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While initial assays were technically complex and tedious women's health clinic gillette wy 60caps menosan with visa, and were therefore restricted to menopause pain menosan 60caps visa the analysis of only small numbers of sera breast cancer awareness day order menosan 60caps on-line, they allowed the definition of neutralizing epitopes by monoclonal antibodies (see also Section 1 womens health vitamin d diet buy discount menosan 60caps. Recent developments suggest that the high-throughput analysis that is needed for large epidemiological and vaccination studies may be feasible. Methods that apply full-length E6 or E7 proteins that present conformational epitopes, i. As seen for antibodies to L1 and also to E6 and E7 proteins, assays that use proteins that also present conformational epitopes need to be developed before this question can be analysed appropriately. The basic steps that lead from the normal cervix to cancer are well established (see Figure 8). Oriel (1971) reported that 64% of sexual partners of individuals who had genital warts developed genital warts themselves after a mean interval of 2–3 months. Moreover, transmission may take place in one anogenital site, such as the introitus, and the infection may be spread by self-inoculation to another site (Winer et al. The possible non-sexual routes include vertical transmission, fomites and skin contact (Mindel & Tideman, 1999; Frega et al. Results from studies of transmission in infants are not consistent, and do not provide a clear indication of the rate of infection among neonates who are exposed perinatally. Differences in samples and techniques may be the reasons for the variability and inconsistency in these results. Age of the mother, birth order of the infant and mode of delivery are considered to be important determinants of transmission. Most infants who develop juvenile-onset recurrent respiratory papillomatosis are the first-born single or twin infant of women who tend to be younger than other mothers who gave birth at the same institutions (Kashima et al. Even if anogenital infections with high viral load are rare in babies, exposure at birth could influence immune response later in life at the time of sexual exposure (Mant et al. There seems to be consensus, however, that perinatal transmission is generally a rare event (Winer & Koutsky, 2004). Because the basic tenet of analytical epidemiology is the observation of individual subjects, several methodological challenges need to be overcome in studies of couples or of infection that begins with an index subject and is eventually transmitted to partners and spread from that point. These studies are very important because they can estimate the probabilities of infective contact per sexual act and partner. It is uncertain whether sexual intercourse near menarche is uniquely prone to establishing infection (or persistence and progression). The type specificity of serological responses supports this conclusion (Wideroff et al. Recently, studies of sexual couples revealed a beneficial effect of condoms on the regression of flat penile lesions (Bleeker et al. However, further studies of multiple infections could be important to guide strategies on vaccines. In some populations, age-specific prevalences decline sharply and reach very low levels at older ages, which is consistent with viral transience as well as lower incidence at older ages (see Figure 9). Different primers were included and varied to some extent in type-specific sensitivity. In general, the prevalence is highest in Africa and South America, lowest in Europe and intermediate in Asia. These data suggest that repeated exposures may contribute to high prevalence over a wide age range, at least in the anal canal. Studies that focus on older women and their male partners are also needed, particularly cohort studies with repeated measurements that assess male and female sexual practices and immunity. Confirmation of this hypothesis, however, would require that preserved specimens of representative samples from different eras be tested at the same time with the same sensitive testing technology, a proposition that could not be easily implemented. Age Method of detection Prevalence (%) Prevalence of specific high-risk types (%) Prevalence of specific low-risk types (%) study area at range risk (years) Overall High Low 16 18 31 33 35 39 45 51 52 56 58 59 66 6 11 34 40 42 43 53 54 73 risk risk Kjaer et al. Tables 13 and 14 show the main characteristics of these studies and illustrate the estimates of incidence and duration by type, respectively. Presumably, they are cleared completely by the cell-mediated immune system, are self-limited or are suppressed into long-term latency. However, this question cannot easily be answered by the measurement technologies currently available to epidemiologists. However, it is not known how frequently this occurs in immunocompetent individuals, how long it lasts, what causes re-emergence into a detectable state or what fraction of cancers arises after a period of latency. There is no consensus as to the length of time that implies persistence, but at least 6 months to 1 year is the time frame that is usually chosen. This approach is complemented by a study of longer-term infection with a median follow-up of 5. There is considerable uncertainty concerning the importance of measurements of viral load or the presence of associated, microscopically evident abnormalities with respect to the duration of persistence. The sparse data are conflicting as to whether the presence or the absence of any one type alters the duration of any other type-specific infection (analogous to whether types influence the acquisition of each other as mentioned above) (Thomas et al. The fraction depends on the thresholds of the molecular and microscopic tests and clinical