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Nerve Injury

Back Clinic Nerve Injury Team. Nerves are fragile and can be damaged by pressure, stretching, or cutting. Injury to a nerve can stop signals to and from the brain, causing muscles not to work properly and losing feeling in the injured area. The nervous system manages a great majority of the body’s functions, from regulating an individual’s breathing to controlling their muscles as well as sensing heat and cold. But, when trauma from an injury or an underlying condition causes nerve injury, an individual’s quality of life may be greatly affected. Dr. Alex Jimenez explains various concepts through his collection of archives revolving around the types of injuries and condition which can cause nerve complications as well as discuss the different form of treatments and solutions to ease nerve pain and restore the individual’s quality of life.

General Disclaimer *

The information herein is not intended to replace a one-on-one relationship with a qualified healthcare professional or licensed physician and is not medical advice. We encourage you to make your own health care decisions based on your research and partnership with a qualified health care professional. Our information scope is limited to chiropractic, musculoskeletal, physical medicines, wellness, sensitive health issues, functional medicine articles, topics, and discussions. We provide and present clinical collaboration with specialists from a wide array of disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system. Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and support, directly or indirectly, our clinical scope of practice.* Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.

We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.

Dr. Alex Jimenez DC, MSACP, CCST, IFMCP*, CIFM*, ATN*

email: coach@elpasofunctionalmedicine.com

Licensed in: Texas & New Mexico*

 


Understanding the Life and Death of a Neuron

Understanding the Life and Death of a Neuron

For many years, most neuroscientists believed we were born with all the neurons we were ever going to carry in our brains. As children, we may develop new neurons to help create the pathways, known as neural circuits, which function as information highways between different regions of the brain. However, scientists believed that after a neural circuit was created, developing any new neurons could interrupt the flow of information and disable the brain’s communication system. �

 

Introduction to Brain Basics

 

In 1962, scientist Joseph Altman questioned this belief when he saw evidence of neurogenesis, or the birth of neurons, in a region of an adult rat’s brain known as the hippocampus. He then reported that newborn neurons migrated from their birthplace in the hippocampus to other regions of the brain. In 1979, another scientist, Michael Kaplan, proved Altman’s findings in the rat brain and in 1983, Kaplan found neural precursor cells in the forebrain of an adult monkey. �

 

In the early 1980s, a scientist attempting to explain how birds learn how to sing suggested that neuroscientists should once again analyze neurogenesis in the adult brain and start to determine how it can make sense. In several experiments, Fernando Nottebohm and his team revealed that the numbers of neurons in the forebrains of male canaries tremendously increased during the mating season. This was the same time in which the birds had to learn new songs to attract females. �

 

However, why did these bird’s brains create new neurons during such a vital time in learning? Nottebohm believed it was because new neurons helped keep new song patterns inside the neural tissues of the forebrain, or the region of the brain which regulates complex behaviors. These new neurons made learning possible. If birds developed new neurons to help them remember and learn new song patterns, Nottebohm believed that the brains of mammals may also be able to do the same. �

 

Elizabeth Gould discovered evidence of newborn neurons in a different region of the brain in monkeys. Fred Gage and Peter Eriksson also demonstrated that the adult human brain developed new neurons in a similar region. For several neuroscientists, neurogenesis in the adult brain is still an unproven theory. However, other neuroscientists believe that the evidence provides interesting possibilities associated with the role of adult-generated neurons in memory and learning. �

 

Architecture of the Neuron

 

The central nervous system, which includes the brain and the spinal cord, consists of two primary types of cells: the neurons and the glia. Glia outnumber neurons in several regions of the brain, however, neurons are the key structures in the brain. Neurons are information messengers. They utilize electrical impulses and chemical signals to transfer information between different regions of the brain and between the brain and the rest of the nervous system. Everything we think, feel, and do would be impossible without the utilization of neurons and the glial cells, known as astrocytes and oligodendrocytes. �

 

Neurons have three primary parts including a cell body and two extensions known as an axon and a dendrite. Within the cell body is a nucleus, which regulates the cell’s activities and holds the cell’s genetic material. The axon is characterized by a very long tail and it transfers messages from the cell. Dendrites are characterized similar to that of the branches of a tree and they receive messages from the cell. Neurons communicate with one another by sending chemicals, known as neurotransmitters, across a very small region, known as a synapse, found between the axons and the dendrites of adjacent neurons. � There are three types of neurons:

 

  • Sensory neurons: Transfer information from the sense organs, such as the eyes and ears, to the brain.
  • Motor neurons: Manage voluntary muscle activity and transfer messages from nerve cells in the brain to muscles.
  • All other neurons are known as interneurons.

