Back Clinic Chiropractic. This is a form of alternative treatment that focuses on the diagnosis and treatment of various musculoskeletal injuries and conditions, especially those associated with the spine. Dr. Alex Jimenez discusses how spinal adjustments and manual manipulations regularly can greatly help both improve and eliminate many symptoms that could be causing discomfort to the individual. Chiropractors believe among the main reasons for pain and disease are the vertebrae’s misalignment in the spinal column (this is known as a chiropractic subluxation).
Through the usage of manual detection (or palpation), carefully applied pressure, massage, and manual manipulation of the vertebrae and joints (called adjustments), chiropractors can alleviate pressure and irritation on the nerves, restore joint mobility, and help return the body’s homeostasis. From subluxations, or spinal misalignments, to sciatica, a set of symptoms along the sciatic nerve caused by nerve impingement, chiropractic care can gradually restore the individual’s natural state of being. Dr. Jimenez compiles a group of concepts on chiropractic to best educate individuals on the variety of injuries and conditions affecting the human body.
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases. �
An understanding of the mechanisms underlying TBI and neurodegenerative diseases is fundamental to determine the possible connection between these health issues, to allow the safe and effective diagnosis and treatment. In the following article, we discuss the pathological mechanisms of neurodegenerative diseases and how they’re associated with traumatic brain injury (TBI), including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
Pathological Mechanisms of Neurodegenerative Diseases
Although many neurological diseases may have different symptoms, AD, PD, and ALS have several common characteristics. Each neurodegenerative disease is caused by genetic risk factors, however, most cases are idiopathic or unknown. The pathological mechanisms of these health issues are ultimately characterized by the degeneration of brain cells or neurons together with several common symptoms. Moreover, abnormal clusters or dysfunction of the substances amyloid-? (A?), ?-synuclein, and superoxide dismutase (SOD1) are generally found in AD, PD. Although the exact pathological mechanisms of neurodegenerative diseases have not been fully determined, it has been suggested that oxidative stress, glutamatergic excitotoxicity, and neuroinflammation play fundamental roles in neurological diseases such as AD, PD, and ALS. �
AD has a tremendous prevalence among older adults which can greatly decrease their rate of survival and their overall quality of life. In 2008, as many as 24 million people worldwide had dementia, where most had AD, a number which is expected to double every 20 years as the population ages. The pathological mechanisms of AD include the presence of neuritic plaques and the loss of cholinergic neurons or brain cells in the human brain, however, the underlying risk factors leading to these events are still unclear. Neurodegeneration in AD is believed to happen due to the accumulation of amyloid ?-peptide (A?) in plaques in the brain tissue however its aggregation and toxicity are still completely misunderstood. �
Research studies have demonstrated that oxidative stress may play a fundamental role in the pathogenesis of AD because of increased neurotoxic markers of lipid peroxidation, such as 4-hydroxynonenal, in human participants, increased brain protein oxidation in AD, increased nuclear DNA oxidation in the brain of AD patients, 30 percent increased activity of the free radical scavenging enzyme SOD-1 in cell lines of AD patients, and considerable evidence that beta amyloid creates free radical peptides. In addition, it has been demonstrated that free radicals and lipid peroxidation caused by A? can ultimately result in neuronal death in AD. In vitro and animal research studies have demonstrated that the antioxidant effect of cannabinoids was able to prevent neurodegeneration in the neurological disease, suggesting the role of oxidative stress in AD. �
Neuroinflammation has also been associated wit A? toxicity which has likewise been connected to oxidative stress by inflammatory cytokine activity. The purpose of inflammation is to restore cellular homeostasis and balance redox equilibrium, however, inflammation changes with co-localized A? deposits, inflammatory-related proteins, and activated microglial cells in AD. Microglia and astroglia recognize misfolded proteins which can trigger an immune response that may be responsible for the progression and severity of the neurodegenerative disease. The microglial cells promote A? clearance and support neuroprotective properties in early stages of AD, but as the health issue progresses, inflammatory cytokines downregulate A? clearance genes and promote A? accumulation, ultimately causing neurodegeneration. Moreover, cytokines can trigger the creation of arachidonic acid which aggravates neurodegeneration by increasing extracellular levels of glutamate, known to cause excitotoxicity in AD as well as causing the creation of superoxide free radicals which are responsible for cellular death. Furthermore, research studies suggest that non-enzymatically glycated tau causes oxidative stress which results in cytokine gene expression and release of A?-peptide in AD, demonstrating pathological mechanisms between cytokines and oxidative stress which causes the progression and severity of AD. In addition, oxidative damage from reactive oxygen species and lipid peroxidation products, such as 4-hydroxy-2-nonenal (HNE), can restrict glutamate transporters, causing a decreased glutamate uptake that is fundamental for neuronal survival, an increased glutamate concentration in the synaptic cleft, and subsequent excitotoxicity which ultimately causes neurodegeneration in AD. �
Neurodegenerative Diseases in Functional Neurology
