral sensitivity to pressure. In my mind that indicates that their localized ambulatory pain symptoms were unlikely attributed to CNS or peripheral sensitization.

    Would you agree with that?

    Cheers Martin


     
  12. gingerphysio

    gingerphysio Member

    The only way to positively rule out a referred event Martin , is, as my protocol describes, find and treat any relevant spinal protective activity first. Very few heel/achilles/plantar area pain problems in my care ,fail to respond with lasting resolution in this way. I realise this may be impossible for you do do effectively, so the whole idea might remain in the realms of interweb chat. Pity.
    In answer to your question about my methods having been researched, truth is , I don't know. I did spend a decade attempting to organise this, loads of net searching, years of web chats, relentless writing about my findings in places that didn't achieve much. I am , as stated, a clinician. Not a researcher, not an academic and don't wish to become one.
    The daily joys that occur for me are in the realm of effective treatment . I have no wish to abandon that in favour of the perils and anxieties of academia.
    Happy to share and discuss however.
    Cheers
     
  13. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    High Volume Image Guided Injections with or without steroid for mid-portion Achilles Tendinopathy: A Pilot Study
    (Running title: HVIGI with or without steroid in Achilles tendinopathy)

    Hatim Abdulhussein et al
    Source
     
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