Tennis Elbow

[alophysio]

Hi Rana Sh,

I am sorry but electrotherapy and modalities etc are just a band-aid - why not fix the problem rather than just the relieve the symptoms temporarily.

We have already discussed that "epicondylitis" is not the proper term because there is no inflammation present - this is proven with microdialysis of the extensor tendons.

If you want a protocol based on research, look in this post - i have posted it up higher.

Your patient's will not think "wow" when you relieve their pain for up to 1 hour. They will think you are wonderful if you actually fix their problem.

I am just studying "patient satisfaction" at the moment and there are 3 factors that are incorporated into the care of a patient:
1. Information - they want to know what is wrong
2. Caring - they want to know you care about what is wrong
3. Effectiveness - they want your treatment to work - you don't need a degree to put on a hot pack or ice or even put on TENS etc. Anyone can look up the book and put a machine on. Medical reps do it all the time. What you have a degree in is "using your brain".

Sorry about sounding like a rant! I just get frustrated when people can't see the big picture...

[rana_sh]

hi..about concidering tennise elbow an inflamatory disease, lots of books look at it as an inflamatory, one of this book, is theraputic exersice for carolyn kisner. there is a whole stage of inflamation mintained from 7 to 14 days, depent on the case it self, and there is signs of inflamation and tenderness. about the electro therapy, and as one of the thing i well know, that one of our aims as a physiotherapist it to redused the pain cased by any disease.. by the way in my post i didn't mintion any electrical modalities. i mintioned ultra sound and modulity used to decrease spasm and will known to breake down the adhesion. as i know the second stage of the course of tennise elbow is the fibroplasia, when new collagen formed, and as i know the collagen fibers formed in this stage are badly orianted, and if the case is a chronic case the bad oriantation of the colagen may be progress and adhesion or a bad spasm developed, so we need modalites to breake down the adhesions and re-organized this fibers, these modalites help.. i work out with many cases of tennise and golfer's elbow, and these modalites give me the result i want.. i do respect my paitent, and i'm saying things based on books i read.. Thanks alot

[alophysio]

Hi rana sh,

I meant no disprespect...

Textbooks are a source of good information - i have recommended many of them.

However, in terms of evidence based medicine, they tend to represent Level 4 evidence (opinion of respected clinicians) unless they present evidence from the body of published research.

Alfredson et al (2000) in the journal acta orthopaedica scandinavia 71(5):475-9 reports that microdialysis of the Ext carpi radialis brevis in 4 tennis elbow patients compared to 4 controls showed high levels of glutamate but no protaglandin E2. In other words, glutamate (a neurotransmitter) was probably mediating the pain and there was not any inflammation.

Here is the abstract for those of you (like me) who can't be bothered to look up references!

We used the microdialysis technique to study concentrations of substances in the extensor carpi radialis brevis (ECRB) tendon in patients with tennis elbow. In 4 patients (mean age 41 years, 3 men) with a long duration of localized pain at the ECRB muscle origin, and in 4 controls (mean age 36 years, 2 men) with no history of elbow pain, a standard microdialysis catheter was inserted into the ECRB tendon under local anesthesia. The local concentrations of the neurotransmitter glutamate and prostaglandin E2 (PGE2) were recorded under resting conditions. Samplings were done every 15 minutes during a 2-hour period. We found higher mean concentrations of glutamate in ECRB tendons from patients with tennis elbow than in tendons from controls (215 vs. 69 micromoL/L, p < 0.001). There were no significant differences in the mean concentrations of PGE2 (74 vs. 86 pg/mL). In conclusion, in situ microdialysis can be used to study certain metabolic events in the ECRB tendon of the elbow. Our findings indicate involvement of the excitatory neurotransmitter glutamate, but no biochemical signs of inflammation (normal PGE2 levels) in ECRB tendons from patients with tennis elbow.

Now he has done the same thing in people with Achilles tendon problems. It is a fairly well known and accepted fact nowadays that Achilles tendinopathy is not an inflammatory problem after the first couple of weeks and there is even some debate as to whether it is present at all!

As for U/S, i consider that electrotherapy but i take your point. The studies on the effectiveness of electrotherapy are equivocal (they go both ways) but one thing to remember from our clinical experience is that what we see as worthwhile and working may not be working for the reasons we think.

For example, asprin is the classic example. The ancients used to think that because inflammation is "hot", they put something cold like willowbark into the system by chewing on it to counter-act the effects of the "heat" of inflammation. Hippocrates mentions it in his writings hundreds of years before Christ but it had been known for thousands of years before that.

But it was only since the 1800s when bayer was able to isolsate the salicin compund that we have asprin in it's form today and we know why it works - it is not because it is "cool".

What i am trying to say is that using ice is great for inflammation. When the cardinal signs of inflammation are present (pain, redness, loss of function, swelling, heat) then you have to treat it as "inflammation".

Pain in itself is not actually a "sign" but a "symptom" so having pain alone is not an indication of inflammation. We also know that pain can be present where there is no inflammation.

Loss of function is often also present wherever pain is present so these 2 on their own aren't good enough for me to be called "inflammation".

I need to see the redness, feel the heat and swelling.

