Back Clinic Treatments. There are various treatments for all types of injuries and conditions here at Injury Medical & Chiropractic Clinic. The main goal is to correct any misalignments in the spine through manual manipulation and placing misaligned vertebrae back in their proper place. Patients will be given a series of treatments, which are based on the diagnosis. This can include spinal manipulation, as well as other supportive treatments. And as chiropractic treatment has developed, so have its methods and techniques.
Why do chiropractors use one method/technique over another?
A common method of spinal adjustment is the toggle drop method. With this method, a chiropractor crosses their hands and pressed down firmly on an area of the spine. They will then adjust the area with a quick and precise thrust. This method has been used for years and is often used to help increase a patient’s mobility.
Another popular method takes place on a special drop table. The table has different sections, which can be moved up or down based on the body’s position. Patients lie face down on their back or side while the chiropractor applies quick thrusts throughout the spinal area as the table section drops. Many prefer this table adjustment, as this method is lighter and does not include twisting motions used in other methods.
Chiropractors also use specialized tools to assist in their adjustments, i.e., the activator. A chiropractor uses this spring-loaded tool to perform the adjustment/s instead of their hands. Many consider the activator method to be the most gentle of all.
Whichever adjustment method a chiropractor uses, they all offer great benefits to the spine and overall health and wellness. If there is a certain method that is preferred, talk to a chiropractor about it. If they do not perform a certain technique, they may recommend a colleague that does.
Unfortunately, there are no stretches for� Root canals or Kidney stones. But there are stretches for Piriformis syndrome.
These ailments are painful and no fun! Piriformis syndrome�is especially a pain, in the butt, no pun intended.
Seriously, people suffering from Piriformis syndrome have frequent and sometimes severe pain and numbness through the buttocks and down their legs. This occurs when the Piriformis muscle spasms. When this happens, it�can end up also aggravating the sciatic nerve, which compounds the pain with tingling and numbness.
The Piriformis�is a short, small�muscle deep inside our hips, and helps rotate our legs both outward and inward. Because of its proximity to the sciatic nerve, this little body part can cause big problems, and hinder our ability to run, or even walk, through our daily activities with ease.
Fortunately, there are a variety of exercises that help stretch and relax the Piriformis muscle, giving sufferers much-needed relief from the pain and numbness it causes. If you are dealing with Piriformis syndrome, try these stretches to get yourself back on your feet and moving, pain-free.
Stretches
The “Knee Up” Stretch
Lie on the floor, use a mat or thick rug for comfort, on your back. Stretch both legs out, with your arms to your sides.�Bend one of your legs at the knee and use your hand to pull it toward the opposite shoulder Hold for ten to thirty seconds.�Straighten out that leg, and then do the same motion with the opposite leg and shoulder.
The “Cross Arm” Stretch
Arrange yourself in a sitting position. The bottoms of your feet should be touching each other, with your arms crossed and your hands resting on the opposite leg. Push both knees down toward the floor until you feel the stretch inside your thighs. Hold the position for a count of 30, then relax for a few seconds and repeat up to five more times.
The “Standing” Stretch
This is a handy exercise you can do in the bathroom at work, in a hotel, or anywhere that you would rather not lie on the floor.
Begin in a standing position with both feet flat on the floor, with your feet a shoulder-length apart.��Don’t lock your knees, and keep your back straight.�Lift one knee up and grasp it with both hands. Make sure you keep the knee parallel to the corresponding hip. Use your hands to pull your knee toward the opposite shoulder until you feel a pull along the side of your buttocks. Hold up to one minute, or as long as you can balance. Repeat the action with the other leg. Try to do it three times for each leg.
The “Sit and Bend” Stretch
This is another convenient�exercise that doesn’t require getting on the floor. Choose a solid, straight-backed chair that doesn’t roll,�sit, and bring one leg across the other, resting your ankle on your other leg. Slowly lean forward until you feel a pull along the crossed leg. Hold for up to 30 seconds. Repeat with the other leg, stretching each side 3 times.
Remember that consistency is key. Perform these exercises at least once a day, every day, until your pain and numbness is gone.
These four simple exercises�help you make great strides in recovering from Piriformis syndrome. However, if you perform these for several days and still have pain, or experience pain while attempting the stretches, it is a good idea to make an appointment with a professional chiropractor. He or she will be able to evaluate your condition and offer a comprehensive treatment plan to treat the Piriformis so it doesn’t get worse, or cause additional issues with your sciatic nerve.
You try to stand up from a seated position and feel a stab of pain in your lower back. It may even shoot through your hip, buttock, or down the back of your thigh. The pain may even get worse then you walk uphill or sit for a long period of time. While these symptoms could mean a pinched nerve, lumbar disc herniation, hip bursitis, or degenerative hip disease, it could also be sacroiliac joint dysfunction.
What Is Sacroiliac Joint Dysfunction?
The sacroiliac (SI) joint is located in the pelvis. It is very strong as it is a weight bearing joint connecting the pelvis to the sacrum. It is surrounded by tough ligaments that reinforce it, providing added support.
There is an SI joint located on each side of the sacrum and they work together, moving as a single unit to act as a shock absorber for the spine and for transmitting force of the upper body. Just like any other joint in the body, the SI joint can be injured or diseased, causing it to become unstable and inflamed, causing pain and limited mobility.
What Causes SI Joint Inflammation?
While doctors have not established how the pain is generated, it is believed that it is due to a change in the normal motion of the joint. This could occur due to:
Hypermobility (Instability or Too Much Movement) � This can cause the pain to reside in the lower back. It can also be felt in the hip or both the hip and lower back and may even radiate into the groin.
Hypomobility (Fixation or Too Little Movement) � This can cause the pain to reside in the lower back or buttocks and may radiate down one leg, usually in the back of the thigh. It usually doesn�t reach the knee, but sometimes can even reach the ankle and foot. In this way, the condition mimics sciatica.
Sacroiliac joint dysfunction typically affects women who are young or middle aged. Older women and men are rarely affected although it does happen.
What Are Treatment Options For Sacroiliac Joint Pain?
When SI joint pain is initially diagnosed the treatment is usually fairly conservative. Medication, physical therapy, and injections are used by doctors for pain management.
NSAIDs and other similar medications decrease inflammation and reduce pain, while physical therapy can readjust the SI joint in cases where it is dislocated or immobilized. It also includes exercises that stabilize the joint for pain management over the long term.
Steroid injections directly into the sacroiliac joint can help with the reduction of inflammation and pain while making physical therapy more effective. When steroid injections are effective but the effects are temporary there is another non-surgical treatment that is sometimes used called RFA, or radiofrequency ablation.
In cases where the conservative methods do not achieve the desired results there are surgical options that provide pain reduction and stabilization on a more permanent scale. SI fusion involves fusing the joint, providing relief.
However, there is a treatment option that is non-invasive, doesn�t involve steroids or medications that could have harmful side effects � chiropractic.
Spinal manipulation � This is the traditional chiropractic adjustment that is also known as high-velocity, low-amplitude (HVLA) thrust.
