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.
Muscle Relaxants? Nearly everyone, more than 80 percent of the world�s population, will experience back pain at some point in their lifetime. Just ask the 31 million Americans suffering from low back pain at any given time.
In fact, globally it is the leading cause of disability. It is the most common reason that people miss work and the second more common reason for doctor�s office visits. In the United States alone more than $50 billion is spent each year trying to relieve back pain, but even that figure is not complete, but only based on trackable, identifiable costs.
There have been studies published over the years that unequivocally show chiropractic as a viable and extremely effective treatment for back pain. Several of these studies plainly show that chiropractic is better than muscle relaxants.
Muscle Relaxants & Chiropractic Study
One study that is one of the most notable was conducted at Life University in Georgia. It has been cited in several journals and used as a catalyst for proving the efficacy of chiropractic treatment for back pain and its superiority to muscle relaxants.
Study Parameters
The study involved 192 subjects who had been experiencing lower back pain for a period of time ranging from two to six weeks. The subjects were separated into three groups:
Group One – Chiropractic adjustments combined with placebo medication
Group Two � Muscle relaxants combined with sham chiropractic adjustments
Group Three � Control Group � received both placebo medication and sham chiropractic adjustments
All groups were given the same length of care, four weeks, with an evaluation of progress at the two-week mark and the four-week mark. The pain was assessed using the Zung Self-Rating for Depression scale, the Oswestry Low Back Pain Disability Questionnaire, and the Visual Analog Scale (VAS). Upon admission into the study during the initial visit as well as at the two-week evaluation, Shober�s Test for Lumbar Flexibility was also administered.
The subjects in all three groups were also allowed to take acetaminophen for pain. This was an additional evaluative measure to assess the need for additional self-medication.
During the course of the study there was a two-week treatment period where the subjects in the chiropractic adjustment group received a total of seven adjustments. These adjustments were tailored to each patient�s specific needs and included pelvic adjustments, sacral (lower back), or lumbar and upper cervical (neck and back).
The sham treatments mimicked all aspects of an actual chiropractic adjustment including dialog, normal visit length, and procedures. However, no actual adjustments were performed.
Study Results
At the conclusion of the study, the subjects who received chiropractic treatment reported a significant decrease in pain and an increase in flexibility. Of the groups that did not receive chiropractic treatment there were no significant differences noted. There was a decrease in disability and depression across all three groups, indicating that muscle relaxants are effective in treating back pain, but overall chiropractic care is the more effective option for treating back pain and disability.
What Does This Mean For Patients With Back Pain?
Patients suffering from back pain can receive greater relief without the undesirable side effects of muscle relaxants by seeking chiropractic care. Patients who are using muscle relaxants to treat their back pain should talk to their chiropractor and doctor about incorporating chiropractic treatment into their patient care regimen. Patients experiencing back pain should pursue chiropractic care before resorting to more aggressive methods including muscle relaxants.
Chiropractic care is a safe, non-invasive treatment for back pain. It also facilitates healing, increases flexibility, and improves mobility. Patients who are looking for a healthy treatment option that focuses on overall wellness, Chiropractic could be the answer.
Neurogenic inflammation, or NI, is the physiological process where mediators are discharged directly from the cutaneous nerves to commence an inflammatory response. This results in the creation of local inflammatory reactions including, erythema, swelling, temperature increase, tenderness, and pain. Fine unmyelinated afferent somatic C-fibers, which respond to low intensity mechanical and chemical stimulations, are largely responsible for the release of these inflammatory mediators.
When stimulated, these nerve pathways in the cutaneous nerves release energetic neuropeptides, or substance P and calcitonin gene related peptide (CGRP), rapidly into the microenvironment, triggering a series of inflammatory responses. There is a significant distinction in immunogenic inflammation, that’s the very first protective and reparative response made by the immune system when a pathogen enters the body, whereas neurogenic inflammation involves a direct connection between the nervous system and the inflammatory responses. Even though neurogenic inflammation and immunologic inflammation can exist concurrently, the two are not clinically indistinguishable. The purpose of the article below is to discuss the mechanism of neurogenic inflammation and the peripheral nervous system’s role in host defense and immunopathology.
Neurogenic Inflammation � The Peripheral Nervous System�s Role in Host Defense and Immunopathology
Abstract
The peripheral nervous and immune systems are traditionally thought of as serving separate functions. This line is, however, becoming increasingly blurred by new insights into neurogenic inflammation. Nociceptor neurons possess many of the same molecular recognition pathways for danger as immune cells and in response to danger, the peripheral nervous system directly communicates with the immune system, forming an integrated protective mechanism. The dense innervation network of sensory and autonomic fibers in peripheral tissues and high speed of neural transduction allows for rapid local and systemic neurogenic modulation of immunity. Peripheral neurons also appear to play a significant role in immune dysfunction in autoimmune and allergic diseases. Therefore, understanding the coordinated interaction of peripheral neurons with immune cells may advance therapeutic approaches to increase host defense and suppress immunopathology.
Introduction
Two thousand years ago, Celsus defined inflammation as involving four cardinal signs � Dolor (pain), Calor (heat), Rubor (redness), and Tumor (swelling), an observation indicating that activation of the nervous system was recognized as being integral to inflammation. However, pain has been mainly thought of since then, only as a symptom, and not a participant in the generation of inflammation. In this perspective, we show that the peripheral nervous system plays a direct and active role in modulating innate and adaptive immunity, such that the immune and nervous systems may have a common integrated protective function in host defense and the response to tissue injury, an intricate interaction that also can lead to pathology in allergic and autoimmune diseases.
Survival of organisms is critically dependent on the capacity to mount a defense against potential harm from tissue damage and infection. Host defense involves both avoidance behavior to remove contact with a dangerous (noxious) environment (a neural function), and active neutralization of pathogens (an immune function). Traditionally, the role of the immune system in combating infective agents and repairing tissue injury has been considered quite distinct from that of the nervous system, which transduces damaging environmental and internal signals into electrical activity to produce sensations and reflexes (Fig. 1). We propose that these two systems are actually components of a unified defense mechanism. The somatosensory nervous system is ideally placed to detect danger. Firstly, all tissues that are highly exposed to the external environment, such as epithelial surfaces of the skin, lungs, urinary and digestive tract, are densely innervated by nociceptors, high threshold pain-producing sensory fibers. Secondly, transduction of noxious external stimuli is almost instantaneous, orders of magnitude quicker than the mobilization of the innate immune system, and therefore may be the �first responder� in host defense.
Figure 1: Noxious stimuli, microbial and inflammatory recognition pathways trigger activation of the peripheral nervous system. Sensory neurons possess several means of detecting the presence of noxious/harmful stimuli. 1) Danger signal receptors, including TRP channels, P2X channels, and danger associated molecular pattern (DAMP) receptors recognize exogenous signals from the environment (e.g. heat, acidity, chemicals) or endogenous danger signals released during trauma/tissue injury (e.g. ATP, uric acid, hydroxynonenals). 2) Pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and Nod-like receptors (NLRs) recognize Pathogen associated molecular patterns (PAMPs) shed by invading bacteria or viruses during infection. 3) Cytokine receptors recognize factors secreted by immune cells (e.g. IL-1beta, TNF-alpha, NGF), which activate map kinases and other signaling mechanisms to increase membrane excitability.
