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High velocity, low-amplitude (HVLA) spinal mobilization is one of the most popular chiropractic methods for addressing both lower and middle back pain. An evidence report compiled in 2010 by Bronfot et al. noted that spinal mobilization was also effective in adults for migraine, cervicogenic dizziness, and neck pain.^[1]There are three schools of technique of HVLA spinal mobilization, as described below:

1. Diversified technique: The most common of the three HVLA methodologies, a diversified technique is generally used to restore full range of motion to restricted joints. One short, high-velocity thrust is applied to the joint of interest to create an unlocking effect. Multiple adjustments can be made in a single appointment if more than one joint is restricted. Manipulation of patient body positioning may be necessary to allow for the ideal angle and leverage for diversified HVLA. 
2. Palmer-Gonstead adjustment: The Palmer-Gonstead adjustment is similar to the diversified technique in both duration and magnitude of force, but places greater emphasis on isolating an exact spinal location for ideal joint adjustment. Location can be determined through palpation (both with motion and static), visualization, instrumentation, and X-ray analysis. A wide variety of specially-designed tables, chairs, and other equipment are employed to alter body configuration and create optimal angles for spinal adjustment. 
3. Drop technique: Also known as the Thompson Terminal Point technique, the drop technique focuses specifically on facilitating the movement of the restricted joint during HVLA mobilization. Patients are placed on specialized tables that have the ability to drop a short distance during the physician’s or chiropractor’s thrust. Occasionally, the drop of the table along is sufficient to free the restricted joint. The drop technique is often used as a complement to the diversified technique.

Little research has been done to compare the relative efficacy of these techniques to each other; however, preliminary findings suggest they may perform similarly.^[2] Regardless, it has been found that overall, successful HVLA spinal mobilization results in significantly superior patient outcomes as compared to placebos,^[3] and should be considered a useful method for treating a variety of back-related issues.

References

^[1] Bronfort G, Haas M, Evans R, Leininger B, Triano J. Effectiveness of manual therapies: the UK evidence report. Chiropr Osteopat. 2010 Feb 25;18:3. doi:10.1186/1746-1340-18-3. PMID: 20184717; PMCID: PMC2841070.

^[2] Cao DY, Reed WR, Long CR, Kawchuk GN, Pickar JG. Effects of thrust amplitude and duration of high-velocity, low-amplitude spinal manipulation on lumbar muscle spindle responses to vertebral position and movement. J Manipulative Physiol Ther. 2013;36(2):68-77. doi:10.1016/j.jmpt.2013.01.004.

^[3] von Heymann WJ, Schloemer P, Timm J, Muehlbauer B. Spinal high-velocity low amplitude manipulation in acute nonspecific low back pain: a double-blinded randomized controlled trial in comparison with diclofenac and placebo. Spine (Phila Pa 1976). 2013 Apr 1;38(7):540-8. doi:10.1097/BRS.0b013e318275d09c. PMID: 23026869.

Low back pain is one of the most prevalent chronic conditions world-wide, affecting adults as young as 18, and worsens with age [4]. Typical interventions for alleviating low back pain involve adjustments in life-style factors such as workload, social support, and physical therapy, with very rare cases requiring admission to an emergency room [2]. However, severe back pain can also be a symptom of a lesser known or misdiagnosed condition [3][4]. For instance, Cauda Equina Syndrome (CES) is a rare condition that typically requires immediate surgical treatment in order to avoid serious excretory complications (incontinence) and permanent nerve damage [5][7]. 

The cauda equina, Latin for “horse’s tail”, is a bundle of spinal nerve roots originating near the distal end of the spinal cord that send and receive nerve impulses to pelvic organs and lower limbs [3][4][7]. Damage to the cauda equina can result in sudden and severe symptoms that disrupt motor and sensory functions of the lower extremities, bladder and bowels [3][5]. Typically, this damage arises from compression and inflammation of the nerve roots, caused by a herniated disc in the lumbar region [3][7]. Common causes of a lumbar disc herniation include excessive pressure from loading or strain from sudden twisting movements [6]. Other causes include but are not limited to spinal infections and inflammation, lumbar spine trauma, spinal lesions and tumors, lumbar spinal stenosis, and spinal hemorrhages [5][7]. 

The severity of symptoms varies depending on the degree of compression and number of nerves injured [5][6]. For some patients, the onset of cauda equina symptoms can develop within 24 hours (acute onset) or over weeks and months (gradual onset) [5]. Typical symptomatic indicators of CES include severe low back pain, weakness, tingling, or sharp, hot pain in one or both legs and/or “saddle region” (groin, buttocks, genitals, upper thighs), recent onset of bladder and bowel dysfunction and/or incontinence, and loss of reflexes in the lower extremities [3-7]. Patients are typically classified into two categories: CES-R (urinary retention) and CES-I (an incomplete syndrome) [4]. In addition to a diagnostic screening with an MRI, Gardner et al. suggests implementation of a trigone sensitivity test in order to discern “genuine” neurological deficits of bladder retention [4].

As mentioned above, CES usually requires immediate hospitalization and prompt decompression surgery in order to reduce the symptoms of neurological dysfunction and avoid incontinence and permanent paralysis [3][4]. As with most neurological conditions, the sooner the diagnosis and subsequent treatment, the better the chance of recovery with minimal lasting neurological damage [1][4][5]. Ideally, CES is treated early within 24 to 48 hours for the best chance of complete sensory recovery [1][4]. However, surgery does not necessarily eradicate the possibility of irreversible outcomes [6]. It is important to note that the rarity and variability of CES contributes to misdiagnosis and delay of treatment, contributing to its “prominent position in the medico-legal field” [4]. While attention of CES has increased in the medical field, it is crucial for patients and doctors to be informed and aware of this rare syndrome.

