Name: El Paso Back Clinic | Spine Specialists - El Paso, TX
Price range: $$

Clinical Neurophysiology

Back Clinic Clinical Neurophysiology Support. El Paso, TX. Chiropractor, Dr. Alexander Jimenez discusses clinical neurophysiology. Dr. Jimenez will explore the clinical significance and functional activities of peripheral nerve fibers, the spinal cord, brainstem, and brain in the context of visceral and musculoskeletal disorders. Patients will gain an advanced understanding of the anatomy, genetics, biochemistry, and physiology of pain in relation to various clinical syndromes. Nutritional biochemistry related to nociception and pain will be incorporated. And the implementation of this information into therapy programs will be emphasized.

Our team takes great pride in bringing our families and injured patients only proven treatment protocols. By teaching complete holistic wellness as a lifestyle, we also change not only our patients’ lives but their families as well. We do this so that we may reach as many El Pasoans who need us, no matter the affordability issues. For answers to any questions you may have please call Dr. Jimenez at 915-850-0900.

Pain Modulation Pathway Mechanisms in El Paso, TX

by Dr Alex Jimenez | Chiropractic, Chronic Pain, Clinical Neurophysiology, Treatments

Most, if not all, ailments of the body trigger pain. Pain is interpreted and sensed in the brain. Pain is modulated by two key types of drugs which operate on the brain: analgesics and anesthetics. The term analgesic refers to a medication that relieves pain without loss of consciousness. The expression central anesthesia refers to a medication that depresses the CNS. It’s distinguished by the lack of all perception of sensory modalities, for instance, loss of consciousness without loss of critical functions.

Opiate Analgesia (OA)

The most successful clinically used drugs for producing temporary analgesia and relief from pain are the opioid family, which includes morphine, and heroin. There are currently no additional powerful pain therapeutic options to opiates. Several side effects caused by opiate use include tolerance and drug dependence or addiction. In general, these drugs modulate the incoming pain information in the spine and central nervous system, in addition to relieve pain temporarily, and can also be called opiate producing analgesia (OA). Opiate antagonist is a drug that antagonizes the opioid effects, such as naloxone or maltroxone, etc.. They are competitive antagonists of opiate receptors. However, the brain has a neuronal circuit and endogenous substances which modulate pain.

Endogenous Opioids

Opioidergic neurotransmission is located throughout the brain and spinal cord and is believed to influence many functions of the central nervous system, or CNS, such as nociception, cardiovascular functions, thermoregulation, respiration, neuroendocrine functions, neuroimmune functions, food consumption, sexual activity, competitive locomotor behaviour as well as memory and learning. Opioids exert marked effects on mood and motivation and produce a sense of euphoria.

Three classes of opioid receptors are identified: ?-mu, ?-delta and ?-kappa. All 3 classes are widely dispersed in the brain. The genes encoding each one of these have been cloned and found to function as members of the G protein receptors. Moreover, three major types of endogenous opioid peptides that interact with the above opiate receptors have been recognized in the central nervous system, including, ?-endorphins, enkephalins and the dynorphins. These 3 opioid peptides are derived from a large protein receptor by three different genes, such as the proopiomelanocortin, or POMC, gene, the proenkephalin gene and the prodynorphin gene.�The opioid peptides modulate nociceptive input in two ways: first, they block neurotransmitter release by inhibiting Ca2+ influx into the presynaptic terminal, or second, they open potassium channels, which hyperpolarizes neurons and inhibits spike activity. They act on various receptors within the brain and spinal cord.

Enkephalins are considered the putative ligands for the ? receptors, ? endorphins for its ?-receptors, and dynorphins for the ? receptors. The various types of opioid receptors are distributed differently within the peripheral and central nervous system, or CNS. There’s evidence for functional differences in these receptors in various structures. This explains why many undesirable side effects occur after opiate treatments. For instance, mu (?) receptors are widespread in the brain stem parabrachial nuclei, where a respiratory center and inhibition of these neurons may cause what’s known as respiratory depression.

Central or peripheral terminals of nociceptive afferent fibers feature opiate receptors in which exogenous and endogenous opioids could act to modulate the capability to transmit nociceptive information. Additionally, high densities of opiate receptors are found in periaqueductal gray, or PAG, nucleus raphe magnus, or NRM, and dorsal raphe, or DR, from the rostral ventral medulla, in the spinal cord, caudate nucleus, or CN, septal nucleus, hypothalamus, habenula and hippocampus.�Systemically administered opioids at analgesic dosages activate spinal and supraspinal mechanisms via ?, ?, and ? type opioid receptors and regulate pain signals to modulate symptoms.

Neuronal Circuits and Pain Modulation

For many decades it was suggested that somewhere in the central nervous system there is a circuit which can modulate incoming pain details. The gate control theory and the ascending/descending pain transmission system are two suggestions of such a circuit. Below, we will discuss both in further detail.

Gate Control Theory

The initial pain modulatory mechanism known as the gate control theory, has been proposed by Melzack and Wall in the mid 1960’s. The notion of the gate control theory is that non-painful input closes the gates to painful input, which results in avoidance of the pain sensation from travel into the CNS, for example, non-noxious input, or stimulation, suppresses pain.

The theory implies that collaterals of the large sensory fibers carrying cutaneous sensory input activate inhibitory interneurons, which inhibit and regulate pain transmission data carried from the pain fibers. Non-noxious input inhibits pain, or sensory input, and closes the gate to noxious input. The gate control theory demonstrates that in the spinal cord level, non-noxious stimulation will create presynaptic inhibition on dorsal root nociceptor fibers that synapse on nociceptors spinal neurons (T). This presynaptic inhibition will also prevent incoming noxious information from reaching the CNS, for example, it will shut the gate to incoming toxic information.

The gate control theory was the rationale for the idea behind the production and utilization of the transcutaneous electrical nerve stimulation, or TENS, for pain relief. In order to be effective, the TENS unit generates two different present frequencies below the pain threshold that can be taken by the patient. This process has found a degree of achievement in chronic pain treatment.

Pain Modulation: Gate Control Theory

Stimulation Produced Analgesia (SPA)

Evidence for an inherent analgesia system was found by intracranial electrical stimulation of certain discrete brain regions. These areas would be the periaqueductal gray, or PAG, and nucleus raphe magnus, or NRM, dorsal raphe, or DR, caudate nucleus, or CN, septal nucleus, or Spt, along with other nuclei. Such stimulation or sensory signals, inhibits pain, making analgesia without behavioral suppression, while the touch, temperature and pressure sensation stays intact. According to research studies, SPA, or stimulation produced analgesia, is more pronounced and continues for a longer period of time after stimulation in humans than in experimental animals. Additionally, during SPA, the subjects, however, still respond to nonpainful stimulation like temperature and touch within the circumscribed region of analgesia. The most effective CNS, or central nervous system regions for SPA to occur, would be in the PAG and the raphe nuclei, or RN.

Electrical stimulation of PAG or NRM inhibits spinal thalamic cells, or spinal neurons that project monosynaptically to the thalamus, in laminae I, II and V to ensure the noxious information from the nociceptors which are ultimately modulated in the level of the spinal cord. Furthermore, PAG has neuronal connections to the nucleus raphe magnus, or NRM.

The activity of the PAG most likely occurs by activation of the descending pathway from NRM and likely also by activation of ascending connections acting on greater subcortical levels of the CNS. In addition, electric stimulation of PAG or NRM produces behavioral analgesia, or stimulation produced analgesia. Stimulation produced analgesia, or SPA causes the release of endorphins which can be blocked by the opiate antagonist naloxone.

During PAG and/or RN stimulation, serotonin, also medically referred to as 5-HT, can also be discharged from ascending and descending axons from subcortical nuclei, in spinal trigeminal nuclei and in the spinal cord. This release of 5-HT modulates and regulates pain transmission by inhibiting or blocking incoming neural action. Depletion of 5-HT by electrical lesion of the raphe nuclei or with a neurotoxic lesion made by local injection of a chemical agent such as parachlorophenylalanine, or PCPA, results in blocking the power of opiate, both intracranial and systemic, as well as that of electrical stimulation in order to produce analgesia.

To confirm if the electric stimulation produced analgesia via the release of opiate and dopamine, then the region is locally microinjected with morphine or 5-HT. All these microinjections ultimately create analgesia. These processes also provide a way of identifying brain areas related to pain suppression and assist to produce a map of pain centers. The most effective way of producing opiate analgesia, or OA, is by intracerebral injection of morphine into the PAG.

The PAG and RN as well as other brain structures in which analgesia is produced, are also rich in opiate receptors. Intracerebral opioid administration produced analgesia and SPA can be blocked by systemic or from local microinjections of naloxone, the morphine antagonist, into the PAG or RN. For that reason, it’s been suggested that the two, both OA and SPA, operate by a frequent mechanism.

If OA and SPA behave through the same intrinsic system, then the hypothesis that opiates activate a pain-suppression mechanism is much more likely. As a matter of fact, current evidence suggests that microinjections of an opiate into the PAG activate an efferent brainstem system which inhibits pain transmission at segmental spinal cord levels. These observations imply that analgesia elicited from the periaqueductal gray, or PAG, demands a descending pathway into the spinal cord.

Dr. Alex Jimenez’s Insight

Pain modulation occurs through the process of electrical brain stimulation which occurs due to the activation of descending inhibitory fibers, which regulate or inhibit the input and output of certain neurons. What has been described as opioid and serotonergic antagonists, is believed to reverse both local opiate analgesia and brain-stimuli generated analgesia. The sensory signals or impulses in the central nervous system are ultimately controlled by both ascending and descending inhibitory systems, utilizing endogenous opioids or other endogenous substances, such as serotonin as inhibitory mediators. Pain is a complex perception which can also be influenced by a variety of other factors, including emotional state.

