Back Clinic Nerve Injury Team. Nerves are fragile and can be damaged by pressure, stretching, or cutting. Injury to a nerve can stop signals to and from the brain, causing muscles not to work properly and losing feeling in the injured area. The nervous system manages a great majority of the body’s functions, from regulating an individual’s breathing to controlling their muscles as well as sensing heat and cold. But, when trauma from an injury or an underlying condition causes nerve injury, an individual’s quality of life may be greatly affected. Dr. Alex Jimenez explains various concepts through his collection of archives revolving around the types of injuries and condition which can cause nerve complications as well as discuss the different form of treatments and solutions to ease nerve pain and restore the individual’s quality of life.
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.
Sciatica is a collection of symptoms in the low back, which radiate down one or both legs. Sciatica is generally caused by the compression or irritation of the sciatic nerve, the largest nerve in the human body. One of the most common health issues that cause sciatic nerve pain is called piriformis syndrome. The piriformis muscle stretches from the front of the sacrum, the triangle-shaped bone between the hipbones on the pelvis.
The piriformis muscle extends to the top of the femur around the sciatic nerve. The femur, as previously mentioned, is the large bone in the upper leg. The piriformis muscle functions by helping the thigh move from side to side. A piriformis muscle spasm, or any other type of injury and/or condition along the piriformis muscle, can place pressure on the sciatic nerve and cause pain and discomfort. The result is piriformis�syndrome.
Piriformis Syndrome Causes and Symptoms
Sciatic nerve pain,�or sciatica, is one of the most prevalent�symptoms of piriformis syndrome. The pain and discomfort, however, may be felt in another part of the body. This is known as referred pain. Other common symptoms of piriformis syndrome include tingling sensations and numbness; tenderness;�difficulty sitting along with�pain while sitting and pain in the buttocks and thighs with physical activities.
The piriformis muscle can easily become damaged or injured from periods of inactivity or an excessive amount of exercise. Some common causes of piriformis syndrome include overuse; repetitive movements involving the legs; sitting for lengthy periods of time; lifting heavy objects; and extensive stair climbing. Sports injuries or automobile accident injuries can also harm the piriformis muscle and cause it to compress the sciatic nerve.�
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Piriformis Syndrome Diagnosis
A doctor appointment for diagnosis of piriformis syndrome may include a review of the patient’s health history, their symptoms, and other probable causes of their pain and discomfort. If you recall straining a muscle during physical activity, be sure to share that information with your doctor. The�doctor may also perform a physical exam. The patient will participate in a series of range of movements to determine the cause of symptoms.
Some imaging tests may also be essential to help rule out other causes of piriformis syndrome. A CT scan or an MRI scan may help the healthcare professional determine whether even a herniated disc or arthritis is causing the patient’s pain and discomfort. An ultrasound of the piriformis muscle may also be helpful in diagnosing the problem if it seems that piriformis syndrome is causing the patient’s overall symptoms.
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Piriformis syndrome is a health issue associated with the compression or impingement of the sciatic nerve around the piriformis muscle. Symptoms may include pain and discomfort, tingling sensations and numbness along the low back, or sciatica. Chiropractic care is a well-known alternative treatment option which can help reduce the compression of the sciatic nerve and improve piriformis syndrome.
Dr. Alex Jimenez D.C., C.C.S.T.
Piriformis Syndrome Treatment
Piriformis syndrome may often not need any treatment to�relieve its symptoms. Just avoiding the physical activities which caused the pain and discomfort to manifest and rest can help improve the health issue. If symptoms do persist, however, alternating between ice and heat can help decrease pain. Apply ice for 15 to 20 minutes then use a heating pad on the affected area. Try that every couple of hours to help relieve symptoms.
Over-the-counter painkillers�may also help decrease pain and discomfort. The symptoms associated with piriformis syndrome can go away with no additional treatment, however, if it doesn’t, the patient might benefit from alternative treatment options, such as chiropractic care or physical therapy. Chiropractic care is a treatment approach which utilizes spinal adjustments and manual manipulations to treat a variety of injuries and/or conditions.
A chiropractor,�or doctor of chiropractic, may also provide piriformis syndrome relief through the use of transcutaneous electrical nerve stimulator, or TENS, treatment. A TENS device is a handheld unit which sends electrical charges directly to the affected region of the piriformis muscle. The nerves are then stimulated by the electric energy, which interferes with pain signals being transmitted to the brain.
The chiropractor or physical therapist may also recommend a series of lifestyle modifications, including physical activity guidance and nutritional advice. Various stretches and exercises can help improve the strength, flexibility, and mobility of the�piriformis muscle. In severe cases of piriformis syndrome, corticosteroid injections or even surgical interventions may be required to help alleviate the symptoms.�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Chiropractic for Athletes with Back Pain
Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
I’m definitely able to do day-to-day stuff a lot easier. It’s just like a much happier life with less pain. Just doing anything like working out or any type of activity that a person would take for granted if you don’t have pain, it’s different when you have pain, and so to get pain relief is amazing.