References

1. Bečulić, H., Skomorac, R., Jusić, A., Alić, F., Imamović, M., Mekić-Abazović, A., Efendić, A., Brkić, H., & Denjalić, A. (2016). Impact of timing on surgical outcome in patients with cauda equina syndrome caused by lumbar disc herniation. Medicinski Glasnik : official publication of the Medical Association of Zenica-Doboj Canton, Bosnia and Herzegovina, 13(2), 136–141. https://doi.org/10.17392/861-16

2. Buruck, G., Tomaschek, A., Wendsche, J., Ochsmann, E., & Dörfel, D. (2019). Psychosocial areas of work life and chronic low back pain: a systematic review and meta-analysis. BMC musculoskeletal disorders, 20(1), 480. https://doi.org/10.1186/s12891-019-2826-3

3. Cauda Equina Syndrome. American Association of Neurological Surgeons.https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Cauda-Equina-Syndrome

4. Gardner, A., Gardner, E., & Morley, T. (2011). Cauda equina syndrome: a review of the current clinical and medico-legal position. European Spine Journal: official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society, 20(5), 690–697. https://doi.org/10.1007/s00586-010-1668-3

5. Hoy, D., Bain, C., Williams, G., March, L., Brooks, P., Blyth, F., Woolf, A., Vos, T., & Buchbinder, R. (2012). A systematic review of the global prevalence of low back pain. Arthritis and Rheumatism, 64(6), 2028–2037. https://doi.org/10.1002/art.34347

6. Kapetanakis, S., Chaniotakis, C., Kazakos, C., & Papathanasiou, J. V. (2017). Cauda Equina Syndrome Due to Lumbar Disc Herniation: a Review of Literature. Folia Medica, 59(4), 377–386. https://doi.org/10.1515/folmed-2017-0038

7. Villavicencio, A. Cauda Equina Syndrome (2016). Cauda Equina Syndrome. Spine-Health. https://www.spine-health.com/conditions/lower-back-pain/cauda-equina-syndrome

Osteoarthritis (OA) is the most common form of arthritis and the most common joint disorder in the United States, affecting approximately 1 in 7 adults [1]. OA is a disease that is caused and worsened by the continual inflammation of joint cartilage along with the surrounding bone and synovium [2] [3]. OA is caused primarily by joint injury and overuse, as these occurrences trigger the production of inflammatory mediators—such as cytokines and chemokines—in the synovium and chondrocytes (cartilage cells). During later stages of OA, cartilage fragments can fall into the synovium, exacerbating the process. Those who are older, obese, and work more physically demanding jobs are more likely to develop OA, as these factors all increase the use of or stress on joints. OA also disproportionately affects women; of those over the age of 60, women are almost twice as likely to develop the condition (18.0% of women over 60 versus 9.6% of men) [4]. OA can develop in any joint, but most commonly occurs in the knees, hips, hands, and spine.

Common symptoms of OA include joint pain, stiffness, swelling, decreased range of motion, and fatigue. This often results in intense discomfort during use, and can inhibit function of the joint, leading to an inability to walk if OA is present in the hip, knee, or foot. However, an individual’s level of pain or discomfort does not translate to the structural deterioration of the joint—thus, OA is often difficult to diagnose symptomatically, especially when pain is less present in its early stages [5]. OA has no cure; its end-stage involves the irreversible damage of joint cartilage, necessitating surgical joint replacement. As such, early diagnosis of OA—through an analysis of symptoms and X-ray or MRI screenings—is imperative for preventive treatment [6]. The presence of developing osteophytes (bone outgrowths), along with narrowing of joint space and deformity are indications of OA. 

Management of OA is largely dependent on the patient and severity. Mild OA can be managed through simple exercises that do not stress the joints, such as aerobics and light muscle-strengthening exercises [1] [7] [8]. Patients with obesity are often given weight loss suggestions, and almost all patients are suggested to attend self-management education courses, which are designed to instruct patients to adopt practices to mitigate daily pain and discomfort. These practices range from identifying unhealthy exercise habits to stress management techniques to improving sleep schedules and diet. Most of all, these courses aim to support patients with the emotional toll of OA, as deteriorating joint function often leads to frustration and depression [1] [4]. Simple analgesics assist patients with day-to-day activities and if needed, topical or oral NSAIDs (non-steroidal anti-inflammatory drugs) can also be prescribed [9]. Physiotherapy is also often recommended. In severe cases, supportive devices like crutches and canes or intra-articular corticosteroid injections may become necessary for function and, as previously stated, end-stage OA requires joint replacement. Although not empirically proven, alternative medicine methods—like acupuncture—have also been reported to improve OA symptoms. 

Hence, it is vital that those who are high-risk of developing OA consult medical professionals in a timely manner to catch symptoms before the OA develops and causes irreversible damage. Individuals who attribute mild joint pain or stiffness solely to the aging process may mistakenly overlook a developing case of OA. When diagnosed early, OA can be alleviated through proper self-management and exercise practices, leading to a superior quality of life. 

