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May Journal Club Case – Double Crush
Apologies for the length of this post. This pt has a lot going on and I included a lot of findings that may seem less pertinent, however, help to illustrate how easily her post/lat hip pain was reproduced, even distally. I listed the O* that I used to assess/re-assess as well to narrow things down.
There are 2 articles, with the primary article talking about the UQ. There is very limited PT intervention specific research on this subject (except for dural tension testing and nerve glides). I don’t expect you to read both. The information from the primary article will be the focus of the presentation.Demographics: 47 y/o female, works with horses, like to ride horses recreationally
Body Chart:
• Pain over low back over L3-S1 area to L post/lat hip along iliac crest and down along proximal 2/3 of lateral thigh
• Pain along proximal 1/3 of L anterior thigh and along proximal 2/3 of lateral thigh
• Pain across anterior aspect of L knee
• Numbness over L proximal 1/3 lateral calf
• Numbness around L lateral malleolusBody Chart Initial Hypothesis:
• L5 radiculopathy with mechanical knee painSubjective Exam:
• LBP: constant, variable, deep aching pain
• Posterior/lateral and anterior radiating pain: intermittent, variable, deep aching pain with occasional sharp pain
o (+) Relationship: radiating pain into thigh with increased LBP and always from low back into the thigh proximally to distally
• Anterior knee: intermittent, variable, deep brief sharp pain followed by lingering ache
• Proximal lateral calf (over proximal tib-fib joint): constant, non-variable numbness since November 2015
• Inferior and posterior to lateral malleolus: intermittent, variable numbness since November 2015
• No changes in bowel and bladder function, saddle anesthesia, changes in gait, night pain, changes in appetite, unexplained weight gain/loss
• NPRS=5-7-9/10; states she has a high pain toleranceAggs
• Increased anxiety/stress
• Prolonged standing, sitting >1-2 hours, sitting in deep chair, driving
• In/out of car – driver’s side only
• L side lying
• Prolonged hip adduction when in R side lying -> interrupts sleep, needs to reposition
• Helping Farrier – pulling/holding horses, lifting/carrying, shoveling, prolonged bending
• Ascending/descending stairs (knee)Eases
• Decreased anxiety – medication, relaxing
• Stretching (previous HEP, hamstring stretch/nerve glide)
• Changing position, moving when stiff
• Sit upright with lumbar support
• Heat/ice – temporary relief <2 hours24 hour
• Mostly activity dependent
• Better/worse in am depending on sleeping position (see above)HPI
• Chronic LBP since teens (slip and fall), insidious onset sciatica in 20s, insidious onset L hip pain in 30s
• 5-6 Years ago – gradually worsening LBP after starting work in retail requiring heavier and more frequent lifting
• Decreased pain and improved function after PT approximately 10 months ago
• Previous PT focus on L/S and hip mobility and trunk/lumbopelvic motor control exercises and LE resistance training
• L inversion ankle sprain in 2010
• L mid 1/3 quad – kicked by horse – localized pain and ST restrictions sincePMH
• Hx of anxiety – medicated and monitored by MD; pt states that she does not require additional counseling and feels like anxiety is well managed
• Hx of bladder cancer in 2005 – sx, no chemo/radiation; successful, oncologist cleared pt last year, no more check ups requiredSpecial tests
• MRI – no severe findings; min to mod foraminal stenosis left L4-5 (pt repeatedly asked whether I saw the MRI report)Objective Exam
• Lumbar ROM:
o FLX hands to knees – decreased localized LBP
o EXT 20 deg – local LBP and min radiating pain into post/lat hip
o R and L SB finger tips to distal 1/3 thigh; L SB – local LBP and post/lat hip
o R EXTQ – clear
o L EXTQ – local LBP and post/lat hip -> further peripheralizing with sustained positioning and OP
o Decreased reproduction of pain with L EXTQ with L foot on 4” stool
• Localized LBP with compression – decreased pain with post pelvic tilt
• Slump: R=(+) reproduction of LBP; L=(-)
• SLR: post/lat hip at 45 deg hip FLX
• Modified SLR – DF/INV before SLR: onset of post/lat hip syx with DF/INV alone; increased at 30 deg hip FLX
• Myotomes/MMT in supine: hip FLX=4/5, knee EXT=4/5, EV/INV=4/5
