Author: Superadmin

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 

Low back pain (LBP) is the most common musculoskeletal condition affecting the adult population and a leading cause of disability worldwide, with a prevalence of 84%.¹ Chronic LBP has a significant impact on functional capacity and occupational activities, is a major cause of absenteeism, and represents a major social and economic burden.¹  One study estimates the cost of chronic LBP at $10 billion annually due to reduced productivity, while another study estimates a total of $100 billion annually due to healthcare costs, lost wages, and reduced productivity combined.² Considering the many physiological, neurological, and psychological factors implicated in LBP, the diagnostic evaluation of patients is very challenging and requires complex clinical decision-making.³ Nevertheless, identifying the source of pain is of fundamental importance in determining a therapeutic approach for patients with LBP.³

LBP can derive from many different anatomical sources, such as muscle, bones, joints, nerve roots, fascial structures, intervertebral discs (IVDs), and organs within the abdominal cavity.³ In addition, symptoms may emerge from aberrant neurological pain processing causing neuropathic LBP.^4-5 During the evaluation, the clinician must also consider the possible influence of psychological factors, such as stress, depression, and anxiety.^6-7 In diagnosing LBP, clinical information is the key element as opposed to MRI. In fact, the American College of Radiology advises against MRI in the first 6 weeks (unless red flags appear) because imaging data is weakly related to symptoms. Overall, chronic LBP may arise from multiple pain generators simultaneously and therefore requires a multidisciplinary diagnosis with an accompanying multimodal treatment plan.⁸

The type of LBP depends on the pain generator. One example is radicular pain, which refers to pain due to ectopic discharges from an inflamed or lesioned dorsal root or its ganglion.³ Typically, pain radiates from the back and buttock into the leg in a dermatomal pattern. The most common pathophysiological cause of radicular pain is disc herniation, which results in inflammation at the nerve. Furthermore, radicular pain differs from radiculopathy in that the latter impairs conduction down a spinal nerve, leading to numbness and muscle weakness.³ Although the two often accompany each other, radicular pain can appear in the absence of radiculopathy and vice versa.³

Another example is facet joint syndrome, which accounts for up to 30% of chronic LBP cases.⁹ The lumbar zygapophyseal joints are formed from the inferior process of upper vertebra and the superior articular process of lower vertebra; furthermore, these joints have a large amount of free and encapsulated nerve ending, which activate nociceptive afferents.³ Patients with facet joint syndrome typically complain of LBP, sometimes with somatic referred pain in the legs and often radiating to the thigh or groin. Back pain tends to be off-center and of lower intensity than leg pain; pain also increases with hyperextension, rotation, lateral bending, and uphill walking.³ Lastly, patients may report back stiffness, especially during the morning.

Other pain generators associated with LBP include sacroiliac joint pain (SIJ), lumbar spinal stenosis (LSS), and discogenic pain. SIJ is well recognized as a source of pain in patients with chronic LBP. Pain associated with SIJ can arise from ligamentous or capsular tension, altered joint mechanics, extraneous compression or shear forces, hypermobility, and myofascial or kinetic chain dysfunction leading to inflammation.¹⁰ LSS is determined by progressive narrowing of the central spinal canal and lateral recesses, which consequently leads to compression of neurovascular structures.³ Most cases of LSS are degenerative and associated with structural changes in the spine due to aging. Lastly, disc degeneration is the pain generator in 39% of chronic LBP cases.³ In terms of the pathophysiology, disc degeneration is characterized by degradation of the nucleus pulposus matrix with accompanying radial and concentric fissures in the annulus fibrosus.³ Overall it is critical that clinicians perform a thorough evaluation to accurately diagnosis the cause of LBP and develop an effective multimodal treatment plan that rapidly alleviates symptoms.

References

1) Balagué F, Mannion AF, Pellisé F, et al.: Non-specific low back pain. Lancet. 2012;379(9814):482–91.

2) Montgomery W, Sato M, Nagasaka Y, Vietri J. The economic and humanistic costs of chronic lower back pain in Japan. Clinicoecon Outcomes Res. 2017;9:361–371.

3) Allegri M, Montella S, Salici F, et al. Mechanisms of low back pain: a guide for diagnosis and therapy. F1000Res. 2016;5: F1000 Faculty Rev-1530.

4) Smart KM, Blake C, Staines A, et al. : Mechanisms-based classifications of musculoskeletal pain: part 1 of 3: symptoms and signs of central sensitization in patients with low back (+/- leg) pain. Man Ther. 2012;17(4):336–44.

5) Garland EL: Pain processing in the human nervous system: a selective review of nociceptive and biobehavioral pathways. Prim Care. 2012;39(3):561–71.

6)  Besen E, Young AE, Shaw WS: Returning to work following low back pain: towards a model of individual psychosocial factors. J Occup Rehabil. 2015;25(1):25–37.