References

1. Centers for Disease Control and Prevention (CDC). (2020). A National Public Health Agenda for Osteoarthritis: 2020 Update. https://www.cdc.gov/arthritis/docs/oaagenda2020.pdf
2. Berenbaum, F. (2013). Osteoarthritis as an inflammatory disease (osteoarthritis is not osteoarthrosis!). Osteoarthritis and cartilage, 21(1), 16-21.
3. Goldring, M. B., & Otero, M. (2011). Inflammation in osteoarthritis. Current opinion in rheumatology, 23(5), 471.
4. Arthritis Foundation. (2019). Arthritis by the Numbers: Book of Trusted Facts & Figures.https://www.arthritis.org/getmedia/e1256607-fa87-4593-aa8a-8db4f291072a/2019-abtn-final-march-2019.pdf
5. Glyn-Jones, S., Palmer, A. J. R., Agricola, R., Price, A. J., Vincent, T. L., Weinans, H., & Carr, A. J. (2015). Osteoarthritis. The Lancet, 386(9991), 376-387.
6. Zhang, Y., & Jordan, J. M. (2010). Epidemiology of osteoarthritis. Clinics in geriatric medicine, 26(3), 355-369.
7. Fransen, M., McConnell, S., Harmer, A. R., Van der Esch, M., Simic, M., & Bennell, K. L. (2015). Exercise for osteoarthritis of the knee. Cochrane database of systematic reviews, (1).
8. Fransen, M., McConnell, S., Hernandez‐Molina, G., & Reichenbach, S. (2014). Exercise for osteoarthritis of the hip. Cochrane Database of Systematic Reviews, (4).
9. Dieppe, P. A., & Lohmander, L. S. (2005). Pathogenesis and management of pain in osteoarthritis. The Lancet, 365(9463), 965-973.

Chiropractic has a long history of serving the public by healing people through the use of natural methods.⁶ Founded by David Daniel Palmer in September 1985, chiropractic has become one of the most commonly used complementary and alternative medicine therapies in the world.² Currently, chiropractors practice in over 100 countries, in which 90 have established national chiropractic associations.² Worldwide, billions are spent each year for their services.¹ In the United States alone, there are over 60,000 licensed chiropractors, making chiropractic a major stakeholder in the healthcare expenditures of the nation.² Knowing the foundations of chiropractic will assist in the understanding of this growing profession. 

Originating from an ancient Greek phrase meaning “done by hand,” chiropractic was viewed by Palmer as an integration of science, art, and philosophy.³ Early chiropractic displayed many aspects of a religion, declaring that there existed an “innate intelligence” that enabled the body to heal itself.¹ The “innate” regulated all body functions, but was hindered by “vertebral subluxations.”^1,5 People were well when the “innate” had unobstructed freedom to act throughout the body.⁵ Diseases were caused by a lack of normal transmission of the “innate.”⁵ The role of chiropractors was to correct subluxations through manual adjustments of the spine and, therefore, restore the flow of the “innate.”^1,5 Early chiropractic was advertised as a cure for many ailments like insanity, sexual dysfunction, measles, and influenza.¹ Chiropractic soon became known as “a science of healing without drugs.”¹ 

Today, chiropractic is defined by the World Health Organization as a health care profession concerned with the diagnosis, treatment, and prevention of disorders of the neuromusculoskeletal system, with an emphasis on manual corrections of misalignments of the vertebrae.⁴ Modern chiropractic philosophy views health as an expression of biological, psychological, social, and spiritual factors.⁷ At the very center of chiropractic is the belief that the body is self-regulating and capable of healing itself.⁶ This perspective represents a holistic biopsychosocial philosophy of health, in contrast to the biomedical one typically shared by medical doctors.⁷ Chiropractic embraces three main principles.¹ First, there is a symbiotic relationship between the spine and health.¹ Second, subluxations negatively affect health.¹ Third, correction of subluxations by spinal manipulation improves health.¹ 

Chiropractors address patients’ health and wellness by using conservative and natural methods, as opposed to prescription drugs and surgery.⁶ They are mainly focused on the relationship between structure, primarily the spine and musculoskeletal system, and function, as directed by the nervous system.⁷ Chiropractors propose that neurological disturbances in the spine and other areas can cause dysfunction to appear in remote organs and tissues.⁶ Since the nervous system has an influence on all bodily functions, chiropractors argue that corrections of dysfunctional areas of the spine and other parts of the body improves health.⁶ They utilize chiropractic manipulations, also known as adjustments, to bring relief to patients most commonly suffering from back and neck pain, headache, sports injuries, and neuromusculoskeletal disorders.⁶ Chiropractic manipulations involve applying specific and controlled movements to various joints in the body to help restore normal structure and function.⁶ In addition to providing adjustments to patients, chiropractors may also provide patients with rehabilitation exercises and counsel patients on healthy lifestyle and nutritional habits.⁷ 

It is important for healthcare professionals to understand the fundamentals of chiropractic. Patient visit to chiropractors are becoming increasingly popular, accounting for 30% of all visits made to complementary and alternative practitioners.⁶ As the percentage of patients receiving chiropractic care each year continues to grow, healthcare professionals should be knowledgeable about the profession and be prepared to answer questions patients may have.⁶ 

References 

1. Ernst, Edzard. 2008. “Chiropractic: A Critical Evaluation”. Journal of Pain and Symptom Management 35 (5): 544-562. doi:10.1016/j.jpainsymman.2007.07.004. 

