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5 Best CBD Oils for Sleep and Insomnia (2019 Updated Review)

and Inflammation Pain



  • and Inflammation Pain
  • A brief comparison of the pathophysiology of inflammatory versus neuropathic pain
  • 1. Introduction
  • In the fight against pain from inflammation, your diet can be an effective weapon. Learn how you can fight back by incorporating these healthy foods into your. Other painful conditions of the joints and musculoskeletal system that may not be associated with inflammation include osteoarthritis. It is not believed that inflammation plays a major role in osteoarthritis. Other painful conditions of the joints and musculoskeletal system that are.

    and Inflammation Pain

    Around the edges of the joint, bony and cartilaginous overgrowths or "spurs," called osteophytes may develop in non weight-bearing areas of the joint. Osteoarthritis has previously been considered a non-inflammatory form of arthritis. It is our theory that the underlying origin, like all other pain syndromes is inflammation and the inflammatory response.

    The changes that occur within the joint are due to inflammation and the inflammatory response. Inflammation is aggravated by the introduction of bone and cartilage breakdown products into the synovial fluid. These products are phagocytized by cells in the synovium, resulting in chronic, low-grade inflammation.

    Consequently, the synovial membrane becomes thickened. Inflammation of the synovial membrane may be absent in the earlier stages of Osteoarthritis; however, as the disease progresses, some degree of synovitis usually exists.

    Once mild synovial inflammation is established, the synovium becomes a source of cartilage-degrading enzymes e. These substances diffuse through the synovial fluid and cause further degradation of articular cartilage. IL-1 and TNF-alpha stimulate the chondrocytes to produce more degrading enzymes, and the process continues in a vicious cycle. Nitric oxide NO is found at higher levels in osteoarthritic cartilage than in normal cartilage.

    A form of NO can be expressed after the activation of chondrocytes by cytokines. Studies have shown that IL-1 derived from the osteoarthritic cartilage stimulates the production of prostaglandin E 2 PGE 2. PGE 2 also has important pro-inflammatory properties and contributes to vasodilation and pain in patients with Osteoarthritis.

    TNF-alpha and Interleukin 1-beta play an important role in rheumatoid arthritis by mediating cytokines that cause inflammation and joint destruction. TNF-alpha, Interleukin 1-beta and Substance P are elevated in the joint fluids in patients with rheumatoid arthritis 2. These inflammatory mediators are also elevated in the joint fluid in patients with osteoarthritis albeit to a far less extent.

    Along with mechanical factors, growth factors and cytokines such as TGF beta 1, IL-1 alpha, IL-1 beta and TNF-alpha may be involved in the formation and growth of osteophytes, since these molecules can induce growth and differentiation of mesenchymal cells. The incidence and size of osteophytes may be decreased by inhibition of direct or indirect effects of these cytokines and growth factors on osteoid deposition in treated animals 3 , 4. Inhibition of IL-1 receptor also decreases the production of metalloproteinase enzymes collagenase-1 and stomelysin-1 in the synovial membrane and cartilage.

    These enzymes are involved in connective tissue breakdown 5. Back and neck pain most commonly results from injury to the muscle, disk, nerve, ligament or facet joints with subsequent inflammation and spasm. Degeneration of the disks or joints produces the same symptoms and occurs subsequent to aging, previous injury or excessive mechanical stresses that this region is subjected to because of its proximity to the sacrum in the lower back.

    Herniation of disk tissue nucleus pulposus produces a profound inflammatory reaction with release of inflammatory chemical mediators especially Tumor Necrosis Factor Alpha. Subsequent to release of TNF-alpha, there is an increase in the formation of inflammatory mediator prostaglandin and Nitric Oxide. It is now known that Tumor Necrosis Factor Alpha is synthesized by herniated or degenerate disk tissue nucleus pulposus , and contributes to the nerve injury and behavioral manifestations of experimental sciatica associated with herniated lumbar discs 6.