 

Scientists believe that neurons are the most varied type of cell in the human body. Within these three types of neurons are hundreds of different types of neurons, each with specific message-carrying abilities. The way these neurons communicate with one another by establishing connections is ultimately what makes people unique in how we think, feel, and act. �

 

Birth of the Neuron

 

The range to which new neurons are created in the brain has been a controversial topic among neuroscientists for many years. Meanwhile, although nearly all neurons are currently present in our brains by the time we’re born, there’s recent evidence to support that neurogenesis, or the scientific word utilized to describe the birth of neurons, is a lifelong procedure. Neurons are born in regions of the brain which are full of neural precursor cells, known as neural stem cells. These cells have the potential to develop all, if not all, of the different types of neurons and glia found in the brain. Neuroscientists have discovered how neural precursor cells function in the laboratory. Although this may not be exactly how these cells behave when they are in the brain, it gives us data about how they may function when they are in the brain’s environment. �

 

The science of stem cells is still very recent and could ultimately change with further discoveries, however, researchers have discovered enough evidence to support as well as to be able to demonstrate how neural stem cells create the other cells of the brain. Neuroscientists refer to this as a stem cell’s lineage and it is similar in principle to the concept of a family tree. �

 

Neural stem cells increase by dividing into two and creating two new stem cells, two early progenitor cells, or one of each. When a stem cell divides to create another stem cell, it is believed to self-renew. This new cell has the potential to make more stem cells. When a stem cell divides to create an early progenitor cell, it is said to differentiate. Differentiation is when a new cell is more technical in structure and function. An early progenitor cell doesn’t have the potential of a stem cell to create several different types of cells. It can only make cells within their distinct lineage. Early progenitor cells may self-renew or go in either of two ways. One type will develop astrocytes. The other type will develop neurons or oligodendrocytes. �

 

Migration of the Neuron

 

Once a neuron is born, it must go to the region of the brain where it will function. But, how does a neuron understand where to go? And, what helps it get there? Neuroscientists have determined that neurons utilize two different methods to travel:

 

  • Several neurons migrate by following the long fibers of cells known as radial glia. These fibers extend from the inner layers to the outer layers of the brain. Neurons glide along the fibers until they reach their destination.
  • Neurons also travel by using chemical signals. Scientists have found special molecules on the surface of neurons, known as adhesion molecules, which bind with similar molecules on nearby glial cells or nerve axons. These chemical signals will also ultimately help guide the neuron to its final destination in the brain.

 

Not all neurons are successful in their journey. Scientists believe that only one-third of these neurons will reach their destination. Some cells die during the process of neuronal growth. Some neurons may also survive, but end up where they don’t belong. Mutations in the genes which regulate migration create regions of misplaced or abnormal neurons which can cause disorders, such as epilepsy. Scientists believe that schizophrenia is partially caused by misguided neurons. �

 

Differentiation of the Neuron

 

When a neuron reaches its destination, then it must begin to perform its initial function. This final measure of differentiation is one of the most misunderstood sections of neurogenesis. Neurons are in charge of the transfer and uptake of neurotransmitters, or chemicals which deliver information between cells. Depending on its location, a neuron may perform the role of a sensory neuron, a motor neuron, or an interneuron, sending and receiving specific neurotransmitters. �

 

In the developing brain, a neuron depends on molecular signals from other cells, including astrocytes, to determine its form and location, the type of transmitter it creates, and to which other neurons it can connect. These newborn cells establish neural circuits, or data pathways that connect from neuron to neuron, which is determined during adulthood. However, in the mature brain, neural circuits are already developed and neurons must find a way to fit in. As a new neuron settles in, it starts to look like enclosing cells. It then develops an axon and dendrites and begins to communicate with its neighbors. �

 

Death of the Neuron

 

Although neurons are the longest living cells within the human body, large numbers of them often die during migration and differentiation. The lives of some neurons can sometimes take unexpected turns. Several health issues associated with the brain, the spinal cord, and the nerves are the consequence of the unnatural deaths of neurons and supporting cells. �

 

  • In Parkinson’s disease, neurons which create the neurotransmitter dopamine die off at the basal ganglia, a region of the brain which controls body movements. This causes difficulty initiating movement.
  • In Huntington’s disease, a genetic mutation causes the over-production of a neurotransmitter known as glutamate, which kills neurons in the basal ganglia. As a result, individuals twist and writhe uncontrollably.
  • In Alzheimer’s disease, unusual proteins build up in and around neurons in the neocortex and hippocampus, sections of the brain which manage memory. When these neurons die, people lose their ability to remember and perform regular tasks. Physical damage to the brain and other regions of the central nervous system can also kill nerves.