2. Beliveau, Peter J. H., Jessica J. Wong, Deborah A. Sutton, Nir Ben Simon, André E. Bussières, Silvano A. Mior, and Simon D. French. 2017. “The Chiropractic Profession: A Scoping Review of Utilization Rates, Reasons for Seeking Care, Patient Profiles, And Care Provided”. Chiropractic & Manual Therapies 25 (1). doi:10.1186/s12998-017-0165-8. 

3. Senzon, Simon. 2018. “An Integral Approach to Unifying the Philosophy of Chiropractic”. Journal of Conscious Evolution 2 (2). 

4. Glucina, Tanja T., Christian U. Krägeloh, Panteá Farvid, and Kelly Holt. 2020. “Moving Towards A Contemporary Chiropractic Professional Identity”. Complementary Therapies in Clinical Practice 39: 101105. doi:10.1016/j.ctcp.2020.101105. 

5. Palmer, B. J. 1920. The Science of Chiropractic. Davenport, Iowa: Palmer School of Chiropractic. 

6. Hawk, Cheryl. 2017. The Praeger Handbook of Chiropractic Health Care. Santa Barbara: ABC-CLIO, LLC. 

7. Hawk, Cheryl, and John Weeks. 2017. Careers in Chiropractic Health Care: Exploring A Growing Field. Santa Barbara: ABC-CLIO, LLC. 

When athletes experience an anterior cruciate ligament (ACL) injury, physical activity becomes highly restricted1. Following an ACL surgery, there are many factors that medical professionals have to consider when allowing athletes or other patients with ACL injuries to begin resuming physical activity1. If incorrect recommendations are made for resuming full activity, the patient can experience additional injuries by adding pressure to the injured ACL, which can be even more dangerous1. As such, figuring out when a patient can resume full activity after an ACL surgery is an incredibly difficult task for many medical professionals.

Zaffagnini et al. (2015) outlines the various intrinsic and extrinsic factors that physicians often consider when making the decision to allow patients to return to a full range of physical activity1. The intrinsic factors include genetics, which is how a patient biologically responds to an ACL surgery, as well as the type of ACL injury and the patient’s motivation or psychological attitude towards resuming full activity1. The extrinsic factors are often the ones that the physician is able to better control. These factors include the technique used during an ACL reconstruction surgery, the type of graft used, and the rehabilitation support that is provided1. Clearly, there are several variables involved in a physician’s decision to allow a patient to resume full activity after an ACL surgery. This creates a challenge for the medical professional as there is no one solution that can be applied to all patients.

To see these factors in play, McCullough et al. (2014) carried out a retrospective cohort study with football players that had experienced an ACL injury2. Looking at both high school and collegiate players, the researchers found that approximately 50% of students did not return to resuming full activity of their sport after their injury2. Some of the factors that influenced players’ ability to resume full activity include the aforementioned extrinsic factors such as the type of graft; however, it seems that a majority of the decision to resume full activity relied on the intrinsic factors2. Interestingly, psychological attitude and motivation were two factors that played a large role, but literature on this matter and how these factors can be used to increase the percentage of players resuming full activity is quite scant2.

Ardern et al. (2014) is just one of the small handful of studies that investigates how psychological factors can influence a player’s return to full activity following an ACL injury3. Using a cross-sectional study design, the researchers looked at factors such as self-efficacy, psychological readiness, and fear of reinjury to assess how a patient’s psychological attitude might have influenced their recovery3. The results revealed that athletes who had completely resumed full activity after surgery were those who

initially had more positive attitudes indicating higher psychological readiness3. For players who had not resumed full activity, the researchers found that players often had a fear of reinjury or a lack of trust in their own body’s abilities3. Ardern et al. (2014) provides rather interesting insights as information on the effect of psychological factors can help physicians then create better interventions and programs for patients to resume full activity.

These studies are critical as a medical professional’s decision to allow their patient to resume full activity after an ACL surgery relies on a large variety of variables. More research similar to Ardern et al. (2014) exploring different factors in greater detail are needed in order for physicians to develop more successful rehabilitation plans for their patients.

References:

(1) Zaffagnini S, Grassi A, Serra M, Marcacci M. Return to sport after ACL reconstruction: how, when and why? A narrative review of current evidence. Joints. 2015;3(1):25‐30. Published 2015 Jun 8.

(2) McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523‐2529. doi:10.1177/0363546512456836

(3) Ardern CL, Österberg A, Tagesson S, Gauffin H, Webster KE, Kvist J. The impact of psychological readiness to return to sport and recreational activities after anterior cruciate ligament reconstruction. Br J Sports Med. 2014;48(22):1613‐1619. doi:10.1136/bjsports-2014-093842

Fibromyalgia syndrome (FMS) refers to a chronic condition causing pain, tenderness, and stiffness in the muscles, joints, and tendons. This pain is typically widespread, affecting the neck, buttocks, shoulders, arms, upper back, and chest on both sides of the body. Patients also report having “tender points”, which refer to localized areas of the body that cause widespread pain and muscle spasms when touched.¹ FMS is also characterized by restlessness, tiredness, fatigue, anxiety, depression, and impaired bowel function.² Despite experiencing severe pain, patients do not develop tissue damage or deformities because there is no inflammation associated with FMS, which makes it difficult to elucidate the mechanisms of this condition.³ FMS commonly arises in young and middle-aged females in the form of persistent pain, fatigue, stiffness, cognitive difficulties, anxiety, depression, and functional impairment. Furthermore, the prevalence in the United States is 6% to 15%, with women being five times as likely as men to develop FMS.⁴