specimens examined, and can range widely from 5 to 30% (Schiffman & Kjaer, 2003). Microscopic diagnoses are prone to subjectivity and lack of interobserver reproducibility, particularly when mild or equivocal changes are involved. However, other aspects of infection may contribute to the likelihood that an infection will progress, such as type, load and concurrent abnormalities. This might also represent a misclassification of cytology or histology or rapid transit through the mildly abnormal phase. These hypotheses can be addressed only through very intensive longitudinal studies that combine visual, microscopic and molecular measurements. The critical step for most women might be whether a precancerous lesion develops as an uncommon outcome of infection (Figure 8). Within this group, viral characteristics, host factors and behavioural co-factors that increase the risk of progression or decrease the probability of viral clearance need to be determined. More rapid progression does occur and should be studied, but it may not be possible to study the full extent of the latency process prospectively. For a balanced interpretation of these data, the following caveats must be considered for most of these studies: the small sample size, the highly selected study population, the insufficient follow-up time, the reporting of crude rates of progression and regression without a precise actuarial analysis of cumulative risk over time and the variability of methods to detect the development of lesions during follow-up. In particular, detection methods that use cytology cannot provide reliable estimates of rates of lesions and those that use histology may have altered the course of the natural history of the disease because frequent cervical biopsies may remove the entire lesion. Overall, these problems tend to affect the comparability of results across studies. A substantial proportion of lesions were biopsied, including cone biopsies, and were classified as persistent without further qualification as to the duration of the sojourn time within each grade, i. Regarding the latter progression figure, 10% of the lesions progressed to carcinoma in situ and 1% to invasive cancer. Within the latter probability, progression to carcinoma in situ was 14% and that to invasive cancer was 1. Progression rates to invasive cancer for studies that followed up only patients with carcinoma in situ by biopsy ranged from 29 to 36%. In a meta-analysis of studies published since 1970 that included more than 27 000 patients who were followed without treatment, Melnikow et al. Cumulative progression rates to invasive cancer at 24 months by cytological abnormality were 0. The following average rates of regression to a normal Pap smear were estimated: 68. The size of the precancerous lesion can be used as a proxy for risk of invasion but prospective proof cannot be obtained for obvious ethical reasons. Improvements in cytology and serology have been less extensive but very important. In future cohort studies that multiply the number of measurements taken over time, the importance of optimized methods will be even greater if observation and interpretation of the patterns of viral clearance, persistence, possible recurrence and progression are to be anticipated. The assays are reasonably type-specific and are usually negative in individuals who have never been infected (Dillner, 1999; Kjaer et al. Two important caveats must be recognized for the interpretation of sero-epidemiological studies.

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Therefore menstruation anemia cheap menosan 60caps with visa, validated protocols pregnancy test meme buy menosan 60caps visa, reagents and reference samples assure the best test performance in different settings women's health center phone number buy 60caps menosan otc. Several studies have evaluated these and other possibilities women's health magazine healthy skin tips 60 caps menosan with amex, some of which are presented here. However, such competitive assays usually have lower analytical sensitivity compared with direct binding assays. Recently, this type of assay has been adapted to fluorescent bead technology which allows the fast analysis of antibodies against many different (theoretically up to 100) proteins in parallel using only minute amounts of serum (Chen et al. Similar results were obtained previously using purified virions isolated directly from lesions (Steele & Gallimore, 1990; Bonnez et al. An alternative method for assaying type-specific antibodies is based on the fact that they are usually present at higher titres than crossreactive antibodies. The sensitivity of assays is measured using panels of serum samples obtained from individuals with a documented infection with the virus in question, i. A heavy infection may produce more viral protein that may induce a more effective antibody response. Transient infections may not be present in the body long enough to evoke an antibody response. Whereas disrupted or partially disrupted viruses expose epitopes that are broadly cross-reactive or even group specific (Jenson et al. Seroprevalence from different studies and laboratories must be compared with caution due to interlaboratory variation in assays and different definitions of cut-off. Especially important factors include the use of different groups of sera as a basis for determination of cut-off and different mathematical definitions of cut-off. The first is the cross-reactivity and relatively low sensitivity in terms of types and the second is the fact that infections in other mucosal sites of the body. Prevalence in neonates and primary school children (anal smear or foreskin) showed very low percentages (< 1%). Oral 61 20–79 Normal Consensus 0 (1995), smear individuals primer Denmark Nasal 48 2. Their significance was not appreciated at the time, but these changes were later