In addition to orthodromic inputs to the spinal cord and brain from the periphery, action potentials in nociceptor neurons can also be transmitted antidromically at branch points back down to the periphery, the axon reflex. These together with sustained local depolarizations lead to a rapid and local release of neural mediators from both peripheral axons and terminals (Fig. 2) 1. Classic experiments by Goltz (in 1874) and by Bayliss (in 1901) showed that electrically stimulating dorsal roots induces skin vasodilation, which led to the concept of a �neurogenic inflammation�, independent of that produced by the immune system (Fig. 3).
Figure 2: Neuronal factors released from nociceptor sensory neurons directly drive leukocyte chemotaxis, vascular hemodynamics and the immune response. When noxious stimuli activate afferent signals in sensory nerves, antidromic axon reflexes are generated that induce the release of neuropeptides at the peripheral terminals of the neurons. These molecular mediators have several inflammatory actions: 1) Chemotaxis and activation of neutrophils, macrophages and lymphocytes to the site of injury, and degranulation of mast cells. 2) Signaling to vascular endothelial cells to increase blood flow, vascular leakage and edema. This also allows easier recruitment of inflammatory leukocytes. 3) Priming of dendritic cells to drive subsequent T helper cell differentiation into Th2 or Th17 subtypes.
Figure 3: Timeline of advances in understanding of the neurogenic aspects of inflammation from Celsus to the present day.
Neurogenic inflammation is mediated by the release of the neuropeptides calcitonin gene related peptide (CGRP) and substance P (SP) from nociceptors, which act directly on vascular endothelial and smooth muscle cells 2�5. CGRP produces vasodilation effects 2, 3, whereas SP increases capillary permeability leading to plasma extravasation and edema 4, 5, contributing to the rubor, calor and tumor of Celsus. However, nociceptors release many additional neuropeptides (online database: www.neuropeptides.nl/), including Adrenomedullin, Neurokinins A and B, Vasoactive intestinal peptide (VIP), neuropeptide (NPY), and gastrin releasing peptide (GRP), as well as other molecular mediators such as glutamate, nitric oxide (NO) and cytokines such as eotaxin 6.
We now appreciate that the mediators released from sensory neurons in the periphery not only act on the vasculature, but also directly attract and activate innate immune cells (mast cells, dendritic cells), and adaptive immune cells (T lymphocytes) 7�12. In the acute setting of tissue damage, we conjecture that neurogenic inflammation is protective, facilitating physiological wound healing and immune defense against pathogens by activating and recruiting immune cells. However, such neuro-immune communications also likely play major roles in the pathophysiology of allergic and autoimmune diseases by amplifying pathological or maladaptive immune responses. In animal models of rheumatoid arthritis for example, Levine and colleagues have shown that denervation of the joint leads to a striking attenuation in inflammation, that is dependent on neural expression of substance P 13, 14. In recent studies of allergic airway inflammation, colitis and psoriasis, primary sensory neurons play a central role in initiating and augmenting the activation of innate and adaptive immunity 15�17.
We propose therefore, that the peripheral nervous system not only plays a passive role in host defense (detection of noxious stimuli and initiation of avoidance behavior), but also an active role in concert with the immune system in modulating the responses to and combat of harmful stimuli, a role that can be subverted to contribute to disease.
Shared Danger Recognition Pathways in the Peripheral Nervous and Innate Immune Systems
Peripheral sensory neurons are adapted to recognize danger to the organism by virtue of their sensitivity to intense mechanical, thermal and irritant chemical stimuli (Fig. 1). Transient receptor potential (TRP) ion channels are the most widely studied molecular mediators of nociception, conducting non-selective entry of cations upon activation by various noxious stimuli. TRPV1 is activated by high temperatures, low pH and capsaicin, the vallinoid irritant component of chili peppers 18. TRPA1 mediates the detection of reactive chemicals including environmental irritants such as tear gas and industrial isothiocyanates 19, but more importantly, it is also activated during tissue injury by endogenous molecular signals including 4-hydroxynonenal and prostaglandins 20, 21.
Interestingly, sensory neurons share many of the same pathogen and danger molecular recognition receptor pathways as innate immune cells, which enable them also to detect pathogens (Fig. 1). In the immune system, microbial pathogens are detected by germline encoded pattern recognition receptors (PRRs), which recognize broadly conserved exogenous pathogen-associated molecular patterns (PAMPs). The first PRRs to be identified were members of toll-like receptor (TLR) family, which bind to yeast, bacterial derived cell-wall components and viral RNA 22. Following PRR activation, downstream signaling pathways are turned on that induce cytokine production and activation of adaptive immunity. In addition to TLRs, innate immune cells are activated during tissue injury by endogenous derived danger signals, also known as damage-associated molecular patterns (DAMPs) or alarmins 23, 24. These danger signals include HMGB1, uric acid, and heat shock proteins released by dying cells during necrosis, activating immune cells during non-infectious inflammatory responses.
PRRs including TLRs 3, 4, 7, and 9 are expressed by nociceptor neurons, and stimulation by TLR ligands leads to induction of inward currents and sensitization of nociceptors to other pain stimuli 25�27. Furthermore, activation of sensory neurons by the TLR7 ligand imiquimod leads to activation of an itch specific sensory pathway 25. These results indicate that infection-associated pain and itch may be partly due to direct activation of neurons by pathogen-derived factors, which in turn activate immune cells through peripheral release of neuronal signaling molecules.
A major DAMP/alarmin released during cellular injury is ATP, which is recognized by purinergic receptors on both nociceptor neurons and immune cells 28�30. Purinergic receptors are made up of two families: P2X receptors, ligand-gated cation channels, and P2Y receptors, G-protein coupled receptors. In nociceptor neurons, recognition of ATP occurs through P2X3, leading to rapidly densensitizing cation currents and pain 28, 30 (Fig. 1), while P2Y receptors contribute to nociceptor activation by sensitization of TRP and voltage-gated sodium channels. In macrophages, ATP binding to P2X7 receptors leads to hyperpolarization, and downstream activation of the inflammasome, a molecular complex important in generation of IL-1beta and IL-18 29. Therefore, ATP is a potent danger signal that activates both peripheral neurons and innate immunity during injury, and some evidence even suggests that neurons express parts of the inflammasome molecular machinery 31.
The flip side of danger signals in nociceptors is the role of TRP channels in immune cell activation. TRPV2, a homologue of TRPV1 activated by noxious heat, is expressed at high levels in innate immune cells 32. Genetic ablation of TRPV2 led to defects in macrophage phagocytosis and clearance of bacterial infections 32. Mast cells also express TRPV channels, which may directly mediate their degranulation 33. It remains to be determined whether endogenous danger signals activate immune cells in a similar manner as nociceptors.