• Single leg heel raise L=80% of R – subjective report of strength
• Dermatomes/light touch: decreased sensation in L1-2 dermatomal distribution
• DTRs L3-5, S1 B=2+
• Hypomobility, post/lat hip pain with FADDIR, IR, ER, ABD; hip EXT and PA
• Hypomobility, post/lat hip pain with PROM DF and TCJ AP
• Hypomobility, post/lat hip pain with knee EXT OP
• Reproduction of ant/lat thigh symptoms with femoral nn test (prone)
• Localized and post/lat hip pain with L5>L4 CPA and L UPA
• Hypomobility and localized pain with T12-L2 CPA, bilateral UPA
• Palpation distal and mid quad – increased tone; localized pain and distal to proximal radiating pain ant thigh to post/lat hipObjective asterisk list used for re-assessment:
• Lumbar AROM + EXTQ
• Toe raise, hip/quad MMT
• Mod SLR: DF/INV -> SLR
• Hip FADDIR
• TFJ EXT OP in DF
• TCJ AP
• L5 CPA and L UPA; TLJ CPASubsequent visits: SIJ, prox/distal tib fib, more specific palpation along fibula, Tinel’s, Psoas palpation
Day 1 treatment (4/20)
Gr III right side lying L5-S1 ROT gapping -> high irritability
Gr III right side lying FLX PPIVM
Gr III L hip inf and lat with belt
TE: supine – pelvic tilts, alternating hip flexion (knee tucks), bent knee drop out, lumbar rotationDay 2 (4/25)
S: increased soreness/irritability for 1-2 days after eval; decreased irritability and overall pain since
O: no significant changes with O* testing; pt reports decreased severity of symptoms
Treatment – same as day 1: increased tolerance to techniques
TE: same as initial
O: decreased irritability with all O*Day 3(4/28)
S: further decreased irritability, overall pain
O: only localized pain with L EXTQ – post/lat hip with sustained position and OP; increased ROM with mod SLR (40 deg); rest same as post-tx day 2
Treatment – same as day 1-2; addition quad STM, knee EXT OP + DF, TCJ AP
TE: initial + recumbent bike, resistance with L/S ROT
O: further decreased irritability; localized pain L EXTQ – no post/lat hip with sustained position and axial compression; mod SLR -> 60 degArticles:
1. Clinical conundrums in a case of upper quadrant dysfunction Clinical conundrums in a case of upper quadrant dysfunction.
2. The Pseudoradicular Syndrome: A Case Report Implicating Double Crush Mechanisms in Peripheral Nerve Tissue of the Lower ExtremityThe primary article was chosen due to having been published more recently and its in depth discussion of proposed neurodynamic and physiologic mechanisms. The secondary article was chosen due to relevance to this case, as well as further illustration of clinical reasoning process based on findings.
Questions:
1. What objective measures would you have added during the evaluation, or follow up visits?
2. Based on the information given, how would you estimate the % involvement of the different components (L/S, hip, knee, ankle, quad)?
3. How would you go about educating a patient with similar presentation about their condition, preferably without inducing fear, or concerns about multiple injuries/problems? Would you use the term “double crush” with your patient?
4. How would you communicate your findings and hypothesis of peripheral soft tissue and PAM contributors to the referring physician/insurance in your assessment? Especially considering the very limited evidence for “double crush”.
5. Within the context of EBP (research, expertise, patients), how do you weigh case studies/series compared to RTC, or other higher-level research, in regards to complex cases? Consider lack of specificity of many RTCs in regards to patient presentation in inclusion/exclusion criteria. -
Your articles point out neurodynamic mobilizations. Which particular neurodynamic technique did you have the most positive result?
Education: I try to make an explanation as simple as possible. His irritation is L extension quadrant and I would show that motion on a skeleton and tell him how that irritates the nerve. I wouldn’t say anything about double crush because that sounds intimidating.
After the Grade 3 R SL flexion PPIVM, did that improve his left extension quadrant? If so, I would use that as an educational tool saying we can make a difference and we want to find what specific exercises would be best to tailor his presentation. Since his symptoms improved I might transition to a femoral nerve glide and see how his system responds?
