Inflammatory & Neuropathic Pain

Research in neuropathic pain in endometriosis:
 

"Women with endometriosis and pelvic pain almost always have fine, unmyelinated nerve fibers present in the functional layer of endometrium, and these nerve fibers are also greatly increased in the myometrium. Women without endometriosis almost never have these nerve fibers. These nerve fibers may also play a role in pain generation."  http://www.livingwithendometriosis.org/2010/03/28/nerve-clusters-without-myelin-sheath-found-as-culprit-in-endometriosis/

"Hormones and chemicals released by endometriosis tissue also may irritate nearby tissue and cause the release of other chemicals known to cause pain....Some endometriosis lesions have nerves in them, tying the patches directly into the central nervous system. These nerves may be more sensitive to pain-causing chemicals released in the lesions and surrounding areas. Over time, they may be more easily activated by the chemicals than normal nerve cells are. Patches of endometriosis might also press against nearby nerve cells to cause pain."  https://www.nichd.nih.gov/health/topics/endometri/conditioninfo/Pages/symptoms.aspx

"Blood vessels are innervated by sensory and sympathetic fibres; thus when blood vessels branch to vascularise developing lesions, termed angiogenesis, nerves innervating those blood vessels may also branch (neural sprouting), thereby enabling nerves to invade lesions. Zhang et al suggest that endometriosis is a neurovascular condition much like headache, a concept that was also suggested clinically....Prolonged noxious stimulation of the viscera, for example in a distended bladder, which is normally not a painful stimulus, can evoke increased excitability of viscerosomatic neurones in the spinal cord and subsequently cause pain. Once triggered, this central sensitisation is sustained despite the termination of noxious input, demonstrating that pain may be experienced even in the absence of peripheral noxious stimuli....This establishes central hypersensitivity whereby normal sensory stimuli, in a magnified form, are perceived as pain. This may also result in muscle hyperalgesia, as muscles are closely related to viscera and the nerves. There is also an implication of chemical changes, for example in the central neuromodulator N-Methyl-D-aspartate.
There is also evidence that painful endometriosis can be classified as a mixed inflammatory and neuropathic pain condition or a neurovascular condition, both of which open new avenues for pain relief."  http://bjp.sagepub.com/content/early/2013/03/21/2049463713481191.full

"Although about ten years ago it had been noted that pain can be more severe in patients whose ectopic growths are located near or in richly innervated anatomical sites (rectovaginal septum, uterosacral ligaments) than in patients whose growths invaded less densely innervated tissue (peritoneum and/or ovaries) [4], [5], scant attention was paid to this finding regarding nerves; research and drug development remained focused on the ectopic growths and their immediate external environment (e.g., peritoneal fluid and local inflammation) as the source of the pain....Our group discovered that ectopic growths harvested from ENDO rats and women with established endometriosis develop their own C-fiber (sensory afferent) and sympathetic (autonomic efferent) nerve supply. The supply is derived from nerve fibers innervating nearby territories that sprout branches into the growths [10], [11]. This discovery suggests that, rather than the growths alone, it is the ectopic growth's own innervation that is a major contributor to the maintenance and modulation of pain in established endometriosis [12]. It remains unknown, however, whether this sprouted and thereby abnormal innervation contributes to the initial development of endometriosis-associated pain. If so, painful endometriosis, now recognized as an inflammatory condition [3], could also be considered within the realm of neural dysfunction, i.e., a mixed inflammatory and neurogenic pain, which would alter clinical approaches to the pain.... Our findings strongly support the hypothesis that the invasion of the cysts by sensory and sympathetic fibers is a major contributor to the development of endometriosis-associated pain, which suggests an aggressive clinical strategy of prevention."  http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0031758

In reference to the above study, this article was written by Chandler Marrs, PHD for HormonesMatter.com: 

"If the innervation is associated with endometrial pain, it is possible that curtailing the nerve growth could eliminate, even prevent the pain, but only if this disease process is identified early enough.
In the rat model, innervation developed in phases.  Within the first two weeks of the tissue implant, a cyst developed and initial sensory and sympathetic nerves sprouted.  Over the next weeks, the nerve sprouts became functional and neurogenic inflammation developed. Finally, over weeks four and five, the cysts became wholly populated by functional sympathetic and sensory nerve fibers. Pain ensued. Researchers found that removing the cysts before they reached the functional stage prevented the development of neuropathic pain- the vaginal hyperalgesia.

Although it is not clear what the time course of cyst innervation would be in human women -for rats the entire estrous cycle is 4-5 days, significantly shorter than the female menstrual cycle- it is clear that efforts should be made to identify and diagnose endometriosis significantly sooner than is currently the average.

That would require investigating the causes of dysmenorrhea and not automatically attributing the pain with menstruation to normal premenstrual or menstrual cramping, as is so often the case. Currently, the average time to diagnose endometriosis is nine years. Research suggests that 90% of adolescent girls have dysmenorrhea and 25-38% of adolescent girls with chronic pelvic pain have endometriosis.

If cyst development stages could be identified in women and if endometriosis diagnosed earlier, then removing or treating cysts before fully innervated could prevent a lifetime of what we now know to be neuropathic pain....Though many are loathe to admit it, hormones are likely involved. In many regions of the brain hormones elicit and modulate neurogenesis. Research also demonstrates a role for hormones in spinal and peripheral nerve functioning. As results from this study suggest, hormones may also influence somatosensory nerve growth in the uterine and extra-uterine endometrial tissue. Understanding the role of hormones in the innervation of endometrial tissue could open up entirely new therapeutic options."  http://www.hormonesmatter.com/endometriosis-and-neuropathy/

So what's Europe doing?

Here's a link to the European Society of Human Reproduction and Embryology's guidelines for the management of women with endometriosis:

http://humrep.oxfordjournals.org/content/early/2014/01/15/humrep.det457.full.pdf+html

Excerpts:
""Are hormonal therapies effective for painful symptoms associated with endometriosis? Currently, hormonal contraceptives, progestagens and anti-progestagens, GnRHagonists and antagonists and aromatase inhibitors are in clinical use. With no overwhelming evidence to support particular treatments over others, it is important that the decisions involved in any treatment plan
are individual, and that a woman is able to make these based on an informed choice and a good understanding of what is happening to her body. GnRHagonists, with and without add-back therapy, are effective in the relief of endometriosis-associated pain, but can be associated with severe side effects, which should be discussed with the woman when offering treatment. No evidence exists on the effectiveness of GnRH antagonists for endometriosis-associated pain (Brown et al., 2010). Due to the severe side effects, aromatase inhibitors should only be prescribed to women after all other options for medical or surgical treatment are exhausted."

"Excision of lesions could be preferential with regard to the possibility of retrieving samples for histology. Furthermore, ablative techniques are unlikely to be suitable for advanced forms of endometriosis....Based on the current evidence, the GDG concluded that there is no proven benefit of post-operative hormonal therapy (within 6 months after surgery), if this treatment is prescribed with the sole aim of improving the outcome of surgery (Furness et al., 2004). However, there is also no proven harm of prescribing hormonal therapy after surgery; hence some forms of post-operative hormonal therapy could be prescribed for other indications, as contraception or secondary prevention."