A key means of communication between immune cells and nociceptor neurons are through cytokines. Upon activation of cytokine receptors, signal transduction pathways are activated in sensory neurons leading to downstream phosphorylation of membrane proteins including TRP and voltage-gated channels (Fig. 1). The resulting sensitization of nociceptors means that normally innocuous mechanical and heat stimuli can now activate nociceptors. Interleukin 1 beta and TNF-alpha are two important cytokines released by innate immune cells during inflammation. IL-1beta and TNF-alpha are directly sensed by nociceptors which express the cognate receptors, induce activation of p38 map kinases leading to increased membrane excitability 34�36. Nerve growth factor (NGF) and prostaglandin E(2) are also major inflammatory mediators released from immune cells that act directly on peripheral sensory neurons to cause sensitization. An important effect of nociceptor sensitization by immune factors is an increased release of neuropeptides at peripheral terminals that further activate immune cells, thereby inducing a positive feedback loop that drives and facilitates inflammation.
Sensory Nervous System Control of Innate and Adaptive Immunity
In early phases of inflammation, sensory neurons signal to tissue resident mast cells and dendritic cells, which are innate immune cells important in initiating the immune response (Fig. 2). Anatomical studies have shown a direct apposition of terminals with mast cells, as well as with dendritic cells, and the neuropeptides released from nociceptors can induce degranulation or cytokine production in these cells 7, 9, 37. This interaction plays an important role in allergic airway inflammation and dermatitis 10�12.
During the effector phase of inflammation, immune cells need to find their way to the specific site of injury. Many mediators released from sensory neurons, neuropeptides, chemokines, and glutamate, are chemotactic for neutrophils, eosinophils, macrophages, and T-cells, and enhance endothelial adhesion which facilitates immune cell homing 6, 38�41 (Fig. 2). Furthermore, some evidence implies that neurons may directly participate in the effector phase, as neuropeptides themselves may have direct antimicrobial functions 42.
Neuronally derived signaling molecules can also direct the type of inflammation, by contributing to the differentiation or specification of different types of adaptive immune T cells. An antigen is phagocytosed and processed by innate immune cells, which then migrate to the nearest lymph node and present the antigenic peptide to na�ve T cells. Depending on the type of antigen, costimulatory molecules on the innate immune cell, and the combinations of specific cytokines, na�ve T cells mature into specific subtypes that best serve the inflammatory effort to clear the pathogenic stimulus. CD4 T cells, or T helper (Th) cells, can be divided into four principle groups, Th1, Th2, Th17, and T regulatory cells (Treg). Th1 cells are mainly involved in regulating immune responses to intracellular microorganisms and organ-specific autoimmune diseases; Th2 are critical for immunity against extracellular pathogens, such as helminths, and are responsible for allergic inflammatory diseases; Th17 cells play a central role in protection against microbial challenges, such as extracellular bacteria and fungi; Treg cells are involved in maintaining self tolerance and regulating immune responses. This T cell maturation process appears to be heavily influenced by sensory neuronal mediators. Neuropeptides, such as CGRP and VIP, can bias dendritic cells towards a Th2-type immunity and reduce Th1-type immunity by promoting the production of certain cytokines and inhibiting others, as well as by reducing or enhancing dendritic cell migration to local lymph nodes 8, 10, 43. Sensory neurons also contribute considerably to allergic (mainly Th2 driven) inflammation 17. In addition to regulating Th1 and Th2 cells, other neuropeptides, such as SP and Hemokinin-1, can drive the inflammatory response more toward Th17 or Treg 44, 45, which means that neurons may also be involved in regulating inflammatory resolution. In immunopathologies such as colitis and psoriasis, blockade of neuronal mediators like substance P may significantly dampen T cell and immune mediated damage 15�17, although antagonizing one mediator may by itself only have a limited effect on neurogenic inflammation.
Considering that signaling molecules released from peripheral sensory nerve fibers regulate not only small blood vessels, but also the chemotaxis, homing, maturation, and activation of immune cells, it is becoming clear that neuro-immune interactions are much more intricate than previously thought (Fig. 2). Furthermore, it is quite conceivable that it is not individual neural mediators but rather specific combinations of signaling molecules released from nociceptors that influence different stages and types of immune responses.
Autonomic Reflex Control of Immunity
A role for a cholinergic autonomic nervous system �reflex� circuit in the regulation of peripheral immune responses also appears prominent 46. The vagus is the chief parasympathetic nerve connecting the brainstem with visceral organs. Work by Kevin Tracey and others point to potent generalized anti-inflammatory responses in septic shock and endotoxemia, triggered by an efferent vagal nerve activity leading to a suppression of peripheral macrophages 47�49. The vagus activates peripheral adrenergic celiac ganglion neurons innervating the spleen, leading to the downstream release of acetylcholine, which binds to alpha-7 nicotinic receptors on macrophages in the spleen and gastrointestinal tract. This induces activation of the JAK2/STAT3 SOCS3 signaling pathway, which powerfully suppresses TNF-alpha transcription 47. The adrenergic celiac ganglion also directly communicates with a subset of acetylcholine producing memory T cells, which suppress inflammatory macrophages 48.
Invariant natural Killer T cells (iNKT) are a specialized subset of T cells that recognize microbial lipids in the context of CD1d instead of peptide antigens. NKT cells are a key lymphocyte population involved in the combat of infectious pathogens and regulation of systemic immunity. NKT cells reside and traffic mainly through the vasculature and sinusoids of the spleen and liver. Sympathetic beta-adrenergic nerves in the liver directly signal to modulate NKT cell activity 50. During a mouse model of stroke (MCAO), for example, liver NKT cell mobility was visibly suppressed, which was reversed by sympathetic denervation or beta-adrenergic antagonists. Furthermore, this immunosuppressive activity of noradrenergic neurons on NKT cells led to increases in systemic infection and lung injury. Therefore, efferent signals from autonomic neurons can mediate a potent immuno-suppression.
Dr. Alex Jimenez’s Insight
Neurogenic inflammation is a local inflammatory response generated by the nervous system. It is believed to play a fundamental role in the pathogenesis of a variety of health issues, including, migraine, psoriasis, asthma, fibromyalgia, eczema, rosacea, dystonia and multiple chemical sensitivity. Although neurogenic inflammation associated with the peripheral nervous system has been extensively researched, the concept of neurogenic inflammation within the central nervous system still needs further research. According to several research studies, however, magnesium deficiencies are believed to be the main cause for neurogenic inflammation. The following article demonstrates an overview of the mechanisms of neurogenic inflammation in the nervous system, which may help healthcare professionals determine the best treatment approach to care for a variety of health issues associated with the nervous system.