Spinal mobilization � This is a less forceful, gentle chiropractic adjustment also known as low-velocity, low-amplitude thrust.
Chiropractic is proven to be an effective, non-invasive, gentle method for relieving the pain and inflammation of SI joint dysfunction. No medication, no surgery, just relief.
So if you�ve been suffering from sacroiliac joint dysfunction, give us a call! Our Doctor of Chiropractic is here to help!
Injury Medical Clinic: Sciatica Treatments & Recoveries
Antioxidants are scientifically referred to as compounds which restrict the oxidation process in the human body, that if left unchecked, it can create free radicals which can develop numerous chain reactions that may cause cellular damage. Fortunately, the human body can create such built-in immune mechanisms, however, when mounting reactive oxygen species, or ROS, are unable to be neutralized, envision a tiny flame which gets out of control when infused with oxygen, harm is bound to occur.
To continue expanding on the metaphor of the flame, the final product of not having the ability to neutralize the impact of ROS, or reactive oxygen species, is damage as well as inflammation, in other words, the human body is quite literally on fire. The fantastic thing is there are antioxidants which can tremendously help fight this health issue and this antioxidant is glutathione. Though found in 1889, glutathione’s antioxidant effect has become one of the most interesting topics in modern research studies.
Master of Antioxidants: Glutathione
The powerful�substance is a tripeptide that develops from cysteine, glutamic acid, and glycine. Because of its capability to protect the human body against the creation of free radicals, glutathione can ultimately help promote a healthy immune system. Based on Scientific Reports in 2015, it was determined that glutathione’s capacity to function synergistically with peroxiredin and catalase helps guard cells against hydrogen peroxide. This synergistic formula functions against reactive oxygen species, or ROS. Glutathione, peroxidredin and catalase are essential elements in the increase of cellular homeostasis, which is an essential process of healthy cells, tissues and organs altogether.
Additionally, glutathione increases overall immune system structure and function utilizing its important effect on lymphocyte functions. According to the Department of Immunochemistry, properly supplementing levels of glutathione in the human body can greatly enhance immune reactions. By way of example, two randomized placebo-controlled trials demonstrated that the therapeutic treatment of immune-compromised patients with N-acetyl-cysteine, or NAC, resulted, in both cases, in a substantial growth in most immunological processes which included an entire rejuvenation of natural killer cell activity. N-acetyl-cysteine, or NAC, uses the sulfur from glutathione and combines it with poisonous molecules, which then become water-soluble and are discharged in the human body.
Glutathione also has the capability to revitalize lipoic acid as well as to recycle Vitamin C and E, which are necessary in order to initiate certain system processes by sending electrons to neutralize free radicals. Based on a research study from PLOS ONE, glutathione affected patients with diabetes metillus, or T2DM, and mycobacterium tuberculosis. Normally, individuals with weak immune systems have a tendency to show greater exposure to M. tb, or mycobacterium tuberculosis, disease or infection. Furthermore, individuals with Type 2 diabetes metilllus, or T2DM, are two to three times more prone to TB than people without T2DM. The research study also suggested that boosting the levels of glutathione in macrophages isolated from patients with T2DM led to improved control of M.Tb disease or infection. These results demonstrate that lower levels of glutathione in patients with T2DM contributes to a heightened chance of M. tb disease or infection. Moreover, dependent on Dietro Ghezzi in Brighton and Sussex Medical School, oxidative stress can ultimately cause poor immune system structure and function.
Fortunately, glutathione plays an essential role in strengthening and controlling immunity. By way of instance, glutathione is essential for innate and adaptive processes within the immune system, including T-lymphocyte proliferation, phagocytic activity of polymorphonuclear neutrophils, and dendritic cell functions, which can be fundamental because these are made-up of antigen-presenting cells. Cell-meditated immunity includes protein antigens which initially begin to degenerate in the endocytic vesicles of macrophages and dendritic cells, therefore, the smaller peptides are demonstrated on the surface to activate proliferation of antigen-specific T cells. In addition, glutathione helps with the creation of cytokines, and it is necessary to maintain interferon-gamma production by dendritic cells, which is important towards protecting against intracellular pathogens including mycobacteria.
N-acetyl-cysteine, or NAC, scientifically referred to as the precursor of glutathione, is also a very powerful cellular antioxidant used as a free radical scavenger antioxidant. Commonly recognized for its role in averting acetaminophen toxicity, NAC, or�N-acetyl-cysteine, has been demonstrated to possess several health and wellness benefits. According to Cell Journal, NAC helps support a healthy inflammatory response and may positively impact human term and preterm labors. The research study concluded that in women with previous preterm birth and bacterial vaginosis, 0.6 gram of NAC per day taken orally together with progesterone after week 16 of pregnancy shielded against preterm birth recurrence and improved neonatal outcome. In conclusion, NAC’s positive effects on muscle building was also detected. After three minutes of persistent contractions, there was a 15 percent enhanced output, demonstrating how NAC plays a fundamental role in improving muscle building and reducing overall fatigue during labour.
Researchers also discovered that NAC, or�N-acetyl-cysteine, may benefit those who have polycystic ovarian syndrome, or PCOS. PCOS, or�polycystic ovarian syndrome, is a common endocrine glands-related disease which impacts approximately 5 to 10 percent of reproductive-age women. In such patients, there is a greater risk of experiencing metabolic syndrome, where the use of NAC helped restore healthy insulin levels and sensitivity.
Dr. Alex Jimenez’s Insight
Glutathione has been referred to as the “master of antioxidants” due to its fundamental role in achieving and maintaining overall health and wellness. While the human body is capable of producing its own glutathione, poor nutrition, pollution, toxins, excessive use of drugs and/or medications, stress, trauma, aging, disease and radiation can all decrease our natural levels of glutathione. This can in turn make individuals more susceptible to cell damage from oxidative stress, free radicals, infections and cancer. Glutathione supplementation can therefore have tremendous benefits on the human body. Together with alternative treatment options, such as chiropractic care, glutathione levels can once again be regulated to improve well-being.
Additionally, healthcare professionals have suggested implementing the use of glutathione supplementation together with other alternative treatment options, such as chiropractic care, to further improve overall health and wellness. Antioxidants are important towards maintaining maximum well-being as well as to inhibit the chain reaction of free radicals that cause cell harm or damage. Powerful antioxidants like glutathione, as previously mentioned above, ultimately help regulate the development of these free radicals and provide a healthier immune system response. Research studies have found that chiropractic care may also play an essential role in this process, naturally boosting the activity of antioxidants in the human body. Chiropractic care is a safe and effective treatment approach which utilizes spinal adjustments and manual manipulations to correct spinal misalignments, or subluxations, in order to allow the human body to naturally heal itself without the use of drugs/medications and/or surgical interventions.