"As a consequence, the lack of clear-cut evidence leads to many research questions. We propose that future research on clinical aspects of endometriosis should include at least: (i) The effectiveness of surgical excision of AFS/ASRM Stage III–IV endometriosis in the treatment of infertility in comparison to direct referral toART, (ii) the diagnostic value of laparoscopy with or without histological verification, (iii) the best way of secondary prevention of endometriosis, (iv) the best management, with respect to both reproductive outcome and pain, of ovarian endometrioma
and of deep endometriosis in women with an active child wish, (v) the use of biomarkers for diagnosis and disease monitoring in endometriosis, (vi) the benefit of anti-adhesion agents in surgery for endometriosis-associated pain, (vii) the clinical management of endometriosis in adolescents, (viii) the psychosocial impact of endometriosis and how this should be addressed: patient-centred care, couple-centred interventions, interventions to improve quality of life, (ix) the definition of
the prerequisites of centres of expertise in the management of endometriosis, and finally, (x) the achievement of an earlier diagnosis of the disease, by raising the awareness amongst primary care specialists, gastroenterologists and internal medicine specialists."

"Several studies have reported a long delay in the diagnosis of endometriosis. Recent studies report, specifically for Europe, an overall diagnostic delay of 10 years in Germany and Austria, 8 years in the UK and Spain, 7 years in Norway, 7–10 years in Italy and 4–5 years in Ireland and Belgium (Ballard et al., 2006; Nnoaham et al., 2011; Hudelist et al., 2012)."











      

Pain Sensivity Related to Brain Structure

 Medscape Medical News

 

"An individual's sensitivity to pain appears to be related to the amount of grey matter in certain regions of the brain, a new study suggests.

"This is the first time that a relationship has been shown between pain sensitivity and brain structure. This initial discovery adds to our basic understanding of brain mechanisms and could lead to clinical implications in pain management," senior author, Robert Coghill, PhD, Wake Forest Baptist Medical Center, commented to Medscape Medical News....

Results showed that individuals with higher pain intensity ratings had less grey matter in the posterior cingulate cortex, precuneus, and areas of the posterior parietal cortex — areas of the brain that contribute to internal thoughts and control of attention.

Pain is very good at getting your attention, but it may be possible to change your pain sensitivity by practicing directing your thoughts elsewhere," Dr. Coghill told Medscape Medical News. "For example, meditation and mindfulness training, in which you learn how to better control your thoughts, has been shown to be associated with a remarkable reduction in pain intensity."

In addition, he said, individuals who have meditated over the long term have been shown to have more grey matter in certain areas. "So it does seem possible to build up grey matter, and train the brain to be less sensitive to pain," he said." http://www.medscape.com/viewarticle/819556?nlid=45823_1882&src=wnl_edit_dail&uac=118924EX

 

Links for tips about mindfulness meditation:

 

http://www.shambhalasun.com/index.php?id=2125&option=content&task=view

 

http://marc.ucla.edu/body.cfm?id=22

 

http://www.ted.com/talks/andy_puddicombe_all_it_takes_is_10_mindful_minutes.html

 

http://meditationscience.weebly.com/what-is-mindfulness-meditation.html

 

http://www.youtube.com/watch?v=yMz_UagXkFk

 

http://www.youtube.com/watch?v=QsFIV4LLYRI

 

http://www.youtube.com/watch?v=hrTeEkXrlQ4

 

 

Endometrial Polyps

"Endometrial polyps are a localized endometrial intrauterine

overgrowth that may be single or multiple, may measure

from a few millimeters to centimeters, and may be sessile or

pedunculated [1]. Endometrial polyps consist of endometrial

glands, stroma, and blood vessels [2]....

There appears to be an association between the finding of

endometrial polyps and other benign diseases including

myomas, cervical polyps, and endometriosis [11,18–20]."  http://www.aagl.org/wp-content/uploads/2013/03/aagl-Practice-Guidelines-for-the-Diagnosis-and-Management-of-Endometrial-Polyps.pdf
 "Polyps: polyps or other growths inside the uterus can act as an obstruction to the outflow of blood during menses. This can increase clotting. These growths can also bleed themselves." http://centerforendo.com/articles/clots.htm 

"Spotting between menstrual cycles is a common symptom of this condition. The menstruation periods may also be very heavy and prolonged in duration. A women with endometrial polyps who has already been through menopause may discover unexpected spotting. Pelvic pain in the presence or absence of menstruation may also be experienced. In some incidences, especially large polyps may cause infertility."  http://www.wisegeek.com/what-are-endometrial-polyps.htm

What does the Endomarch mean to me?

I suffered from endometriosis long before I knew what it was or that I had it. No one should have to go through years of pain, thinking or being told it was "normal." No one should have to go 7-9 years with multiple misdiagnoses before accurate diagnosis is made. No one should have to go through inadequate and at times harmful treatments and yet still end up with the same pain and affliction.

My story, in short form, goes like this:

I had hard times with periods but thought that was normal.
I functioned for a few years, but college found me being more incapacitated.
It got bad enough I finally had to quit a demanding job and find one that was part time with less call.
I still didn't realize how abnormal it was to be that incapacitated. I guess I thought I was weak.

My pain worsened and stretched beyond my period days. "Irritable bowel" symptoms worsened.
The doctor thought of a few diagnoses and tried to treat them but they didn't help.

Friends and family finally convinced me I needed further care.
I saw a nurse practioner who tried a few things and suspected endometriosis.
At this point, my pain was month long with acute episodes during periods- not to mention fatigue, bowel symptoms, etc.- that left me barely able to work at all and bedbound for about 3 days with no sleep because of intractable peritoneal pain.
I was referred to an ob/gyn who could perform surgery.

The ob/gyn wasn't convinced it was endo, but after about passing out, I told the doctor it was time for surgery.
The ob/gyn performed surgery and, to my relief, found endometriosis.
I say relief because there was an explanation for my pain. It had a name.

He ablated the endo he found in the posterior cul de sac and put me on continuous birth control.
I was amazingly better but still had some symptoms.
Unfortunately, those symptoms crept back up again.

After doing all he could for me, he referred me to another doctor who performed excision and did more surgeries on endo patients.
I had another surgery where endo was found on my bladder, uterus, peritoneum, round ligament, and uterosacral ligaments.
My story doesn't end there though.

Years of terrible pain had left me with pelvic floor dysfunction (hypertonic). I still have symptoms that might indicate adenomyosis. I still get uterine polyps. I might still have some endometriosis. I still have some hormonal imbalances. The evil of endometriosis is that it rarely travels alone. It brings its malevolent friends along- pelvic floor dysfunction, interstitial cystitis, adenomyosis, hormonal imbalances, and the list goes on. It has kept me from having the educational, professional, and quality of life opportunities that I would wish for. It's a long and winding road with no end in sight. That's why I march.

I was blessed that my doctors believed my pain and suffering. They kept searching to figure it out and offer treatments to help beyond "take a pill." There are so many myths and misinformation out there. Things that modern research has long since rebutted. I've been told by acquaintances to get pregnant or have a hysterectomy and that would cure me. Endo also seems to be shrouded by silence of being a "female" issue- the way breast cancer once was. If every other commercial seems to be for erectile dysfunction and October can be engulfed in pink, I think endometriosis can be talked about without embarrassment. I believe it is past time for the myths to be dispelled, the misinformation to be corrected, for research to be funded, treatments to be advanced, and better education to the medical community. This is why I march.