    This has been confirmed by numerous animal studies and research wherein application of disk tissue nucleus pulposus to a nerve results in nerve fiber injury, with reduction of nerve conduction velocity, intracapillary thrombus formation, and the intraneural edema formation 7 8. One study demonstrated that disk tissue nucleus pulposus increases inducible nitric oxide synthetase activity in spinal nerve roots and that nitric oxide synthetase inhibition reduces nucleus pulposus-induced swelling and prevents reduction of nerve-conduction velocity.

    Tumor Necrosis Factor Alpha and other inflammatory mediators induce phospholipase A2 activation. High levels of phospholipase A2 previously have been demonstrated in a small number of patients undergoing lumbar disc surgery. Phospholipase A2 is the enzyme responsible for the liberation of arachidonic acid from cell membranes at the site of inflammation and is considered to be the limiting agent in the production of inflammatory mediator prostaglandins and leukotrienes Culture media from the herniated lumbar discs show-increased levels of matrix metalloproteinase activity, nitric oxide, prostaglandin E2, and interleukin-6 compared with the control discs 11 Subsequent to the release of inflammatory mediators, activation of motor nerves that travel from the spinal cord to the muscles results in excessive muscle tension, spasm and pain.

    Back or neck pain with or without herniated disk is due to inflammation and the inflammatory response. Most cases can be treated medically in accordance with the principles that we have outlined and do not require surgery. Surgery is indicated when there is compression of the nerve roots producing continuous release of inflammatory mediators, significant muscle weakness and or urinary or bowel incontinence.

    Fibromyalgia is a chronic, painful musculoskeletal disorder characterized by widespread pain, pressure hyperalgesia, morning stiffness, sleep disturbances including restless leg syndrome, mood disturbances, and fatigue. Other syndromes commonly associated with fibromyalgia include irritable bowel syndrome, interstitial cystitis, migraine headaches, temporomandibular joint dysfunction, dysequilibrium including nerve mediated hypotension, sicca syndrome, and growth hormone deficiency.

    Fibromyalgia has been proposed to be due to neurogenic inflammation induced by an inflammatory response to allergens, infectious agents, irritants, chemical exposures or emotional stress Several studies have shown that there are increased levels of the inflammatory transmitter Substance P SP and calcitonin gene related peptide CGRP in the spinal fluid of patients with fibromyalgia syndrome FMS 14 15 The levels of platelet serotonin are also abnormal Furthermore, in patients with fibromyalgia, the level of pain intensity is related to the spinal fluid level of arginine, which is a precursor to the inflammatory mediator nitric oxide NO Another study found increases over time in blood levels of cytokines Interleukin -6, Interleukin -8 and Interleukin -1R antibody IL-1Ra whose release is stimulated by substance P.

    The study authors concluded that because Interleukin-8 promotes sympathetic pain and Interleukin -6 induces hypersensitivity to pain, fatigue and depression, both cytokines play a role in producing Fibromyalgia symptoms Interstitial cystitis is a severe debilitating bladder disease characterized by unrelenting pelvic pain and urinary frequency. This sterile painful bladder disorder is associated with a defective glycosaminoglycan bladder mucosal layer and an increased number of activated mast cells.

    Mast cells are ubiquitous cells derived from the bone marrow and are responsible for allergic reactions as they release numerous vasodilatory, nociceptive and pro-inflammatory mediators in response to immunoglobulin E IgE and specific antigen. Mast cell secretion is also triggered by a number of peptides, such as bradykinin and substance P, and may also be involved in the development of inflammatory responses SP-containing nerve fibres are increased in the submucosa of the urinary bladder of interstitial cystitis IC patients and are frequently seen in juxtaposition to Mast cells 21 , There is enhanced sympathetic innervation of the bladder in the submucosa and detrusor muscle.

    In interstitial cystitis the number of neurons positive for inflammatory mediator vasoactive intestinal polypeptide and neuropeptide Y is higher compared with control subjects These peptides potentiate the responses to the purinergic component of the neurogenic stimulation that part of the contractile response that remains after treatment with atropine and potentiate the responses to exogenously applied adenosine triphosphate ATP Significant elevations in Interleuken-2, Interleukin -6, and Interleukin -8 have also been found in the urine of subjects with active interstitial cystitis compared with subjects with interstitial cystitis in remission and control subjects Migraine headache is caused by activation of trigeminal sensory fibers by known and unknown migraine triggers.