Mechanisms of Pain Modulation

Ascending and Descending Pain Suppression Mechanism

The primary ascending pain fibers, such as the A ? and C fibers, reach the dorsal horn of the spinal cord from peripheral nerve areas in order to innervate the nociceptor neurons in Rexed laminae I & II. Cells from Rexed lamina II make synaptic connections in Rexed layers IV to VII. Cells, particularly within laminae I and VII of the dorsal horn, give rise to ascending spinothalamic tracts. In the spinal level, opiate receptors are located in the presynaptic endings of their nocineurons and in the interneural level layers IV to VII from the dorsal horn.

Activation of opiate receptors at the interneuronal level produces hyperpolarization of the neurons, which lead to the the inhibition of activation as well as the release of substance P, a neurotransmitter involved in pain transmission, thus preventing pain transmission. The circuit which consists of the periaqueductal gray, or PAG, matter in the upper brain stem, the locus coeruleus, or LC, the nucleus raphe magnus, or the NRM, and the nucleus reticularis gigantocellularis, or Rgc,� leads to the descending pain suppression pathway, which inhibits incoming pain data at the spinal cord level.

As stated before, opioids interact with the opiate receptors in distinct central nervous system levels. These opiate receptors are the normal target regions for hormones and endogenous opiates, such as the endorphins and enkephalins. Due to binding at the receptor in subcortical websites, secondary changes which result in some change in the electrophysiological properties of the neurons and regulation of their ascending pain information.

What activates the PAG to exert its consequences? It was discovered that noxious stimulation triggers neurons in the nucleus reticularis gigantocellularis, or RGC. The nucleus Rgc innervates both PAG and NRM. The PAG sends axons into the NRM, and nerves in the NRM send their axons to the spinal cord. Additionally, bilateral dorsolateral funiculus, or DLF, lesions, referred to as DLFX, block the analgesia produced by both electrical stimulation and by microinjection of opiates directly into the PAG and NRM, but they just attenuate the systemic analgesic effects of opiates. These observations support the hypothesis that discrete descending pathways from the DLF are necessary for both OA and SPA.

The DLF is comprised of fibers originating from several brainstem nuclei, which can be serotonergic, or 5-HT, from nerves located inside the nucleus raphe magnus, or NRM; dopaminergic neurons originating from ventral tegmental area, or VTA, and adrenergic neurons originating from the locus coeruleus, or LC. These descending fibers suppress noxious input in the nociceptive spinal cord neurons in laminae I, II, and V.

Opiate receptors have also been discovered in the dorsal horn of the spinal cord, chiefly in Rexed laminae I, II, and V, and such spinal opiate receptors mediate inhibitory effects on dorsal horn neurons transmitting nociceptive information. The action of morphine seems to be exerted equally in the spinal cord and brainstem nuclei, including the PAG and NRM. Systemic morphine acts on both brain stem and spinal cord opiate receptors to produce analgesia. Morphine binds the brainstem opiate receptors, which triggers the brainstem descending serotonergic pathway into the spinal cord as well as the DLF, and these have an opioid-mediated synapse at the level of the spinal cord.

This observation demonstrates that noxious stimuli, instead of non-noxious stimulus, determine the gate control theory, which are critical for the activation of the descending pain modulation circuit where pain inhibits pain via the descending DLF pathway. In addition, there are ascending connections in the PAG and the raphe nuclei into the PF-CM complex. These thalamic regions are a part of the ascending pain modulation at the diencephalon degree.

Stress Induced Analgesia (SIA)

Analgesia may be produced in certain stressful circumstances. Exposure to many different stressful or painful events generates an analgesic response. This phenomenon is known as stress induced analgesia, or SIA. Stress induced analgesia has been believed to give insight into the physiological and psychological factors that trigger endogenous pain control and opiate systems. By way of instance, soldiers injured in battle or athletes hurt in sports sometimes report that they don’t feel pain or discomfort during the battle or game, nevertheless, they will go through the pain afterwards once the specific situation has stopped. It’s been demonstrated in animals that electrical shocks cause stress-induced analgesia. Based on these experiments, it is assumed that the pressure the soldiers and the athletes experienced suppressed the pain which they would later experience.

It’s believed that endogenous opiates are produced in response to stress and inhibit pain by triggering the midbrain descending system. Furthermore, some SIA exhibited cross tolerance with opiate analgesia, which indicates that this SIA is mediated via opiate receptors. Experiments using different parameters of electrical shock stimulation demonstrate such stress induced analgesia and some of those anxieties that produce analgesia could be blocked by the opioid antagonist naloxone, whereas others were not blocked by naloxone. In conclusion, these observations lead to the decision that both opiate and non-opiate forms of SIA exist.

Somatovisceral Reflex

The somatovisceral reflex is a reflex in which visceral functions are activated or inhibited by somatic sensory stimulation. In experimental animals, both noxious and innocuous stimulation of somatic afferents are proven to evoke reflex changes in sympathetic efferent activity and, consequently, effector organ function. These phenomena have been shown in such regions as the gastrointestinal tract, urinary tract, adrenal medulla, lymphatic cells, heart and vessels of the brain and peripheral nerves.

Most frequently, incisions are elicited experimentally by stimulation of cutaneous afferents, even though some work has also been conducted on muscle and articular afferents, including those of spinal cells. The ultimate responses will represent the integration of multiple tonic and reflex influences and might exhibit laterality and segmental trends as well as variable excitability in line with the afferents involved. Given the complexity and multiplicity of mechanisms involved in the last expression of the reflex response, attempts to extrapolate to clinical situations should most likely be conducted in favor of further systematic physiological studies.

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.

EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Neurophysiology Of Pain | El Paso, TX. | Part II

by Dr Alex Jimenez | Clinical Neurophysiology

Neurophysiology: There are two ways that nociceptive information reaches the central nervous system. One is the neospinothalamic tract for quick pain and two is the paleospinothalamic tract for slow pain that increases.

Neurophysiology Of Pain Part II

Intensity, Location & Quality of Pain…

… involve Spinothalamic and Trigeminal Pathways

The trigeminal pathway brings information from the face area.
The spinothalamic pathway brings information from the rest of the body.
Both these pathways project to the sensory cortex, which also receives information on innocuous stimuli such as touch, pressure and warmth via a separate pathway.

2 Pain Transmission Pathways For Location Intensity Quality

Neuroscience Purves et al.

Spinothalamic pathway
(Anterolateral Pathway)
Trigeminal pathway

Unpleasant Quality & Autonomic Affective Motivational Pathway For Pain

Brain Areas Involved In Processing Of Nociceptive Signals

The Anterior Cingulate & Insula Cortex Are Activated In Human Subjects

… in connection with an intense burning sensation following hand contact with the thermal grill.

Adapted from Craig et al. 1994, 1996. From Principles of Neural Science, Kandell et al.

Control Of Pain Perception

There is difference between the objective and subjective aspects of injury and pain.
Despite similar injury, people can differ in how much pain they feel.
Depending on the context, pain may not be felt despite injury, e.g. battlefield injury, during intense sports.
This suggests that there is a physiological mechanism that controls the transmission of nociceptive signals to the brain or modifies the interpretation of pain.
The pain control system can also explain the placebo effect.

Pain Modulation Pathway

Nerve signals are sent form the somatic sensory cortex and hypothalamus to the periaqueductal gray matter (PAG).
PAG sends signals to the parabrachial nucleus, medullary reticular formation, locus coeruleus, and Raphe neulei.
These in turn can control the in the transmission of nociceptive signals from the spinal cord to the brain.
This involves different involves different neurotransmitters.

Endogenous Opioids

Internally produced molecules with opioid-like action which regulate transmission of nociceptive signals.

Three classes of these molecules have been identified. All are peptide molecules

Enkephalins
Endorphins
Dynorphins

Despite these being powerful, endogenous modifiers of nociceptive signals, it has been difficult to produce and administer them in a way than can used in clinical practice.

Location Of Nerve Cells With Endogenous Opioid Receptors

Spinal cord, Medulla, Periaqueductal gray matter (PAG)
In the spinal cord, endogenous opioids can prevent transmission between 1st order nerve cells (bringing signals from the periphery) and 2nd order spinal nerve cells that transmit the signals to the brain.
Also can prevent the increased synaptic efficiency, which plays a role in hyperalgesia.

(Center for Brain Research, Uni Vienna)

Modulation Of Pain Signal Transmission In The Spinal Cord

Connections in the spinal cord where opiates act.

Neurotransmitters � serotonin (5- HT) and norephinephrine (noradrenaline) � in the spinal cord can block transmission of pain signals to the brain.

Inflammatory Soup – Hyperalgesia

Tissue damage results in the release of a number of chemicals.
These increase nociceptors� response to a stimulus (=hyperalgesia) & produce inflammation.
Hyperalgesia = when the magnitude of the response to a nociceptive stimulus is higher than normal.

Julius-D & Basbaum-AI, Nature 2001;413:203

Clinical Application

Knowing the molecules involved in the �inflammatory soup� and how they are synthesized provides possible targets for pain reduction.
e.g. prostaglandins are produced by the COX enzyme. The activity of this enzyme is blocked by non-steroidal anti- inflammatory drugs (NSAIDs) such as ibuprofen, diclofenac.

Allodynia

A condition when normally non- painful stimuli cause pain, e.g., touch, light pressure, cold.
Involves changes in the synaptic sensitivity of the nociceptive neurons in the spinal cord (central sensitization).
Drugs such as ketamine, block NMDA receptors and so reduce transmisison of the nociceptive stimuli.