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repeated blunt force impacts to the head with the transfer of acceleration and deceleration forces to the brain or repetitive mild traumatic brain injuries, although the central pathological mechanisms for the development of neurodegeneration in CTE has not been discovered. CTE has been associated with behavioral and personality changes, parkinsonism, and dementia. Research studies demonstrated similarities between CTE and Alzheimer�s disease but these were different in the predominance of tau protein deposition over amyloid. The tau protein deposition in CTE has been previously demonstrated to restrict kinesin-dependent transport of peroxisomes and the loss of peroxisomes makes the cells vulnerable to oxidative stress, ultimately causing neurodegeneration. This tau protein deposition, which occurs in AD, also restricts the transport of amyloid precursor protein (APP) in axons or dendrites, causing its accumulation in the cell body. Along with tau proteins, portions of TDP43, a nuclear RNA/DNA binding protein which controls the transcription of thousands of genes, have been demonstrated in AD, PD, ALS, and CTE, which cause the misfolding of SOD1, affecting the surrounding cells with free-radical damage. The research studies have also demonstrated the purpose of oxidative stress in CTE neurodegeneration and in other neurological diseases. �
Chronic inflammation has also been demonstrated in CTE and AD, which is believed to aggravate neurodegeneration and, as previously mentioned, it is ultimately associated with oxidative stress though inflammatory cytokines. Moreover, it has been demonstrated that after the initial head trauma in CTE, microglia activate and release toxic levels of cytokines and excitotoxins, such as glutamate, where the excitotoxins restrict phosphatases, resulting in hyperphosphorylated tau, neurotubule dysfunction, and neurofibrillary tangle deposition, all of which are fundamental factors of CTE. Research studies have also demonstrated a synergy between proinflammatory cytokines and glutamate receptors which increase reactive oxygen species and worsens neurodegeneration in the injured brain associated with TBI and neurological diseases. �
Parkinson�s disease is the second most prevalent neurodegenerative disease with a prevalence of approximately 0.3 percent of the older adult population. PD is characterized by the development of ?-synuclein rich Lewy bodies and subsequent death of the dopaminergic neurons of the substantia nigra. Several genetic risk factors have also been demonstrated, including mutations to the ubiquitin-proteasome system. Although the pathological mechanisms which trigger dopaminergic degeneration in non-hereditary PD are still unclear, it has been suggested that oxidative modification or carbonylation of the lysine-rich N-terminus and the non-amyloid factor of ?-synuclein may ultimately cause an ?-synuclein aggregation. �
The reactive carbonyls created as secondary products in oxidative stress have been demonstrated to develop lysine adducts and promote ?-synuclein aggregation in vitro. Additionally, animal models of PD utilizing agents, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, have demonstrated the increased development of superoxide in dopaminergic cells associated with the cortex. Furthermore, mitochondrial localization of ?-synuclein has been demonstrated to promote oxidative stress in vitro. Neuroinflammation is believed to be a partial cause for the oxidative stress in PD with activated microglial cells demonstrated in the substantia nigra and striatum of deceased PD patients. Activated microglia were also demonstrated in rhesus monkeys up to 14 years after model induction. In addition, glutamatergic excitotoxicity is believed to play a fundamental role in PD. Rotigotine, an FDA approved dopamine receptor agonist, has been suggested to improve the efficiency of glutamate transporter 1 (GLT-1) and has been demonstrated to support neuroprotection against glutamatergic excitotoxicity in dopaminergic cell culture as well as a variety of other functions in the human brain in Parkinson’s disease. �
ALS is a fatal neurodegenerative disease characterized by the death of motor neurons in the central nervous system (CNS) and it is the most common motor neuron disease. Approximately 10 percent of all ALS cases have been associated with genetic causes while the majority are idiopathic or of unknown cause. Mutations affecting superoxide dismutase (SOD1) are responsible for almost 20 percent of all familial cases, however, this is responsible for only 2 percent of all overall cases. Despite the characterized mutations, the exact pathological mechanisms of ALS have yet to be fully determined. �
Research studies utilizing SOD1 mutant mouse models have demonstrated the development of SOD1 aggregates. Given the fundamental role of SOD1 in detoxification of superoxide radicals, it has been previously mentioned that loss of function could cause increased cellular exposure to reactive oxygen species, however, this hypothesis has been challenged by outcome measures in the normal development of SOD1 deficient mice in the absence of considerable traumatic injuries. Furthermore, research studies demonstrated that SOD1 mutant animals ultimately demonstrated no considerable improvement in symptomatic progression with knockout or coexpression of wild type SOD1 which suggests that the mutation results not in the loss of function but rather in the gain of toxic properties. Research studies in rats and human patients suggest that, similar to ?-synuclein and A?, SOD1 mutation cause the development of potentially cytotoxic protein aggregates even in patients without SOD1 mutations. Additionally, the catalysis changes achieved by several mutant variants causes decreased astroglial reuptake of glutamate through restriction of GLT-1. Riluzole, an FDA approved treatment for ALS, has been suggested to help improve glutamatergic excitotoxicity with increased glutamate uptake through GLT-1 and blockade of sensitive channels. Oxidative stress is also involved in neuronal death and in the progression of ALS. �
Given its fundamental role in maintaining and regulating damage from neuroinflammation and excitotoxicity, it is possible that oxidative stress also plays a fundamental role in the pathophysiology of AD, PD, and ALS in a similar fashion to TBI. As such, addressing oxidative stress in neurodegeneration could serve as an effective treatment strategy in neuroprotection. �
Conclusion