    There is subsequent release of inflammatory mediators from the trigeminal nerve. This leads to distention of the large meningeal blood vessels in the skull and brain and the development of a central sensitization within the trigeminal nucleus caudalis TNC. Genetic abnormalities may be responsible for altering the response threshold to migraine specific trigger factors in the brain of a migraineur compared to a normal individual The painful neurogenic vasodilation of meningeal blood vessels is a key component of the inflammatory process during migraine headache.

    The cerebral circulation is supplied with two vasodilator systems: A clear association between migraine and the release of inflammatory mediator calcitonin gene-related peptide CGRP and substance P SP has been demonstrated. Jugular plasma levels of the potent vasodilator, calcitonin gene-related peptide CGRP have been shown to be elevated in migraine headache.

    CGRP-mediated neurogenic dural vasodilation is blocked by anti-migraine drug dihydroergotamine, triptans, and opioids In cluster headache and in chronic paroxysmal hemicrania, there is additional release of inflammatory mediator vasoactive intestinal peptide VIP in association with facial symptoms nasal congestion, runny nose In addition, there are studies reporting the occurrence of putative neurotransmitters such as cholecystokinin, dynorphin B, galanin, gastrin releasing peptide, vasopressin, neurotensin, and somatostatin.

    The nerves occur as a longitudinally oriented network around large cerebral arteries. There is often a richer supply of nerve fibers around arteries than veins. The origin of these nerve fibers has been studied by retrograde tracing and denervation experiments. These techniques, in combination with immunocytochemistry, have revealed a rather extensive innervation pattern.

    Several ganglia, such as the superior cervical ganglion, the sphenopalatine ganglion, the otic ganglion, and small local ganglia at the base of the skull, contribute to the innervation. Sensory fibers seem to derive from the trigeminal ganglion, the jugular-nodose ganglionic complex, and from dorsal root ganglia at the cervical spine level C2.

    The noradrenergic and most of the NPY fibers derive from the superior cervical ganglion. A minor population of the NPY-containing fibers contains vasoactive intestinal peptide VIP , instead of NA and emanates from the sphenopalatine ganglion. The cholinergic and the vasoactive intestinal peptide VIP -containing fibers derive from the sphenopalatine ganglion, the otic ganglion, and from small local ganglia at the base of the skull.

    Minor contributions may emanate from the jugular-nodose ganglionic complex and from the spinal dorsal root ganglia. Neuropeptide Y NPY , is a potent vasoconstrictor in vitro and in situ. Meningeal blood vessels are involved in the generation of migraine pain and other headaches. Classical experiments have shown that blood vessels of the cranial dura mater are the most pain-sensitive intracranial structures.

    Dural blood vessels are supplied by trigeminal nerve fibers, and dilate in response to activation of the trigeminal nerves and release of neuropeptide cytokines such as substance P SP and calcitonin gene-related peptide CGRP CGRP can be released experimentally from dural nerve fibers, and there is evidence that this occurs also during migraine attacks.

    Stimulation of dural nerve fibers causes vasodilatation and an increase in dural arterial flow, which depends on the release of CGRP but not SP. SP, on the other hand, is known to mediate plasma leakage extravasation from small veins in the dura mater. The dural arterial flow depends also on the formation of cell wall nitric oxide. The introduction of serotonin 5-HT 1 receptor agonists such as sumatriptan changed the treatment strategies for migraine.

    Sumatriptan and other triptans may inhibit the release of inflammatory mediators from the trigeminal nerve. Sumatriptan has been shown to block the release of vasoactive cytokines from trigeminal nerves that surround the blood vessels in the dura mater during migraine.

    Sumatriptan blocks nerve fiber induced plasma extravasation but has only minor effects on nerve fiber mediated vasodilatation and dural arterial flow. Women tend to react to histamine-containing foods more frequently than men do, on account of a deficiency in an enzyme diamine oxidase that breaks histamine down. Taking supplemental B6 has been shown to be helpful in migraine, as it can increase diamine oxidase activity. Nociceptive pain is mediated by receptors on A-delta and C nerve fibers, which are located in skin, bone, connective tissue, muscle and viscera.