Please join me and the other women for

Endomarch on March 13, 2014.

http://www.millionwomenmarch2014.org/

 

EndoMarch 2014

 

A lot of people may have heard of endometriosis but really have no idea what it is or the impact it has on the lives of those with it. Many myths and misconceptions abound. Most endometriosis patients have a delay of 7-9 years before a correct diagnosis is made. Inadequate treatments can leave sufferers with continuing pain and other symptoms that progress over time. It's time for a change.

 

What is it? When is it?

In order to raise awareness and campaign for better research, treatment options, and early detection, a march is being organized for March 13, 2014.

(to see its specific goals see here: http://www.millionwomenmarch2014.org/our-goals-2/)

 

Where is it?

The march is being organized worldwide with the one in the United States taking place in Washington DC.

 

Who is sponsoring it?

 

Drs. Nezhat and the Nezhat Family Foundation
The American Society for Reproductive Medicine (ASRM )
The American College of OB Gyn (ACOG)
The Society of Laparoendoscopic Surgeons (SLS)
The World Endometriosis Society (WES)
American Association of Gynecologic Laparoscopists (AAGL)
American Medical Association (AMA)
World Symposium on Endometriosis (WSE)

 

How can I join?

It's easy and it's free! Simply register online. There are precinct managers for each country/state that you can contact for more information and how you can get involved.

Go here for more information: http://www.millionwomenmarch2014.org/

 

I hope to see you there. Even if you can't come, please participate by spreading the word.

 