Gate Control Theory of Pain

Mother says to child, �Come I will rub the area which is painful and this will make it feel better.�
After stubbing a toe, we instinctively rub the area; this reduces the sensation of pain.
Ronald Melzack and Patrick Wall in 1962 provided an possible explanation for this effect.

Ascending Tracts | Pain Modulation: Gate Control Theory

Gate Theory

Rubbing the area that hurts stimulates receptors of innocuous stimuli like touch, pressure and vibration.

These mechano-receptors send signals along the A? nerve fibers that:

(1) stimulate spinal nerves (inhibitory inter-neurons) that in turn inhibit signaling in the 2nd order neurons (projection neuron) and (2) directly inhibit the 2nd order neuron to reduce or stop pain signal from being sent to the brain

wikidoc.org/images/f/fe/Gate_control_A_firing.png

Clinical Application

Transcutaneous Nerve Stimulation (TENS) is based on the Gate Control Theory. Nerves of the innocuous sensory system are stimulated and they in turn, inhibit transmission of nociceptive stimuli in the spinal cord.

Abnormalities Of Pain System

Phantom Pain

Patients with amputation often have burning or tingling pain in the body part removed.
One possible cause is that nerve fibers at the stump are stimulated and the brain interprets the signals as originating in the amputated portion.
The other is the rearrangement within the cortical areas so that area say for the hand now responds to signals from other parts of the body but still interprets them as coming for the amputated hand.

Peripheral Sensitization

Peripheral sensitization represents a reduction in the threshold and/or an increase in magnitude of responsiveness at the peripheral ends of sensory nerve fibers.
This occurs in response to chemical mediators released by nociceptors and non-neuronal cells (e.g. mast cells, basophils, platelets, macrophages, neutrophils, endothelial cells, keratinocytes and fibroblasts) at the site of tissue injury or inflammation.
Basically, it is an increased sensitivity to an afferent nerve stimuli.

Central Sensitization

Peripheral & Central Sensitisation

A condition of the nervous sytem that is associated with the development and maintenance of chronic pain.
Known as �wind-up� or persistent high reactivity.
�Plastiticity in pain pathways� or the persistence of pain even after an injury has healed.
Is this negative or positive plasticity?

Central Sensitization & C Fibers

Two Main Characteristics Of Central Sensitization:

� Allodynia � occurs when a person experiences pain with things that are normally not painful, ie, soft touch causes pain.

� Hyperalgesia � occurs when a stimulus that is typically painful is perceived as more painful that it should be, ie, a simple bump.

Both are due to hyperreactivity of the nervous system.

Somatosensory Cortex Organization

Cortical Reorganization

Neuroscience. 2nd edition. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Fig 25.14

Referred Pain

Often originates from a visceral organ.
May be felt in a part of the body remote from the site of the pathology.
The mechanisms may be spinal convergence of visceral and somatic afferent fibers on spinothalamic neurons.
Common manifestations: cutaneous and deep hyperalgesia, tenderness, muscular contractions.

Pain Sensation Referred From Visceral Organs …

… to another part of the body surface

Pain Hypersensitivity Mechanisms At A Glance

Neurophysiology Of Pain | El Paso, TX. | Part I

by Dr Alex Jimenez | Clinical Neurophysiology

Neurophysiology of pain: Pain�defined is the unpleasant sensation that accompanies injury or near injury to tissues, though it can also occur in the absence of such damage if the nociception system is not functioning. Nociception means the system that carries pain signals of injury from the tissues. This is the physiological incident that comes with pain.

Neurophysiology Of Pain

Objectives

Basics of the nervous system
Synaptic function
Nerve impulses
Transduction of peripheral painful stimuli
Central pathways
Central Sensitization
PeripheralSensitization
Control or modulation of pain signals
Pathophysiology of pain signaling pathway

Definition Of Pain

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”.

(The International Association for the Study of Pain)

The Nervous System

It is important to know the basic structure of the nervous system.
This will help in:
� Understanding the mechanism by which nociceptive signals are produced.
� Know the different regions of the nervous system involved in processing these signals.
� Learn how the different medications and treatment for pain management work.

Nervous System

Central nervous system (CNS)

Brain and Spinal Cord

Peripheral Nervous System (PNS)

Nerve fibers go to all parts of the body.
Send signals to the different tissues and send signals back to the CNS.

Nerve Cells

The nervous system is made up of nerve cells which send long processes (axons) to make contact with other cells.

Nerve Cell-To-Nerve Cell Communication

Nerve cells communicate with other cells by releasing a chemical from the nerve endings � Neurotransmitters

Basic Steps In Synaptic Transmission

Synaptic Transmission

Steps in the passage of signal from one nerve cell to other.

Drugs are used to block the transmission of signals from one nerve cell to other.

These drugs can effect:

Ca2+ ion channel to prevent Ca2+ inflow which is essential for neurotransmitter (NT) release, e.g., the action of gabapentin.
Release of NT.
Prevent NT from binding to its receptor so stop further transmission of the signal.

Electrical Impulse

Signals move along a nerve process (axon) as a wave of membrane depolarization called the Action Potential.
The inside of all nerve cells has a negative electrical potential of around � 60 mV.
When stimulated this negative electrical potential becomes positive and then negative again in milliseconds.
The action potential moves along the nerve process (axon) to the nerve ending where it cause release of NT.

Action Potential

When there is no stimulation the membrane potential is at its Resting Potential.
When stimulated, channels in the nerve membrane open allowing the flow of sodium ions (Na+) or calcium ions (Ca2+) into the nerve or cell. This makes the inside less negative and in fact positive -the peak of the action potential (+40 mV).
These channels than close and by the opening of K+ channels the membrane potential returns to its resting level.

Stopping Action Potentials To Stop Nociceptive Stimuli

Nociceptive stimuli are those that will create a sensation of pain after they are processed in the CNS.
Nociceptive signals can be prevented from reaching the CNS by blocking the action of the channels that control the movement of ions across the nerve membrane.
A number of anesthetic agents stop Na+ channel from working and hence stop the generation of actions potentials and transmission of signals to the CNS.

Sensory Systems

The sensory system that can be divided into two divisions:

A Sensory System that transmits innocuous stimuli such as touch, pressure, warmth.
A System that transmits stimuli that indicate that tissues have been damaged = nociceptive .

These two systems have different receptors and pathways in the PNS & CNS

Skin Receptors

Neuroscience. 2nd edition. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001.

Nociceptors

Nociceptors are free nerve endings that respond to stimuli that can cause tissue damage or when tissue damage has taken place.
Present in membrane of free nerve endings are receptors (protein molecules) whose activity changes in the presence of painful stimuli.
(Note the use of the same term receptor is used for cell or organs or molecules that involved in transduction of a stimuli.)

Transduction

Transduction is the process of converting the stimuli into a nerve impulse.
For this to occur the flow of ions across the nerve membrane has to change to allow entry of either Na+ or Ca2+ ions to cause depolarization of the membrane potential.
This involves a receptor molecule that either directly or indirectly opens the ion channels.

Chemical Agents…

… which can cause the membrane potential at the free nerve ending (nociceptor) to produce an action potential.

Fields HL. 1987. Pain. New York: McGraw-Hill.

Summary Of Transduction Process At The Periphery

TRP Channels

Many stimuli � mechanical, chemical and thermal � give rise to painful sensation making transduction a complex process.
Recently receptor molecules have been identified�� Transient Receptor Potential (TRP) channels � that respond to a number of strong stimuli.
TRP receptors are also involved in transmitting the burning sensation of chili pepper.
In time, drugs that act on these receptors will be developed to control pain.

Different TRP Channels

Capsasin, the active ingredient in chili pepper, is used in patches for relief of pain.
Menthol and peppermint gels are used to relieve muscle pain.

Motor Output & Sensory Input To Spinal Cord

Sensory nerves have their cell body outside the spinal cord in the dorsal root ganglia ( = 1st order neurons).
One process goes to the periphery, the other goes to the spinal cord where it makes synaptic contact with nerve cells in the spinal cord ( = 2nd order neurons).
The 2nd order neuron sends processes to other nerve cells in the spinal cord and to the brain.

2nd Order Nerve Cells Send Nerve Fibers In The Spinal Cord White Matter

Transmission Of Nociceptive Signals From The Periphery To The Brain

Silverthorn

A Delta (?) & C Nerve Fibers

Nerve fibers are classified according to the:

� (1) diameter of the nerve fiber and
� (2) whether myelinated or not.

A? and C nerve fiber endings respond to strong stimuli.
A? are myelinated and C are not.
Action potentials are transmitted 10 times faster in the A?
(20 m/sec) fibers than in C fibers (2 m/sec).

A? & C fibers

A? fibers respond mainly to mechanical and mechno-thermal stimuli.
C fibers are polymodal, i.e. the nerve ending responds to several modalities � thermal, mechanical and chemical
This polymodal ability is due to the presence of different receptor molecules in a single nerve ending.

Fast & Slow Pain

Most people when they are hit by an object or scrape their skin, feel a sharp first pain (epicritic) followed by a second dull, aching, longer lasting pain (protopathic).
The first fast pain is transmitted by the myelinated A? fibers and the second pain by the unmyelinated C fibers.

Central Pain Pathways

Nociceptive signals are sent to the spinal cord and then to different parts of the brain where sensation of pain is processed.

There are a pathways/regions for assessing the:

Location, intensity, and quality of the noxious stimuli
Unpleasantness and autonomic activation (fight-or-flight response, depression, anxiety).

