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Hi, my name's Jo Gibson. I'm a clinical physiotherapy specialist working at the Liverpool Upper Limb Unit in Liverpool in the UK. Tonight is just a quick 10-minute taster about an unusual case that came to the Accident and Emergency Department about three weeks ago.
Those of you that have already been able to watch our free videos at www.clinicaledge.co/shoulder may already know the answer, but we'll see how much you took on.
But really this was just about an unusual case of shoulder pain that had presented acutely. So, very definitely acute onset shoulder pain. So, let me tell you a little bit about this guy. 30-year-old guy presents to A&E because of the severity of his pain. He has a two-week history, sudden onset, woke up with it. So, woke up in the early hours of the morning with severe shooting pain. He describes pain as constant, it's shooting, it's severe, it's only on one side, is in his upper arm posteriorly, not up into his neck, but there's some around his supraspinatus fossa and around his trapezius.
When asked about his history, he said he had been working out in the gym and because of lockdown, he'd perhaps done a little bit more body weight stuff, but there was no particular instance where he felt anything go. No particular onset of sharp pain, and he didn't have anything at all until he woke up with this sharp pain.
In terms of his medical history, he has Crohn's disease, but he says that's well managed and he's very careful with his diet. In terms of how the pain behaves, he says, "It's very difficult to get comfortable. There's not really any particular positional aggravating and easing factors, but it's definitely worse at night." All his movements are uncomfortable, but he particularly dislikes abduction.
In terms of questing more about his pain, he definitely doesn't have any scapular pain and there doesn't seem to be a very specific dermatomal spread of his pain, if you like. He obviously can't take nonsteroidals because of his Crohn's, so he's just taking paracetamol at the moment and that's not really touching his pain at the moment. He's a little bit worried. He's tried to manage it himself at home. He's tried to keep exercising, but he's now a little bit worried because he feels that the shape of his shoulder has started to change, and he feels that he's starting to lose a little bit of strength. So, he's very, very anxious about getting some help. So, what can we do in terms of assessing him? Well, this was at the beginning of COVID, so we were very limited in terms of handling and stuff. So, what can we look at?
Well, he was very reluctant to lift his arm up because everything was so sore, but we could look at his rotation in neutral and he didn't have any significant restriction of external rotation in neutral or internal rotation in neutral. So, just looking at this and then arms down his side. In terms of doing resisted movements, he had some pain on resisted abduction, but it was very painful, but if he supported his arm himself, it felt a little bit stronger. As I say, there was no neck pain and his neck range of movement was really good. Combined rotation and extension didn't provoke anything at all. And there was absolutely no doubt that when you looked at the back of his shoulder, there was definitely some wasting over his infraspinatus fossa, but also over his posterior deltoid. Now, what are you thinking already?
Okay, because I've given you quite a lot of clues, but I've also thrown some red herrings in there, very deliberately. And Sam was quick off the mark and actually has already got the answer, but if you didn't spot that, I'm just going to go through some things that are relevant in this guy's history. Now, one of the first things about that waking up with acute pain, that's a really key point, because this guy, because he's got Crohn's, he's actually more likely to get an acute calcific tendinitis. So, that was very deliberate putting the Crohn's in there because the increasing evidence about calcific tendinitis is that actually, if you have any background of absorption issues with your stomach or any metabolic issues, at a younger age, you're far more likely to get calcific tendinitis. However, it's very easy to do an X-ray and there was no calcific deposit on this guy's X-ray.
So, what are the next things? Well, certainly we'd want to think about potentially some sort of cervical nerve root, but again, the difference in this guy is he hasn't got a clear dermatomal pattern.
He doesn't have scapular pain, he doesn't have neck pain and his symptoms aren't provoked by doing any combined cervical spine movements. So, that allows us to rule that out. One suggestion was thoracic outlet, but again, this guy doesn't have an acute history. There's no doubt if he had symptoms that were provoked with overhead or arms down by his side, he was able to give us some precipitating mechanism, that might be a road we'd go down, but certainly there's nothing about this guy's history that would be suggestive of that. In terms of having wasting over his infraspinatus, he hasn't got a history of trauma. There's no instance of anything that he did in the gym, but when I'm questioning him, he's telling the story. He does tell me that about two years ago, he had an injury to his shoulder when he was climbing. He had an overreach injury where he slipped and the whole of the weight of his body went on that arm.
So, again, I've got that in the back of my brain, but there's nothing to suggest any further issues from that incident two years ago, it was sore for a few weeks, settled down, and it's never stopped him doing anything since. So, what have I got so far? I'm pretty confident it's not his neck because it's not provoked by neck movements. It doesn't follow a key pattern. He hasn't got any scapular pain and he's not able to describe any particular unloading position. He doesn't have any systemic factors in terms of any worrying things, in terms of night sweats, weight loss, any history of anything nasty, other than his Crohn's, that might make me worry about a tumor or any malignancy. The reason I mentioned the injury two years ago is purely because we do know that people who get SLAP lesions from some sort of overreach or stretch injury, and climbing's a really common mechanism.