Gale Grijalva
Head and neck injuries are health issues commonly caused by�automobile accidents. Due to the force of the impact, a�moderate fender bender can sometimes even jerk a victim enough to make them hit their head inside the vehicle. The brain�can be very susceptible to suffering damage�after an auto accident, leading to neurological issues which can have lasting effects.
Nerve damage is a prevalent consequence after a car crash, and it can�cause debilitating symptoms, such as pain, headaches, and mental health issues, among others, ultimately making it difficult for anyone to go about their everyday activities.�When it comes to nerve damage, the most common types of automobile accident injuries include:
Whiplash, an intense jerking motion of the head and neck which can cause the nerves to stretch or be pinched;
Blunt-force trauma, hitting your head, arms, or legs on a hard surface inside or outside the vehicle, compressing the nerves; and
Lacerations, deep cuts into the skin sustained during an automobile accident that can sever the nerves in the affected region.
Several signs and symptoms can help indicate when nerves are damaged. These include�pain; partial or full paralysis of limbs and appendages like fingers and/or toes; muscular fatigue; twitching or uncontrolled movements of muscles; a prickling sensation; tingling or numbness on the skin or in limbs; or increased sensitivity to cold and hot temperatures on the surface. Below, we will discuss the effects of nerve damage after an auto accident.
Neuropathy After Auto Injuries
Neuropathy, or nerve damage, may be brought on by sports injuries, work-related injuries, automobile accident injuries, or repetitive motion injuries. These scenarios may cause the nerves to be completely or partially compressed, stretched or even severed. Dislocated or broken, fractured, bones may also place an unnecessary quantity of pressure on the nerves, where slipped intervertebral discs can compress the nerve fibers.
Neuropathy,�a term used to describe nerve damage, usually involves�the peripheral nerves instead of the central nervous system, or the brain and spinal cord. This health issue may not only develop due to the causes�explained above,�but nerve damage can also occur for many other reasons. The most prevalent nerves to be affected by neuropathy include the motor nerves, the autonomic nerves, and the sensory nerves.
The motor nerves enable movement and power;
The autonomic nerves control the systems of the body; and
The sensory nerves control feeling.
Diagnosing neuropathy to determine the best treatment options can help a victim regain a healthy lifestyle. The healthcare professional will begin their evaluation by reviewing the patient’s medical history, including general health, signs and symptoms, any other�type of neuropathy in the family, current or recent prescriptions used, any exposure to poisons or toxins, alcohol consumption, and sexual history.
They will then diagnose the cause of the neuropathy by checking the skin, taking their pulse in different places, examining for feeling, such as analyzing vibration sensations with a tuning fork and evaluating tendon reflexes. The healthcare professional may determine your precise treatment options once the source of the neuropathy is narrowed down. The proper treatment approach can help manage the symptoms.
Radiculopathy After Auto Injuries
Radiculopathy is the medical term used to describe compression or irritation of a nerve in the spine. It is not a specific condition, but instead, a description of a general health issue in which or more nerves are affected, causing symptoms. Radiculopathy may cause pain, tingling sensations, numbness, or fatigue. This condition can occur in any portion of the spine, although it may be more common in some areas than others.
It is most common in the lower back (lumbar radiculopathy);
And in the neck (cervical radiculopathy);
It is�less common in the middle portion of the spine (thoracic radiculopathy), but it’s still tremendously debilitating.
Cervical radiculopathy is pain and other symptoms resulting from any condition which affects the nerves in the cervical, thoracic, or lumbar spine. Degeneration of the cervical region of the spine may lead to a myriad of conditions that might result in problems. These are usually divided between problems that come from health issues originating from pinched or irritated nerves as well as other underlying problems in the neck.
Lumbar radiculopathy causes pain which occurs in the lower back. Damage or injuries to the lumbar spine and compression or impingement of the nerve roots can cause pain, tingling sensations, and numbness. Automobile accident injuries can result in very significant pathologies including damage to the intervertebral discs, muscles, tendons, and ligaments as well as to the nerves traveling down the length of the spine.
Like neuropathy, a diagnosis for radiculopathy begins with a review of a patient’s medical history and a physical evaluation by the healthcare professional. The doctor might be able to determine the source of the symptoms by evaluating the patient’s muscle strength, sensation, and reflexes. These tests often comprise of a CT scan, an MRI or X-rays. The exam may also include an electromyogram or a nerve conduction study which analyzes the current threshold of sensibility in patients.
Millions of people are involved in automobile accidents every year, many of which result in long-term injuries and disability. Chiropractic care is one of the most frequently considered forms of treatment after an auto accident. Through the use of spinal adjustments and manual manipulations, a doctor of chiropractic can help restore normal function to the nervous system in order to allow the body to naturally heal itself.
Dr. Alex Jimenez D.C., C.C.S.T.