I think evidence is great as it helps shape practice. I try to use it “judiciously”. If we see something that looks like it will help our patient then I say let’s try it. The case report you choose might help guide your treatment based on similar subjective and objective findings. I try not to disregard evidence if my patient does not fit all the inclusion or exclusion or if it’s expert opinion. There was very limited evidence for one of my patients with morton’s neuroma. He was not a success story and I worked hard working to address the impairments. I reviewed EBP, talked to my colleagues, listened to my patient (only wanted plantar soft tissue), and left his surgeon messages. I think it’s great to have some sort of resource to go to. I can’t fix everyone, but at least I tried and didn’t give up.
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Alex,
You apologized, and I forgive you for the lengthy post.
In all seriousness, it certainly seems like you were fairly thorough in your exam. The only thing I might have thrown in would be a brief functional movement or two – probably something as simple as a double/single leg squat. Just to get a sense for her willingness to move and also to add greater load to knee structures, if you were suspecting local knee pathology.
I certainly would not use the term “double crush,” to a patient. In fact, I would probably never use the word, “crush,” with a patient. If I felt that the idea of double crush was present, and it was necessary for the patient to understand their condition/buy in to my treatment approach, then I would try and explain it as simply and understandably as possible, “I think we can get the best results if we work both on A and on B.” If it wasn’t necessary for patient buy in or critical for them to understand, I might not even explain it.
I feel I have come to appreciate more readily case series/reports since starting this residency. They are often more practical, with greater attention given to clinical reasoning. The RCT’s usually contain methodological flaws that limit specific applicability anyway, and therefore while I wouldn’t make the case series the gold standard of treatment, it certainly has great value.
What was the patients affect/fear level during the exam? What is your interpretation of the reproduction of hip pain with ankle DF, TCJ PA, and knee extension? Did she complete a FABQ and what was your take in this regard to the patient?
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No need to apologize – more details, the better. Of course, I have more questions…
To clarify the HPI, the insiduous onset of sciatica in her 20s’s – this was similar symptoms to her current complaint? Same with the hip pain in her 30’s? And with my understanding, she has been experiencing all these symptoms for the past 5-6 years since retail job, got better with physical therapy, but then has had a recent worsening of symptoms in November?
When was the horse kick?
Does she currently ride and did she ever mention any problems with riding on a horse?
What specific surgery did she have for bladder cancer?
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The case is certainly interesting and tough to wrap my brain around, especially with the neurodynamic testing that you performed with a negative slump, however positive SLR and positive modified SLR. On top of all that, it seems like you weren’t able to reproduce or change the numbness (correct me if I’m wrong).
During the initial evaluation, did you reassess any of your asterisks after the treatments to see the changes of the lumbar spine or hip treatments? Sometimes I find that if I do too many different treatments and they are no better, worse, or better, I don’t know what I did that specifically made a difference. I probably would have picked only lumbar spine or hip, reassessed, then added more at the next follow up visit to avoid muddy-ing the waters.
Where do you think that the “double crush” is happening with her? If I truly think that there is a mechanical irritation or sensitivity at two different points, I talk to patients about their nervous system and how it connects to every point in our bodies. In our daily lives, we don’t just move at single joints we move as a system and if we have a weaker link proximally, it might affect the way our joints and muscles move at a distal point. To agree what Nick said, I would say that we have a good chance of helping you more if we focus on both areas. I tend to avoid using the term “double crush” with patients as well. The imagery that could come to mind of anything in our bodies that is “crushed” cannot be healthy.
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I don’t want to beat this drum again, but I just can’t imagine that treating ANY of those multitude of impairments, special tests, movement dysfunction will ever get better unless she understands that her pain is not from the tissues.
These are incredibly hard patients to treat, but us not seeing all the signs and changing our evaluation and treatment, communication to addressing the biopyschosocial components after clearing red flags, needs to be the primary focus of treatment.
