Back Clinic Neuropathy Treatment Team. Peripheral neuropathy is a result of damage to peripheral nerves. This often causes weakness, numbness, and pain, usually in the hands and feet. It can also affect other areas of your body. The peripheral nervous system sends information from the brain and spinal cord (central nervous system) to the body. It can result from traumatic injuries, infections, metabolic problems, inherited causes, and exposure to toxins. One of the most common causes is diabetes mellitus.
People generally describe the pain as stabbing, burning, or tingling. Symptoms can improve, especially if caused by a treatable condition. Medications can reduce the pain of peripheral neuropathy. It can affect one nerve (mononeuropathy), two or more nerves in different areas (multiple mononeuropathies), or many nerves (polyneuropathy). Carpal tunnel syndrome is an example of mononeuropathy. Most people with peripheral neuropathy have polyneuropathy. Seek medical attention right away if there is unusual tingling, weakness, or pain in your hands or feet. Early diagnosis and treatment offer the best chance for controlling your symptoms and preventing further damage to the peripheral nerves. Testimonies http://bit.ly/elpasoneuropathy
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.
Until only several decades ago, neuroscientists believed that the brain stopped creating new neural connections, meaning that your memory starts to become irreversibly worse when the human body stopped developing, which is generally in your early 20s.� Neuroscientists also understood that neurons weaken and die as we age. The loss of brain function due to neural breakdown was believed to be a normal part of aging until recent research studies demonstrated the opposite of this belief. �
Over the last several years, it has become evident to neuroscientists that you can, as a matter of fact, create new neurons and develop new neural connections starting in your early 20s and continuing well into your old age. As the older regions of the brain start to wear out, you can ultimately rewire your brain and improve your overall brain health. But, how can you improve brain health? In the following article, we will discuss 5 ways you can improve your brain health and promote your well-being. �
Eat Healthy Foods
You are what you eat, or at least, your brain can be affected by the types of foods you eat. Eating junk food can have a tremendous impact on your brain health because trans fats and saturated fats, frequently found in processed foods, can negatively alter the brain’s synapses. Synapses connect the brains neurons and are fundamental for memory and learning. But, a balanced diet rich in omega-3 fatty acids, which are found in salmon, walnuts, and kiwi, can provide the synapses with a boost which can ultimately help fight against neurological diseases, including depression, dementia, and Alzheimer’s disease. �
Participate in Exercise
Participating in exercise and physical activity can also help boost your memory and help you think more clearly, reducing the risk of developing neurological diseases. Because exercise and some physical activity is a moderate stressor to the body, which uses energy needed by the brain, it triggers the release of substances, known as growth factors, which make the brain’s neurons fitter and stronger. Participating in 30 minutes of exercise or physical activity every other day can help improve brain health, and don’t forget to stretch. Stretching can help reduce anxiety, which can affect overall brain health. �
Mental Stimulation
Make sure to also give your brain a workout with brainteasers, crossword puzzles, and memory games. Research studies have demonstrated that using these tools to remain mentally active can help reduce the risks of developing dementia and other neurological diseases by building and maintaining a reserve of stimulation on your brain. Mental stimulation can help boost the regions of your brain which control and regulate learning and attention, which are hard-wired into the brain. �
Memory Training
Maintaining information stored in your memory banks and retaining that memory with age may also be a simple matter of mind control. By way of instance, confidence in your cognitive abilities might actually influence how well your memory works, especially for the elderly. Because many older adults tend to blame memory lapses on age, regardless of whether or not that is the reason, they may often be keeping themselves out of even trying to remember. Prediction can also enhance memory. If you have an idea of the information you have to remember afterward, you’re more likely to remember it. �
Get Enough Sleep
Getting enough sleep can help improve your overall well-being, especially your brain health. Sleep gives your brain an opportunity to match the memories of the day and combine them for long-term storage. One research study demonstrated that the brain can perform its reviewing much quicker when you are asleep than when you’re wide awake. A 90-minute mid-afternoon nap can help store long-term memories, such as events or skills you are attempting to master. Research studies have demonstrated that developing Alzheimer’s disease and other types of dementia are generally due to genetics. �
One research study, presented in July at the Alzheimer’s Association’s International Conference on Alzheimer’s Disease, demonstrated a connection between moms who develop Alzheimer’s disease and the chances that their children will develop the health issue in older age. Another research study suggests that a pattern of proteins is a risk factor for neurological disease. But, no one can predict who will develop dementia. While neuroscientists discover better treatments for these health issues, following ways to improve brain health is probably the best you can do to promote your overall well-being. �
Many neuroscientists once believed that the brain stopped developing new neurons and new neural connections as soon as you reached adulthood. However, recent research studies have demonstrated that we can create new neurons and new neural connection which can continue well into your old age.�In the following article, we discuss 5 ways you can improve your brain health and promote your well-being. From eating healthy foods to getting enough sleep, maintaining your overall well-being can help improve your brain health. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
The purpose of the article above is to demonstrate 5 ways which can ultimately help improve your overall brain health. 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�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. �
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�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. �
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. �
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�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. �
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
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
Polyphasic MUPS
Increased amplitude and duration can be the result of reinnervation after chronic denervation
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
Positive Sharp Waves
DO NOT occur in normally functioning fibers
Spontaneous depolarization due to increased resting membrane potential
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
Useful in assessing demyelinative peripheral neuropathies
Sources
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
Day, Jo Ann. �Neuroradiology | Johns Hopkins Radiology.� Johns Hopkins Medicine Health Library, 13 Oct. 2016, www.hopkinsmedicine.org/radiology/specialties/ne uroradiology/index.html.
Neurogenic inflammation, or NI, is the physiological process where mediators are discharged directly from the cutaneous nerves to commence an inflammatory response. This results in the creation of local inflammatory reactions including, erythema, swelling, temperature increase, tenderness, and pain. Fine unmyelinated afferent somatic C-fibers, which respond to low intensity mechanical and chemical stimulations, are largely responsible for the release of these inflammatory mediators.
When stimulated, these nerve pathways in the cutaneous nerves release energetic neuropeptides, or substance P and calcitonin gene related peptide (CGRP), rapidly into the microenvironment, triggering a series of inflammatory responses. There is a significant distinction in immunogenic inflammation, that’s the very first protective and reparative response made by the immune system when a pathogen enters the body, whereas neurogenic inflammation involves a direct connection between the nervous system and the inflammatory responses. Even though neurogenic inflammation and immunologic inflammation can exist concurrently, the two are not clinically indistinguishable. The purpose of the article below is to discuss the mechanism of neurogenic inflammation and the peripheral nervous system’s role in host defense and immunopathology.