Conclusions
What are the respective specific roles of the somatosensory and autonomic nervous systems in regulating inflammation and the immune system (Fig. 4)? Activation of nociceptors leads to local axon reflexes, which locally recruit and activate immune cells and is therefore, mainly pro-inflammatory and spatially confined. In contrast, autonomic stimulation leads to a systemic immunosuppression by affecting pools of immune cells in liver and spleen. The afferent signaling mechanisms in the periphery leading to the triggering of the immunosuppressive vagal cholinergic reflex circuit are poorly understood. However, 80�90% of vagal fibers are primary afferent sensory fibers, and therefore signals from the viscera, many potentially driven by immune cells, may lead to activation of interneurons in the brainstem and through them to an output in efferent vagal fibers 46.
Figure 4: Sensory and autonomic nervous systems modulate local and systemic immune responses respectively. Nociceptors innervating epithelial surfaces (e.g. skin and lung) induce localized inflammatory responses, activating mast cells and dendritic cells. In allergic airway inflammation, dermatitis and rheumatoid arthritis, nociceptor neurons play a role in driving inflammation. By contrast, autonomic circuits innervating the visceral organs (e.g. spleen and liver) regulate systemic immune responses by blocking macrophage and NKT cell activation. In stroke and septic endotoxemia, these neurons play an immunosuppressive role.
Typically, the time course and nature of inflammation, whether during infection, allergic reactions, or auto-immune pathologies, is defined by the categories of immune cells involved. It will be important to know what different types of immune cells are regulated by sensory and autonomic signals. A systematic assessment of what mediators can be released from nociceptors and autonomic neurons and the expression of receptors for these by different innate and adaptive immune cells might help address this question.
During evolution, similar danger detection molecular pathways have developed for both innate immunity and nociception even though the cells have completely different developmental lineages. While PRRs and noxious ligand-gated ion channels are studied separately by immunologists and neurobiologists, the line between these two fields is increasingly blurred. During tissue damage and pathogenic infection, release of danger signals are likely to lead to a coordinated activation of both peripheral neurons and immune cells with complex bidirectional communication, and an integrated host defense. The anatomical positioning of nociceptors at the interface with the environment, the speed of neural transduction and their ability to release potent cocktails of immune-acting mediators allows the peripheral nervous system to actively modulate the innate immune response and coordinate downstream adaptive immunity. Conversely, nociceptors are highly sensitive to immune mediators, which activate and sensitize the neurons. Neurogenic and immune-mediated inflammation are not, therefore, independent entities but act together as early warning devices. However, the peripheral nervous system also plays an important role in the pathophysiology, and perhaps etiology, of many immune diseases like asthma, psoriasis, or colitis because its capacity to activate the immune system can amplify pathological inflammation 15�17. Treatment for immune disorders may need to include, therefore, the targeting of nociceptors as well as of immune cells.
Acknowledgements
We thank the NIH for support (2R37NS039518).
In conclusion,�understanding the role of neurogenic inflammation when it comes to host defense and immunopathology is essential towards determining the proper treatment approach for a variety of nervous system health issues. By looking at the interactions of the peripheral neurons with immune cells, healthcare professionals may advance therapeutic approaches to further help increase host defense as well as suppress immunopathology. The purpose of the article above is to help patients understand the clinical neurophysiology of neuropathy, among other nerve injury 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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Chiropractic Care: Tracy Ludech, club director and coach of the El Paso Diggers, expresses how much of a difference the fitness program at PUSH has done for her athletes. Working cohesively and diligently together with the staff and trainers at PUSH, Tracy Ludech has witnessed tremendous improvements in her athlete’s strength, mobility and flexibility. Tracy Ludech encourages others to experience the benefits that a fitness program can have on young athletes.
Chiropractic Care Power & Rehabilitation
Physical wellness is a condition of health and well-being and, more especially, the ability to do aspects of sport, jobs and daily activities. Physical fitness is generally accomplished through proper nourishment, moderate-vigorous physical exercise, and sufficient rest. An extensive fitness program tailored to someone normally concentrates on one or more specific skills, and on medical needs like bone health. Many sources also cite psychological, social and emotional wellbeing as an significant part overall wellbeing. Physical fitness may also prevent or treat several chronic health conditions brought on by unhealthy lifestyle or aging.
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.
Concussions are traumatic brain injuries that affect brain function. Effects from these injuries are often temporary but can include headaches, problems with concentration, memory, balance and coordination. Concussions are usually caused by a blow to the head or violent shaking of the head and upper body. Some concussions cause loss of consciousness, but most do not. And it is possible to have a concussion and not realize it. Concussions are common in contact sports, such as football. However, most people gain a full recovery after a concussion.
Can also happen due to excessive shaking of the head or acceleration/deceleration
Mild injuries (mTBI/concussions) are the most common type of brain injury
Glasgow Coma Scale
Common Causes Of Concussion
Motor vehicle collisions
Falls
Sports injuries
Assault
Accidental or intentional discharge of weapons
Impact with objects
Prevention
Prevention of concussive injuries can be paramount
Encourage Patients To Wear Helmets
Competitive sports, especially boxing, hokey, football and baseball
Horseback riding
Riding bicycles, motorcycles, ATVs, etc.
High elevation activates such as rock climbing, zip lining
Skiing, snowboarding
Encourage Patients To Wear Seatbelts
Discuss the importance of wearing seatbelts at all times in vehicles with all of your patients
Also encourage use of appropriate booster or car seats for children to ensure adequate fit and function of seat belts.
Driving Safely
Patients should never drive while under the influence of drugs, including certain medications or alcohol
Never text and drive
Make Spaces Safer For Children
Install baby gates and window latches in the home
May in areas with shock-absorbing material, such as hardwood mulch or sand
Supervise children carefully, especially when they�re near water
Prevent Falls
Clearing tripping hazards such as loose rugs, uneven flooring or walkway clutter
Using nonslip mats in the bathtub and on shower floors, and installing grab bars next to the toilet, tub and shower
Ensure appropriate footwear
Installing handrails on both sides of stairways
Improving lighting throughout the home
Balance training exercises
Balance Training
Single leg balance
Bosu ball training
Core strengthening
Brain balancing exercises
Concussion Verbiage
Concussion vs. mTBI (mild traumatic brain injury)
mTBI is the term being used more commonly in medical settings, but concussion is a more largely recognized term in the community by sports coaches, etc.