Research pathogenesis of endometriosis

Current Concepts and Research in the Pathogenesis of Endometriosis Erkut Attar, M.D. Istanbul University, Istanbul Medical School, Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility P.O.30,CAPA,34272 Istanbul, Turkey Tel/Fax : +90-216-3273245 e-mail: erkutattar@usa.net  Keywords: Endometriosis, Etiology, Pathogenesis, Research Objective: To review the recent basic research and literature from different disciplines as genetics, environmental science, cancer biology and immunology for better understanding the current status of endometriosis. Abstract: Endometriosis is a complex gynecologic disorder that affects nearly 1 in 7 women of reproductive age. Ectopic dissemination of endometrial cells and their subsequent implantation are the mechanisms involved in the development of endometriosis. Despite extensive investigation the pathogenesis of endometriosis is poorly understood. Research on the pathogenesis of endometriosis currently interfaces with four areas of basic research: 1) Genetics; 2) Environmental Science; 3) Cancer Biology; 4) Immunology. In this article current research of these disciplines and their pertinence to endometriosis research were reviewed. Data from these disciplines relevant to endometriosis were summarized and conjunctions were highlighted to provide a better understanding of the pathogenesis Introduction Endometriosis is a chronic disease that affects nearly 1 in 7 women of reproductive age (1). Sampson first described the disease formally in 1921. Then he proposed the hypothesis that the origin of peritoneal endometrial implants was tissue delivered by the retrograde menstruation (2). Retrograde menstruation is a nearly universal phenomenon among cycling women (3,4), but it is not clear why endometrial tissue will implant and grow in the peritoneal cavity of only a subgroup of women. These endometrial cells can respond to ovarian hormones and, therefore undergo cyclic menstrual changes with periodic bleedings. Despite extensive investigation the pathogenesis of endometriosis is poorly understood. Research on the pathogenesis of endometriosis currently interfaces with four areas of basic research:        1) Genetics; 2) Environmental Science; 3) Cancer Biology; 4) Immunology. In this article current research of these disciplines and their relevance to endometriosis research are reviewed. 1. Genetics: 1.1 Oxford Endometriosis Gene Study (OXEGENE) There is increasing evidence that endometriosis has genetic basis. Endometriosis is probably a complex trait, like diabetes mellitus, hypertension and asthma, which implies that the disease is caused by an interaction between multiple genes and environment. Such conditions do not have a clear Mendelian pattern of inheritance and multiple gene loci conferring susceptibility to the condition interact with each other and the environment to produce the phenotype. Oxford Endometriosis Gene Study (OXEGENE) is designed to discover whether there is a genetic cause for endometriosis, and to identify susceptibility loci involved in the development of endometriosis using the linkage analysis. DNA from sisters with surgically confirmed r-AFS stage II-IV disease and their parents are being collected to perform a genome-wide screen. There were 571 Families, 886 patients and 65 collaborators involving this study until the time that this manuscript was in preparation. 1.2 Candidate Genes Nevertheless, the use of linkage analysis alone is often insufficient to localize susceptibility genes in complex traits because of the limited resolution of the method for fine mapping. As a complementary approach, candidate genes need to be investigated in association studies by comparing the frequency of marker alleles in affected cases and normal controls. There are two genetic associations with endometriosis have been reported: 1) Polymorphism in galactose-1-phosphate uridyl transferase (GALT) (5);  2) Null mutation in Glutathione S-transferase M1 (GSTM1)(6,7). Enzymes belonging to the glutathione S-transferase family are involved in the two stage of detoxification of2,3,7,8-Tetraachlorodibenzo-p-Dioxin (Dioxin) which is a potential pollutant for endometriosis development. 1.3  Familial Clustering in Rhesus Monkeys Oxford Group recently made some publications using the epidemiological data that they have collected. Familial tendency of disease supporting the hypothesis that endometriosis has a genetic basis was deserved in these studies(8,9). However, defining the familial tendency more thoroughly in whole population is difficult because surgery is required to establish the diagnosis. The clinical features appearance at surgery and histological characteristics of the disease in the rhesus monkey mimic those in human (10). Therefore, the clearer understanding of the epidemiology and inheritability of the disease may emerge from studying spontaneous endometriosis in rhesus monkey colonies (Macaca Mulatta). Oxford Group is collaborating with California Regional Primate Research Center (CRPRC) and Wisconsin Regional Primate Research Center (WRPRC) to study the epidemiology and inheritability of endometriosis. They have identified 121 (8.3%) affected rhesus monkeys among the autopsy records of the 1459 female animals that they died, aged 4 years of more, in the colony between 1982-1996 at CRPRC. They are trying to determine the familial tendency in these affected animals by analyzing the entire colony records over 9000 females from 1965-1977  (11). Hadfield et al studied the autopsy records of 399 rhesus monkeys that died in the WRPRC colony between 1980 and 1995 and reported a prevalence rate of 20% in animals aged 4 years or older at death and 29% in animals aged 10 years or older at death (12). 2.      Environmental Science 2.1 Dioxin Dioxin is a potent chemical toxicant, which serves as the reference compound for a large class of halogenated aromatic hydrocarbons. The dioxin connection to endometriosis was discovered almost by accident. The aim of the original study was to investigate the long-term reproductive effects of  exposure to dioxin in the rhesus monkeys. Twelve years after the initiation of this work, in 1989 endometriosis was discovered at the autopsy of a dioxin exposed animal. The major source of dioxin in the environment (95%) comes from incinerators burning chlorinated wastes. Dioxin pollution is also affiliated with paper mills, which use chlorine bleaching in their process and with the production of Polyvinyl Chloride (PVC) plastics. The major sources of dioxin are in diet. Since dioxin is fat-soluble, it bioaccumulates up the food chain and it is mainly (97.5%) found in meat and dairy products. Men have no ways to get rid of dioxin other than letting it break down according to its chemical half-lives. Women, on the other hand, have two ways which it can exit their bodies: It crosses the placenta into the growing infant causing recurrent pregnancy loss and it is present in the fatty breast milk, which is also a route of exposure which doses the infant. 2.2 Experimental endometriosis in Rhesus Monkeys Now new thinking about endometriosis has been stimulated by research linking dioxin exposure to the disease in rhesus monkeys. In rhesus monkeys the disease develops spontaneously and resembles the human disease both anatomically and clinically. Scientists who have been studying the disease for two decades or more, unsuccessfully seeking a cause consider the recognition of dioxin as a contributor to the disease in rhesus monkeys a exciting breakthrough. It seems that there is a dose response relationship between the dioxin and severity of endometriois(13) Reproductivity of these monkeys was also affected when they exposed to high levels of dioxin. Fetotoxicity was also reported in rhesus monkeys exposed to dioxin (14) 2.3 Genetics and Dioxin Target genes for the action of dioxin include cytochrome p450 and growth regulatory genes involved in both inflammation and differentiation, including plasminogen  activator inhibitor-2 and interleukin-1b. (15,16). As it was previously stated in this chapter, glutathione S-transferase M1 (GSTM1) is responsible for detoxification of dioxin that is a candidate gene for endometriosis development.  2.4  Reproductive System and Dioxin Dioxin is also modulates various hormone receptor systems which play a role in uterine function, including estrogenreceptor, progesterone receptor, epidermal growth factor  receptor and prolactin receptor (17,18) . Moreover this toxin alters the action of estrogen in reproductive organs in a manner which is both age-dependent and target organ specific (18,19). It modulates steroid receptor expression resulting in altered tissue specific responses to hormone(18) . 2.5 Immune System and Dioxin In addition to effects on the reproductive system, dioxin is also adversely effect immuncompetence(20,21,22,23,24) Dioxin shows immunosuppressive activities and is a potent inhibitor of T-lymphocyte function(22,23,24). 3. Cancer Biology While it is not a malignant disorder, endometriosis exhibits cellular proliferation and invasion. Invasive phenotype in endometriosis shares aspects with tumor metastasis (25). T cell mediated invasion may be similar to that which occurs with metastatic neoplasia, where in immune surveillance systems are inadequate or unable to respond the seeding tissue (26,27). Accumulation of various growth factors and the occurrence of angiogenesis to produce a self contained blood supply are the features that implicate the relationship of cancer biology and ectopic endometriotic tissue development. 