Dr. Sletten Discussing Central Sensitization Syndrome (CSS)

Gate Control Theory and Pain Management in El Paso, TX

by Dr Alex Jimenez | Chiropractic, Chronic Pain, Clinical Neurophysiology, Treatments

Pain perception varies across different people based on their mood, psychological condition and previous experience, even when pain is brought on by similar physical stimulation and ends in a similar level of damage. In 1965, Ronald Melzack and Patrick Wall summarized a scientific theory about the psychological influence on pain perception; known as the gate control theory.

If it wasn’t for this theory, pain perception would still be connected to the intensity of the pain stimulation and the degree of damage caused to the affected tissue. But Melzack and Wall made it clear that pain perception is far more complicated than we believe.

Based on the gate control theory, pain signals aren’t free to travel to the brain as soon as they’re generated in the region of the damaged or injured tissues. These first need to encounter specific neural gates found at the level of the spinal cord level, where these gates ascertain whether the pain signals should reach the brain or not. To put it differently, pain is perceived when the gate gives way to the pain signals and it is not as intense or it is not sensed at all when the gate closes for the signs to pass through.

This theory provides the explanation for why people find relief by massaging or rubbing a damage, injured or painful site. Although the gate control theory cannot demonstrate the whole picture of the fundamental system which underlies pain, it’s visualized the mechanism of pain perception and it has created a pathway to various pain management treatment approaches.

Nerve Fibers in Transmission of Sensory Signals

Every organ, or portion of the human body, has its own nerve supply which are in charge of carrying electric impulses generated in reaction to several senses, such as touch, temperature, pressure and pain. These nerves, which make up the peripheral nervous system, transmit these sensory signals, to the central nervous system, or the brain and the spinal cord. These impulses are then translated and perceived as senses. The peripheral nerves send signals to the dorsal horn of the spinal cord and from there, the sensory signals are transmitted into the brain through the spinothalamic tract. Pain is a sensation which alarms a person that a tissue or certain portion of the human body has been damaged or injured.

Due to their axonal diameter and their conduction speed, nerve fibers can be categorized into three different types, nerve fibers A, B and C. The C fibers are considered to be the smallest among the three different types. Moreover, there are four subtypes within the A fibers: A-alpha, A-beta, A-gamma and A-delta. From the A fiber subtypes, the A-alpha fibers are the largest and the A-delta fibers are the smallest.

The A fibers which are larger compared to the A-delta fibers, carry sensations, such as touch, pressure, etc., into the spinal cord. The A-delta fibers as well as the C fibers carry pain signals into the spinal cord. A-delta fibers are faster and carry sharp pain signals while the C fibers are slower and carry diffuse pain signals.

When thinking about that the conduction velocity of nerve fibers, the A-alpha fibers, which are the biggest A nerve fibers, have greater conduction speed compared to A-delta fibers and C fibers, which are considered to be the smallest nerve pathways. When a tissue is damaged or injured, the A-delta fibers are activated first, followed by the activation of the C fibers. These nerve fibers have a tendency to carry the pain signals to the spinal cord and then to the brain. However, the pain signals are transmitted through a much more complex process than what is simply explained above.

Ascending Tracts | Pain Modulation: Gate Control Theory

What is the Gate Control Theory of Pain?

The gate control theory implies that the sensory signals or impulses which are transmitted by the nerve fibers encounter neural gates at the level of the spinal cord and these will need to get cleared through those gates to reach the brain. Various factors determine how the pain signals ought to be treated in the neurological gates, including:

The intensity of the pain signals
The degree of another sensory signal, such as touch, temperature and pressure, if produced at the site of damage or injury
The message from the brain itself to deliver the pain signals or not

As previously mentioned, the nerve fibers, both large and small, carrying the sensory signals, end in the dorsal horn of the spinal cord from where the impulses are transmitted into the brain. According to the original postulate of Melzack and Wall, the nerve fibers project to the substantia gelatinosa, or SG, of the dorsal horn and the initial central transmission (T) cells of the spinal cord. The SG consists of inhibitory interneurons that behave as the gate and ascertain which sensory signals should get to the T cells then go further throughout the spinothalamic tract to finally reach the brain.

When the pain signals carried by the small nerve fibers, or the A-delta fibers and the C fibers, are somewhat less intense compared to another non-pain sensory signal like touch, temperature and pressure, the inhibitory neurons stop the transmission of the pain signals through the T cells. The non-pain signals override the pain signals and therefore the pain is not perceived by the brain. When the pain signals are somewhat more intense compared to the non-pain signals, the inhibitory neurons are inactivated and the gate is opened. The T cells transmit the pain signals into the spinothalamic tract which carries those impulses to the brain. As a result, the neurological gate is influenced by the relative amount of activity from the large and the small nerve fibers.

How Emotions and Thoughts Affect Pain

The gate control theory also suggests that the pain signal transmission could be affected by thoughts and emotions. It’s well known that people do not feel that a chronic pain or, more appropriately, the pain does not disturb them if they concentrate on other activities which interest them. Whereas, people who are depressed or anxious may often feel intense pain and can also find it challenging to cope with. This is due to the fact that the brain sends messages through descending nerve fibers which stop, reduce or enhance the transmission of pain signals through the gate, depending on the emotions and thoughts someone may be going through.

Gate Control Theory in Pain Management

The gate control theory has caused a radical revolution within the field of pain management. The theory suggested that pain management can be accomplished by influencing the larger nerve fibers that carry non-pain stimulation. The concept has also paved way for more research on cognitive and behavioral strategies to achieve pain relief.

Among the most tremendous advances in pain management research is the arrival of Transcutaneous Electrical Nerve Stimulation (TENS). The gate control theory forms the cornerstone of TENS. In this procedure, the selective stimulation of the large diameter nerve fibers taking non-pain sensory stimulation from a particular region nullifies or reduces the impact of pain signals from the region. TENS is a non-invasive and affordable pain control strategy that has been widely used for the treatment of chronic and intractable pain by various healthcare professionals, which may otherwise have been non-responsive to analgesics and surgical interventions. TENS is tremendously advantageous over pain drugs from the aspect that it does not have the problem of medication interactions and toxicity.

For instance, many doctors of chiropractic, or chiropractors, utilize TENS and other electrotherapeutic procedures in their practice. These are generally utilized along with spinal adjustments and manual manipulations to increase circulation as well as to aid in the support of chiropractic care. Several other invasive and noninvasive electrical stimulation techniques are discovered to be helpful in several chronic pain conditions such as arthritic pain, diabetic neuropathy, fibromyalgia, etc.. The theory has also been extensively studied in treating chronic back pain and cancer pain. However, favorable results are not attained in some conditions and the long term efficacy of these techniques based on the theory still remains under consideration.

Dr. Alex Jimenez’s Insight

Chiropractic care is widely utilized to benefit patients with chronic pain. Symptoms of persistent pain and discomfort have become a big health issue in the United States where many years of research have found that drugs and/or medications are not necessarily a solution to the problem. The gate control theory, which was first proposed over half a century ago, has offered healthcare professionals new insights on the perception of pain, providing a variety of pain management treatment methods, such as the use of transcutaneous electrical nerve stimulation, or TENS, as well as other electrotherapeutic procedures. Chiropractors can help with pain management through spinal adjustments and manual manipulations, and through the use of TENS.

Nevertheless, the gate control theory has radically revolutionized the area of pain research and it has achieved to get numerous studies which aim at presenting a pain-free lifestyle into the patients who suffer from chronic pain. 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

EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

What is Central Sensitization? | El Paso, TX Chiropractor

by Dr Alex Jimenez | Chiropractic, Clinical Neurophysiology

Central sensitization is a state of the nervous system that’s related to the development and maintenance of chronic pain. When central sensitization occurs, the nervous system goes through a procedure known as wind-up and gets regulated in a constant condition of increased reactivity. This persistent, or regulated, state of reactivity decreases the threshold for what causes pain and subsequently learns to keep pain after the initial injury has healed. Central sensitization has two major characteristics. Both have an increased sensitivity to pain and to the feeling of touch. These are referred to as allodynia and hyperalgesia.

Allodynia occurs when an individual experiences pain with circumstances that are normally not supposed to be painful. For instance, chronic pain patients often experience pain even with things as simple as touch or a massage. In these situations, nerves in the region which has been touched sends signals through the nervous system into the brain. Because the nervous system is in a constant condition of heightened reactivity, the brain doesn’t generate a mild feeling of touch as it should, given that the stimulus that initiated it was an easy touch or massage. Instead, the brain produces a feeling of pain and discomfort.

Hyperalgesia occurs when a stimulus that’s usually considered to be somewhat painful is perceived as a much more debilitating pain than it ought to be. For instance, chronic pain patients that experience a simple bump, which generally would be mildly painful, will often feel intense pain. Again, once the nervous system is in a constant condition of high reactivity, it amplifies pain.

Peripheral and Central Sensitization

Chronic pain patients sometimes believe they might be suffering from a mental health issue because they understand from common sense that touch or simple bumps produce tremendous amounts of pain or discomfort. Other times, it’s not the patients themselves who feel this way, but their friends and family members. Individuals who don’t suffer with chronic pain may witness others who have central sensitization experience pain at the slightest touch or cry out at the simplest bump. However, because they don’t have the condition, it may be difficult for them to understand what someone who does is going through.