Also, how long does it take for your treatments to "cure" their pain to less than 50% for more than an hour or two??

With the stated procedure above, you can achieve results using manual therapy within minutes that last for more than an hour or two. This may take a little while depending on their chronicity but you can see significant drops in pain and increases in strength, function and satisfaction within one week.

If your treatments take longer than 6 weeks to get better, then could it not just be that natural recovery has run its course?

About shortwave - i consider this electrotherapy as well - i think it is because it requires electricity to make it work!!! (my mistake if this is wrong!).

Is muscle spasm the main problem in epicondylalgia? Because if it is, surely massaging and frictions and releases would be all that is required to make this problem better. Anyone can massage their own arm. Yet we can see that this is not a solution. It cannot simply be sorting out the muscle spasm that is the solution.

I am interested to hear more of what you believe. Obviously i cannot know who you are or what you believe in only a few short posts!

[Dugal]

I'm not gonna jump on a high horse.

I'd check out the Cx spine if I were you.

Read Bill's masterclass - it's illuminating

[alophysio]

You are right, i am sorry.

It is, of course, only an opinion (what i believe that is)

[asha]

Short Wave Diathermy for Tennis Elbow? !!!!! Its unheard of. Not done.
asha

[ginger]

"tennis elbow" is not an elbow problem at all , which explains why so many have trouble with this. "Lateral epicondyliitis" used to be the popular name for this, till it was discovered that no inflammatory conditions were present at the condyle. This condition is , in most cases , entirely referred from C567. Mobilsisation at those levels , as well as similar attention at adjacent levels of the vertebral spine, will entirely eliminate this problem, without attention to the arm at all , provided therapists use Continuous Mobilisation ( CM ) and resolve hypertonicity around these facet joints. By doing so the inflammaory event that does exixt , at the joint and nerve root , will also resolve , and remove the irritation giving rise to elbow symptoms. This approach has been working well for me and my many students , for many years.

[Dugal]

This is not true.

Lateral epicondylALGI shows distinct tissue degradation of the extensor muscles, particularly ECRB. Look for papers by Alfredson et al.

I agree that LE isn't just about the elbow, but I don't think it is all about the Cx. I think that chronic LE is a pain state with the concurrent tissue degradation. Your Cx glides, in my opinion, provide pain relief for patients with LE to exercise in pain free manner, similar the the lateral glide MWM presented by Mulligan and evidenced by Vicenzino et al.

[ginger]

Dugal , that would sound plausible , along with the other highly credentialled arguments alluding to protein and cartilage breakdown, presence of chemical irritants etc etc , what I'm saying is however that in the period during which I have managed so called LE, ( more than twenty years ) since I stopped treating the elbow and became alert to the neuralgic events , my success rate with this otherwise perplexing issue has risen to near 100 percent . All without touching the elbow at all. One to three treatments, all to the relevant facet behaviour, some to dural length if indicated, but esssentially no exercise at all . Results are immediate, at the time of treatment, prove to be very long term ( years ) and able to be learned by anyone with the willingness to think beyond pathology and become alert to neurology and its relationship to hypomobile facet joints.

[alophysio]

Hi Ginger,

Perhaps in your clinical experience you have come across patients who have been incorrectly labelled "LE". I too believe in treating the C/S, mobilisation of the lower C/S, the nerves and fascia. All of that is part of the usual assessment of LE (it is posted around here somewhere...)

However, there is no doubt that there are patients who really have a mechanical problem at the elbow. A simple way to find out is to treat the C/S only and find that their pain and dysfunction has not changed. Also, it would seem that treating the C/S only is not revolutionary - if it really worked that well for LE (nearly 100%), then surely it would have been reported many times over and researched thoroughly.

I do believe however that many practitioners focus too much on the elbow and not on the whole patient.

What is your particular background? What treatment styles do you use? e.g. Maitland, Mulligan, Nordic, etc

[ginger]

You are quite right of course , it is important to exclude from the group I alluded to, those whose elbow pain can be attributed to trauma. Though I do not exclude those whose "trauma" is listed or described as "overuse ", A notion I find most unsatisfactory in the aetiological considerations of this and any other MSK condition .
There is a difference in my aproach , I use a method I call Continuous Mobilisation to deal with the protective responses at the spine and restore normal facet mobility. The method has been developed over many years , and now occupies most of my clinical time.
CM was developed out a frustration with the somewhat mechanical and formula driven types of Mobs , such as Maitland. This approach can be read about in detail on the Rehabedge site under Manual therapies.
For the group that has no major trauma ( but may include "overuse', including those who actually play sport ) , my success rate does indeed approach 100 percent.
I am keen to pursue the kind of research that you have mentioned , however as a private practitioner, the resources needed and time required have always stopped me. This does not mean I have not been out there putting my method on the line as it were. This forum is one of a number that I contribute to , learn from and am otherwise encouraged by .I also lecture and teach whenever I can in Victoria.
If you are interested I'm happy to share any details you want to know about.


Thanks for your interest.