Finally, antioxidants demonstrate their biological properties through a great deal of health benefits, which might be necessary now more than ever with the every so increasing onslaught of stress, disease and pollution in our modern world, which all contribute to cell harm and/or damage. Glutathione and its precursor, NAC, or�N-acetyl-cysteine, continue to show their powerful status in the realm of antioxidants. Together with alternative treatment options, such as chiropractic care, people can take advantage of all the benefits that this powerful antioxidant has to offer. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
Curcumin is the main active ingredient found in turmeric, a bright yellow aromatic powder obtained from the rhizome of a plant in the ginger family commonly utilized for flavoring and coloring in a variety of Asian cuisines, as well as a very strong antioxidant which additionally has powerful anti-inflammatory effects. While turmeric has been consumed for generations due to its medicinal properties, it’s curcumin content is actually not that high. Therefore, if you want to experience its full benefits, it may be best to take a supplement that contains significant amounts of curcumin, or better yet, a supplement specially formulated to bring out the benefits of this naturally occurring chemical compound.
Curcumin is ultimately found in turmeric, the key ingredient in curry, and as a powerful antioxidant that offers numerous health benefits, curcumin helps support joint health and cardiovascular function, and it helps maintain a normal inflammatory reaction in the human body. Individuals throughout Asia have benefited from the healthful effects of curcumin for centuries.�Whether taken as a nutritional supplement or from meals, however, curcumin is usually poorly absorbed into the bloodstream.
Fortunately, global experts in botanical extract technologies have uncovered the key to curcumin absorption: phytosome technology. Meriva curcumin phytosome is an exceptional curcumin extract that’s significantly better absorbed than other curcumin extracts. Curcumin nutrients which have previously been remarkable in “test tube” experiments are extremely poorly absorbed when taken orally by people. The product Curcumin Phytosome comprising Meriva� unites curcumin with another bioactive nutrient, thereby dramatically improving its absorption and releasing its overall health and wellness potential.�Meriva is a unique, patented, time-release curcumin product.
Meriva Product Overview
Phytosomes are plant extracts bound to phosphatidylcholine, or PC, an important component of individual cells. The human body can create PC, or phosphatidylcholine, but it can even be obtained from food and/or supplements. When taken orally, PC is very well absorbed.�PC is a significant building block for membranes, the most metabolically dynamic zones of our cells. PC most likely transfers the curcumins in the bloodstream until they arrive in cell membranes. Researchers found a way to attach a curcumin extract to PC for superior absorption, leading to Meriva.�Curcumin phytosome is a curcumin molecule bonded to a molecule of PC. Unlike curcumin alone, PC is excellently absorbed orally.
When consumers utilize Meriva curcumin phytosome, the body absorbs the PC as well as the attached curcumin, leading to more curcumin reaching the cells which can benefit more from it. After the curcumin phytosomes are accepted as a dietary supplement, PC protects its connected curcumin and economically transports it across the intestinal lining and into the circulating blood. Curcumins at phytosomes are over 29 times better absorbed than curcumin alone. PC itself has proven benefits for the liver, intestines, and lungs, and its existence in the Meriva curcumin phytosome amplifies the benefits available from the curcumin alone.
Dr. Alex Jimenez’s Insight
Turmeric contains four major curcuminoids: curcumin, demethoxycurcumin, bisdemethoxycurcumin and cyclocurcumin. These chemical compounds have been demonstrated to have tremendous benefits, which is why turmeric has been a fundamental addition in Asian cooking. However, curcumin, as well as all the other curcuminoids, are poorly absorbed by the human body when taken orally. Researchers developed Meriva curcumin phytosome, a curcumin compound which is bonded to the molecule phosphatidylcholine, or PC, which promotes the proper absorption of curcumin. Meriva curcumin phytosome can provide a variety of health benefits, including vision and eye health, joint health and even prostrate benefits, among other medicinal properties.
Meriva Curcumin Phytosome Research
Curcumin phytosome with Meriva� is a powerful antioxidant which protects cells and tissues by fighting free radicals. It’s also known to support healthy joint function, eye health and small vessel circulatory health. The curcumin is extracted from turmeric and provides a curcumin complex including, curcumin, bisdemethoxy curcumin and demethoxy curcumin. Meriva� curcumin phytosome is made utilizing the patented Phytosome� technology that enhances the absorption of those curcumins. Comprehensive research over the previous quarter of a century suggests that curcumin helps counter toxins, in addition to influencing cell survival through other means.
Although curcumins are poorly absorbed, Phytosome� technology helps improve bioavailability. The technology evolves every curcumin molecule with one or more atoms of the nutrient phosphatidylcholine, or PC, to create molecular complexes called phytosomes. Curcumin molecules at the Meriva� phytosome complexes are more stable against breakdown and combine far better into water in order for them to be better absorbed when taken orally. The PC molecules in the phytosomes serve as a “delivery vehicle” or even “chaperone”, which not only chemically protects the curcumin molecules but also markedly increases their absorption. A human absorption research discovered that the curcumins were absorbed when taken as Meriva� curcumin phytosomes, in comparison to their basic molecular forms.
The numerous beneficial effects attributed to turmeric root are linked to the antioxidant properties of the curcumins it contains. This antioxidant activity can neutralize free radicals which threaten the integrity of mobile structures. Free radicals may lead to “oxidative stress,” a process that can activate cell damage. In addition, oxidative stress is considered to play a role in the development of a variety of diseases. Because curcumins are poorly absorbed when taken orally, this can tremendously restrict their biological actions. The Phytosome� technology used with Meriva� curcumin phytosome creates phytosome complexes which are proven to be absorbed better.
A 2007 study published in the journal, Cancer Chemotherapy and Pharmacology, revealed Meriva’s exceptional bioavailability in contrast to ordinary curcumin. Liver levels of curcumin were also higher with Meriva supplementation. A recent human research study also demonstrated that Meriva curcumin phytosome has 29-times higher bioavailability. Meriva supplementation also resulted in higher plasma concentrations of curcumin from a much smaller dose compared to ordinary curcumin. In a recent eight-month human trial, Meriva was shown to encourage a healthy inflammatory reaction. People experienced improvements in clinical and biochemical end-points associated with joint health.
Several studies have shown curcumin’s hepatoprotective effects, causing researchers to suggest its use in protecting the liver from exogenous insults due to environmental toxins. Curcumin also has the capacity to increase both the circulation and solubility of bile. Curcumin’s hepatoprotective effects are due in part to lead free-radical scavenging; however, curcumin also enhances the body’s natural antioxidant system, which raises glutathione levels, thus aiding in hepatic detoxification and inhibiting nitrosamine formation. Furthermore, research studies have demonstrated several other health benefits of Meriva curcumin phytosome, including its support in joint health, eye health, vision and circulation, as well as several prostrate benefits, among others.
Supports Joint Health – Two Clinical Trials
In two double-blind trials with subjects having knee problems, Meriva, taken at about 1,000 mg/day, enhanced treadmill walk space by 345 percent after eight months. It improved joint pain, stiffness, swelling and joint work. Intakes of over-the-counter medications fell 63 percent and their adverse effects dropped by 67 percent. The subjects’ medical prices fell 45 percent after 8 months. C-Reactive Protein, or CRP, levels were reduced into a more healthy variety. After eight months, the Karnofsky Scale of well-being moved into “able to perform ordinary activity.”