    These receptors serve a biologically useful role at localizing noxious chemical, thermal and mechanical stimuli. Nociceptive pain can be somatic or visceral in nature. Somatic pain tends to be well-localized, constant pain that is described as sharp, aching, throbbing, or gnawing.

    Visceral pain, on the other hand, tends to be vague in distribution, spasmodic in nature and is usually described as deep, aching, squeezing and colicky in nature.

    Examples of nociceptive pain include: Neuropathic pain in contrast to nociceptive pain, is described as "burning", "electric", "tingling", and "shooting" in nature. It can be continuous or paroxysmal in presentation. Whereas nociceptive pain is caused by the stimulation of peripheral A-delta and C-polymodal pain receptors, by peripheral release of inflammatory mediators, e. The hallmarks of neuropathic pain are chronic allodynia and hyperalgesia.

    Allodynia is defined as pain resulting from a stimulus that ordinarily does not elicit a painful response e. Hyperalgesia is defined as an increased sensitivity to normally painful stimuli. Examples of neuropathic pain include carpal tunnel syndrome, trigeminal neuralgia, post herpetic neuralgia, phantom limb pain, complex regional pain syndromes and the various peripheral neuropathies. Mechanisms of Pain Is it mechanical, nerve or centralized pain? Osteoarthritis Pain Learn the origins of OA pain.

    Musculoskeletal Pain Soft tissue as a source of pain. Back Pain Recognize the many causes of spinal pain. Centralized Pain Understand widespread, escalating pain. Comorbid Conditions and Pain Other diseases may contribute to your pain. Your Pain Management Plan. Heterozygote mice are viable and relatively normal. All of these conditional knockout animals showed deficits to some degree in acute and chronic pain, although the phenotypes do not completely overlap [ 76 - 78 ].

    In all cases, attenuated nociception is associated with reduced firing of superficial dorsal horn neurons or c-fos expression, confirming a key role for glutamate release from the central terminals. VGLUT3 is expressed in a small group of DRG neurons, with their central afferents terminating in the superficial layer of spinal dorsal horn. VGLUT3 knockout animals do not develop mechanical hypersensitivity in models of inflammatory pain and neuropathic pain, while noxious heat sensation is largely intact.

    In addition, VGLUT3 appears to be primarily responsible for transport of glutamate into astrocyte vesicles [ 79 ], which can subsequently be released by astrocyte activation. Release of glutamate in the spinal dorsal horn leads to activation of a variety of ionotrophic receptors. The importance of this release is indicated by the fact that AMPA receptor blockade results in a virtual complete block of acute post-synaptic excitation while blockade of the NMDA receptor has little effect upon acute excitation, but can markedly diminish the initiation of the enhanced response of spinal neurons to repetitive small afferent input e.

    In response to peripheral inflammation and increased primary afferent traffic, synaptic efficacy in the spinal cord dorsal horn is strengthened, which in part results from the enhanced function of postsynaptic glutamate receptors [ 27 ].

    Changes in channel properties are extensively studied for AMPA receptors. Dorsal horn nociceptive neurons are under powerful inhibitory control. Intrathecal strychnine glycine receptor antagonist or bicuculline GABA A receptor antagonist evokes immediate tactile allodynia, but had no effect upon thermal escape thresholds [ 9 ], suggesting that tonic or evoked glycinergic or GABAergic inhibition in the spinal cord is crucial to the encoding of low threshold mechanical tactile stimuli as a non-aversive stimulus.

    This mechanism is implicated in both inflammatory pain and neuropathic pain [ 85 ]. Reduced spinal expression of KCC2 is noticed following intraplantar formalin [ 86 ] or CFA [ 87 ], as well as nerve injury [ 28 ]. Fast phosphorylation of dorsal horn NKCC1 is seen within 10 min after intracolonic capsaicin injection [ 88 ]. The phosphorylation likely promotes membrane trafficking of NKCC1 and might play a role in referred mechanical hyperalgesia. Intraplantar capsaicin produced a significant enhancement in spike frequency in both wide dynamic range WDR and nociceptive specific neurons in dorsal horn.