 

Injury to the brain, or damage caused by a stroke, can kill nerves completely or gradually starve them of the oxygen and nutrients they need to survive. Spinal cord injury may disrupt communications between the brain and nerves when these lose their link to axons located under the site of injury. These neurons survive but they may lose their ability to communicate. �

 

Conclusion to Brain Basics

 

Scientists hope that by understanding more about the life and death of neurons, they could develop treatment options and perhaps even cures for brain diseases and disorders which ultimately affect the lives of many people in the United States. �

 

The most current research studies suggest that neural stem cells can generate many, if not all, of the several types of neurons located in the brain and the nervous system. Determining how to control these stem cells from the laboratory into specific types of neurons can develop a new supply of brain cells to replace the ones which have been damaged or died. �

 

Treatment approaches may also be created to take advantage of growth factors and other signaling mechanisms within the brain which tells precursor cells to make new neurons. This will make it easy to fix, reshape, and renew the brain from within. �

 

A neuron is characterized as a nerve cell which is considered to be the basic building block of the central nervous system. Neurons are similar to other cells in the human body, however, neurons are responsible for transferring and transmitting information throughout the human body. As previously mentioned above, there are also several different types of neurons which are in charge of a variety of functions. Understanding the life and death of neurons is essential to help understand the mechanisms of neurological diseases and hopefully their treatment and cure.� – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article is to understand the life and death of neurons and how these relate with neurological diseases. Neurological diseases are associated with the brain, the spine, and the nerves. 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.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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 Annual Cost of Neurological Disease in the US

The Annual Cost of Neurological Disease in the US

Neurological diseases are characterized as health issues associated with the brain, the spine, and the nerves which connect them. Neurological disease is considered to be one of the most prevalent health issues with a high burden to the patients, their families, and society. However, there are now estimates of the burden of neurological diseases in the United States. �

 

Neurological Disease Prevalence and Costs

 

The most prevalent and costly neurological diseases, according to several recent research studies, include Alzheimer disease and other dementias, chronic low back pain, stroke, traumatic brain injury, migraine headaches, epilepsy, multiple sclerosis, spinal cord injury, and Parkinson’s disease. Many other neurological diseases were excluded due to their mixed etiologies. �

 

The most common neurological disorders described above cost the United States approximately $789 billion in 2014, which may increase as the elderly population increases between 2011 and 2050, according to a research study published in the Annals of Neurology. The research study demonstrates the price of the serious annual financial burden in the US and has been demonstrated as healthcare professionals have suggested budget reductions for federally-funded research studies. �

 

According to these demographic statistics, the American Neurological Association, or the ANA, commissioned a research study by former ANA marketing committee and public advocacy committee chair Clifton L. Gooch, MD, currently professor and chair of the Department of Neurology in the University of South Florida’s Morsani College of Medicine in Tampa. �

 

The research study, the Burden of Neurological Disease in the United States: A Summary Report and Call to Action, demonstrated the annual cost of the most prevalent neurological diseases, including Alzheimer’s disease and other dementias, chronic low back pain, stroke, traumatic brain injury, migraine headaches, epilepsy, multiple sclerosis, spinal cord injury, and Parkinson’s disease. Neurological disease ultimately affects an estimated 100 million people in the United States every year and, together with the costs of stroke and dementia alone, these are estimated to total over $600 billion by 2030. �

 

Figure demonstrating the annual costs of the most common neurological diseases.

 

Funding for Neurology in the United States

 

The tremendous and sustained capital investments made in cardiovascular and cancer research studies beginning in the 1970s have considerably increased lifespan. Ironically, however, the number of older adults who have a higher chance of developing neurological diseases have increased, which has developed a growing outbreak among healthcare professionals. �

 

“Preliminary research studies, including those of cancer, focus considerable research study investment to the neurological diseases which are impacting the quality of life and mortality of more and more people in the United States every year,” stated Gooch, referring to the $1.8 billion in funding for cancer and neurology research approved by Congress in 2016. �

 

“We hope the findings of the report will serve as a wake-up call to Congress to improve much needed clinical and basic research funding necessary to discover treatments which can mitigate, and finally cure, the considerable amount of neurological diseases which have developed profound consequences in our patients as well as for the national economy.” �

 

“The future of funding for neurological research studies was an issue in 2012 when the ANA voted to support this particular research study,” stated ANA President Barbara G. Vickrey, MD, MPH. “With the reductions now being suggested to the NIH funding from the President of the United States, this has become of even greater concern today. As representatives of the scholars working to eradicate these health issues, we feel we must raise our collective perceptions, armed with the facts.” �

 

Annual Cost of Neurological Disease Overview

 

Researchers gathered the information from the research study through a complete review of the world literature among the most prevalent and costly neurological diseases in the United States. To be conservative, researchers focused on the prevalence and cost estimates they considered to be the most comprehensive and accurate, excluding neurological diseases, such as depression and chronic pain, which frequently have mixed etiologies beyond primary nervous system injury. �

 

“A complete accounting of all neurological diseases would considerably increase price tag estimates,” wrote the authors of the research study. Indirect and direct costs for the most common neurological diseases previously mentioned above, have been demonstrated in the research study and were estimated according to maintenance standards for each health issue. �

 

Alzheimer’s disease and other dementias accounted for $243 billion of their $789 billion total, while chronic lower back pain represented $177 billion, and stroke represented $110 billion.�As well as documenting the fiscal costs of neurological disease, Gooch and his USF colleagues ultimately recommend an action plan for reducing the burden of these health issues through infrastructure investment in neurological research and enhanced clinical management of neurological disorders. �

 

Many research studies have demonstrated how several of the most common neurological diseases pose a serious annual financial burden in the United States. The most prevalent and costly neurological health issues, such as Alzheimer’s disease and other dementias, chronic low back pain or sciatica, as well as stroke, among other common neurological diseases mentioned above, have been estimated to have an annual cost totalling $789 billion in 2014, according to research studies. These annual costs have also been demonstrated to considerable increase further over time.� – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

The purpose of the article is to demonstrate the annual cost of several of the most prevalent neurological diseases. Neurological diseases are associated with the brain, the spine, and the nerves. 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.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

Why Pinched Nerves Respond So Well To Chiropractic Care | El Paso, Tx.

Why Pinched Nerves Respond So Well To Chiropractic Care | El Paso, Tx.

Pinched nerves are a common complaint that can cause a wide variety of symptoms. In many cases the condition can be resolved quickly through chiropractic care; sometimes with just one session. However, chiropractic should be treated as an ongoing practice for better health and wellness.

Not only can chiropractic care help you better manage pain and resolve many health problems it can also help prevent injuries and certain conditions from developing. This often means that seeking chiropractic for a pinched nerve is a wise decision and can bring a quick resolution.

What is a Pinched Nerve?

A pinched nerve is the result of excessive pressure being applied to a nerve. This pressure can come from muscles, bones, tendons, or cartilage and causes a disruption in the nerve�s ability to function. This causes a variety of symptoms including pain, numbness, tingling, and weakness.

In the spine, a herniated disc can put pressure on the nerve root, causing pain and discomfort. In the wrist, it can cause a condition known as carpal tunnel syndrome.

Why is a Pinched Nerve such a Challenge?

The issue with a pinched nerve is finding the source. When a nerve is pinched, the pain and other symptoms may not be at the actual site. Instead, the pain and other sensations can travel to other parts of the body, including down the leg or through the arm. This can make it difficult to treat, but an experienced, knowledgeable chiropractor can assess the situation and treat the condition, bringing relief to the patient.

a pinched nerve and chiropractic care el paso tx.

Symptoms of a Pinched Nerve?

A pinched nerve can manifest with many different symptoms, often depending on its location in the body. They may worsen while the patient is sleeping. Some of the most common symptoms include:

  • Pain that is aching or sharp
  • Lower or mid back pain
  • Neck pain
  • Shoulder pain
  • General spinal pain
  • Pain that radiates down the leg or arm
  • Numbness or tingling in the legs, arms, fingers, or toes
  • Burning sensation in the legs, arms, fingers, or toes
  • Muscle weakness in the legs or back
  • Headaches
  • Frequently feeling like a hand or food is �asleep�

When the nerve is not pinched for very long, it typically does not leave the patient with any permanent damage. When the pressure is relieved, normal function returns rather quickly. On the other hand, if the pressure is not relieved, it can cause permanent damage to the nerve, leading to chronic pain.

Causes of a Pinched Nerve?

A pinched nerve can have a number of causes. Wrist or rheumatoid arthritis is a common cause, but others may include:

  • Injury
  • Repetitive motion that places stress on parts of the body
  • Obesity
  • Sports activities
  • Certain hobbies that require repetitive motion

Treatments for a Pinched Nerve?

The first line of treatment for a pinched nerve is rest. Medications may be recommended or prescribed, such as NSAIDs and muscle relaxers, but remember every drug has side effects so make sure you talk to your medical doctor before moving forward.

Physical therapy is another common treatment. The patient is taught certain exercises that stretch and strengthen muscles around the pinched nerve so that it relieves pressure. They are also given self-management techniques that they can do at home to get relief. However, if the pinched nerve is do to a misalignment in the spine, it doesn�t matter how many exercises you do; they won�t fix the problem. In severe cases, surgery may be recommended. This is usually a last resort.

Does Chiropractic for a Pinched Nerve Really Work?

Chiropractic care is a very effective treatment for pinched nerve because it addresses the root cause and works toward fixing the problem through spinal manipulation and very specific chiropractic adjustments. By bringing the body into alignment, pressure on the nerves is relieved. This helps relieve the pain but also facilitates healing allowing the patient to return to their normal daily activities and experience less downtime.

El Paso, TX Piriformis Syndrome Chiropractic Treatment

Piriformis Syndrome Management

Piriformis Syndrome Management

Sciatica is a collection of symptoms in the low back, which radiate down one or both legs. Sciatica is generally caused by the compression or irritation of the sciatic nerve, the largest nerve in the human body. One of the most common health issues that cause sciatic nerve pain is called piriformis syndrome. The piriformis muscle stretches from the front of the sacrum, the triangle-shaped bone between the hipbones on the pelvis.

