An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve.
Amount of stimulation required before the sensation of pain is experienced.
Peripheral AFFERENT NEURONS which are sensitive to injuries or pain, usually caused by extreme thermal exposures, mechanical forces, or other noxious stimuli. Their cell bodies reside in the DORSAL ROOT GANGLIA. Their peripheral terminals (NERVE ENDINGS) innervate target tissues and transduce noxious stimuli via axons to the CENTRAL NERVOUS SYSTEM.
Scales, questionnaires, tests, and other methods used to assess pain severity and duration in patients or experimental animals to aid in diagnosis, therapy, and physiological studies.
A water-soluble extractive mixture of sulfated polysaccharides from RED ALGAE. Chief sources are the Irish moss CHONDRUS CRISPUS (Carrageen), and Gigartina stellata. It is used as a stabilizer, for suspending COCOA in chocolate manufacture, and to clarify BEVERAGES.
An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.
Introduction of therapeutic agents into the spinal region using a needle and syringe.
Act of eliciting a response from a person or organism through physical contact.
Compounds capable of relieving pain without the loss of CONSCIOUSNESS.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
An antigen solution emulsified in mineral oil. The complete form is made up of killed, dried mycobacteria, usually M. tuberculosis, suspended in the oil phase. It is effective in stimulating cell-mediated immunity (IMMUNITY, CELLULAR) and potentiates the production of certain IMMUNOGLOBULINS in some animals. The incomplete form does not contain mycobacteria.
Presence of warmth or heat or a temperature notably higher than an accustomed norm.
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.
A subgroup of TRP cation channels named after vanilloid receptor. They are very sensitive to TEMPERATURE and hot spicy food and CAPSAICIN. They have the TRP domain and ANKYRIN repeats. Selectivity for CALCIUM over SODIUM ranges from 3 to 100 fold.
Compounds with activity like OPIATE ALKALOIDS, acting at OPIOID RECEPTORS. Properties include induction of ANALGESIA or NARCOSIS.
Sensation of making physical contact with objects, animate or inanimate. Tactile stimuli are detected by MECHANORECEPTORS in the skin and mucous membranes.
Neurons in the SPINAL CORD DORSAL HORN whose cell bodies and processes are confined entirely to the CENTRAL NERVOUS SYSTEM. They receive collateral or direct terminations of dorsal root fibers. They send their axons either directly to ANTERIOR HORN CELLS or to the WHITE MATTER ascending and descending longitudinal fibers.
The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle.
Any of several BRASSICA species that are commonly called mustard. Brassica alba is white mustard, B. juncea is brown or Chinese mustard, and B. nigra is black, brown, or red mustard. The plant is grown both for mustard seed from which oil is extracted or used as SPICES, and for its greens used as VEGETABLES or ANIMAL FEED. There is no relationship to MUSTARD COMPOUNDS.
Disease or damage involving the SCIATIC NERVE, which divides into the PERONEAL NERVE and TIBIAL NERVE (see also PERONEAL NEUROPATHIES and TIBIAL NEUROPATHY). Clinical manifestations may include SCIATICA or pain localized to the hip, PARESIS or PARALYSIS of posterior thigh muscles and muscles innervated by the peroneal and tibial nerves, and sensory loss involving the lateral and posterior thigh, posterior and lateral leg, and sole of the foot. The sciatic nerve may be affected by trauma; ISCHEMIA; COLLAGEN DISEASES; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1363)
Increased sensitivity to cutaneous stimulation due to a diminished threshold or an increased response to stimuli.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
The observable response an animal makes to any situation.
Sensing of noxious mechanical, thermal or chemical stimuli by NOCICEPTORS. It is the sensory component of visceral and tissue pain (NOCICEPTIVE PAIN).
A type of pain that is perceived in an area away from the site where the pain arises, such as facial pain caused by lesion of the VAGUS NERVE, or throat problem generating referred pain in the ear.
The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included.
Specialized afferent neurons capable of transducing sensory stimuli into NERVE IMPULSES to be transmitted to the CENTRAL NERVOUS SYSTEM. Sometimes sensory receptors for external stimuli are called exteroceptors; for internal stimuli are called interoceptors and proprioceptors.
Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from DRUG RESISTANCE wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from MAXIMUM TOLERATED DOSE and NO-OBSERVED-ADVERSE-EFFECT LEVEL.
Pain originating from internal organs (VISCERA) associated with autonomic phenomena (PALLOR; SWEATING; NAUSEA; and VOMITING). It often becomes a REFERRED PAIN.
A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.
The distal extremity of the leg in vertebrates, consisting of the tarsus (ANKLE); METATARSUS; phalanges; and the soft tissues surrounding these bones.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
A class of nerve fibers as defined by their nerve sheath arrangement. The AXONS of the unmyelinated nerve fibers are small in diameter and usually several are surrounded by a single MYELIN SHEATH. They conduct low-velocity impulses, and represent the majority of peripheral sensory and autonomic fibers, but are also found in the BRAIN and SPINAL CORD.
Contractions of the abdominal muscles upon stimulation of the skin (superficial abdominal reflex) or tapping neighboring bony structures (deep abdominal reflex). The superficial reflex may be weak or absent, for example, after a stroke, a sign of upper (suprasegmental) motor neuron lesions. (Stedman, 25th ed & Best & Taylor's Physiological Basis of Medical Practice, 12th ed, p1073)
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.
Methods of PAIN relief that may be used with or in place of ANALGESICS.
Drugs that act on neuronal sensory receptors resulting in an increase, decrease, or modification of afferent nerve activity. (From Smith and Reynard, Textbook of Pharmacology, 1991, p367)
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
A subclass of analgesic agents that typically do not bind to OPIOID RECEPTORS and are not addictive. Many non-narcotic analgesics are offered as NONPRESCRIPTION DRUGS.
The sensory fibers innervating the viscera.
A class of cell surface receptors for TACHYKININS with a preference for SUBSTANCE P. Neurokinin-1 (NK-1) receptors have been cloned and are members of the G protein coupled receptor superfamily. They are found on many cell types including central and peripheral neurons, smooth muscle cells, acinar cells, endothelial cells, fibroblasts, and immune cells.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The forcing into the skin of liquid medication, nutrient, or other fluid through a hollow needle, piercing the top skin layer.
An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.
A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.
Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen.
Agents inhibiting the effect of narcotics on the central nervous system.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.
NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.
A highly reactive aldehyde gas formed by oxidation or incomplete combustion of hydrocarbons. In solution, it has a wide range of uses: in the manufacture of resins and textiles, as a disinfectant, and as a laboratory fixative or preservative. Formaldehyde solution (formalin) is considered a hazardous compound, and its vapor toxic. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p717)
The caudal portion of the nucleus of the spinal trigeminal tract (TRIGEMINAL NUCLEUS, SPINAL), a nucleus involved with pain and temperature sensation.
Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.
The lower portion of the BRAIN STEM. It is inferior to the PONS and anterior to the CEREBELLUM. Medulla oblongata serves as a relay station between the brain and the spinal cord, and contains centers for regulating respiratory, vasomotor, cardiac, and reflex activities.
Injuries to the PERIPHERAL NERVES.
Disease or trauma involving a single peripheral nerve in isolation, or out of proportion to evidence of diffuse peripheral nerve dysfunction. Mononeuropathy multiplex refers to a condition characterized by multiple isolated nerve injuries. Mononeuropathies may result from a wide variety of causes, including ISCHEMIA; traumatic injury; compression; CONNECTIVE TISSUE DISEASES; CUMULATIVE TRAUMA DISORDERS; and other conditions.
A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant & Hackh's Chemical Dictionary, 5th ed)
The endogenous peptides with opiate-like activity. The three major classes currently recognized are the ENKEPHALINS, the DYNORPHINS, and the ENDORPHINS. Each of these families derives from different precursors, proenkephalin, prodynorphin, and PRO-OPIOMELANOCORTIN, respectively. There are also at least three classes of OPIOID RECEPTORS, but the peptide families do not map to the receptors in a simple way.
A class of opioid receptors recognized by its pharmacological profile. Mu opioid receptors bind, in decreasing order of affinity, endorphins, dynorphins, met-enkephalin, and leu-enkephalin. They have also been shown to be molecular receptors for morphine.
A family of hexahydropyridines.
Mechanical compression of nerves or nerve roots from internal or external causes. These may result in a conduction block to nerve impulses (due to MYELIN SHEATH dysfunction) or axonal loss. The nerve and nerve sheath injuries may be caused by ISCHEMIA; INFLAMMATION; or a direct mechanical effect.
Pain during the period after surgery.
Pain in the facial region including orofacial pain and craniofacial pain. Associated conditions include local inflammatory and neoplastic disorders and neuralgic syndromes involving the trigeminal, facial, and glossopharyngeal nerves. Conditions which feature recurrent or persistent facial pain as the primary manifestation of disease are referred to as FACIAL PAIN SYNDROMES.
A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.
Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator.
A condition where damage to the peripheral nervous system (including the peripheral elements of the autonomic nervous system) is associated with chronic ingestion of alcoholic beverages. The disorder may be caused by a direct effect of alcohol, an associated nutritional deficiency, or a combination of factors. Clinical manifestations include variable degrees of weakness; ATROPHY; PARESTHESIAS; pain; loss of reflexes; sensory loss; diaphoresis; and postural hypotension. (From Arch Neurol 1995;52(1):45-51; Adams et al., Principles of Neurology, 6th ed, p1146)
Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
A G-protein-coupled, proteinase-activated receptor that is expressed in a variety of tissues including ENDOTHELIUM; LEUKOCYTES; and the GASTROINTESTINAL TRACT. The receptor is activated by TRYPSIN, which cleaves off the N-terminal peptide from the receptor. The new N-terminal peptide is a cryptic ligand for the receptor. The uncleaved receptor can also be activated by the N-terminal peptide present on the activated THROMBIN RECEPTOR and by small synthetic peptides that contain the unmasked N-terminal sequence.
A form of acupuncture with electrical impulses passing through the needles to stimulate NERVE TISSUE. It can be used for ANALGESIA; ANESTHESIA; REHABILITATION; and treatment for diseases.
Painful sensation in the muscles.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
A class of opioid peptides including dynorphin A, dynorphin B, and smaller fragments of these peptides. Dynorphins prefer kappa-opioid receptors (RECEPTORS, OPIOID, KAPPA) and have been shown to play a role as central nervous system transmitters.
A protein kinase C subtype that was originally characterized as a CALCIUM-independent, serine-threonine kinase that is activated by PHORBOL ESTERS and DIACYLGLYCEROLS. It is targeted to specific cellular compartments in response to extracellular signals that activate G-PROTEIN-COUPLED RECEPTORS; TYROSINE KINASE RECEPTORS; and intracellular protein tyrosine kinase.
Cell membrane proteins that bind opioids and trigger intracellular changes which influence the behavior of cells. The endogenous ligands for opioid receptors in mammals include three families of peptides, the enkephalins, endorphins, and dynorphins. The receptor classes include mu, delta, and kappa receptors. Sigma receptors bind several psychoactive substances, including certain opioids, but their endogenous ligands are not known.
A broad group of eukaryotic six-transmembrane cation channels that are classified by sequence homology because their functional involvement with SENSATION is varied. They have only weak voltage sensitivity and ion selectivity. They are named after a DROSOPHILA mutant that displayed transient receptor potentials in response to light. A 25-amino-acid motif containing a TRP box (EWKFAR) just C-terminal to S6 is found in TRPC, TRPV and TRPM subgroups. ANKYRIN repeats are found in TRPC, TRPV & TRPN subgroups. Some are functionally associated with TYROSINE KINASE or TYPE C PHOSPHOLIPASES.
A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.
Aching sensation that persists for more than a few months. It may or may not be associated with trauma or disease, and may persist after the initial injury has healed. Its localization, character, and timing are more vague than with acute pain.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
The time from the onset of a stimulus until a response is observed.
Dull or sharp aching pain caused by stimulated NOCICEPTORS due to tissue injury, inflammation or diseases. It can be divided into somatic or tissue pain and VISCERAL PAIN.
Surgical interruption of a spinal or cranial nerve root. (From Dorland, 28th ed)
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Elements of limited time intervals, contributing to particular results or situations.
Traumatic injuries to the TRIGEMINAL NERVE. It may result in extreme pain, abnormal sensation in the areas the nerve innervates on face, jaw, gums and tongue and can cause difficulties with speech and chewing. It is sometimes associated with various dental treatments.
A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.
Absent or reduced sensitivity to cutaneous stimulation.
Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines.
Region of the back including the LUMBAR VERTEBRAE, SACRUM, and nearby structures.
An eph family receptor found primarily in the nervous system. In the embryonic BRAIN EphB1 receptor expression occurs in the mantle layer and increases with the progression of embryogenesis. In adult brain it is found in the several regions including the CEREBELLUM; CEREBRAL CORTEX; and CAUDATE NUCLEUS; and PUTAMEN.
A potent narcotic analgesic, abuse of which leads to habituation or addiction. It is primarily a mu-opioid agonist. Fentanyl is also used as an adjunct to general anesthetics, and as an anesthetic for induction and maintenance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1078)
Intravenous anesthetics that induce a state of sedation, immobility, amnesia, and marked analgesia. Subjects may experience a strong feeling of dissociation from the environment. The condition produced is similar to NEUROLEPTANALGESIA, but is brought about by the administration of a single drug. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed)
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Disease of the TIBIAL NERVE (also referred to as the posterior tibial nerve). The most commonly associated condition is the TARSAL TUNNEL SYNDROME. However, LEG INJURIES; ISCHEMIA; and inflammatory conditions (e.g., COLLAGEN DISEASES) may also affect the nerve. Clinical features include PARALYSIS of plantar flexion, ankle inversion and toe flexion as well as loss of sensation over the sole of the foot. (From Joynt, Clinical Neurology, 1995, Ch51, p32)
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Rapidly decreasing response to a drug or physiologically active agent after administration of a few doses. In immunology, it is the rapid immunization against the effect of toxic doses of an extract or serum by previous injection of small doses. (Dorland, 28th ed)
A subclass of cannabinoid receptor found primarily on immune cells where it may play a role modulating release of CYTOKINES.
Forceful administration under the skin of liquid medication, nutrient, or other fluid through a hollow needle piercing the skin.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
A voltage-gated sodium channel subtype that is expressed in nociceptors, including spinal and trigeminal sensory neurons. It plays a role in the transmission of pain signals induced by cold, heat, and mechanical stimuli.
A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.