Anybody who's here and suddenly has an overstretch, if they get a superior labral tear that allows the fluid in the shoulder joint to communicate outside the joint, then we can actually develop a synovial cyst. And somewhere between two and three years after the injury, patients can actually present with weakness rather than pain. They may have a posterior ache, but it's not the sharp pain that this guy is describing and that can because the cyst starts to press on the nerve.
So, commonly those cysts from SLAP lesions will press on the suprascapular nerve, but if they're big enough, they can actually take out the posterior branch of the axillary nerve as well. So, again, those were very deliberate red herrings in his history. Now, what does that leave us with? Well, several of you have got the answer already in terms of Parsonage Turner Syndrome.
Now, I've very deliberately put this in as an unusual cause of shoulder pain, because some people would argue that it's actually getting more attention than it deserves these days. It's been much more described in the literature. And the key thing with this guy is, he's got a normal X-ray, but he has got frank weakness and he has got frank muscle wasting. So, the very typical descriptor you'll see in all the literature about this condition is people wake up in the early hours with horrible pain. The pain can last anywhere up to four to six weeks, with most people by two to four weeks, the pain just goes and they're left with this really frank weakness and muscle wasting. So, the muscle wasting, again, can start anytime from two days to four weeks after the onset of pain. Now, that's the very typical presentation and definitely something you need to consider in your acute shoulder pain patients.
Now, Parsonage Turner has lots of different names. It's also referred to as neuralgic amyotrophy, brachial plexus neuritis, brachial plexopathy, lots of different terms, but the key thing is it tends to take out the upper and middle plexus. Now, again, if you read some of the early literature, it tends to suggest that it mainly takes out the long thoracic nerve, but I don't think that that's well supported and it's certainly not what we see in our practice. The most common thing we see is actually that it takes out the suprascapular nerve and often in conjunction with either the axillary nerve or the musculocutaneous nerve, but I would definitely say the suprascapular nerve is the most prevalent. We have seen patients with the anterior interosseous nerve involved, but that's much, much rarer. Again, if you look at the literature, there's two key types, there's a hereditary type and there's an idiopathic i.e., we don't really know the cause type.
The idiopathic type is far, far more common. As I say, if you had somebody with this presentation, and their pain hadn't gone away by the three-month mark, you could almost exclude Parsonage Turner because it's so typical that that pain goes away and is replaced by this muscle wasting and weakness. Now, I say, in terms of causes, we don't really know. As I say, the idiopathic cause is nine times more prevalent than the hereditary. If you look at postulated causes, there's no doubt things like immunisations, people that are immunosuppressed. So, again, our guy with Crohn's, if perhaps he'd not been so well, again, he might be a little bit more vulnerable. Exercise, strenuous exercise has been shown to be an issue, a lovely study done by Clarke et al, who's part of Len Funk's group, actually showed quite a high prevalence in people who did overhead sport, whether that was professionally or just for fun. Hepatitis E is a risk factor. And the Hepatitis E can actually get an association with their phrenic or laryngeal nerve so they can get hoarseness or problems with shortness of breath, rheumatic diseases, any viral overload, and actually after surgery, again, they think it's because patients are potentially immuno-suppressed. So, quite a few potential factors. Now, interestingly, that Clarke study that I was just referring to before, by Len Funk and his group, actually suggests that it might be over diagnosed and the trouble is because it's had so much more coverage in the literature that people have stopped being suspicious about other diagnosis. So, what would we do? Really, it's a diagnosis of exclusion, for me this guy is young, he doesn't have a history of trauma. I can't reproduce or change anything with his neck. He doesn't have any clear signs that are consistent with a cuff, and again, doesn't have that history. And as we know, history is absolutely everything. An X-ray is going to rule out a calcific tendinitis.
I can do an X-ray of his neck if I thought it was relevant, but I don't in this case, though you would have to say, in terms of the nerve involvement in the frank weakness, you'd have to rule out some sort of plexus involvement. When you do MRI on these patients, what you actually see is a series of mononeuropathies involving the trunk and the nerve. It doesn't take out the whole plexus. So, it's a really, really interesting condition. You'll often pick up fatty edema and edema in the muscles that are affected, and certainly now MR neurography is getting more common.
So, your testing can be useful. Nerve conduction studies can be useful. They're not infallible if you use them too early in the process. And what's really interesting, there's a massive spectrum of how well these patients do. Some papers will tell you that 80% will be better in two to three years.
And so, sequential nerve conduction studies may have some use, or EMGs to monitor that improvement. But actually, some of the more recent studies would actually suggest that patients can have symptoms that persist quite significant functional restriction, and certainly, things like pain and fatigue by up to 30% of patients. Now, there's a specialist group in the Netherlands, ones that they work with Maastricht University in terms of their research. And they've certainly been doing some interesting work looking at effective management. Now, it's like every nerve injury, it's very difficult to look at our interventions and know what we're actually influencing and also what is just natural recovery. But they certainly looked at using left/right judgment as an assessment tool and shown correlations in terms of changes in central representation, which clearly, if we're not getting normal input, that's very likely. And there's no doubt that in terms of the most proactive things we can do, we certainly look at things like left/right judgment and mirror therapy.