Supports Eye Health, Vision, Circulation – Three Clinical Trials
One frequent eye problem is a really persistent redness that keeps coming back even when it is cleared. At a clinical trial, 106 patients obtained Meriva, taken at about 1,200 mg/day, for a single year. There were 86 percent fewer returns of this reddening, and in 82 percent of these patients, approximately 87 from 106, it didn’t return at all. In another study, Meriva, taken at about 1,000 mg/day, improved retinal blood circulation, retinal swelling, and eyesight. In only four weeks, visual sharpness improved from an initial average of 20/122-155 to 20/32-78. Meriva also improved circulation elsewhere in the body. In areas with foot blood circulation issues, it substantially reduced immunity, increased oxygen consumption, and enhanced nerve control over the capillary networks. The subjects’ Karnofsky Score of well-being improved, from “normal activity, with effort” into “normal activity.”
Breakthrough Prostate Benefits with Meriva
In a clinical trial on middle-aged men with prostate troubles, Meriva, taken at 1,000 mg/day, significantly enhanced: sense of incomplete bladder emptying, urination frequency, flow stop/start, feeble stream, straining and getting up at night, urinary block, and PSA levels. Quality of life and sexual activity were also considerably improved. The Meriva curcumin phytosome breakthrough guarantees that curcumins are effectively delivered to human cells, in functional mix with PC, or phosphatidylcholine. Multiple effective clinical trials have established curcumin phytosome comprising of Meriva� as the “gold standard” one of curcumin supplements.
In conclusion,�Meriva curcumin phytosome is bound to phosphatidylcholine, or PC, for increased absorption and bioavailability, ultimately protecting DNA against damage by free radicals and reactive oxygen species, among providing a variety of other health benefits. With its enhanced absorption through an improved curcumin absorb delivery system, Meriva curcumin phytosome is clinically documented to promote joint health, eye health, vision and circulation, and even has prostrate benefits. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
Biomarkers (short for biological markers) are biological measurements of a biological condition. By definition, a biomarker is “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes or pharmacological responses to a therapeutic intervention” Biomarkers are the measurements utilized to perform a clinical evaluation like blood pressure or cholesterol level and therefore are used to monitor and forecast health conditions in individuals or across populations so that appropriate treatment options could be proposed. Biomarkers may be used by itself or in combination to assess the health or disease state of an individual.
Variety of Biomarkers
A wide selection of biomarkers are used now. Every biological system, such as the cardiovascular system, metabolic system or the immune system, has its own specific biomarkers. Many of these biomarkers are rather easy to quantify and form part of regular medical examinations. By way of instance, a general health check may include assessment of blood pressure, heart rate, cholesterol, triglycerides and fasting glucose levels. Body dimensions such as weight, body mass index, or BMI, and waist-to-hip ratio are routinely used for assessing conditions like obesity and metabolic disorders, among others. These varieties in biomarkers can ultimately be useful in the diagnosis of a variety of health issues.
Attributes of a Perfect Biomarker
An ideal biomarker has particular characteristics that make it suitable for assessing a particular disease or condition. Ideally, an ideal marker should possess the following features, as it should be:
Safe and simple to measure
Cost effective to follow up
Modifiable with treatment
Consistent across gender and cultural groups
Biomarkers as Health and Disease Predictors
Biomarkers are used to predict significant ailments like diabetes and cardiovascular disease, among others. Each individual biomarker indicates whether there’s a disease or health condition and can be combined to offer a thorough demonstration of how healthy an individual is and whether further diagnosis needs to be made. Biomarkers ultimately serve as health and disease predictors, capable of determining a potential onset of disease or illness, such as that of cancer.
Biomarkers in Cancer Detection and Drug Development
The principles of biomarkers in disease have been applied to the discovery, screening, diagnosis, treatment and monitoring of cancer. Traditionally, anti-cancer drugs and/or medications were agents that eliminated both cancer cells and healthy cells. However, more targeted therapies have now been developed that can be instructed to kill cancer cells only, while sparing healthy cells. The evaluation of a typical biomarker in cancer will help in the development of therapies that may target the biomarker. This can minimize the risk of toxicity and reduce the cost of treatment. In cancer research, genetic studies are valuable because genetic abnormalities so often underlie the evolution of cancer. Certain DNA or RNA markers might therefore help in the treatment and detection of specific cancers. The purpose of the following article, however, is to demonstrate the biomarkers involved in low back pain, disc degeneration and other chronic pain health issues, such as neuropathic pain.
Inflammatory Biomarkers of Low Back Pain and Disc Degeneration: a Review
Abstract
Biomarkers are biological characteristics that can be used to indicate health or disease. This paper reviews studies on biomarkers of low back pain (LBP) in human subjects. LBP is the leading cause of disability, caused by various spine-related disorders, including intervertebral disc degeneration, disc herniation, spinal stenosis, and facet arthritis. The focus of these studies is inflammatory mediators, because inflammation contributes to the pathogenesis of disc degeneration and associated pain mechanisms. Increasingly, studies suggest that the presence of inflammatory mediators can be measured systemically in the blood. These biomarkers may serve as novel tools for directing patient care. Currently, patient response to treatment is unpredictable with a significant rate of recurrence, and, while surgical treatments may provide anatomical correction and pain relief, they are invasive and costly. The review covers studies performed on populations with specific diagnoses and undefined origins of LBP. Since the natural history of LBP is progressive, the temporal nature of studies is categorized by duration of symptomology/disease. Related studies on changes in biomarkers with treatment are also reviewed. Ultimately, diagnostic biomarkers of LBP and spinal degeneration have the potential to shepherd an era of individualized spine medicine for personalized therapeutics in the treatment of LBP.
Biomarkers for Chronic Neuropathic Pain and their Potential Application in Spinal Cord Stimulation: a Review
Abstract
This review was focused on understanding which substances inside the human body increase and decrease with increasing neuropathic pain. We reviewed various studies, and saw correlations between neuropathic pain and components of the immune system (this system defends the body against diseases and infections). Our findings will especially be useful for understanding ways to reduce or eliminate the discomfort, chronic neuropathic pain brings with it. Spinal cord stimulation (SCS) procedure is one of the few fairly efficient remedial treatments for pain. A follow-up study will apply our findings from this review to SCS, in order to understand the mechanism, and further optimize efficaciousness.