called carcinoma in situ and described precursors of cervical cancer. Reagan and Hamonic (1956) introduced the term ‘dysplasia’ to designate cervical epithelia that contained cytologically atypical cells but lacked the full-thickness of differentiation. Dysplasias were further divided into mild, moderate and severe, depending on their degree of differentiation. From this terminology, it was implicit that the higher the grade, the closer the lesion was in aggregate to invasion. This assumption was based upon the observation that higher-grade dysplasias resembled carcinoma in situ and invasive cancer more closely than those of a lower grade. However, carcinoma in situ remained in the minds of clinicians as the only true precursor of cancer. Patients with this disease were generally treated by total hysterectomy and those with lesser degrees of epithelial change — dysplasias — were either treated by cervical conization or followed prospectively without treatment (reviewed in Younge, 1965). It was particularly difficult for pathologists to distinguish between severe dysplasia and carcinoma in situ, and clinicians became increasingly sceptical of the rationale for therapy that was dictated by the classification system for dysplasia–carcinoma in situ. In view of this, and after the completion of a number of laboratory and clinical studies that were begun in the 1960s, it became apparent that severe dysplasia and carcinoma in situ could not be distinguished reproducibly at any level and that the lesser degrees of atypia — particularly mild and moderate dysplasia — merged imperceptibly in objective measurements with the higher-grade lesions (Richart, 1987). The clinical impact of this new terminology was that presumed precursor lesions should be treated based on their size and location. However, it was emphasized that the diagnostic decision should be taken at an operational level as well as at a morphological level so that the clinician could infer accurately from the diagnosis whether the pathologist believed that the lesion being diagnosed was a true precursor of cancer or not. This meeting concluded that molecular data are more consistent with a two-tiered, rather than a three-tiered system. The terminology used was agreed after a review process in which more than 400 cyto-/histopathologists, gynaecologists, cytotechnologists, epidemiologists, health physicians and lawyers were involved. This simple but important observation led to the concept that cancers were preceded by a precursor state that could be recognized histologically. The invention of the colposcope by Hinselmann (1925) allowed gynaecologists to recognize clinically alterations in the cervical epithelium that could be diagnosed by punch biopsy as carcinoma in situ. These alterations could then be treated to prevent the development of invasive cancer. However, it was not until Papanicolaou and Traut (1943) published their observations on exfoliated cells that it was discovered that these early histological and colposcopical observations could be used as part of mass screening programmes and be translated into schemes for cancer prevention. Subsequent observers noted that the mean age at diagnosis of mild, moderate and severe dysplasia, carcinoma in situ and invasive cancer increased progressively and that this increase was accompanied by an increase in the size of the lesion. This increase was in turn found to be accompanied by an increase in gland and canal involvement; in addition, the larger lesions were more likely to contain areas of invasion. These tongues of microinvasive carcinoma may be single or multiple and are generally accompanied by a local inflammatory infiltrate and a desmoplastic response. In the cervix, the risk of metastasis depends upon the degree of stromal penetration. Similar observations were made by Kottmeier (1961) who followed 31 women with carcinoma in situ prospectively for at least 12 years; 72% of these women developed invasive cancer. These observations of the natural history of carcinoma in situ suggest that, in the majority of the patients, once this disease is established, it rarely regresses spontaneously. There is therefore a discrepancy between the cumulative incidence of carcinoma in situ observed in the natural history studies conducted in British Columbia (Canada), the Netherlands and Denmark, which suggested that a high proportion of carcinomas in situ do regress without treatment, and the cumulative incidence of invasive cancer seen in earlier observational studies (Smith & Pemberton, 1934; Kottmeier, 1961; McIndoe et al. The natural history of cervical precursor lesions of a lower histological grade than carcinoma in situ has been studied by Ho et al. About 50% of low-grade lesions regress within 1 year, while a smaller proportion of high-grade lesions regress. Operationally, it is a lesion that is thought by pathologists to be the result of a productive viral infection and not to represent a true precursor of cancer. However, this productive stage is restricted to postmitotic, differentiated cells in the suprabasal layers of the epithelium that are withdrawn from the cell cycle. The basal and parabasal layers characteristically have little cytological atypia, are arranged in a uniform fashion on the basal lamina and are not highly disorganized. The combination of nuclear atypia and perinuclear halo formation is referred to as koilocytosis or koilocytotic atypia (Koss & Durfee, 1955). It should be emphasized that perinuclear halos may be produced as a result of other cervical or vaginal infections or may accompany repair or metaplastic processes. The result of this interference with the mitotic process is the formation of biand multinucleated cells and enlarged atypical nuclei, accompanied by heteroploidization. Mitotic figures are generally increased in low-grade lesions but are mainly confined to the