false
Catalog
New Frontiers in Chronic Pelvic Pain, Myofascial P ...
New Frontiers in Chronic Pelvic Pain, Myofascial P ...
New Frontiers in Chronic Pelvic Pain, Myofascial Pain Syndrome and Central Sensitization: Advances in the Pain Sciences Inform Management Strategies
Back to course
[Please upgrade your browser to play this video content]
Video Transcription
Hello, my name is Jay Shaw and on behalf of my co-presenters Colleen Fitzgerald and Cecily DiStefano, we wish to thank the Academy for inviting us to give this presentation titled New Frontiers in Chronic Pelvic Pain, Myofascial Pain Syndrome and Central Sensitization, Advances in the Pain Sciences in Form Management. So I am the first speaker and the title of my presentation is Traditional Insights Regarding Central Sensitization and Myofascial Dysfunction and Chronic Pelvic Pain from Endometriosis. As you know, active myofascial trigger points are powerful sources of nociceptive bombardment into the dorsal horn, including trigger points from the abdominal and pelvic musculature, and one of the things that this will lead to is the opening of the postsynaptic neuron and release of glutamate and substance P with consequent postsynaptic changes occurring. So we have to keep in mind that it's both the persistent bombardment from the nociceptor as well as from the viscera which can cause further sensitization. And why do these two interact so powerfully? Because of this structure right here, the wide dynamic range neuron in lamina 5 of the dorsal horn, allowing communication between the soma and viscera and the viscera and soma. So one of the results of this is pain, as you know, and this pain can be located in the abdominal area, in the visceral tissues, internally, externally, etc. And how do we know the subjects are sensitized? Because we see signs of allodynia to a pinch and roll test, as well as hyperalgesia to a pinwheel, giving us some clue about the degree of central sensitization occurring in these subjects. So this is a tremendous conundrum in terms of understanding endometriosis. So for example, in chronic pelvic pain associated endometriosis, there is poor correlation between severity of disease and severity of pain, and there's poor correlation, excuse me, there's poor correlation between severe disease and severity of pain, and poor correlation between location of pain and location of ectopic growths. And in addition to that, hormonal therapies and surgery target ectopic endometrial lesions, which may control the extent of the disease, unfortunately often fail to alleviate the associated chronic pelvic pain. And even when these treatments are helpful, the return of pain is not necessarily associated with the return of disease, contributing to this conundrum. So why are active trigger points so commonly found in women with chronic pelvic pain? And this is a fascinating study done by Jarrell, who asked this question, why do 25 to 40 percent of laparoscopy cases done for pelvic pain fail to demonstrate an identifiable visceral cause for the pain? In his study of 55 consecutive patient subjects, he found that the presence or absence of a myofascial trigger point in the abdominal wall helps to determine whether there is evidence of current or previously treated visceral disease. In fact, he demonstrated that the presence of an abdominal wall trigger point predicted evidence of visceral disease in 90 percent of subjects, and the absence of that trigger point, of a trigger point which is associated with no visceral disease, in 64 percent of subjects. So this was very intriguing. So what our group, led by Dr. Pam Stratton, who's a gynecologist at the NIH, we sought to determine, to evaluate sensitization, myofascial trigger points in quality of life in women with chronic pelvic pain, with and without endometriosis. So we performed a cross-sectional prospective study of women aged 18 to 50 years, with pain suggestive of endometriosis, and a group of healthy pain-free volunteers without a history of endometriosis. The examiner was blinded, that's myself, to the clinical status of the subjects. The subjects underwent a neuromusculoskeletal assessment of clinical signs of sensitization from T9 to S2, and palpation of trigger points in paired muscles and the abdominal pelvic region. Pain symptoms, psychosocial, and quality of life measures were also assessed. All participants with pain underwent laparoscopic incision of suspicious lesions to confirm endometriosis diagnosis by histologic evaluation. So what did we find? Patients including 18 with current biopsy-proven endometriosis, 11 with pain only, and 20 healthy volunteers. The prevalence of sensitization as measured by regional alidin and hyperhidrosia was similar in both groups, 83 and 82 percent, but much lower among healthy volunteers who were pain-free. Nearly all women with pain had trigger points, 94 and 91 percent. Adjusting for study group, those with high anxiety and depression were more likely to have sensitization. And interestingly, pain patients with any history of endometriosis had the highest proportion of sensitization compared with others, 87 percent compared to 67 percent of chronic pelvic pain with or without endometriosis compared with healthy volunteers at only 15 percent. So conclusion, sensitization and trigger points were common in women with pain regardless of whether they had endometriosis at surgery. Those with any history of endometriosis were more likely to have sensitization, and traditional methods of classifying endometriosis-associated pain based on disease, duration, and anatomy are inadequate and should be replaced by a mechanism-based evaluation. So what's very important to realize is that there is direct innervation of ectopic lesions by sensory and sympathetic fibers, and this has been conferred in a rat model and in women with endometriosis. Furthermore, their presence correlates with the severity of pelvic pain and dysmenorrhea. And the perineal fluid of women with endometriosis contains elevated levels of interleukin-1-beta, TNF-alpha, IL-6, IL-8, IL-10, neuropeptides, nerve growth factor, all substances which can directly activate and sensitize local nociceptors, sending increased bombardment into the dorsal horn, leading to more sensitization of the entire neuraxis. Now, these sensory fibers that innervate endometrial lesions and surrounding muscle include CGRP-positive C-fiber nociceptors. Why is this significant? Because when these tissues, whether they be the viscera or the myofascial trigger points, are sources of persistent bombardment, they will not only lead to increased input into the dorsal horn, causing more sensitization, more pain, but you will see the antedromic release of these neuropeptides down the axon into the peripheral tissue, which can potentially exacerbate the local pain and inflammation and sensitization in the tissue. So, we understand now that these active trigger points, whether they be in the musculoskeletal region or in the visceral region, the point being is that they are a source of persistent bombardment and, as we said, this antedromic release will result in increased release of neuropeptides like substance P and CGRP. And please understand that there's a lower pH in this area, elevated levels of inflammatory mediators. This will lead to sensitization and everything that that nerve segment innervates can potentially be more sensitized, and this can lead to expansion of the receptive field of pain, alidinia and hyperalgesia, and in addition, more central sensitization and changes in higher brain centers. Okay, so again, there is this bi-directional communication between the nociceptor and the spinal cord at higher centers, and this is what allows for this type of