3.1 Angiogenesis Endometrial tissue develops its own vascular supply and becomes an independent, growing mass. In ways similar to the spread of neoplasm, a piece of implanted tissue may subsequently break off from the primary site and travel elsewhere in the peritoneal cavity, setting up a peritoneal location or may enter a blood or lymph vessel and disseminate to distant body sites. As the free floating pieces of endometrial tissue themselves implant, grow, and develop their own blood supply, the process repeats itself. Endometriosis is one of the family of angiogenic diseases and excessive endometrial angiogenesis is proposed as an important mechanism in the pathogenesis of endometriosis. Evidence is reviewed for the hypothesis that the endometrium of  women with endometriosis has an increased capacity to proliferate, implant and grow in the peritoneal cavity. Data is summarized indicating that the endometrium of patients with endometriosis shows enhanced endothelial cell proliferation. Results are also reviewed indicating that the cell adhesion molecule integrin alpha(v)betha3 is expressed in more blood vessels in the endometrium of women with endometriosis when compared with normal women (28). Taken together, these results provide evidence for increased endometrial angiogenesis in women with endometriosis when compared with normal subjects (29). Endometrium is a rich source of growth factors which promote angiogenesis including the fibroblast growth factors, FGF1 and FGF2 and the vascular endometrial growth factor (VEGF) (30,31,32). Dysmenorrhoea is associated with increased plasma levels of vasopresssin (33,34). Vasopressin induced uterine contractions, but also increases contractility of the uterine resistance artery (35). In addition other peptides including oxytocin, endothelin and noradrenalin contribute to this action on blood levels. The consequence is a large reduction in blood flow in the uterus particularly to the endometrium during uterine contractions. Hypoxia is a critical activator of genes, especially for VEGF and results increased translation for VEGF protein in glandular and stromal cells of endometrium (36) . Thus, the greater hypoxia in the uteri of women with severe dysmenorrhoea results in increased production of VEGF, facilitating angiogenesis at the implantation site of desquamated endometrium. (fig 1) figure 1 3.2 Extracellular Matrix Remodeling Essential features of endometrial physiology involve extracellular matrix (ECM). In the pathogenesis of endometriosis interactions of endometriosis cells with ECM can be postulated. Indeed, it has been shown that extracellular matrix (ECM) turnover in the patients with endometriosis is altered (37). A group of enzymes, matrix mettaloproteinases (MMP) are responsible for extracellular matrix and endometrium remodeling. Tumor promotors, growth factors, cytokines, steroids and oncogenes regulate them. Suppression of MMP inhibits establishment of ectopic lesions by human endometrium (38). It has been shown that MMP-1 expression is correlated with the activity of endometriotic tissue suggesting its involvement in tissue remodeling and reimplantation of endometriotic lesion (39) and endometriotic implants express the protease enabling the invasion of surrounding tissue (40). Adhesion to peritoneum has to occur with subsequent implantation and proliferation. Therefore, specific cell adhesion receptors and their extracellular matrix ligands are being investigated to understand the invasive features of endometriosis. Cell adhesion molecules fall into 4 major groups including cadherins, selectins, members of immunoglobulin superfamily and integrins that each may potentially play a role in the development and progression of disease(41,42). 3.3 Apoptosis Programmed cell death (apoptosis) has been implicated in the pathogenesis of endometrium. Several investigations have revealed that uterine endometrium in mammals can be regulated by apoptosis. It has been suggested that decreased susceptibility of endometrial tissue to apoptosis contributes to the etiology or pathogenesis of endometriosis (43). The increased proportion of Bcl-2 positive macrophages found in women with endometriosis may predispose these cells to resist apoptosis (44) . The continued survival of these active cells could have important consequences for the survival and proliferation of the ectopic tissue. Decreased apoptosis in endometrial cells of  the patients with endometriosis may lead to acquiring the capacity to utilize the products of an activated immune system to establish ectopic foci of disease. 4.  Immunology There are many immune and inflammatory changes relevant to endometriosis that can be considered as a cause and/or result of the disease development. Genetic characteristics and environmental (dioxin) factors could be responsible for the altered immune functions and disease development in patients with endometriosis. Because the ectopic implants of endometrial tissue are destroyed by a variety of immune and inflammatory reactions, research on cancer biology is a part of the  full understanding of the disease development as it was emphasized in section 3, previously. Nonetheless, altered macrophage functions itself and the role of peritoneal fluid have a special impact on the current endometriosis research. 4.1 Altered Macrophage Functions Unlike the situation seen in women without endometriosis, in women with endometriosis the macrophages do not appear to be as active in the phagocytosis ad cellular debris. They do, however secrete high concentration of substances as growth factors that restrict natural killer activity, increase angiogenesis and fibrosis and induce endometrial cell proliferation in vitro. As a cause of infertility in the patients with endometriosis, these changes in peritoneal milieu could also be responsible for the failure of fertilization, embryo development and implantation. 4.2 Paracrine Changes in the peritoneal environment of women with endometriosis Macrophage derived substances such as prostanoids, cytokines, growth factors and angiogenic factors have been detected in the peritoneal fluid of women with endometriosis. In paricular growth-promoting and angiogenic factors are considered to be substantially involved in the pathogenesis of endometriosis (fig.2). figure 2 Interleukin 8 (IL-8) is a chemoattractant and activating factor for human neutrophils and a potent angiogenic agent. IL-8 concentrations in peritoneal fluid show higher levels in patients with endometriosis according to the stage of the disease compared to the control. However potential source of IL-8 in peritoneal fluid are not only the macrophages but also mesothelial cells of the peritoneum and endometrium itself. We found that cultured mesothelial cells constitutively express IL-8 mRNA and secrete IL-8 protein, and the expression of IL-8 from mesothelial cells is modulated by other cytokines such as  IL-1, TNFa . These latter cytokines appear to play some role in the constitutive secretion of IL-8 as well as being capable of greatly stimulating further production and secretion (45). Peritoneal macrophages therefore play an important role in the initiation of the pathogenic cascade as a sources of IL-1 and TNF-a.   Monocyte Chemotatctic Protein-1 (MCP-1) is also an active participant in the pathogenesis of endometriosis.  The level of the MCP-1 levels was found significantly higher in patients with severe disease. We have observed that the elevated MCP-1 levels in peritoneal fluid of the patients with endometriosis  may play a role in growth and maintenance of ectopic endometrial tissue by directly stimulating endometrial cell proliferation (46). VEGF is a growth factor related to angiogenesis and released in response to hypoxia. The role of VEGF on endometriosis was discussed previously in this article. Thus, it may reflect a connection between the retrograde menstruation and /or dysmenorrhoea and changes in peritoneal fluid. Activated macrophages in the peritoneal cavity produce large amount of VEGF. (47) 5. Conclusion It is likely that endometriosis is a common multifactorial disease, caused by an interaction between multiple gene loci and environment. Causes of immune or inflammatory deficiency may be related to the effects of stress on immune functioning, or may be genetically determined. Environmental factors such as Dioxin can be responsible for immunosuppressive activities in patients with endometriosis. In addition this toxin modulates steroid receptor expression resulting in altered tissue specific responses to hormones. Chronic immunosuppression in combination with hormonal regulation may have facilitated the aberrant growth of endometrial tissue with in the peritoneum. Basic research on the field of cancer biology currently interfaces with the pathogenesis of endometriosis and this may lead to a better understanding of disease etiology. It seems that the genetical, environmental, immunological and hormonal (Autocrine and Paracrine) factors interfere each other and, implicating that a circle occurred could be responsible for the development and progression of endometriosis. However, the mechanism appears to require endometrium and retrograde menstruation in most cases of disease. In conclusion, we have just started to bring together the more obvious clinical observations as retrograde menstruation and/or dysmenorrhoea and results of the basic research on genetics, cancer biology and immunology to explain the  disease (fig. 3).  