Neurogenic Inflammation � The Peripheral Nervous System�s Role in Host Defense and Immunopathology
Abstract
The peripheral nervous and immune systems are traditionally thought of as serving separate functions. This line is, however, becoming increasingly blurred by new insights into neurogenic inflammation. Nociceptor neurons possess many of the same molecular recognition pathways for danger as immune cells and in response to danger, the peripheral nervous system directly communicates with the immune system, forming an integrated protective mechanism. The dense innervation network of sensory and autonomic fibers in peripheral tissues and high speed of neural transduction allows for rapid local and systemic neurogenic modulation of immunity. Peripheral neurons also appear to play a significant role in immune dysfunction in autoimmune and allergic diseases. Therefore, understanding the coordinated interaction of peripheral neurons with immune cells may advance therapeutic approaches to increase host defense and suppress immunopathology.
Introduction
Two thousand years ago, Celsus defined inflammation as involving four cardinal signs � Dolor (pain), Calor (heat), Rubor (redness), and Tumor (swelling), an observation indicating that activation of the nervous system was recognized as being integral to inflammation. However, pain has been mainly thought of since then, only as a symptom, and not a participant in the generation of inflammation. In this perspective, we show that the peripheral nervous system plays a direct and active role in modulating innate and adaptive immunity, such that the immune and nervous systems may have a common integrated protective function in host defense and the response to tissue injury, an intricate interaction that also can lead to pathology in allergic and autoimmune diseases.
Survival of organisms is critically dependent on the capacity to mount a defense against potential harm from tissue damage and infection. Host defense involves both avoidance behavior to remove contact with a dangerous (noxious) environment (a neural function), and active neutralization of pathogens (an immune function). Traditionally, the role of the immune system in combating infective agents and repairing tissue injury has been considered quite distinct from that of the nervous system, which transduces damaging environmental and internal signals into electrical activity to produce sensations and reflexes (Fig. 1). We propose that these two systems are actually components of a unified defense mechanism. The somatosensory nervous system is ideally placed to detect danger. Firstly, all tissues that are highly exposed to the external environment, such as epithelial surfaces of the skin, lungs, urinary and digestive tract, are densely innervated by nociceptors, high threshold pain-producing sensory fibers. Secondly, transduction of noxious external stimuli is almost instantaneous, orders of magnitude quicker than the mobilization of the innate immune system, and therefore may be the �first responder� in host defense.
Figure 1: Noxious stimuli, microbial and inflammatory recognition pathways trigger activation of the peripheral nervous system. Sensory neurons possess several means of detecting the presence of noxious/harmful stimuli. 1) Danger signal receptors, including TRP channels, P2X channels, and danger associated molecular pattern (DAMP) receptors recognize exogenous signals from the environment (e.g. heat, acidity, chemicals) or endogenous danger signals released during trauma/tissue injury (e.g. ATP, uric acid, hydroxynonenals). 2) Pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and Nod-like receptors (NLRs) recognize Pathogen associated molecular patterns (PAMPs) shed by invading bacteria or viruses during infection. 3) Cytokine receptors recognize factors secreted by immune cells (e.g. IL-1beta, TNF-alpha, NGF), which activate map kinases and other signaling mechanisms to increase membrane excitability.
In addition to orthodromic inputs to the spinal cord and brain from the periphery, action potentials in nociceptor neurons can also be transmitted antidromically at branch points back down to the periphery, the axon reflex. These together with sustained local depolarizations lead to a rapid and local release of neural mediators from both peripheral axons and terminals (Fig. 2) 1. Classic experiments by Goltz (in 1874) and by Bayliss (in 1901) showed that electrically stimulating dorsal roots induces skin vasodilation, which led to the concept of a �neurogenic inflammation�, independent of that produced by the immune system (Fig. 3).
Figure 2: Neuronal factors released from nociceptor sensory neurons directly drive leukocyte chemotaxis, vascular hemodynamics and the immune response. When noxious stimuli activate afferent signals in sensory nerves, antidromic axon reflexes are generated that induce the release of neuropeptides at the peripheral terminals of the neurons. These molecular mediators have several inflammatory actions: 1) Chemotaxis and activation of neutrophils, macrophages and lymphocytes to the site of injury, and degranulation of mast cells. 2) Signaling to vascular endothelial cells to increase blood flow, vascular leakage and edema. This also allows easier recruitment of inflammatory leukocytes. 3) Priming of dendritic cells to drive subsequent T helper cell differentiation into Th2 or Th17 subtypes.
Figure 3: Timeline of advances in understanding of the neurogenic aspects of inflammation from Celsus to the present day.
Neurogenic inflammation is mediated by the release of the neuropeptides calcitonin gene related peptide (CGRP) and substance P (SP) from nociceptors, which act directly on vascular endothelial and smooth muscle cells 2�5. CGRP produces vasodilation effects 2, 3, whereas SP increases capillary permeability leading to plasma extravasation and edema 4, 5, contributing to the rubor, calor and tumor of Celsus. However, nociceptors release many additional neuropeptides (online database: www.neuropeptides.nl/), including Adrenomedullin, Neurokinins A and B, Vasoactive intestinal peptide (VIP), neuropeptide (NPY), and gastrin releasing peptide (GRP), as well as other molecular mediators such as glutamate, nitric oxide (NO) and cytokines such as eotaxin 6.
We now appreciate that the mediators released from sensory neurons in the periphery not only act on the vasculature, but also directly attract and activate innate immune cells (mast cells, dendritic cells), and adaptive immune cells (T lymphocytes) 7�12. In the acute setting of tissue damage, we conjecture that neurogenic inflammation is protective, facilitating physiological wound healing and immune defense against pathogens by activating and recruiting immune cells. However, such neuro-immune communications also likely play major roles in the pathophysiology of allergic and autoimmune diseases by amplifying pathological or maladaptive immune responses. In animal models of rheumatoid arthritis for example, Levine and colleagues have shown that denervation of the joint leads to a striking attenuation in inflammation, that is dependent on neural expression of substance P 13, 14. In recent studies of allergic airway inflammation, colitis and psoriasis, primary sensory neurons play a central role in initiating and augmenting the activation of innate and adaptive immunity 15�17.
We propose therefore, that the peripheral nervous system not only plays a passive role in host defense (detection of noxious stimuli and initiation of avoidance behavior), but also an active role in concert with the immune system in modulating the responses to and combat of harmful stimuli, a role that can be subverted to contribute to disease.
Shared Danger Recognition Pathways in the Peripheral Nervous and Innate Immune Systems
Peripheral sensory neurons are adapted to recognize danger to the organism by virtue of their sensitivity to intense mechanical, thermal and irritant chemical stimuli (Fig. 1). Transient receptor potential (TRP) ion channels are the most widely studied molecular mediators of nociception, conducting non-selective entry of cations upon activation by various noxious stimuli. TRPV1 is activated by high temperatures, low pH and capsaicin, the vallinoid irritant component of chili peppers 18. TRPA1 mediates the detection of reactive chemicals including environmental irritants such as tear gas and industrial isothiocyanates 19, but more importantly, it is also activated during tissue injury by endogenous molecular signals including 4-hydroxynonenal and prostaglandins 20, 21.