[Physio Bed]

Hi guys,

The other thing to think about is PIN (posterior interosseous nerve) entrapment as a diagnosis. It presents with very similar objective signs as would LE and often would exist concurrently. This responds well to radial nerve mobilisations and may go some way to explaining your success too Ginger...!!

[ginger]

The position I have found to be the most effective , in MSK treatment, is to assume referred events are taking place till proven otherwise, by thorough attention to the relevant facet joints with CM.
It is rare to find a peripheral joint pain problem not caused by direct trauma , that does not have a significant component of cause , by neuralgic means. certainly in cases where trauma has been a feature , this remains true, though there are cases obviously where local pathology plays a role. The point I make as I apply myself, is to remove that which can be easily removed first ( referred pain and other altered behaviours and sensations ) , such that effective testing may not then be blurred by false neuralgic positives. In most cases the pain and dysfunction ,certainly in LE, and numerous other peripheral joint problems , is entirely eliminated by this attention . Thus by hindsight , I have been able to show in many hundreds of cases over many years, that referred pain is , according at least to my own clinical evidence , the most common cause of MSK problems.

[Physio Bed]

"It is rare to find a peripheral joint pain problem not caused by direct trauma , that does not have a significant component of cause , by neuralgic means".....


So how do you explain OA of the hip or knee (not due to trauma) where symtoms are relieved dramatically with arthroplasties?? You also, mention that your thoughts are based a lot on your clinical experience, which is important. Do you have any recent research that would support your above statement relating to peripheral pathology being so rare??

[ginger]

It is as well to remember that diagnoses , by and large made without the benefit of the patient being a corpse and being examined by a coroner, are best guesses, based , we would hope , on best available evidence , common sense and the science of medicine. Many diagnoses offered to physiotherapists are clearly wrong , or at best , offered without the kind of tactile relationship consistant with examination protocols common to physiotherapy. It is fair to assume that in many cases where the "OA" and other pathological explanations are given for hip and knee pain , that the kind of thorough , manual therapy inclined examinations and post treatment testing routinely done by physios , are left out of the diagnostic routines of many GPs.
This is not a negative or disrespectful position to take , we all ( we would hope ) take our own brand of skillfullness to the table when we examine and assess, not someone elses.
Gps are generalists, physios who regularly work in the MSK arena , if not initially , then with practice , become akin to specialists. Particularly so when able to cross the floor as it were and discuss cases with both medical and paramedical colleagues. Who amongst the practitioners regularly seeing orthopaedic cases regularly, would not say words to the effect, It is as well that physiotherapy stands somewhere between Gps and surgeons , to filter and reduce those who without such attention , by themselves and others , would ultimately find their way , wrongly, prematurely or both , to the surgeons table .
OA certainly does occur , to joints, adding to the distress of those unfortunate to have progressed to the point of pain and disability. No doubt about it . My point , Mr Bed, is, are we keen and alert to the prospect that diagnoses like these are skewed by a lack of the very sensitivity and understanding that goes hand in hand with a willingness , indeed reson dete, to percieve pain as a companion to pathology , rather than to dysfunction.
We occupy a special position in the medical team . A position not so rigidly defined by issues of safety by exclusion , of pathological threats to life and limb. We are the group , who by our interest in function , will often see alternatives to surgery , to pills and potions , to bed rest , to the otherwise ultrconservative regimens predicted by medicines answers,. particularly to MSK problems.
This, really ,is our reason to be.
Referred pain is the most commonly mistreated , misdiagnosed, and misunderstood issue in medicine . By remaining alert to the prospect , even under the shadow of a confirmed diagnosis of OA related breakdown, I am able to offer significant problem solving to many whose future had been considerably altered by the prospect of only medical or surgical answers to MSK problems. I recommend readers become skilled in and alert to spinal neuralgic events in their assessments for this reason.

[Physio Bed]

Ginger,

I certainly agree that the CNS has an overwhelming contribution to someones pain state and adapts itself to an ongoing pain state. What I am trying to suggest is that pathology also may exist concurrently with the central signs. Obviously these exist in different proportions in different patients groups.

However... are you telling me that someone who walks into your clinic with a diagnosis of hip OA and objective signs that support this would be treated by mobilisations of the PIV joints?????

[ginger]

I'm sure I just said that, but, yes , that is exactly what I do . No need to reiterate the position I have already made clear. Were I not to do this , I would not know , and could not know, what contribution was made to pain and dysfunction from neuralgic means. Clearing tests are virtually useless, have always been so. One cannot percieve referred pain in a way that would identify it as such, tests for joint function routinely offer false postives when blurred by neural interference. The logic of spine first makes more sense of course once you have seen this approach work over and over again. With the experience of having reduced and eliminated pain and dysfunction hundreds and hundreds of times in the face of diagnoses including OA, tenosynovitis , frozen shoulder , PFS, migraine, achilles tendinosis, shin splints , tennis elbow, Ilio tibial band synd. etc etc etc . It is clear to those who approach MSK problems this way , that desigated pathology does not , by itself, exclude the possibility that these signs are less relevant , in the aetiology of pain , than neurology . One only has to treat a few people with so called iliotibial band syndrome by twenty minutes of L4 mobs to witness the elimination of this referred event to have a taste for this approach.