Cardiovascular and neuronal responses to head stimulation reflect central sensitization and cutaneous allodynia in a rat model of migraine. (1/2095)

Reduction of the threshold of cardiovascular and neuronal responses to facial and intracranial stimulation reflects central sensitization and cutaneous allodynia in a rat model of migraine. Current theories propose that migraine pain is caused by chemical activation of meningeal perivascular fibers. We previously found that chemical irritation of the dura causes trigeminovascular fibers innervating the dura and central trigeminal neurons receiving convergent input from the dura and skin to respond to low-intensity mechanical and thermal stimuli that previously induced minimal or no responses. One conclusion of these studies was that when low- and high-intensity stimuli induce responses of similar magnitude in nociceptive neurons, low-intensity stimuli must be as painful as the high-intensity stimuli. The present study investigates in anesthetized rats the significance of the changes in the responses of central trigeminal neurons (i.e., in nucleus caudalis) by correlating them with the occurrence and type of the simultaneously recorded cardiovascular responses. Before chemical stimulation of the dura, simultaneous increases in neuronal firing rates and blood pressure were induced by dural indentation with forces >/= 2.35 g and by noxious cutaneous stimuli such as pinching the skin and warming > 46 degrees C. After chemical stimulation, similar neuronal responses and blood pressure increases were evoked by much smaller forces for dural indentation and by innocuous cutaneous stimuli such as brushing the skin and warming it to >/= 43 degrees C. The onsets of neuronal responses preceded the onsets of depressor responses by 1.7 s and pressor responses by 4.0 s. The duration of neuronal responses was 15 s, whereas the duration of depressor responses was shorter (5.8 s) and pressor responses longer (22.7 s) than the neuronal responses. We conclude that the facilitated cardiovascular and central trigeminal neuronal responses to innocuous stimulation of the skin indicate that when dural stimulation induces central sensitization, innocuous stimuli are as nociceptive as noxious stimuli had been before dural stimulation and that a similar process might occur during the development of cutaneous allodynia during migraine.  (+info)

Cytokine-mediated inflammatory hyperalgesia limited by interleukin-4. (2/2095)

1. The effect of IL-4 on responses to intraplantar ( carrageenin, bradykinin, TNFalpha, IL-1beta, IL-8 and PGE2 was investigated in a model of mechanical hyperalgesia in rats. Also, the cellular source of the IL-4 was investigated. 2. IL-4, 30 min before the stimulus, inhibited responses to carrageenin, bradykinin, and TNFalpha, but not responses to IL-1beta, IL-8 and PGE2. 3. IL-4, 2 h before the injection of IL-1beta, did not affect the response to IL-1beta, whereas IL-4, 12 or 12+2 h before the IL-1beta, inhibited the hyperalgesia (-30%, -74%, respectively). 4. In murine peritoneal macrophages, murine IL-4 for 2 h before stimulation with LPS, inhibited (-40%) the production of IL-1beta but not PGE2. Murine IL-4 (for 16 h before stimulation with LPS) inhibited LPS-stimulated PGE2 but not IL-1beta. 5. Anti-murine IL-4 antibodies potentiated responses to carrageenin, bradykinin and TNFalpha, but not IL-1beta and IL-8, as well as responses to bradykinin in athymic rats but not in rats depleted of mast cells with compound 40/80. 6. These data suggest that IL-4 released by mast cells limits inflammatory hyperalgesia. During the early phase of the inflammatory response the mode of action of the IL-4 appears to be inhibition of the production TNFalpha, IL-1beta and IL-8. In the later phase of the response, in addition to inhibiting the production of pro-inflammatory cytokines, IL-4 also may inhibit the release of PGs.  (+info)

The effects of inflammation and inflammatory mediators on nociceptive behaviour induced by ATP analogues in the rat. (3/2095)

1. We have studied the behavioural effects of intraplantar injections of adenosine 5'-triphosphate (ATP) and related compounds in freely moving rats and investigated whether these nociceptive effects are augmented in the presence of inflammatory mediators. 2. We find that in normal animals ATP and analogues produce dose-dependent nocifensive behaviour (seen as bursts of elevation of the treated hindpaw), and localized thermal hyperalgesia. The rank order of potency was: alpha,beta-methyleneadenosine 5'-triphosphate (alpha,beta-methylene ATP) > 2-methylthioadenosine triphosphate (2-methylthio ATP) > ATP. After neonatal treatment with capsaicin, to destroy small calibre primary sensory neurones, nocifensive behaviour was largely absent. 3. The effects of ATP analogues were assessed in three models of peripheral sensitization: 2 h after dilute intraplantar carrageenan (0.25% w v(-1)); 24 h after irradiation of the hindpaw with ultraviolet (U.V.) B; immediately following prostaglandin E2 (PGE2) treatment. In all models the effect of alpha,beta-methylene ATP was greatly augmented. After carrageenan, significant hindpaw-lifting behaviour activity was induced by injection of only 0.05 nmol of alpha,beta-methylene ATP, some 100 times less than necessary in normal skin. 4. Our data suggest that it is much more likely that endogenous levels of ATP will reach levels capable of exciting nociceptors in inflamed versus normal skin. Our data also suggest the involvement of P2X3 receptor subunits in ATP-induced nociception.  (+info)

Role of protein kinase A in the maintenance of inflammatory pain. (4/2095)

Although the initiation of inflammatory pain (hyperalgesia) has been demonstrated to require the cAMP second messenger signaling cascade, whether this mechanism and/or other mechanisms underlie the continued maintenance of the induced hyperalgesia is unknown. We report that injection of adenylyl cyclase inhibitors before but not after injection of direct-acting hyperalgesic agents (prostaglandin E2 and purine and serotonin receptor agonists) resulted in reduction in hyperalgesia, evaluated by the Randall-Selitto paw-withdrawal test. In contrast, injection of protein kinase A (PKA) inhibitors either before or after these hyperalgesic agents resulted in reduced hyperalgesia, suggesting that hyperalgesia after its activation was maintained by persistent PKA activity but not by adenylyl cyclase activity. To evaluate further the role of PKA activity in the maintenance of hyperalgesia, we injected the catalytic subunit of PKA (PKACS) that resulted in hyperalgesia similar in magnitude to that induced by the direct-acting hyperalgesic agents but much longer in duration (>48 vs 2 hr). Injection of WIPTIDE (a PKA inhibitor) at 24 hr after PKACS reduced hyperalgesia, suggesting that PKACS hyperalgesia is not independently maintained by steps downstream from PKA. In summary, our results indicate that, once established, inflammatory mediator-induced hyperalgesia is no longer maintained by adenylyl cyclase activity but rather is dependent on ongoing PKA activity. An understanding of the mechanism maintaining hyperalgesia may provide important insight into targets for the treatment of persistent pain.  (+info)