The two terms describe the same basic thing, mTBI is a better term to use in your charting
Evaluating Concussion
Remember that there does not always have to be loss of consciousness for there to be a concussion
Post-Concussion Syndrome can occur without LOC as well
Symptoms of concussion may not be immediate and could take days to develop
Monitor for 48 post head injury watching for red flags
Blurred eyesight or other vision problems, such as dilated or uneven pupils
Confusion
Dizziness
Ringing in the ears
Nausea or vomiting
Slurred speech
Delayed response to questions
Memory loss
Fatigue
Trouble concentrating
Continued or persistent memory loss
Irritability and other personality changes
Sensitivity to light and noise
Sleep problems
Mood swings, stress, anxiety or depression
Disorders of taste and smell
Mental/Behavioral Changes
Verbal outbursts
Physical outbursts
Poor judgment
Impulsive behavior
Negativity
Intolerance
Apathy
Egocentricity
Rigidity and inflexibility
Risky behavior
Lack of empathy
Lack of motivation or initiative
Depression or anxiety
Symptoms In Children
Concussions can present differently in children
Excessive crying
Loss of appetite
Loss of interest in favorite toys or activities
Sleep issues
Vomiting
Irritability
Unsteadiness while standing
Amnesia
Memory loss and failure to form new memories
Retrograde Amnesia
Inability to remember things that happened before the injury
Due to failure in recall
Anterograde Amnesia
Inability to remember things that happened after the injury
Due to failure to formulate new memories
Even short memory losses can be predictive of outcome
Amnesia may be up to 4-10 times more predictive of symptoms and cognitive deficits following concussion than is LOC (less than 1 minute)
Return To Play Progression
Baseline: No Symptoms
As the baseline step of the Return to Play Progression, the athlete needs to have completed physical and cognitive rest and not be experiencing concussion symptoms for a minimum of 48 hours. Keep in mind, the younger the athlete, the more conservative the treatment.
Step 1: Light Aerobic Activity
The Goal: Only to increase an athlete�s heart rate.
The Time: 5 to 10 minutes.
The Activities: Exercise bike, walking, or light jogging.
Absolutely no weight lifting, jumping or hard running.
Step 2: Moderate activity
The Goal: Limited body and head movement.
The Time: Reduced from typical routine.
The Activities: Moderate jogging, brief running, moderate-intensity stationary biking, and moderate-intensity weightlifting
Step 3: Heavy, non-contact activity
The Goal: More intense but non-contact
The Time: Close to typical routine
The Activities: Running, high-intensity stationary biking, the player�s regular weightlifting routine, and non- contact sport-specific drills. This stage may add some cognitive component to practice in addition to the aerobic and movement components introduced in Steps 1 and 2.
Step 4: Practice & full contact
The Goal: Reintegrate in full contact practice.
Step 5: Competition
The Goal: Return to competition.
Microglial Priming
After head trauma microglial cells are primed and can become over active
To combat this, you must mediate the inflammation cascade
Prevent repeated head trauma
Due to priming of the foam cells, response to follow-up trauma may be far more severe and damaging
What Is Post-Concussion Syndrome (PCS)?
Symptoms following head trauma or mild traumatic brain injury, that can last weeks, months or years after injury
Symptoms persist longer than expected after initial concussion
More common in women and persons of advanced age who suffer head trauma
Severity of PCS often does not correlate to severity of head injury
PCS Symptoms
Headaches
Dizziness
Fatigue
Irritability
Anxiety
Insomnia
Loss of concentration and memory
Ringing in the ears
Blurry vision
Noise and light sensitivity
Rarely, decreases in taste and smell
Concussion Associated Risk Factors
Early symptoms of headache after injury
Mental changes such as amnesia or fogginess
Fatigue
Prior history of headaches
Evaluation Of PCS
PCS is a diagnosis of exclusion
If patient presents with symptoms after head injury, and other possible causes have been ruled out => PCS
Use appropriate testing and imaging studies to rule out other causes of symptoms
Headaches In PCS
Often �tension� type headache
Treat as you would for tension headache
Reduce stress
Improve stress coping skills
MSK treatment of the cervical and thoracic regions
Constitutional hydrotherapy
Adrenal supportive/adaptogenic herbs
Can be migraine, especially in people who had pre-existing migraine conditions prior to injury
Reduce inflammatory load
Consider management with supplements and or medications
Reduce light and sound exposure if there is sensitivity
Dizziness In PCS
After head trauma, always assess for BPPV, as this is the most common type of vertigo after trauma
Dix-Hallpike maneuver to diagnose
Epley�s maneuver for treatment
Light & Sound Sensitivity
Hypersensitivity to light and sound is common in PCS and typically exacerbates other symptoms such as headache and anxiety
Management of excess mesencephalon stimulation is crucial in such cases
Sunglasses
Other light blocking glasses
Earplugs
Cotton in ears
Treatment Of PCS
Manage each symptom individually as you otherwise would
Manage CNS inflammation
Curcumin
Boswelia
Fish oil/Omega-3s � (***after r/o bleed)
Cognitive behavioral therapy
Mindfulness & relaxation training
Acupuncture
Brain balancing physical therapy exercises
Refer for psychological evaluation/treatment
Refer to mTBI specialist
mTBI Specialists
mTBI is difficult to treat and is an entire specialty both in the allopathic and complementary medicine
Primary objective is to recognize and refer for appropriate care
Pursue training in mTBI or plan to refer to TBI specialists
Sources
�A Head for the Future.� DVBIC, 4 Apr. 2017, dvbic.dcoe.mil/aheadforthefuture.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
�Heads Up to Health Care Providers.� Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 16 Feb. 2015, www.cdc.gov/headsup/providers/.
�Post-Concussion Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 28 July 2017, www.mayoclinic.org/diseases-conditions/post- concussion-syndrome/symptoms-causes/syc-20353352.
Neuropathic pain is a complex, chronic pain condition that is generally accompanied by soft tissue injury. Neuropathic pain is common in clinical practice and also poses a challenge to patients and clinicians alike. With neuropathic pain, the nerve fibers themselves may be either damaged, dysfunctional or injured. Neuropathic pain is the result of damage from trauma or disease to the peripheral or central nervous system, where the lesion may occur at any site. As a result, these damaged nerve fibers can send incorrect signals to other pain centers. The effect of a nerve fiber injury consists of a change in neural function, both at the region of the injury and also around the injury. Clinical signs of neuropathic pain normally include sensory phenomena, such as spontaneous pain, paresthesias and hyperalgesia.
Neuropathic pain, as defined by the International Association of the Study of Pain or the IASP, is pain initiated or caused by a primary lesion or dysfunction of the nervous system. It could result from damage anywhere along the neuraxis: peripheral nervous system, spinal or supraspinal nervous system. Traits that distinguish neuropathic pain from other kinds of pain include pain and sensory signs lasting beyond the recovery period. It’s characterized in humans by spontaneous pain, allodynia, or the experience of non-noxious stimulation as painful, and causalgia, or persistent burning pain. Spontaneous pain includes sensations of “pins and needles”, burning, shooting, stabbing and paroxysmal pain, or electric-shock like pain, often associated with dysesthesias and paresthesias. These sensations not only alter the patient’s sensory apparatus, but also the patient’s well-being, mood, attention and thinking. Neuropathic pain is made up of both “negative” symptoms, such as sensory loss and tingling sensations, and “positive” symptoms, such as paresthesias, spontaneous pain and increased feeling of pain.