sensitization and expanded neuroplastic changes to occur, and communication between the viscera and the muscle. So in addition, we understand that this persistent bombardment creates not just central sensitization, but facilitation of segments in the dorsal horn, the ventral horn, etc., and as we already discussed, these very profoundly important somato-visceral and visceral somatic interactions, and potentially we can see dysfunction or loss of segmental inhibitory neurons. And again, this can occur in this activity-dependent manner, so the more bombardment coming in from the muscle, the viscera, the more likely you are to see this type of sensitization occurring. So, what is spinal facilitation? Well, basically what you can see here is this bombardment coming from the dorsal horn, will activate not from the peripheral tissue, will activate not only the dorsal horn, but will activate the ventral horn, which will increase the activity, and that segment, in terms of the musculature, being tightened, being shortened, being activated, it can activate the intermediate horn, which will activate the autonomic ganglia, and potentially involving the sympathetic nervous system, and what we also see is an increased, what's called a dorsal horn outflow, or dorsal root reflex, and what will this do? This will exacerbate that very same neurogenic inflammation process that I just showed you, and that will lead to more pain and sensitization in the trigger point and any other tissue innervated by that segment. So, now we start to appreciate that the input can come in from endometrial tissue or other visceral organs, and as I said, this can lead to inputs increasing the dorsal horn, and this will affect not just the ventral horn, but the lateral horn, and again, increase the dorsal root reflex and affect the tissue and make the pain worse at the endometrial area, and as I will show you, it can also affect the opposite side as well, and the manifestations could be in the viscera, they could be in the myofascial tissue, or it could originate in one of those structures and then affect the other. It could also originate in the joint, so the principles are the same. So, speaking of the joint, so let's say the bombardment is coming in from the L3-L4 facet joint, and that will cause sensitization of the dorsal horn, increased activity of the myotome of that segment, so that will affect the muscles, the paraspinal muscles, and the rectus femoris, for example. It will also affect the dermatome, so now, if you were to do a pinch-and-roll test of the L3-L4 segments in the periphery or paraspinally, you will see allodynia. If you do a pinwheel test, you will see hyperalgesia, so these are signs of that sensitization, spinal segmental sensitization. We can also see the sclerotomal structures being affected as well, ligaments, tendons, and BCs, etc. So, these are often findings on physical exam, and what we have to determine is whether they are the primary cause or their secondary manifestation of something like segmental sensitization. And so, we under-appreciate now that the persistent source of bombardment could be from the joint, it could be from a trigger point, it could also be from a visceral tissue such as like endometriosis, and regardless of what the origin is, once you have sensitization developing, even if you do a treatment, let's say you do an injection to block the peripheral source of bombardment, the patient can still be sensitized. Why? Because those changes that have occurred have resulted in neuroplastic changes in the dorsal horn, which can continue to reverberate and cause more pain and sensitization and dysfunction, so we need to also deactivate and treat these dysfunctional segments and the segmental sensitization. So, Dr. Seyfried Mensah mentions this in his studies and says that we have to keep in mind that even though two structures, let's say the Achilles tendon and the sacroiliac joint, are so far apart from each other, the neurons that control those structures can communicate with each other, such that synapses that were previously ineffective can now become effective ones, and that can lead to expansion of the receptive field of pain, aledinia, hyperalgesia, etc. So, because this is a PM in our audience, I think it's helpful to show this in the context of a classic musculoskeletal presentation and then draw in some of our lessons of what we're learning about segmental findings as it relates to the viscera and endometrial tissue. So, let's say you have a patient who has pain that first starts in the gastroxilius muscle, and this is a trigger point there, and then they develop pain in the sacroiliac joint. Now, what you, of course, you want to know is there some type of SI joint dysfunction? Is there radiculopathy that perhaps could explain pain in both these locations, perhaps? Let's say you rule both those conditions out, but you do find that there is a trigger point in the trigger point manual, for example, that does refer pain in both these two very disparate and remote from each other locations. What could be happening based upon our understanding of Jarrell's work and our work in terms of sensitization? Well, this is what Dr. Mensah hypothesizes, and basically it is looking at the pain as being a result of the segmental involvement in sensitization. So, what you can see here is the neurons for that gastroxilius muscle, due to an active trigger point there, I'm showing in red. Why? Because there is spontaneous pain in this region. The neurons for the SI joint are initially quiescent, so I have it in this fuchsia or purple color. So, these are those ineffective synapses that the Mensah described, and what can happen is that you can have the release of those neuropeptides, which can convert those ineffective synapses into effective ones, and look what can happen. Lo and behold, now the patient can begin to complain of pain in the SI joint, even though the tissue and the joint are completely normal, and there is no local nociceptor being activated there. Now, you could do a treatment, as we just said a couple slides ago, and you could deactivate that trigger point, and that would be great. You could eliminate that pain, but you potentially can still have pain in this region. Why? Because this area is sensitized. Now, how would you know it? Because you would then, you would examine for aledinia and hyperalgesia, and you must be asking the question, well, could it affect other neurons? Absolutely. So, it could affect the L3, L4 neuron, in which case the patient would complain of pain in the knee. It could also occur on the contralateral side, and by extension, it could affect, this could be a somatovisceral effect, so that the visceral tissues, the endometrial, as well as the muscles, such as their sphincter ane, levator ane, and coccygeus, which are innervated from S2, S2, S5, could be sensitized and be a source, could be a manifestation of this pain process. So, we need to understand these concepts to understand better what might be happening in our patients with chronic pelvic pain, myofascial pain, and segmental symptoms. So, I'm going to turn it over to Kelly and Fitzgerald to talk a little bit about the clinical PM&R and the diagnosis and medical management of chronic pelvic pain. So, Kelly, I'm going to turn it over to you to talk about the clinical PM&R and the diagnosis and medical management of chronic pelvic pain. Thank you very much for your attention. Hi, everyone. It's so nice to see my fellow physiatrists. Thank you, Dr. Shaw, for an amazing presentation, as always. My name is Kelly Fitzgerald, and I'm going to talk about the clinical PM&R perspective and the diagnosis and medical management of chronic pelvic pain. For those of you who don't