    Spinal blockade of NKCC1 normalized the spike frequency to baseline levels, suggesting that NKCC1 plays a key role in the sensitization of dorsal horn neurons [ 89 ]. It is increasingly recognized that glias, especially microglias play important roles in the generation of chronic pain [ 90 - 92 ]. Mice deficient in PGE 2 production have impaired dorsal horn activation of microglia and do not exhibit mechanical allodynia after peripheral nerve injury [ 93 ].

    In addition, IL6 activates microglial p38 MAPK pathway—mediated expression of fractalkine receptor CX3CR1 [ 95 ], thereby promoting the interaction between dorsal horn neurons and microglia. Proinflammatory cytokines release from activated microglia modulates neuronal synaptic transmission. In addition to its role in cytokine production, activated microglia could assume an amoeboid shape and act similar to a macrophage.

    Following peripheral nerve injury, microglia in lamina II-III were shown to engulf both injured and uninjured myelinated axons, a phenomenon not observed in the normal dorsal horn [ 97 ]. The engulfment of axons likely induces injuries to spinal cord neurons, as indicated by the dorsal horn expression of ATF3. Thus microglia activation may introduce central pain components to an existing peripheral neuropathic pain.

    There is no doubt that inflammatory pain and neuropathic pain share common mechanisms, although the time course and relative contribution of each of these mechanisms might be different. A more precise depiction of these differences is critical in providing the rationale for a timely intervention, which might prevent the transition from acute pain to a persistent, chronic state.

    It becomes clear that a successful approach is likely to involve not only analgesics, but also means that may modify the progression of pain as a disease. This is a PDF file of an unedited manuscript that has been accepted for publication.

    As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

    National Center for Biotechnology Information , U. Author manuscript; available in PMC Aug 1. Qinghao Xu 1 and Tony L. Qinghao Xu 1 Dept. Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Curr Opin Anaesthesiol. See other articles in PMC that cite the published article. Abstract Purpose of review The aetiologies of inflammatory pain and neuropathic pain are fundamentally different.

    Recent findings The increased pain sensation following tissue and nerve injury results from several mechanisms, including altered ion channel expression in DRG neurons, enhanced dorsal horn glutamate release from primary afferents, enhanced glutamate receptor function in second order neurons, disinhibition in the dorsal horn and glia cell activation.

    Summary Recognition of mechanisms common to both inflammatory pain and neuropathic pain might shed light on the understanding of the transition from acute pain to persistent pain.

    Introduction Heuristically, the pain experience has been divided into three principal categories based on the initiating conditions and the anticipated underlying mechanisms: Acute nociception Acute transient high intensity stimuli yield a somatotopically limited pain sensation that resolves upon the removal of the stimuli. Tissue injury Tissue injury arising from ongoing exposure to high-intensity stimului leads to a pain sensation continuing beyond the removal of the originating stimulus. The systems underlying this spinal facilitation include: Spinobulbospinal pathway Afferent input activates caudal midline raphe-spinal serotonergic neurons which terminate in dorsal horn neurons to facilitate the activity in deep dorsal horn projection systems [ 7 - 8 ].

    Loss of local inhibition Local dorsal horn neuronal excitability is under the tonic control of local inhibitory GABAergic and glycinergic interneurons. Local non neuronal cell systems Peripheral inflammation leads to both acute and chronic indices of activation of spinal microglia and astrocytes.

    Migration of non-neuronal inflammatory cells into the DRG Peripheral inflammation results in the appearance of macrophages in the DRG, but not the spinal cord [ 12 ].

    Peripheral nerve injury Injury to the peripheral nerve leads to a pain state with persistency and components of hyperalgesia and allodynia aversive sensation generated by an otherwise innocuous stimulus referred to the distribution of the injured nerve. The peripheral and spinal mechanisms underlying this increased spontaneous activity are broadly summarized in terms of: Migration of nonneuronal inflammatory cells into the DRG After nerve injury, increased macrophages and neutrophils have been shown in the DRG [ 24 - 25 ].