Chronic neuropathic pain disorders represent a common long-term disability in the United States, as well as, globally. They affect 1 in 4 Americans. Chronic neuropathic pain treatment has limited success because of poor understanding of the mechanisms that lead to the initiation and maintenance. Additionally, the effectiveness of neuropathic pain management regimens and procedures has been difficult to determine in the past, due to the subjectivity related to pain perception, and a lack of standardized assessment of neuropathic pain. However, one of the most effective management strategies in recent times is spinal cord stimulation (SCS). The main goals of spinal cord stimulation are to improve physical function and quality of life in the patients afflicted with chronic neuropathic pain associated with complex regional pain syndrome (CRPS), failed back syndrome, and other chronic neuropathic pain syndromes [1�2]. Despite limited knowledge of how people benefit from SCS, more than 20,000 stimulators are implanted each year, with more than a half-billion dollars in revenue [3]. While it is generally believed that spinal cord stimulation inhibits pain transmission in the dorsal horn, the exact mechanisms by which SCS relieves neuropathic pain is unknown. Chronic neuropathic pain is caused often by inflammation and/or nerve injury. The advances have shown that inflammation and nerve injury produce changes in the expression of cytokines, neurotransmitters, and structural proteins [4]. It is very likely that there are changes in the body�s serum biomarkers of neuropathic pain before SCS and after SCS. Such a study would contribute greatly to the field of neuromodulation, as objective quantifiers of neuropathic pain control before and after SCS have not yet been investigated. Such definitive data regarding the effectiveness of SCS in relieving neuropathic pain and improving function will be important in future use of SCS.
In preparation for the launching of this study, the authors� goal with this transcript is to provide a review of the literature regarding known biomarkers for chronic neuropathic pain, and then prepare a role for biomarker analysis in the prediction of therapy success in SCS.
Data
The expression of certain genes is altered under chronic pain conditions. This alteration has helped provide an insight into the identification of potential biomarkers [5]. Current advanced research suggests that genetic expression of cytokines, positively or negatively, correlates with the experience of chronic pain. This negative or positive correlation primarily depends on the nature of the cytokine. Cytokines are signaling proteins which mediate the activation, differentiation, and proliferation of immune cells. They can be pro-inflammatory or anti-inflammatory. A misaligned balance between pro-inflammatory and anti-inflammatory cytokines has been common in most of the studies conducted (Table 1). Pro-inflammatory cytokines such as IL-1?, IL-6, IL-2, IL-33, CCL3, CXCL1, CCR5, and TNF-?, have been found to play significant roles in the amplification of chronic pain states. In studies involving discogenic pain, Complete Freund�s adjuvant (CFA)-induced discogenic pain in animal models has been observed to coincide with a sustained up-regulation of the above named cytokines [6]. In a more recent study, chronic constriction injury (CCI)-induced rats (neuropathic pain induction) were shown to have increased serum levels of CCL3 and CCR5. Even more interesting, an intrathecal injection of the anti-inflammatory cytokine, IL-4, and the CCL3-neutralizing antibody, reduced the CCI-induced neuropathic pain, estimated by a plantar test [7]. Other studies have also shown that the selective genetic impairment of the highlighted pro-inflammatory cytokines attenuated nerve-injury induced pain behavior, observed in neuropathic pain models [8]. Particularly, Zarpelon et al. revealed that CCI-induced rats showed reduced mechanical hyperalgesia when the IL-33 receptor gene, IL-33R (ST2), was knocked out, compared to the wild-type mice [9].
On the other hand, one study showed that blood levels of anti-inflammatory cytokines (such as IL-10 and IL-4) of Complex Regional Pain Syndrome (CRPS) patients were lower compared to the control [10]. A recent study also shows a distinction of the significant increases of pro-inflammatory cytokines based on the part of the back affected. There were more significant elevations (p<0.05, student�s t test) of pro-inflammatory cytokines in the plasma of lower back pain patients than in upper back patients, when compared to controls [11]. There has also been a study focusing on the levels of the aforementioned cytokines in patients with painful neuropathy in contrast with painless neuropathy and healthy control subjects. Patients with a painful neuropathy had about double the level of IL-2 expression (p = 0.001), TNF expression (p < 0.0001) and protein levels (p = 0.009) than the controls. The study further indicated there was about double the IL-2 and TNF level expression (p = 0.03; p = 0.001) and protein levels in painful neuropathy (p = 0.04; p = 0.04) than patients with painless neuropathy. On the contrary, levels of mRNA expression of the anti-inflammatory cytokines, IL-10 and IL-4 were considerably lower in patients with painful neuropathy than in patients with painless neuropathy (p =0.001) [12].
Several other studies, focused on the antagonist and agonist effects of some drugs targeting pro-inflammatory and anti-inflammatory cytokines, also have pointed out their significance with pain. Certain known analgesics were seen to reduce the levels of pro-inflammatory cytokines in the studies reviewed. There was a study about (CCI)-induced rats, in which case, this induced injury significantly, elevated the levels of pro-inflammatory cytokines, and decreased the serum levels of anti-inflammatory cytokines. Omeprazole, a known remedy for stomach pain, was observed to reduce the levels of pro-inflammatory cytokines (TNF-?, IL-1?, and IL-6) to normal, compared with the CCI control. It is important to note that this was while curbing the CCI-induced neuropathic pain, measured with the paw withdrawal latency [13]. Zhou et al. also highlighted the significance of certain drugs in determining the correlation between cytokines and neuropathic pain. CCI was again, used to induce neuropathic pain on rat models; and in turn, Paenoflorin, an established analgesic [14] was administered. Once Paenoflorin was introduced, significant decreases in serum levels of pro-inflammatory cytokines of CCI-induced rats (IL-1?, IL-6, TNF-?, and CXCL1) were observed, compared to the CCI-control [15]. The cytokines identified here, are the ones that showed correlation in various studies reviewed.
Even though cytokines are the key chronic pain biomarkers, according to the studies reviewed, there are still other proteins and nucleotides that have been observed to associate with chronic pain disorder. Two studies laid emphasis on regulatory microRNAs (miRNAs), which are small non-coding RNA molecules involved in post-transcriptional gene regulation. miRNAs achieve this by binding to mRNAs and degrading them or repressing their functions. Orlova et al. showed that 60% of CRPS patients in their study showed a significant down-regulation of 18 different miRNAs. The rest of the patients, however, showed variable (contradicting) miRNA levels. miRNA levels show variability, depending on the gene being regulated [5]. Tao et al. revealed that an increased inflammatory stimulation by the cytokine IL-1? in normal and osteoarthritis chondrocytes produced a significant down-regulation of the miRNA, miR-558, and a significant up-regulation of miR-21 in DRG neurons. A connection between IL-1? and miR-21 was attributed to AP-1, which is a transcription factor located in the promoter site of the mRNA, and is activated by IL-1? [4]. siRNAs have the same features as miRNAs, in the sense, that they are regulatory nucleotides. They also show variability, depending on the gene being regulated. SIRT1, a deacetylase, functions in regulating various pathways, including inflammation. It was observed that an intrathecal injection of SRT170, an SIRT1 agonist, reduced serum levels of NF-?B, a transcription factor for pro-inflammatory cytokines, in CCI-induced rat models. When SRT170-siRNA (a regulator of the regulator) was administered before SRT170, there was no agonistic effect [16].