Primary and secondary hyperalgesia in a rat model for human postoperative pain. (5/2095)

BACKGROUND: Previously, the authors developed and characterized a rat model for postoperative pain to learn more about pain produced by incisions. In this study, the responses to heat and mechanical stimuli were evaluated directly on or adjacent to the incision and at varying distances from the incision. METHODS: Rats were anesthetized with halothane and incisions were made at different locations in the plantar aspect of the foot. The response frequency to a blunt mechanical stimulus, the withdrawal threshold to von Frey filaments (15-522 mN), and the withdrawal latency to radiant heat were measured. Rats were tested before surgery, 2 h later, and then daily through postoperative day 9. RESULTS: After plantar incision, persistent hyperalgesia was observed immediately adjacent to or directly on the incision to punctate and blunt mechanical stimuli, respectively. The withdrawal threshold to punctate stimuli applied 1 cm from the incision was decreased through postoperative day 1. In a transitional area, between the distant and adjacent sites, the withdrawal threshold was intermediate and the duration of hyperalgesia was transient. Heat hyperalgesia was persistent but present when the stimulus was applied to the site of injury but not to a distant site. CONCLUSION: Robust primary hyperalgesia to punctate and blunt mechanical stimuli was present. Hyperalgesia distant to the wound, or secondary hyperalgesia, occurred in response to punctate mechanical stimuli, was short-lived, and required greater forces. These results suggest that the most persistent pain behaviors in this model are largely primary hyperalgesia.  (+info)

The novel analgesic compound OT-7100 (5-n-butyl-7-(3,4,5-trimethoxybenzoylamino)pyrazolo[1,5-a]pyrimid ine) attenuates mechanical nociceptive responses in animal models of acute and peripheral neuropathic hyperalgesia. (6/2095)

We investigated the effects of OT-7100, a novel analgesic compound (5-n-butyl-7-(3,4,5-trimethoxybenzoylamino)pyrazolo[1,5-a]pyrimidi ne), on prostaglandin E2 biosynthesis in vitro, acute hyperalgesia induced by yeast and substance P in rats and hyperalgesia in rats with a chronic constriction injury to the sciatic nerve (Bennett model), which is a model for peripheral neuropathic pain. OT-7100 did not inhibit prostaglandin E2 biosynthesis at 10(-8)-10(-4) M. Single oral doses of 3 and 10 mg/kg OT-7100 were effective on the hyperalgesia induced by yeast. Single oral doses of 0.1, 0.3, 1 and 3 mg/kg OT-7100 were effective on the hyperalgesia induced by substance P in which indomethacin had no effect. Repeated oral administration of OT-7100 (10 and 30 mg/kg) was effective in normalizing the mechanical nociceptive threshold in the injured paw without affecting the nociceptive threshold in the uninjured paw in the Bennett model. Indomethacin had no effect in this model. While amitriptyline (10 and 30 mg/kg) and clonazepam (3 and 10 mg/kg) significantly normalized the nociceptive threshold in the injured paw, they also increased the nociceptive threshold in the uninjured paw. These results suggest that OT-7100 is a new type of analgesic with the effect of normalizing the nociceptive threshold in peripheral neuropathic hyperalgesia.  (+info)

Nitric oxide mediates the central sensitization of primate spinothalamic tract neurons. (7/2095)

Nitric oxide (NO) has been proposed to contribute to the development of hyperalgesia by activating the NO/guanosine 3',5'-cyclic monophosphate (cGMP) signal transduction pathway in the spinal cord. We have examined the effects of NO on the responses of primate spinothalamic tract (STT) neurons to peripheral cutaneous stimuli and on the sensitization of STT cells following intradermal injection of capsaicin. The NO level within the spinal dorsal horn was increased by microdialysis of a NO donor, 3-morpholinosydnonimine (SIN-1). SIN-1 enhanced the responses of STT cells to both weak and strong mechanical stimulation of the skin. This effect was preferentially on deep wide dynamic range STT neurons. The responses of none of the neurons tested to noxious heat stimuli were significantly changed when SIN-1 was administered. Intradermal injection of capsaicin increased dramatically the content of NO metabolites, NO-2/NO-3, within the dorsal horn. This effect was attenuated by pretreatment of the spinal cord with a nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). Sensitization of STT cells induced by intradermal injection of capsaicin was also prevented by pretreatment of the dorsal horn with the NOS inhibitors, L-NAME or 7-nitroindazole. Blockade of NOS did not significantly affect the responses of STT cells to peripheral stimulation in the absence of capsaicin injection. The data suggest that NO contributes to the development and maintenance of central sensitization of STT cells and the resultant mechanical hyperalgesia and allodynia after peripheral tissue damage or inflammation. NO seems to play little role in signaling peripheral stimuli under physiological conditions.  (+info)

Epinephrine produces a beta-adrenergic receptor-mediated mechanical hyperalgesia and in vitro sensitization of rat nociceptors. (8/2095)

Hyperalgesic and nociceptor sensitizing effects mediated by the beta-adrenergic receptor were evaluated in the rat. Intradermal injection of epinephrine, the major endogenous ligand for the beta-adrenergic receptor, into the dorsum of the hindpaw of the rat produced a dose-dependent mechanical hyperalgesia, quantified by the Randall-Selitto paw-withdrawal test. Epinephrine-induced hyperalgesia was attenuated significantly by intradermal pretreatment with propranolol, a beta-adrenergic receptor antagonist, but not by phentolamine, an alpha-adrenergic receptor antagonist. Epinephrine-induced hyperalgesia developed rapidly; it was statistically significant by 2 min after injection, reached a maximum effect within 5 min, and lasted 2 h. Injection of a more beta-adrenergic receptor-selective agonist, isoproterenol, also produced dose-dependent hyperalgesia, which was attenuated by propranolol but not phentolamine. Epinephrine-induced hyperalgesia was not affected by indomethacin, an inhibitor of cyclo-oxygenase, or by surgical sympathectomy. It was attenuated significantly by inhibitors of the adenosine 3',5'-cyclic monophosphate signaling pathway (the adenylyl cyclase inhibitor, SQ 22536, and the protein kinase A inhibitors, Rp-adenosine 3',5'-cyclic monophosphate and WIPTIDE), inhibitors of the protein kinase C signaling pathway (chelerythrine and bisindolylmaleimide) and a mu-opioid receptor agonist DAMGO ([D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin). Consistent with the hypothesis that epinephrine produces hyperalgesia by a direct action on primary afferent nociceptors, it was found to sensitize small-diameter dorsal root ganglion neurons in culture, i. e., to produce an increase in number of spikes and a decrease in latency to firing during a ramped depolarizing stimulus. These effects were blocked by propranolol. Furthermore epinephrine, like several other direct-acting hyperalgesic agents, caused a potentiation of tetrodotoxin-resistant sodium current, an effect that was abolished by Rp-adenosine 3',5'-cyclic monophosphate and significantly attenuated by bisindolylmaleimide. Isoproterenol also potentiated tetrodotoxin-resistant sodium current. In conclusion, epinephrine produces cutaneous mechanical hyperalgesia and sensitizes cultured dorsal root ganglion neurons in the absence of nerve injury via an action at a beta-adrenergic receptor. These effects of epinephrine are mediated by both the protein kinase A and protein kinase C second-messenger pathways.  (+info)