    Activity-induced facilitation The ongoing afferent traffic is believed to contribute importantly to the initiation of a central sensitization state with several components including activation of the NMAD receptors and increased AMPA subunit expression [ 26 - 27 ]. Spinobulbospinal facilitatory pathways As noted above, spinobulbospinal pathways lead to the activation through the caudal midline raphe of serotonergic projections, which terminate in dorsal horn neurons to activate dorsal horn projection systems.

    Activation of non-neuronal cells After nerve injury there are trophic changes in the appearance of microglia and astrocytes, suggesting increased activity of non-neuronal cells [ 11 ]. Migration of non-neuronal inflammatory cells into dorsal horn Peripheral nerve injury produces segmentally organized disruption of the blood brain barrier [ 33 ] and the influx of T cells and macrophages [ 34 ].

    Separation of tissue vs. Pharmacology As show in table 1 , in preclinical models, inflammatory hyperalgesia are frequently sensitive to agents such as NSAIDs and opiates whereas neuropathic pain states are not. Table 1 Analgesic pharmacology of nerve and tissue injury pain states. Open in a separate window. Comparison of tissue vs.

    Mechanims mediating persistent pain following tissue injury or nerve injury Following tissue injury or nerve injury, pathological changes that might lead to persistent pain in the DRG 1 and the spinal cord dorsal horn 2.

    Voltage-gated sodium channels VGSCs control the propagation of nerve impulses and are therefore essential for the excitability of neurons. Voltage-gated calcium channels VGCCs are critical in controlling neurotransmitter release. Post synaptic activation Release of glutamate in the spinal dorsal horn leads to activation of a variety of ionotrophic receptors. Disinhibition Dorsal horn nociceptive neurons are under powerful inhibitory control. Involvement of spinal glia It is increasingly recognized that glias, especially microglias play important roles in the generation of chronic pain [ 90 - 92 ].

    Conclusion There is no doubt that inflammatory pain and neuropathic pain share common mechanisms, although the time course and relative contribution of each of these mechanisms might be different. Inflammatory pain and neuropathic pain can be distinguished from the following characteristics: Mechanisms common to both inflammatory and neuropathic pain include altered expression of cytokines, cytokine receptors and VGSCs in the DRG, enhanced glutamate release and receptor functions, disinhibition and glia activation and invasion in the spinal dorsal horn.

    Nerve injury marker ATF3 is observed in the DRG neurons following prolonged peripheral inflammation, suggesting the pain of inflammatory origin may evolve into a condition that resembles neuropathic pain. Footnotes This is a PDF file of an unedited manuscript that has been accepted for publication.

    An SCN9A channelopathy causes congenital inability to experience pain. Chen L, Huang LY. In vivo recruitment by painful stimuli of AMPA receptor subunits to the plasma membrane of spinal cord neurons. MAP kinase and pain. Spinal phospholipase A2 in inflammatory hyperalgesia:

    A brief comparison of the pathophysiology of inflammatory versus neuropathic pain

    Chronic, subtle, systemic inflammation is a possible factor in stubborn musculoskeletal pain. It can have many underlying causes, from bad. People will feel pain, stiffness, discomfort, distress, and even agony, depending on the severity of the inflammation. Inflammatory arthritis is the term used to describe conditions characterized by pain, swelling, tenderness and warmth in the joints, as well as morning stiffness.

    1. Introduction



    Chronic, subtle, systemic inflammation is a possible factor in stubborn musculoskeletal pain. It can have many underlying causes, from bad.


    People will feel pain, stiffness, discomfort, distress, and even agony, depending on the severity of the inflammation.


    Inflammatory arthritis is the term used to describe conditions characterized by pain, swelling, tenderness and warmth in the joints, as well as morning stiffness.


    When you have arthritis, your body is in an inflammatory state. Learn more about these 8 food ingredients that can cause inflammation.


    Inflammation is initiated upon tissue injury and sets off a cascade of biochemical reactions that prime the nervous system for pain sensing.

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