7) Deyo RA, Bryan M, Comstock BA, et al.: Trajectories of symptoms and function in older adults with low back disorders. Spine (Phila Pa 1976). 2015;40(17):1352–62.

8) Boden SD, Davis DO, Dina TS, et al.: Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am. 1990;72(3):403–8.

9) van Kleef M, Vanelderen P, Cohen SP, et al.: 12. Pain originating from the lumbar facet joints. Pain Pract. 2010;10(5):459–69.

10)  Dreyfuss P, Dreyer SJ, Cole A, et al.: Sacroiliac joint pain. J Am Acad Orthop Surg. 2004;12(4):255–65.

Manipulation under anesthesia (MUA) was originally practiced by orthopedic and osteopathic physicians for the management of spinal pain since the 1930s. Today, the practice is currently acceptable for management of several other conditions including: arthrofibrosis, reduction of fractures, contractures and pain management of musculoskeletal conditions. This article will briefly discuss the indications, relevant physiology, risks, benefits, and steps of MUA for the management of several musculoskeletal conditions.

The practice of MUA requires an understanding of the effects of anesthesia on neuro-musculoskeletal innervation, signal transduction, and tissue manipulation. Systemic anesthesia will impair the protective innate tissue reflexes that exist in muscle tissue as well as attenuate the transduction of pain signals centrally. After administration of a sufficient dose of anesthesia to cause either full or conscious sedation, the practitioner can begin to engage in anatomical range of motion of the area of interest. This can also occur intra-operatively. Anesthesia will allow for the reduction of innate muscle stretch reflexes and signal transduction of pain.

Manipulation treatments can include progressive stretch, high-velocity thrust, local deep tissue injections as well as aiding in positioning for targeted injection therapy. Often a single treatment session is needed. Benefits such as range of motion improvement and pain reduction can be seen immediately. Risks associated with this procedure include those associated with anesthetic administration as well as those carried by specific manipulation treatments.

Certain indications for MUA include pain in a restricted joint that is unresponsive to conservative care. One example of this is Adhesive Capsulitis (commonly referred to as Frozen Shoulder). This is as omni-directional pain and range of motion reduction of the shoulder after injury, metabolic and endocrine insults, or prolonged subluxation after conferring local tissue structural changes. MUA can be trialed after the patient has tried other conservative and interventional measures. MUA can aid in reducing tissue fibrosis and improving range of motion with attention paid to patient comfort.

MUA can also be offered for the reduction of fractures. Long bone fractures often require manipulation of the fractured bone under anesthesia to optimal healing position before fixation. In some cases, manipulation of the broken limb into optimal placement followed by casting is sufficient alone. It is important to note that there is less evidence to support the use of MUA for acute and chronic axial pain conditions.

Contracture of an extremity can be seen after prolonged range of motion restriction of an affected extremity either from neurological or traumatic causes. Less commonly, it can be seen post arthroplasty. One cause of contracture is Heterotopic Ossification and this is seen after significant neurological or skin trauma. Findings will typically include range of motion restriction, pain with use, decreased outcomes with post-illness rehabilitation, and serum biomarker elevation of bone metabolic activity. The most common joints affected are the hip, shoulder, and elbow. MUA can allow for a more aggressive range of motion therapy, which will aid in breaking up contracted elements.

In conclusion, MUA is a long-standing treatment plan for the management of musculoskeletal pain conditions. It involves the use of anesthesia to reduce innate neuro-musculoskeletal reflexes as well as patient discomfort for the management of range of motion restriction, fracture, and positioning of limbs for interventional treatment. Risks associated with treatment include those associated with anesthesia as well as specific manipulations and interventions. It is essential to weigh the risks and benefits of treatment and pursue more conservative treatments if available.

References

1. American Chiropractic Association. Spinal manipulation policy statement. Updated 2003. Accessed October 3, 2019: http://www.acatoday.org/SearchResults?Search=Spinal+manipulation+policy+statement

2. American Association of Manipulation Under Anesthesia Providers. Guidelines for the practice and performance of manipulation under anesthesia. Feb 3, 2014. Chiropr Man Therap. 2014; 22: 7.

3. Antuna SA, Morrey BF, Adams RA, O’Driscoll SW. Ulnohumeral arthroplasty for primary degenerative

arthritis of the elbow: long-term outcome and complications. J Bone Joint Surg Am. 2002Dec: 84-A(12):2168-73.

4. Araghi A, Celli A, Adams R, Morrey B. The outcome of examination (manipulation) under anesthesia on the stiff elbow after surgical contracture release. Shoulder Elbow Surg. 2010 Mar;19(2):202-8.

5. Assendelft WJJ, Morton SC, Yu EI, Suttorp MJ, Shekelle PG. Spinal manipulative therapy for low-back pain. The Cochrane Database of Systematic Reviews 2005 Issue 4. In: The Cochrane Library, Issue 4, 2005.