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Hey Alex,
Nice job completing your final Journal Club presentation. It definitely sounds like a tough patient case. I just wanted to follow-up with a point that stuck out to me during your presentation. From my understanding it sounds you agree there is a central component to this patient’s presentation and you are pleased with the fact that she is getting better, regardless of whether or not her improvement is a result of your manual techniques, exercise or the education you are providing. I agree, it’s great that she is improving. The point I would like to make is that I think it’s very important that the patient understand why she is improving, especially with a case involving a central sensitization component. In cases that have an apparent central component, even if there are still mechanical signs and symptoms that make sense, I want to focus all my energy on educating them on their pathology, set their mind at ease and see if that has an impact. If my education has a significant influence at relaxing the patient and their symptoms and movement significantly improve, it’s huge that they realize what helped them improve so they can manage the condition themselves. There are times that my strategies for a patient who have even a hint of a central sensitization component are to spend most of my time educating and begin low level, healthy movement and to be hands-off initially. I want to empower them to manage their condition independently and I want to avoid giving them the impression that they need me to perform treatment technique on them. Obviously this is a case-by-case basis. I realize that some hands-on techniques are completely warranted at times for a patient such as this and it’s difficult for me to say whether or not your patient would or not. Regardless, I want the patient and myself to know if she improves from my education, from my exercise or from my manual treatment, and to do that I feel like I need to perform minimal treatment initially to make that determination if I am initially unsure. To start, I need to make a determination of what component is the most heavily weighed and start there.
Thanks for presenting! It’s great to reflect on patients like this -
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Great job with your presentation Alex and thanks for sharing a particularly tough case.
From my understanding:
Double crush = proximal compression of a nerve that decreases ability of a nerve to withstand compression at a distal site. Central sensitization = impaired inhibition of nociception in the pathways that lead to/from and augmentation of pain perception within the brain (short version). ALSO, after sensitization has been set in place, further peripheral perceptions of harm can sustain or worsen the sensitivity. I can’t imagine that they cannot both happen in the same patient, but it comes down to what, how, and when to approach each. Do you initially start with 1) pain education, ensuring their maximal understanding of what is causing their pain, and making sure they have some management strategies set in place OR 2) mechanical/neurodynamic approach addressing impairments OR 3) both at the same time?I struggle at times when I have initiated treatment with a patient who I think could benefit from a mechanical focus, realizing they have components of central sensitization, then having to back track and sometimes contradict myself because I’ve already started treating him with a mechanical, peripheral focus. I realize that you have to “roll with resistance” and if they don’t buy in at first, sometimes you have to layer it in as you can when the patient develops trust. But’s not like adding in a certain exercise or manual technique, it’s the entire concept of what they are feeling and why. I understand the importance of addressing this FIRST, but lately I’ve been finding that it’s hard to do this smoothly.
With the case report you presented, I was surprised to only read one sentence at the end of the discussion on possible involvement of his biopsychosocial components with his case, despite chronicity, fear, widespread symptoms. I’d be curious to find how much of a long-term change he sustained after treatment.
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My thoughts keep going back to function with this patient – assessing functional movement; aggravating factors, sometimes an emphasis more on functional work/activity related movement assessment can be a more effective way to weave in education, and assess other biopsychosocial components may come out.
Who cares what her UPA at L4 on the (L) is, if she has to hold a horse’s hoof for 3 hours/day; then rides for 20 hours/week. Sometimes stepping away from our battery of “Special Tests” which have limited reliability/validity, and can just be provocative; as well as fear inducing when some are positive in non organic ways (TC post glide reproduce proximal hip sxs), then we are stuck trying to further explain those findings.
Bit of a ramble, but hopefully makes some sense and facilitates some additional discussion
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I hope not to blindly beat the drum I have been thinking about in recent days, but it is simply so hard to appreciate the unique personality of the patient and the quality and nature of patient-therapist interaction via a discussion board/powerpoint presentation, which undoubtedly is a huge aspect of treatment. Reproduction of lateral hip pain with knee extension + DF overpressure in one patient could signal significant fear, kinesiophobia, and catastrophizing in one patient, marked central and/or peripheralization in another, or something merely mechanical/neural in another. Determining which of the three is happening seems to be heavily based on patient personality as a whole as well specific interaction and response during testing. This is simply so hard to convey on a discussion board.
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