|
 
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| SPECIAL ARTICLE |
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| Year : 2020 | Volume
: 3
| Issue : 4 | Page : 101-105 |
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Advanced interventions for common pain conditions in women
Areerat Suputtitada1, Carl P C Chen2, Mark Young3, Neil A Segal4, Bryan O’Young5
1 Department of Rehabilitation Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Bangkok, Thailand
2 Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital at Linkou and College of Medicine, Chang Gung University, Guishan District, Taoyuan City, Taiwan
3 Department of Physical Medicine and Rehabilitation, Maryland Rehabilitation Center, USA
4 Department of Rehabilitation Medicine, University of Kansas Medical Center, Kansas City, KS, USA
5 Department of Physical Medicine and Rehabilitation, Lewis Katz School of Medicine at Temple University, PA, USA
| Date of Submission | 02-Jun-2020 |
| Date of Decision | 08-Jul-2020 |
| Date of Acceptance | 30-Jul-2020 |
| Date of Web Publication | 12-Nov-2020 |
Correspondence Address:
Prof. Areerat Suputtitada
Department of Rehabilitation Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Rama 4 Road, Patumwan, Bangkok 10330
Thailand
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jisprm.jisprm_25_20
Pain syndromes affecting women have a significant global impact. There is increasing evidence that chronic pain affects a higher proportion of women than men around the world; unfortunately, women are less likely to receive treatment. Moreover, women generally experience more recurrent pain, more severe pain and longer-lasting pain than men. Pain conditions are more prevalent in women such as fibromyalgia, chronic pelvic pain and lumbopelvic pain during pregnancy and postpartum. Gender differences in pain sensitivity, pharmacological therapy, and nonpharmacological pain interventions have also been reported. It is becoming evident that gender differences in pain and its relief arise from an interaction of genetic, anatomical, physiological, neuronal, hormonal, psychological and social factors that modulate pain differently.
Keywords: Common pain syndrome, fibromyalgia, lumbopelvic pain, pelvic pain, postpartum, pregnancy, women
How to cite this article:
Suputtitada A, Chen CP, Young M, Segal NA, O’Young B. Advanced interventions for common pain conditions in women. J Int Soc Phys Rehabil Med 2020;3:101-5 |
How to cite this URL:
Suputtitada A, Chen CP, Young M, Segal NA, O’Young B. Advanced interventions for common pain conditions in women. J Int Soc Phys Rehabil Med [serial online] 2020 [cited 2023 May 29];3:101-5. Available from: https://www.jisprm.org/text.asp?2020/3/4/101/300597 |
| Introduction | |  |
Accumulating scientific evidence indicates that chronic pain affects a higher proportion of women than men around the world; yet unfortunately, women are less likely to receive treatment.[1],[2],[3] Moreover, women generally experience more recurrent pain, more severe pain and chronic pain than men.[1],[2],[3] Pain conditions that are more prevalent in women include fibromyalgia (FM), chronic pelvic pain (CPP), prenatal and postpartum musculoskeletal conditions.[1],[2],[3],[4] FM and irritable bowel syndrome are common disorders that are often found in women with CPP.[4] Women with CPP have a higher prevalence of FM and irritable bowel syndrome than the general population.[4] Aberrant pain processing and psychosocial stressors are implicated in the co-occurrence of these pain syndromes called chronic overlapping pain conditions.[5],[6],[7] Advances in neuroscience have demonstrated that male and female brains are different.[5],[6] Human bodies maintain and adjust to a careful balance of sex-specific hormonal cocktails that influence biology.[1],[2],[3] Gender differences in pain sensitivity, pharmacological therapy, and nonpharmacological pain interventions have also been reported.[1],[2],[3] It is becoming evident that gender differences in pain and its relief arise from an interaction of genetic, anatomical, physiological, neuronal, hormonal, psychological and social factors, which modulate pain differently.[1],[2],[3],[4],[5],[6],[7] Chronic pain is associated with central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults.[7],[8] It is also stimulated by neuroinflammation in the peripheral and central nervous system (CNS). A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines which are powerful neuromodulators and cause hyperalgesia and allodynia after CNS administration.[5],[6],[7]