The piriformis muscle extends to the top of the femur around the sciatic nerve. The femur, as previously mentioned, is the large bone in the upper leg. The piriformis muscle functions by helping the thigh move from side to side. A piriformis muscle spasm, or any other type of injury and/or condition along the piriformis muscle, can place pressure on the sciatic nerve and cause pain and discomfort. The result is piriformis�syndrome.

Piriformis Syndrome Causes and Symptoms

Sciatic nerve pain,�or sciatica, is one of the most prevalent�symptoms of piriformis syndrome. The pain and discomfort, however, may be felt in another part of the body. This is known as referred pain. Other common symptoms of piriformis syndrome include tingling sensations and numbness; tenderness;�difficulty sitting along with�pain while sitting and pain in the buttocks and thighs with physical activities.

The piriformis muscle can easily become damaged or injured from periods of inactivity or an excessive amount of exercise. Some common causes of piriformis syndrome include overuse; repetitive movements involving the legs; sitting for lengthy periods of time; lifting heavy objects; and extensive stair climbing. Sports injuries or automobile accident injuries can also harm the piriformis muscle and cause it to compress the sciatic nerve.�

 

Piriformis Syndrome Diagnosis

A doctor appointment for diagnosis of piriformis syndrome may include a review of the patient’s health history, their symptoms, and other probable causes of their pain and discomfort. If you recall straining a muscle during physical activity, be sure to share that information with your doctor. The�doctor may also perform a physical exam. The patient will participate in a series of range of movements to determine the cause of symptoms.

Some imaging tests may also be essential to help rule out other causes of piriformis syndrome. A CT scan or an MRI scan may help the healthcare professional determine whether even a herniated disc or arthritis is causing the patient’s pain and discomfort. An ultrasound of the piriformis muscle may also be helpful in diagnosing the problem if it seems that piriformis syndrome is causing the patient’s overall symptoms.

 

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Piriformis syndrome is a health issue associated with the compression or impingement of the sciatic nerve around the piriformis muscle. Symptoms may include pain and discomfort, tingling sensations and numbness along the low back, or sciatica. Chiropractic care is a well-known alternative treatment option which can help reduce the compression of the sciatic nerve and improve piriformis syndrome.

Dr. Alex Jimenez D.C., C.C.S.T.

Piriformis Syndrome Treatment

Piriformis syndrome may often not need any treatment to�relieve its symptoms. Just avoiding the physical activities which caused the pain and discomfort to manifest and rest can help improve the health issue. If symptoms do persist, however, alternating between ice and heat can help decrease pain. Apply ice for 15 to 20 minutes then use a heating pad on the affected area. Try that every couple of hours to help relieve symptoms.

Over-the-counter painkillers�may also help decrease pain and discomfort. The symptoms associated with piriformis syndrome can go away with no additional treatment, however, if it doesn’t, the patient might benefit from alternative treatment options, such as chiropractic care or physical therapy. Chiropractic care is a treatment approach which utilizes spinal adjustments and manual manipulations to treat a variety of injuries and/or conditions.

A chiropractor,�or doctor of chiropractic, may also provide piriformis syndrome relief through the use of transcutaneous electrical nerve stimulator, or TENS, treatment. A TENS device is a handheld unit which sends electrical charges directly to the affected region of the piriformis muscle. The nerves are then stimulated by the electric energy, which interferes with pain signals being transmitted to the brain.

The chiropractor or physical therapist may also recommend a series of lifestyle modifications, including physical activity guidance and nutritional advice. Various stretches and exercises can help improve the strength, flexibility, and mobility of the�piriformis muscle. In severe cases of piriformis syndrome, corticosteroid injections or even surgical interventions may be required to help alleviate the symptoms.�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

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Additional Topics: Chiropractic for Athletes with Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience 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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EXTRA IMPORTANT TOPIC: Piriformis Syndrome Chiropractic Treatment

Neurological Health Issues After Auto Injuries

Neurological Health Issues After Auto Injuries

I’m definitely able to do day-to-day stuff a lot easier. It’s just like a much happier life with less pain. Just doing anything like working out or any type of activity that a person would take for granted if you don’t have pain, it’s different when you have pain, and so to get pain relief is amazing.

Gale Grijalva

Head and neck injuries are health issues commonly caused by�automobile accidents. Due to the force of the impact, a�moderate fender bender can sometimes even jerk a victim enough to make them hit their head inside the vehicle. The brain�can be very susceptible to suffering damage�after an auto accident, leading to neurological issues which can have lasting effects.

Nerve damage is a prevalent consequence after a car crash, and it can�cause debilitating symptoms, such as pain, headaches, and mental health issues, among others, ultimately making it difficult for anyone to go about their everyday activities.�When it comes to nerve damage, the most common types of automobile accident injuries include:

  • Whiplash, an intense jerking motion of the head and neck which can cause the nerves to stretch or be pinched;
  • Blunt-force trauma, hitting your head, arms, or legs on a hard surface inside or outside the vehicle, compressing the nerves; and
  • Lacerations, deep cuts into the skin sustained during an automobile accident that can sever the nerves in the affected region.