Treatment After Auto Injuries
The force that’s often placed on the�neck and the spine during an auto accident can cause nerve damage.�If you experience any signs and symptoms after being involved in a car crash, it’s essential to seek immediate medical attention from a healthcare professional, such as a chiropractor, to receive the proper diagnosis and treatment. Chiropractic care is a popular treatment for automobile accident injuries.
Chiropractic care is an alternative treatment approach which focuses on the diagnosis, treatment, and prevention of a variety of injuries and/or conditions associated with the musculoskeletal and nervous system. Through the use of spinal adjustments and manual manipulations, a chiropractor can carefully correct any spinal misalignments�which may be placing unnecessary amounts of stress on the nerves.�
By naturally restoring the original integrity of the spine, chiropractic care has become one of the most common treatments for a variety of injuries and conditions, including nerve damage associated with automobile accident injuries. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Central Sensitization After Auto Injuries
Central sensitization is a health issue affecting the nervous system which is commonly associated with the development of chronic pain. With central sensitization, the nervous system experiences a “wind-up” process that causes it to become regulated in a constant state of high reactivity. This constant, or persistent, state of high reactivity lowers the threshold for what should be causing pain in the human body, ultimately maintaining pain even after the initial injury has healed. Central sensitization is identified by two main characteristics, both of which involve a heightened sensitivity to pain and the sensation of touch, known as allodynia and hyperalgesia.
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.
Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves. The causes of neuropathy, or nerve damage, can vary greatly among each individual and these may be caused by a number of different diseases, injuries, infections and even vitamin deficiency states. However, neuropathy can most commonly affect the nerves that control the motor and sensory nerves. Because the human body is composed of many different kinds of nerves which perform different functions, nerve damage is classified into several types. Neuropathy can also be classified according to the location of the nerves being affected and according to the disease causing it. For instance, neuropathy caused by diabetes is called diabetic neuropathy. Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest as a result. Below we will discuss several specific types of neuropathies clinically treated by chiropractors, physical therapists and physical medicine doctors alike, as well as briefly describing their causes and their symptoms.
Brachial Plexopathies
Brachial plexopathy is a type of peripheral neuropathy, which affects the nerves that transmit messages from the brain and the spinal cord to the rest of the body. This kind of nerve damage occurs when harm affects the brachial plexus, a region found on each side of the neck where nerve roots from the spinal cord branch out into each arm’s nerves. Damage, injury or a condition that impacts these nerve roots can result in pain, decreased mobility and reduced sensation in the arm and shoulder. In some cases, no cause can be identified.
Erb’s Palsy
Erb’s Palsy, also known as�Erb�Duchenne palsy or Waiter’s tip palsy, is identified as a paralysis of the arm caused by damage or injury to the nerves in the neck which form part of the brachial plexus. The most common mechanism of injury in adults with Erb’s Palsy is a patient who fell forward while holding onto something behind them. Erb�Duchenne palsy can also happen to an infant during childbirth, most commonly, but not exclusively, from shoulder dystocia during a difficult birth. To be more precise, this type of brachial plexopathy results from damage to the C5-C6 nerve roots along the brachial plexus in the neck. Symptoms of Erb’s Palsy include dermatomal distribution of sensory disruption followed by weakness or paralysis in the deltoid, biceps, and brachialis muscles, leading to the �waiter�s tip� position associated with this type of neuropathy. While many infants can recover on their own from this type of brachial plexopathy, some may require rehabilitation.
Klumpke’s Palsy
Klumpke’s Palsy, also known as Klumpke’s paralysis or�Dejerine�Klumpke palsy, is a partial palsy in the nerve roots of the brachial plexus located along the cervical spine, or neck. It is named after�Augusta D�jerine-Klumpke, an American-born French medical doctor acknowledged for her work in neuroanatomy. Klumpke’s Palsy is characterized as a form of paralysis involving the muscles of the forearm and hand, which occurs to�infants during childbirth if their arm is pulled overhead.�Dejerine�Klumpke palsy can also occur to adults with overhead traction injuries caused by harm to the C8-T1 nerve roots in the brachial plexus and upper thoracic region of the spine. Symptoms of Klumpke’s paralysis include dermatomal distribution of sensory disruption, weakness or paralysis, in the wrist flexors and pronators as well as in the muscles of the hand. This type of brachial plexopathy may often lead to Horner�s syndrome, a collection of symptoms which manifest when a set of nerves, known as the sympathetic trunk, are damaged or injured due to T1 involvement. This form of neuropathy is identified by resulting�in a �claw hand� appearance, where the forearm is supinated with the wrist hyperextended, together with finger flexion.
Entrapment Neuropathies
Entrapment neuropathy, also known as nerve compression syndrome or compression neuropathy, is best-known as nerve damage or a type of neuropathy caused by direct pressure on a nerve. Common symptoms include pain and discomfort, tingling or burning sensations, numbness and muscle weakness which affects only a particular part of the human body, depending on which nerve is affected. A nerve can become compressed as a result of a constant external force or due to a lesion, such as a tumor. Additionally, some conditions can make the nerves more susceptible to compression, including diabetes, where the nerves are rendered more sensitive to minor degrees of compression due to their already compromised supply of blood. Nerve damage caused by a single episode of harm can be considered an entrapment neuropathy, however, it is generally not classified under this group of compression neuropathy or nerve compression syndrome.