Interestingly, sensory neurons share many of the same pathogen and danger molecular recognition receptor pathways as innate immune cells, which enable them also to detect pathogens (Fig. 1). In the immune system, microbial pathogens are detected by germline encoded pattern recognition receptors (PRRs), which recognize broadly conserved exogenous pathogen-associated molecular patterns (PAMPs). The first PRRs to be identified were members of toll-like receptor (TLR) family, which bind to yeast, bacterial derived cell-wall components and viral RNA 22. Following PRR activation, downstream signaling pathways are turned on that induce cytokine production and activation of adaptive immunity. In addition to TLRs, innate immune cells are activated during tissue injury by endogenous derived danger signals, also known as damage-associated molecular patterns (DAMPs) or alarmins 23, 24. These danger signals include HMGB1, uric acid, and heat shock proteins released by dying cells during necrosis, activating immune cells during non-infectious inflammatory responses.
PRRs including TLRs 3, 4, 7, and 9 are expressed by nociceptor neurons, and stimulation by TLR ligands leads to induction of inward currents and sensitization of nociceptors to other pain stimuli 25�27. Furthermore, activation of sensory neurons by the TLR7 ligand imiquimod leads to activation of an itch specific sensory pathway 25. These results indicate that infection-associated pain and itch may be partly due to direct activation of neurons by pathogen-derived factors, which in turn activate immune cells through peripheral release of neuronal signaling molecules.
A major DAMP/alarmin released during cellular injury is ATP, which is recognized by purinergic receptors on both nociceptor neurons and immune cells 28�30. Purinergic receptors are made up of two families: P2X receptors, ligand-gated cation channels, and P2Y receptors, G-protein coupled receptors. In nociceptor neurons, recognition of ATP occurs through P2X3, leading to rapidly densensitizing cation currents and pain 28, 30 (Fig. 1), while P2Y receptors contribute to nociceptor activation by sensitization of TRP and voltage-gated sodium channels. In macrophages, ATP binding to P2X7 receptors leads to hyperpolarization, and downstream activation of the inflammasome, a molecular complex important in generation of IL-1beta and IL-18 29. Therefore, ATP is a potent danger signal that activates both peripheral neurons and innate immunity during injury, and some evidence even suggests that neurons express parts of the inflammasome molecular machinery 31.
The flip side of danger signals in nociceptors is the role of TRP channels in immune cell activation. TRPV2, a homologue of TRPV1 activated by noxious heat, is expressed at high levels in innate immune cells 32. Genetic ablation of TRPV2 led to defects in macrophage phagocytosis and clearance of bacterial infections 32. Mast cells also express TRPV channels, which may directly mediate their degranulation 33. It remains to be determined whether endogenous danger signals activate immune cells in a similar manner as nociceptors.
A key means of communication between immune cells and nociceptor neurons are through cytokines. Upon activation of cytokine receptors, signal transduction pathways are activated in sensory neurons leading to downstream phosphorylation of membrane proteins including TRP and voltage-gated channels (Fig. 1). The resulting sensitization of nociceptors means that normally innocuous mechanical and heat stimuli can now activate nociceptors. Interleukin 1 beta and TNF-alpha are two important cytokines released by innate immune cells during inflammation. IL-1beta and TNF-alpha are directly sensed by nociceptors which express the cognate receptors, induce activation of p38 map kinases leading to increased membrane excitability 34�36. Nerve growth factor (NGF) and prostaglandin E(2) are also major inflammatory mediators released from immune cells that act directly on peripheral sensory neurons to cause sensitization. An important effect of nociceptor sensitization by immune factors is an increased release of neuropeptides at peripheral terminals that further activate immune cells, thereby inducing a positive feedback loop that drives and facilitates inflammation.
Sensory Nervous System Control of Innate and Adaptive Immunity
In early phases of inflammation, sensory neurons signal to tissue resident mast cells and dendritic cells, which are innate immune cells important in initiating the immune response (Fig. 2). Anatomical studies have shown a direct apposition of terminals with mast cells, as well as with dendritic cells, and the neuropeptides released from nociceptors can induce degranulation or cytokine production in these cells 7, 9, 37. This interaction plays an important role in allergic airway inflammation and dermatitis 10�12.
During the effector phase of inflammation, immune cells need to find their way to the specific site of injury. Many mediators released from sensory neurons, neuropeptides, chemokines, and glutamate, are chemotactic for neutrophils, eosinophils, macrophages, and T-cells, and enhance endothelial adhesion which facilitates immune cell homing 6, 38�41 (Fig. 2). Furthermore, some evidence implies that neurons may directly participate in the effector phase, as neuropeptides themselves may have direct antimicrobial functions 42.
Neuronally derived signaling molecules can also direct the type of inflammation, by contributing to the differentiation or specification of different types of adaptive immune T cells. An antigen is phagocytosed and processed by innate immune cells, which then migrate to the nearest lymph node and present the antigenic peptide to na�ve T cells. Depending on the type of antigen, costimulatory molecules on the innate immune cell, and the combinations of specific cytokines, na�ve T cells mature into specific subtypes that best serve the inflammatory effort to clear the pathogenic stimulus. CD4 T cells, or T helper (Th) cells, can be divided into four principle groups, Th1, Th2, Th17, and T regulatory cells (Treg). Th1 cells are mainly involved in regulating immune responses to intracellular microorganisms and organ-specific autoimmune diseases; Th2 are critical for immunity against extracellular pathogens, such as helminths, and are responsible for allergic inflammatory diseases; Th17 cells play a central role in protection against microbial challenges, such as extracellular bacteria and fungi; Treg cells are involved in maintaining self tolerance and regulating immune responses. This T cell maturation process appears to be heavily influenced by sensory neuronal mediators. Neuropeptides, such as CGRP and VIP, can bias dendritic cells towards a Th2-type immunity and reduce Th1-type immunity by promoting the production of certain cytokines and inhibiting others, as well as by reducing or enhancing dendritic cell migration to local lymph nodes 8, 10, 43. Sensory neurons also contribute considerably to allergic (mainly Th2 driven) inflammation 17. In addition to regulating Th1 and Th2 cells, other neuropeptides, such as SP and Hemokinin-1, can drive the inflammatory response more toward Th17 or Treg 44, 45, which means that neurons may also be involved in regulating inflammatory resolution. In immunopathologies such as colitis and psoriasis, blockade of neuronal mediators like substance P may significantly dampen T cell and immune mediated damage 15�17, although antagonizing one mediator may by itself only have a limited effect on neurogenic inflammation.