lower third of the epithelium, as are undifferentiated or basal-type cells, and are characteristically absent from the upper layers of the epithelium. Most of the mitotic figures have a normal appearance, but cells with tripolar mitosis or tetraploid-dispersed metaphases may also be seen (Winkler et al. These two types of abnormal mitotic figure are also commonly found in polyploid lesions in other organs. As the nuclei enlarge, the nuclear cytoplasmic ratio is altered in favour of the nucleus and the cell borders, which commonly contain visible desmosomes in low-grade lesions, become indistinct and difficult to define. In contrast to low-grade lesions, expression of the viral oncogenes E6 and E7 in high-grade lesions also occurs in the dividing, immature, metaplastic basal stem cells. Other abnormal mitotic figures that are commonly seen include the two-group metaphase, multipolar mitoses in excess of three, lagging metaphase chromosomes, coarsely clumped chromosomes and highly abnormal, bizarre mitotic figures. In the presence of an abnormal mitotic figure, a lesion is consistently aneuploid and is a true precursor of cancer. In the absence of abnormal mitotic figures, other histological features commonly used to classify these lesions should be taken into account. Areas of microinvasion infiltrate in an irregular fashion and split collagen bundles. Microinvasive foci are commonly accompanied by an inflammatory and desmoplastic response. Microinvasion is defined as a lesion that invades the cervical stroma to a depth of no more than 5 mm; frank invasive cancer has a histological appearance similar to that of microinvasive cancer but has invaded more than 5 mm into the cervical stroma. Moreover, because of the incomplete overview of the endocervical canal and the poorer prognosis of adenocarcinoma of the cervix compared with squamous-cell carcinoma, clinicians always remove intraepithelial lesions of the glandular cells and data on the natural history of these lesions are therefore lacking (Boon et al. Adenocarcinoma in situ is characterized by a complex gland formation in the distribution of the normal endocervical glands, cytological atypia, an increased mitotic rate and a gland-within-gland pattern. Cytological alterations similar to those seen in other aneuploid cell populations are present and abnormal mitotic figures are common.

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Other research priorities included size estimations of trans populations and documenting risk factors and protective factors that build resilience menstruation headaches nausea purchase 60 caps menosan amex, alongside human rights 60 3 obligations and violations womens health center xenia ohio purchase 60 caps menosan fast delivery. Finally breast cancer awareness month 2014 generic 60caps menosan, Winter emphasised the need to pregnancy 15 weeks 60 caps menosan with visa document examples of trans-positive, competent, comprehensive, and accessible healthcare. This need to better understand diferent subpopulations within trans communities is also matched by an imperative to research the particular experiences of trans people in the Pacifc. At the same time, the level of acceptance of gender diversity within some parts of the Pacifc may inform culturally appropriate care for the many Pacifc trans people living in New Zealand and Australia. Compared to other regions, the size and linguistic diversity of Asia and the Pacifc is likely to mean there are fewer opportunities for networking amongst health professionals, academics, and trans health advocates interested in trans health research. Both a human rights approach and sound research practice would suggest that trans people need to be actively involved in identifying research priorities. No one should be forced to undergo medical procedures, including sex reassignment surgery, sterilisation or hormonal therapy, as a requirement for legal recognition of their gender identity. No status, such as marriage or parenthood, may be invoked as such to prevent the legal recognition of a person’s gender identity. Trans people face marginalisation when they are required to use a birth certifcate, passport, or other identity verifcation document that does not match their gender identity or gender expression. This discrimination may involve threats to a trans person’s safety or exclusion from vital health services, housing, employment, school, or social assistance. When trans people are disowned by their families this can have a signifcant impact on their attempts to gain legal gender recognition, particularly if parental permission is required to change or obtain identity documents. Many trans people are forced to leave their own region or country to start a new life. In addition, Article 8 of the Convention on the Rights of the Child requires states to “respect the right of the child to preserve his or her identity. In these circumstances, trans people who do not have identity documents that match their gender identity or expression may be turned away from essential services. Below are two recent examples from the earthquake disasters in Japan and Nepal in 2011 and 2015, respectively. The Social Inclusion Support Center, a community-based organisation, set up a telephone support service in October 2011 in response to the ongoing needs of disaster survivors. This Yorisoi Hotline became a nationwide service after receiving some government support in March 2012. Callers could select a specifc option if they had diffculties related to sexual orientation, gender identity or gender expression issues. Of the 10,878,227 calls made to the Yorisoi Hotline between 1 April 2012 and 31 March 2013, 3. Typically, trans people living in the areas affected by the disaster had not openly disclosed their gender identity prior to the disaster. Many were forced to do so because of the public nature of