Several signs and symptoms can help indicate when nerves are damaged. These include�pain; partial or full paralysis of limbs and appendages like fingers and/or toes; muscular fatigue; twitching or uncontrolled movements of muscles; a prickling sensation; tingling or numbness on the skin or in limbs; or increased sensitivity to cold and hot temperatures on the surface. Below, we will discuss the effects of nerve damage after an auto accident.

Neuropathy After Auto Injuries

Neuropathy, or nerve damage, may be brought on by sports injuries, work-related injuries, automobile accident injuries, or repetitive motion injuries. These scenarios may cause the nerves to be completely or partially compressed, stretched or even severed. Dislocated or broken, fractured, bones may also place an unnecessary quantity of pressure on the nerves, where slipped intervertebral discs can compress the nerve fibers.

Neuropathy,�a term used to describe nerve damage, usually involves�the peripheral nerves instead of the central nervous system, or the brain and spinal cord. This health issue may not only develop due to the causes�explained above,�but nerve damage can also occur for many other reasons. The most prevalent nerves to be affected by neuropathy include the motor nerves, the autonomic nerves, and the sensory nerves.

  • The motor nerves enable movement and power;
  • The autonomic nerves control the systems of the body; and
  • The sensory nerves control feeling.

Diagnosing neuropathy to determine the best treatment options can help a victim regain a healthy lifestyle. The healthcare professional will begin their evaluation by reviewing the patient’s medical history, including general health, signs and symptoms, any other�type of neuropathy in the family, current or recent prescriptions used, any exposure to poisons or toxins, alcohol consumption, and sexual history.

They will then diagnose the cause of the neuropathy by checking the skin, taking their pulse in different places, examining for feeling, such as analyzing vibration sensations with a tuning fork and evaluating tendon reflexes. The healthcare professional may determine your precise treatment options once the source of the neuropathy is narrowed down. The proper treatment approach can help manage the symptoms.

Radiculopathy After Auto Injuries

Radiculopathy is the medical term used to describe compression or irritation of a nerve in the spine. It is not a specific condition, but instead, a description of a general health issue in which or more nerves are affected, causing symptoms. Radiculopathy may cause pain, tingling sensations, numbness, or fatigue. This condition can occur in any portion of the spine, although it may be more common in some areas than others.

  • It is most common in the lower back (lumbar radiculopathy);
  • And in the neck (cervical radiculopathy);
  • It is�less common in the middle portion of the spine (thoracic radiculopathy), but it’s still tremendously debilitating.

Cervical radiculopathy is pain and other symptoms resulting from any condition which affects the nerves in the cervical, thoracic, or lumbar spine. Degeneration of the cervical region of the spine may lead to a myriad of conditions that might result in problems. These are usually divided between problems that come from health issues originating from pinched or irritated nerves as well as other underlying problems in the neck.

Lumbar radiculopathy causes pain which occurs in the lower back. Damage or injuries to the lumbar spine and compression or impingement of the nerve roots can cause pain, tingling sensations, and numbness. Automobile accident injuries can result in very significant pathologies including damage to the intervertebral discs, muscles, tendons, and ligaments as well as to the nerves traveling down the length of the spine.

Like neuropathy, a diagnosis for radiculopathy begins with a review of a patient’s medical history and a physical evaluation by the healthcare professional. The doctor might be able to determine the source of the symptoms by evaluating the patient’s muscle strength, sensation, and reflexes. These tests often comprise of a CT scan, an MRI or X-rays. The exam may also include an electromyogram or a nerve conduction study which analyzes the current threshold of sensibility in patients.

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Millions of people are involved in automobile accidents every year, many of which result in long-term injuries and disability. Chiropractic care is one of the most frequently considered forms of treatment after an auto accident. Through the use of spinal adjustments and manual manipulations, a doctor of chiropractic can help restore normal function to the nervous system in order to allow the body to naturally heal itself.

Dr. Alex Jimenez D.C., C.C.S.T.

Treatment After Auto Injuries

The force that’s often placed on the�neck and the spine during an auto accident can cause nerve damage.�If you experience any signs and symptoms after being involved in a car crash, it’s essential to seek immediate medical attention from a healthcare professional, such as a chiropractor, to receive the proper diagnosis and treatment. Chiropractic care is a popular treatment for automobile accident injuries.

Chiropractic care is an alternative treatment approach which focuses on the diagnosis, treatment, and prevention of a variety of injuries and/or conditions associated with the musculoskeletal and nervous system. Through the use of spinal adjustments and manual manipulations, a chiropractor can carefully correct any spinal misalignments�which may be placing unnecessary amounts of stress on the nerves.�

By naturally restoring the original integrity of the spine, chiropractic care has become one of the most common treatments for a variety of injuries and conditions, including nerve damage associated with automobile accident injuries. 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

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Additional Topics: Central Sensitization After Auto Injuries

Central sensitization is a health issue affecting the nervous system which is commonly associated with the development of chronic pain. With central sensitization, the nervous system experiences a “wind-up” process that causes it to become regulated in a constant state of high reactivity. This constant, or persistent, state of high reactivity lowers the threshold for what should be causing pain in the human body, ultimately maintaining pain even after the initial injury has healed. Central sensitization is identified by two main characteristics, both of which involve a heightened sensitivity to pain and the sensation of touch, known as allodynia and hyperalgesia.