figure 3 LITERATURE 1.      Klotz M.M.: Dysmenorrhea, endometriosis and pelvic pain . In: Lemcke D.P., Pattison J., Marshall L., Cowley D.S., eds. Primary care of women . Norwalk: Appleton & Lange, 1995:26 2.      Sampson J..A: Peritoneal endometriosis due to dissemination due to menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 1927; 14:422-69 3.      Halme J., Hammond M., Hulka J., Raj S., Talbert L.: Retrograde menstruation in healthy women and in patients with endometriosis. Obstetrics and Gynecology, 1984; 64:151-154 4.      Kliman H.J., Arici A., Olive D., Meaddough E.L., Ahn K.S., Comite F., Attar E.: Endometrial glandular cells are found equally in the peritoneal fluid of women with or without endometriosis. American Society for Reproductive Medicine, Seattle, WA, October,1995 5.      Cramer D.W., Hornstein M.D., Ng W.G., Barbieri R.L. Endometriosis associated with the N314D mutation of galactose-1-phosphate uridyl transferase (GALT). Mol Hum Reprod 1996; 2:149-52 6.      Baranova H., Botorishvilli R., Canis M., et al. Glutathioe S-transferase M1 gene polymorphism and susceptibility to endometriosis in a French population. Mol Hum Reprod 1997;3:775-80          7.      Baranov V.S., Ivaschenko T., Bakay B.., et al.  Proportion of the GSTM1 0/0 phenotype in some Slavic populations and its correlation with cystic fibrosis and some multifactorial diseases. Hum Genet 1996;97:516-20) 8.      Kennedy S., Mardon H., Barlow D.: Familial endometriosis, J Assist Reprod Genet 1995;12(1):32-4         9.      Kennedy S., Hadfield R., Mardon H., Barlow D. Age of onset of pain symptoms in non-twin sisters concordant for endometriosis, Hum Reprod 1996;11:403 10.  MacKenzie W.F., Casey H.W. Animal model of human disease. Endometriosis. Animal Model: endometriosis in rhesus monkeys. Am J Pathol 1975; 80:341-4 11.  Stephen K Smith. Genetic factors in Endometriosis pathogenesis and work-up. In Female Infertility Therapy Current Practice, Eds Shoham Z., Howles V.M., Hackobs H.S., London 1997 Martin Dunitz LTD 363-371 12.  Hadfield R.M., Yudkin P.L., Coe C.L., et al. Risk Factors for endometriosis in the rhesus monkey (Macaca Mulatta). A case control study. Hum Reprod Update 1997;3:109-15 13.  Sherry E. Rier at all: Endometriosis in rhesus monkeys (Macaca Mullata) following chronic exposure to 2,3,7,8-Tetraachlorodibenzo-p-Dioxin. Fundamental and applied toxicology ,1993;21:433-441 14.  McNauly W.P. Fetotoxicity of 2,3,7,8-Tetraachlorodibenzo-p-Dioxin (TCDD) for rhesus macaques (Macaca Mulatta). Am J Primatol, 1984;6:41-47 15.  Whitlock J.P.: Genetic and molecular aspects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin. Ann Rev Pharmacol 1990; 30:251-2         16.  SutterT.R., Guzman K. Dold K. M. And Greenlee W.F.: Targets for dioxin: Genes for plasminogen activator inhibitor-2 and interleukin-1b. Science 1991; 254:415-419 17.  Jones M.K., Weinsenburger W.P., Sipes I.G. and Russel D.H.: Circadian alterations in prolactin, corticosterone and thyroid hormone levels and downregulation of prolactin receptor activity 2,3,7,8-Tetrachlorodibenzo-p-dioxin. Toxicol Appl Pharmacol 1987;87:337-352              18.  Safe S., Astrorff B., Harris M., Zacharewski T., Dickerson R., Romkes M. And Biegal L: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related compounds as antiestrogens: Characterization and mechanism of action. Pharmacol Toxicol 1991;69: 400-409 19.  DeVito M.J., Thomas T., Martin E., Umbreit T.H., and Gallo M.A.: Antiestrogenic action of 2,3,7,8-Tetrachlorodibenzo-p-dioxin: Tissue-specific regulation of estrogen receptor in CDI mice. Toxicol Appl Pharmacol 1992;113:284-292 20.  Allen J.R., Barsotti L.K., Lambrecht L.K. And Van Miller J.P. Reproductive effects of halogenated aromatic hydrocarbons on non human primates. Ann NY Acad Sci 320:419-425,           21.  Bowman R.E., Schnatz S.L., Weerasinghe N.C.A., Gross M. and Barsotti D.: Chronic dietary intake of 2,3,7,8-Tetraachlorodibenzo-p-Dioxin (TCDD) at 5 or 25 parts Per trillion in the monkey: TCDD kinetics and dose-effect estimated reproductive toxicity, 1989;18:243-252                          22.  Holsapple M.P., Snyder N.K., Wood S.C., and Morris D.L.: A review of 2,3,7,8-Tetraachlorodibenzo-p-Dioxin-iduced changes in immunocompetence: 1991 update. Toxicology 1991;69:219-255        23.  Neubert R., Jackob-Muller U., Stahlmann R., Helge H. and Neubert D.: Poyhlogenated dibenzo-p-dioxins and dibenzofurans and the immune system. Arch Toxicol 1991;65:213-219        24.  Tomar RS.  Kerkvliet N.I.: Reduced T-helper cell function in mice exposed to 2,3,7,8-Tetraachlorodibenzo-p-Dioxin (TCDD). Toxicol Lett 1991;57:55-64 25.  Starzinski-Powitz A., Gaetje R., Zeitvogel A., et al: Tracking cellular and molecular mechanisms involved in endometriosis. Hum Reprod Update 1998 Sep-Oct; 4(5):730-5 26.  Gaetjii R., Lotzian S., Hermann G., et al.: Invasiveness of the endometriotic cells in vitro. Lancet 1995; 346:1463-64  27.  Dmowski W.P., Braun D., Gebel : The immun system in endometriosis. In: Rock J., ed. Modern Approaches to Endometriosis. New York: Kluver Academic Publishers, 1991:97 28.  Hii L.L., Rogers P.A. Endometrial vascular and glandular expression of integrin alpha(v)beta3 in women with and without endometriosis. Hum Reprod 1998;13(4):1030-5 29.  Healy D.L., Rogers P.A., Hii L., Wingfield M.: Angiogenesis: a new theory for endometriosis. Hum Reprod Update 1998 ; Sep-Oct; 4(5):736-40 30.  Ferriani R.A., Charnock-Jones D.S., Prentice A., Thomas E.J., Smith S.K. Immunohistochemical localization of acidic and basic fibroblast growth factor in human normal human endometriun and ednometriosis and the detection of their mRNA by polymerase chain reaction. Hum Reprod 1003;8:11-16.             31.  Charnock Jones D.S., Sharkey A.M., Rajput-Williams A.C. et al: Identification and localization of alternately spliced mRNAs for vascular endohelial growth factor in human uterus and steroid regulation in endometrial carcinoma cell lines. Biol Reprod 1993; 48:1120-8 32.  Sangha R.K., Xiao Feng L., Shams M., Ahmed A. Fibroblast growth factor receptor-1 is a critical component for endometrial remodeling: Localization and expression of basic fibroblast growth factor and FGF-R1 in human endometrium during the menstrual cycle and decreased FGF-R1 expression in menorrhagia. Lab Invest, 1997;77389-402 33.  Akerlund M., Stromberg P., Forsling M-L., Primary dysmenorrhoea and vasosupresssion. Br Obstet Gynaecol. 1979;86:484-7            34.  Ekstrom P., Akerlund M., Forsling M., et al. Stimulation of vasopressin releases in women with primary dysmenorrhoea and after oral contraceptive treatment-effect on uterine contractility. Br J Obstet Gynaecol 1992;99:680-4 35.  Ekstrom P., Alm P., Akerlund M. Differences in vasomotor responses between main stem and smaller branches of the human artery Acta Obstet Gynaecol Scand 1991;47:484-7 36.  Dmowski W.P.: Immunological aspect of endometriosis. Int J Gynaecol Obstet 1995;50 (supp1):S3-10 37.  Sillem M., Prifiti S., Neher M., Runnebaum B.: Extracellular matrix remodeling in the endometrium and its possible relevance to the pathogenesis of endometriosis. Hum Reprod Update 1998 Sep-Oct; 4(5):730-5 38.  Bruner K.L., Matrisian L.M., Rodgers W.H., Gorstein F., Osteen K.G. . Suppression of MMP inhibits establishment of ectopic lesions by human endometrium in nude mice. J Clin Invest 1997;15;99(12);2851-7 39.  Kokorine I., Nisolle M., Donnez J., Eeckhout Y., Courtoy P.J., Marbaix E. Expression of interstitial colagenase (matrix metalloproteinase-1) is related to the activiti of human endometriotic lesions. Fertil Steril 1997;68(2):246-51 40.  Wenzl R.J., Heinzl H. Localization of matrix metalloproteinase-2 in uterine endometrium ad ectopic implants. Gynecol Obstet Invest 1998;45(4):253-7 41.  Lessey B.A., Young S.L. Integrins and other cell adhesion molecules in endometrium and endometriosis. Semin Reprod Endocrinol 1997;15(3):291-9             42.  Regidor P.A.,Vogel C., Regidor M., Schindler A.E., Winterhager E. Expression pattern of  integrin adhesion molecules in endometriosis and human endometrium. Hum Reprod Update1998;4(5):710-8 43.  Gebel H.M., Braun D.P., Tambur A., Frame D., Rana N., Dmowski W.P. Spontaneous apoptosis of endometrial tissue is impaired in women with endometriosis. Fertil Steril 1998;69(6):104-7 44.  McLaren J., Prentice A., Charnock Jones D.S., Sharkey A.M., Smith S.K. Immunolocalization of the apoptosis regulating proteins Bcl-2 and Bax in human endometrium and isolated peritoneal fluid macrophages in endometriosis. Hum Reprod 1997;12(1):146-52 45.  Arici A., Tazuke S.I., Attar E., Kliman H.J. and Olive D.L. Interleukin-8 concentration in peritoneal fluid of patients with endometriosis and modulation of interleukin-8 expression in human mesothelial cell. Mol Hum Reprod 1996;2:40-45 46.  Arici A., Oral E., Attar E., Tazuke S.I. and Olive D.L. Monocyte Chemotactic Protein-1 concentration in peritoneal fluid of women with endometriosis and its modulation of expression in mesothelial cell. Fertil Steril 1997;67(6):1065-1072 47.  McLaren J., Prentice A., Charnock-Jones D.S., Smith S.K.. Vascular endothelial growth factor (VEGF concentrations are elevated in peritoneal fluid of women with endometriosis. Hum Reprod 1996;11:220 From endometriosiszone.org