know me, I'm a professor in physical medicine and rehabilitation at Loyola University, Chicago. I am housed in the Department of Obstetrics and Gynecology in the Division of Female Pelvic Medicine. I have a couple other roles in the chronic pelvic pain program here and also as director of the Clinical Research Office. But hopefully, what I present to you will be clinical and practical, and I'm excited to be here with you. Our main objective is to really better understand the patient management and the implications for the objective findings of central sensitization in pelvic floor myofascial pain, specifically in women with chronic pelvic pain. And the sub-bullets towards that objective are really to look at the differential diagnosis of chronic pelvic pain, to understand the importance of the comprehensive pelvic floor physical examination, to review current pelvic floor muscle diagnostics, and then to discuss multidisciplinary non-surgical pharmacologic and non-pharmacologic treatments with a focus specifically on myofascial pain. I won't speak too much to pelvic floor physical therapy because my colleague will speak on that topic after my presentation. So, just in general, we know that pelvic pain has multifactorial etiology. There are multiple stakeholders. Depending on what specialty we train in, we see the patient with the lens of that of which we've trained, right? Physical medicine is a little late to the game in terms of taking care of these patients, and our colleagues in OB-GYN, GI, and urology have long been caring for women with pelvic pain. And what's difficult is that the precision of diagnosis is really limited because of the convergence of the somatic and visceral pain afferents. And we know that these patients take a significant amount of time to see and to treat in our clinics, so we have a lot of pressure to do it quickly, yet it cannot be done quickly. We also don't have, even in PM&R, although we're well trained in pain management, we have inadequate training as it relates to pelvic pain in general. And to top it all off, there's not great evidence for effective and durable treatments, which makes our job more difficult. The definition of chronic pelvic pain by the OB-GYNs is this, non-cyclic pain of six or more months duration that localizes to the anatomic pelvis, the anterior abdominal wall, and as they say, at or below the umbilicus. So it's really a widespread area and they include in that definition lumbosacral back pain or buttock pain. They say, not unsimilar to the physiatrist, that the pain should be severe enough to cause some level of disability. But most studies, if you look at this, just broadly define chronic pelvic pain and fail to even describe the location and duration of symptoms. And to make it more complicated, most of the studies that discuss chronic pelvic pain describe visceral etiologies. And yet, in our own literature, in PM&R, we really speak of pelvic girdle pain, which by definition is musculoskeletal pelvic pain. And that definition, as put forth by Bleming and colleagues in 2008, is defined as pain experienced between the posterior iliac crest to the gluteal fold, particularly in the region of the sacroiliac joint. And that that pain may radiate into the posterior thigh and occur in conjunction with or separately in the pubic symphysis. And what we know about pelvic girdle pain is very specifically the endurance capacity for standing, walking, and sitting is diminished. So this is pelvic pain that is brought on somehow by movement and is relieved by lack of movement. So this overlaps with our OBGYN colleagues and neurology colleagues as it relates to visceral pain. And so when Dr. Jarrell spoke about the differential diagnosis of chronic pelvic pain, he broke it down by system. And I think this still rings true today. What I can tell you is that now we know that if you have one diagnosis, you typically have more than one across the systems. So for example, if a gynecologist is diagnosing endometriosis, we commonly see overlapping pelvic floor myofascial pain, irritable bowel syndrome, interstitial cystitis or painful bladder syndrome, and then comorbid depression and anxiety, not unlike other diagnoses in chronic pain. And this is well described in some recent papers that you can see here. And interestingly, the level of disease that we can sometimes see in patients is often not there. So in this picture, ulcerative interstitial cystitis, for example, is only seen about 10% of the time in women with bladder pain syndrome. And these lesions here on the right showing endometriosis, we know from that literature that those lesions do not correlate with the severity of pain or the level of disability. So what we do know from the work of these great authors on the bottom is that though if you have one diagnosis of chronic pelvic pain, you typically have another diagnosis. And that also overlaps with fibromyalgia, which we commonly see in our world. And this is actually substantiated now with neuroimaging studies. Our colleagues at Northwestern led this charge, Dr. Farmer. They looked at women with interstitial cystitis or painful bladder syndrome, and they compared it to normal healthy controls, and they showed numerous white matter abnormalities that actually correlated with clinical symptoms, which is really helpful. And that included pain severity, urinary symptoms, and impaired quality of life. So this is the first hallmark, at least in some of the clinical work, that there was actual biomarker that correlated with that central sensitization. We know well in the musculoskeletal world that the pelvis is really important in terms of function and movement, and that the pelvis provides the base of stability for the kinetic chain for head, arm, and trunk complex. And that movement, that base allows for transmitting and absorbing forces from top to bottom. We know that the pelvis does rotate during walking to create that rhythmic swing for smooth translation of the trunk to the lower extremities, and the pelvis provides obviously a broad area of support for muscular attachments. And so just to review a little bit of that, we're going to again focus on pelvic floor, but these muscles are also really important. So you can see the iliopsoas here, along with the adductor muscles. And the reason I bring it up is because it's common that when we have pelvic floor myofascial pain in chronic pelvic pain, that we see that these other muscles kick in and try to help out, and they become their own pain generator. We also see problems concomitantly with the piriformis, and especially with the obturator muscles, both the obturator externus and internus. So I'm going to show you how closely linked the obturator internus is to the pelvic floor of the levator ani. We know that from also the work of Lemming that it's very important that we understand both form and force closure within the pelvis, form closure being how naturally the bony elements of the pelvis work together in concert, and force closure, how the ligaments and muscular structures and motor control actually help support that level of stability. But we know especially that the pelvic floor is the floor of the core, and for those of you who know me, I've been saying this for years. We know that the pelvic floor muscles co-activate with other key abdominal and core muscles during many voluntary exercises to maintain lumbopelvic stability. We know that when we take our first step, as I tell the medical students and the residents, the pelvic floor muscles are the first group of muscles to kick in, and that when we sit more upright and seated, we can recruit the pelvic floor muscles more appropriately. We also know from some other work out of the Netherlands that