Considering that signaling molecules released from peripheral sensory nerve fibers regulate not only small blood vessels, but also the chemotaxis, homing, maturation, and activation of immune cells, it is becoming clear that neuro-immune interactions are much more intricate than previously thought (Fig. 2). Furthermore, it is quite conceivable that it is not individual neural mediators but rather specific combinations of signaling molecules released from nociceptors that influence different stages and types of immune responses.
Autonomic Reflex Control of Immunity
A role for a cholinergic autonomic nervous system �reflex� circuit in the regulation of peripheral immune responses also appears prominent 46. The vagus is the chief parasympathetic nerve connecting the brainstem with visceral organs. Work by Kevin Tracey and others point to potent generalized anti-inflammatory responses in septic shock and endotoxemia, triggered by an efferent vagal nerve activity leading to a suppression of peripheral macrophages 47�49. The vagus activates peripheral adrenergic celiac ganglion neurons innervating the spleen, leading to the downstream release of acetylcholine, which binds to alpha-7 nicotinic receptors on macrophages in the spleen and gastrointestinal tract. This induces activation of the JAK2/STAT3 SOCS3 signaling pathway, which powerfully suppresses TNF-alpha transcription 47. The adrenergic celiac ganglion also directly communicates with a subset of acetylcholine producing memory T cells, which suppress inflammatory macrophages 48.
Invariant natural Killer T cells (iNKT) are a specialized subset of T cells that recognize microbial lipids in the context of CD1d instead of peptide antigens. NKT cells are a key lymphocyte population involved in the combat of infectious pathogens and regulation of systemic immunity. NKT cells reside and traffic mainly through the vasculature and sinusoids of the spleen and liver. Sympathetic beta-adrenergic nerves in the liver directly signal to modulate NKT cell activity 50. During a mouse model of stroke (MCAO), for example, liver NKT cell mobility was visibly suppressed, which was reversed by sympathetic denervation or beta-adrenergic antagonists. Furthermore, this immunosuppressive activity of noradrenergic neurons on NKT cells led to increases in systemic infection and lung injury. Therefore, efferent signals from autonomic neurons can mediate a potent immuno-suppression.
Dr. Alex Jimenez’s Insight
Neurogenic inflammation is a local inflammatory response generated by the nervous system. It is believed to play a fundamental role in the pathogenesis of a variety of health issues, including, migraine, psoriasis, asthma, fibromyalgia, eczema, rosacea, dystonia and multiple chemical sensitivity. Although neurogenic inflammation associated with the peripheral nervous system has been extensively researched, the concept of neurogenic inflammation within the central nervous system still needs further research. According to several research studies, however, magnesium deficiencies are believed to be the main cause for neurogenic inflammation. The following article demonstrates an overview of the mechanisms of neurogenic inflammation in the nervous system, which may help healthcare professionals determine the best treatment approach to care for a variety of health issues associated with the nervous system.
Conclusions
What are the respective specific roles of the somatosensory and autonomic nervous systems in regulating inflammation and the immune system (Fig. 4)? Activation of nociceptors leads to local axon reflexes, which locally recruit and activate immune cells and is therefore, mainly pro-inflammatory and spatially confined. In contrast, autonomic stimulation leads to a systemic immunosuppression by affecting pools of immune cells in liver and spleen. The afferent signaling mechanisms in the periphery leading to the triggering of the immunosuppressive vagal cholinergic reflex circuit are poorly understood. However, 80�90% of vagal fibers are primary afferent sensory fibers, and therefore signals from the viscera, many potentially driven by immune cells, may lead to activation of interneurons in the brainstem and through them to an output in efferent vagal fibers 46.
Figure 4: Sensory and autonomic nervous systems modulate local and systemic immune responses respectively. Nociceptors innervating epithelial surfaces (e.g. skin and lung) induce localized inflammatory responses, activating mast cells and dendritic cells. In allergic airway inflammation, dermatitis and rheumatoid arthritis, nociceptor neurons play a role in driving inflammation. By contrast, autonomic circuits innervating the visceral organs (e.g. spleen and liver) regulate systemic immune responses by blocking macrophage and NKT cell activation. In stroke and septic endotoxemia, these neurons play an immunosuppressive role.
Typically, the time course and nature of inflammation, whether during infection, allergic reactions, or auto-immune pathologies, is defined by the categories of immune cells involved. It will be important to know what different types of immune cells are regulated by sensory and autonomic signals. A systematic assessment of what mediators can be released from nociceptors and autonomic neurons and the expression of receptors for these by different innate and adaptive immune cells might help address this question.
During evolution, similar danger detection molecular pathways have developed for both innate immunity and nociception even though the cells have completely different developmental lineages. While PRRs and noxious ligand-gated ion channels are studied separately by immunologists and neurobiologists, the line between these two fields is increasingly blurred. During tissue damage and pathogenic infection, release of danger signals are likely to lead to a coordinated activation of both peripheral neurons and immune cells with complex bidirectional communication, and an integrated host defense. The anatomical positioning of nociceptors at the interface with the environment, the speed of neural transduction and their ability to release potent cocktails of immune-acting mediators allows the peripheral nervous system to actively modulate the innate immune response and coordinate downstream adaptive immunity. Conversely, nociceptors are highly sensitive to immune mediators, which activate and sensitize the neurons. Neurogenic and immune-mediated inflammation are not, therefore, independent entities but act together as early warning devices. However, the peripheral nervous system also plays an important role in the pathophysiology, and perhaps etiology, of many immune diseases like asthma, psoriasis, or colitis because its capacity to activate the immune system can amplify pathological inflammation 15�17. Treatment for immune disorders may need to include, therefore, the targeting of nociceptors as well as of immune cells.
Acknowledgements
We thank the NIH for support (2R37NS039518).
In conclusion,�understanding the role of neurogenic inflammation when it comes to host defense and immunopathology is essential towards determining the proper treatment approach for a variety of nervous system health issues. By looking at the interactions of the peripheral neurons with immune cells, healthcare professionals may advance therapeutic approaches to further help increase host defense as well as suppress immunopathology. The purpose of the article above is to help patients understand the clinical neurophysiology of neuropathy, among other nerve injury health issues. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
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Neuropathic pain is a complex, chronic pain condition that is generally accompanied by soft tissue injury. Neuropathic pain is common in clinical practice and also poses a challenge to patients and clinicians alike. With neuropathic pain, the nerve fibers themselves may be either damaged, dysfunctional or injured. Neuropathic pain is the result of damage from trauma or disease to the peripheral or central nervous system, where the lesion may occur at any site. As a result, these damaged nerve fibers can send incorrect signals to other pain centers. The effect of a nerve fiber injury consists of a change in neural function, both at the region of the injury and also around the injury. Clinical signs of neuropathic pain normally include sensory phenomena, such as spontaneous pain, paresthesias and hyperalgesia.