In addition to allodynia and hyperalgesia, central sensitization has other well-known features, though they may occur less commonly. Central sensitization may lead to heightened sensitivities throughout all senses, not only the feeling of touch. Chronic pain patients can sometimes report sensitivities to light, smell and sound. As such, regular levels of light may seem overly bright or even the perfume aisle in the department shop can produce a headache. Central sensitization can also be associated with cognitive deficits, such as poor concentration and poor short-term memory. Central sensitization also interferes with increased levels of psychological distress, particularly fear and axiety. After all, the nervous system is responsible for not merely senses, like pain, but also emotions. If the nervous system is trapped in a constant condition of reactivity, patients are going to be nervous or anxious. Lastly, central sensitization is also correlated with sick role behaviors, such as resting and malaise, and pain behavior.

Central sensitization has long been known as a potential consequence of stroke and spinal cord injury. However, it is increasingly believed that it plays a part in several different chronic pain disorders. It may happen with chronic low back pain, chronic neck pain, whiplash injuries, chronic tension headaches, migraine headaches, rheumatoid arthritis, osteoarthritis of the knee, endometriosis, injuries sustained in an automobile accident, and even following surgeries. Fibromyalgia, irritable bowel syndrome, and chronic fatigue syndrome, all appear to occur due to central sensitization as well.

Central Sensitization and C Fibers

What Causes Central Sensitization?

Central sensitization involves specific changes to the nervous system. Changes in the dorsal horn of the spinal cord and in the brain occur, particularly at the cellular level, such as at the receptor sites. As mentioned previously, it has long been proven that fractures and spinal cord injuries can cause central sensitization. It stands to reason. Strokes and spinal cord injuries cause harm to the central nervous system, including the brain, in the event of strokes, and the spinal cord, in the case of spinal cord injuries. These injuries change the sections of the nervous system which are involved in central sensitization.

However, what about the other, more prevalent, types of chronic pain disorders, recorded above, such as headaches, chronic back pain, or pain in the extremities? The accidents or conditions which lead to these kinds of chronic pain are not direct injuries to the brain or spinal cord. Rather, they include injuries or condition which affect the peripheral nervous system, particularly in that are of the nervous system which lies outside the spinal cord and brain. How can health issues associated with the peripheral nervous system contribute to modifications in the central nervous system and cause chronic pain in the isolated area of the initial injury? In summary, how can isolated migraine headaches eventually become chronic daily headaches? How can an acute low back lifting injury become chronic low back pain? How does an injury to the hand or foot turn into a complex regional pain syndrome?

There are probably multiple factors that cause the development of central sensitization in these ‘peripheral’ chronic pain disorders. These variables may be divided into two classes:

Factors that are associated with the state of the central nervous system before onset of the initial pain or injury condition
Factors that are associated with the central nervous system following onset of the initial pain or injury condition

The first group involves those factors that might predispose individuals to developing central sensitization once an accident occurs and the next group involves antecedent factors that boost central sensitization once pain begins.

Dr. Alex Jimenez’s Insight

Chronic pain can often modify the way the central nervous system itself functions, so much so that a patient may become more sensitive to pain with less provocation. This is what’s referred to as central sensitization and it generally involves changes in the central nervous system, or CNS, more specifically, in the brain and the spinal cord. Central sensitization has been associated with several common diseases and it’s even been reported to develop with something as simple as a muscle ache. Central sensitization has also been documented to persist and worsen even in the absence of obvious provocation. Several factors have also been attributed with the development of central sensitization, although the true cause is still unknown.

Predisposing Factors for Central Sensitization

There are probably biological, emotional, and environmental predisposing factors for central sensitization. Low and higher sensitivity to pain, or pain thresholds, are perhaps in part due to numerous genetic factors. While there’s absolutely no research as of yet to support a causal link between pre-existing pain thresholds and following development of central sensitization after an incident, it’s largely assumed that it will be eventually found.

Psychophysiological factors, like the stress-response, are also apt to play a part in the development of central sensitization. Direct experimental evidence on animals and humans, as well as prospective studies on humans, have demonstrated a connection between stress and the decrease of pain thresholds. Similarly, different kinds of pre-existing anxiety about pain is consistently related to higher pain sensitivities. All these psychophysiological aspects suggest that the preexisting state of the nervous system is also an important determinant of creating central sensitization after the onset of pain. If the stress response has made the nervous system responsive prior to injury, then the nervous system might be more prone to become sensitized once onset of pain happens.

There is considerable indirect evidence for this theory as well. A prior history of anxiety, physical and psychological trauma, and depression are predictive of onset of chronic pain later in life. The most common denominator between chronic pain, anxiety, nervousness, injury, and depression, is the nervous system. They’re all states of the nervous system, especially a persistently changed, or dysregulated, nervous system.

It’s not that such pre-existing health issues make individuals more vulnerable to injury or the onset of illness, as injury or illness is apt to happen on a somewhat random basis across the populace. Instead, these pre-existing health issues are more inclined to make people prone to the development of chronic pain once an injury or disease occurs. The dysregulated nervous system, at the time of injury, for instance, may interfere with the normal trajectory of healing and thereby stop pain from subsiding once tissue damage is healed.

Factors Resulting in Central Sensitization After Onset of Pain

Predisposing factors may also be part of the development of central sensitization. The onset of pain is frequently associated with subsequent development of conditions, such as depression, fear-avoidance, nervousness or anxiety and other phobias. The stress of those responses can, in turn, further exacerbate the reactivity of the nervous system, leading to central sensitization.�Inadequate sleep is also a frequent effect of living with chronic pain. It’s associated with increased sensitivity to pain as well. In what’s technically known as operant learning, interpersonal and environmental reinforcements have long been proven to lead to pain behaviors, however, it is also evident that such reinforcements may lead to the development of central sensitization.

Mayo Clinic Discusses Central Sensitization

Treatments of Central Sensitization

Treatments for chronic pain syndromes that involve fundamental sensitization typically target the central nervous system or the inflammation which corresponds with central sensitization. All these often generally include antidepressants and anticonvulsant medications, and cognitive behavioral treatment. While usually not considered to target the central nervous system, regular mild aerobic exercise changes structures in the central nervous system and contributes to reductions in the pain of many ailments which are mediated by central sensitization. As such, moderate aerobic exercise is used to treat chronic pain syndromes marked by central sensitization. Non-steroidal anti-inflammatories are utilized for the inflammation associated with central sensitization.

Finally, chronic pain rehabilitation programs are a standard, interdisciplinary treatment that employs each of the above-noted therapy strategies in a coordinated manner. They also make the most of the research on the role of operant learning from central sensitization and also have developed behavioral interventions to reduce the pain and discomfort associated with the health issue. Such applications are typically considered the most effective treatment option for chronic pain syndromes.�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

blog picture of cartoon paperboy big news

EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Blank

References

1.�Phillips, K. & Clauw, D. J. (2011). Central pain mechanisms in chronic pain states � maybe it is all in their head.�Best Practice Research in Clinical Rheumatology, 25, 141-154.

2.�Yunus, M. B. (2007). The role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain.�Best Practice Research in Clinical Rheumatology, 21, 481-497.

3.�Curatolo, M., Arendt-Nielsen, L., & Petersen-Felix, S. (2006). Central hypersensitivity in chronic pain: Mechanisms and clinical implications.�Physical Medicine and Rehabilitation Clinics of North America, 17, 287-302.

4.�Wieseler-Frank, J., Maier, S. F., & Watkins, L. R. (2005). Immune-to-brain communication dynamically modulates pain: Physiological and pathological consequences.�Brain, Behavior, & Immunity, 19, 104-111.

5.�Meeus M., & Nijs, J. (2007). Central sensitization: A biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome.�Clinical Journal of Rheumatology, 26, 465-473.

6. Melzack, R., Coderre, T. J., Kat, J., & Vaccarino, A. L. (2001). Central neuroplasticity and pathological pain.�Annals of the New York Academy of Sciences, 933, 157-174.

7.�Flor, H., Braun, C., Elbert, T., & Birbaumer, N. (1997). Extensive reorganization of primary somatosensory cortex in chronic back pain patients.�Neuroscience Letters, 224, 5-8.

8. O�Neill, S., Manniche, C., Graven-Nielsen, T., Arendt-Nielsen, L. (2007). Generalized deep-tissue hyperalgesia in patients with chronic low-back pain.�European Journal of Pain, 11, 415-420.

9.�Chua, N. H., Van Suijlekom, H. A., Vissers, K. C., Arendt-Nielsen, L., & Wilder-Smith, O. H. (2011). Differences in sensory processing between chronic cervical zygapophysial joint pain patients with and without cervicogenic headache.�Cephalalgia, 31, 953-963.

10.�Banic, B, Petersen-Felix, S., Andersen O. K., Radanov, B. P., Villiger, P. M., Arendt-Nielsen, L., & Curatolo, M. (2004). Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and fibromyalgia.�Pain, 107, 7-15.

11.�Bendtsen, L. (2000). Central sensitization in tension-type headaches � possible pathophysiological mechanisms.�Cephalalgia, 20, 486-508.

12. Coppola, G., DiLorenzo, C., Schoenen, J. & Peirelli, F. (2013). Habituation and sensitization in primary headaches. Journal of Headache and Pain, 14, 65.

13.�Stankewitz, A., & May, A. (2009). The phenomenon of changes in cortical excitability in migraine is not migraine-specific � A unifying thesis.�Pain, 145, 14-17.

14.�Meeus M., Vervisch, S., De Clerck, L. S., Moorkens, G., Hans, G., & Nijs, J. (2012). Central sensitization in patients with rheumatoid arthritis: A systematic literature review.�Seminars in Arthritis & Rheumatism, 41, 556-567.

15.�Arendt-Nielsen, L., Nie, H., Laursen M. B., Laursen, B. S., Madeleine P., Simonson O. H., & Graven-Nielsen, T. (2010). Sensitization in patients with painful knee osteoarthritis.�Pain, 149, 573-581.