actually over 50% of women with postpartum lumbopelvic pain had some level of pelvic floor muscle dysfunction, and the research is quickly catching up to also show this in other musculoskeletal conditions. This is a great study that was done early on, also out of the Netherlands, where cadaveric models were actually looked at and compared between the male and female pelvices. The pelvic floor muscles were removed and replaced with springs, and then those springs were tightened to look at actually what happens to the sacroiliac joints. And with simulating that tension of the pelvic floor muscles, or stiffness, or contraction if you will, the SI joints were more stable by 8.5% in the female cadavers, but this level of stiffness was not seen in the male cadavers. So just sort of showing the importance of the pelvic floor muscles as it relates to external musculoskeletal structures. So again, the floor, the core, the pelvic floor, yes, the male pelvis also has pelvic floor, but we're going to focus a little bit more on the female pelvis today. Here's both the superficial and deep layer that you can see here on the right, female model. The superficial layer comprised of, also called the urogenital diaphragm, comprised of the ischiocavernosus, the bulbocavernosus, and the transverse peroneal muscles. The deep layer, also known as a levator ani, the Kegel or Kegel musculature, is also threefold, but they work in concert. Just to show you, this is the arcus tendineus here on the left-hand side, and you can see that there, if you go most medial, you have the puborectalis, followed by pubococcygeus, and lateral to that, the iliococcygeus, and very lateral to that, we can see the obturator internus, as well as the piriformis muscle, as previously mentioned. I like the picture on the right, because it really shows that beautiful pelvic sling that connects the anterior musculoskeletal pelvis to the posterior musculoskeletal pelvis, and not just the importance of those muscles to maintain visceral support, but really to connect the musculoskeletal pelvis as a whole. The innervation to the pelvic floor muscles is from the sacral efferents, so mainly S2 through 4. Those direct efferents go right to the levator ani, and then we have the branch of the pudendal coming from there, which dives deep into the pelvis through this little break in the fascia called Alpax canal, comes anteriorly in three branches to innervate the anterior component of the pelvic floor muscles. Those three branches are the nerve to the clitoris, the nerve to the perineum, and then the inferior hemorrhoidal branch. The pelvic floor muscles, and there's some really nice work, and I gave you a reference here from Dr. Tuttle that shows that mainly these muscles are slow twitch type 1 endurance fibers, 70% of the component, the main component of the pelvic floor is that. And it makes sense because these are muscles that always have to be at a low level of contraction to maintain continence. The other component are the fast twitch type 2 fibers, which are the muscle group, of course, that has to act quickly with a sudden movement, with a cough, sneeze, particularly in your athletes that have high increases in interabdominal pressure in order to maintain that continence during that high impact activity. So in general, think of these muscles as muscles that provide not only a protection for continence, but they are muscles that provide support to the visceral structures of the pelvis. They're muscles that are involved in sexual appreciation because they do contract with sexual activity. And also, like any other muscle in the body, right, as I've said to many of you in the past, they can be a source of pain. And that's where we're going to talk about myofascial pain of the pelvic floor. So if you look at what is the normal function of the pelvic floor, it's sort of threefold, right? There's the static baseline activity that provides tonic support. There's contraction and there's relaxation. And we break that down into both voluntary and involuntary contraction and relaxation. The voluntary contraction that everyone knows, the kegel or the kegel, can be performed to prevent urination and defecation. We can teach a patient how to do that. The involuntary contractions, though, is when you cough, sneeze, and naturally we have an increased reflexic activity of the pelvic floor muscles, including the urethral sphincter to maintain continence. Relaxation occurs twofold, voluntarily when you let go of that contraction and then involuntarily when you strain or valsalva to allow for voiding and defecation. So what is the prevalence of pelvic floor myofascial pain? Well, it's really interesting. And I want to just point, with each one of these bullet points, there's a reference for your knowledge. So overall, how common is female chronic pelvic pain? It's about 25% if you look at multiple studies across the board. And this nice article from Lamboo really just summarizes that. But as we move through time, you can see that the better we got at actually assessing the pelvic floor, the more commonly we found it. And I think that's why we're seeing higher levels of prevalence over time. So originally, in the early work by Dr. Tooth, it was documented that in about 900 patients that they examined, that 22% of them had pelvic floor myofascial pain. In a separate urogynecology clinic with Adam's group, they found about 24%. In our own work, we found about 60% of patients who present to a chronic pelvic pain clinic have pelvic floor myofascial pain. And even more recent work, when we combine PM&R with female pelvic medicine and reconstructive surgery, and even teach the urogynecologist how to do a more detailed exam, we have prevalence rates as high as 80%, 85%. So really impressive numbers if we look at these patients. So what is the etiology for pelvic floor myofascial pain? So there's been a lot of discussion about this. We heard from Dr. Shah, the visceral pathology and the convergence of the nerves. So we know that patients who have irritable bowel, that have chronic bladder pain, that have endometriosis, also have pelvic floor myofascial pain. And whether that's a somatic response to the visceral etiology, or the somatic pain generator that creates visceral symptoms is still a hot topic of debate. We also know from the literature that underlying weakness or pelvic floor muscle dysfunction, perhaps over time, can lead to strain. And then over a significant period of time can lead to myofascial pain. We see myofascial pain and overuse injuries, just like other rehab populations where there's overactivity or hypertonicity of the pelvic floor from overusing the muscle. And then we see strain and myofascial pain. And certainly, where it's well described is in trauma and injury, particularly the injury of vaginal delivery. And I'm going to show you some of that data. We know that in women who have had a forceps delivery, when they've had significant third and fourth degree peroneal lacerations, and they've had an eccentric contraction injury, perhaps, they are more likely to have ongoing myofascial pain. We see myofascial pain after numerous abdominal and pelvic surgeries, and of course, after any kind of trauma to the bony pelvis itself. We also think that perhaps pelvic floor myofascial pain is the result of a compensatory response to other musculoskeletal pain. And you've seen from literature of our colleagues and those with hip pathology and lumbar pathology. And from the work that we've done, we know that pregnant women with sacroiliac joint We know that pregnant women with sacroiliac joint pain and postpartum women also have pelvic floor myofascial pain. So there's a difference really between pelvic floor muscle