Dr. Alex Jimenez’s Insight
A biomarker is most accurately defined as any measurement which demonstrates an interaction between a biological system and the possibility of a chemical, physical or biological hazard. However, biomarkers are often most commonly associated with medicine. In this setting, these can be utilized to determine the effects a particular treatment may have on a patient as well as for determining the risk a patient may have of developing certain health issues. An example of a diagnostic use of biomarkers includes the measurement of biomarkers in blood to evaluate the severity of a heart attack. In the same manner, blood samples can be analyzed and biomarkers can be measured in the instance of chronic pain.
Discussion
Chronic neuropathic pain affects a tremendous amount of the population. There are few effective therapies. However, outcomes are hard to determine due to the subjective nature of pain. We would like to devise a strategy that would establish objectivity of pain assessment. After review of various studies relating to pain biomarkers, we found that serum levels of pro-inflammatory cytokines and chemokines, such as IL-1?, IL-6, IL-2, IL-33, CCL3, CXCL1, CCR5, and TNF-?, were significantly up-regulated during chronic pain experience. On the other hand, anti-inflammatory cytokines such as IL-10 and IL-4 were found to show significant down-regulation during chronic pain state. Regulatory miRNAs, siRNAs, and deacetylases that coincide with these cytokines, also showed negative correlation, corresponding to the cytokine they were regulating.
The authors would like to apply this knowledge to SCS, a therapy for chronic neuropathic pain, in an attempt to develop a biomarker profile to help predict success. This study will be a prospective study including patients scheduled for SCS. One month before SCS surgery, patients will complete a survey assessing their subjective level of pain on the visual analog scale and subjective level of function. Patients will also have venipuncture performed, and serum will be analyzed for levels of pain biomarkers. After SCS surgery, patients will be followed at 6 more time points: 2 weeks, 1 month, 3 months, 6 months, 1 year, and 2 years. At each time point, the survey will be re-administered and blood work will be repeated. By evaluating patients pre-operatively and post-operatively, we will be able to assess subjective and objective levels of pain, allowing us to analyze trends in pain biomarkers in the context of patient-reported pain measurement. The duration of this study will be 4 years. Each subject will participate in this study for a total period of 25 months, which will allow us to follow these patients for 2 years postoperatively.
Conclusion
The review of various studies relating to inflammation- and/or nerve injury-induced chronic pain disorder led us to hypothesize that the application of the spinal cord stimulation procedure should relatively reduce serum pro-inflammatory cytokines, and relatively increase serum levels of anti-inflammatory cytokines. This should, in turn, help us understand the mechanism of spinal cord stimulation, thereby optimizing the efficaciousness of the procedure, and perhaps allow us to make predictions regarding therapy success. A follow-up prospective study regarding serum biomarker profile in SCS patients is currently being undertaken.
Footnotes
Author Disclosure:The authors declare no conflicts of interest.
Disclosure of Funding:This work was supported by grants from the University of Medicine and Dentistry of New Jersey and the National Institutes of Health, Bethesda, Maryland (grant numbers: NS072206, HL117684, and DA033390).
In conclusion,�diagnostic biomarkers have the potential of leading new personalized therapeutics in the treatment of chronic pain health issues, such as low back pain, disc degeneration and neuropathic pain. Several research studies like the ones above have been established to ultimately help healthcare professionals understand better ways to reduce or eliminate the pain and discomfort associated with these chronic pain problems. Furthermore, biomarkers can be essential diagnostic tools for the evaluation and treatment of a variety of health issues. Information referenced from the National Center for Biotechnology Information (NCBI).�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
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14.�Yin D, Liu YY, Wang TX, Hu ZZ, Qu WM, Chen JF, Cheng NN, Huang ZL. Paeoniflorin exerts analgesic and hypnotic effects via adenosine A1 receptors in a mouse neuropathic pain model.�Psychopharmacology (Berl)�2016 Jan;233(2):281�93.�[PubMed]
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17.�Kraychete DC, et al. Serum Cytokine Levels in Patients with Chronic Low Back Pain due to Herniated Disc: Analytical Cross-Sectional Study.�Sao Paulo Med J.�2010;128(5):259�292.�[PubMed]
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Arthritis pain is a complex phenomenon involving intricate neurophysiological processing at all levels of the pain pathway. The treatment options available to alleviate joint pain are fairly limited, and most arthritis patients report only modest pain relief with current treatments. A better understanding of the neural mechanisms responsible for musculoskeletal pain and identifying new targets will help develop future pharmacological therapies. This article reviews some of the latest research into factors that contribute to joint pain and covers areas such as cannabinoids, proteinase-activated receptors, sodium channels, cytokines, and transient receptor potential channels. The emerging hypothesis that osteoarthritis may have a neuropathic component is also discussed.
Introduction
The world health organization ranks musculoskeletal disorders as the most frequent cause of disability in the modern world, affecting one in three adults [1]. Even more alarming is that the prevalence of these diseases is rising while our knowledge of their underlying causes is fairly rudimentary.
Fig. 1 A schematic illustrating some of the targets known to modulate joint pain. Neuromodulators can be released from nerve terminals as well as mast cells and macrophages to alter afferent mechanosensitivity. Endovanilloids, acid, and noxious heat can activate transient receptor potential vanilloid type 1 (TRPV1) ion channels leading to the release of algogenic substance P (SP), which subsequently binds to neurokinin-1 (NK1) receptors. Proteases can cleave and stimulate protease-activated receptors (PARs). Thus far, PAR2and PAR4have been shown to sensitize joint primary afferents. The endocannabinoid anandamide (AE) is produced on demand and synthesized from N-arachidonoyl phosphatidylethanolamine (NAPE) under the enzymatic action of phospholipases. A portion of AE then binds to cannabinoid-1 (CB1) receptors leading to neuronal desensitization. Unbound AE is rapidly taken up by an anandamide membrane transporter (AMT)before being broken down by a fatty acid amide hydrolase (FAAH)into ethanolamine (Et) and arachidonic acid (AA). The cytokines tumor necrosis factor-?(TNF-?), interleukin-6 (IL-6) and interleukin1-beta (IL-1?) Can bind to their respective receptors to enhance pain transmission. Finally, tetrodotoxin (TTX)-resistant sodium channels (Nav1.8) are involved in neuronal sensitization.
Patients yearn for their chronic pain to disappear; however, currently prescribed analgesics are largely ineffective and are accompanied by a wide range of unwanted side effects. As such, millions of people worldwide are suffering from the debilitating effects of joint pain, for which there is no satisfactory treatment [2].
More than 100 different forms of arthritis have osteoarthritis (OA) being the most common. OA is a progressively degenerative joint disease that causes chronic pain and loss of function. Commonly, OA is the inability of the joint to repair damage effectively in response to excessive forces being placed on it. The biological and psychosocial factors that comprise chronic OA pain are not well understood, although ongoing research unravels the complex nature of disease symptoms [2]. Current therapeutics, such as non-steroidal anti-inflammatory drugs (NSAIDs), provide some symptomatic relief, reducing the pain for short periods of time, but do not alleviate pain across the patient’s lifespan. Furthermore, high-dose NSAIDs cannot be taken repeatedly over many years, as this can lead to renal toxicity and gastrointestinal bleeding.