Neuropathic pain, as defined by the International Association of the Study of Pain or the IASP, is pain initiated or caused by a primary lesion or dysfunction of the nervous system. It could result from damage anywhere along the neuraxis: peripheral nervous system, spinal or supraspinal nervous system. Traits that distinguish neuropathic pain from other kinds of pain include pain and sensory signs lasting beyond the recovery period. It’s characterized in humans by spontaneous pain, allodynia, or the experience of non-noxious stimulation as painful, and causalgia, or persistent burning pain. Spontaneous pain includes sensations of “pins and needles”, burning, shooting, stabbing and paroxysmal pain, or electric-shock like pain, often associated with dysesthesias and paresthesias. These sensations not only alter the patient’s sensory apparatus, but also the patient’s well-being, mood, attention and thinking. Neuropathic pain is made up of both “negative” symptoms, such as sensory loss and tingling sensations, and “positive” symptoms, such as paresthesias, spontaneous pain and increased feeling of pain.
Conditions frequently related to neuropathic pain can be classified into two major groups: pain due to damage in the central nervous system and pain because of damage to the peripheral nervous system. Cortical and sub-cortical strokes, traumatic spinal cord injuries, syringo-myelia and syringobulbia, trigeminal and glossopharyngeal neuralgias, neoplastic and other space-occupying lesions are clinical conditions that belong to the former group. Nerve compression or entrapment neuropathies, ischemic neuropathy, peripheral polyneuropathies, plexopathies, nerve root compression, post-amputation stump and phantom limb pain, postherpetic neuralgia and cancer-related neuropathies are clinical conditions that belong to the latter group.
Pathophysiology of Neuropathic Pain
The pathophysiologic processes and concepts underlying neuropathic pain are multiple. Prior to covering these processes, a review of ordinary pain circuitry is critical. Regular pain circuitries involve activation of a nociceptor, also known as the pain receptor, in response to a painful stimulation. A wave of depolarization is delivered to the first-order neurons, together with sodium rushing in via sodium channels and potassium rushing out. Neurons end in the brain stem in the trigeminal nucleus or in the dorsal horn of the spinal cord. It is here where the sign opens voltage-gated calcium channels in the pre-synaptic terminal, allowing calcium to enter. Calcium allows glutamate, an excitatory neurotransmitter, to be released into the synaptic area. Glutamate binds to NMDA receptors on the second-order neurons, causing depolarization.
These neurons cross through the spinal cord and travel until the thalamus, where they synapse with third-order neurons. These then connect to the limbic system and cerebral cortex. There is also an inhibitory pathway that prevents pain signal transmission from the dorsal horn. Anti-nociceptive neurons originate in the brain stem and travel down the spinal cord where they synapse with short interneurons in the dorsal horn by releasing dopamine and norepinephrine. The interneurons modulate the synapse between the first-order neuron as well as the second-order neuron by releasing gamma amino butyric acid, or GABA, an inhibitory neurotransmitter. Consequently, pain cessation is the result of inhibition of synapses between first and second order neurons, while pain enhancement might be the result of suppression of inhibitory synaptic connections.
The mechanism underlying neuropathic pain, however, aren’t as clear. Several animal studies have revealed that lots of mechanisms may be involved. However, one has to remember that what applies to creatures may not always apply to people. First order neurons may increase their firing if they’re partially damaged and increase the amount of sodium channels. Ectopic discharges are a consequence of enhanced depolarization at certain sites in the fiber, resulting in spontaneous pain and movement-related pain. Inhibitory circuits might be diminished in the level of the dorsal horn or brain stem cells, as well as both, allowing pain impulses to travel unopposed.
In addition, there might be alterations in the central processing of pain when, because of chronic pain and the use of some drug and/or medications, second- and third-order neurons can create a “memory” of pain and become sensitized. There’s then heightened sensitivity of spinal neurons and reduced activation thresholds. Another theory demonstrates the concept of sympathetically-maintained neuropathic pain. This notion was demonstrated by analgesia following sympathectomy from animals and people. However, a mix of mechanics can be involved in many chronic neuropathic or mixed somatic and neuropathic pain conditions. Among those challenges in the pain field, and much more so as it pertains to neuropathic pain, is the capability to check it. There is a dual component to this: first, assessing quality, intensity and advancement; and second, correctly diagnosing neuropathic pain.
There are, however, some diagnostic tools that may assist clinicians in evaluating neuropathic pain. For starters, nerve conduction studies and sensory-evoked potentials may identify and quantify the extent of damage to sensory, but not nociceptive, pathways by monitoring neurophysiological responses to electrical stimuli. Additionally, quantitative sensory testing steps perception in reaction to external stimuli of varying intensities by applying stimulation to the skin. Mechanical sensitivity to tactile stimuli is measured with specialized tools, such as von Frey hairs, pinprick with interlocking needles, as well as vibration sensitivity together with vibrameters and thermal pain with thermodes.
It is also extremely important to perform a comprehensive neurological evaluation to identify motor, sensory and autonomic dysfunctions. Ultimately, there are numerous questionnaires used to distinguish neuropathic pain in nociceptive pain. Some of them include only interview queries (e.g., the Neuropathic Questionnaire and ID Pain), while others contain both interview questions and physical tests (e.g., the Leeds Assessment of Neuropathic Symptoms and Signs scale) and the exact novel tool, the Standardized Evaluation of Pain, which combines six interview questions and ten physiological evaluations.
Treatment Modalities for Neuropathic Pain
Pharmacological regimens aim at the mechanisms of neuropathic pain. However, both pharmacologic and non-pharmacologic treatments deliver complete or partial relief in just about half of patients. Many evidence-based testimonials suggest using mixtures of drugs and/or medications to function for as many mechanisms as possible. The majority of studies have researched mostly post-herpetic neuralgia and painful diabetic neuropathies but the results may not apply to all neuropathic pain conditions.
Antidepressants
Antidepressants increase synaptic serotonin and norepinephrine levels, thereby enhancing the effect of the descending analgesic system associated with neuropathic pain. They’ve been the mainstay of neuropathic pain therapy. Analgesic actions might be attributable to nor-adrenaline and dopamine reuptake blockade, which presumably enhance descending inhibition, NMDA-receptor antagonism and sodium-channel blockade. Tricyclic antidepressants, such as TCAs; e.g., amitriptyline, imipramine, nortriptyline and doxepine, are powerful against continuous aching or burning pain along with spontaneous pain.
Tricyclic antidepressants have been proven significantly more effective for neuropathic pain than the specific serotonin reuptake inhibitors, or SSRIs, such as fluoxetine, paroxetine, sertraline and citalopram. The reason may be that they inhibit reuptake of serotonin and nor-epinephrine, while SSRIs only inhibit serotonin reuptake. Tricyclic antidepressants can have unpleasant side effects, including nausea, confusion, cardiac conduction blocks, tachycardia and ventricular arrhythmias. They can also cause weight gain, a reduced seizure threshold and orthostatic hypotension. Tricyclics have to be used with care in the elderly, who are particularly vulnerable to their acute side effects. The drug concentration in the blood should be monitored to avoid toxicity in patients who are slow medication metabolizers.