16.�Bajaj, P., Bajaj, P., Madsen, H., & Arendt-Nielsen, L. (2003). Endometriosis is associated with central sensitization: A psychophysical controlled study.�The Journal of Pain, 4, 372-380.

17.�McLean, S., Clauw, D. J., Abelson, J. L., & Liberzon, I. (2005). The development of persistent pain and psychological morbidity after motor vehicle collision: Integrating the potential role of stress response systems into a biopsychosocial model.�Psychosomatic Medicine, 67, 783-790.

18.�Fernandez-Lao, Cantarero-Villanueva, I., Fernandez-de-Las-Penas, C, Del-Moral-Avila, R., Arendt-Nielsen, L., Arroyo-Morales, M. (2010). Myofascial trigger points in neck and shoulder muscles and widespread pressure pain hypersensitivity in patients with post-mastectomy pain: Evidence of peripheral and central sensitization.�Clinical Journal of Pain, 26, 798-806.

19.�Staud, R. (2006). Biology and therapy of fibromyalgia: Pain in fibromyalgia syndrome.�Arthritis Research and Therapy, 8, 208.

20. Verne, V. N., & Price, D. D. (2002). Irritable bowel syndrome as a common precipitant of central sensitization.�Current Rheumatology Reports, 4, 322-328.

21.�Meeus M., & Nijs, J. (2007). Central sensitization: A biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome.�Clinical Journal of Rheumatology, 26, 465-473.

22.�Schwartzman, R. J., Grothusen, R. J., Kiefer, T. R., & Rohr, P. (2001). Neuropathic central pain: Epidemiology, etiology, and treatment options.�Archives of Neurology, 58, 1547-1550.

23.�Alexander, J., DeVries, A., Kigerl, K., Dahlman, J., & Popovich, P. (2009). Stress exacerbates neuropathic pain via glucocorticoid and NMDA receptor activation.�Brain, Behavior and Immunity, 23, 851-860.

24. Imbe, H., Iwai-Liao, Y., & Senba, E. (2006). Stress-induced hyperalgesia: Animal models and putative mechanisms.�Frontiers in Bioscience, 11, 2179-2192.

25. Kuehl, L. �K., Michaux, G. �P., Richter, S., Schachinger, H., & Anton F. (2010). Increased basal mechanical sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.�Pain, 194, 539-546.

26. Rivat, C., Becker, C., Blugeot, A., Zeau, B., Mauborgne, A., Pohl, M., & Benoliel, J. (2010). Chronic stress induces transient spinal neuroinflammation, triggering sensory hypersensitivity and long-lasting anxiety-induced hyperalgesia.�Pain, 150, 358-368.

27.�Slade, G. D., Diatchenko, L., Bhalang, K., Sigurdsson, A., Fillingim, R. B., Belfer, I., Max, M. B., Goldman, D., & Maixner, W. (2007). Influence of psychological factors on risk of temporomandibular disorders.�Journal of Dental Research, 86, 1120-1125.

28.�Hirsh, A. T., George, S. Z., Bialosky, J. E., & Robinson, M. E. (2008). Fear of pain, pain catastrophizing, and acute pain perception: Relative prediction and timing of assessment.�Journal of Pain, 9, 806-812.

29. Sullivan, M. J. Thorn, B., Rodgers, W., & Ward, L. C. (2004). Path model of psychological antecedents to pain experience: Experimental and clinical findings.�Clinical Journal of Pain, 20, 164-173.

30.�Nahit, E. S., Hunt, I. M., Lunt, M., Dunn, G., Silman, A. J., & Macfarlane, G. J. (2003). Effects of psychosocial and individual psychological factors on the onset of musculoskeletal pain: Common and site-specific effects.�Annals of Rheumatic Disease, 62, 755-760.

31. Talbot, N. L., Chapman, B., Conwell, Y., McCollumn, K., Franus, N., Cotescu, S., & Duberstein, P. R. (2009). Childhood sexual abuse is associated with physical illness burden and functioning in psychiatric patients 50 years of age or older.�Psychosomatic Medicine, 71, 417-422.

32. McLean, S. A., Clauw, D. J., Abelson, J. L., & Liberzon, I. (2005). The development of persistent pain and psychological morbidity after motor vehicle collision: Integrating the potential role of stress response systems into a biopsychosocial model.�Psychosomatic Medicine, 67, 783-790.

33. Hauser, W., Galek, A., Erbsloh-Moller, B., Kollner, V., Kuhn-Becker, H., Langhorst, J… & Glaesmer, H. (2013). Posttraumatic stress disorder in fibromyalgia syndrome: Prevalence, temporal relationship between posttraumatic stress and fibromyalgia symptoms and impact on clinical outcome.�Pain, 154, 1216-1223.

34.�Diatchenko, L., Nackley, A. G., Slade, G. D., Fillingim, R. B., & Maixner, W. (2006). Idiopathic pain disorders � Pathways of vulnerability.�Pain, 123, 226-230.

35.�Azevedo, E., Manzano, G. M., Silva, A., Martins, R., Andersen, M. L., & Tufik, S. (2011). The effects of total and REM sleep deprivation on laser-invoked potential threshold and pain perception.�Pain, 152, 2052-2058.

36. Chiu, Y. H., Silman, A. J., Macfarlane, G. J., Ray, D., Gupta, A., Dickens, C., Morris, R., & McBeth, J. (2005). Poor sleep and depression are independently associated with a reduced pain threshold: Results of a population based study.�Pain, 115, 316-321.

37.�Holzl, R., Kleinbohl, D. & Huse, E. (2005). Implicit operant learning of pain sensitization.�Pain, 115, 12-20.

38. Baumbauer, K. M., Young, E. E., & Joynes, R. L. (2009). Pain and learning in spinal system: Contradictory outcomes from common origins.�Brain Research Reviews, 61, 124-143.

39. Becker, S., Kleinbohl, D., Baus, D., & Holzl, R. (2011). Operant learning of perceptual sensitization and habituation is impaired in fibromyalgia patients with and without irritable bowel syndrome.�Pain, 152, 1408-1417.

40.�Hauser, W., Wolfe, F., Tolle, T., Uceyler, N. & Sommer, C. (2012). The role of antidepressants in the management of fibromyalgia: A systematic review and meta-analysis.�CNS Drugs, 26, 297-307.

41.�Hauser, W., Bernardy, K., Uceyler, N., & Sommer, C. (2009). Treatment of fibromyalgia syndrome with gabapentin and pregabalin � A meta-analysis of randomized controlled trials.�Pain, 145, 169-181.

42. Straube, S., Derry, S., Moore, R. A., & McQuay, H. J. (2010). Pregabalin in fibromyalgia: Meta-analysis of efficacy and safety from company clinical trial reports.�Rheumatology, 49, 706-715.

43. Tzellos, T. G., Toulis, K. A., Goulis, D. G., Papazisis, G., Zampellis, Z. A., Vakfari, A., & Kouvelas, D. (2010). Gabapentin and pregabalin in the treatment of fibromyalgia: A systematic review and meta-analysis.�Journal of Clinical Pharmacy and Therapeutics, 35, 639-656.

44.�Thieme, K. Flor, H., & Turk, D. C. (2006). Psychological pain treatment in fibromyalgia syndrome: Efficacy of operant behavioral and cognitive behavioral treatments.�Arthritis Research & Therapy, 8, R121.

45. Lackner, J. M., Mesmer, C., Morley, S., Dowzer, C., & Hamilton, S. (2004). Psychological treatments for irritable bowel syndrome: A systematic review and meta-analysis.�Journal of Clinical and Consulting Psychology, 72, 1100-1113.

46. Salomons, T. V., Moayedi, M. Erpelding, N., & Davis, K. D. (2014). A brief cognitive-behavioral intervention for pain reduces secondary hyperalgesia. Pain, 155, 1446-1452. doi: 10.1016/j.pain.2014,02.012

47.�Erickson, K. I., Voss., M. W., Prakesh, R. S., et al. (2011). Exercise training increases size of hippocampus and improves memory.�Proceedings of the National Academy of Sciences, 108, 3017-3022.

48. Hilman, C. H., Erickson, K. I., & Kramer, A. F. (2008). Be smart, exercise your heart: Exercise effects on brain and cognition.�Nature Reviews Neuroscience, 9, 58-65.

49.�Busch, A. J., Barber, K. A., Overend, T. J., Peloso, P. M., & Schachter, C. L. (Updated August 17, 2007). Exercise for treating fibromyalgia. In Cochrane Database Reviews, 2007, (4). Retrieved May 16, 2011, from The Cochrane Library, Wiley Interscience.

50.�Fordyce, W. E., Fowler, R. S., Lehmann, J. F., Delateur, B. J., Sand, P. L., & Trieschmann, R. B. (1973). Operant conditioning in the treatment of chronic pain.�Archives of Physical Medicine and Rehabilitation, 54, 399-408.

51. Gatzounis, R., Schrooten, M. G., Crombez, G., & Vlaeyen, J. W. (2012). Operant learning theory in pain and chronic pain rehabilitation.�Current Pain and Headache Reports, 16, 117-126.

52.�Hauser, W., Bernardy, K., Arnold, B., Offenbacher, M., & Schiltenwolf, M. (2009). Efficacy of multicomponent treatment in fibromyalgia syndrome: A meta-analysis of randomized controlled clinical trials.�Arthritis & Rheumatism, 61, 216-224.

53. Flor, H., Fydrich, T. & Turk, D. C. (1992). Efficacy of multidisciplinary pain treatment centers: A meta-analytic review.�Pain, 49, 221-230.