dysfunction, which is abnormal muscle activation patterns versus pelvic floor myofascial pain. And I think it's really important when you're doing your exam that you differentiate the two. Is there tenderness indicative of myofascial pain? And then are there problems with contract, relax, and baseline tone? So these are kind of the types of pelvic floor muscle dysfunction that were defined by Abrams in the standardization report of lower urinary tract symptoms. So these were the people that came together and decided, okay, what's normal muscle function? However, they were thinking it more as it relates to lower urinary tract symptoms, not pain. But they nicely defined that a non-contracting or underactive pelvic floor, which more commonly happens with increasing age and parity, it leads to things like incontinence, which makes sense, leads to things like pelvic organ prolapse potentially as one factor. But the non-relaxing overactive pelvic floor also can potentially lead to stress urinary incontinence, for example, in perhaps a female athlete that's over activating to prevent incontinence. And then the most common thing we see is the non-contracting, non-relaxing pelvic floor, the pelvic floor that also has myofascial pain, and that's the classic chronic pelvic pain patient. These are risk factors for pelvic floor muscle dysfunction. I already kind of talked about them as it relates to etiology of myofascial pain in general. And one thing I just want to point out is that aging also potentially can lead to muscle dysfunction and menopause as it affects, as the lack of estrogen affects the fascia, which therefore can affect myofascial pain. And there are modifiable risk factors for treating at least some of the consequences of these muscle issues. So these things can be used to mitigate the lower urinary tract symptoms. But I love this picture from University of Michigan that shows what happens at the time of vaginal delivery to the pelvic floor muscles and what leads to a pelvic floor muscle injury. So to orient you, you have the pubic symphysis. This blue ball is the fetal head. This red, this red sling here is representing the pubococcygeus and then the other muscles here, and this is showing the vaginal canal where the ball or the fetal head comes out and then also the anal sphincter. And what basically we know from this work is that the pubococcygeus itself has to stretch three times its normal length to accommodate a fetal head. And so what we know because of that is that there are delivery-associated perineal injuries or also known as OASIS in the OB-GYN literature. This work came from Dr. Lewicki Gap, who's now at Northwestern and trained at University of Michigan, and she was able to show that there's an increased risk for OASIS with the instrument of delivery and that pelvic floor myofascial pain was significantly higher in those that sustained those injuries or third or fourth degree tears. It was also higher in patients, as you would expect, that had associated wound problems or infection, and that pain after 12 weeks is not known because this study only went to the 12-week mark. So I'm talking a lot about pelvic floor myofascial pain intentionally because this is something that we haven't trained in as well in PM&R, but we know that it's a part of all the other things we consider in the differential diagnosis of musculoskeletal pelvic pain. It tops the list in terms of myofascial etiology, but we are always trying to rule out other problems, skeletal and joint, SI joint pain, ruling out lumbar and hip pathology, considering neurologic etiologies as listed here, and then also as I previously mentioned, the visceral somatic overlap with other visceral diagnoses. I want to show you that this intake form that I think you'll find really helpful if you go to the International Pelvic Pain Society website, which is free, and you can download, even if you're not a member, you can download these intake forms, which is, they're very comprehensive and really get at the history, description, and contributing factors of pelvic pain and details around relevant history that can affect pelvic pain. So I'm not going to go into that too much because I want to focus on the exam, but I want you to take a look at that when you have time. So the pelvic floor muscle exam is really important. Recently a paper was published in the American Journal of Obstetrics and Gynecology detailing this exam. And what we're doing is a vaginal and sometimes a rectal exam to assess the pelvic floor muscles for tenderness, the quality and coordination of contraction and relaxation both voluntarily and involuntarily, as well as assessing for strength. And we know just in general that chronic pelvic pain typically involves poor relaxation, poor contraction, and tenderness. And we use this pelvic clock to talk to our physical therapy colleagues as we describe where we see the problems. We also inspect, we check sacral sensation, reflexes, the Q-tip test for vulvodynia, and this nicely delineates the different components that as a physiatrist you would go through to make your overall assessment. We know from some earlier work that we did about 10 years ago that when we were blinded to a pain status we could really tell who had pelvic floor myofascial pain and who didn't. That the women who self-reported chronic pelvic pain were more likely to have pelvic floor muscle tenderness on exam. But interestingly in this study at least not necessarily weakness. We also found in an adjunct study to this that those same women were more likely to have diffusely abnormal musculoskeletal findings than women who did not have pain. We took this to an objective level a few years later where we wanted to look at a pain pressure threshold at the level of the pelvic floor. This is a finger showing a pain algometer, a pressure algometer that we use to examine the pelvic floor muscles. We compared women with pain, 14 women, to healthy women. And we were able to show that the mean of pain pressure thresholds for all the sites we tested within the pelvic floor was significantly lower on women who had pain compared to their counterparts who did not. And that was even after we controlled for differences in age and menopausal status. We now have taken it to a second generation model. We're currently in the process of looking at this data. And this device actually not only measures pain pressure threshold which you can see here in the red part of the figure, but also measures EMG or muscle activation patterns. And this is showing in a normal healthy control a nice volitional Kegel. Then when I put place pressure in the red we don't see an increase in pelvic floor muscle contraction because this patient does not have pain. This device is still not available for clinical use, but we're hoping that it gives us some idea of how we might study the muscles more objectively in time. There are some newer devices though that are very exciting. Looking at surface EMG, a couple recent papers, the MAPLE device which you see here on the left has shown to be reliable for not only sidedness, but for location of the pelvic floor muscles. It's only been studied so far in overactive bladder. It was used as a biofeedback like device. It's not yet been studied in pain, but we're hoping to do that. And then a more recent study that just came out this year looked at high definition surface EMG using a very similar probe in women with interstitial cystitis. And they were able to show that those women had a higher resting tone compared with control women. As far as imaging, plain radiographs really don't help us obviously as we're diagnosing pelvic floor myofascial pain. We rely on our exam to do that, but we use the radiographs just to rule out