Evidence reveals significant gender differences in the association between gray matter (GM) metrics and pain-related psychosocial characteristics.[5],[6],[7] These findings indicate that, in women, reduced GM area and volume of several central brain regions (i.e., paracentral, postcentral, precentral, and supramarginal) associate to a greater extent with perceived negative consequences of the illness, perceived emotional representations, and pain catastrophizing, compared to men.[5],[6] Also, the more women perceive chronicity, the less GM thickness in the lateral orbitofrontal cortex. In men with nonspecific chronic spinal pain, precentral area GM and insula volume are inversely related to perceived personal control of the illness. GM area and volume of the precuneus cortex relates more positively with perceived personal control and more negatively with kinesiophobia in men compared to women. Finally, perceived symptom fluctuations are inversely associated with precentral volume in men, whereas they are more positively associated with lingual thickness in women.[5],[6],[7]
FM affects more women than men. The treatment is quite challenging, since there are multiple symptoms besides severe chronic widespread pain. Its pathophysiology is related to central sensitization, involving both brain and spinal mechanisms. Greater brain activation in response to pain-related upregulation of ascending facilitation pathways and deficits in descending spinal inhibitory influences have been found in FM.[8],[9] Typical FM symptoms such as allodynia or hyperalgesia can be explained by central sensitization.[8],[9] The diagnostic criteria, combining a widespread pain index (WPI) and severity scale (SS) for fatigue, nonrestful sleep and cognitive problems, with WPI >7, SS >5 OR WPI 4–6, SS >9 had 88.1% accuracy for the diagnosis of FM.[9],[10],[11] Once a diagnosis of FM has been confirmed, a multidisciplinary treatment strategy has been recommended. The first-line and most commonly used pharmacological treatments are pregabalin, duloxetine and milnacipran. Treatment is challenging because the symptoms of FM vary by patient. A multidisciplinary approach, including medications, acupuncture, low-level laser therapy, transcutaneous electrical stimulation exercise and cognitive behavior therapy, is recommended to manage FM patients.[9],[10],[11] Moderate evidence shows that higher pain intensity and pressure pain sensitivity are related to decreased regional GM volume in brain regions encompassing the cingulate cortex, the insula, and the superior frontal and temporal gyrus.[9],[10],[11],[12] Further, some evidence exists that longer disease duration is correlated with decreased total GM volume. Structural and functional brain alterations within regions involved in somatosensory, affective, and cognitive pain processing play a crucial role in the persistent pain of chronic MSKP patients.[5],[6],[7],[8],[13] Accordingly, these brain alterations have to be taken into account when assessing and treating patients with chronic pain. Two methods of noninvasive brain stimulation, repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) have been recommended. The stimulation at M1 was more effective in pain reduction than the stimulations at the primary sensory cortex or supplementary motor areas with navigation-guided rTMS.[13] The analgesic effects of M1 stimulation can change thalamic and subthalamic nuclei and modulate the affective component of pain.[14] Dorsolateral prefrontal cortex (DLPFC) stimulation coupled with the limbic system can modulate pain processing and perception. Pain inhibition mediated by descending fibers through the prefrontal cortex has been proposed. Level A (definite efficacy) for analgesic effect of high-frequency (HF) rTMS of the primary motor cortex (M1) contralateral to the pain area and the antidepressant effect of HF-rTMS of the left DLPFC.[13],[14] Level B recommendation (probable efficacy) of tDCS is endorsed for: (i) anodal electrode applied at the left primary motor cortex (M1) and cathodal electrode applied at the right orbitofrontal area in FM; (ii) anodal electrode applied at the left DLPFC and cathodal electrode applied at the right orbitofrontal area in cognitive function, major depressive episode without drug resistance. [15] FM is caused by dysfunction of the CNS but current treatments are mostly ineffective.[16] tDCS, a neuromodulation technique that targets the CNS, may offer a new line of treatment. A Systematic review of the most up-to-date literature including a meta-analysis of the effects of tDCS on pain intensity in FM. Fourteen clinical studies were analyzed. Ten were controlled trials and 4 were within-subject crossover studies. Meta-analysis of data found that tDCS is a safe intervention with the potential to lower pain intensity in FM. However, the high heterogeneity and risk of bias across studies suggest a need for further empirical research.[17] rTMS is an emerging therapeutic option for this condition. A comprehensive systematic review and meta-analysis of randomized clinical trials comparing rTMS (irrespective of the stimulation protocol) to sham for treating FM pain intensity, depression, and/or quality of life (QoL) were analyzed. The outcomes assessed closest to the 30th day after rTMS treatment were extracted. rTMS demonstrated superior effect on QoL. This effect, may involve pain modulation. The level of evidence is 1b.[18]