Thoracic Outlet Syndromes
Thoracic outlet syndromes are a group of disorders which develop when the nerves or blood vessels between the collarbone and the thoracic outlet, located in the region of the first rib, are compressed. As a result, this can cause pain and discomfort in the neck and shoulders as well as numbness in the fingers. There are a number of types of thoracic outlet syndromes, including neurogenic, or neurological, thoracic outlet syndrome, specifically caused by the compression of the brachial plexus, vascular thoracic outlet syndrome, which is caused specifically by the compression of the veins, known as venous thoracic outlet syndrome, or arteries, known as arterial thoracic outlet syndrome, and nonspecific-type thoracic outlet syndrome, which is considered to be idiopathic and has been described to worsen with activity. Several healthcare professionals believe that nonspecific-type thoracic outlet syndrome doesn’t exist, while others claim it to be a common disorders. However, the majority of thoracic outlet syndromes are often classified as neurogenic.
Thoracic outlet syndromes are caused by the compression of the cervical rib, an extra “rib” in the seventh cervical vertebra, subclavius muscle tension, improper posture or�excessive thoracic kyphosis, physical trauma, repetitive activity, obesity and pregnancy. Thoracic outlet syndromes can vary depending on which structures are compressed. Thoracic outlet syndromes can be diagnosed using tests, such as the Adsons test, the Allen maneuver, the Costoclavicular maneuver, the Halstead maneuver, the�Reverse bakody maneuver, the Roos test, the Shoulder compression test and the Wright test. Thoracic outlet syndromes can cause permanent neurological damage if not diagnosed and treated early.
Median Nerve Entrapment
Median nerve entrapment or median nerve entrapment syndrome, is a mononeuropathy, a condition that impacts only a single nerve or nerve group outside the brain and spinal cord, which affects the movement of or sensation in the hand. Median nerve entrapment is caused by the compression of the median nerve found in the elbow or distally in the forearm or wrist. Symptoms include sensory disruption in the lateral portion of the palmar aspect of the hand and dorsal finger tips of the same fingers. In addition, motor fibers may also be affected in the forearm, if applicable, including the muscles of the thenar eminence, such as the abductor pollicis brevis, the opponens pollicis, and the flexor pollicis brevis. Other forms of median nerve entrapment syndromes include: pronator teres syndrome and carpal tunnel syndrome.
Pronator teres syndrome is characterized as the compression of the median nerve at the elbow. It is considered rare compared to carpal tunnel syndrome. Pronator teres syndrome is caused by repetitive movement, pronator teres muscle inflammation and thickened bicipital aponeurosis. Clinical findings for this type of neuropathy include, tenderness with palpation of the pronator teres muscle, pain with resisted pronation of the arm, flexor pollicus longus and flexor digitorum profundus involvement, otherwise, symptoms manifestations for pronator teres syndrome may appear similar to carpal tunnel syndrome but without positive wrist orthopedics.
Carpal tunnel syndrome is characterized as the compression of the median nerve at the wrist. Carpal tunnel syndrome is identified by symptoms of pain and discomfort, tingling sensations in the thumb, index finger, middle finger and the thumb side of the ring fingers, and numbness. These can generally start gradually and may extend up the arm. Advanced instances of carpal tunnel syndrome may cause weakened grip strength where the muscles at the base of the thumb may waste away if left untreated for an extended period of time. In many cases, carpal tunnel syndrome may affect both hands or arms. Carpal tunnel syndrome is caused by repetitive movements, hypothyroidism, obesity, rheumatoid arthritis, diabetes and pregnancy. Orthopedic tests utilized to diagnose carpal tunnel syndrome include the use of the Tinel�s Sign, positive if tapping over the median nerve reproduces/exacerbates symptoms, the�Phalen�s Maneuver/Prayer Sign, performed by bringing the hands together, with wrists flexed, and is repeated in reverse with the wrists extended, for at least 60 seconds, and is considered positive if tests reproduce/exacerbate symptoms, and the�Wringing Test, if wringing a towel produces paresthesia.
Ulnar Nerve Entrapment
Ulnar nerve entrapment is a condition where the ulnar nerve itself becomes physically trapped or pinched, resulting in symptoms of pain, numbness and weakness which extends throughout the little finger, the ulnar half of the ring finger and throughout the intrinsic muscles of the hand. Symptoms or ulnar nerve entrapment ultimately involve sensory disruption in the medial two digits of the palmar and dorsal aspects of the hand. Symptoms of ulnar nerve entrapment may vary depending on the specific location of the ulnar nerve compression or impingement. These may also be classified as motor, sensory or both, depending on the location of the injury. If motor fibers are affected in the hand, all fingers, besides the thumb, may become weakened, described as general hand weakness. The most common location of ulnar nerve entrapment is within the cubital tunnel. Other forms of ulnar nerve entrapment include: cubital tunnel syndrome and tunnel of Guyon syndrome.