Conditions frequently related to neuropathic pain can be classified into two major groups: pain due to damage in the central nervous system and pain because of damage to the peripheral nervous system. Cortical and sub-cortical strokes, traumatic spinal cord injuries, syringo-myelia and syringobulbia, trigeminal and glossopharyngeal neuralgias, neoplastic and other space-occupying lesions are clinical conditions that belong to the former group. Nerve compression or entrapment neuropathies, ischemic neuropathy, peripheral polyneuropathies, plexopathies, nerve root compression, post-amputation stump and phantom limb pain, postherpetic neuralgia and cancer-related neuropathies are clinical conditions that belong to the latter group.
Pathophysiology of Neuropathic Pain
The pathophysiologic processes and concepts underlying neuropathic pain are multiple. Prior to covering these processes, a review of ordinary pain circuitry is critical. Regular pain circuitries involve activation of a nociceptor, also known as the pain receptor, in response to a painful stimulation. A wave of depolarization is delivered to the first-order neurons, together with sodium rushing in via sodium channels and potassium rushing out. Neurons end in the brain stem in the trigeminal nucleus or in the dorsal horn of the spinal cord. It is here where the sign opens voltage-gated calcium channels in the pre-synaptic terminal, allowing calcium to enter. Calcium allows glutamate, an excitatory neurotransmitter, to be released into the synaptic area. Glutamate binds to NMDA receptors on the second-order neurons, causing depolarization.
These neurons cross through the spinal cord and travel until the thalamus, where they synapse with third-order neurons. These then connect to the limbic system and cerebral cortex. There is also an inhibitory pathway that prevents pain signal transmission from the dorsal horn. Anti-nociceptive neurons originate in the brain stem and travel down the spinal cord where they synapse with short interneurons in the dorsal horn by releasing dopamine and norepinephrine. The interneurons modulate the synapse between the first-order neuron as well as the second-order neuron by releasing gamma amino butyric acid, or GABA, an inhibitory neurotransmitter. Consequently, pain cessation is the result of inhibition of synapses between first and second order neurons, while pain enhancement might be the result of suppression of inhibitory synaptic connections.
The mechanism underlying neuropathic pain, however, aren’t as clear. Several animal studies have revealed that lots of mechanisms may be involved. However, one has to remember that what applies to creatures may not always apply to people. First order neurons may increase their firing if they’re partially damaged and increase the amount of sodium channels. Ectopic discharges are a consequence of enhanced depolarization at certain sites in the fiber, resulting in spontaneous pain and movement-related pain. Inhibitory circuits might be diminished in the level of the dorsal horn or brain stem cells, as well as both, allowing pain impulses to travel unopposed.
In addition, there might be alterations in the central processing of pain when, because of chronic pain and the use of some drug and/or medications, second- and third-order neurons can create a “memory” of pain and become sensitized. There’s then heightened sensitivity of spinal neurons and reduced activation thresholds. Another theory demonstrates the concept of sympathetically-maintained neuropathic pain. This notion was demonstrated by analgesia following sympathectomy from animals and people. However, a mix of mechanics can be involved in many chronic neuropathic or mixed somatic and neuropathic pain conditions. Among those challenges in the pain field, and much more so as it pertains to neuropathic pain, is the capability to check it. There is a dual component to this: first, assessing quality, intensity and advancement; and second, correctly diagnosing neuropathic pain.
There are, however, some diagnostic tools that may assist clinicians in evaluating neuropathic pain. For starters, nerve conduction studies and sensory-evoked potentials may identify and quantify the extent of damage to sensory, but not nociceptive, pathways by monitoring neurophysiological responses to electrical stimuli. Additionally, quantitative sensory testing steps perception in reaction to external stimuli of varying intensities by applying stimulation to the skin. Mechanical sensitivity to tactile stimuli is measured with specialized tools, such as von Frey hairs, pinprick with interlocking needles, as well as vibration sensitivity together with vibrameters and thermal pain with thermodes.
It is also extremely important to perform a comprehensive neurological evaluation to identify motor, sensory and autonomic dysfunctions. Ultimately, there are numerous questionnaires used to distinguish neuropathic pain in nociceptive pain. Some of them include only interview queries (e.g., the Neuropathic Questionnaire and ID Pain), while others contain both interview questions and physical tests (e.g., the Leeds Assessment of Neuropathic Symptoms and Signs scale) and the exact novel tool, the Standardized Evaluation of Pain, which combines six interview questions and ten physiological evaluations.
Treatment Modalities for Neuropathic Pain
Pharmacological regimens aim at the mechanisms of neuropathic pain. However, both pharmacologic and non-pharmacologic treatments deliver complete or partial relief in just about half of patients. Many evidence-based testimonials suggest using mixtures of drugs and/or medications to function for as many mechanisms as possible. The majority of studies have researched mostly post-herpetic neuralgia and painful diabetic neuropathies but the results may not apply to all neuropathic pain conditions.
Antidepressants
Antidepressants increase synaptic serotonin and norepinephrine levels, thereby enhancing the effect of the descending analgesic system associated with neuropathic pain. They’ve been the mainstay of neuropathic pain therapy. Analgesic actions might be attributable to nor-adrenaline and dopamine reuptake blockade, which presumably enhance descending inhibition, NMDA-receptor antagonism and sodium-channel blockade. Tricyclic antidepressants, such as TCAs; e.g., amitriptyline, imipramine, nortriptyline and doxepine, are powerful against continuous aching or burning pain along with spontaneous pain.
Tricyclic antidepressants have been proven significantly more effective for neuropathic pain than the specific serotonin reuptake inhibitors, or SSRIs, such as fluoxetine, paroxetine, sertraline and citalopram. The reason may be that they inhibit reuptake of serotonin and nor-epinephrine, while SSRIs only inhibit serotonin reuptake. Tricyclic antidepressants can have unpleasant side effects, including nausea, confusion, cardiac conduction blocks, tachycardia and ventricular arrhythmias. They can also cause weight gain, a reduced seizure threshold and orthostatic hypotension. Tricyclics have to be used with care in the elderly, who are particularly vulnerable to their acute side effects. The drug concentration in the blood should be monitored to avoid toxicity in patients who are slow medication metabolizers.
Serotonin-norepinephrine reuptake inhibitors, or SNRIs, are a new class of antidepressants. Like TCAs, they seem to be more effective than SSRIs for treating neuropathic pain because they also inhibit reuptake of both nor-epinephrine and dopamine. Venlafaxine is as effective against debilitating polyneuropathies, such as painful diabetic neuropathy, as imipramine, in the mention of TCA, and the two are significantly greater than placebo. Like the TCAs, the SNRIs seem to confer benefits independent of their antidepressant effects. Side effects include sedation, confusion, hypertension and withdrawal syndrome.