other musculoskeletal problems like you see here like pubic symphysis separation, osteitis pubis on the bottom, any coccyx injuries such as a fracture. MRI is our best test for diagnosing anything else in the musculoskeletal pelvis, but again does not seem yet to be helpful as it relates to myofascial pain. And these are just images showing things like a sacral insufficiency fracture, degenerative disc disease, tendinopathy, pubic rami, stress fracture, and stress reaction. This is also MR imaging that's not typically done clinically, but has been done in the research realm. Also at University of Michigan, this is an image showing at the top pubic body, urethra, vagina, and rectum and showing the levator ani complex they call it. And evidence of what is a levator ani tear or avulsion on the right, bilateral complete levator ani avulsion. Similarly, transperineal ultrasound is really gaining a lot of excitement. Originally it was more in the pelvic floor disorders world, but now it's being looked at more closely in women who had pain, specifically pelvic girdle pain or SI joint pain. And Britt Stueke was able to show with transperineal ultrasound that women who had pain actually had a significantly smaller levator hiatus area. So this line across kind of able to show that idea of pelvic floor muscle tightness or a non-relaxing pelvic floor. So we're moving towards these objective measures of the pelvic floor, which I hope in clinical practice will be much more useful going forward. So I'm just going to run through some of the treatment options you should be considering. I want to point out that in the American Urologic Association, they have treatment guidelines and algorithm, if you will, for painful bladder syndrome. And after some of the things that we know well in rehabilitation, like patient education, behavioral modification, stress management, the second line treatment is physical therapy. And this was shown in a level one study, a randomized controlled trial in women who had pelvic floor physical therapy compared to global massage. And it was found to be significantly better than just the sham control. You're going to hear more about that in the subsequent lecture. So I'll move on to some of the other medical management. But here's some nice references for you. I want you to think about pelvic floor physical therapy as having the greatest amount of evidence for the treatment of pelvic floor myofascial pain. First line treatment, it's typically one session per week for about 12 sessions focused on myofascial release, muscle retraining, biofeedback. We know there are issues with some groups of women who are less likely to participate in pelvic floor PT and be compliant. And so that body of evidence is growing and hopefully we can get better with that over time. The medical treatment of pelvic floor myofascial pain is really not well studied at all. It was really limited to no evidence, or at least randomized controlled trials specific to pelvic floor myofascial pain. There have been studies on neuropathic agents for painful bladder, for example, for vulvodynia. We use all of our tricks as we do in other chronic pain populations, but wide open for research as it relates to pelvic floor myofascial pain. Probably the most common drugs that we use are muscle relaxants and neuromodulators. There was a recent movement looking at a vaginal diazepam, a suppository that's compounded. But that study, a randomized controlled trial last year showed not only is there systemic absorption, but it's probably no better than placebo. And all these topical agents that we use have very little to no evidence to support their use in pelvic floor myofascial pain. What does have more evidence are the injectable options for pelvic floor myofascial pain. So trigger point injections either with saline, with bupivacaine or repivacaine or lidocaine or botulinum toxin. So you can see, and I know I'm running out of time here, but multiple authors have looked at this. And a recent systematic review by Meister in 2020 showed significant promise, particularly with botulinum toxin as it relates to the treatment of pelvic floor myofascial pain. Both significant reductions in pain as well as secondary outcomes like sexual activity and bowel and bladder habits. There are no randomized controlled trials for any of these other types of injections in the treatment of pelvic floor myofascial pain. Although they're widely discussed and utilized, there again is not good evidence to support their use, at least as it relates to pelvic floor myofascial pain. Acupuncture has been studied more in the male pelvic pain literature with actually very good results. We just completed a randomized controlled trial looking at this and specific to women with bladder pain. And there's a fair amount of evidence, particularly in the vulvodynia chronic pelvic pain world for cognitive behavioral therapy. Again, not unlike our other chronic pain populations. So in summary, there's a large differential diagnosis for chronic pelvic pain. We know there's peripheral and central contributing factors. And if you have one pelvic pain diagnosis, you're more likely to have another. But really think about pelvic floor myofascial pain as topping your list for these patients. I think the evidence is mounting that that is true. Our physical exam is getting better and our treatment options are starting to grow. But multidisciplinary multimodal treatment is also really key and particularly including pelvic floor physical therapy, which you'll hear about next. So thank you so much for your time and attention. I really appreciate being involved with AAPMNL. Thank you, Dr. Shaw and Dr. Fitzgerald. I'll be talking about how pelvic health physical therapy can enhance your outcomes and your patients with chronic pelvic pain. I have no relevant financial relationships to disclose. I'm the owner of a private practice, Optimal Motion Physical Therapy in Herndon. I'm also an adjunct professor at the Health Administration and Policy Department at Mason University in Fairfax and a co-investigator with Dr. Shaw at George Mason and also in collaboration with NIH and currently serving as the president of the Academy of Pelvic Health Physical Therapy. As we've kind of talked about, we don't talk about pelvic health enough. Often it gets lost in our clinical care, and what that does is it causes our clients to take a long time to get care, which increases their prevalence of chronic pelvic pain. If we can get to them sooner and get them the treatment they need sooner, their outcomes are better. So Dr. Fitzgerald did a fantastic job of going over the local anatomy and the pelvic floor muscles. We just want to remember when we're screening the sacroiliac joint that the pelvic floor muscles are innervated as 2 to 5, and also don't forget about the abdominals and their innervation in the thoracic spine. So we'll want to do a thoracic spine screen as well, and she talked a little bit, I think, their pudendal alcox canal where the pudendal nerve comes through the obturator fascia and obturator internus. This is the local anatomy, but as Dr. Shaw eloquently described, we want to make sure we're looking neurosegmentally, viscerally, and at the somatic tissue as well. In your history taking, make sure you're also reviewing the red flag questions. Is there any bleeding, any signs of infection, noticeable masses, nocturnal pain or fever, any history of malignancy? What else can we do? So as I mentioned, we're going to do some thoracic spine screening, thoracolumbar, sacral dysfunction. What's getting better? What's not getting better? What's been missed so far? Also talking to them a little bit about their breathing in conjunction with their thoracic