Cubital tunnel syndrome is identified by the compression or impingement of the ulnar nerve in the cubital tunnel at the elbow. It is considered to be the second most common entrapment neuropathy which affects the upper extremities, following carpal tunnel syndrome. Symptoms of cubital tunnel syndrome are characterized by pain and discomfort along the region of the ulnar nerve entrapment, along with sensory impairment, paresis and paresthesia.�Causes of cubital tunnel syndrome include, repetitive movements, hypothyroidism, obesity, diabetes, physical trauma or injury to the cubital tunnel, and prolonged sitting with pressure on bent elbow.
Tunnel of Guyon syndrome, or Guyon’s canal syndrome, is identified by the compression or impingement of the ulnar nerve at the wrist, particularly along an anatomical space in the wrist known as Guyon’s canal. Guyon’s canal syndrome may also be referred to as ulnar tunnel syndrome. Symptoms of tunnel of Guyon syndrome are similar to those of cubital tunnel syndrome with slight variations depending on the region of ulnar nerve entrapment.�Causes of tunnel of Guyon syndrome include, repetitive movements, long term crutch use, fracture of the hamate, a carpal bone, due to a ganglion cyst, hypothyroidism, obesity, rheumatoid arthritis and diabetes.�Orthopedic tests utilized to diagnose Guyon’s canal syndrome include the use of the�Tinel�s Sign, positive if test over the ulnar nerve at the wrist elicits symptoms, the Wartenberg Sign, positive if the 5th digit abducts when patient performs hard grip strength test or attempts to squeeze fingers together and reduced two-point discrimination in the hand.
Radial Nerve Entrapment
Radial nerve entrapment, also known as radial tunnel syndrome, is a condition caused by the compression of the radial nerve, which travels from the brachial plexus, to the hand and wrist. Healthcare professionals believe that radial tunnel syndrome occurs because the radial nerve becomes irritated or inflamed due to the friction caused by the impingement of the muscles in the forearm. Radial nerve entrapment manifests symptoms of sensory disruption in the lateral three and a half digits of the dorsal aspect of the hand. Motor�fibers may also be affected along the�posterior arm and extensor compartment of the forearm, and wrist drop may be seen. Other forms of radial tunnel syndrome include: spiral groove entrapment, where all radial nerve innervated muscles below entrapment are affected,�Saturday night palsy caused due to sleeping on your own arm and the brachioradialis & triceps reflexes are both diminished, supinator syndrome, caused by the compression at the arcade of Frohse with no change in reflexes. Posterior interosseous syndrome, or radial tunnel syndrome, also elicits no change in reflexes.
Sciatic Nerve Entrapment
Sciatic nerve entrapment is a condition caused by the compression of the sciatic nerve, the longest and largest nerve in the human body, which travels from the low back, down through the buttocks, thighs, legs and into the foot. The collection of symptoms which manifest as a result of sciatic nerve entrapment, including pain and discomfort, tingling and burning sensations, and numbness as well as weakness in the lower extremitites, is commonly known as sciatica. Sciatic nerve entrapment, or sciatica, can be caused by a variety of injuries and/or aggravated conditions which can lead to the compression of the sciatic nerve, including, but not limited to, disc herniation and spinal stenosis. However, symptoms of sciatic nerve entrapment may vary depending on the location of the compression of the sciatic nerve. Other conditions caused by the compression of the sciatic nerve include: piriformis syndrome, peroneal nerve entrapment and tarsal tunnel syndrome.
Piriformis syndrome is a condition which occurs due to the compression of the sciatic nerve as a result of the irritation or inflammation of the piriformis muscle. Symptoms of piriformis syndrome may include pain and discomfort, followed by numbness in the buttocks and down the leg. Symptoms may worsen with regular activities, such as sitting and running. Piriformis syndrome is caused by anatomic variation or due to piriformis overuse/tension. Piriformis syndrome diagnosis exams include, a positive Lase?gue test, where the healthcare professional�extends the patient�s leg passively, while the patient is lying supine,�test is positive if the maneuver is limited by pain, and through the use of tenderness and palpable tension in piriformis muscle which elicits symptoms.
Peroneal nerve entrapment is a condition which occurs when the peroneal or the fibular branch of the sciatic nerve are compressed at the fibular head. Tinel�s sign may be present at the fibular region of the head and/or neck. Peroneal nerve entrapment generally affects the common peroneal nerve, therefore, motor and sensory symptoms may manifest, including, weakness of the ankle dorsiflexion and eversion, or the tibialis anterior. Other symptoms of peroneal nerve entrapment may include sensory disruption on the dorsum of the foot and lateral aspect of the calf. Common peroneal nerve entrapement at the fibular head is the most common nerve entrapment syndrome in the lower extremities.