Neuropathic pain affects 7-10% of people, but responds poorly to pharmacotherapy, indicating a need for better treatments. Mechanistic research on neuropathic pain frequently uses human surrogate models of the secondary hyperalgesia that is a common feature of neuropathic pain. Experimentally induced secondary hyperalgesia has been manipulated with pharmacological and non-pharmacological methods to clarify the relative contributions of different mechanisms to secondary hyperalgesia. However, this literature has not been systematically synthesised. The aim of this systematic review is to identify, describe, and compare methods that have been used to manipulate experimentally induced secondary hyperalgesia in healthy humans. A systematic search strategy will be supplemented by reference list checks and direct contact with identified laboratories to maximise the identification of data reporting the experimental manipulation of experimentally induced secondary hyperalgesia in healthy humans. Duplicated
A method to measure cutaneous hyperalgesia to thermal stimulation in unrestrained animals is described. The testing paradigm uses an automated detection of the behavioral end-point; repeated testing does not contribute to the development of the observed hyperalgesia. Carrageenan-induced inflammation resulted in significantly shorter paw withdrawal latencies as compared to saline-treated paws and these latency changes corresponded to a decreased thermal nociceptive threshold. Both the thermal method and the Randall-Selitto mechanical method detected dose-related hyperalgesia and its blockade by either morphine or indomethacin. However, the thermal method showed greater bioassay sensitivity and allowed for the measurement of other behavioral parameters in addition to the nociceptive threshold.
Hyperalgesia (/ˌhaɪpərælˈdʒiziə/ or /-siə/; hyper from Greek ὑπέρ (huper, over), -algesia from Greek algos, ἄλγος (pain)) is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves. Prostaglandins E and F are largely responsible for sensitizing the nociceptors. Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection. Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have established that it is possible to experience a learned hyperalgesia of the latter, diffuse form. The focal form is typically associated with injury, and is divided into two subtypes: Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues. Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues. Opioid-induced hyperalgesia may develop as a result of long-term ...
Interleukin-17 (IL-17) and tumour necrosis factor-α (TNF) are critical in the pathogenesis of arthritis but their relationship during inflammatory pain has received limited attention. We aimed to establish whether IL-17 can induce hyperalgesia in acute conditions, and investigated the role of TNF in mediating the pain response. Hyperalgesia was elicited in C57BL/6 mice by injection of recombinant IL-17, TNF or vehicle into the plantar tissue. Elevated pain was measured by the Hargreaves test for thermal hyperalgesia and Linton incapacitance tester for weight-bearing change. Cellular infiltration during hyperalgesia was determined by histological analysis and myeloperoxidase assay. IL-17 was found to induce hyperalgesia, but this was dependent on neutrophil migration and TNF binding to TNF receptor 1 (TNFR1). Because TNF-induced hyperalgesia was also dependent on neutrophil migration, the relationship between the resident fibroblasts, the cytokines and the migrating neutrophils was further investigated.
This project investigates the phenomenon of opioid-induced hyperalgesia (OIH). Opioid analgesics, in addition to their therapeutic anti-nociceptive effects, under some conditions produce pro-nociceptive effects. This phenomenon of pain or pain sensitivity being increased by prior opioid administration is called opioid-induced hyperalgesia. It is thought to be relevant both to pain management complications and to complications of opioid dependence and its treatment. This study investigated the time-course of opioid-induced hyperalgesia development in healthy normal volunteers (N=12 completers), using a series of acute alfentanil administrations (15 mg/kg mg intramuscular (IM) per day) spaced at 3-4 day intervals, with testing for pain tolerance using the cold pressor test (CPT), and mechanical quantitative sensory testing (MQST) each administered repeatedly over time within each testing day. The goal was to determine the time course of OIH development following acute opioid administration, and to ...
One of the key findings of this study is that whereas metformins sex differential effect on neuropathic pain (Inyang et al., 2019) can also be observed in the incisional pain model, other AMPK activators did not have a sex-specific effect on pain in our experiments. NCLS, ZLN-024, and MK 8722 all had the same level of efficacy on hyperalgesic priming in male and female mice. Metformin had a robust initial antihyperalgesic effect and blocked hyperalgesic priming in male mice but showed no effect in female mice. These sex differences are not readily explained by the pharmacokinetics of metformin. In fact, female mice had higher plasma and brain levels of metformin than did male mice. Although we do not have an explanation for the sex differences in metformins efficacy in incisional or neuropathic pain models in mice, our work does illustrate that other AMPK activators can be effective in the incisional model in both sexes. A possible mechanism that can be explored in future work is sexual ...
Hermal hyperalgesia at 1 or 7 days right after CFA injection, the plantar test was MedChemExpress Acacetin performed around the mice at 30 min after DHA or
Blockade of prostaglandin (PG) production by COX inhibitors is the treatment of choice for inflammatory pain but is also prone to severe side effects. Identification of signaling elements downstream of COX inhibition, particularly of PG receptor subtypes responsible for pain sensitization (hyperalgesia), provides a strategy for better-tolerated analgesics. Here, we have identified PGE2 receptors of the EP2 receptor subtype as key signaling elements in spinal inflammatory hyperalgesia. Mice deficient in EP2 receptors (EP2-/- mice) completely lack spinal PGE2-evoked hyperalgesia. After a peripheral inflammatory stimulus, EP2-/- mice exhibit only short-lasting peripheral hyperalgesia but lack a second sustained hyperalgesic phase of spinal origin. Electrophysiological recordings identify diminished synaptic inhibition of excitatory dorsal horn neurons as the dominant source of EP2 receptor-dependent hyperalgesia. Our results thus demonstrate that inflammatory hyperalgesia can be treated by ...
Exaggerated pain and hyperalgesia are major issues after surgery and can lead to chronic pain. Opioid are parts of pain sensitization processes but remain absolutely necessary in the intraoperative period. NMDA receptor antagonists succeed in reducing this pain sensitization process. Recent studies show that in pain and opioid-experienced rats (POER) fentanyl ultra low doses do not induce analgesia, as observed in naive rats, but hyperalgesia. This is the first demonstration that a drug can induce opposite effect depending on individual history. We also observed a strong correlation between this hyperalgesic response in POER and the intensity of hyperalgesia they develop later, after inflammatory or surgical pain. The main aim of this study is to measure the dose effect response to fentanyl ultra low doses on human volunteers nociceptive threshold, to determine if such an opposite response profile can be revealed ...
Experimental and clinical studies showed that intraoperative infusionof remifentanil has been associated with postoperative hyperalgesia. Previous reports suggested that spinal N-methyl-D-aspartate (NMDA) receptors may contribute to the development and maintenance of opioid-induced hyperalgesia. In the present study, we used a rat model of postoperative pain to investigate the role of tyrosine phosphorylation of NMDA receptor 2B (NR2B) subunit in spinal cord in the postoperative hyperalgesia induced by remifentanil and the intervention of pretreatment with ketamine. Intraoperative infusion of remifentanil (0.04 mg/kg, subcutaneous) significantly enhanced mechanical allodynia and thermal hyperalgesia induced by the plantar incision during the postoperative period (each lasting between 2 h and 48 h), which was attenuated by pretreatment with ketamine (10 mg/kg, subcutaneous). Correlated with the pain behavior changes, immunocytochemical and western blotting experiments in our study revealed that there was
TY - JOUR. T1 - Spinal and supraspinal mechanisms of neuropathic pain. AU - Ossipov, Michael H.. AU - Lai, Josephine. AU - Malan, T. Philip. AU - Porreca, Frank. PY - 2000. Y1 - 2000. N2 - Neuropathic pain is associated with abnormal tactile and thermal responses that may be extraterritorial to the injured nerve. Importantly, tactile allodynia and thermal hyperalgesia may involve separate pathways, since complete and partial spinal cord lesions have blocked allodynia, but not hyperalgesia, after spinal nerve ligation (SNL). Furthermore, lesions of the dorsal column, and lidocaine microinjected into dorsal column nuclei block only tactile allodynia. Conversely, thermal hyperalgesia, but not tactile allodynia was blocked by desensitizatin of C-fibers with resiniferotoxin. Therefore, it seems that tactile allodynia is likely to be mediated by large diameter AP fibers, and not susceptible to modulation by spinal opioids, whereas hyperalgesia is mediated by unmyelinated C-fibers, and is sensitive to ...
Adam Hargreaves is the son of Roger Hargreaves, creator of the popular childrens book series Mr. Men and Little Miss. After his fathers death he has continued the franchise. He is also active as a painter. Adam Hargreaves was born in 1963 in Surrey as son of Roger Hargreaves, a concept artist in an advertising company whod become famous from 1971 on as...
The present study was designed to clarify whether the recently detected IKKε is involved in inflammatory nociception and, if yes, whether this process is mediated by modulation of NF-κB activity. We showed that IKKε mRNA and protein are expressed in DRG and spinal cord and are upregulated during paw inflammation. Neurons and glia apparently contribute to this adaptation because we observed an upregulation of IKKε protein in primary cultured neurons, astrocytes, and microglia upon inflammatory stimulation. IKKε-deficient mice show attenuated nociceptive behavior in inflammatory models. This effect could be mimicked pharmacologically in C57BL/6 mice by treatment with the IKKε inhibitor BX795. From these results, we inferred that IKKε at basal levels is involved in early inflammatory nociception, as shown in the formalin test, whereas its upregulation contributes to the sensitization of the nervous system during inflammation and the manifestation of hyperalgesia, as observed in the late ...
Insights into components governing image resolution of inflammatory pain happen to be of great importance for many long-term pain-associated disorders. IL-1β- and carrageenan-induced inflammatory hyperalgesia. Just lately we exhibited that IL-1β- and carrageenan-induced hyperalgesia is certainly significantly long term in LysM-GRK2+/? mice which may have reduced degrees of G-protein-coupled radio kinase a couple of (GRK2) in LysM+ myeloid cells. In this article we demonstrate that adoptive transfer of wild-type although not of GRK2+/? bone marrow-derived monocytes normalizes ARL-15896 the image resolution of IL-1β-induced hyperalgesia in LysM-GRK2+/? rats. Adoptive copy of IL-10? /? cuboid marrow-derived monocytes failed to stabilize the life long IL-1β-induced hyperalgesia in LysM-GRK2+/? mice. We all show that GRK2+/ mechanistically? macrophages develop less IL-10 in vitro. In addition intrathecal IL-10 treatment attenuated IL-1β-induced hyperalgesia in LysM-GRK2+/? rats whereas zero ...