spine and their intra-abdominal pressure. Like everything else, pelvic pain is affected by their genetics, their current lifestyle, and their environment. So we want to make sure we're doing a thorough history of their family as well as what's going on with them, cutting down on their stress if need be, caffeine, alcohol, and bladder pain diaries so we can better understand the nature of their pain symptoms. One of the things that I've found helpful and that's also been shown in some of the recent literature regarding testosterone, low testosterone, and bladder pain is that I work with my team to make sure that the patients are looking at their hormones as well. And as we are noticing in our research, the inflammatory analytes can be helpful too. Dr. Fitzgerald did a wonderful job talking about what's happening in the research regarding injections and medications and how to refer appropriately depending on what you're finding in your differential diagnosis. Other questions that we talk about that I think I highlighted anxiety and depression and overall health function is because sometimes we miss this in our looking at the different systems. We look at the GI system, we look at urology, but sometimes we'll miss the anxiety and depression that goes with the chronic pain. And so we'll want to make sure that that's being addressed as well. Other questions that I like to ask is to make sure are they waking up to go to the bathroom in the middle of the night? Have they had any falls or trauma resulting in any other injury besides childbirth to their pelvic floor? If they did have any falls and trauma, were they at night while they were getting up related to increased frequency at night? Do they have any repetitive stress as was discussed earlier by Dr. Fitzgerald, cycling, horseback riding, running, anything that might impact the pelvic floor? Do they have a history of UTIs? Is going to the bathroom painful? What other medications are they on? Sometimes other medications that they're on can be impacting their pelvic health, so it's good to think about the implications of that. Do they have pain during, before, and or after sex in their pelvic floor? Is the pain with sitting or standing? Is the pain can we reproduce that pain? We talked to them about their nutrition as well as their exercise and ask if there's any abuse in their history. What's their menstrual history like besides their pregnancies itself? We talked to them about did they have any abdominal surgeries and how was their pregnancy as well as their childbirth experience? Have they had any other images or testing so that we can rule out what's already been looked at and where we need to go next? I talked to them a lot about their bladder behaviors, urgency, frequency, their fluid intake, and their bowel behaviors, and we measure that through a Bristol scale for them. Do they have constipation which can often impact the pelvic floor and create pelvic pain as well as hip symptom? As we've discussed, there's no specific diagnostic tests that are conclusive. One diagnostic test that's conclusive for chronic pelvic pain but identification and exclusion can help give us some inkling of where we need to go next. Common local referral sites as Dr. Fitzgerald talked about, the levator ani will look more perennial pain. If the coccygeus is involved, often the patient will describe that they feel like they have a full bowel movement and they have more of rectal pain versus vaginal pain. The obturator internus often they'll describe a choking feeling in their hip or a golf ball feeling in their rectum. They have hamstring referral pain. Often they come into me, they've been getting their hamstring treated, but in fact their obturator internus is the driver. As Dr. Fitzgerald pointed out on her anatomy slides, the adductor magnus can be a factor as well and will show pain in the perineum, bladder pain, again that golf ball in the rectum description has also come through, and the pudendal nerve itself will have similar presentation with the golf ball. They'll have pain with bowel movements, constipation, pain with urination, pain with sex. The Monday morning applicable examination as we've talked about, we'll take it through clinical history and physical examination so we can rule things in or out, rule out complications with their sacroiliac joint, lumbar spine, other hip injuries. What do you believe is the primary versus the secondary driver? We do active range of motion, passive range of motion, and strength testing. One of the things that I look at is are they hyper or hypo mobile because either one on either end of the spectrum has been shown to be a factor. Patient reported outcomes measures and quantitative sensory testing as both Dr. Shaw and Dr. Fitzgerald pointed out. Algometry can give you a sense of how sensitized they are to pressure. Aledinia and hyperalgesia, looking at the ultrasound imaging, the MRI studies, the analytes, and the hormones. Here are some questionnaires that I like to use in my practice to help hone in on what is actually causing the pain and to give us some important objective measures. I like the patient-specific functional scale because the patients can really hone in on what's important to them which helps us be able to identify functional treatments that go along with what their functional goals are. What does the recent research show? I think Dr. Fitzgerald did a nice job of talking about physical therapy and what physical therapy can do. The research supports this, that exercise and manual therapy provided under the care of a physical therapist leads to positive outcomes for these patients. Manual therapy, biofeedback, taping and exercise do help in multiple different studies. So what does a pelvic health physical therapy examination entail? So you can help give your patients a look as to what they'll be expecting when they go to physical therapy. We examine the perineum, the vulva, the rectum externally to identify any asymmetries or scarring tissue abnormalities visual or palpable as well as inflammation and sensitization as Dr. Shaw has discussed. to identify tightness, tenderness, the angle of the coccyx may also be a factor. Do they have any trigger points that are identifiable? How's their strength and endurance in their pelvic floor? Can we reproduce their pain on the vaginal or rectal exam? What are the first layer of muscles vaginally or rectally look like as well as the deep muscle layers? Muscle endurance, how many seconds can they hold? Quick contractions, how many quick contractions can they do in 10 seconds? We do a brink score and as Dr. Fitzgerald pointed out, we too look at the pelvic clock and the nice thing is we can all correlate our findings together for a better result for the patient. What does the resting tone look like and the quality of the rest itself? As she pointed out, rest is very important in the pelvic floor so we want to make sure we're assessing not just the contraction but also the de-recruitment and relaxation of the pelvic floor as well. We look at the fascial integrity and one of our collaborators that Dr. Shaw and I collaborate with, Dr. Stucco talks about the importance of the fascial connection and the fascial integrity as well. So what I use in my practice is I use an ultrasound to look at the quality of movement and the tissue texture as well as the sliding and gliding of the tissue. As you can see here, the this is the bladder on the ultrasound and the pelvic floor is underneath it. In the middle what you can see is the patient is contracting and there's a bit of an out pouching on the right side of the screen. So what you can do is correlate that with your clinical findings to see is their hip dysfunction. That's where the