While the mechanistic underpinnings remain unclear, there is a characteristic pathophysiology associated with FMS. Namely, patients commonly experience changes in their sleep patterns and neuroendocrine transmitters – such as serotonin, substance P, growth hormone, and cortisol – which indicates that regulation of the autonomic and neuroendocrine systems serves as the biological basis of the condition.⁵ Although FMS is not life-threatening, it is characterized by debilitating, chronic pain that may result from a variety of interconnected mechanisms. More specifically, patients with FMS may experience aberrant pain processing due to central sensitization; this refers to the blunting of inhibitory pain pathways and associated changes in neurotransmitter levels. Due to aberrant neurochemical processing of sensory signals, the threshold of pain is significantly lowered in patients with FMS.⁶ Therefore, many of the symptoms associated with FMS may be explained by alterations in the autonomic, neuroendocrine, and pain processing systems.

Management of FMS is often patient-centered and can involve a variety of therapeutic approaches. Pain medications used to treat FMS include paracetamol, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetaminophen. In addition to analgesics, other drugs such as antidepressants, anticonvulsants, dopamine agonists, and growth hormones, can be useful in the management of FMS.⁷ A combination of tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) can produce mild to moderate improvement in symptoms of FMS. In addition, duloxetine, a serotonin and norepinephrine reuptake inhibitor, has shown promise in patients with FMS.

Lifestyle modifications are a powerful method to alleviate the symptoms of FMS. For example, patients can practice stress management to avoid increased levels of stress and feelings of depression, anxiety, and frustration. Cognitive behavioral therapy, relaxation training, group therapy, and biofeedback are all effective treatment options that can help patients reduce their stress levels.⁸ Exercise such as walking, jogging, or sports, is another lifestyle change that can help alleviate symptoms by further reducing stress. Additionally, there are several alternative therapies for FMS, such as Chinese herbal medications, Chinese herbal tea, acupuncture, and Tai-chi.⁸

In summary, FMS is a common condition characterized by widespread pain and stiffness, sleep disturbances, anxiety, and depression, among other symptoms. Although there are many theories of etiology, the biological underpinnings of FMS are not fully understood. With the proper treatment from a skilled chiropractor who can assist in developing an effective exercise plan and implementing appropriate lifestyle changes, patients with FMS can alleviate pain and improve their quality of life.

References

1. Mease PJ, Clauw DJ, Arnold LM, Goldenberg DL, Witter J, Williams DA, et al. Fibromyalgia syndrome. J Rheumatol 2005. Nov;32(11):2270-2277.
2. Shleyfer E, Jotkowitz A, Karmon A, Nevzorov R, Cohen H, Buskila D. Accuracy of the diagnosis of fibromyalgia by family physicians: is the pendulum shifting? J Rheumatol 2009. Jan;36(1):170-173.
3. Schmidt-Wilcke T, Clauw DJ. Fibromyalgia: from pathophysiology to therapy. Nat Rev Rheumatol 2011. Sep;7(9):518-527.
4. Wolfe F, Ross K, Anderson J, Russell IJ, Hebert L. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum 1995. Jan;38(1):19-28.
5. Arnold LM, Hudson JI, Keck PE, Auchenbach MB, Javaras KN, Hess EV. Comorbidity of fibromyalgia and psychiatric disorders. J Clin Psychiatry 2006. Aug;67(8):1219-1225.
6. Yunus MB. Role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain. Best Pract Res Clin Rheumatol 2007. Jun;21(3):481-497.
7. Katz RS, Wolfe F, Michaud K. Fibromyalgia diagnosis: a comparison of clinical, survey, and American College of Rheumatology criteria. Arthritis Rheum 2006. Jan;54(1):169-176.
8. Culpepper L. Nonpharmacologic care of patients with fibromyalgia. J Clin Psychiatry 2010. Aug;71(8):e20.

Despite yearly healthcare expenditures totaling billions of dollars, the annual prevalence of low back pain (LBP) remains near 40% in the adult population¹ and the condition continues to be a prominent cause of physical disability and psychological distress.²  Recent findings have indicated a high prevalence of sleep disturbance in patients suffering from chronic and acute LBP³ which may further worsen physical and psychological symptoms of LBP in addition to contributing to the development of other chronic diseases such as obesity, type-2 diabetes, hypertension, and coronary artery disease.^3,4

A meta-analysis, consolidating data across severalmajor LBP studies, determined that nearly 60% of LBP patients reported “yes” to the questionnaire item: “I sleep less well because of my back”.³  Although this constitutes quantitative evidence of a significant association between LBP and sleep disturbance, the directionality of that relationship is not yet well understood.⁵   

Commonly, pain is perceived to be the agent responsible for reduced quality sleep⁶ but there is, in fact, cause to believe that the relationship between LBP and sleep disturbance is bidirectional.⁵  This conclusion is supported by recent clinical evidence that has suggested that sleep and pain exist in a reciprocal relationship,^6,7 leading to the proposition that LBP and sleep disturbance may exacerbate each other.  Multiple laboratory experiments have demonstrated that the disturbance of normal sleep patterns may induce musculoskeletal pain in healthy subjects and worsen pain intensity in those who suffer from existing musculoskeletal or osteoarthritic pain.^8,9,10  These findings, which illustrate the important analgesic role that sleep may have in mediating existing pain, have resulted in the proposition that LBP and sleep disturbance exist in a reciprocal, cyclical relationship, in which LBP contributes to poor sleep quality which, in turn, may worsen the intensity of LBP.⁵