Serotonin-norepinephrine reuptake inhibitors, or SNRIs, are a new class of antidepressants. Like TCAs, they seem to be more effective than SSRIs for treating neuropathic pain because they also inhibit reuptake of both nor-epinephrine and dopamine. Venlafaxine is as effective against debilitating polyneuropathies, such as painful diabetic neuropathy, as imipramine, in the mention of TCA, and the two are significantly greater than placebo. Like the TCAs, the SNRIs seem to confer benefits independent of their antidepressant effects. Side effects include sedation, confusion, hypertension and withdrawal syndrome.
Antiepileptic Drugs
Antiepileptic drugs can be utilized as first-line treatment especially for certain types of neuropathic pain. They act by modulating voltage-gated calcium and sodium channels, by improving the inhibitory effects of GABA and by inhibiting excitatory glutaminergic transmission. Anti-epileptic medications have not been demonstrated to be effective for acute pain. In chronic pain cases, antiepileptic drugs seem to be effective only in trigeminal neuralgia. Carbamazepine is routinely employed for this condition. Gabapentin, which functions by inhibiting calcium channel function through agonist actions at the alpha-2 delta subunit of the calcium channel, is also known to be effective for neuropathic pain. However, gabapentin acts centrally and it might cause fatigue, confusion and somnolence.
Non-Opioid Analgesics
There is a lack of strong data supporting using non-steroidal anti inflammatory medications, or NSAIDs, in the relief of neuropathic pain. This may be due to the lack of an inflammatory component in relieving pain. But they have been utilized interchangeably with opioids as adjuvants in treating cancer pain. There have been reported complications, though, especially in severely debilitated patients.
Opioid Analgesics
Opioid analgesics are a subject of much debate in relieving neuropathic pain. They act by inhibiting central ascending pain impulses. Traditionally, neuropathic pain has been previously observed to be opioid-resistant, in which opioids are more suitable methods for coronary and somatic nociceptive types of pain. Many doctors prevent using opioids to treat neuropathic pain, in large part because of concerns about drug abuse, addiction and regulatory issues. But, there are many trials that have found opioid analgesics to succeed. Oxycodone was superior to placebo for relieving pain, allodynia, improving sleep and handicap. Controlled-release opioids, according to a scheduled basis, are recommended for patients with constant pain to encourage constant levels of analgesia, prevent fluctuations in blood glucose and prevent adverse events associated with higher dosing. Most commonly, oral preparations are used because of their greater ease of use and cost-effectiveness. Trans-dermal, parenteral and rectal preparations are generally used in patients who cannot tolerate oral drugs.
Local Anesthetics
Nearby acting anesthetics are appealing because, thanks to their regional action, they have minimal side effects. They act by stabilizing sodium channels at the axons of peripheral first-order neurons. They work best if there is only partial nerve injury and excess sodium channels have collected. Topical lidocaine is the best-studied representative of the course for neuropathic pain. Specifically, the use of this 5 percent lidocaine patch for post-herpetic neuralgia has caused its approval by the FDA. The patch seems to work best when there is damaged, but maintained, peripheral nervous system nociceptor function from the involved dermatome demonstrating as allodynia. It needs to be set directly on the symptomatic area for 12 hours and eliminated for another 12 hours and may be used for years this way. Besides local skin reactions, it is often well tolerated by many patients with neuropathic pain.
Miscellaneous Drugs
Clonidine, an alpha-2-agonist, was shown to be effective in a subset of patients with diabetic peripheral neuropathy. Cannabinoids have been found to play a role in experimental pain modulation in animal models and evidence of the efficacy is accumulating. CB2-selective agonists suppress hyperalgesia and allodynia and normalize nociceptive thresholds without inducing analgesia.
Interventional Pain Management
Invasive treatments might be considered for patients who have intractable neuropathic pain. These treatments include epidural or perineural injections of local anesthetics or corticosteroids, implantation of epidural and intrathecal drug delivery methods and insertion of spinal cord stimulators. These approaches are reserved for patients with intractable chronic neuropathic pain who have failed conservative medical management and also have experienced thorough psychological evaluation. In a study by Kim et al, it was shown that a spinal cord stimulator was effective in treating neuropathic pain of nerve root origin.
Dr. Alex Jimenez’s Insight
With neuropathic pain, chronic pain symptoms occur due to the nerve fibers themselves being damaged, dysfunctional or injured, generally accompanied by tissue damage or injury. As a result, these nerve fibers can begin to send incorrect pain signals to other areas of the body. The effects of neuropathic pain caused by nerve fiber injuries includes modifications in nerve function both at the site of injury and at areas around the injury. Understanding the pathophysiology of neuropathic pain has been a goal for many healthcare professionals, in order to effectively determine the best treatment approach to help manage and improve its symptoms. From the use of drugs and/or medications, to chiropractic care, exercise, physical activity and nutrition, a variety of treatment approaches may be used to help ease neuropathic pain for each individual’s needs.
Additional Interventions for Neuropathic Pain
Lots of patients with neuropathic pain pursue complementary and alternative treatment options to treat neuropathic pain. Other well-known regimens used to treat neuropathic pain include acupuncture, percutaneous electrical nerve stimulation, transcutaneous electrical nerve stimulation, cognitive behavioral treatment, graded motor imagery and supportive treatment, and exercise. Among these however, chiropractic care is a well-known alternative treatment approach commonly utilized to help treat neuropathic pain. Chiropractic care, along with physical therapy, exercise, nutrition and lifestyle modifications can ultimately offer relief for neuropathic pain symptoms.
Chiropractic Care
What is known is that a comprehensive management application is crucial to combat the effects of neuropathic pain. In this manner, chiropractic care is a holistic treatment program that could be effective in preventing health issues associated with nerve damage. Chiropractic care provides assistance to patients with many different conditions, including those with neuropathic pain. Sufferers of neuropathic pain often utilize non-steroidal-anti-inflammatory medications, or NSAIDs, such as ibuprofen, or heavy prescription painkillers to help ease neuropathic pain. These may provide a temporary fix but need constant use to manage the pain. This invariably contributes to harmful side effects and in extreme situations, prescription drug dependence.
Chiropractic care can help improve symptoms of neuropathic pain and enhance stability without these downsides. An approach such as chiropractic care offers an individualized program designed to pinpoint the root cause of the issue. Through the use of spinal adjustments and manual manipulations, a chiropractor can carefully correct any spinal misalignments, or subluxations, found along the length of the spine, which could lower the consequences of nerve wracking via the realigning of the backbone. Restoring spinal integrity is essential to keeping a high-functioning central nervous system.