evacuation centres or in order to regain access to hormone treatment after medical clinics and hospitals were destroyed. Some avoided going to the toilet or washing because they did not know if they would be safe in sex-segregated washrooms or public baths. With little or no privacy, some did not change their clothes—including trans men scared of showing they were wearing chest binders. There were positive experiences too, such as a trans woman who was accepted as a woman at a refuge, given access to a women’s dressing room and bathroom, and supported by other women when men harassed her for being trans (Yamashita and Gomez, 2015). When relief camps were quickly set up, people without families were segregated into male and female camps. Also, basic facilities such as toilets and bathrooms in emergency shelters are typically divided into male and female venues. Having to share toilets, particularly at night, put trans people at risk of violence and rape. Gender considerate disaster risk reduction is essential, and transgender people need to be included in preparation planning. Their voices must be heard and their issues must be addressed in the current post disaster risk assessment. In many countries, there are no laws or policies allowing a trans person’s gender marker to be changed. This is the situation in all Pacifc countries, though a small number of countries, including Niue, Guam, Fiji, and Tonga, do allow someone to legally change their name. Tere are also no laws or policies enabling gender recognition in Thailand, the Philippines, Viet Nam, or Malaysia. Tere have been individual cases in Malaysia, Indonesia, and the Philippines in which a court has enabled a trans woman to change her gender marker afer gender-afrmation surgery. However, as recently as 2012, the Prime Minister’s Ofce told Parliament that such changes are not permitted in Malaysia (Human Rights Watch, 2014). A 2007 Supreme Court decision in the Philippines removed the right previously held by trans people to apply to the Regional Trial Court for gender recognition (Winter, 2012; Open Society Foundations, 2015). In other countries, laws and policies limit gender recognition to a minority of trans people, with strict stipulations that violate other human rights. One of these is requiring trans people to undergo all gender-afrming medical surgeries— ofen discussed in laws as “full sex reassignment surgery. Although many trans people wish to medically transition, the steps involved mean it is ofen a long-term goal. For other trans people, it is never a possibility because of fnancial, medical, or personal reasons. This is particularly true for trans men, as creating male genitals involves multiple stages of surgery; frequent technical difculties and postoperative complications mean only a small minority of trans men have such operations (Coleman et al. If legal gender recognition requires such medical steps, trans people can be forced to spend many years, or all of their lives, with no legal verifcation of their gender identity. Typically, these trans people had tried to change their gender markers so they could marry their partners. In one 2011 case from Central Java, a 26-year-old trans man known as Rega was jailed for 18 months afer the family of his 17 year-old bride “discovered” on the day of his wedding that he was “born a woman. In Thailand, it is mandatory for legal documents to have an honorifc or title that matches a person’s sex at birth. This title cannot be changed, even if a trans person has had gender afrmation/sex reassignment surgeries. In some countries that have a medical threshold for changing sex or gender details, the type of medical interventions required are not always clearly stated. She noted “It is not satisfactory that ofcials can impose their own interpretations. Since 2008, trans people in mainland China who have had these surgeries and met the other criteria detailed below have been able to change their household registration records (Hu Kou). Additional barriers to gender recognition in South Korea and Japan are requirements that a trans person be over the age of 20, unmarried (and required to divorce if already married), and have no children. Meeting all of these criteria is very difcult for trans people, especially given that sex work is both illegal and the main form of employment for many trans women in China. No country in Asia enables trans children and young people to amend their sex details on legal documents, even with parental consent. In the few countries in Asia and the Pacifc where a trans person has the right to marry, it is permitted only afer surgeries that result in sterilisation. Tese restrictions undermine trans people’s rights to recognition before the law and infringe on their rights to privacy, fnding (or raising) a family, and non-discrimination (Open Society Foundations, 2015). Across Asia, trans people ofen do not know whether or how they can apply to change their gender markers. A December 2013 media report indicated that Taiwan was considering removing any medical requirements (Yiu, 2013). In Japan, the parenting restriction has been lessened slightly, stipulating that trans people are not eligible if their children are under the age of 20. As discussed later in this section, some are very aware of world-leading gender recognition laws in Argentina and Malta that focus on the right to self-determination. It “urges governments to eliminate unnecessary barriers, and to institute simple and accessible administrative procedures for transgender people to obtain legal recognition of gender, consonant with each individual’s identity. Furthermore, it maintains that trans youth and trans people in prison or other institutions also require legal gender recognition. Registrar of Marriages, fnally allowed a trans woman who had undergone “sex reassignment surgery” to marry her boyfriend.