Tarsal tunnel syndrome, also known as posterior tibial neuralgia, is a condition caused by the compression of the tibial nerve as it travels through the tarsal tunnel, found along the region of the inner leg, posterior to the medial malleolus, or the bump on the inside of the ankle. Tarsal tunnel syndrome can manifest symptoms of pain and discomfort, burning or tingling sensations, and numbness along the big toe and the first three toes. However, symptoms may vary slightly depending on the area of compression, where the entire foot may manifest the symptoms previously described. Other symptoms associated with posterior tibial neuralgia include sensory changes in the sole of the foot. Tinel�s sign may be present with percussion posterior to the medial malleolus. The exact cause of tarsal tunnel syndrome may be difficult to determine and it is essential to receive a proper diagnosis to determine the source of the symptoms.
Radiculopathy
Radiculopathy is a mononeuropathy,�a condition that impacts only a single nerve or nerve group outside the brain and spinal cord, which affects the movement of or sensation in one specific area. It is often associated with neuropathy involving spinal nerve roots and presents as changes in sensory and/or motor function affecting a single or a few nerve root level(s). The most common types of radiculopathies include: sciatica and cervical radiculopathy. The most prevalent causes of radiculopathy include, disc herniation, osteophytes, spinal stenosis, trauma, diabetes, epidural abscess or metastasis, nerve sheath tumors, such as schwannomas and neurofibromas, Guillain-Barre? syndrome, Herpes Zoster, or shingles, Lyme disease, cytomegalovirus, myxedema and/or thyroid disorder, and idiopathic neuritis.
Narrowing down some of the most common causes of radiculopathy, symptoms can manifest due to disc herniation which most commonly affects the nerve roots along the C6, C7, L5 & S1 vertebrae of the spine, spinal stenosis and lumbar stenosis which may produce neurogenic claudication, and pain and weakness with ambulation. Cervical stenosis may present with mixed radiculopathy and myelopathy due to long tract involvement. Symptoms may also manifest due to trauma, because it may lead to compression, trauma or avulsion of the nerve roots, diabetes, which is most�likely to cause a polyneuropathy, but mononeuropathy is possible, and Herpes Zoster, or shingles, most often on the trunk, accompanied by vesicular lesions in a single dermatome. If pain persists past vesicular regression, radiculopathy may instead be considered post-herpetic neuralgia.
Patients with a history of radiculopathy will often complain of burning pain or tingling sensations which radiates or shoots down an affected area in a “dermatomal” pattern. Occasionally, patients will complain of motor weakness, however if onset is recent, there is often no motor involvement. The diagnosis of radiculopathy can depend on a variety of exams.�Most often, hypoesthesia may be present in the affected dermatome level. It’s recommended to�evaluate for pain, as light touch can be difficult for these patient�s to distinguish. Fasciculations and/or atrophy may be seen if radiculopathy is chronic, due to the lower motor neuron being compressed or impinged. Motor weakness may be seen in muscles innervated by the same root level. Orthopedic tests for the diagnosis of radiculopathy may include: the straight-leg raise test (SLR), where pain between 10 to 60 degrees likely indicates nerve root compression, the�Well-leg raise/Crossed straight-leg raise test (WLR), where if positive, 90 percent specificity for L/S nerve root compression may be present, the Valsalva Maneuver, where its considered positive if there is an increase in radicular symptoms, and spinal percussion, where pain may indicate metastatic disease, abscess or osteomyelitis.
Specific radiculopathy patterns may also develop as a result of different regions being affected. Radiculopathy along the T1 can cause Horner�s syndrome, a combination of symptoms caused by the disruption of a nerve pathway from the brain to the face and eye on one side of the body. This is due to its effect on cervical sympathetic ganglia, includind ptosis, miosis, anhidrosis. Radiculopathy below the L1, can cause Cauda Equina syndrome, a condition caused by damage or injury to the bundle of nerves found below the end of the spinal cord, known as the cauda equina. This type of radiculopathy may manifest symptoms of saddle anesthesia, sensory loss in the S2-S5 distribution, urinary retention or overflow incontinence, constipation, decreased rectal tone or fecal incontinence, and loss of erectile function. Individuals with these signs and symptoms must be referred for emergency care immediately to prevent permanent dysfunction.
Other patterns of neuropathy can include the cape/shawl distribution of symptoms, identified by an intramedullary lesion, such as syringomyeli, intramedullary tumor and central cord damage. Stocking and glove distribution of symptoms may manifest as a result of diabetes mellitus,�B12 deficiency, alcoholism and/or hepatitis,�HIV, and thyroid dysfunction and/or myxedema.