Previous studies suggest that cholecystokinin (CCK) is implicated in the modulation of pain sensitivity and the development of neuropathic pain. We used CCK(2) receptor deficient (CCK(2) (-/-)) mice and assessed their mechanical sensitivity using Von Frey filaments, as well as the development and time course of mechanical hyperalgesia in a model of neuropathic pain. We found that CCK(2) (-/-) mice displayed mechanical hyposensitivity, which was reversed to the level of wild-type animals after administration of naloxone (0.1-10 mg/kg). On the other hand, injection of L-365260 (0.01-1 mg/kg), an antagonist of CCK(2) receptors, decreased dose-dependently, mechanical sensitivity in wild-type mice. The mechanism of reduced mechanical sensitivity in CCK(2) (-/-) mice may be explained by changes in interactions between CCK and opioid systems. Indeed, CCK(2) (-/-) mice natively expressed higher levels of lumbar CCK(1), opioid delta and kappa receptors. Next, we found that CCK(2) (-/-) mice did not ...
In the present study, we observed early microglial hyperactivation at 1-3 d after CCI-ION, followed by a prolonged astrocytic hyperactivation in the RVM lasting at least for 28 d, with a peak expression at 14 d. As expected, inhibition of local glial hyperactivation in the RVM using propentofylline significantly attenuated mechanical hyperalgesia/allodynia at both 3 and 14 d after nerve injury. Interestingly, microinjection of the microglial inhibitor minocycline in the RVM blocked CCI-induced hyperalgesia/allodynia at the early phase (3 d) but not the later phase (14 d). In contrast, fluorocitrate, when used at lower doses in the RVM, only attenuated behavioral hypersensitivity at the later phase. Consistent with our finding, studies with disruption of spinal microglial function by intrathecal injection or local application of minocycline suggest that spinal microglial hyperactivation is required for the initiation, but not the maintenance of nerve injury-induced hyperalgesia (Ledeboer et al., ...
EXPERIMENTAL APPROACH: After 14 consecutive days of intraperitoneal CBDA-ME administration at 0.01, 0.1, and 1 μg/kg, commencing one day after surgically implanting a sciatic nerve-constricting cuff to induce NEP, the anti-nociceptive efficacy of this cannabinoid was assessed in male and female Sprague-Dawley rats relative to vehicle-treated counterparts. In females, 2 and 4 μg/kg daily doses of CBDA-ME were also evaluated. Behavioural tests were performed for hind paw mechanical and thermal withdrawal thresholds once a week for eight weeks. At endpoint, in vivo electrophysiological recordings were obtained to characterize soma threshold changes in primary sensory neurons ...
Our primary aim is to determine whether perioperative NMDA-receptor antagonism has differential effects on postoperative pain, hyperalgesia and morbidity in younger and older patients. In order to achieve this aim, we propose to conduct the first randomized, double-blind placebo-controlled study designed to investigate age differences in the effects of perioperative oral administration of an NMDA-receptor antagonist (amantadine) in men undergoing radical prostatectomy. In addition, age differences in psychosocial factors and the pharmacological properties of amantadine and morphine will be measured to control for, and clarify, their contribution to the differences found. ...
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One of the mechanisms used to describe the genesis of chronic pain is peripheral sensitisation. This constitutes a decreased threshold and increased responsiveness of nociceptors due to post-translational changes in, and altered trafficking of, transducer receptors and ion channels. Clinincal characteristics of peripheral clinical pain are pain after the end of a stimulus and a spread of sensitivity to normal tissue induced by local inflammatory mediators. This is referred to as the zone of primary hyperalgesia.1. In contrast, in chronic neuropathic pain the mechanically sensitive skin area often extends beyond the area of the initially involved root or nerve to create a zone of secondary hyperalgesia. This area is unaffected by the primary nerve lesion, which often becomes independent of the initial noxious event.. ...
IB4-saporin attenuates acute and eliminates chronic muscle pain in the rat.. Alvarez P, Gear RW, Green PG, Levine JD.. Exp Neurol 233(2):859-865, 2012.. In order to clarify the roles of isolectin B4-positive and IB4-negative nociceptors in inflammatory and ergonomic muscle pain, the authors administered 3.2 µg of IB4-SAP (Cat. #IT-10) into the intrathecal space of rats. Although the baseline mechanical nociceptive threshold was not affected in the lesioned animals, mechanical hyperalgesia had a shorter duration. In the ergonomic models peak hyperalgesia was attenuated, and prolongation of PGE2-induced mechanical hyperalgesia was completely prevented.. Age-related Accumulation of Non-heme Ferric and Ferrous Iron in Mouse Ovarian Stroma Visualized by Sensitive Non-heme Iron Histochemistry.. Asano Y.. J Histochem Cytochem 60(3):229-242, 2012.. The mammalian ovary engages in continuous growth and cellular differentiation as long as the animal is capable of reproduction. During these processes iron ...
In the present study, we investigated the in vivo contribution of TRPC5 to the local inflammatory changes that occur in arthritis using pharmacogenomic approaches. We show that genetic deletion or blockade of TRPC5 in arthritic mice resulted in marked exacerbation of hyperalgesia and, critically, increased localised inflammation in the synovium characterised by increased cellular infiltration, secretion of early response cytokines and enhanced synovial vascularisation. This provides the first in vivo evidence to show that TRPC5 acts as a regulatory channel to protect the joint against inflammatory insults.. Joint pain remains an unmet clinical need,1 and patients with RA exhibit symmetry in both their clinical symptoms and pain. Peripheral and central sensitisation, characterised by pain radiating to an unaffected site, is a common feature.4 ,15 ,23 We designed experiments to investigate this by inducing unilateral arthritis, which resulted in primary hyperalgesia, in addition to symmetrical ...
This page contains the abstract Joint Manipulation Reduces Hyperalgesia By Activation of Monoamine Receptors But Not Opioid or GABA Receptors in the Spinal Cord
Neuropathic pain is a difficult to treat disorder arising from central or peripheral nervous system lesions. The etiology of neuropathic pain consists of several overlapping pathways converging into an exaggerated pain state with symptoms such as allodynia and hyperalgesia. One of these pathways involves activation of spinal cord microglia and astrocytes, which drive and maintain the inflammatory response following the lesion. These cells are a potential target for drugs for neuropathic pain relief. In this current study, we investigated the dose-effect relationship of the tissue protective peptide ARA 290, derived from the tertiary structure of erythropoietin, on allodynia and concurrent spinal cord microglia and astrocytes. Following a spared nerve injury in rats, vehicle or ARA290 (administered in either one of 4 doses: 3, 10, 30 and 60 μg/kg) was administered on days 1, 3, 6, 8 and 10. ARA290 exerted a dose-response effect by significantly reducing mechanical allodynia up to 20 weeks when compared
Mechanical hyperalgesia Paw withdrawal mechanical threshold (PWMT) was determined by applying a von Frey hair filament (Stoelting Co., Chicago, IL, USA) to the hind paw until a positive indicator of pain behavior was elicited (19). Evaluation thresholds were as follows: The mid-plantar paw was assessed in the area of the sciatic nerve, avoiding the footpads. The von Frey filaments with logarithmically incremental stiffness (0.4-15.1 g) were applied serially to the paw via the up-down method. The hairs were presented in ascending order of strength, perpendicular to the plantar surface with sufficient force to cause slight bending against the paw, and were held for 6-8 sec. A positive response was recorded if the paw was sharply withdrawn. Flinching immediately upon removal of the hair was also considered a positive response. A 15.1 g hair was selected as the upper limit for testing. If there was no response at 15.1 g pressure, rats were assigned the upper limit value. A bending force able to ...
Researchers using siRNA complexed with our i-Fect ™ transfection regent have successfully knocked down ASIC3 Receptors in vivo. This publication joins the growing parade (starting with Luo et al, 2005) that reference successful modulation of receptors involved in pain using siRNA complexes. These studies all share animal behavior studies showing a marked change in response to pain stimuli after treatment.. In this study, Dr. Eric Lingueglia and his team found Peripheral ASIC3 channels are thus essential sensors of acidic pain and integrators of molecular signals produced during inflammation where they contribute to primary hyperalgesia.. Emmanuel Deval, Jacques Noël, Nadège Lay, Abdelkrim Alloui, Sylvie Diochot, Valérie Friend, Martine Jodar, Michel Lazdunski and Eric Lingueglia. ASIC3, a sensor of acidic and primary inflammatory pain. The EMBO Journal advance online publication 16 October 2008; doi: 10.1038/emboj.2008.213. Cy3-labelled siRNA no. 1121 and its corresponding scramble (no. ...
Infection, we discovered infection with each mid-log and stationary phase S. aureus-induced comparable levels of both spontaneous pain and mechanical hyperalgesia (Supplementary Fig. 2). For that reason, reside S. aureus infection induces instant, dose-dependent spontaneous pain, followed by robust mechanical and thermal hyperalgesia that lasts for days post infection. The agr locus mediates pain and nociceptor neuron activation. We subsequent compared diverse virulent strains of S. aureus in their abilities to create discomfort. USA300 and USA500, two epidemic strains of MRSA15,17, created substantial levels of spontaneous discomfort upon infection that were related in magnitude to each other (Fig. 1d). The methicillin-sensitive Newman strain, which expresses lower levels of virulence determinants than USA300 or USA50017, also produced spontaneous pain, although not drastically above PBS injection (Fig. 1d). These information indicate pain may be connected to the expression of virulence ...
Mr David Hargreaves is a specialist consultant at Spire Southampton Hospital. Get in touch now for expert advice and treatments provided at Spire Healthcare.
Diana Hargreaves, Ph.D. is currently a postdoctoral scholar in the laboratory of Gerald Crabtree at Stanford University. She is investigating the function of a…
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Just read an interesting article by our friends at Work Comp Roundup on Opioid-Induced Hyperalgesia (OIH). In cases where an individual is taking large
Inflammation causes an increased synthesis of COX-2-dependent prostaglan- dins, which sensitize peripheral nociceptor terminals and produce localized pain hypersensitivity. Prostaglandins regulate the sensitivity of so-called poly- modal nociceptors that are ...
An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve ...
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Last Tuesday, after whingeing at my GP by email about the inordinate length of time and multiple appointments(8), I had undergone, still without resolution of my angina problems, I received a surprise phone call from my cardiologists secretary, saying they could finally operate to insert a stent in the artery of my heart as an urgent procedure that Friday (15th) at 7.30am at the Manchester Royal Hospital. Yippee quoth I, had they finally cut-to- the-chase after seven months of, what was to me, wasting time and NHS resources on a condition that was already identified and quantified. My cancer consultant and my GP had both made clear the need for speed at the outset, because of the likelihood of me requiring chemotherapy imminently. But seven months and eight inconclusive appointments had so far not resolved the matter and it looked as though another few weeks waiting was likely.. But nonetheless I was delighted to be finally getting done. So as Friday 15th August dawned at 5am, Jane and I ...