 

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EXTRA IMPORTANT TOPIC: Neck Pain Chiropractic Treatment

 

Neurological Advanced Studies

Neurological Advanced Studies

After a neurological exam, physical exam, patient history, x-rays and any previous screening tests, a doctor may order one or more of the following diagnostic tests to determine the root of a possible/suspected neurological disorder or injury. These diagnostics generally involve neuroradiology, which uses small amounts of radioactive material to study organ function and structure and ordiagnostic imaging, which use magnets and electrical charges to study organ function.

Neurological Studies

Neuroradiology

  • MRI
  • MRA
  • MRS
  • fMRI
  • CT scans
  • Myelograms
  • PET scans
  • Many others

Magnetic Resonance Imaging (MRI)

Shows organs or soft tissue well
  • No ionizing radiation
Variations on MRI
  • Magnetic resonance angiography (MRA)
  • Evaluate blood flow through arteries
  • Detect intracranial aneurysms and vascular malformations
Magnetic resonance spectroscopy (MRS)
  • Assess chemical abnormalities in HIV, stroke, head injury, coma, Alzheimer’s disease, tumors, and multiple sclerosis
Functional magnetic resonance imaging (fMRI)
  • Determine the specific location of the brain where activity occurs

Computed Tomography (CT or CAT Scan)

  • Uses a combination of X-rays and computer technology to produce horizontal, or axial, images
  • Shows bones especially well
  • Used when assessment of the brain needed quickly such as in suspected bleeds and fractures

Myelogram

Contrast dye combined with CT or Xray
Most useful in assessing spinal cord
  • Stenosis
  • Tumors
  • Nerve root injury

Positron Emission Tomography (PET Scan)

Radiotracer is used to evaluate the metabolism of tissue to detect biochemical changes earlier than other study types
Used to assess
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease
  • Epilepsy
  • Cerebrovascular accident

Electrodiagnostic Studies

  • Electromyography (EMG)
  • Nerve Conduction Velocity (NCV) Studies
  • Evoked Potential Studies

Electromyography (EMG)

Detection of signals arising from the depolarization of skeletal muscle
May be measured via:
  • Skin surface electrodes
  • Not used for diagnostic purposes, more for rehab and biofeedback
Needles placed directly within the muscle
  • Common for clinical/diagnostic EMG

neurological studies el paso tx.Diagnostic Needle EMG

Recorded depolarizations may be:
  • Spontaneous
  • Insertional activity
  • Result of voluntary muscle contraction
Muscles should be electrically silent at rest, except at the motor end-plate
  • Practitioner must avoid insertion in motor end-plate
At least 10 different points in the muscle are measured for proper interpretation

Procedure

Needle is inserted into the muscle
  • Insertional activity recorded
  • Electrical silence recorded
  • Voluntary muscle contraction recorded
  • Electrical silence recorded
  • Maximal contraction effort recorded

Samples Collected

Muscles
  • Innervated by the same nerve but different nerve roots
  • Innervated by the same nerve root but different nerves
  • Different locations along the course of the nerves
Helps to distinguish the level of the lesion

Motor Unit Potential (MUP)

Amplitude
  • Density of the muscle fibers attached to that one motor neuron
  • Proximity of the MUP
Recruitment pattern can also be assessed
  • Delayed recruitment can indicated loss of motor units within the muscle
  • Early recruitment is seen in myopathy, where the MUPs tend to be of low amplitude short duration

neurological studies el paso tx.Polyphasic MUPS

  • Increased amplitude and duration can be the result of reinnervation after chronic denervation

neurological studies el paso tx.Complete Potential Blocks

  • Demyelination of multiple segments in a row can result in a complete block of nerve conduction and therefore no resulting MUP reading, however generally changes in MUPs are only seen with damage to the axons, not the myelin
  • Damage to the central nervous system above the level of the motor neuron (such as by cervical spinal cord trauma or stroke) can result in complete paralysis little abnormality on needle EMG

Denervated Muscle Fibers

Detected as abnormal electrical signals
  • Increased insertional activity will be read in the first couple of weeks, as it becomes more mechanically irritable
As muscle fibers become more chemically sensitive they will begin to produce spontaneous depolarization activity
  • Fibrillation potentials