The cape/shawl pattern of neuropathy is characterized by symptoms occurring due to an intramedullary lesion, such as a tumor, syringomyelia or a hyperextension injury in patient with C/S spondylosis. It can also be characterized by loss of pain and temperature sensation in C/T dermatomes because of the arrangement of the lateral spinothalamic tract. The stocking and glove pattern may progress gradually depending on its specific stage. It can also be characterized as a symmetrical polyneuropathy, where the feet and legs are generally affected first, followed by the hands and arms. A vibration-like sensation in the smallest toes are also typically the first to go and the neuropathy symptoms may progress across the foot to the big toe and then upward through the ankle and leg, then hands, arms and finally to the trunk if the condition becomes severe. The most likely cause of this pattern may be attributed to diabetes mellitus, but other possible causes include, B12 deficiency, alcoholism, HIV, chemotherapy treatment, thyroid dysfunction and multiple other causes.
Diabetic Neuropathy
Diabetic neuropathy is medically defined as a collection of nerve damaging disorders associated with diabetes. These conditions are believed to occur as a result of a diabetic microvascular injury involving the small blood vessels, known as the vasa nervorum, which supply the nerves. Additionally, macrovascular conditions have also been considered to accumulate and cause diabetic neuropathy.�Diabetic neuropathy often presents as a polyneuropathy, or the simultaneous damage or disease of many peripheral nerves throughout the body, but it can also present as a mononeuropathy, usually with acute onset. Diabetic neuropathy most commonly affects the CN III, femoral and sciatic nerves. Diabetic neuropathy can affect all peripheral nerves, including the sensory neurons, motor neurons and, although rarely, the autonomic nervous system. As a result, diabetic neuropathy can affect all organs and systems, as these are all innervated. Diabetic neuropathy can manifest into a wide array of symptoms, including, but not limited to, pain, burning or tingling sensations, numbness, dizziness and trouble with balance.
Demyelinating Neuropathies
Demyelinating neuropathies can be individually defined by its two types: Acute inflammatory demyelinating polyneuropathy, best known as�Guillain-Barre? syndrome, or Chronic inflammatory demyelinating polyneuropathy.�Guillain-Barre? syndrome, abbreviated as AIDP, is identified as a rapid-onset muscle weakness caused when the immune system damages, harms or destroys the peripheral nervous system. Onset has been reported by around one to two weeks following viral infection with progressive weakness, loss of DTRs/areflexia, paresthesia in the hands and feet, more motor involvement than sensory, potential autonomic fiber involvement, elevated CSF protein, and EMG/NCV studies indicating demyelination.�Guillain-Barre? syndrome may require treatment with plasmapheresis or IV Ig therapy.�Chronic inflammatory demyelinating polyneuropathy, abbreviated as CIDP,�is identified as an acquired immune-mediated inflammatory disorder of the peripheral nervous system which appears similar to AIDP but does not follow infection. Symptoms must be present for at least 8 weeks for this diagnosis to be considered positive.�Anti-inflammatory treatments may help treat CIDP.
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: Sciatica
Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.
The vast array of symptoms caused by neuropathy, also known as peripheral neuropathy, reflect the fact that it may be caused by an equally broad range of ailments involving disease and damage to peripheral nerves.
Signs and Symptoms of Neuropathy
Depending on the reason and unique to each patient, signs and symptoms of neuropathy can include:�pain; tingling, burning or prickling sensations; increased sensitivity to touch; muscle weakness or wasting;�temporary or permanent numbness; paralysis; dysfunction in glands or organs; or impairment in urination and sexual functioning.
Such signs and symptoms are dependent on whether autonomic, sensory, or motor nerves, as well as a combination of them, are ultimately affected. Autonomic nerve damage can influence physiological functions like blood pressure or create gastrointestinal problems and issues. Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while harm to motor nerves may affect movement and reflexes. When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.
Diabetic Neuropathy Symptoms
Diabetic peripheral neuropathy, which affects between 12 and 50 percent of individuals with diabetes, is one of the most common types of neuropathy. Many times, symptoms include a gradual change in sensation, as well as pain and weakness in the feet and, although less commonly, the hands. As the neuropathy develops further, it can lead to a loss of sensation in the affected regions.
This lack of feeling raises the odds of harm to the affected areas, explains Matthew Villani, doctor of podiatric medicine at Central Florida Regional Hospital at Lake Mary. Without the pain to signal when there’s an issue, individuals with diabetic neuropathy may allow modest abrasions or blisters on their feet, for instance, to fester as sores or ulcers. “The ulcers can become infected since they are open wounds, which can also progress to bone infection. Unfortunately, it frequently requires amputations if it does progress to that point”, states Dr. Matthew Villani.
Chemotherapy-Associated Neuropathy Symptoms
Cancer patients may suffer with neuropathy induced by chemotherapy as well as by other drugs and/or medications used to treat the disease. Symptoms can include intense pain, impaired movement, changes in heart rate and blood pressure, issues with balance, difficulty breathing, paralysis, and even organ failure. After chemotherapy is done, the symptoms frequently abate swiftly, but occasionally they last more, or these may not go away at all.