Will systematic screening of a major drug database identify new candidates for ME/CFS treatment? And does fibromyalgia-like central pain sensitization
TY - JOUR. T1 - Role of spinal cord alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors in complete Freunds adjuvant-induced inflammatory pain. AU - Park, Jang Su. AU - Yaster, Myron. AU - Guan, Xiaowei. AU - Xu, Ji Tian. AU - Shih, Ming Hung. AU - Guan, Yun. AU - Raja, Srinivasa N.. AU - Tao, Yuan Xiang. PY - 2008/12/30. Y1 - 2008/12/30. N2 - Spinal cord α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) mediate acute spinal processing of nociceptive and non-nociceptive information, but whether and how their activation contributes to the central sensitization that underlies persistent inflammatory pain are still unclear. Here, we examined the role of spinal AMPARs in the development and maintenance of complete Freunds adjuvant (CFA)-induced persistent inflammatory pain. Intrathecal application of two selective non-competitive AMPAR antagonists, CFM-2 (25 and 50 μg) and GYKI 52466 (50 μg), significantly attenuated mechanical and thermal hypersensitivities ...
Background: Diabetes mellitus in some clinical cases is accompanied with hyperalgesia. In this study, we evaluated the possible beneficial effect of chronic pelargonidin (PG) treatment on hyperalgesia in streptozotocin (STZ)-diabetic neuropathic rat. Methods: Male Wistar rats (n = 56) were divided into seven groups, i.e. control, diabetic, PG-treated control, PG (single- ...
Any form of hyperalgesia manifests itself by increased pain, which is intensified by stimulation or application of the nociceptor. This is the case when one suffers from dental neuralgia, gingivitis and some cases of otitis. The same applies to all innervated parts of the body, on which manifestations of hyperalgesia are particularly acute, even without applying pressure on the painful area or stimulating it in any way whatsoever. Some types of hyperalgesia may result in severe pain caused by the slightest body movement or the stimulation of a proprioceptor (bones, muscles, ligaments, joints). But there also are other types of hyperalgesia that affect organs like the stomach, liver, kidneys and even the intestines. This is known as colic or abdominal hyperalgesia.. ...
Hyperalgesia was induced by injecting complete Freunds adjuvant (CFA, 0.08 ml, 40 μg Mycobacterium tuberculosis) into one hind paw of each rat. EA treatment, 10 Hz at 3 mA, was given at acupoint GB30 twice for 20 min each, once immediately post-CFA and again 2 hours later. Paw withdrawal latency (PWL) was tested before (-48 h) and 2 and 24 hours after CFA to assess behavioral hyperalgesia. IL-17 antibody (0.2-2 µg/rat) was given intrathecally (i.t.) 24 h before CFA to block the action of basal IL-17 and 2 hours prior to each of two PWL tests to block CFA-induced IL-17. I.t. recombinant IL-17 (10-400 ng/rat) was administered to naive rats to determine its effects on PWL and phosphorylation of NR1 (p-NR1). P-NR1 is known to modulate N-methyl-D-aspartate receptor (NMDAR) activity and to facilitate pain. Spinal cords were removed for immunostaining of IL-17, double immunostaining of IL-17/cell markers and IL-17 receptor subtype A (IL-17RA)/NR1, and western blot to measure p-NR1 and IL-17RA. ...
Peripheral inflammatory hyperalgesia depends on the sensitization of primary nociceptive neurons. Inflammation drives molecular alterations not only locally but also in the dorsal root ganglion (DRG) where interleukin-1 beta (IL-1β) and purinoceptors are upregulated. Activation of the P2X7 purinoceptors by ATP is essential for IL-1β maturation and release. At the DRG, P2X7R are expressed by satellite glial cells (SGCs) surrounding sensory neurons soma. Although SGCs have no projections outside the sensory ganglia these cells affect pain signaling through intercellular communication. Therefore, here we investigated whether activation of P2X7R by ATP and the subsequent release of IL-1β in DRG participate in peripheral inflammatory hyperalgesia. Immunofluorescent images confirmed the expression of P2X7R and IL-1β in SGCs of the DRG. The function of P2X7R was then verified using a selective antagonist, A-740003, or antisense for P2X7R administered in the L5-DRG. Inflammation was induced by CFA,
Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This seems to occur via immune cells interacting with the peripheral nervous system and releasing pain-producing chemicals (cytokines and chemokines).[4]. One unusual cause of focal hyperalgesia is platypus venom.[5]. Long-term opioid (e.g. heroin, morphine) users and those on high-dose opioid medications for the treatment of chronic pain, may experience hyperalgesia and experience pain out of proportion to physical findings, which is a common cause for loss of efficacy of these medications over time.[3][6][7] As it can be difficult to distinguish from tolerance, opioid-induced hyperalgesia is often compensated for by escalating the dose of opioid, potentially worsening the problem by further increasing sensitivity to pain. Chronic hyperstimulation of opioid receptors results in altered homeostasis of pain signalling pathways in the body with several mechanisms of action ...
Peripheral neuropathic pain is characterized by an increased activation of afferent nociceptors and sensitized afferent information through spinal processing [4, 24]. Mechanical allodynia, a central sensitization caused by peripheral noxious barrage to the spinal cord, is characterized by a painful sensation evoked by light touch, a normally innocuous stimulation. Touch-evoked pain is a hallmark of neuropathic pain and is triggered by spontaneous ectopic discharges from injured peripheral nerves to sensitized spinal dorsal horn cells. Although mechanisms of allodynia are not entirely understood, they may involve A-beta myelinated afferents [25], activated microglia and astrocytes [26-30], and dorsal horn neuron cells [28]. It has been shown that sodium channel blockers applied to the injured site [31], DRG [32] or the spinal cord [33] all effectively decrease neuropathic pain and attenuate hyperalgesia and allodynia. The present study demonstrates that intrathecal pretreatment with ...
β-Caryophyllene (BCP) is known as a common constitute of the essential oils of numerous food plants and primary component in Cannabis. In this study, we investigated the effect of local intraplantar ( injection of BCP on mechanical hypersensitivity induced by partial sciatic nerve ligation (PSNL) in mice. Relative to sham operation controls, mice with the PSNL displayed a maximum level of hyperresponsiveness to von Frey metallic filament on post-operative day 7. PSNL-induced allodynia was seen in the ipsilateral side of nerve ligation, but not in the contralateral side. The injection of BCP into the ipsilateral hindpaw to PSNL attenuated mechanical allodynia in a dose-dependent manner. BCP injection into the contralateral hindpaw did not produce anti-allodynic effects, suggesting a local peripheral anti-allodynic effect of BCP. Anti-allodynic effects induced by injection of BCP were prevented by pretreatment with the cannabinoid (CB2) receptor antagonist AM630, but not by the CB1
Pioglitazone attenuates tactile allodynia and thermal hyperalgesia in mice subjected to peripheral nerve injury. - Takehiko Maeda, Norikazu Kiguchi, Yuka Kobayashi, Masanobu Ozaki, Shiroh Kishioka
Several research papers on various aspects of SCI mechanisms and therapeutic applications have been published. Some of these publications evaluated WNK1, cation-dependent chloride transporters activation (NKCC1) and inhibition by bumetanide, cannabinoid receptors specially CB2 (anti-hyperalgesic effect of WIN 55,212-2), anti-hyperalgesic effects of bradykinin (B1) and vanilloid-1 (TRPV1) receptor antagonists, rolipram (specific PDE4 inhibitor) effect on thermal hyperalgesia, cyclooxygenase-2 (Cox2) inhibitor (meloxicam) and PPAR-gamma induction and ghrelin for control of SCI-induced neuropathic pain. I also presented the research findings at six national and three international meetings. I regularly supervise the undergraduate and med students working in the SCI lab. My research expertise encompasses all aspects of the present proposal including induction of SCI, monitoring functional recovery, measurements of neuropathic pain and evaluating the molecular mechanisms. In this project, I will ...
While protein kinase C epsilon has been shown to contribute to acute and chronic mechanical hyperalgesia, its upstream signaling pathway has received little attention. Since phospholipase C can signal to PKC epsilon and has been implicated in nociceptor sensitization, we tested if it is upstream of …
Methods: Using male and female Sprague-Dawley rats, spinal cord injuries were induced using a clip compression model at mid-thoracic levels. To assess neuropathic pain symptoms, we evaluated the development of tactile allodynia, cold allodynia, and heat hyperalgesia. First, we conducted dose-response analyses for both drugs using a battery of behavioral tests including the Von Frey test, the acetone evaporation test, and the Hargreaves test. Rats were tested at baseline and every 30 minutes for 2 hours post-injection. If some analgesic effects remained, they were again tested at 5- and 24-hours post-drug administration. CBD was tested at 0.1-5 mg/kg (ip) and BCP was orally administered (oral gavage) at 10-50 mg/kg. We then assessed for potential synergism using isobolographic analysis based on ratios of the single drug A50 values.. Results: Both CBD and BCP administered individually reduced cold and tactile hypersensitivity in both male and female rats. The combination of CBD and BCP produced ...
Allodynia (Ancient Greek άλλος állos other and οδύνη odúnē pain) refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain. Temperature or physical stimuli can provoke allodynia, which may feel like a burning sensation, and it often occurs after injury to a site. Allodynia is different from hyperalgesia, an extreme, exaggerated reaction to a stimulus which is normally painful. There are different kinds or types of allodynia: Mechanical allodynia (also known as tactile allodynia) Static mechanical allodynia - pain in response when touched Dynamic mechanical allodynia - pain in response to stroking lightly Thermal (hot or cold) allodynia - pain from normally mild skin temperatures in the affected area Movement allodynia - pain triggered by normal movement of joints or muscles Allodynia is a clinical ...
The results from this study show that injection of kaolin and carrageenan into the knee joint of the rat results in an acute arthritis which is characterized by secondary heat hyperalgesia, swelling of the knee joint and spontaneous pain. Microdialysis infusion of S-(+)-3-IBG or R-(−)-3-IBG through the dorsal horn of the spinal cord after inflammation of the knee joint reduced the amount of heat hyperalgesia and the spontaneous pain observed in a dose-dependent manner, but did not alter the amount of swelling of the knee joint when compared with rats treated with aCSF. Microdialysis infusion of either enantiomer for 1.5 h before the injection of kaolin and carrageenan (pretreatment) did not change the baseline responses to the noxious radiant heat stimulus. However, pretreatment with either enantiomer reduced the amount of swelling observed and blocked the development of secondary hyperalgesia and spontaneous pain normally observed after inflammation.. The antihyperalgesic effects of ...