Fibrillation Potentials

  • DO NOT occur in normal muscle fibers
  • Fibrillations cannot be seen with the naked eye but are detectable on EMG
  • Often caused by nerve disease, but can be produced by severe muscle diseases if there is damage to the motor axons

neurological studies el paso tx.Positive Sharp Waves

  • DO NOT occur in normally functioning fibers
  • Spontaneous depolarization due to increased resting membrane potential

neurological studies el paso tx.Abnormal Findings

  • Findings of fibrillations and positive sharp waves are the most reliable indicator of damage to motor axons to the muscle after one week up to 12 months after the damage
  • Often termed �acute� in reports, despite possibly being visible months after onset
  • Will disappear if there is complete degeneration or denervation of nerve fibers

Nerve Conduction Velocity (NCV) Studies

Motor
  • Measures compound muscle action potentials (CMAP)
Sensory
  • Measures sensory nerve action potentials (SNAP)

Nerve Conduction Studies

  • Velocity (Speed)
  • Terminal latency
  • Amplitude
  • Tables of normal, adjusted for age, height and other factors are available for practitioners to make comparison

Terminal Latency

  • Time between stimulus and the appearance of a response
  • Distal entrapment neuropathies
  • Increased terminal latency along a specific nerve pathway

Velocity

Calculated based on latency and variables such as distance
Dependent on diameter of axon
Also dependent on thickness of myelin sheath
  • Focal neuropathies thin myelin sheaths, slowing conduction velocity
  • Conditions such as Charcot Marie Tooth Disease or Guillian Barre Syndrome damage myelin in large diameter, fast conducting fibers

Amplitude

  • Axonal health
  • Toxic neuropathies
  • CMAP and SNAP amplitude affected

Diabetic Neuropathy

Most common neuropathy
  • Distal, symmetric
  • Demyelination and axonal damage therefore speed and amplitude of conduction are both affected

Evoked Potential Studies

Somatosensory evoked potentials (SSEPs)
  • Used to test sensory nerves in the limbs
Visual evoked potentials (VEPs)
  • Used to test sensory nerves of the visual system
Brainstem auditory evoked potentials (AEPs)
  • Used to test sensory nerves of the auditory system
Potentials recorded via low-impedance surface electrodes
Recordings averaged after repeated exposure to sensory stimulus
  • Eliminates background �noise�
  • Refines results since potentials are small and difficult to detect apart from normal activity
  • According to Dr. Swenson, in the case of SSEPs, at least 256 stimuli are usually needed in order to obtain reliable, reproducible responses

Somatosensory Evoked Potentials (SSEPs)

Sensation from muscles
  • Touch and pressure receptors in the skin and deeper tissues
Little if any pain contribution
  • Limits ability to use testing for pain disorders
Velocity and/or amplitude changes can indicate pathology
  • Only large changes are significant since SSEPs are normally highly variable
Useful for intraoperative monitoring and to assess the prognosis of patients suffering severe anoxic brain injury
  • Not useful in assessing radiculopathy as individual nerve roots cannot be easily identified

Late Potentials

Occur more than 10-20 milliseconds after stimulation of motor nerves
Two types
  • H-Reflex
  • F-Response

H-Reflex

Named for Dr. Hoffman
  • First described this reflex in 1918
Electrodiagnostic manifestation of myotatic stretch reflex
  • Motor response recorded after electrical or physical stretch stimulation of the associated muscle
Only clinically useful in assessing S1 radiculopathy, as the reflex from the tibial nerve to triceps surae can be assessed for velocity and amplitude
  • More quantifiable that Achilles reflex testing
  • Fails to return with after damage and therefore not as clinically useful in recurrent radiculopathy cases

F-Response

So named because it was first recorded in the foot
Occurs 25 -55 milliseconds after initial stimulus
Due to antidromic depolarization of the motor nerve, resulting in a orthodromic electrical signal
  • Not a true reflex
  • Results in a small muscle contraction
  • Amplitude can be highly variable, so not as important as velocity
  • Reduced velocity indicates slowed conduction
Useful in assessing proximal nerve pathology
  • Radiculopathy
  • Guillian Barre Syndrome
  • Chronic Inflammatory Demyelinating Polyradiculopathy (CIDP)
Useful in assessing demyelinative peripheral neuropathies

Sources

  1. Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
  2. Day, Jo Ann. �Neuroradiology | Johns Hopkins Radiology.� Johns Hopkins Medicine Health Library, 13 Oct. 2016, www.hopkinsmedicine.org/radiology/specialties/ne uroradiology/index.html.
  3. Swenson, Rand. Electrodiagnosis.

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The Role of Neurogenic Inflammation

The Role of Neurogenic Inflammation

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 Activation Triggers of the Peripheral Nervous System | El Paso, TX Chiropractor

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 | El Paso, TX Chiropractor

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 Neurogenic Inflammation | El Paso, TX Chiropractor

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: http://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.

 

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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 | El Paso, TX Chiropractor

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

 

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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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EXTRA IMPORTANT TOPIC: Low Back Pain Management

 

MORE TOPICS: EXTRA EXTRA:�Chronic Pain & Treatments

 

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