Traditionally, arthritis research has focused largely on the articular cartilage as a primary target for the therapeutic development of novel OA drugs for disease modification. This chondrogenic focus has shed new light on the intricate biochemical and biomechanical factors that influence chondrocyte behavior in diseased joints. However, as the articular cartilage is aneural and avascular, this tissue is unlikely to be the source of OA pain. This fact, coupled with the findings that there is no correlation between the damage of articular cartilage and pain in OA patients [3,4] or preclinical models of OA [5], has caused a shift in focus to develop drugs for effective pain control. This article will review the latest findings in joint pain research and highlight some of the emerging targets that may be the future of arthritis pain management (summarized in Fig. 1)
Cytokines
The actions of various cytokines in joint neurophysiology studies have featured quite prominently recently. Interleukin-6 (IL-6), for example, is a cytokine that typically binds to the membrane-bound IL-6 receptor (IL-6R). IL-6 can also signal by binding with a soluble IL-6R (SIL-6R) to produce an IL-6/sIL-6R complex. This IL-6/sIL-6R complex subsequent lybinds to a transmembrane glycoprotein subunit 130(gp130), thereby allowing IL-6 to signal in cells that do not constitutively express membrane-bound IL-6R [25,26]. IL-6 and SIL-6R are key players in systemic inflammation and arthritis, as upregulation of both has been found in RA patients’ serum and synovial fluid [27,29]. Recently, Vazquez et al.observed that co-administration of IL-6/sIL-6R into rat knees caused inflammation-evoked pain, as revealed by an increase in the response of spinal dorsal horn neurons to mechanical stimulation of the knee and other parts of the hindlimb [30]. Spinal neuron hyperexcitability was also seen when IL-6/sIL-6R was applied locally to the spinal cord. Spinal application of soluble gp130 (which would mop up IL-6/sIL-6R complexes, thereby reducing trans-signaling) inhibited IL-6/sIL-6R-induced central sensitization. However, acute application of soluble gp130 alone did not reduce the neuronal responses to already established joint inflammation.
The transient receptor potential (TRP) channels are non-selective cation channels that act as integrators of various physiological and pathophysiological processes. In addition to thermosensation, chemosensation, and mechanosensation, TRP channels are involved in the modulation of pain and inflammation. For example, TRP vanilloid-1 (TRPV1) ion channels have been shown to contribute to joint inflammatory pain as thermal hyperalgesia was not evocable in TRPV1 mono arthritic mice [31]. Similarly, TRP ankyrin-1 (TRPA1)ion channels are involved in arthritic mechano hypersensitivity as blockade of the receptor with selective antagonists attenuated mechanical pain in the Freunds complete adjuvant model inflammation [32,33]. Further evidence thatTRPV1 may be involved in the neurotransmission of OA pain comes from studies in which neuronal TRPV1 expression is elevated in the sodium monoiodoacetate model of OA [34]. In addition, systemic administration of the TRPV1 antagonist A-889425 reduced the evoked and spontaneous activity of spinal-wide dynamic range and nociception-specific neurons in the monoiodoacetate model [35]. These data suggest that endovanilloids could be involved in central sensitization processes associated with OA pain.
There are currently known to be at least four polymorphisms in the gene that encodes TRPV1, leading to an alteration in the structure of the ion channel and impaired function. One particular polymorphism (rs8065080) alters the sensitivity of TRPV1 to capsaicin, and individuals carrying this polymorphism are less sensitive to thermal hyperalgesia [36]. A recent study examined whether OA patients with the rs8065080 polymorphism experienced altered pain perception based on this genetic anomaly. The research team found that patients with asymptomatic knee OA were more likely to carry the rs8065080 gene than patients with painful joints [37]. This observation indicates that OA patients with normal functioning; TRPV1 channels have an increased risk of joint pain and re-affirms the potential involvement of TRPV1 in OA pain perception.
Conclusion
While the hurdle of treating arthritis pain effectively remains, great leaps are being made in our understanding of the neurophysiological processes responsible for the generation of joint pain. New targets are being discovered continually, while the mechanisms behind known pathways are being further defined and refined. Targeting one specific receptor or ion channel is unlikely to be the solution to normalizing joint pain, but rather a polypharmacy approach is indicated in which various mediators are used in combination during specific phases of the disease. Unraveling the functional circuitry at each level of the pain pathway will also improve our knowledge of how joint pain is generated. For example, identifying the peripheral mediators of joint pain will allow us to control nociception within the joint and likely avoid the central side effects of systemically administered pharmacotherapeutics.
FACETOGENIC PAIN
FACET SYNDROME & FACETOGENIC PAIN
Facet syndrome is an articular disorder related to the lumbar facet joints and their innervations and produces both local and radiating facetogenic pain.
Excessive rotation, extension, or flexion of the spine (repeated overuse) can result in degenerative changes to the joint’s cartilage. In addition, itt may involve degenerative changes to other structures, including the intervertebral disc.
CERVICAL FACET SYNDROME & FACETOGENIC PAIN
Axial neck pain (rarely radiating past the shoulders), most common unilaterally.
Pain with and/or limitation of extension and rotation
Tenderness upon palpation
Radiating facetogenic pain locally or into the shoulders or upper back, and rarely radiate in the front or down an arm or into the fingers as a herniated disc might.
LUMBAR FACET SYNDROME & FACETOGENIC PAIN
Pain or tenderness in the lower back.
Local tenderness/stiffness alongside the spine in the lower back.
Pain, stiffness, or difficulty with certain movements (such as standing up straight or getting up from a chair.
Pain upon hyperextension
Referred pain from upper lumbar facet joints can extend into the flank, hip, and upper lateral thigh.
Referred pain from lower lumbar facet joints can penetrate deep into the thigh, laterally and/or posteriorly.
L4-L5 and L5-S1 facet joints can refer to pain extending into the distal lateral leg, and in rare instances, to the foot
EVIDENCE-BASED MEDICINE
Evidence-based Interventional Pain Medicine according to Clinical Diagnoses
12. Pain Originating from the Lumbar Facet Joints
Abstract
Although the existence of a facet syndrome had long been questioned, it is now generally accepted as a clinical entity. Depending on the diagnostic criteria, the zygapophysial joints account for between 5% and 15% of cases of chronic, axial low back pain. Most commonly, facetogenic pain results from repetitive stress and/or cumulative low-level trauma, leading to inflammation and stretching of the joint capsule. The most frequent complaint is axial low back pain with referred pain perceived in the flank, hip, and thigh. No physical examination findings are pathognomonic for diagnosis. The strongest indicator for lumbar facetogenic pain is pain reduction after anesthetic blocks of the rami mediales (medial branches) of the rami dorsales that innervate the facet joints. Because false-positive and, possibly, false-negative results may occur, results must be interpreted carefully. In patients with injection-confirmed zygapophysial joint pain, procedural interventions can be undertaken in the context of a multidisciplinary, multimodal treatment regimen that includes pharmacotherapy, physical therapy, and regular exercise, and, if indicated, psychotherapy. Currently, the gold standard for treating facetogenic pain is radiofrequency treatment (1 B+). The evidence supporting intra-articular corticosteroids is limited; hence, this should be reserved for those who do not respond to radiofrequency treatment (2 B1).