The interplay of specific leukocyte subpopulations, resident cells and proalgesic mediators results in pain in inflammation. Proalgesic mediators like reactive oxygen species (ROS) and downstream products elicit pain by stimulation of transient receptor potential (TRP) channels. The contribution of leukocyte subpopulations however is less clear. Local injection of neutrophilic chemokines elicits neutrophil recruitment but no hyperalgesia in rats. In meta-analyses the monocytic chemoattractant, CCL2 (monocyte chemoattractant protein-1; MCP-1), was identified as an important factor in the pathophysiology of human and animal pain. In this study, intraplantar injection of CCL2 elicited thermal and mechanical pain in Wistar but not in Dark Agouti (DA) rats, which lack p47phox, a part of the NADPH oxidase complex. Inflammatory hyperalgesia after complete Freunds adjuvant (CFA) as well as capsaicin-induced hyperalgesia and capsaicin-induced current flow in dorsal root ganglion neurons in DA were comparable to
1) Charles Roger Hargreaves (9 May 1935 - 11 September 1988) was born at a private hospital in Cleckheaton, West Yorkshire, England.. 2) Roger Hargreaves always wanted to be a cartoonist and wrote his firs Mr. Men book, Mr. Tickle, while working as a creative director for an advertising agency.. 3) He had a difficult time finding a publisher, however once published the books were an instant success selling over one million copies in three years.. 4) He published his first Mr. Men book in 1971, by 1976 he quit his day job. The Little Miss book series appeared in 1981.. 5) Mr. Hargreaves wrote many other stories for children, including a series of 25 books called Timbuctoo.. ...
Neuropathic pain syndromes, i.e., pain after a lesion or disease of the peripheral or central nervous system, are clinically characterized by spontaneous pain (ongoing, paroxysms) and evoked types of pain (hyperalgesia, allodynia). A variety of distinct pathophysiological mechanisms in the peripheral and central nervous system operate in concert: In some patients the nerve lesion triggers molecular changes in nociceptive neurons that become abnormally sensitive and develop pathological spontaneous activity (upregulation of sodium channels and receptors, e.g., vanilloid TRPV1 receptors, menthol-sensitive TRPM8 receptors, or alpha-receptors). These phenomena may lead to spontaneous pain, shooting pain sensations, as well as heat hyperalgesia, cold hyperalgesia, and sympathetically maintained pain. Spontaneous activity in damaged large nonnociceptive A-fibers may lead to paresthesias. All these changes may also occur in uninjured neurons driven by substances released by adjacent dying cells and ...
What exactly is Hyperalgesia youre asking? Well, if you ask C. Scott McMillin, and what his credentials to be hypothesizing on chronic pain treatment are, I do not know, he would tell you that Hyperalgesia is when Opioid pain medication makes a patients pain worse despite having been on a stable dose. The problem with…
neuropathic pain - MedHelps neuropathic pain Center for Information, Symptoms, Resources, Treatments and Tools for neuropathic pain. Find neuropathic pain information, treatments for neuropathic pain and neuropathic pain symptoms.
TY - JOUR. T1 - Chronic Neuropathic Pain Following Hand Burns. T2 - Etiology, Treatment, and Long-Term Outcomes. AU - Klifto, Kevin M.. AU - Yesantharao, Pooja S.. AU - Dellon, A. Lee. AU - Hultman, C. Scott. AU - Lifchez, Scott D.. N1 - Funding Information: We thank Carrie Cox, MS, RN, and Vidhi Javia, BS, for assistance with coordinating clinical research at The Johns Hopkins Burn Center. Without their assistance our work would not be possible.. PY - 2021/1. Y1 - 2021/1. N2 - Purpose: Chronic neuropathic pain (CNP) after burn injury to the hand/upper extremity is relatively common, but not well described in the literature. This study characterizes patients with CNP after hand/upper extremity burns to help guide risk stratification and treatment strategies. We hypothesize that multiple risk factors contribute to the development of CNP and refractory responses to treatment. Methods: Patients older than 15 years admitted to the burn center after hand/upper extremity burns, from January 1, 2014, ...
0006]Many different neurotransmitter systems, ion channels and enzymes have been implicated in pain transmission, processing and controlling. Among them, serotonin (5-hydroxtryptamine [5-HT]), produced by central and peripheral serotonergic neurons but also by platelets and mast cells after tissue injury, has been described to exert algesic or analgesic effects depending on the site of action and the receptor subtype it acts on (Eide and Hole, 1993; Millan, 2002). At the peripheral level, after nerve injury, 5-HT is released in increased amounts and interacts with different 5-HT receptors present on C-fibers (Sommer, 2004). Acting in combination with other inflammatory mediators, 5-HT may ectopically excite and sensitize afferent nerve fibers, thus contributing to peripheral sensitization and hyperalgesia following inflammation and nerve injury (Beck and Handwerker, 1974; Obata et al., 2000). The central serotonin system has also been the subject of considerable research over the last twenty ...
GAINESVILLE - Florida DB Vernon Hargreaves is the latest to join an injury list of Gators from the Tampa Bay area.Hargreaves sprained his shoulder Wednesday and is expected to miss five to seve
The effects of capsaicin pretreatment of adult rats was investigated on consequences of unilateral paw inflammation induced by inoculation with Freunds adjuvant. Decrease in mechanical nociceptive threshold in the inflamed paw, as measured by the paw pressure test, was dose-dependently inhibited by …
Effects of ONO-4057 on pain behavior in the formalin test. Time course of pain behavior in mice pretreated with intraperitoneal (i.p.) (A), intraplantar (ipl.)
Persistent postoperative pain is a very common phenomenon which severely affects the lives of patients who develop it following common surgical procedures. activated protein kinase CGP60474 (MAPK) activation. To CGP60474 test this hypothesis rats were implanted with subcutaneous osmotic minipumps on day zero releasing saline or morphine for seven days preceding or seven days preceding and following paw incision surgery which was completed on day seven. Thermal hyperalgesia and mechanical allodynia were assessed postoperatively every three days. Chronic morphine attenuated the resolution of postoperative thermal hyperalgesia and mechanical allodynia through day twenty. However no changes in Iba1 or GFAP expression were observed in the spinal cord dorsal horn between groups. Assessment of MAPK protein phosphorylation revealed that chronic morphine administration enhanced both p38 and extracellular receptor kinase (pERK) phosphorylation compared to saline on day twenty. p-p38 and pERK ...
Ultiva® is commonly administered intravenously through standard anaesthesia. IbrutinibIts key constituent is remifentanil, a potent small-performing μ-opioid receptor agonist. Despite the fact that behavioural research in rats counsel that intrathecal administration of remifentanil induces profound analgesia, Ultiva® is not authorized for epidural or intrathecal use in medical observe.The medical formulation of Ultiva® is made up of glycine as an acidic buffer. Glycine is a main inhibitory neurotransmitter in the central anxious system, and is also an significant N-methyl-D-aspartate receptor co-activator with glutamate the latter motion is proposed as a likely mechanism for opioid-induced hyperalgesia. It has also been suggested that remifentanil by itself may well straight boost NMDA receptor-mediated responses in the dorsal horn and market hyperalgesia.Though these results counsel that intrathecal administration of Ultiva® might have contrary professional-nociceptive and anti-nociceptive ...
Ultiva® is commonly administered intravenously through standard anaesthesia. IbrutinibIts key constituent is remifentanil, a potent small-performing μ-opioid receptor agonist. Despite the fact that behavioural research in rats counsel that intrathecal administration of remifentanil induces profound analgesia, Ultiva® is not authorized for epidural or intrathecal use in medical observe.The medical formulation of Ultiva® is made up of glycine as an acidic buffer. Glycine is a main inhibitory neurotransmitter in the central anxious system, and is also an significant N-methyl-D-aspartate receptor co-activator with glutamate the latter motion is proposed as a likely mechanism for opioid-induced hyperalgesia. It has also been suggested that remifentanil by itself may well straight boost NMDA receptor-mediated responses in the dorsal horn and market hyperalgesia.Though these results counsel that intrathecal administration of Ultiva® might have contrary professional-nociceptive and anti-nociceptive ...
Ethyl pyruvate (EP) possesses anti-inflammatory activity. However, the potential anti-nociceptive value of EP for the treatment of the inflammatory nociception is largely unknown. We investigated whet
0241] The effect of siRNAs against Nav1.8, formulated with iFECT, on complete Freunds adjuvant-induced tactile hypersensitivity was evaluated in rats (FIG. 5). Adult male Sprague-Dawley rats received an injection of CFA (150 uL) into the hindpaw on day 0. siRNAs against Nav1.8 were then administered by intrathecal bolus to the lumbar region of the spinal cord on days 1, 2 and 3; specifically, for each bolus injection, 2 ug of siRNA was complexed with iFECT transfection reagent (Neuromics, Minneapolis Minn., USA) at a ratio of 1:4 (w:v) in a total volume of 10 uL. Five groups of rats (with 5 rats per group) were treated with either siRNA (AL-DP-6049, AL-DP-6209, AL-DP-6217 or AL-DP-6218; Table 1), or PBS, in the presence of iFECT. Tactile hypersensitivity was expressed as tactile withdrawal thresholds which were measured by probing the hindpaw with 8 calibrated von Frey filaments (Stoelting, Wood Dale Ill., USA) (0.41 g to 15 g). Each filament was applied to the plantar surface of the paw. ...
URB937 is a peripherally restricted inhibitor of the anandamide-deactivating enzyme fatty-acid amide hydrolase (FAAH). Despite its limited access to the CNS, URB937 produces marked antinociceptive effects in rodents. URB937 is actively extruded from the CNS by the ATP-binding cassette (ABC) membrane transporter, Abcg2. Tissue Abcg2 levels are markedly different between males and females, and this transporter is known to limit the access of xenobiotics to the fetoplacental unit in gestating female rodents. In the present study, we investigated the tissue distribution and antinociceptive properties of URB937 in female mice and rats.We studied the systemic disposition of URB937 in female mice and the antinociceptive effects of this compound in models of visceral (acetic acid-induced writhing) and inflammatory nociception (carrageenan-induced hyperalgesia) in female mice and rats. Furthermore, we evaluated the interaction of URB937 with the blood-placenta barrier in gestating mice and rats.Abcg2 ...
Takeshi Ono, Makato Inoue, Hiroshi Ueda, Koji Sumikawa; Room B, 10/16/2000 2: 00 PM - 4: 00 PM (PS) The Role of Receptor Subtypes in Bradykinin Hyperalgesia in Neuropathic Mice : A-923. Anesthesiology 2000; 93:A-923 doi: Download citation file:. ...
Objective: The objective of this study was to investigate the influence of gender and obesity on analgesic modulation of tramadol in Wistar rats.Methods: This study was carried out in two sets of experiments. In Set I experiment - 48 rats (body weight ≤150 g), 24 each male and female rats were randomly divided into two groups (n=6/group) (Group I - Control; 0.9% NaCl; 1 ml/kg/day i.p. and Group II - Tramadol 10 mg/kg/day i.p.) for each nociception model - plantar test and acetic acid-induced writhing test. The treatment duration was of 5 days. On the last day of treatment (i.e., on the 5th day), paw withdrawal latency (PWL) was assessed using plantar test, and writhing movements were observed following dministration of 0.8% acetic acid; 10 ml/kg i.p. Set II experiment was repeated like Set I experiment among rest 48 high- at diet-fed rats (body weight ≥300 g).Results: For both males and females, PWL was significantly decreased (p,0.05) in obese control groups compared to lean control groups. ...
Azarpazhooh, A., Diogenes, A. R., Fouad, A. F., Glickman, G. N., Kang, M. K., Kishen, A., Levin, L., Roda, R. S., Sedgley, C. M., Tay, F. R. & Hargreaves, K. M., Jan 2020, In : Journal of endodontics. 46, 1, p. 1-2 2 p.. Research output: Contribution to journal › Editorial ...