hip fascia comes in to play here to the pelvic floor and you can see does that correlate to a weakness on one side or a tightness on the other side which is helpful. And that visual imagery can be very helpful to the patients to be able to train themselves to be able to recruit or de-recruit the muscles of the pelvic floor as well as breathing. Gives you a nice image of the bladder too so they can see how the pelvic floor supports the bladder. And then we look at the sliding and gliding of the abdominal muscles, the transverse abdominis here and the fascial insertions as well as the internal oblique and external oblique. Other things that we do that help give us a full clinical picture, we look at whether something's dysfunctional or functional, painful or non-painful regarding their active range of motion of their upper and lower extremities, strength and endurance of the core and lower extremities. Some recent studies have shown that the pelvic floor in isolation and treating the pelvic floor in isolation does not yield as positive a result as also incorporating core and hip function. For example, abdominal function and glute med function to improve stability around the pelvic floor to help support the pelvic floor. We check myotomes and dermatomes and reflexes, allodynia, hyperalgesia as we've discussed, and the mobility and stability of the sacroiliac joint. And as I mentioned, I'm a big fan of the Bate and Brighton for hypermobility. And here it is if you're not familiar with it. Here's the one that we use in our study. An example of a case presentation because these clients, you know, with chronic pelvic pain can be tricky and can have long-standing symptoms even with multiple treatment avenues. This is a 55-year-old nurse, a mom of two with chronic pelvic pain for 20 years that initially began after a lifting injury at work as a nurse. It was compounded shortly after that by a cycling injury where she was hit by a car. Her images were negative for her lumbar and sacroiliac testing. She was unable to work secondary to her increasing chronic pain, unable to sit, walk, drive or stand for more than 15 minutes without severe pain. And like I said, this went on for many, many years and she had tried multiple different treatments to no avail. She finally got in for physical therapy and we basically assessed her motor control from the top to the bottom. She did have some associated hypermobility. She had, we treated her with some autonomic quieting. At that point she was pretty ramped up and sensitized. We worked on strengthening the hips and the abdominals that were weak. We did some stretching which is pretty common for her iliopsoas and external rotators. As Dr. Shaw and Dr. Lynn Gerber have shown in their prior research, dry needling can be a great way to treat patients with chronic pain. So we did some dry needling with her and it was vastly helpful as well as some postural re-education. As Dr. Fitzgerald pointed out, that can be very important. Changing their posture can engage or quiet the pelvic floor based on your positioning. We utilized the ultrasound very effectively as well as some graded motor imagery. She had had pain so long that she felt like she had really smudged these body parts, her pelvis off her brain map. She wasn't really able to access it and helping her with some mirror therapy and improved her sensitization. And we also referred her, she as many of these patients had some comorbidities related to her GI system and her urology. So we referred her to a urologist and gastroenterologist as well. Other things that helped her was getting some internal biofeedback or intimate fitness as we started calling it. She did really well with the myofascial and the manual treatment as well as vibration. And of course, pain science education has been shown to be helpful in these clients as well. Exercise, I didn't put it on here but it's an obvious one in the literature. Exercise really helps these patients and I want to mention that other clients, we're focusing mainly on females but the male pelvic pain population, there was a study that came out of NIH in May of this year and it showed that daily Cialis was helpful for the smooth muscle and they had a hundred percent positive result with all of their participants in that study. So in a male patient, a male pelvic pain patient that sort of was similar to this patient, that helped him as we coordinated with his doctor to get him on that. And also I have a lot of these clients do self-authoring if they've had trauma, self-authoring by James Pennebaker out of University of Texas. His research has been helpful as well. The take-home basically is that patients can have a good result such as this client here. She is now able to ride horses for two hours a day, shop and have dinner with her family without pain which she wasn't able to do prior to this. I want to applaud you for putting the pelvis back in the body and really appreciate you listening to our talk and hopefully going in Monday morning of next week or tomorrow whenever you're watching this and treating these clients with a good prognosis for you and your clients. The prognosis is best the earlier it's caught. If the client is motivated and active and has intermittent pain relief, if they have limited sitting and are continuing to have sex and have a lot of support, if you're able to provoke their pain and it's non-progressive. Here are some more references in addition to the ones we talked about earlier. I want to thank you. I want to thank our clients. I'd like to thank the Academy, Dr. Shaw and Dr. Fitzgerald as well as again you for putting the pelvis back in the body. I hope your coffee, your pelvic floor, your intuition, and your self-appreciation be strong. Thank you.
Video Summary
The presentation titled "New Frontiers in Chronic Pelvic Pain, Myofascial Pain Syndrome, and Central Sensitization: Advances in the Pain Sciences and Form Management" covers various topics related to chronic pelvic pain. The first speaker discusses traditional insights regarding central sensitization and myofascial dysfunction in chronic pelvic pain from endometriosis. The speaker explains how active myofascial trigger points contribute to nociceptive bombardment and the release of substances that lead to pain and sensitization. They also highlight the poor correlation between disease severity and pain intensity in endometriosis cases and the limited effectiveness of hormonal therapies and surgery in alleviating chronic pelvic pain. The speaker suggests that a mechanism-based evaluation is needed to better understand endometriosis-associated pain. <br /><br />The second speaker focuses on the diagnosis and medical management of chronic pelvic pain from a clinical PM&R perspective. They emphasize the importance of a comprehensive pelvic floor physical examination and discuss the prevalence of pelvic floor myofascial pain in women with chronic pelvic pain. They also summarize the limited evidence for various treatments, including physical therapy, medications, and injections. The speaker highlights the need for further research to better understand and treat pelvic floor myofascial pain. <br /><br />Overall, the presentations provide insights into the complex nature of chronic pelvic pain, including the role of myofascial dysfunction and central sensitization. They stress the importance of a multidisciplinary approach and call for more research to improve diagnostic and treatment strategies for this condition.
Keywords
Chronic pelvic pain
Myofascial pain syndrome
Central sensitization
Pain sciences
Form management
Endometriosis
Active myofascial trigger points
Hormonal therapies
Surgery
Pelvic floor myofascial pain
×
Please select your language
1
English