HIV- and AIDS-Associated Neuropathy Symptoms
Individuals being treated for HIV or AIDS can develop neuropathy from effects of the virus and the drugs and/or medications used to treat it as well. Common symptoms include stiffness, burning, prickling, tingling, and loss of feeling in the toes and soles of their feet. Sometimes the nerves in the fingers, hands, and wrists are also affected. The drugs Videx (didanosine), Hivid (zalcitabine), and Zerit (stavudine) have been most commonly associated with neuropathic symptoms.
Inflammation-Associated Neuropathy Symptoms
Inflammation caused by infections, like herpes zoster (also known as shingles), Lyme disease, or hepatitis B and hepatitis C, may lead to neuropathy, as may inflammation caused by autoimmune disorders, such as vasculitis, sarcoidosis, or autoimmune disease. In such situations, the signs and symptoms generally include burning and tingling sensations or numbness.
Other Causes of Neuropathy Symptoms
Additional causes of neuropathy and associated signs and symptoms include metabolic disorders, such as hypoglycemia or kidney failure; autoimmune disorders, such as rheumatoid arthritis, lupus, Sjogren’s syndrome, and Guillain-Barr� syndrome; toxicity; hereditary disorders, such as Charcot-Marie-Tooth disorder; hormonal disorders; alcoholism; vitamin deficiencies; physical trauma or injury; compression; and repetitive stress. In addition, many individuals may experience idiopathic neuropathy signs and symptoms, meaning that healthcare professionals may not know the reason for their neuropathy.
Dr. Alex Jimenez’s Insight
Neuropathy can be caused by a variety of injuries and/or aggravated conditions, often manifesting into a plethora of associated signs and symptoms. While every type of neuropathy, such as diabetic neuropathy or autoimmune disease-associated neuropathy, develops its own unique group of signs and symptoms, many patients will often report common complaints. Individuals with neuropathy generally describe their pain as stabbing, burning or tingling in character. If you experience unusual or abnormal tingling or burning sensations, weakness and/or pain in your hands and feet, it’s essential to seek immediate medical attention in order to receive a proper diagnosis of the cause of your specific signs and symptoms. Early diagnosis may help prevent further nerve injury.
What are the Common Signs and Symptoms of Neuropathy?
“Although there’s a wide array of signs and symptoms associated with neuropathy, the type of pain that people encounter may be common in many aspects of the disorder”, notes Vernon Williams, MD, a sports neurologist and director of the Center for Sports Neurology and Pain Medicine at Cedars-Sini Kerlan-Jobe Institute in Los Angeles. “The character and quality of neuropathic pain will often be pain that is burning or electric in character.” Furthermore, he describes that the pain will frequently be associated with different symptoms, like paresthesia, or a lack of normal sensation associated with pain; allodynia, or a painful reaction to a stimulus that wouldn’t normally trigger pain signals; and hyperalgesia, or a striking or severe pain in response to a stimulus that normally causes moderate pain.
How is Neuropathy Diagnosed?
If you think you’re having any of the above neuropathy signs and symptoms, consult a healthcare professional. A number of tests can be done to diagnose neuropathy. “There are certain patterns of complaints that indicate neuropathy,” stated Dr. Williams, “so taking down a patient’s history which includes a description of these complaints is an important first step.”
“After that, your healthcare professional can perform a physical evaluation, including checking motor and sensory function, assessing deep tendon reflexes, as well as looking for signs and symptoms like allodynia and hyperalgesia,” Williams says. “Then we can even perform electrodiagnostic testing; the most common being electromyography and nerve conduction testing, where we can stimulate nerves and document responses, calculate the rate at which signals are being transmitted and see whether there are some areas where nerves are not transmitting signals normally,” Williams continues.
With needle tests, Williams states, “We can put modest needles into human muscles, and, according to what we see and listen together with all the needle in the muscle, we get details about the way the nerves supplying those muscle tissues are functioning. There are a number of unique tests that could be handy to identifying neuropathy, in addition to localizing where the abnormality is the most likely to be coming from”, concluded Dr.�Vernon Williams.
Often, blood tests may test for elevated blood glucose to see whether your neuropathy signs and symptoms could possibly be associated to type 2 diabetes, nutritional deficiencies, toxic elements, hereditary disorders, and evidence of an abnormal immune response. Your healthcare professional may also do a nerve biopsy, which normally involves removing a small segment of a sensory nerve to search for abnormalities, or even a skin biopsy to see if there’s a reduction in nerve endings.
To give yourself the best chance of an accurate diagnosis as well as relief from your neuropathy signs and symptoms, be prepared to describe everything you are experiencing in detail, even when you experience them, how long an episode persists, and the amount of pain, discomfort or loss of sensation or movement you experience. The more specific you are on the signs and symptoms you’re experiencing, the easier it’ll be for your doctor to understand what’s happening. 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: Sciatica
Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.
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Diagnostic Needle EMG
Polyphasic MUPS
Complete Potential Blocks
Positive Sharp Waves
Abnormal Findings