A chiropractor can also be a long-term treatment towards enhancing your overall well-being. Besides spinal adjustments and manual manipulations, a chiropractor may offer nutritional advice, such as prescribing a diet rich in antioxidants, or they may design a physical therapy or exercise program to fight nerve pain flair-ups. A long-term condition demands a long-term remedy, and in this capacity, a healthcare professional who specializes in injuries and/or conditions affecting the musculoskeletal and nervous system, such as a doctor of chiropractic or chiropractor, may be invaluable as they work to gauge favorable change over time.
Physical therapy, exercise and movement representation techniques have been demonstrated to be beneficial for neuropathic pain treatment. Chiropractic care also offers other treatment modalities which may be helpful towards the management or improvement of neuropathic pain. Low level laser therapy, or LLLT, for instance, has gained tremendous prominence as a treatment for neuropathic pain. According to a variety of research studies, it was concluded that LLLT had positive effects on the control of analgesia for neuropathic pain, however, further research studies are required to define treatment protocols that summarize the effects of low level laser therapy in neuropathic pain treatments.
Chiropractic care also includes nutritional advice, which can help control symptoms associated with diabetic neuropathy. During a research study, a low fat plant-based diet was demonstrated to improve glycemic control in patients with type 2 diabetes. After about 20 weeks of the pilot study, the individuals involved reported changes in their body weight and electrochemical skin conductance in the foot was reported to have improved with the intervention. The research study suggested a potential value in the low-fat plant-based diet intervention for diabetic neuropathy. Moreover, clinical studies found that the oral application of magnesium L-threonate is capable of preventing as well as restoring memory deficits associated with neuropathic pain.
Chiropractic care can also offer additional treatment strategies to promote nerve regeneration. By way of instance, enhancing the regeneration of axons has been suggested to help improve functional recovery after peripheral nerve injury. Electrical stimulation, together with exercise or physical activities, was found to promote nerve regeneration after delayed nerve repair in humans and rats, according to recent research studies. Both electrical stimulation and exercise were ultimately determined to be promising experimental treatments for peripheral nerve injury which seem ready to be transferred to clinical use. Further research studies may be needed to fully determine the effects of these in patients with neuropathic pain.
Conclusion
Neuropathic pain is a multifaceted entity with no particular guidelines to take care of. It’s best managed using a multidisciplinary approach. Pain management requires ongoing evaluation, patient education, ensuring patient follow-up and reassurance. Neuropathic pain is a chronic condition that makes the option for the best treatment challenging. Individualizing treatment involves consideration of the impact of the pain on the individual’s well-being, depression and disabilities together with continuing education and evaluation. Neuropathic pain studies, both on the molecular level and in animal models, is relatively new but very promising. Many improvements are anticipated in the basic and clinical fields of neuropathic pain hence opening the doorways to improved or new treatment modalities for this disabling condition. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
When the sensory system is affected by injury or disease, the nerves within that system can’t work properly to transmit sensations and feelings into the brain. This frequently contributes to a feeling of numbness, or lack of sensation. However, in certain cases, when this system is damaged, people may experience pain in the affected area.
Neuropathic pain does not start abruptly or resolve quickly; it’s a chronic pain condition which leads to persistent pain symptoms. For most individuals, the intensity of their symptoms may wax and wane throughout the day. Although neuropathic pain is supposed to be related to peripheral nerve health issues, like neuropathy caused by diabetes or spinal stenosis, injuries to the brain or spinal cord may also lead to chronic neuropathic pain. Neuropathic pain is also referred to as nerve pain.
Neuropathic pain may be contrasted to nociceptive pain. Neuropathic pain does not develop to any specific circumstance or outside stimulus, but rather, the symptoms occur simply because the nervous system may not be working accordingly. As a matter of fact, individuals can also experience neuropathic pain even when the aching or injured body part is not actually there. This condition is called phantom limb pain, which may occur in people after they’ve had an amputation.
Nociceptive pain is generally acute and develops in response to a specific circumstance, such as when someone experiences a sudden injury, like hammering a finger with a hammer or stubbing a toe when walking barefoot. Moreover, nociceptive pain tends to go away once the affected site heals. The body contains specialized nerve cells, known as nociceptors, which detect noxious stimuli that could damage the body, such as extreme heat or cold, pressure, pinching, and exposure to chemicals. These warning signals are then passed along the nervous system to the brain, resulting in nociceptive pain.
What are the Risk Factors for Neuropathic Pain?
Anything that contributes to a lack of function within the sensory nervous system can lead to neuropathic pain. As such, nerve health issues from carpal tunnel syndrome, or similar conditions, can ultimately trigger neuropathic pain. Trauma, resulting in nerve injury, may lead to neuropathic pain. Other conditions which could predispose individuals to developing neuropathic pain include: diabetes, vitamin deficiencies, cancer, HIV, stroke, multiple sclerosis, shingles, and even some cancer treatments.
What are the Causes of Neuropathic Pain?
There are many causes from which individuals may develop neuropathic pain. But on a cellular level, one explanation is an increased release of certain receptors that indicate pain, together with a diminished ability of the nerves to modulate these signals, leads to the sensation of pain originating from the affected region. Additionally, in the spinal cord, the region which exerts painful signs is rearranged with corresponding changes in hormones and loss of normally-functioning mobile bodies. Those alterations result in the perception of pain in the absence of external stimulation. In the brain, the ability to block pain can be affected following an injury, such as stroke or trauma from an injury. As time passes, additional cell damage happens and the feeling of pain continues. Neuropathic pain is also related to diabetes, chronic alcohol intake, certain cancers, vitamin B deficiency, diseases, other nerve-related diseases, toxins, and specific drugs.
What are the Symptoms of Neuropathic Pain?
Contrary to other neurological conditions, identification of neuropathic pain can be challenging. However, several, if any, objective signals may be present. Healthcare professionals have to decipher and translate an assortment of words which patients use to describe their pain. Patients may describe their symptoms as sharp, dull, hot, cold, sensitive, itchy, deep, stinging, burning, among a variety of other descriptive terms. Additionally, some patients may experience pain through light touch or pressure.
In an effort to help identify how much pain patients could be undergoing, different scales are often used. Patients are asked to rate their pain according to a visual scale or numerical graph. Many examples of pain scales exist, such as the one demonstrated below. Often, pictures of faces depicting a variety of levels of pain may be helpful when individuals have a difficult time describing the quantity of pain they are experiencing.
Chronic Pain and Mental Health
For many, the impact of chronic pain may not be limited to the pain ; it may also negatively influence their mental state. New research studies conducted by scientists at the Northwestern University in Chicago can explain why individuals who have chronic pain also suffer with seemingly unrelated health issues, such as depression, stress, lack of sleep and difficulty concentrating.