Pelvic Floor Spasm

You hear a lot about strengthening the pelvic floor muscles, but for many of us this does harm. The pelvic floor muscles may be weak due to them being too tight!

"...the very large oversight is that tight or hypertonic pelvic floor muscle will register as “weak” because it is unable to generate force due to the fact that this muscle is already in its tightest (and shortest) position." http://www.katysays.com/atootightpelvicfloor/

(There is a lot that goes on in the pelvis.)

So why does this happen?

"When the brain perceives an irritation in the pelvis it sends a signal down to the pelvic floor muscle to "protect" your pelvis. This signal puts your pelvic floor muscle in an involuntary contraction.
The irritation may start with a bladder infection, vaginitis, endometriosis, recent surgery, irritable bowel, or interstitial cystitis (breakdown of the bladder lining). Sometimes, the brain sends an exaggerated response. Other times the brain continues to send a dysfunctional signal to the pelvic floor to stay in contraction, even after the original problem has cleared up, healed or been controlled. This dysfunctional continuous signal is believed to happen because the brain perceives the discomfort of the contraction as an irritation and it becomes a vicious cycle of involuntary nerve and muscle response. (In actual fact, it is not so much a signal to contract, but lack of a signal NOT to contract).
Over time the pelvic floor muscle becomes tender from being in a chronic tetanic contracted state, a condition we call pelvic floor spasm."  http://www.whconnection.com/bladder-problems-and-pelvic-prolapse/pelvic-floor-problems/what-is-pelvic-floor-spasm

"Many women with endometriosis have tight painful pelvic muscles. Sometimes pain from spasm in these muscles is worse than the pain from their endometriosis. It can be confusing, too, because painful muscles don’t show at a laparoscopy or on an ultrasound scan. They are a good example of a pain you can’t see. When the muscles around the opening of the vagina are tight, sex becomes painful. It may also be painful using a tampon, or having a cervical smear test. When the muscles on the side of the pelvis become tight, there may be sudden sharp pains on one side. The pain can come at any time, can make it difficult to walk, may also be felt down the leg on that side and is often better with a heat-bag or hot bath...." http://www.drsusanevans.com.au/physiotherapy-for-pelvic-pain-with-dr-patricia-neumann-and-ms-sonia-scharfbillig/

This can lead to problems with chronic pain, spasms, trouble with peeing or defecating, and so on.

"Nonrelaxing pelvic floor dysfunction is not widely recognized. Unlike in pelvic floor disorders caused by relaxed muscles (eg, pelvic organ prolapse or urinary incontinence, both of which often are identified readily), women affected by nonrelaxing pelvic floor dysfunction may present with a broad range of nonspecific symptoms. These may include pain and problems with defecation, urination, and sexual function, which require relaxation and coordination of pelvic floor muscles and urinary and anal sphincters. These symptoms may adversely affect quality of life. Several terms such as pelvic floor tension myalgia, piriformis syndrome, and levator ani syndrome³ have been used to describe this entity, but the term nonrelaxing pelvic floor dysfunction may be preferable because it will help the clinician identify a recognizable pattern of symptoms....Women with these disorders tend to have the dysfunctions diagnosed and managed by specialists who usually focus on symptoms pertaining to their expertise (eg, urologists for bladder problems, gastroenterologists for defecatory problems, physiatrists for low back or pelvic pain)....Pelvic floor rehabilitation with neuromuscular education is the cornerstone of therapy for women with nonrelaxing pelvic floor dysfunction. Therapy is ideally provided by a physical therapist with training in pelvic floor dysfunction. The specific therapy used is guided by symptoms and usually includes strategies to optimize lumbopelvic and spinal function and to improve bowel, bladder, and sexual function. Manual techniques may include trigger point massage, myofascial release, strain-counterstrain, and joint mobilization, among others.³¹, ³⁷ In addition, exercises to strengthen and stabilize the core muscles usually are included with pelvic floor physical therapy. A resource to help clinicians identify physical therapists who specialize in pelvic floor dysfunction may be found at the American Physical Therapy Association's Web site (www.womenshealthapta.org/plp/)."  http://www.mayoclinicproceedings.org/article/S0025-6196(11)00024-3/fulltext

 

"A patient with high-tone pelvic-floor muscle dysfunction experiences sudden and involuntary contractions of the levator ani muscles, or pelvic-floor muscles, which hold the bladder, uterus, vagina and rectum in place like a hammock. These spasms also can occur in the obturator internus muscles, which control the rotation of the leg and are closely related to the levator ani muscles....Patients who have interstitial cystitis, endometriosis, vulvodynia or fibromyalgia also appear more susceptible...."  http://www.christianacare.org/pelvicfloormuscledysfunction

 

(Did anyone else at first glance think it looked like the gloved hand was punching the pelvic floor??)

Here is a good article on pelvic floor spasm and its treatment:

Pelvic Floor Spasm: The missing link in chronic pelvic pain

Publish date: OCT 01, 2012

 

By: Patrice M. Weiss, MD and Jennifer Rich, MS, PT and Eric Swisher, MD

"Acute or chronic pelvic pain is often due to musculoskeletal disorders, which may go unrecognized during a traditional pelvic examination. Proper evaluation facilitates the diagnosis of spasm or trigger points, and physical therapy often achieves a major improvement in quality of life for these women....

The pelvic floor consists of striated muscles, ligaments, and connective tissues that support the pelvic organs against gravity and intraabdominal pressure. The pelvic diaphragm is composed of the coccygeus muscle posteriorly and the levator ani anterolaterally. Although they are not fully distinct, the components of the levator ani consist of the iliococcygeus, the pubococcygeus, and the puborectalis muscle group. The pelvic floor must allow relaxation of this support at the urogenital hiatus during voiding and parturition while maintaining the anatomic position of pelvic structures. The complex mechanics of its bimodal function and frequent insults to the integrity of the pelvic diaphragm from gravity, daily activities, and vaginal birth contribute to the pelvic musculature’s vulnerability to damage and injury. Lying within the pelvic cavity are the piriformis, and obturator muscles, which are not elements of the pelvic diaphragm but may contribute to pelvic pain when injured.⁵

Pelvic floor hypertonus may be the primary cause of pelvic pain in some patients; in others it may simply be a response to the underlying pelvic disorder.⁶ Several mechanisms of injury may lead to spasm of the pelvic floor. These include, but are not limited to, traumatic vaginal delivery, pelvic surgery, positional insults such as prolonged driving or occupations that require prolonged sitting, gait disturbances, traumatic injury to the back or pelvis, and sexual abuse. Malalignment of the pelvis, especially in the sacroiliac joint, due to trauma, poor posture, pelvic floor deconditioning, muscular asymmetry, or excessive athletics also may contribute to muscular dysfunction of the pelvis.

Injury leading to myofascial pain begins with an acute phase, characterized by inflammatory and immune responses. The injury may perpetuate itself with spasm promoting further inflammation, neurotransmitter release, and central nervous system sensitization. As the injury evolves, the second stage is the musculodystrophic stage, during which fibrosis develops and the process favors a chronic syndrome.

Pelvic floor dysfunction can also arise in response to other common chronic pain syndromes, such as endometriosis, irritable bowel disease, vulvodynia, and interstitial cystitis. A prospective evaluation of patients with chronic pelvic pain of various etiologies found abnormal musculoskeletal findings in 37%, versus 5% of controls.⁷ For this reason, the pelvic floor should be included in any evaluation regardless of the suspected source of pelvic pain....

The treatment of symptomatic pelvic floor hypertonus begins with rehabilitation of the neuromuscular unit or neuromuscular reeducation using biofeedback, muscle relaxation techniques, and soft-tissue manipulation. During the therapist’s manipulation of the affected pelvic floor musculature, the patient is asked to contract and relax. Verbal and tactile cues are used to help the patient recognize when she has appropriately controlled the pelvic floor. External or intravaginal electrodes may be used to monitor the electrical activity of the pelvis and provide visual or auditory biofeedback as the patient attempts to contract or relax. A key objective of neuromuscular reeducation is to improve the patient’s proprioceptive awareness of the pelvic floor. Once a woman is able to recognize contracted versus relaxed pelvic musculature, she is better able to control the pelvic floor.

Physical therapy modalities for chronic pelvic pain also include massage, ultrasound, and myofascial release. Therapists may perform intravaginal soft tissue work as well as manual stretching, although these techniques are most beneficial in the presence of trigger points, banding, or contractures. Massage tools allow self-treatment at home on a more frequent basis. A crystal wand is one of the most commonly used devices for independent therapy of the pelvic floor. In some cases, therapeutic exercise may address musculoskeletal imbalances, and neuromuscular stimulation is used to relieve persistent spasm.