CPP occurs more commonly in women.[8],[9],[12],[19],[20],[21],[22] There are many causes, all requiring accurate diagnoses to develop an appropriate treatment plan to reduce the pain. Vulvodynia and deeper pelvic issues such as pelvic floor myalgia and tendinopathy have been traditionally difficult to diagnose and adequately treat.[19] In addition, women with CPP have a higher prevalence of FM and irritable bowel syndrome than the general population.[8],[9],[12],[19] Aberrant pain processing and psychosocial stressors are implicated in the co-occurrence of these pain syndromes (chronic overlapping pain conditions).[8],[9],[12],[19] More evidence regarding the diagnosis and treatment of these and other chronic overlapping pain conditions are needed to improve care for women.[8],[9],[12],[19] Interventional procedures can play an important diagnostic and therapeutic role in different types of pelvic pain syndromes, including: pudendal neuralgia, piriformis syndrome, and “border nerve” syndrome (ilioinguinal, iliohypogastric, and genitofemoral nerve neuropathy).[8],[9],[12],[19],[20] Ultrasonography allows visualization of the muscles and nerves and provides opportunities for real-time injections. Pudendal neuralgia commonly presents as chronic debilitating pain in the penis, scrotum, labia, perineum, or anorectal region.[19],[20],[21],[22],[23],[24],[25] The experts' consensus and low-level evidence suggests that treatments provided by physical therapists for patients with CPP are therapeutic exercises, manual therapy (internal and/or external), biofeedback, breathing techniques, and electrical stimulation to improve muscle function and decrease pain. Traditional medical treatments for CPP include oral analgesics (nonsteroidal anti-inflammatory drugs [NSAIDs] and opioids), hormonal suppression, tricyclic antidepressants, muscle relaxants, and even anticonvulsants. Additional interventions include injection therapy (using anesthetics or botulinum toxin A), neuromodulation, and surgery.[19]
In patients with pelvic floor musculoskeletal pain, several injection treatments can be performed using musculoskeletal ultrasound guidance.[19],[20],[21],[22],[23],[24],[25] Caudal epidural injection is the administration of medications into the epidural space via the sacral hiatus proven efficacy for CPP.[19],[20] This injection technique is used for the treatment of low back pain caused by lumbosacral nerve root compression. Successful caudal epidural injection relies on the accurate placement of a needle into the epidural space (sacral canal) through the sacral hiatus.[21] Medial branch blocks to the lumbosacral area have proven to be effective for CPP.[19],[20] Accurate medial branch blocks can be performed using ultrasound guidance.[20],[22] A curvilinear transducer is preferred for medial branch blocks. The patient is placed in the prone position and the transducer is placed in the transverse plane in relation to the lumbosacral spine. In this plane, the facet joint and the transverse process can be clearly seen. The medial branch is located at the 90° angle between the facet joint (superior articular process) and the transverse process. In-plane injection is performed in a lateral to medial approach. Under in-plane guidance, the needle can be clearly visualized during the entire injection process. [20,22.23] Pudendal nerve injection has been shown to be effective in treating pelvic floor pain.[19],[20] With the patient in the prone position, the curvilinear transducer is preferred for pudendal nerve injection. The transducer is placed in a transverse plane in relation to the sacrum. The transducer is then moved in a proximal to distal direction. Distal to the ischial spine, two hypoechoic bands can be visualized under ultrasound. One is the sacrotuberous ligament, and the other one is the sacrospinous ligament. The needle is then inserted in a medial to lateral direction, injected into the space between these two ligaments as the pudendal nerve is located here.[25] Positioning a patient for ultrasound-guided examination and injection of the piriformis muscle. The patient assumes the prone position during ultrasound-guided examination. A curvilinear transducer is preferred. The sacral hiatus is identified first; afterward, the transducer is moved in a lateral direction towards the greater trochanter. The piriformis muscle is located between the lateral border the sacrum and the greater trochanter. The piriformis muscle appears as a hyperechoic band deep in the gluteus maximus muscle. The sciatic nerve appears as an oval-shaped structure deep in the piriformis muscle.[26]