54. Gatchel, R., J., & Okifuji, A. (2006). Evidence-based scientific data documenting the treatment and cost-effectiveness of comprehensive pain programs for chronic non-malignant pain.�Journal of Pain, 7, 779-793.

55. Turk, D. C. (2002). Clinical effectiveness and cost-effectiveness of treatments for patients with chronic pain.�The Clinical Journal of Pain, 18, 355-365.

Close Accordion

ART and PNF Treatment for Sciatica in El Paso, TX

by Dr Alex Jimenez | Chiropractic, Clinical Neurophysiology, Sciatica, Sciatica Nerve Pain, Treatments

Low back pain occurs due to a variety of causes, which is why it is often poorly diagnosed and treated. As there are many mechanisms by which lower back pain happens, such as trauma, overuse from weight lifting for example, and repetitive motion, it’s important to mention that this article will only focus on sciatic nerve pain, or sciatica.

Sciatica refers to pain and other symptoms which radiate or travel down the leg, associated with numbness, tingling or burning sensations, and weakness in one or both lower extremities. Many patients complain of sharp, intense pain and discomfort when sitting and driving, affecting their capacity to bear weight properly when one has to walk or move. Their pain can shoot down the length of the sciatic nerve, into the buttocks, down the back of the leg, into the calf, and lastly, into the ankle and foot. The sciatic nerve, which is the longest nerve in the body, can become compressed or entrapped by certain muscles leading to sciatica.

Based on the location of this impingement, the individual will present with a variety of symptoms. If the health issue is diagnosed to originate in the low back, then the problem normally occurs around the hole in which the nerve exits the spine, resulting in symptoms surrounding the entire lower extremity. If the health issue is correctly diagnosed to originate from the buttocks, it most often includes the piriformis muscle because the sciatic nerve travels beneath it as it makes its way down the length of the leg. The source of this type of sciatica may involve different muscles just below the piriformis, otherwise known as a group of muscles called the hip rotators.

If the health issue is not in the lower back, or buttocks, then the problem is very likely to have occurred in the hamstrings, primarily at one of the muscles where the plantar nerve divides the hamstrings at the back of the thigh. The sciatic nerve may also manifest symptoms when compressed in the calf, however, these symptoms will often only be reported below the knee.

ART and PNF Treatment for Sciatic Nerve Pain

In regards to treatment, sciatica can be worked out by performing active release techniques, or ART, through the release of the entire nerve where it is being compressed. The objective when using ART for sciatic nerve pain would be to maneuver the nerve while trapping the muscle(s) in their own position. The nerve is then pulled from beneath the muscle. Also, using rehabilitation exercises through specific stretches and strengthening exercises of the muscle groups involved may allow for faster healing alongside chiropractic care to boost the communication between the spine and the positioning of the nerve entrapment/compression.

One of the most common stretching methods for sciatica is PNF or proprioceptive neuromuscular facilitation. PNF is a sort of stretch that produces a rebound relaxation of the muscle. PNF is a more advanced kind of flexibility training that involves both the contraction and stretching of the muscle group being targeted. PNF is a stretching technique utilized to increase range of motion and flexibility. PNF increases range of motion by increasing the length of the muscle and increasing neuromuscular efficiency. PNF stretching has been found to increase ROM in trained, as well as untrained, individuals. Effects can last 90 minutes or more after the stretching has been completed. PNF stretching was initially created as a form of rehabilitation, and to that effect, it is very effective. It’s also excellent for targeting specific muscle groups as well as increasing flexibility and enhancing muscle power and strength.

Four theoretical physiological mechanisms for increasing range of motion were identified using PNF stretching: autogenic inhibition, reciprocal inhibition, stress relaxation, and the gate control theory.�Autogenic Inhibition is what occurs in a contracted or stretched muscle in the form of a decrease in the excitability because of inhibitory signals sent from the same muscle.�Reciprocal inhibition is what occurs in the TM when the opposing muscle is contracted voluntarily in the form of decreased neural activity. It occurs when an opposing muscle is contracted in order to maximize its contraction force, and it relaxes.�Stress relaxation is what occurs when the musculotendinous unit (MTU), which involves the muscles and the connected tendons, is under a constant stress.�The gate control theory is what occurs when two kinds of stimuli, such as pain and pressure, activate their respective receptors at the same time.

How to Perform a PNF Stretch

The practice of doing a PNF stretch involves the next steps. The muscle group to be stretched is first placed so that the muscles are stretched and under pressure. The individual then contracts the muscle, using a band for 5 to 6 seconds while a partner, or immovable object, applies sufficient resistance to inhibit motion. Please be aware, the effort of contraction ought to be relevant to the individual’s amount of conditioning. The contracted muscle group is then relaxed and a controlled stretch is used for approximately 20 to 30 seconds. The muscle band is then allowed 30 seconds to recover and the process is repeated 2 to 4 more times.

Information differs marginally regarding time recommendations for PNF stretching, determined by which healthcare professional you’re speaking to. Although there are conflicting responses to the question of how long should a patient contract the specific muscle group for and how long should they rest for between each stretch, it’s been found through a study of research and patient experience, that the above timing recommendations offer the most advantages from proprioceptive neuromuscular facilitation stretching.

Furthermore, certain precautions will need to be taken when performing PNF stretches because they may put additional stress on the targeted muscle group, which can boost the possibility of soft tissue injury. To reduce this risk, it’s essential for the patient to include a conditioning phase before a maximum, or intense effort is utilized.

About the Active Release Technique or ART

The active release technique, or ART, is among the newest treatments in the world of chiropractic. ART is used to target muscle, nerve, and tendon problems. It is also used to treat blood vessel problems. Quite a few studies have been conducted and these have generated positive results which reveal that ART is really an effective treatment method. A lot of individuals nowadays try ART since so many are experiencing muscle problems.

Oftentimes, individuals, particularly the older ones, wake up and they feel that their body is quite hard to move. There are also those who start to feel their range of motion getting more and more limited with time. A number of the most common body parts that suffer from limited selection of motion include the neck, the arms, and the back. For many individuals, there is also restricted range of motion. There are numerous factors that cause restricted range of movement. The active release technique can be used to improve limited mobility as well as improve sciatica symptoms associated with a variety of health issues.

How ART Affects Limited Range of Motion

ART therapists initial assess the muscles that they are supposed to take care of. They check the texture, the stiffness, and needless to say, their freedom. Since the groundwork is conducted, the therapists would then attempt to elongate the muscles so as to break the adhesions. The stretching is usually conducted with the management of vein in consideration. Also, the practitioner would need to ask the patient to move the affected body parts in ways prescribed by the practitioner. So essentially, ART is a joint-venture. Practitioner and patients work together in order to generate great medical outcomes.

Dr. Alex Jimenez’s Insight

The active release techniques, or ART, and the proprioceptive neuromuscular facilitator, or PNF, stretches are therapeutic procedures commonly utilized for the common practice of releasing tension in the soft tissues as well as increasing the range of motion of the human body. Although a variety of treatment options are available to help treat sciatica, ART and PNF can be used by qualified and experienced healthcare professionals to safely and effectively improve and manage sciatic nerve pain. Moreover, alternative treatment options, such as chiropractic care, and strengthening exercises can also be used in combination with these therapeutic methods to help speed up the recovery process.

The Future of ART and PNF

It’s important to remember that both ART and PNF should only be run by accredited practitioners. Healthcare professionals are not just expected to find basic instruction and permit but they are also expected to have attended numerous workshops and seminars about the subject. In some countries, credential tests even must be passed. In addition, it ought to be noted that ART and PNF must be conducted on muscle stiffness not due to blunt trauma. The condition should also not involve inflammation.

There are many healthcare professionals who focus on ART and PNF. A few of these include chiropractors, physical therapists, massage therapists, medical physicians, and even athlete trainers. The active release technique and the proprioceptive neuromuscular facilitation stretches helps people do things that they used to do. It helps them become more efficient at work as well as be practical in their daily lives. Due to the health benefits of ART and PNF, more and more people from the medical and therapeutic world are learning how to concentrate on it. 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

EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Active Release Technique for Sciatica in El Paso, TX

by Dr Alex Jimenez | Chiropractic, Clinical Neurophysiology, Sciatica, Sciatica Nerve Pain, Treatments

Active release therapy, more specifically referred to as the active release technique, is a patented system designed by Dr. P. Michael Leahy which focuses on the treatment of developed scar tissue in damaged muscles all across the human body. When Dr. Leahy first developed the technique about two decades ago, he realized that the damage in the complex soft tissues of the muscles might perhaps be able to be sensed as well as addressed directly through movement in the form of specialized techniques. With its proven ability to cure pain, its own acronym, ART, provides the active release therapy with some ironical link to being a true art form in chiropractic care.

When athletes overwork their muscles from playing sports or even through just everyday activities, many individuals don’t understand how scar tissue can develop on our muscles in the first place. The scar issue forms in order to help heal damaged muscles, however, it can ultimately create painful symptoms which may last long after these have healed. Scar tissue most commonly develops as a result of pulled muscles or muscle tears, or even from a lack of oxygen, called hypoxia.

As the scar tissue builds in the damaged or injured muscles, if the individual does not maintain a proper level of mobility in the affected area, it can progressively cause muscles to become stiff or tight and weak, eventually leading to health issues such as tendonitis or nerve problems. This explains why some people with pain or limited range of motion, often will need to visit a healthcare professional immediately. Fortunately, many doctors are certified to treat these type of problems using active release therapy.