Despite the prevalence of TBI the significant neurological sequelae associated with such injuries, diagnosis, and treatment of TBI remains greatly misunderstood. In addition, the causing factors connected to TBI and neurodegenerative diseases, such as AD, PD, ALS, and CTE, have not been fully determined. Several processes, including oxidative stress and neuroinflammation, have also been found to be common between secondary TBI and several neurodegenerative diseases. In particular, oxidative stress appears to be the key mechanism connecting neuroinflammation and glutamatergic excitotoxicity in both TBI and neurological diseases. It is possible that the oxidative cascade caused by TBI ultimately causes and results in the characteristic pathologies of neurodegenerative diseases through oxidation or carbonylation of essential proteins. �
Due to the high prevalence of TBI and neurodegenerative diseases, the development of new safe and effective treatment approaches for TBI is fundamental. Given the essential role that oxidative stress plays in connecting secondary injury and neurodegeneration, detection of ROS and key byproducts could serve as a method or technique for the diagnosis and treatment of potential cellular damage. Finally, these reactive species may serve as a viable therapeutic target for reducing long-term neurodegenerative disease risk following TBI, helping to reduce the disability and death as well as improve the quality of life of individuals in the United States that suffer from traumatic brain injury (TBI) and other health issues. �
TBI is among one of the most common causes of disability and death among the general population in the United States. According to a variety of research studies, mild, moderate, and severe traumatic brain injury has been associated with neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, as well as a variety of other neurodegenerative diseases. It is fundamental to understand the pathophysiological mechanisms of neurodegenerative diseases while further research studies are still required to determine the association between TBI and neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may cause a variety of neurodegenerative diseases and health issues, such as Alzheimer’s disease (AD). The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
When we look at our patients, we try to figure out what is causing their ailments from living their best lives. Some practitioners would prescribe medications to alleviate pain. While other practitioners will start trying to figure out what is causing the patient to have these ailments. Here at Injury Medical Clinic, we talk to our patients about the importance of functional medicine and how it can benefit them. In this article, we will be discussing Connective Tissue Disorder and how it is linked to wheat-related disorders.
What is Connective Tissue Disorder?
CTD (Connective Tissue Disorder) is an autoimmune disorder that can affect the connective tissues such as the collagen and elastin in our skins. This disease is highly inflammatory and can occur alongside with other autoimmune diseases, and it is common if families have a history of Connective Tissue Disorder.
About 3% of the population has a connective tissue disorder, and it is most likely to occur in women than men. In fact, women who are diagnosed with connective tissue disorder have a ration of 10:1, compared to men.
CTD includes (but is not limited to) the following conditions:
Systemic Lupus Erythematosus (SLE): SLE is a widespread and chronic autoimmune condition, for unknown reasons, can cause the immune system to attack the body�s own tissue and organs, including joints, kidneys, heart, lungs, brain, blood, and skin.
Sjogren�s Syndrome: This autoimmune disease causes white blood cells to attack moisture-producing glands, such as the tear ducts and salivary glands. This can make it very difficult for the body to produce tears and saliva.
Systemic sclerosis (scleroderma): This condition causes the skin and connective tissue to harden and tighten.
Rheumatoid arthritis (RA): RA is a chronic inflammatory condition and an autoimmune disorder that can generally affect the lining of the joints, but mostly in the hands and feet. Rheumatoid arthritis causes painful swelling that can eventually lead to deformity and erosion in the joints and bones.
Polymyositis: This is a persistent inflammatory muscle disease that causes weakness in the skeletal muscles, which can affect your body movement.
Dermatomyositis: This is an uncommon inflammatory disease that is marked by muscle weakness and can cause a distinctive skin rash.
These conditions can group together and can be very hard to diagnose because of the research and many tests that the patient is taking. Surprisingly, the average patient suffers from symptoms for 3.6 years before meeting diagnostic criteria. And the systems alone are difficult to classify, and often mimic or overlap other conditions. Some of the symptoms include hair loss, muscle pain, numbness or tingling, inflammation, low-grade fever, weakness and fatigue, joint pain, sensitive skin, and rashes.
Increased Need For Advanced Testing and Early Diagnosis
Sadly though, patients wait longer when they have these conditions, and it can worsen in the process as it takes years to get diagnosed for CDT. Practitioners can use treatments on their patients, but the medications act as a band-aid to mask the symptoms, but it does not adequately address the root causes of the disease. Sometimes the symptoms can progress faster than the current diagnostic test. So if you want to make sure your patients have any autoimmune diseases, run a diagnostic test on them, so you can detect early stages of the disease and start treating them so it can go away.
Antinuclear antibody (ANA) is used as an initial test that can help evaluate a person for an autoimmune disorder that can affect many tissues and organs throughout the body. It is most often used when practitioners are diagnosing patients for systemic lupus erythematosus.
Surprisingly ENA can be more predictive than ANA. However, patients were followed for 2 years, and about 20% of those patients developed positive ENA.
Vibrant Wellness Wheat Zoomer
In�a�previous article, we talked about gluten sensitivity and introduced the wheat zoomer. What the Vibrant Wheat Zoomer does is that it actually runs a test on your microbiomes to determine if you have a wheat sensitivity or a gluten sensitivity. It can actually detect IgG and IgA antibodies as well as detecting if your body has the celiac disease and intestinal permeability.� It pairs well with the Vibrant Gut Zoomer, and here at Injury Medical, we use the Wheat Zoomer on our patients to inform them about what is causing them to have gut inflammation or even leaky gut.