In the first longitudinal study directly evaluating the possibility that LBP and sleep disturbance exist in a bidirectional relationship, evidence was found in support of this hypothesis.⁵  The study measured patients’ rate of sleep disturbance through both subjective measures, defined by subjects’ perception of sleep quantity and quality, and through objective measures, characterized by biometric data obtained while patients slept.  It was found that nights, during which patients experienced higher rates of sleep disturbance, were, on average, followed by days during which patients experienced increased pain intensity.  In turn, higher rates of daytime LBP resulted in lower quality sleep the following night by both subjective and objective measures, thereby supporting the conclusion that there exists a reciprocal, causal relationship between LBP and sleep disturbance.⁵  Further, the relationship was demonstrated to be independent of potential confoundssuch as the chronicity of LBP as well as psychological factors.⁵

While this study constitutes strong evidence for the existence of a bidirectional relationship between the conditions of LBP and sleep disturbance and is supported by several other studies on the general relationship between sleep and musculoskeletal pain,^9,10 it should be noted that there also exist several studies in which patients, with other forms of chronic pain, did not experience a significant pain-sleep relationship.^11,12  Across different studies, it is difficult to standardize the construct of sleep quality and, further, patients’ assessment of pain intensity is subjective; these two factors may account for these conflicting findings.⁵

What is known for certain is that there is a significant association between sleep disturbance and LBP, and that these conditions, more than likely, exacerbate each other in at least some capacity.  Although there have been some promising findings in long-term longitudinal studies, suggesting that reducing sleep problems may improve the long-term prognosis of chronic LBP,¹³ it is imperative that further research be conducted in order to better define the relationship between LBP and sleep disturbance and to develop a better understanding of how to effectively manage both conditions.⁵

References:

1. Hoy, D., Bain, C., Williams, G., March, L., Brooks, P., Blyth, F., … Buchbinder, R. (2012). A systematic review of the global prevalence of low back pain. Arthritis & Rheumatism, 64(6), 2028–2037. https://doi.org/10.1002/art.34347
2. Kelly, G. A., Blake, C., Power, C. K., OʼKeeffe, D., & Fullen, B. M. (2011). The Association Between Chronic Low Back Pain and Sleep. The Clinical Journal of Pain, 27(2), 169–181. https://doi.org/10.1097/ajp.0b013e3181f3bdd5
3. Alsaadi, S. M., McAuley, J. H., Hush, J. M., & Maher, C. G. (2010). Prevalence of sleep disturbance in patients with low back pain. European Spine Journal, 20(5), 737–743. https://doi.org/10.1007/s00586-010-1661-x
4. Haack, Monika, & Mullington, J. M. (2005). Sustained sleep restriction reduces emotional and physical well-being. Pain, 119(1–3), 56–64. https://doi.org/10.1016/j.pain.2005.09.011
5. Alsaadi, S. M., McAuley, J. H., Hush, J. M., Lo, S., Bartlett, D. J., Grunstein, R. R., & Maher, C. G. (2014a). The Bidirectional Relationship Between Pain Intensity and Sleep Disturbance/Quality in Patients With Low Back Pain. The Clinical Journal of Pain, 30(9), 755–765. https://doi.org/10.1097/ajp.0000000000000055
6. Moldofsky, H. (2001). Sleep and pain. Sleep Medicine Reviews, 5(5), 385–396. https://doi.org/10.1053/smrv.2001.0179
7. Haack, M., Scott-Sutherland, J., Santangelo, G., Simpson, N. S., Sethna, N., & Mullington, J. M. (2012). Pain sensitivity and modulation in primary insomnia. European Journal of Pain, 16(4), 522–533. https://doi.org/10.1016/j.ejpain.2011.07.007
8. Kundermann, B., Spernal, J., Huber, M. T., Krieg, J.-C., & Lautenbacher, S. (2004). Sleep Deprivation Affects Thermal Pain Thresholds but Not Somatosensory Thresholds in Healthy Volunteers. Psychosomatic Medicine, 66(6), 932–937. https://doi.org/10.1097/01.psy.0000145912.24553.
9. Smith, M. T., Edwards, R. R., McCann, U. D., & Haythornthwaite, J. A. (2007). The Effects of Sleep Deprivation on Pain Inhibition and Spontaneous Pain in Women. Sleep, 30(4), 494–505. https://doi.org/10.1093/sleep/30.4.494
10. Roehrs, T., Hyde, M., Blaisdell, B., Greenwald, M., & Roth, T. (2006). Sleep Loss and REM Sleep Loss are Hyperalgesic. Sleep, 29(2), 145–151. https://doi.org/10.1093/sleep/29.2.145
11. Tang, N. K. Y., Goodchild, C. E., Sanborn, A. N., Howard, J., & Salkovskis, P. M. (2012). Deciphering the temporal link between pain and sleep in a heterogeneous chronic pain patient sample: a multilevel daily process study. Sleep, 35(5), 675-87A. https://doi.org/10.5665/sleep.1830
12. Lewandowski, A. S., Palermo, T. M., De la Motte, S., & Fu, R. (2010). Temporal daily associations between pain and sleep in adolescents with chronic pain versus healthy adolescents. Pain, 151(1), 220–225. https://doi.org/10.1016/j.pain.2010.07.016
13. Skarpsno, E. S., Mork, P. J., Nilsen, T. I. L., & Nordstoga, A. L. (2019b). Influence of sleep problems and co-occurring musculoskeletal pain on long-term prognosis of chronic low back pain: the HUNT Study. Journal of Epidemiology and Community Health, 74(3), 283–289. https://doi.org/10.1136/jech-2019-212734