Facetogenic Pain emanating from the lumbar facet joints is a common cause of low back pain in the adult population. Goldthwaite was the first to describe the syndrome in 1911, and Ghormley is generally credited with coining the term �facet syndrome� in 1933. Facetogenic pain is defined as pain that arises from any structure that is part of the facet joints, including the fibrous capsule, synovial membrane, hyaline cartilage, and bone.35
More commonly, it is the result of repetitive stress and/or cumulative low-level trauma. This leads to inflammation, which can cause the facet joint to be filled with fluid and swell, resulting in stretching of the joint capsule and subsequent pain generation.27 Inflammatory changes around the facet joint can also irritate the spinal nerve via foraminal narrowing, resulting in sciatica. In addition, Igarashi et al.28 found that inflammatory cytokines released through the ventral joint capsule in patients with zygapophysial joint degeneration may be partially responsible for the neuropathic symptoms in individuals with spinal stenosis. Predisposing factors for zygapophysial joint pain include spondylolisthesis/lysis, degenerative disc disease, and advanced age.5
I.C ADDITIONAL TESTS
The prevalence rate of pathological changes in the facet joints on radiological examination depends on the mean age of the subjects, the radiological technique used, and the definition of abnormality. Degenerative facet joints can be best visualized via computed tomography (CT) examination.49
NEUROPATHIC PAIN
Pain initiated or caused by a primary lesion or dysfunction in the somatosensory nervous system.
Neuropathic pain is usually chronic, difficult to treat, and often resistant to standard analgesic management.
Abstract
Neuropathic pain is caused by a lesion or disease of the somatosensory system, including peripheral fibers (A?, A? and C fibers) and central neurons, and affects 7-10% of the general population. Multiple causes of neuropathic pain have been described. Its incidence is likely to increase due to the aging global population, increased diabetes mellitus, and improved survival from cancer after chemotherapy. Indeed, imbalances between excitatory and inhibitory somatosensory signaling, alterations in ion channels, and variability in how pain messages are modulated in the central nervous system all have been implicated in neuropathic pain. Furthermore, the burden of chronic neuropathic pain seems to be related to the complexity of neuropathic symptoms, poor outcomes, and difficult treatment decisions. Importantly, quality of life is impaired in patients with neuropathic pain due to increased drug prescriptions and visits to health care providers and the morbidity from the pain itself and the inciting disease. Despite challenges, progress in understanding the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain.
PATHOGENESIS OF NEUROPATHIC PAIN
PERIPHERAL MECHANISMS
After a peripheral nerve lesion, neurons become more sensitive and develop abnormal excitability and elevated sensitivity to stimulation.
This is known as…Peripheral Sensitization!
CENTRAL MECHANISMS
As a consequence of ongoing spontaneous activity in the periphery, neurons develop an increased background activity, enlarged receptive fields, and increased responses to afferent impulses, including normal tactile stimuli. This is known as…Central Sensitization!
Chronic neuropathic pain is more frequent in women (8% versus 5.7% in men) and in patients >50 years of age (8.9% versus 5.6% in those <49 years of age), and most commonly affects the lower back and lower limbs, neck and upper limbs24. Lumbar and cervical painful radiculopathies are probably the most frequent cause of chronic neuropathic pain. Consistent with these data, a survey of >12,000 patients with chronic pain with both nociceptive and neuropathic pain types, referred to pain specialists in Germany, revealed that 40% of all patients experienced at least some characteristics of neuropathic pain (such as burning sensations, numbness, and tingling); patients with chronic back pain and radiculopathy were particularly affected25.
The contribution of clinical neurophysiology to the comprehension of the tension-type headache mechanisms.
Abstract
So far, clinical neurophysiological studies on tension-type headache (TTH) have been conducted with two main purposes: (1) to establish whether some neurophysiological parameters may act as markers of TTH, and (2) to investigate the physiopathology of TTH. Regarding the first point, the present results are disappointing since some abnormalities found in TTH patients may also be frequently observed in migraineurs. On the other hand, clinical neurophysiology has played an important role in the debate about the pathogenesis of TTH. Studies on the exteroceptive suppression of the temporalis muscle contraction have detected a dysfunction of the brainstem excitability and suprasegmental control. A similar conclusion has been reached using trigeminocervical reflexes, whose abnormalities in TTH have suggested a reduced inhibitory activity of brainstem interneurons, reflecting abnormal endogenous pain control mechanisms. Interestingly, the neural excitability abnormality in TTH seems to be a generalized phenomenon, not limited to the cranial districts. Defective DNIC-like mechanisms have indeed been evidenced also in somatic districts by nociceptive flexion reflex studies. Unfortunately, most neurophysiological studies on TTH are marred by serious methodological flaws, which should be avoided in future research to clarify the TTH mechanisms better.
References:
Neurophysiology of arthritis pain. McDougall JJ1 Linton P.
Pain originating from the lumbar facet joints. van Kleef M1,Vanelderen P,Cohen SP,Lataster A,Van Zundert J,Mekhail N.
Neuropathic painLuana Colloca,1Taylor Ludman,1Didier Bouhassira,2Ralf Baron,3Anthony H. Dickenson,4David Yarnitsky,5Roy Freeman,6Andrea Truini,7Nadine Attal, Nanna B. Finnerup,9Christopher Eccleston,10,11Eija Kalso,12David L. Bennett,13Robert H. Dworkin,14and Srinivasa N. Raja15
The contribution of clinical neurophysiology to the comprehension of the tension-type headache mechanisms. Rossi P1, Vollono C, Valeriani M, Sandrini G.
Heel Spur: Blanca, born and raised in El Paso, TX, has been suffering from heel spurs for about two years. As a registered nurse, her symptoms significantly affected her ability to work and her overall quality of life. Determined to improve her health, Blanca considered chiropractic care. Once she started treatment with Dr. Alex Jimenez, however, Blanca experienced tremendous relief from her heel spurs, almost instantly. Blanca highly recommends chiropractic care with Dr. Alex Jimenez as the non-surgical choice for treatment of heel spurs.
Chiropractic Heel Spur Treatment
A heel spur is a calcium residue resulting in a bony protrusion on the bottom of the heel bone. Although heel spurs are often painless, they can lead to heel pain. They are often associated with plantar fasciitis, a painful inflammation of the fibrous band of connective tissue (plantar fascia) that runs across the bottom of the foot and also connects the heel bone to the ball of the foot. Heel spurs are usually caused by strains on foot muscles and ligaments, stretching of the plantar fascia, and repeated tearing of the membrane which covers the heel bone. Heel spurs are particularly common among athletes.
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