Celiac Disease and Wheat Allergens
Celiac Disease and Wheat Allergens is an autoimmune disorder in genetically susceptible individuals, and it affects about 1% of the population. In a previous article, we mentioned the hidden problems that gluten does to the body. And surprisingly, any wheat-related disorders can exist on a spectrum, this includes wheat allergy, gluten sensitivity, and wheat sensitivity.
When a person, has the celiac disease, having any traces of wheat can actually upset their intestinal permeability and causing them to have a leaky gut.
The Connection to CTD and Celiac Disease
But how do connective tissue disorder and celiac disease are connected? Well, surprisingly, Rheumatoid arthritis (RA) and celiac disease (CD) share multiple aspects in epidemiology and clinical manifestations. Both disorders have been proven to be influenced by comparable environmental factors and a recent incidental surge of associated antibodies. Even though they have different depositions, both of them are mediated by endogenous enzymes that target different tissues and organs.
Conclusion
However through functional medicine; local chiropractors and health coaches here at Injury Medical Clinic, strive to understand what do our patients need to make their bodies feel better. If we can use functional medicine to prevent leaky gut at the early stages and help our patients with any ailments that they may have, then we can gently push them into the right direction of exercising throughout the week (even if it is about thirty minutes) and eating nutritious, whole, organic foods; as well as, preventing their ailments coming back then their bodies can finally heal.
Piriformis syndrome will cause dull, mild pain in the low back, buttocks and can radiate down the leg.
Hip pain attributed to avascular necrosis will be severe and constant.
Sacroiliac joint pain could be attributed to the hip and the low back because the sacroiliac joints connect the sacrum in the spine to the hip bones.
Symptoms that the Spine Is the Root
Where groin pain is a sign that the pain is linked to the hip when the pain is above the waistline and travels down the body usually indicates a low back issue.
Among the most common degenerative conditions that affect the lumbar spine are:
Herniated discs
Spinal stenosis
Spondylolisthesis
Pain is caused by irritating the low back nerves, which result in pain shooting down the leg/s and:
Weakness
Numbness
Reduced range of motion
Arthritis of the spine brings on pain usually when first getting out of bed or rising up after sitting.
It usually improves after beginning to move.
Spinal stenosis or nerve pressure compression pain worsens with prolonged standing or walking, while relief comes with sitting.
Getting to the Root
When there is pain in the lower body and are not sure whether it’s the back or hip, the first course of action is to visit your doctor or a chiropractor.
They will review your medical history and perform a series of physical exams, such as various movements to get an idea of what is going on.
Your primary doctor may refer you to a doctor/chiropractor who specializes in hip or spinal conditions to make an accurate diagnosis.
The doctor will ask you to describe the:
Pain
Location
When it worsens
When it’s relieved
What the pain feels like (e.g., sharp, dull).
The doctor may have you perform various movements to observe your biomechanics.
The goal is to determine what movements trigger the pain.
For both spine and hip pain, surgery is rarely necessary and only utilized as the last-resort option.
Labrum Tear Hip Treatment El Paso, TX Chiropractor
Andrew Hutchinson turned into chiropractic care and Crossfit rehab after suffering a high ankle sprain and a hip labrum tear for which he moved through with surgery to repair it. After being bedridden for weeks so as to correctly recuperate, Andrew Hutchinson transitioned to chiropractic care and Crossfit rehab to regain his strength, freedom, and flexibility before returning to perform. Although he has suffered other sports accidents, Andrew Hutchinson continues to trust in chiropractic care and Crossfit rehab to keep his spine properly aligned and maintain overall health and wellbeing.
Labrum tears in athletes may occur from a single event or recurring trauma. Running may lead to labrum tears as a result of labrum being used more for weight-bearing and taking excessive forces while at the end-range motion of the leg. Sporting activities are likely causes, especially the ones that require frequent hip rotation or pivoting to some wealthy femur as in ballet or hockey. Continuous hip rotation places increased pressure on the capsular tissue and injury to the iliofemoral ligament. This then causes hip instability placing increased stress on the labrum and resulting in a cool labrum tear.
What’s Afoot
Muscle imbalances in the hip, such as tight hip flexors, can cause low back pain � or at least contribute to it. When the hip flexor muscles are too tight, it causes what is known as an anterior pelvic tilt. In other words, the muscles cause an anterior pull on the pelvis. This affect posture and throws the entire lower body out of alignment. It can also affect the knees and feet if left untreated.
NCBI Resources
Hip flexors can become too tight if the person sits for extended periods of time or engages in activities like cycling and jogging. A chiropractor can guide you through exercises that will help release the tight muscles and stop the micro spams that occur as a result. They will also assess your knees, feet, and ankles to ensure that the issue has not through them out of alignment as well. Correcting the cause of the problem will often correct the associated issues and resolve the pain allowing you to return to your normal activities.