The temporomandibular articulation is composed of a group of anatomical structures including the bilateral, diarthrodial, and temporomandibular joints (TMJs). The TMJ and its associated structures play a key role in mandibular motion and redistributing stress from daily tasks such as chewing, swallowing, and speaking. TMJ disorders, or TMD, refer to a group of conditions that cause pain and dysfunction in the jaw joint and the muscles controlling the jaw.¹ As a degenerative musculoskeletal condition, TMD is associated with morphological and functional deformities including abnormalities in the intra-articular discal position and dysfunction of the surrounding musculature.² Common symptoms include painful joint sounds, restricted range of motion, and orofacial pain.

Although signs of TMD appear in 60-70% of the general population, only one in four individuals actually report symptoms.³ The frequency of severe symptoms (e.g. headaches and facial pain) associated with an urgent need of treatment is 1-2% in children, 5% in adolescents, and 5-12% in adults.⁴ Furthermore, studies in the 1980s found TMD symptoms in 16-59% of the general population, with only 3-7% of the adult population seeking treatment. A major risk factor for TMD is gender as symptoms appear four times as often in females than in males. Females also represent the vast majority of the patient population, with nearly 90% of TMD patients being female.⁴

Nearly 70% of TMD patients suffer from internal derangement, which refers to a malpositioning of the TMJ disc. Although the progression of TMD is not fully understood, the present evidence points to osteoarthritis (for inflammatory states) and osteoarthrosis (for non-inflammatory states) as the primary pathologies.⁵ For example, Bertram et al found that 54.2% of patients with unilateral TMD suffered from osteoarthritis in the affected joint.⁶ In contrast to asymptomatic patients, who show minimal morphological change in the condyle and articular eminence, symptomatic patients with internal derangement show substantial osseous change over time. Osteoarthritic changes associated with TMD may include deterioration of the articular cartilage and thickening of the underlying bone.¹ Once joint breakdown begins, osteoarthritis can become crippling and eventually lead to significant morphological deformity and functional obstruction.

Treatment options for TMD vary with respect to the severity of degeneration. Non-invasive modalities include physical therapy, occlusal splints, and pharmacologics. Physical therapy for TMD involves electrophysical modalities (e.g. transcutaneous electric nerve stimulation) and manual techniques aimed at relieving pain in the joint and improving range of motion.⁷ Physical therapists may also implement behavior changes by altering the patient’s posture, diet, and stress-related habits. In previous studies, manual therapies demonstrated promise in treating TMD, especially when combined with exercise regimens aimed at strengthening the masticatory and cervical spine muscles to enhance mobility.⁸ Pharmacologic agents commonly prescribed to TMD patients include non-steroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants. Minimally invasive therapies for TMD include sodium hyaluronate and corticosteroid injections, arthrocentesis, and arthroscopy.¹ In the 5% of cases where nonsurgical methods fail, open joint surgery is potentially necessary to restore mandibular motion and relieve orofacial pain. Open joint surgery commonly involves discectomy, reshaping the articulating surfaces, and implanting alloplastic materials.⁹ When the negative effects of joint degeneration and pain exceed the potential benefit of less invasive surgical methods, total joint replacement may be required. 

References

1. Zarb GA, Carlsson GE. Temporomandibular disorders: osteoarthritis. J Orofac Pain. 1999;13:295–306.
2. Laskin DM, Greenfield W, Gale E.  The President’s Conference on the Examination, Diagnosis, and Management of Temporomandibular Disorders. Chicago: American Dental Association; 1983.  
3. Graber, Rakosi, Petrovic . In: Dentofacial Orthopedics with Functional Appliances. 2nd ed. St. Louis: Mosby; 2009. Functional analysis- examination of temporomandibular joint and condylar movement; pp. 135–40.
4. Athanasiou AE. Orthodontics and craniomandibular disorders. In: Samire, Bishara, editors. Textbook of orthodontics. 2nd ed. Philadelphia: Saunders; 2003. pp. 478–93.
5. Farrar WB, McCarty WL., Jr The TMJ dilemma. J Ala Dent Assoc. 1979;63:19–26.
6. Bertram S, Rudisch A, Innerhofer K, Pumpel E, Grubwieser G, Emshoff R. Diagnosing TMJ internal derangement and osteoarthritis with magnetic resonance imaging. J Am Dent Assoc. 2001;132:753–61.
7. McNeely ML, Armijo Olivo S, Magee DJ. A systematic review of the effectiveness of physical therapy interventions for temporomandibular disorders. Phys Ther. 2006;86:710–25.
8. Rocabado M. The importance of soft tissue mechanics in stability and instability of the cervical spine: a functional diagnosis for treatment planning. Cranio. 1987;5:130–8.
9. Dolwick MF. The role of temporomandibular joint surgery in the treatment of patients with internal derangement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997;83:150–5.