Antiepileptic Drugs
Antiepileptic drugs can be utilized as first-line treatment especially for certain types of neuropathic pain. They act by modulating voltage-gated calcium and sodium channels, by improving the inhibitory effects of GABA and by inhibiting excitatory glutaminergic transmission. Anti-epileptic medications have not been demonstrated to be effective for acute pain. In chronic pain cases, antiepileptic drugs seem to be effective only in trigeminal neuralgia. Carbamazepine is routinely employed for this condition. Gabapentin, which functions by inhibiting calcium channel function through agonist actions at the alpha-2 delta subunit of the calcium channel, is also known to be effective for neuropathic pain. However, gabapentin acts centrally and it might cause fatigue, confusion and somnolence.
Non-Opioid Analgesics
There is a lack of strong data supporting using non-steroidal anti inflammatory medications, or NSAIDs, in the relief of neuropathic pain. This may be due to the lack of an inflammatory component in relieving pain. But they have been utilized interchangeably with opioids as adjuvants in treating cancer pain. There have been reported complications, though, especially in severely debilitated patients.
Opioid Analgesics
Opioid analgesics are a subject of much debate in relieving neuropathic pain. They act by inhibiting central ascending pain impulses. Traditionally, neuropathic pain has been previously observed to be opioid-resistant, in which opioids are more suitable methods for coronary and somatic nociceptive types of pain. Many doctors prevent using opioids to treat neuropathic pain, in large part because of concerns about drug abuse, addiction and regulatory issues. But, there are many trials that have found opioid analgesics to succeed. Oxycodone was superior to placebo for relieving pain, allodynia, improving sleep and handicap. Controlled-release opioids, according to a scheduled basis, are recommended for patients with constant pain to encourage constant levels of analgesia, prevent fluctuations in blood glucose and prevent adverse events associated with higher dosing. Most commonly, oral preparations are used because of their greater ease of use and cost-effectiveness. Trans-dermal, parenteral and rectal preparations are generally used in patients who cannot tolerate oral drugs.
Local Anesthetics
Nearby acting anesthetics are appealing because, thanks to their regional action, they have minimal side effects. They act by stabilizing sodium channels at the axons of peripheral first-order neurons. They work best if there is only partial nerve injury and excess sodium channels have collected. Topical lidocaine is the best-studied representative of the course for neuropathic pain. Specifically, the use of this 5 percent lidocaine patch for post-herpetic neuralgia has caused its approval by the FDA. The patch seems to work best when there is damaged, but maintained, peripheral nervous system nociceptor function from the involved dermatome demonstrating as allodynia. It needs to be set directly on the symptomatic area for 12 hours and eliminated for another 12 hours and may be used for years this way. Besides local skin reactions, it is often well tolerated by many patients with neuropathic pain.
Miscellaneous Drugs
Clonidine, an alpha-2-agonist, was shown to be effective in a subset of patients with diabetic peripheral neuropathy. Cannabinoids have been found to play a role in experimental pain modulation in animal models and evidence of the efficacy is accumulating. CB2-selective agonists suppress hyperalgesia and allodynia and normalize nociceptive thresholds without inducing analgesia.
Interventional Pain Management
Invasive treatments might be considered for patients who have intractable neuropathic pain. These treatments include epidural or perineural injections of local anesthetics or corticosteroids, implantation of epidural and intrathecal drug delivery methods and insertion of spinal cord stimulators. These approaches are reserved for patients with intractable chronic neuropathic pain who have failed conservative medical management and also have experienced thorough psychological evaluation. In a study by Kim et al, it was shown that a spinal cord stimulator was effective in treating neuropathic pain of nerve root origin.
Dr. Alex Jimenez’s Insight
With neuropathic pain, chronic pain symptoms occur due to the nerve fibers themselves being damaged, dysfunctional or injured, generally accompanied by tissue damage or injury. As a result, these nerve fibers can begin to send incorrect pain signals to other areas of the body. The effects of neuropathic pain caused by nerve fiber injuries includes modifications in nerve function both at the site of injury and at areas around the injury. Understanding the pathophysiology of neuropathic pain has been a goal for many healthcare professionals, in order to effectively determine the best treatment approach to help manage and improve its symptoms. From the use of drugs and/or medications, to chiropractic care, exercise, physical activity and nutrition, a variety of treatment approaches may be used to help ease neuropathic pain for each individual’s needs.
Additional Interventions for Neuropathic Pain
Lots of patients with neuropathic pain pursue complementary and alternative treatment options to treat neuropathic pain. Other well-known regimens used to treat neuropathic pain include acupuncture, percutaneous electrical nerve stimulation, transcutaneous electrical nerve stimulation, cognitive behavioral treatment, graded motor imagery and supportive treatment, and exercise. Among these however, chiropractic care is a well-known alternative treatment approach commonly utilized to help treat neuropathic pain. Chiropractic care, along with physical therapy, exercise, nutrition and lifestyle modifications can ultimately offer relief for neuropathic pain symptoms.
Chiropractic Care
What is known is that a comprehensive management application is crucial to combat the effects of neuropathic pain. In this manner, chiropractic care is a holistic treatment program that could be effective in preventing health issues associated with nerve damage. Chiropractic care provides assistance to patients with many different conditions, including those with neuropathic pain. Sufferers of neuropathic pain often utilize non-steroidal-anti-inflammatory medications, or NSAIDs, such as ibuprofen, or heavy prescription painkillers to help ease neuropathic pain. These may provide a temporary fix but need constant use to manage the pain. This invariably contributes to harmful side effects and in extreme situations, prescription drug dependence.
Chiropractic care can help improve symptoms of neuropathic pain and enhance stability without these downsides. An approach such as chiropractic care offers an individualized program designed to pinpoint the root cause of the issue. Through the use of spinal adjustments and manual manipulations, a chiropractor can carefully correct any spinal misalignments, or subluxations, found along the length of the spine, which could lower the consequences of nerve wracking via the realigning of the backbone. Restoring spinal integrity is essential to keeping a high-functioning central nervous system.
A chiropractor can also be a long-term treatment towards enhancing your overall well-being. Besides spinal adjustments and manual manipulations, a chiropractor may offer nutritional advice, such as prescribing a diet rich in antioxidants, or they may design a physical therapy or exercise program to fight nerve pain flair-ups. A long-term condition demands a long-term remedy, and in this capacity, a healthcare professional who specializes in injuries and/or conditions affecting the musculoskeletal and nervous system, such as a doctor of chiropractic or chiropractor, may be invaluable as they work to gauge favorable change over time.
Physical therapy, exercise and movement representation techniques have been demonstrated to be beneficial for neuropathic pain treatment. Chiropractic care also offers other treatment modalities which may be helpful towards the management or improvement of neuropathic pain. Low level laser therapy, or LLLT, for instance, has gained tremendous prominence as a treatment for neuropathic pain. According to a variety of research studies, it was concluded that LLLT had positive effects on the control of analgesia for neuropathic pain, however, further research studies are required to define treatment protocols that summarize the effects of low level laser therapy in neuropathic pain treatments.