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases. �
A better understanding of the mechanisms underlying TBI and neurodegenerative diseases is ultimately fundamental to determine the possible connection between these health issues to allow safe and effective diagnosis and treatment. In part 1 of the following article, we will discuss the pathological mechanisms of traumatic brain injury (TBI) and how it’s associated with the development of a variety of neurological diseases and other health issues, including Alzheimer’s disease (AD). �
Pathological Mechanisms of Traumatic Brain Injury
In most instances, TBI is caused by a physical blow to the head during traumatic events, such as falls, automobile accidents, or sports-related accidents, although TBI may also be aggravated by exposure to explosive blasts. TBI can be characterized as mild, moderate, or severe according to the symptoms, such as the length of loss of consciousness and post-traumatic amnesia. Mild TBI (mTBI) is prevalent in the majority of cases, however, it may be difficult to diagnose. This difficulty in diagnosis can be a serious concern as a result of severe consequences like instant impact syndrome or other health issues. �
Damage to the nervous tissue can be characterized as the main injury which happens as a direct effect of a physical blow and secondary injury which happens due to pathophysiological processes subsequent to the traumatic event. The injury process occurs from the rapid acceleration-deceleration of the brain which is believed to harm the brain by causing sheer force within tissue resulting in impact and axonal injury with the cranial wall. These injuries can be contralateral or ipsilateral to the physical blow. In more severe instances, the injury may cause intracranial hypertension and intracranial hemorrhage. This increase in pressure not only damages brain tissue but it also causes potential injury and cerebral hypoperfusion. �
Secondary injury in TBI generally happens several days, weeks, and even months following the traumatic circumstance because of the biochemical changes which occur in the nervous tissue. This harm is often mediated by free radicals and reactive oxygen species (ROS) which develop from ischemia-reperfusion damage, glutamatergic excitotoxicity, or neuroinflammation. After the injury, axonal damage from the sheer force of injury can affect membrane balance. Moreover, uptake of calcium through either membrane disruption or activation of the NMDA and the AMPA receptors by glutamate could ultimately cause mitochondrial dysfunction as well as the overproduction of free radicals and the activation of apoptotic caspase signaling. Following inflammatory processes associated with TBI, such as the activation of microglial cells, can cause oxidative stress through the effects of inflammatory cytokines. These radicals can also cause cellular damage through lipid peroxidation and protein modifications which can overwhelm endogenous antioxidant systems. The secondary products of free radical-mediated lipid peroxidation, such as reactive carbonyl species, can also be electrophilic and can further propagate oxidative damage to biomacromolecules, which can be associated with various neurological diseases. �
Clinical and preclinical research studies have demonstrated the presence of oxidative stress and its byproducts following TBI with both serological and histological methods and techniques. In animal research studies, these products have been demonstrated to continue over a recurrent injury and it may increase following a single traumatic event. Spectroscopic evaluations suggest that the endogenous antioxidants glutathione and ascorbic acid may decrease for 3 to 14 days following the injury. Furthermore, the increase of F2-isoprostane, a lipid peroxidation byproduct, was demonstrated in the cerebrospinal fluid of severe TBI patients with increased levels at 1 day following the injury, however, this was primarily an assessment of alternative treatment and didn’t establish a contrast with healthy controls. Lipid peroxidation products like 4-hydroxynoneal were also found to be elevated in the serum of acute TBI patients needing treatment. Although chronic oxidative stress has not currently been detected following single mild injuries in people, it seems possible that oxidative stress and its associated processes may aggravate or prolong post-concussive symptoms. Given the involvement of oxidative stress in excitotoxicity and reperfusion injury, it’s possible that oxidative stress plays a role in cerebral injury after TBI. �
The pathological mechanisms of secondary TBI are particularly interesting due to the ability to prolong cellular injury beyond the initial traumatic event. Some of these characteristic modifications, such as oxidative stress and excitotoxicity, have also been demonstrated in the pathophysiology of neurodegenerative diseases and other health issues which also suggests a possible pathological mechanistic connection between TBI and neurological diseases. Further research studies of the pathological mechanisms in cerebral diseases and TBI may help determine the factors for neurodegenerative diseases. �
Conclusion
Despite the prevalence of TBI the significant neurological sequelae associated with such injuries, diagnosis, and treatment of TBI remains greatly misunderstood. In addition, the causing factors connected to TBI and neurodegenerative diseases, such as AD, PD, ALS, and CTE, have not been fully determined. Several processes, including oxidative stress and neuroinflammation, have also been found to be common between secondary TBI and several neurodegenerative diseases. In particular, oxidative stress appears to be the key mechanism connecting neuroinflammation and glutamatergic excitotoxicity in both TBI and neurological diseases. It is possible that the oxidative cascade caused by TBI ultimately causes and results in the characteristic pathologies of neurodegenerative diseases through oxidation or carbonylation of essential proteins. �
Due to the high prevalence of TBI and neurodegenerative diseases, the development of new safe and effective treatment approaches for TBI is fundamental. Given the essential role that oxidative stress plays in connecting secondary injury and neurodegeneration, detection of ROS and key byproducts could serve as a method or technique for the diagnosis and treatment of potential cellular damage. Finally, these reactive species may serve as a viable therapeutic target for reducing long-term neurodegenerative disease risk following TBI, helping to reduce the disability and death as well as improve the quality of life of individuals in the United States that suffer from traumatic brain injury (TBI) and other health issues. �
Traumatic brain injury is among one of the most prevalent causes of disability and death among the general population in the United States. According to a variety of research studies, mild, moderate, and severe traumatic brain injury has been associated with neurodegenerative diseases, such as Alzheimer’s disease, as well as a variety of other neurological diseases and health issues. It is fundamental to understand the pathophysiological mechanisms of traumatic brain injury while further research studies are still required to determine the association between TBI and neurodegenerative diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may cause a variety of neurodegenerative diseases and health issues, such as Alzheimer’s disease (AD). The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
� �
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
The human nervous system is made up of two parts: the central nervous system, which includes the brain and the spinal cord, and the peripheral nervous system, which includes the connection nerves running from the brain and the spinal cord to the rest of the human body, including the hands and the feet.