Using the Active Release Technique to Relieve Pain

Together with providing tension to the targeted sore muscle and utilizing specific body motions, the painful symptoms associated with scar tissue improves through active release therapy. As of now, there are approximately 500 different active release techniques designed to alleviate the tightness or stiffness and weakness in all of the body’s soft tissues, from the muscles to the nerves. Many of these movements are particularly chosen for each individual based on the specific muscle issue and location.

Active release techniques can also be helpful for small traumatic injuries caused by accumulative trauma or repetitive strain. More specifically, ART functions to break up fibrous tissues called adhesions. These adhesions result from a tear onto a tendon, ligament or muscle. Adhesions commonly develop in different ways, including from trauma as a result of acute injury or from repetitive motion injury caused by overuse, most commonly from sports injuries. It may also be a result of poor posture which has been aggravated by continuous pressure in addition to tension produced in the soft tissues for extended amounts of time.

Such adhesions, when left untreated, can also limit blood flow as well as shorten muscles, causing the well-known symptoms. Worsened symptoms can also result in pain, discomfort or weakness and at times numbness, most notably when scar tissue applies pressure on the nerves. When adhesions occur, the patient will surely complain of distress much more due to the simple fact that they will not be able to engage in the physical activities they were used to performing in before.

What is Active Release Techniques (ART)?

How Does ART work?

The active release technique, or ART,� works by implementing a couple of movements and motions on the affected muscle, tendon or fascia. In comparison to other soft tissue therapies, it’s said to achieve better end results. Primarily, ART aims to help improve the symptoms of the damaged or injured area by applying pressure and force on it. From there, the individual will be tasked to perform a technique which will help release the tension from the treatment. This can essentially improve motion for the treated region.

The combination of this tension out of the active release technique and that of the movement of muscles and its soft tissues will loosen and break up the adhesions. Because of this, there’ll be lesser pain felt on the injured region. This technique works well with active strengthening in addition to biomechanics training. The combination of these therapies will make patients feel improved body awareness, strength, flexibility and mobility even after a few ART sessions.

How Different is ART from Traditional Soft Tissue Treatments?

When compared with traditional manners of soft tissue therapy, ART boasts of a very comprehensive strategy. The active release technique is performed by certified healthcare practitioners who’ve underwent a very rigorous training procedure. Healthcare professionals must participate in sit-in classes and they must also have hands-on testing. Their certificate doesn’t stop after they pass the 90 percent mark on the hands on test though. They’ll also have to maintain their ART certification by getting annual recertification. This may work by honing the healthcare professional’s abilities and at the exact time, this will boil to the benefit of patients undergoing the therapy.

How Successful is ART as a Treatment?

Current research has demonstrated how effective the procedure is when it comes to treating hamstring pain and dysfunction in addition to hip pain, turf toe and lymph nodes. While the efficacy of ART has been demonstrated along these areas, several studies are still being made to check into its potential for treating disorders for other body components.

Using the Active Release Technique for Sciatica

Sciatica is an issue which affects a large number of people. It is essentially a pain syndrome, characterized by a collection of common symptoms which are caused when the sciatic nerve, the largest and most important nerve supplying the lower spine and the lower extremities, is compressed by the small muscles in the pelvis. The piriformis muscle is the one most implicated in the compression of the sciatic nerve, particularly because it moves through this muscle when emerging from the pelvis and entering the lower limbs. The active release technique, or ART, may be used in the treatment of sciatica brought on by piriformis syndrome.

Pathophysiology of Sciatica

When sciatica is caused by the compression of the sciatic nerve by the piriformis muscle, the latter generally goes into a spasm for an extended period of time, leading to the compression of this fundamental nerve. The spasm may result in a compromise in the blood supply to the muscle itself as well as the nerve, which will further complicate the issue. Nerve communications are important in order for the human body to maintain its outmost efficiency. Sciatica often can also be caused by disc injuries and herniations, as generally is a differential diagnosis to piriformis syndrome. Specific orthopedic tests can help, doctors of chiropractic, or chiropractors, evaluate the source of the patient’s sciatica prior to commencing any type treatment.

Consequences of Sciatic Nerve Pain

There are a number of effects that could arise as a result of sciatica. Reduction in overall body ranges of movement can be anticipated, accompanied by searing or sharp pain that can be excruciating. This can make it very difficult for an individual’s quality of life, especially when carrying out daily tasks like going to school and work, might become impossible due to the seriousness of the health issue. When the issue isn’t treated on time, it might cause permanent damage to the sciatic nerve.

Conventional Treatments for Sciatic Nerve Pain

There are a range of conventional treatments that may be utilized based on the intensity of the sciatic nerve pain, or sciatica. One of these is an injection of a drug/medication that can relax the muscle so that it stops compressing the nerve. Additionally, it has been proven that drugs and/or medications, such as steroids, may also have an impact on reducing the pain and impairment related to the symptoms. When the pharmacological methods don’t result in any progress, surgical ones can be attempted. The most usual of these is a surgery to release the nerve from the muscle by cutting away a portion of it. Although these have been listed as conventional treatments which may be used to treat sciatica, alternative treatment options and secondary opinions should be considered before considering surgical interventions. Only when no other treatment has demonstrated any improvements, should surgery be considered by a patient.

The Role of Active Release Techniques for Sciatica

The active release technique, or ART, is a form of therapy that focuses on the manipulation of soft tissues, including nerves, fascia and muscles, so as to achieve relief of painful symptoms, in this case for sciatica. For sciatic nerve pain, ART is utilized to reduce spasm and remove adhesions of the muscle that may be entrapping the sciatic nerve. Since the adhesions are removed through specific manual methods, the nerve can slide under the soft tissues, and sciatica symptoms can solve relatively quickly. There are a range of things that a patient can do in order to increase the efficacy of the active release technique. Early start to treatment assists in long-term resolution of sciatica symptoms.

Dr. Alex Jimenez’s Insight

The active release technique, also known as active release therapy or ART, is a soft tissue treatment based on a series of movement and motion techniques utilized to relieve pain and discomfort as well as promote the healing of muscles, joints and nerves, among other soft tissues. When performed by a certified healthcare professional, including a chiropractor, ART can help break down adhesions which may have developed following scar tissue formation after a damaged or injured muscle has healed. The active release technique has become one of the most common therapy for soft tissue treatment.

ART therapy is usually provided by skilled therapists like chiropractors, who have to keep their accreditation through continuing education on a yearly suface. This treatment is a specialized procedure that needs quite a bit of expertise and skill so as to work and supply rapid results. 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

EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

« Older Entries

Next Entries »

IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine

Online Booking & Appointments 24/7*

Certified Functional Medicine Doctor El Paso — Certified Functional Medicine Provider*
All Providers work within legal jurisdiction and established clinical scope of practice.*

The Injury & Trauma Rehabilitation Specialists

PUSHasRx® Trauma Rehabilitation Center

Health, Wellness & Nutrition Specialists

Opiate Analgesia (OA)

Endogenous Opioids

Neuronal Circuits and Pain Modulation

Gate Control Theory

Stimulation Produced Analgesia (SPA)

Dr. Alex Jimenez’s Insight

Mechanisms of Pain Modulation

Ascending and Descending Pain Suppression Mechanism

Stress Induced Analgesia (SIA)

Somatovisceral Reflex

Additional Topics: Sciatica

Neurophysiology Of Pain Part II

Intensity, Location & Quality of Pain…

2 Pain Transmission Pathways For Location Intensity Quality

Unpleasant Quality & Autonomic Affective Motivational Pathway For Pain

Brain Areas Involved In Processing Of Nociceptive Signals

The Anterior Cingulate & Insula Cortex Are Activated In Human Subjects

Control Of Pain Perception

Pain Modulation Pathway

Endogenous Opioids

Location Of Nerve Cells With Endogenous Opioid Receptors

Modulation Of Pain Signal Transmission In The Spinal Cord

Inflammatory Soup – Hyperalgesia

Clinical Application

Allodynia

Gate Control Theory of Pain

Ascending Tracts | Pain Modulation: Gate Control Theory

Gate Theory

Clinical Application

Abnormalities Of Pain System

Phantom Pain

Peripheral Sensitization

Central Sensitization

Peripheral & Central Sensitisation

Central Sensitization & C Fibers

Two Main Characteristics Of Central Sensitization:

Somatosensory Cortex Organization

Cortical Reorganization

Referred Pain

Pain Sensation Referred From Visceral Organs …

… to another part of the body surface

Neurophysiology Of Pain

Objectives

Definition Of Pain

The Nervous System

Nervous System

Central nervous system (CNS)

Peripheral Nervous System (PNS)

Nerve Cells

Nerve Cell-To-Nerve Cell Communication

Nerve cells communicate with other cells by releasing a chemical from the nerve endings � Neurotransmitters

Basic Steps In Synaptic Transmission

Synaptic Transmission

Steps in the passage of signal from one nerve cell to other.

Electrical Impulse

Action Potential

Stopping Action Potentials To Stop Nociceptive Stimuli

Sensory Systems

Skin Receptors

Nociceptors

Transduction

Chemical Agents…

Summary Of Transduction Process At The Periphery

TRP Channels

Different TRP Channels

Motor Output & Sensory Input To Spinal Cord

2nd Order Nerve Cells Send Nerve Fibers In The Spinal Cord White Matter

Transmission Of Nociceptive Signals From The Periphery To The Brain

A Delta (?) & C Nerve Fibers

A? & C fibers

Fast & Slow Pain

Central Pain Pathways

Dr. Sletten Discussing Central Sensitization Syndrome (CSS)

Nerve Fibers in Transmission of Sensory Signals

What is the Gate Control Theory of Pain?

How Emotions and Thoughts Affect Pain

Gate Control Theory in Pain Management