Cupping therapy is an ancient technique that appears in numerous ancient medical systems, including Chinese, Unani, Korean, Tibetan, and Oriental medicine.¹ The oldest medical text to mention cupping therapy is Eber’s papyrus (1550 BC) from Ancient Egypt. Hippocrates, the ancient Greek physician, mentioned cupping in a collection of medical notes describing the different types of cups and methods of application. Furthermore, cupping therapy was commonly used in Arabic and Islamic countries; physicians such as Ibn Sina (AD 980-1037), Al-Zahrawi (AD 936-1036), and Abu Bakr Al-Razi (AD 854-925) described cupping sites and created illustrations of cupping tools with accompanying diagrams. During the Renaissance, between the 14th and 17th centuries, cupping therapy spread to Italy and, subsequently, all of Europe.¹ Although cupping is an ancient treatment used by various cultures and societies, its mechanism was not well understood until, recently, interest in cupping re-emerged and scientists began investigating in mechanistic underpinnings.² 

There are many types of cupping therapy, but dry and wet cupping are the most common. In dry cupping, skin is pulled into the cup without scarification; in wet cupping, the skin is lacerated so that blood is drawn into the cup.² Each cupping session lasts about 20 minutes. In the first step, the therapist disinfects specific skin points marked for cupping. Next, a suitably sized cup is placed on the selected area, heat or manual suction is applied to create a vacuum inside the cup, and the cup is left for a period of three to five minutes. For wet cupping, a sanitized surgical scalpel, needle, or auto-lancing device is used to create superficial incisions on the skin³; the cup is then reapplied to the skin for three to five minutes, and the area is disinfected with an FDA approved disinfectant and dressed.⁴  

A converging amount of evidence supports the positive effects of cupping. To elaborate, cupping therapy leads to improved pain control by increasing endogenous opioid production in the brain, and promotes comfort and relaxation on a systemic level. Furthermore, researchers propose that cupping therapy improves blood circulation and enhances removal of toxins and waste from the body, which helps in normalizing the patient’s functional state and progressive muscle relaxation.⁵ Cupping also removes noxious materials from interstitial compartments and skin microcirculation. In men, cupping therapy is an effective method of reducing low density lipoprotein and, therefore, may help prevent atherosclerosis and cardiovascular diseases.⁶ Additionally, cupping is known to significantly decrease total cholesterol, and the ratio of low density lipoprotein to high density lipoprotein. According to Hao et al, cupping therapy can lower the number of lymphocytes in the local blood near the affected area and increase the number of neutrophils, which serves as an antiviral mechanism reducing pain sores. Overall, cupping leads to several positive effects with respect to the biochemical properties of the skin, pain modulation, and reduced inflammation.⁸ 

There are several proposed mechanisms of action for cupping. According to the immunomodulation theory, cupping therapy and acupuncture shared the same mechanism. The theory suggests that changes in the microenvironment of the skin, e.g. by stimulation, create biological signals that activate the neuroendocrine immune system.⁹ According to the genetic theory, mechanical stress on the skin – due to sub atmospheric pressure – and local anaerobic metabolism during cupping therapy produces physiological and mechanical signals that modulate gene expression. In wet cupping, for example, superficial scarifications may activate genetic programs for wound-healing.⁹ In summary, cupping therapy is an ancient technique that leads to numerous positive effects on pain modulation, blood circulation, waste removal, and the immune system. The immunomodulation and genetic theories provide possible mechanisms of action, though clinical researchers have not reached a consensus.  

References 

1. N.A. Qureshi, G.I. Ali, T.S. Abushanab, A.T. El-Olemy, M.S. Alqaed, I.S. El-Subai, et al. History of cupping [Hijama]: a narrative review of literature. J Integr Med, 15 (3) (2017 May 31), pp. 172-181 
2. Rozenfeld Evgeni, Kalichman Leonid. New is the well-forgotten old: the use of dry cupping in musculoskeletal medicine. J Bodyw Mov Ther. 2016;20(1):173–178.  
3.  Al-Rubaye K.Q.A. The clinical and Histological skin changes after the cupping therapy (Al-Hujamah)’ J. Turkish Acad. Dermatol. 2012;6:1. 
4. Shaban T.  Professional Guide to Cupping Therapy. first ed. CreateSpace Independent Publishing Platform; 2009. 
5. Yoo Simon S., Tausk Francisco. Cupping: east meets west. Int J Dermatol. 2004;43:664–665. 9.  
6. Niasari Majid, Kosari Farid, Ahmadi Ali. The effect of wet cupping on serum lipid concentrations of clinically healthy young men: a randomized controlled trial. J Alternative Compl Med. 2007;13:79–82.
7. Hao P., Yang Y., Guan L. Effects of bloodletting pricking, cupping and surrounding acupuncture on inflammation-related indices in peripheral and local blood in patients with acute herpes zoster. Zhongguo Zhen Jiu. 2016;36:37–40. 1. 
8. Lin M.L., Lin C.W., Hsieh Y.H.  Bioelectronics and Bioinformatics (ISBB), IEEE International Symposium on. IEEE; 2014. Evaluating the effectiveness of low level laser and cupping on low back pain by checking the plasma cortisol ^level; pp. 1–4. 
9. Y. Guo, B. Chen, D.Q. Wang, M.Y. Li, C.H. Lim, Y. Guo, et al. Cupping regulates local immunomodulation to activate neural-endocrine-immune work net. Complement Ther Clin Pract, 28 (2017 Aug 31), pp. 1-3