Chiropractic care also includes nutritional advice, which can help control symptoms associated with diabetic neuropathy. During a research study, a low fat plant-based diet was demonstrated to improve glycemic control in patients with type 2 diabetes. After about 20 weeks of the pilot study, the individuals involved reported changes in their body weight and electrochemical skin conductance in the foot was reported to have improved with the intervention. The research study suggested a potential value in the low-fat plant-based diet intervention for diabetic neuropathy. Moreover, clinical studies found that the oral application of magnesium L-threonate is capable of preventing as well as restoring memory deficits associated with neuropathic pain.
Chiropractic care can also offer additional treatment strategies to promote nerve regeneration. By way of instance, enhancing the regeneration of axons has been suggested to help improve functional recovery after peripheral nerve injury. Electrical stimulation, together with exercise or physical activities, was found to promote nerve regeneration after delayed nerve repair in humans and rats, according to recent research studies. Both electrical stimulation and exercise were ultimately determined to be promising experimental treatments for peripheral nerve injury which seem ready to be transferred to clinical use. Further research studies may be needed to fully determine the effects of these in patients with neuropathic pain.
Conclusion
Neuropathic pain is a multifaceted entity with no particular guidelines to take care of. It’s best managed using a multidisciplinary approach. Pain management requires ongoing evaluation, patient education, ensuring patient follow-up and reassurance. Neuropathic pain is a chronic condition that makes the option for the best treatment challenging. Individualizing treatment involves consideration of the impact of the pain on the individual’s well-being, depression and disabilities together with continuing education and evaluation. Neuropathic pain studies, both on the molecular level and in animal models, is relatively new but very promising. Many improvements are anticipated in the basic and clinical fields of neuropathic pain hence opening the doorways to improved or new treatment modalities for this disabling condition. 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.
Pain Anxiety Depression�Everyone has experienced pain, however, there are those with depression, anxiety, or both. Combine this with pain and it can become pretty intense and difficult to treat. People that are suffering from depression, anxiety or both tend to experience severe and long term pain more so than other people.
The way anxiety, depression, and pain overlap each other is seen in chronic and in some disabling pain syndromes, i.e. low back pain, headaches, nerve pain and fibromyalgia. Psychiatric disorders contribute to the pain intensity and also increase the risk of disability.
Depression:�A (major depressive disorder or clinical depression) is a common but serious mood disorder. It causes severe symptoms that affect how an individual feels, thinks, and how the handle daily activities, i.e. sleeping, eating and working. To be diagnosed with depression, the symptoms must be present for at least two weeks.
Persistent sad, anxious, or �empty� mood.
Feelings of hopelessness, pessimistic.
Irritability.
Feelings of guilt, worthlessness, or helplessness.
Loss of interest or pleasure in activities.
Decreased energy or fatigue.
Moving or talking slowly.
Feeling restless & having trouble sitting still.
Difficulty concentrating, remembering, or making decisions.
Thoughts of death or suicide & or suicide attempts.
Aches or pains, headaches, cramps, or digestive problems without a clear physical cause and/or that do not ease with treatment.
Not everyone who is depressed experiences every symptom. Some experience only a few symptoms while others may experience several. Several persistent symptoms in addition to low mood are�required�for a diagnosis of major depression. The severity and frequency of symptoms along with the duration will vary depending on the individual and their particular illness. Symptoms can also vary depending on the stage of the illness.
PAIN ANXIETY DEPRESSION
Objectives:
What is the relationship?
What is the neurophysiology behind it?
What are the central consequences?
Brain Changes In Pain
Figure 1 Brain pathways, regions and networks involved in acute and chronic pain
Davis, K. D. et al. (2017) Brain imaging tests for chronic pain: medical, legal and ethical issues and recommendations Nat. Rev. Neurol. doi:10.1038/nrneurol.2017.122
PAIN, ANXIETY AND DEPRESSION
Conclusion:
Pain, especially chronic is associated with depression and anxiety
The physiological mechanisms leading to anxiety and depression can be multifactorial in nature
Pain causes changes in brain structure and function
This change in structure and function can alter the ability for the brain to modulate pain as well as control mood.
Functional short leg is a fairly common condition that typically occurs due to inflexibility or muscle weakness at the pelvis, ankle, and foot complex. Runners sometimes experience the condition when running over certain surfaces that are unstable or not level. It can also occur due to inappropriate footwear.
This condition can cause pain in the lower spine, hips, buttock, and leg. If left untreated, it can lead to balance issues, neck and shoulder problems, and incorrect weight distribution. Chiropractic care has been proven to effectively treat functional leg syndrome.
What Is Functional Short Leg?
Patients with a functional short leg have an apparent short leg although structurally both legs are the same length when measured. The most common method for measuring leg length is from the medial malleolus (inside ankle bone) to the ASIS (front of the pelvis). When the legs are measured in the case of a functional short leg, they are equal in length.
Mothers who always carry a child on one hip or individuals who always sleep on the same side can experience functional short leg syndrome. In fact, any movement, posture, or activity that causes increased stresses on the joints, nerves, and muscles involved can create an imbalance.
Functional Short Leg vs Anatomical Short Leg
Where with functional short leg syndrome one leg is apparently shorter than the other but not structurally so, an anatomical short leg is structurally shorter. This can happen due to growth problems, structural issues, and curvature of the spine.
The differences between the two conditions are significant, particularly when it comes to treatment. Both conditions can be treated by chiropractic for pain. Functional short leg syndrome can greatly benefit from chiropractic care as it helps to realign the body.
Symptoms Of Functional Short Leg
Functional short leg syndrome symptoms can remain confined to the leg, lower back, and hip region, or it can affect the entire body. When walking it can affect the way your feet hit the ground, causing pain in the foot and ankle.
However, it can even affect how you chew your food and how your teeth come together. When a person has short leg syndrome, they will often adjust their body in order to compensate, but that is when the real problems start. Symptoms of functional short leg syndrome include:
Pain in the lower back
Pain in the knee of both the long and short legs
Pain in the leg and lower back due to inflammation or sciatica
The human body is a marvelous, mysterious machine. When part of the machine is not working properly, the body will naturally attempt to fix it. If it cannot fix the problem, it finds a work around to compensate for the problem. This can lead to misalignment of the spine and imbalance in the body.
Chiropractic Treatment For Functional Short Leg
When you go to a chiropractor for functional short leg, he or she will do a thorough exam on you including diagnostic tests like MRI and x-ray. Once a diagnosis has been confirmed, the chiropractor will begin what is usually a multi-faceted approach that incorporates spinal alignment, a heel lift, lifestyle change recommendations, and exercises that you can do at home.
The chiropractic adjustments will return the spine to its natural position and bring the body back into balance. Patients will usually experience a dramatic decrease in pain or the pain will go away completely. They will also enjoy increased mobility and flexibility as well and an overall sense of wellness.
Injury Medical Clinic: Athletic Recovery & Rehabilitation
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