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Be slow and detailed in your search for trigger points; there can be several in this muscle menstrual reg purchase 60 caps menosan fast delivery. They’re not easy to menstruation fatigue cheap menosan 60caps on line massage and your activities may be keeping them under continuous stress menstrual age buy cheap menosan 60caps online. Give serious thought to menstruation every 14 days order menosan 60caps without a prescription changes you can make in the way you use your hands that will give these special muscles a break. Pthomegroup Chapter 7 Chest, Abdominal, and Genital Pain Pthomegroup 156 the Trigger Point Therapy Workbook Chest pain Side pain Abdominal pain Genital pain (both genders) Pthomegroup Chapter 7—Chest, Abdominal, and Genital Pain 157 Pain Guide Chest, Abdominal, and Genital Boldface type indicates a primary pain pattern. Abdominal Genital rectus abdominis (172) pelvic floor muscles (181) abdominal obliques (172) abdominal obliques (172) iliocostalis (195) adductor magnus (236) deep spinal muscles (192) rectus abdominis (172) quadratus lumborum (198) gluteus maximus (201) piriformis (182) Chest psoas (177) pectoralis major (163) pectoralis minor (167) Side scalenes (96) serratus anterior (169) sternocleidomastoid (62) abdominal obliques (172) sternalis (166) intercostals (195) intercostals (195) latissimus dorsi (117) iliocostalis (195) diaphragm (171) subclavius (166) abdominal obliques (172) diaphragm (171) Pthomegroup 158 the Trigger Point Therapy Workbook Other Symptoms Guide Chest, Abdominal, and Genital Belching Colic Ejaculation abdominal obliques (172) rectus abdominis (172) pelvic floor (bulbospongiosus) (181) Bladder Pain or Costochondritis Lying Flat on the Back Frequency pectoralis major (163) pelvic floor (levator ani) (182) adductor magnus (236) serratus anterior (169) Reaching Out and Behind abdominal obliques (172) intercostal (171) pectoralis major (163) piriformis (and other deep diaphragm (171) pectoralis minor (167) lateral rotators) (209) abdominal obliques (172) Rising from a Chair pelvic floor (162) rectus abdominis (172) superficial spinal muscles (195) Breast or Nipple Forward-Head Posture Side Bending (slouching) abdominal obliques (172) Hypersensitivity superficial spinal muscles (195) pectoralis major (163) rectus abdominis (172) serratus anterior (169) abdominal obliques (172) Sitting pectoralis major (163) pelvic floor (levator ani and Cardiac Arrhythmia pectoralis minor (167) coccygeus) (182) pectoralis major (163) sternalis (166) Tw ist i ng sternocleidomastoid (62) intercostals (195) scalenes (96) Cardiac Ischemia or Angina (false) Pain with Breathing, Heartburn pectoralis major (163) Coughing, Sneezing, or upper abdominal obliques (172) pectoralis minor (167) Difficulty Taking a Full rectus abdominis (172) sternalis (166) Breath superficial spinal (195) Impotence scalenes (96) iliocostalis (195) piriformis (182) serratus anterior (169) pelvic floor (bulbospongiosus) pectoralis minor (167) Chronic Pelvic Pain, pectoralis major (163) (181) Gynecological or diaphragm (171) Menstrual Pain intercostals (195) Indigestion abdominal obliques (172) abdominal obliques (172) rectus abdominis (172) rectus abdominis (172) rectus abdominis (172) adductor magnus (236) latissimus dorsi (117) Nausea pelvic floor (162) rectus abdominis (172) piriformis/deep rotators (209) Penis Pain psoas/iliacus (177) rectus abdominis (172) Pain or Trouble with pelvic floor (ischiocavernosus Motion Coccyx (tailbone) Pain or and bulbospongiosus) (181) Tenderness Bending and Lifting rectus abdominis (172) Perineum gluteus maximus (201) multifidi (78) Bowel Movement piriformis (182) pelvic floor (levator ani, pelvic floor (sphincter ani) (182) pelvic floor (levator ani, coccygeus, sphincter ani, and bulbospongiosus, obturator internus) (162) ischiocavenosus) (181) Pthomegroup Chapter 7—Chest, Abdominal, and Genital Pain 159 Pseudo-Appendicitis pelvic floor (bulbospongiosus Vaginal Pain or rectus abdominis (172) and ischiocavernosus) (181) Vulvodynia quadratus lumborum (198) abdominal obliques (172) Rectal Pain and Sense of adductor magnus (236) Urinary Frequency or Fullness pelvic floor (levator ani, adductor magnus (236) Urgency bulbospongiosus, pelvic floor (levator ani, abdominal obliques (172) ischiocavernosus, and obturator internus, and obturator internus) (181) sphincter ani) (182) Urinary Incontinence piriformis (182) pelvic floor (162) Vomiting, Projectile abdominal obliques (172) Scrotum Pain Urinary Retention rectus abdominis (172) quadratus lumborum (198) abdominal obliques (172) psoas/iliacus (177) pelvic floor (bulbospongiosus) Urinary Sphincter Spasm (181) rectus abdominis (172) Testicular Pain abdominal obliques (172) Pthomegroup 160 the Trigger Point Therapy Workbook Pain Illustrations Guide Chest, Abdominal, and Genital Pectoralis major, clavicular Pectoralis major, sternal Pectoralis major, costal Subclavius trigger point section: trigger points section: trigger points section: trigger points and referred pain and referred pain pattern and referred pain pattern and referred pain pattern pattern (p. Trigger points are and referred visceral pain pattern referred visceral pain pattern hidden behind the lowest (p. Pthomegroup Chapter 7—Chest, Abdominal, and Genital Pain 161 Pseudoappendicitis trigger point Lower abdominal trigger points Abdominal trigger points and and referred pain pattern (p. This is especially regrettable because the solutions are so simple when trigger points are to blame. Trigger point therapy is the appropriate treatment for many kinds of symptoms in the chest, back, side, stomach, shoulder, arm, and hand that originate in chest and abdominal muscles (Simons, Travell, and Simons 1999). Trigger points in chest muscles can cause distortions of your posture that promote shallow breathing and shortness of breath. Tenderness, pain, and breathing difficulties caused by these trigger points are often mistaken for symptoms of hiatal hernia or lung disease. Pectoral trigger points can cause chest, shoulder, arm, and back pain; heart arrhythmia; and false heart pain. Their indirect effects on neck and upper back muscles sponsor headaches, jaw pain, and other symptoms of the head, face, and neck. The numbness they cause in hands and fingers can lead to false diagnoses of carpal tunnel syndrome (Simons, Travell, and Simons 1999). Abdominal trigger points can cause abdominal pain, back pain, heartburn, menstrual pain, false appendicitis, diarrhea, nausea, urinary bladder and sphincter spasms, constipation, and even, rarely, projectile vomiting. Just as the internal organs can cause trigger points in muscles, trigger points can mimic disorders of the esophagus, kidneys, bladder, colon, gallbladder, and other internal organs, including the heart. Colic in babies and stomachaches in both children and adults can be produced by abdominal trigger points. They’re even thought to cause bed-wetting in older children (Simons, Travell, and Simons 1999). Myofascial pain from lower abdominal and pelvic floor trigger points is commonly felt in the groin, rectum, ovaries, uterus, vagina, penis, and testes, resulting in much needless worry and discomfort. Prostate symptoms and impotence in males from the effects of pelvic floor trigger points is not unusual. Painful intercourse for both sexes can have the same source (Travell and Simons 1992; Simons, Travell, and Simons 1999). Pthomegroup Chapter 7—Chest, Abdominal, and Genital Pain 163 As shown in figure 7. If something doesn’t seem right, your symptoms keep recurring, your gut is telling you to “worry now! When the physician doesn’t find anything wrong with you, rejoice; it may only be muscle pain! Modern practitioners of Western medicine are really good at prolonging our lives by treating and curing diseases; they just aren’t yet so good at recognizing and resolving muscle pain. In the following sections, you will find advice for what to massage when no other disorder or disease can be detected. When any of these symptoms are caused by myofascial trigger points, you may be able to handle them yourself with massage. Symptoms Pain from pectoralis major trigger points may be felt in the chest and the front of the shoulder; down the inner arm, the inner elbow (figures 7. Symptoms can be referred pain pattern pain pattern mislabeled as thoracic outlet syndrome. The exact location of the pain depends on the location of the trigger point in several sections of this complex muscle. The outer section in front of the armpit can harbor a trigger point that causes breast pain and nipple hypersensitivity (figure 7. A trigger point in the lower border of the pectoralis major can cause an irregular heartbeat (figure 7. You might think a trigger point affecting the heart would be on the left side, nearer to the heart, but this arrhythmia trigger point occurs