The evaluation demonstrated that people with chronic pain show different regions of the brain which are always active, most specifically, the area associated with mood and attention. This continuous action rewires nerve connections from the brain and leaves chronic pain sufferers at greater risk for psychological problems. Researchers suggested that getting pain signals constantly could result in mental rewiring that adversely affects the mind. The rewiring compels their brains to devote mental resources differently to deal with everyday tasks, from mathematics, to recalling a shopping list, to feeling happy.
The pain-brain connection has been well recorded, at least anecdotally, and lots of healthcare professionals say they’ve seen first-hand the way the patient’s mental state can go downhill when they endure chronic pain. Misconceptions about the pain-brain connection may have emerged from a lack of evidence that pain has a measurable, lasting influence on the brain. Researchers expect that with additional research into the mechanisms of how chronic pain makes people more susceptible to mood disorders, people are going to have the ability to better manage their overall well-being.
Culture and Chronic Pain
Many things contribute to the way we experience and express pain, however, it has also been recently suggested by researchers that culture relates directly into the expression of pain. Our upbringing and societal values affect how we express pain and also its own nature, intensity and length. However, these variables aren’t as obvious as socio-psychological values, such as age and sex.
Research states that chronic pain is a multifaceted process and the concurrent interplay between pathophysiology, cognitive, affective, behavioral and sociocultural factors summate to what is referred to as the chronic pain experience. It’s emerged that chronic pain is experienced differently among patients of varied cultures and ethnicities.
Some cultures encourage the expression of pain, particularly in the southern Mediterranean and Middle East. Other individuals suppress it, as in the many lessons to our kids about behaving bravely and not crying. Pain is recognized as part of the human experience. We are apt to assume that communication about pain will seamlessly cross cultural boundaries. But people in pain are subject to the manners their civilizations have trained them to experience and express pain.
Both individuals in pain and healthcare professionals experience difficulties communicating pain across ethnic borders. In a matter like pain, where effective communication can have far-reaching implications for medical care, quality of life and potentially survival, the role of culture in pain communicating remains under-evaluated. Persistent pain is a multidimensional, a composite encounter formed by interweaving and co-influencing biological and psychosocial factors. Knowing the culmination of these factors is critical to understanding the differences of its manifestation and management.
How is Neuropathic Pain Diagnosed?
The diagnosis of neuropathic pain relies upon additional evaluation of an individual’s history. If underlying nerve damage is suspected, then analysis of the nerves together with testing may be justified. The most common means to assess whether or not a nerve is injured is using electrodiagnostic medicine. This medical subspecialty utilizes techniques of nerve conduction studies with electromyelography (NCS/EMG). Clinical evaluation may show evidence of loss of work, and can include evaluation of light touch, the capacity to differentiate sharp out of dull pain and the ability to discern temperature, as well as the evaluation of vibration.
After a thorough clinical examination is completed, the electrodiagnostic analysis could be planned. These studies are conducted by specially trained neurologist and physiatrists. If neuropathy is suspected, a hunt for reversible causes ought to be accomplished. This can include blood function for vitamin deficiencies or thyroid problems, and imaging studies to exclude a structural lesion affecting the spinal cord. Depending on the results of this testing, there might be a means to decrease the intensity of the neuropathy and possibly reduce the pain that a patient is undergoing.
Regrettably, in many conditions, even good control of the underlying cause of the neuropathy can’t reverse the neuropathic pain. This is commonly seen in patients with diabetic neuropathy. In rare instances, there may be signs of changes in the skin and hair growth pattern in an affected region. These alterations may be associated with changes in perspiration. If present, these changes can help identify the likely presence of neuropathic pain related to a condition known as complex regional pain syndrome.
Dr. Alex Jimenez’s Insight
Neuropathic pain is a chronic pain condition which is generally associated with direct damage or injury to the nervous system or nerves. This type of pain is different from nociceptive pain, or the typical sensation of pain. Nociceptive pain is an acute or sudden sensation of pain which causes the nervous system to send signals of pain immediately after the trauma occurred. With neuropathic pain, however, patients may experience shooting, burning pain without any direct damage or injury. Understanding the possible causes of the patient’s neuropathic pain versus any other type of pain, can help healthcare professionals find better ways to treat chronic pain conditions.
What is the Treatment for Neuropathic Pain?
Various medicines are used in an attempt to treat neuropathic pain. The majority of these drugs are utilized off-label, which means that the medicine was approved by the FDA to treat different conditions and was then recognized as being advantageous to treat neuropathic pain. Tricyclic antidepressants, such as amitriptyline, nortriptyline and desipramine, have been prescribed for management of neuropathic pain for several years.
Some individuals find that these may be very effective in giving them relief. Other kinds of antidepressants have been shown to offer some relief. Selective serotonin reuptake inhibitors, or SSRIs, such as paroxetine and citalopram, and other antidepressants , such as venlafaxine and bupropion, have been utilized in certain patients. Another frequent treatment of neuropathic pain incorporates antiseizure medications, including carbamazepine, phenytoin, gabapentin, lamotrigine, and others.
In acute cases of painful neuropathy which don’t respond to first-line brokers, drugs typically utilized to treat heart arrhythmias may be of some benefit; however, these can lead to significant side effects and often have to be monitored closely. Medications applied directly to the skin can offer modest to perceptible benefit for some patients. The forms commonly used include lidocaine (in patch or gel type) or capsaicin.
Treating neuropathic pain is dependent on the underlying cause. If the cause is reversible, then the peripheral nerves can regenerate and the pain will abate; nonetheless, this reduction in pain may take several months to years. Several other alternative treatment options, including chiropractic care and physical therapy, may also be utilized in order to help relieve tension and stress along the nerves, ultimately helping to improve painful symptoms.
What is the Prognosis for Neuropathic Pain?
Many individuals with neuropathic pain are able to get some measure of aid, even when their pain persists. Although neuropathic pain isn’t dangerous to a patient, the presence of chronic pain can negatively affect quality of life. Patients with chronic nerve pain might suffer from sleep deprivation or mood disorders, including depression, anxiety and stress, as previously mentioned above. Because of the inherent alopecia and lack of sensory feedback, patients are at risk of developing injury or infection or unknowingly causing an escalation of a present injury. Therefore, it’s essential to seek immediate medical attention and follow specific guidelines directed by a healthcare professional for safety and caution.
Can Neuropathic Pain be Prevented?
The best way to prevent neuropathic pain is to avoid the development or progression of neuropathy. Monitoring and changing lifestyle options, including restricting the use of alcohol and tobacco; keeping a healthy weight to lower the chance of diabetes, degenerative joint disease, or stroke; and having great ergonomic form at work or when practicing hobbies to lower the risk of repetitive stress injury are strategies to decrease the probability of developing neuropathy and potential neuropathic pain. Make sure to seek immediate medical attention in the case of any symptoms associated with neuropathic pain in order to proceed with the most appropriate treatment approach.�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
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Diagnostic Needle EMG
Polyphasic MUPS
Complete Potential Blocks
Positive Sharp Waves
Abnormal Findings