Many patients with neuropathy may experience a variety of painful symptoms due to nerve damage or injury. But, with the proper treatment approach, neuropathy can be effectively treated and even reversed. Diagnosis of neuropathy is fundamental towards proper treatment. Dr. Alex Jimenez, a chiropractor in El Paso, TX, can help patients with neuropathy.
Peripheral Neuropathy Causes & Symptoms | El Paso, TX (2019)
Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves. The causes of neuropathy, or nerve damage, can vary greatly among each individual and these may be caused by a number of different diseases, injuries, infections, and even vitamin deficiency states. However, neuropathy can most commonly affect the nerves that control the motor and sensory nerves. Because the human body is composed of many different kinds of nerves which perform different functions, nerve damage is classified into several types.
Neuropathy can also be classified according to the location of the nerves being affected and according to the disease-causing it. For instance, neuropathy caused by diabetes is called diabetic neuropathy. Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest as a result. Below we will discuss several specific types of neuropathies clinically treated by chiropractors, physical therapists and physical medicine doctors alike, as well as briefly describing their causes and their symptoms.
Peripheral neuropathy, which is often simply referred to as �neuropathy,� is a state that happens when your nerves become damaged or injured, oftentimes simply disrupted. It�s estimated that neuropathy affects roughly 2.4 percent of the general populace and approximately 8 percent of people older than age 55. However, this quote doesn�t include people affected by neuropathy caused by physical trauma to the nerves.
Types
Neuropathy can affect any of the three types of peripheral nerves:
Sensory nerves, which transmit messages from the sensory organs, eyes, nose to the brain
Motor nerves, which track the conscious movement of the muscles
Autonomic nerves, which regulate the involuntary functions of the body
Sometimes, neuropathy will only impact one nerve. This is medically referred to as mononeuropathy and instances of it include:
Ulnar neuropathy, which affects the elbow
Radial neuropathy, which affects the arms
Peroneal neuropathy, which affects the knees
Femoral neuropathy, which affects the thighs
Cervical neuropathy, which affects the neck
Sometimes, two or more isolated nerves in separate regions of the body can become damaged, injured or disrupted, resulting in mono neuritis multiplex neuropathy. Most often, however, multiple peripheral nerves malfunction at the same time, a condition called polyneuropathy. According to the National Institute for Neurological Disorders and Stroke, or the NINDS, there are over 100 kinds of peripheral neuropathies.
Causes
Neuropathies are often inherited from birth or they develop later in life. The most frequent inherited neuropathy is the neurological disease Charcot-Marie-Tooth disease, which affects 1 in 2,500 people in the USA. Although healthcare professionals are sometimes not able to pinpoint the exact reason for an acquired neuropathy, medically referred to as idiopathic neuropathy, there are many known causes for them, including systemic diseases, physical trauma, infectious diseases, and autoimmune disorders.
A systemic disease is one which affects the whole body. The most frequent systemic cause behind peripheral neuropathy is diabetes, which can lead to chronically high blood glucose levels that harm nerves.
Other systemic issues can cause neuropathy, including:
Kidney disorders, which permit high levels of nerve-damaging toxic chemicals to flow in the blood
Toxins from exposure to heavy metals, including arsenic, lead, mercury, and thallium
Certain drugs and/or medications, including anti-cancer medications, anticonvulsants, antivirals, and antibiotics
Chemical imbalances because of liver ailments
Hormonal diseases, including hyperthyroidism, which disturbs metabolic processes, potentially inducing cells and body parts to exert pressure on the nerves
Deficiencies in vitamins, such as E, B1 (thiamine), B6 (pyridoxine), B12, and niacin, that can be vital for healthy nerves
Alcohol abuse, which induces vitamin deficiencies and might also directly harm nerves
Cancers and tumors that exert damaging pressure on nerve fibers and pathways
Chronic inflammation, which can damage protective tissues around nerves, which makes them more vulnerable to compression or vulnerable to getting inflamed and swollen
Blood diseases and blood vessel damage, which may damage or injure nerve tissue by decreasing the available oxygen supply
Signs and Symptoms of Neuropathy
Depending on the reason and unique to each patient, signs, and symptoms of neuropathy can include:
Pain
Tingling
Burning/prickling sensations
Increased sensitivity to touch
Muscle weakness
Temporary or permanent numbness;
Paralysis
Dysfunction in glands or organs
Impairment in urination and
Sexual function
Such signs and symptoms are dependent on whether autonomic, sensory, or motor nerves, as well as a combination of them, are ultimately affected. Autonomic nerve damage can influence physiological functions like blood pressure or create gastrointestinal problems and issues. Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while harm to motor nerves may affect movement and reflexes. When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.
Complications
Peripheral�neuropathy�may result in several complications, as a result of disease or its symptoms. Numbness from the ailment can allow you to be less vulnerable to temperatures and pain, making you more likely to suffer from burns and serious wounds. The lack of sensations in the feet, for instance, can make you more prone to developing infections from minor traumatic accidents, particularly for diabetics, who heal more slowly than other people, including foot ulcers and gangrene.
Furthermore, muscle atrophy may cause you to develop particular physical disfigurements, such as pes cavus, a condition marked by an abnormally high foot arch, and claw-like deformities in the feet and palms.