Pelvic girdle pain is a specific type of low back pain that commonly arises in relation to pregnancy, affecting an estimated 1 in 5 women.[27],[28],[29] Traditionally, women have been advised that pain is an inevitable part of pregnancy, and little effort has been made on the part of the medical community to offer prevention or treatment strategies. This “grin and bear it” attitude suggests that pain during pregnancy is normal, not treatable, and will resolve completely after delivery. Yet, current research on pain in pregnancy dispels such beliefs as out-of-date myths.[27],[28],[29]
Given that women carry pregnancies, lumbopelvic pain (LPP) during pregnancy and postcaesarean section pain are two important pain syndromes in women. LPP of pregnant women is very frequently left untreated due to care providers and patients assuming that it will spontaneously resolve with delivery. However, LPP is a significant source of lost work and social time.[27],[28],[29] Furthermore, pain persists following delivery in a substantial number of women and can persist for >1–2 years after delivery.[27],[28],[29] Risk factors associated with ongoing LPP include greater severity during pregnancy, earlier onset and inability to return to prepartum weight. This phenomenon is likely insufficiently understood, as the prevalence of low back pain is greater in women than in men and >10% women with chronic low back pain attribuitale to pregnancy.[27],[28],[29]
Evaluation of acute pelvic pain in pregnancy and the postpartum period is difficult. Knowledge of the clinical settings and sonographic features of acute pelvic pain in pregnancy and the postpartum period can lead to accurate diagnosis and appropriate management of the condition.[30] Certain analgesics may increase the risk for adverse fetal and pregnancy outcomes, while inadequate pain management can lead to adverse maternal outcomes such as depression, and hypertension. Paracetamol and NSAIDs are appropriate for mild to moderate pain, but NSAIDs should be avoided in the third trimester because of various risks. Short courses of weaker opioids are generally safe in pregnancy, although neonatal abstinence syndrome must be monitored in the third-trimester administration. Limited safety data for pregabalin and gabapentin indicate that these are unlikely to be major teratogens, and tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors have limited but overall reassuring safety data. Treatment should be tailored to the lowest therapeutic dose and shortest possible duration, and management should involve a discussion of risks and benefits and monitoring for a response. Further research is required to better understand the safety profile of various analgesics in pregnancy.[31]
There is low-quality evidence that exercise (any exercise on land or in water), may reduce pregnancy-related low-back pain.[32] However, there is moderate-to low-quality evidence suggesting that any exercise improves functional disability and reduces sick leave more than usual prenatal care.[32] There is evidence of physical activity interventions enhancing physical activity levels of pregnant women. Furthermore, they are potentially useful in alleviating pregnancy-related pain and psychological symptoms, reducing gestational weight gain, and increasing self-efficacy in enhancing physical activity levels among these individuals.[33]
Another common cause of postpartum pain is caesarean section. While the precise cause of this pain syndrome is incompletely understood. The scar pain, loss of anterior core muscle integrity and dysfunctional uterine bleeding due to a pocket-forming in the uterine scar are potential etiologies.[34],[35],[36] A key to reducing risk for postpartum caesarean section pain becoming chronic is an early and effective treatment.[34],[35],[36]
The common persistent vaginal and perineal pain after vaginal delivery may relate to perineal trauma. History of pregnancy-related and prepregnancy back pain and heavier body weight are risk factors for persistent back pain after pregnancy. Interventional studies targeting the most vigorously associated, targeting modifiable risk factors, such as acute postpartum pain, may lead to strategies for prevention and treatment of chronic back and pelvic pain after pregnancy.[34],[35],[36]
| Conclusion | | |
Gender differences in anatomy, physiology (especially hormonal effects), and psychological responses lead to differences in common pain conditions and management. There are more prevalence of chronic pain in women, especially FM, CPP, and chronic LPP caused by pregnancy. There are evidences supporting advanced chronic pain interventions for FM with tDCS and rTMS, diagnostic ultrasonography and ultrasound guided interventions for CPP, therapeutic exercises, physical activity and analgesic medications during pregnancy and lactation. However, the more well designed researches are needed to confirm the efficacy and safety of these advanced interventions.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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