6. Chao EK, Chen AC, Lee MS, Ueng SW. Surgical approaches for nonneurogenic elbow heterotopic ossification with ulnar neuropathy. J Trauma. 2002 Nov;53(5):928-33.

7. Charalambous CP, Morrey BF. Posttraumatic elbow stiffness. J Bone Joint Surg Am. 2012 Aug 1;94(15):1428-37.

8. Cremata E, Collins S, Clauson W, Solinger AB, Roberts ES. Manipulation under anesthesia: a report of four cases. J Manipulative Physiol Ther. 2005 Sep;28(7):526-33.

Anterior uveitis refers to an inflammatory condition of the iris and ciliary body, while posterior uveitis refers to an inflammatory condition of the choroid.¹ Both conditions cause blurred vision due to opacities in the intraocular fluid. In addition, lesions within the eye cause reduced vision and increased awareness of floaters, dark spots that drift across the field of vision.¹ Children with uveitis may report pain, photophobia, lacrimation, blepharospasm, and disturbed vision – or, the patient may be asymptomatic. Several researchers report correlations between uveitis and other conditions, such as ankylosing spondylitis, sacroilitis, juvenile chronic arthritis, herpes simplex and connective tissue diseases.² Other studies show a correlation between posterior uveitis and disorders of the central nervous system, such as toxoplasmosis. However, one third of patients with uveitis display no association with any other diseases.^2,3

In a case study, a male child aged 5.75 years was diagnosed with anterior and posterior uveitis based on a thorough ophthalmological examination. Visual acuity was 20/100 in the right eye and 20/30 in the left eye; slit lamp examination showed evidence of anterior uveitis with 2+ cells and flare in each anterior chamber; and a broken synechia was identified in the right eye with mild changes of the lens consistent with inflammation.¹ Ophthalmoscopic monitoring continued over a four month course of topical and systemic steroid therapy. However, no significant improvement was observed based on the Snellen eye chart and fundus examination. Therefore, steroid therapy was discontinued and chiropractic treatment was taken into consideration.¹

During the chiropractic consultation, a thorough history was performed. The patient suffered from chronic bronchitis since infancy; at three years, the patient fell from the bed and lacerated his left eyelid; at five years, the patient fell from the bed again and reported leg and knee pain; the patient complained of intermittent neck and back pain and leg, knee, and ankle pain; and lastly the patient complained of pain in the proximal interphalangeal joints of all fingers.² During spinal examination, the patient presented with a mild dextro-scoliosis in the thoracic spine and a mild levoscoliosis in the lumbar spine. Although the range of motion in the cervical spine was normal, pain at C3 to C5 was noted during neck extension.² Furthermore, the patient reported pain at C7 during forward flexion, and pain in the area of the contralateral trapezius muscle during neck rotation.²  Lastly, static and motion palpation of the spine revealed segmental subluxations, muscle induration, fixation, and misalignments at several spinal levels.¹ Therefore, a course of spinal adjustments was commenced.

Spinal adjustments were initially delivered at a frequency of three times per week and later reduced to two times per month after improvement in visual acuity was achieved. After the second visit for spinal adjustment, visual acuity was 20/80 in the right eye and 20/20 in the left eye. After the sixth visit, visual acuity was 20/50 in the right eye and 20/20 in the left eye. A year after chiropractic treatment, an ophthalmologist and optometrist verified improvement in visual acuity (20/30 for the right eye) based on Snellen chart tests.¹

To understand the link between uveitis and spinal adjustment therapy, one must consider the neurological and internal anatomy of the eye. The superior cervical ganglion receives preganglionic fibers from the first thoracic nerve and supplies postganglionic fibers to the internal carotid and cavernous plexuses. In turn, the internal carotid and cavernous plexuses supply sympathetic fibers to the vasculature of the eye. Alteration of the sympathetic nerve supply may lead to tissue neovascularization and increase the possibility of rupture with trauma and histamine release.⁴ Therefore, correction of associated nerve irritation via spinal adjustment may reverse symptoms of uveitis.

References

1) Manuele, J and Fysh, P. “The Effects of Chiropractic Spinal Adjustments in a Case of Bilateral Anterior and Posterior Uveitis.” Journ of Clin Chiro Ped. 2004; 6:334-337.

2) Szanto E, Granfors K, Wretlind B. Acute anterior uveitis, arthritis and enteric antigens. Clin Rheumatol 1991; 4:395-400.

3) Linssen A, et al. “The lifetime cumulative incidence of acute anterior uveitis in a normal population and its relation to ankylosing spondylitis and histocompatibility antigen HLAB27.” Ophthal Vis Sci. 1991; 9:2568-78.

4) Oski, FA. Principles and Practice of Pediatrics, 2nd ed. Philadelphia; Lippincott 1994; 34:891.