We look at using muscle stimulation, just to try and keep some sensory inputs. Prof. Frostick, who's been my mentor, who sadly died this year, he was a great believer that the more you could keep some sensory input to the muscle, the more chance there was of recovery, but the longer that the muscle was out of action, the more damage or deterioration in the motor end plate, fatigue was almost an inevitability in the long-term. And that's quite important when we're setting patient expectations. So, the other things we use are visualisation and cross-education, where you just work the other arm really hard targeting the muscles that are affected and really doing everything you can proactively to keep things healthy and set that road for recovery. But it's a very massive variation, if you like, in how well patients do. The great thing with this condition is you can reassure people that their pain is going to go. The ongoing pain they tend to have relates to the muscles that are compensating for the muscles are weak.
So, it's very common to get periscapular pain and almost like, cuff pain, that's purely secondary to the different muscles are having to overwork because of frank weakness, but nerve conduction studies, really are your friend in trying to identify any sort of improvement. So, why did I choose this guy? Well, really the Clarke paper from Len Funk's group really made me think because it's certainly something I always flag up when I'm talking about differential diagnosis of acute shoulder pain. The reason I bought it in is because it just shows you how vigilant we have to be and how our clinical reasoning is informed by all these things. And it's fun because it's a little bit of detective work. We saw that we had a few red herrings in terms of the Crohn's disease, that previous history of shoulder injury. Immediately, we might think of that calcific tendinitis because of that Crohn's association.
But you can also see how with really simple objective assessment, very simple questions about aggravating and easing and positions, but also just that background history, how we can very quickly rule lots of those things out and then our investigations help. So, really with Parsonage Turner, the other thing we always have to be aware of is any compressive pathology. I talked about the cysts, but also any other nasties or lipomas, or other things that could potentially cause compression, but again, they don't tend to present acutely. So, we never lose that air of suspicion, if things stop progressing the way that we expect them to. But I think this is definitely a condition that we want to consider in our workup.
Now, there was a question from Peter that was just saying, "Would I use a Compex for muscle stimulation?" Now, usually I just use a Neurotech or whatever, but I think what I'm finding when I actually wants to get frank contraction of the muscle, there's no doubt that the Compex seems to have more clinical effect than perhaps using the Neurotech. But again, that is a much more expensive machine and in terms of accessibility for patients, we can get a Neurotech for like a hundred quid, and actually, I think it's down as low as 60 now.
And what is interesting, it would seem some sensory input, probably because of those cortical effects does have some positive effect. And I think if we're honest, it's very difficult to delineate what effect we're having as opposed to natural recovery, but it's a question of managing and being supportive and doing all the things that we can. So, certainly in my nerve injuries after surgery or a frank nerve injury, I definitely use the Compex if I've got access to it. But if I haven't, I think the Neurotech is a good second, just in terms of keeping that sensory input. I think we need more evidence in terms of targeting the particular frequency of the muscle. So, I hope that answers that.
So, Matthew's asked, "Would we treat this as an acute neuritis with a course of prednisolone?" The answer to that is, we wouldn't know, some of the literature reviews do suggest that a short course of steroid is actually useful, but that's not been well supported in the Cochrane Collaboration Reviews. And actually, I would say that the evidence for it is pretty unsupportive. It would seem that patients get more gain if they can take nonsteroidals. They seem to be as effective, if taken at the correct dose for long enough, as opioids, but obviously in this guy's case, he was unable to do that.
So, neuropathic meds, again, if they have persistent pain after that first four week period, that some would suggest neuropathic meds. But again, if you remember that pain generally goes within four to six weeks, most of the patients I've seen, it's very unusual for it longer than that. And often, that reassurance and just some simple strategies with oral meds do seem to be as effective. There's a very small cohort that seemed to actually need the neuropathic meds to support their recovery. But as I say, I think the key thing about this is because this is getting a lot more press, it's very easy to think this is the key issue. We just have to be a little bit careful that we don't always assume.
Now, guys, I said I was going to be here for 10 minutes, and as usual I've gone on for longer than I intended, this was just a quick taster, a quick interesting case that I saw. Showing that very simple things, clinically, actually helped rule in and rule out. But as ever, perhaps telling us that sometimes our investigations are paramount, just in being clear, I haven't got anything nasty and everything fits with my initial preliminary diagnosis.
We'll post some resources on the Facebook page, some interesting papers and certainly to the group in Holland that are doing the most work about this, but definitely that Clarke paper as well, that just may be questions things a little bit. We're really looking forward to sharing some content and looking at some of the controversies that face all of us at the moment, the scapular, cuff tears, when they need operating on, injections, should we still be doing them or shouldn't we? All sorts of exciting things. We've got a good list of things lined up. Thank you to those of you who asked questions. Guys, thank you so much for joining. It's lovely to have you all here. If you haven't had a chance to look at those free videos at Clinical Edge, they're still available at www.clinicaledge.co/shoulder. I’ll talk all about differential diagnosis of acute shoulder pain. Parsonage Turner is in there, but also some other considerations. So, I hope you enjoyed it. Thanks for joining and I'll see you again very soon.