only on the right. The pattern of pain referred from the pectoralis major and other pectoral muscles can be frighteningly like the pain of a heart attack. Long after an afflicted heart has recovered, you can still have severe chest pain that in reality is coming not from the heart but from the muscles of the chest (Simons, Travell, and Simons 1999). Unable to wear the unit at night, she regularly had to take a pain pill to enable her to sleep. Trigger points had shortened her pectoral muscles to such an extent that she couldn’t pull her shoulders back to stand up straight. After her first massage, she was able to go to sleep without taking her pain medication for the first time in years. Though she’s never eager to massage her own pectoral muscles, which are still very tender, her back always feels better when she does. Tightness from trigger points in the pectoralis major keeps the shoulder pulled forward, making it difficult to reach back and putting a constant strain on the upper back muscles. This round-shouldered posture also causes the head and neck to be constantly projected forward, which sponsors trigger points in the sternocleidomastoid, scalene muscles, and back of the neck muscles. This can make the pectoralis major indirectly the ultimate source of the many symptoms that come from these muscles. The overload imposed on shoulder and upper back muscles by a shortened pectoralis major can lead to the development of secondary trigger points in the anterior deltoid, coracobrachialis, rhomboid, and middle trapezius, progressively limiting movement of the arm and lead to trigger points in the subscapularis, latissimus dorsi, and serratus anterior. Eventually, the infraspinatus, teres major, and posterior deltoid develop antagonist trigger points from being continuous and overstretched and the whole dysfunction ends in a frozen shoulder. The round-shouldered posture fostered by pectoral trigger points can have many unanticipated effects, including chronic upper back pain, excessive pressure on spinal disks, compression of nerves, jaw problems, restricted breathing, chronic fatigue, neck pain, and headaches (Simons, Travell, and Simons 1999). Unfortunately, attempts to force a correction of your posture generally fail unless you first find and deactivate the specific trigger points that are keeping the pectoral muscles tight. Efforts to stretch these sensitive muscles without releasing their trigger points can make all your symptoms worse. After the trigger points are gone, stretching and postural retraining are quite appropriate and can be expected to have a beneficial effect. The clavicular (upper) section attaches to the collarbone, the sternal (middle) section to the breastbone, and the costal (lower) section to the ribs and stomach muscles. These attachments allow the pectoralis major to rotate the arm inward and to pull it across the chest. The upper section also helps raise the arm; the lower section helps pull the arm and shoulder down. In vigorous sports activities and many kinds of work, the pectoralis major can be overused by any of these movements done with excessive force or repetition. Carrying a heavy backpack can be a contributing cause, or possibly the sole cause, of trigger points in muscles of the chest, abdomen, upper back, and neck. Part of your trigger point therapy should be to figure out how to lighten your load or find another way to carry it (Simons, Travell, and Simons 1999). In women, the upper half is similarly accessible, but the lower half must be approached through breast tissue or by moving the breast aside as much as possible. Trigger points in the clavicular section send pain to the front of the shoulder (figure 7. Trigger points in the sternal section refer pain to the inner arm and the inner elbow (figure 7. Sensitivity and pain in the breast come from trigger points in the thick lateral border of the muscle (figure 7. Pthomegroup Chapter 7—Chest, Abdominal, and Genital Pain 165 the trigger point for a fluttery kind of benign heart arrhythmia is found between the ribs, a couple of inches to the right of the end of the breastbone (figure 7. Pressing on this one is sharply painful, but the heart rhythm straightens out right away if the trigger point is to blame. There can be a trigger point in the left side of the breastbone, but it does not create arrhythmia or have a specific pain pattern.

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