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Neuropathy can be caused by a variety of injuries and/or aggravated conditions, often manifesting into a plethora of associated signs and symptoms. While every type of neuropathy, such as diabetic neuropathy or autoimmune disease-associated neuropathy, develops its own unique group of signs and symptoms, many patients will often report common complaints. Individuals with neuropathy generally describe their pain as stabbing, burning or tingling in character.
If you experience unusual or abnormal tingling or burning sensations, weakness and/or pain in your hands and feet, it�s essential to seek immediate medical attention in order to receive a proper diagnosis of the cause of your specific signs and symptoms. Early diagnosis may help prevent further nerve injury. Visit www.neuropathycure.org�for more details.
Alzheimer�s disease (AD) is one of the most common types of dementia among older adults. Research studies have demonstrated that pathological changes in the human brain, whether directly or indirectly, can ultimately cause loss of synaptic function, mitochondrial damage, microglial cell activation, and neuronal cell death. However, the pathogenesis of AD is not yet fully understood and there is currently no definitive treatment for the neurological disease. Research studies have demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD. �
A proinflammatory status of the central nervous system (CNS) can also cause changes in the function of the microglial cells or microglia. Neuroinflammation is closely associated with the activation of microglia and astrocytes which are connected to a variety of neurological diseases by the synthesis and secretion of inflammatory mediators such as iNOS, ROS, and proinflammatory cytokines. According to research studies, microglial priming is also caused by the inflammation of the CNS. �
Therefore, whether microglial priming is the result or the cause of neuroinflammation is still controversial. Microglial cell activation commonly causes an increase of A? and tau proteins as well as a decrease of neurotrophic factors, ultimately leading to the loss of healthy brain cells or neurons and the development of neuritic plaques and neurofibrillary tangles which are closely associated with AD. With the progression of Alzheimer’s disease, changes from neuronal dysfunctions which may have no obvious symptoms to memory loss and cognitive impairment may become more noticeable. �
Microglial Priming, Neuroinflammation, and AD
Although the accurate and detailed, fundamental role of the microglial cells continues to be discovered and explained, there is a consensus among many researchers that primed microglia are associated with the inflammatory response of the CNS in AD. It has also been determined that neuroinflammation caused by microglial priming is mainly associated with aging, systemic inflammation, gene regulation, and blood-brain barrier impairment. The purpose of the article below is to discuss how microglial priming and neuroinflammation in Alzheimer’s disease can be caused due to a variety of risk factors. �
Aging
Aging is considered to be one of the main risk factors for AD and it is generally followed by chronic, systemic up-regulation of pro-inflammatory factors and a considerable decrease in an anti-inflammatory response. This change from homeostasis to an inflammatory state occurs through age-related elements which cause an imbalance between anti-inflammatory and pro-inflammatory systems. Microglia is primed into an activated state which can increase the consistent neuroinflammation and inflammatory reactivity in the aged human brain. Research studies have demonstrated that microglia in the brain of rodents developed an activated phenotype during aging characterized by the increased expression of CD11b, CD11c, and CD68. �
Systemic Inflammation
Recent research studies have determined that the neuroinflammation from primed microglial cells can also cause the pathogenesis of AD. Continuous activation of microglia can promote the synthesis and secretion of pro-inflammatory cytokines and trigger a pro-inflammatory response, ultimately causing neuronal damage. Neuroinflammation is an early symptom in the progression of AD. The microglia can have a tremendous effect on the inflammation of the human brain. �
The inflammation and health issues of the CNS can be associated with systemic inflammation through molecular pathways. One research study demonstrated that ROS development of primed microglia decreases the levels of intracellular glutathione and increases nitric oxide in NADPH oxidase subunit NOX2. Moreover, researchers demonstrated that these simultaneously occurring processes ultimately cause the development of more neurotoxic peroxynitrite. This is demonstrated in rodents with peripheral LPS or proinflammatory cytokines, such as TNF-?, IL-1?, and IL-6, IL-33. �
The outcome measures of numerous research studies have demonstrated that systemic inflammation can cause microglial activation. The results of the research studies emphasize the variability of the inflammatory response in the human brain associated with AD and the underlying health issues associated with systemic inflammation and neuroinflammation, as shown in Table 1. MAPK (mitogen-activated protein kinase) signaling pathways regulate mechanisms of the eukaryotic cell and microglial MAPK can also cause an inflammatory response to the aged brain with AD. Furthermore, chronic or continuous systemic inflammation causes neuroinflammation, resulting in the onset and accelerating the progression of AD. �
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Genetic Regulation
In the aging human brain, gene regulation has ultimately been associated with an innate immune response. Recent preclinical, bioinformatics, and genetic data have demonstrated that the activation of the brain immune system is associated with the pathology of AD and causes the pathogenesis of this neurological disease. Genome-wide association studies (GWAS), functional genomics, and even proteomic evaluations of cerebrospinal fluid (CSF) and blood have demonstrated that dysfunctional immune pathways from genic mutation are risk factors in LOAD, which is the vast majority of AD. �
GWAS have become a fundamental tool in the screening of genes as well as demonstrating several new risk genes associated with AD. Apolipoprotein E (APOE) ?4allele is one of the most considerable and well-known risk genes for sporadic AD and this mutation ultimately increases the risk of neurological disease onset by 15 times in homozygous carriers and by three times in heterozygous carriers. Further research studies have demonstrated how microglial cell function can be affected through a variety of rare mutations which have demonstrated to have an increased risk factor of Alzheimer’s disease. �
An extracellular domain mutation of the TREM2 gene has also demonstrated an almost identical extent with APOE?4 in increasing the risk factor of AD. TREM2 is increasingly demonstrated on the surface of microglia and mediates phagocytosis as well as the removal of neuronal debris. Additionally, several other genes, such as PICALM, Bin1, CLU, CR1, MS4A, and CD33 have been demonstrated as risk genes for AD. Most of the risk mutation genes are expressed by microglial cells. �
Blood-Brain Barrier (BBB) Impairment
The blood-brain barrier (BBB) is a specialized barrier commonly developed between the blood and the brain by tight liner sheets consisting of specific endothelial cells and tight junctions or structures which connects a variety of cells together. The CNS is fundamental for the human body, and the BBB is fundamental for the CNS. The BBB and the blood-nerve barrier develop a defense system to control the communications of cells and soluble factors between blood and neural tissue where it plays a considerable role in maintaining and regulating the homeostasis of the CNS and peripheral nervous system. �
With development, continuous inflammation can also cause damage to the BBB. This damage can ultimately cause loss of hypersensitive neurons, neuroinflammatory regions, and focal white matter impairment following the damage. The compromised BBB also allows more leukocytes to enter into the CNS where an immune response can be aggravated by brain microglia under the condition of peripheral inflammation. These processes may ultimately be under the control of chemokine and cytokine signaling which can also have an effect on brain microglial cells as well as other health issues in AD. �
By way of instance, it has been determined that TNF-?, IL-17A, and IL-1? can reduce the tight junctions and eliminate the BBB. Loss of BBB integrity and abnormal expression of tight junctions are associated with neuroinflammation. Several research studies also demonstrated in an animal model of AD that the vulnerability of BBB to inflammation increases. Current evidence has also demonstrated that the BBB integrity is fundamental while further evidence of the BBB may demonstrate a new treatment approach for AD associated with microglial priming as shown in Figure 2 below. �
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Conclusion
Microglia play a fundamental role in maintaining and regulating the homeostasis of the CNS’s micro-environment. If the balance of the homeostasis of the human brain is interrupted, the microglial cells can be activated to restore the balance in the CNS by defending against the stimulation and protecting the structure and function of the brain. However, chronic and continuous stimulation can trigger microglia into a state known as microglial priming, which is more sensitive to potentially minor stimulation, causing a variety of health issues, such as central sensitization, chronic pain, and fibromyalgia. �
Microglial priming mainly causes the boost of A?, tau protein as well as neuroinflammation and reduces neurotrophic factors which can cause the loss of healthy brain cells or neurons as well as the development of neuritic plaques and neurofibrillary tangles which are associated with Alzheimer’s disease. Although this �double-edged sword� plays a fundamental role, it can increase the progression of abnormal protein development and aggravate neuronal loss and dysfunction. However, research studies have ultimately demonstrated that aging can cause the progression of AD and there’s not much we can do about it. �
Microglial cells play a fundamental role as the protectors of the brain and they ultimately help maintain as well as regulate the homeostasis of the CNS microenvironment. However, continuous stimulation can cause the microglia to trigger and activate at a much stronger state which is known as microglial priming. Once the microglial cells go into protective mode, however, primed microglia can become much more sensitive to even minor stimulation and they have a much stronger possibility of reacting towards normal cells. Microglial priming has been associated with neuroinflammation and Alzheimer’s disease (AD) as well as central sensitization and fibromyalgia. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
AD is one of the most common types of dementia among older adults. However, the pathogenesis of AD is misunderstood and there is no definitive treatment for the neurological disease. Research studies have ultimately demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
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These medications help return normal function to the osteoclasts and osteoblasts.
Bisphosphonates can manage the disease and reduce symptoms, but do not cure the disease.
Living with Paget�s
Advanced cases can cause spine problems, which includes spinal fractures.
Most with Paget�s disease have preferable outcomes.
When Paget’s disease is managed with medication, regular doctor visits, chiropractic care, and proper diet, then there shouldn�t be a problem in achieving a healthy quality of life.
El Paso, TX Lower Back Bain Pain Chiropractic Relief
David Garcia, maintenance Centre Employee and a proud Dad in El Paso, TX works at the Region 19 Education Services Center. However, Mr. Garcia’s daily life is frequently influenced by his chronic lower back pain. After undergoing worsening symptoms for a while, David Garcia was advocated to seek chiropractic care with Dr. Alex Jimenez by his sister, a former patient of Dr. Jimenez. Mr. Garcia has since experienced enormous relief out of his lower back pain, and he’s grateful to Dr. Alex Jimenez and his staff for supplying him with schooling regarding his health problems as well as adequately caring for him. David Garcia urges Dr. Alex Jimenez as the non-invasive surgical selection for lower back pain.
NCBI Resources
Several studies show that chiropractic care is a very effective treatment for back pain. The chiropractor will perform spinal manipulation to bring the spine (and body) into proper alignment. He may also offer advice on exercises, stretching, and ways to improve posture as well as recommending lifestyle changes and what to look for in supportive shoes. Chiropractic�s whole-body approach not only helps relieve back pain, but it also helps prevent it as well.
This allows the patient to gain whole body benefits from chiropractic.
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