No single modality for pelvic floor therapy has proved to be superior, perhaps because most physical therapists take a multifaceted approach to this complex disorder. Although most treatment options can be applied to almost any patient, our experience suggests that generalized hypertonus usually responds best to generalized therapy (such as strengthening, stretching, biofeedback, ultrasound), whereas trigger points and other focal anomalies more often require manual therapy (such as myofascial release, crystal wand manipulation, trigger point injection). Substantial overlap exists, and a multimodal approach is therefore typical. Some therapy options, such as intravaginal manual therapy, may not be acceptable to all patients.

Physical therapy is relatively successful for patients with chronic pelvic pain related to pelvic floor dysfunction, especially considering the typical outcome and persistence of symptoms for this patient population as a whole. Only a few prospective randomized trials have been conducted, but FitzGerald et al demonstrated a 57% response rate to myofascial physical therapy for urologic pelvic pain syndrome among patients presenting with pelvic floor tenderness.¹⁰ The same multicenter collaborative group later confirmed these results with a 59% response rate in women treated with myofascial physical therapy for interstitial cystitis and painful bladder syndrome.¹¹ In a study by Glazer et al, patients with vulvar vestibulitis and pelvic hypertonus also demonstrated a 50% response rate to physical therapy and biofeedback.¹²

Finding a physical therapist with the skill and interest to address pelvic floor dysfunction may pose a challenge in some geographic areas. Therapists familiar with women’s health issues and chronic pelvic pain are listed at the American Physical Therapy Association Web site (http://www.apta.org) under the “Find a PT” link.  The Herman & Wallace Pelvic Rehabilitation Institute (http://hermanwallace.com) specializes in pelvic floor rehabilitation training for physical therapists and maintains a database of practitioners.

Pharmacologic management options for pelvic floor dysfunction begin with nonsteroidal anti-inflammatory drugs, cyclobenzaprine, amitriptyline, or baclofen. Narcotics are tempting for patients in extreme discomfort but are a poor long-term solution. Gabapentin and pregabalin have shown promise in patients with pelvic floor myalgia.^8,13 Injection of persistent trigger points with lidocaine, with or without cortisone, is also a successful approach to the myofascial component of pelvic pain.⁸ More recently, purified botulinum toxin (Botox) has been used to treat pelvic floor muscle spasm, with proven success.^8,13 Sacral nerve, pudendal nerve, and posterior tibial nerve stimulation are all developing modalities with therapeutic promise.^8...

 Attention to the pelvic floor musculature during pelvic examinations is an effective and inexpensive diagnostic strategy that can be life-changing for patients with pelvic pain, yet requires minimal time and effort. These patients may have to undergo the usual chronic pelvic pain algorithm without the option of physical therapy if hypertonus goes unrecognized.Physical therapy with or without pharmacologic management offers many patients significant relief or even resolution. Educating patients and using physical therapy to make them active partners in their own care give women with chronic pelvic pain a sense of empowerment and benefit them physically and psychologically."

http://contemporaryobgyn.modernmedicine.com/contemporary-obgyn/news/modernmedicine/modern-medicine-feature-articles/pelvic-floor-spasm-missing-l

"In most cases of pelvic floor disorder, not only is the pelvic floor’s timing off due to chronic tension patterns, tension in the abdomen is also great....Tension in the abdomen has nothing to do with strength (Tattoo this in your mind: Tension does not equal strength). Chronic “sucking your stomach in” habits are found more often in those who feel they have something to hide, right? If you’ve got military posture, been slightly tucking your pelvis to give the appearance of a flatter stomach and butt, lifting your chest (at-ten-tion!), or have simply done one too many core exercise session, the tension in the diaphragm and psoas is higher than it should be.
Lie on your back, placing your hands on your lower abdomen. Cough and see if the lower abdomen bulges. Ideally, a cough should produce an upward motion, not a downward one.
If you find that you measure “positive” for all three assessments, time to relax the belly and release all those tense muscles!...Trigger points, points of extreme tenderness or weird “lumpiness” in the specific parts of the body are common in those with hypertonicity of the pelvic floor. Here’s a picture of some typical areas with excessive sensitivity to pressure and/or lumpiness:

Picture from Rehabilitation of the Short Pelvic Floor

What makes these areas lumpy and sensitive? No one knows how it gets this way, but muscles that are tight and non-innervated tend to pull on connective tissues (called fascia) in a way that gets the fascia all wadded up, so you’ve got this tight, cold (cuz there’s not much blood there), dehydrated, non-uniform muscle/fascia tissue bundled in chunks around your body. When you push on a big wad instead of smooth, supple layers, the pressure on the sensory organs becomes higher, which means you feel it more...
Restoring length to the pelvic floor is a combination of not only what you need to do, but also what you need to do less often.
Here’s my (read: your) to-do list: http://www.katysays.com/tootightpelvicfloor-2/" 

http://www.katysays.com/tootightpelvicfloor-2/

Helpful stretches for patients with pelvic pain

Buttock Stretch 1 Place your right ankle in front of your left knee. Grasp your left thigh with both hands and gently pull it towards you. The stretch is felt in the shaded area on the diagram (buttock and back of thigh). Hold for at least 30 seconds. Repeat on the other side.

Buttock Stretch 2 Draw your left knee towards your right shoulder. Hold for at least 30 seconds. Repeat on the other side.

Rotation Stretch Keep both shoulders on the floor and roll one leg and hip to the opposite side. This stretches your low back area.

 

Happy baby pose

 

Malasana

 

Hip flexor stretch

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

hamstring stretch

 

 

 

 

 

 

 

                                      

 

                                                                                                                                                           

Video of some of these stretches: http://abcnews.go.com/2020/video?id=8277884

(Link for several other stretches: http://www.freewebs.com/trydent78/)

 

"Activities and Exercises to Avoid with Pelvic Floor Muscle Tension

• Pelvic floor exercises or kegel exercises
• Intense core abdominal exercises
• Painful intercourse/ painful vaginal penetration
• Prolonged sitting
• Heavy lifting or heavy activity
• High impact exercise e.g. running
• Stress

How to Promote Pelvic Floor Relaxation- ‘Down Training’ Methods

Treatment for pelvic floor muscle spasm is multifaceted. The following Down Training steps (Shelly 2002) can encourage the pelvic floor relaxation when performed regularly.

• Relax–lie down with a pillow under the knees for 20-30 minutes daily to relax the pelvic floor muscles. Sometimes a warm pack placed over the pubic area or lower abdomen can assist pelvic floor relaxation.
• Employ diaphragmatic breathing – this means breathing into your diaphragm. Slow diaphragmatic breathing (like yoga breathing) is very important for relaxing the pelvic floor muscles.
• Visualise your pelvic floor muscles relaxing and a warmth in the pelvic floor region
• Gentle perineal bulging – this is very gentle bulging of the pelvic floor and should be taught by a pelvic floor physiotherapist. Bearing down too strongly can actually increase spasm so this must be done gently.
• Choose a relaxed environment is important e.g. soft music, surrounding warmth.
• Total body relaxation – relax the muscles of the whole body, this may involve progressive relaxation of the different muscles from the face and neck through to the feet.
• Employ body scanning for any areas of increased muscle tension and aim for complete physical relaxation."  https://www.pelvicexercises.com.au/pelvic-floor-muscle-tension-article/