Mr. Men Sports Day by Roger Hargreaves | Buy Books at Theres going to be a Sports Day in Nonsenseland and all the Mr. Men are invited, but will it be what they are expecting? A silly, fun-filled sports day story featuring lots of your favourite Mr. Men characters showing their sporting prowess ... or not! Mr Men and Little Miss...Find out more
Mr. Cheerful by Roger Hargreaves | Buy Books at Mr Cheerful always woke up in a cheerful mood, with a bright sunny smile on his face. In fact, Mr Cheerful was one of the most cheerful people you are ever likely to meet. He did, however, have one secret that made him sad. But nobody knew about it. The...Find out more
The 617 aa sequence of VGF contains nearly a dozen potential cleavage sites. Functional effects have been reported for several potential proteolytic products contained within the C-terminal 62 aa portion of VGF (Alder et al., 2003; Succu et al., 2005). Recently, TLPQ-21, a VGF-derived peptide located immediately upstream from AQEE-30 within the VGF sequence, was shown to modulate inflammatory pain (Rizzi et al., 2008), and TLPQ-62, a peptide that includes both TLPQ-21 and AQEE-30, produced mechanical allodynia when administered intrathecally in rat (Moss et al., 2008). Our observations of dose-dependent thermal hyperalgesia evoked by intrathecal injection of AQEE-30 and LQEQ-19 provide additional evidence for a role of VGF peptides in nociceptive processing. Notably, the hyperalgesia evoked by VGF peptides exceeded in magnitude and duration the effect of NMDA in the same experimental paradigm (Kitto et al., 1992; Roberts et al., 2005). Although the tail-withdrawal paradigm used in our studies is ...
This unit, which is designed for testing narcotics and strong non-narcotic drugs, offers both Plantar (Hargreaves Method) and Tail Flick testing with a single unit. Either testing system is also available individually.
In this study, we have further investigated whether BV derived phospholipase A2 (bvPLA2) attenuates oxaliplatin-induced cold and mechanical allodynia in mice and its mechanism. The behavioral signs of cold and mechanical allodynia were evaluated by acetone and a von Frey hair test on the hind paw, respectively. The significant allodynia signs were observed from one day after an oxaliplatin injection (6 mg/kg, i.p.). Daily administration of bvPLA2 (0.2 mg/kg, i.p.) for five consecutive days markedly attenuated cold and mechanical allodynia, which was more potent than the effect of BV (1 mg/kg, i.p.). The depletion of noradrenaline by an injection of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP4, 50 mg/kg, i.p.) blocked the analgesic effect of bvPLA2, whereas the depletion of serotonin by injecting DL-p-chlorophenylalanine (PCPA, 150 mg/kg, i.p.) for three successive days did not. Furthermore, idazoxan (α2-adrenegic receptor antagonist, 1 mg/kg, i.p.) completely blocked ...
Painful skin conditions, fibromyalgia, ME, CFS, Lupus, Invisible Disability, Patients First Hand View, Itching skin, burning skin, crawling skin
Tekus V, Bolcskei K, Kis-Varga A, Dezsi L, Szentirmay E, Visegrady A, Horvath C, Szolcsanyi J, Petho G: Effect of transient receptor potential vanilloid 1 (TRPV1) receptor antagonist compounds SB705498, BCTC and AMG9810 in rat models of thermal hyperalgesia measured with an increasing-temperature water bath, EUROPEAN JOURNAL OF PHARMACOLOGY 641: (2-3) pp. 135-141 ...
New research from the University of Adelaide has now shown that this is a result of an exaggerated immune response; and could be overcome by targeting the immune system.. I identified that a gut receptor called TLR4 drives the heightened immune response, says researcher Hannah Wardill.. Deletion of TLR4 in mice provides protection, lowering the severity and duration of diarrhoea and reducing chemotherapy-induced pain.. The results support existing evidence linking gut health with nerve function and sensation, and are consistent with the experiences of many whove been through cancer treatment.. Every year, more than 74,000 Australians in chemotherapy experience severe, sometimes life-threatening diarrhoea.. They also endure heightened sensitivity to pain, known as hyperalgesia.. Current treatments for chemotherapy-induced diarrhoea and hyperalgesia focus not on the cause, but instead on managing the symptoms. They are often ineffective.. With further research, Hannah hopes that a focus on ...
Figure 9. Effect of in vivo endogenous NOV inhibition on MMP-2/-9 expression and mechanical allodynia. In CFA rats, NOV-specific siRNA (2 μg) or control non-silencing siRNA (Ctr) were delivered intrathecally (i.t) daily for 3 consecutive days. (A) NOV protein levels in DHSC. Representative western blot (left panel) and quantification of protein levels normalized to GAPDH (right panel) (**P ,0.01, siNOV versus Ctr, n = 6) (B, C) Levels of MMP-9 and MMP-2 mRNA in DRG (B) and DHSC. (C) Transcript levels were quantified by RT-qPCR and values were normalized to rat S26 mRNA level. Data represent the mean value ± SEM of two independent experiments realized with three rats per condition (*P ,0.05 siNOV versus Ctr). (D) Representative gelatin zymograph showing MMP-9 and MMP-2 activities in DRG (left panel) and quantification of MMP-2 and MMP-9 gelatinolytic bands (right panel). Data represent the mean ± SEM of six rats per group (**P ,0.01 siNOV versus Ctr). (E) Paw withdrawal threshold (g) of CFA ...
Counselling can be sought for many reasons and I believe a close supportive collaboration between therapist and client is of great importance to a...
Above Ground Stack Support Pipe finished externally in a two part red epoxy coating and fully compliant with BS EN 877:1999 + A1:2006. For more specifications please see the table below. Code number(s) for available products are: HS3056, HS4056, HS6056, HS8056. ...
Allodynia is pain that results from even a light touch of the skin. Learn how migraine is often a cause of this phenomenon and how to best manage it.
Pöyhiä R, Vainio A (January 2006). "Topically administered ketamine reduces capsaicin-evoked mechanical hyperalgesia". The ... Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or temperature sensation and/or deep somatic ... hyperalgesia; and decreased/restricted ability and painful movement of affected body part. Drop attacks (falls), almost ... mechanical hyperalgesia) and showed a "significantly increased activation" of not just the S1 cortex (contralateral), S2 ( ...
Lee M, Silverman SM, Hansen H, Patel VB, Manchikanti L (2011). "A comprehensive review of opioid-induced hyperalgesia". Pain ... It may also prevent opioid-induced hyperalgesia and postanesthetic shivering. For chronic pain, ketamine is used as an ... Jianren Mao (19 April 2016). Opioid-Induced Hyperalgesia. CRC Press. pp. 127-. ISBN 978-1-4200-8900-4. Archived from the ...
Shu XQ, Mendell LM (July 1999). "Neurotrophins and hyperalgesia". Proceedings of the National Academy of Sciences of the United ...
Hyperalgesia Opioid-induced hyperalgesia (OIH) has been evident in patients after chronic opioid exposure. Infrequent adverse ... Opioid induced hyperalgesia more commonly occurs with chronic use or brief high doses but some research suggests that it may ... Opioid-induced hyperalgesia - where individuals using opioids to relieve pain paradoxically experience more pain as a result of ... Long-term opioid use can cause opioid-induced hyperalgesia, which is a condition in which the patient has increased sensitivity ...
Pretreatment with MK-801 significantly reduced SP induced hyperalgesia. Intrathecal MK-801 also blocked hyperalgesia resulting ... Allodynia and hyperalgesia were experimentally induced by administration of CCK into the RVM. Spinal administration of SB- ... Behavioral hyperalgesia in inflammatory pain states is closely correlated with phosphorylation of spinal NMDA receptors. To ... Injection of the CCK-saporin conjugate also reversed allodynia and hyperalgesia in a nerve injury model, producing the same ...
"VICTORIAN HALLS Release Hyperalgesia". Mass Movement. 19 May 2015. Retrieved 22 June 2017. "VICTORIAN HALLS announce "All My ... Their second full-length studio album, "Hyperalgesia" was recorded in Gossip Studios, Chicago and released in May 2015 with ... Hyperalgesia, while maintaining the overall characteristic experimental-rock feel of Victorian Halls' music, is a much more ...
Opioid-induced hyperalgesia Kraychete, DC; Sakata, RK (July 2012). "Use and rotation of opioids in chronic non-oncologic pain ...
It is different from hyperalgesia, an exaggerated response from a normally painful stimulus. The term is from Ancient Greek ... Coutaux A, Adam F, Willer JC, Le Bars D (2005). "Hyperalgesia and allodynia: peripheral mechanisms". Joint Bone Spine. 72 (5): ...
... and inflammation-based pain and hyperalgesia. Lipoxins have protective effects in animal models of infection-based inflammation ...
Normally hyperalgesia ceases when inflammation goes down, however, sometimes genetic defects and/or repeated injury can result ... This is commonly known as hyperalgesia. Inflammation is one common cause that results in the sensitization of nociceptors. ...
This can cause allodynia or hyperalgesia. In individuals with chronic pain, EEGs showed altered brain activity, suggesting pain ... opioid-induced hyperalgesia, physical dependence, addiction, abuse, and overdose. Alternative medicine refers to health ...
Evidence for a link between PGE2 and hyperalgesia comes from an antisense deoxynucleotide knockdown of Nav1.8 in the DRG of ... Lai J, Porreca F, Hunter JC, Gold MS (2004). "Voltage-gated sodium channels and hyperalgesia". Annual Review of Pharmacology ... Therefore, Nav1.8 contributes to hyperalgesia (increased sensitivity to pain) and allodynia (pain from stimuli that do not ... hyperalgesia). The increased levels of nerve growth factor and tumour necrosis factor-α (TNF-α) causes the upregulation of ...
It has anti-hyperalgesia effects in animals. SIB-1757 along with other mGluR5 antagonists has been shown to have ...
His studies on the basic mechanisms involved in the development of inflammatory hyperalgesia led to the discovery that a select ... II-Prostaglandins hyperalgesia: the peripheral analgesic activity of morphine, enkephalins and opioid antagonists. ... Bradykinin initiates cytokine mediated inflammatory hyperalgesia. Brazilian Journal of Pharmacological Sciences. vol. 110, p. ... group made a relevant contribution to the role of bradykinin and of cytokines in the development of inflammatory hyperalgesia. ...
Sommer C, Schäfers M, Marziniak M, Toyka KV (June 2001). "Etanercept reduces hyperalgesia in experimental painful neuropathy". ...
People suffering from this probably have hyperalgesia. The Fear of Pain Questionnaire (currently the FPQ-III), a mental health ...
Epub 2015 Mar 31.] The original Hp peptide reduces sensitivity to painful stimuli in an experimental model of hyperalgesia. Hp ... March 2005). "Antinociceptive action of hemopressin in experimental hyperalgesia". Peptides. 26 (3): 431-6. doi:10.1016/j. ...
DuPen A, Shen D, Ersek M (September 2007). "Mechanisms of opioid-induced tolerance and hyperalgesia". Pain Management Nursing. ...
"CXCR4 Signaling Mediates Morphine-induced Tactile Hyperalgesia". Brain, Behavior, and Immunity. 25 (3): 565-73. doi:10.1016/j. ... of CXCR4 signalling by plerixafor has also unexpectedly been found to be effective at counteracting opioid-induced hyperalgesia ...
These patient often have a lower pain threshold with balloon distension of the bowel (visceral hyperalgesia), or they have ... Narcotic bowel syndrome (NBS)/ Opioid-induced GI hyperalgesia E. Gallbladder and Sphincter of Oddi disorders E1. Biliary pain ... Basic and clinical aspects of visceral hyperalgesia. Gastroenterology 1994;107:271-293 Zhou Q, Zhang B, Verne GE. Intestinal ...
It was developed as a potential analgesic, and blocks the development of hyperalgesia following exposure to cold temperatures ... Gong K, Jasmin L (February 2017). "Sustained Morphine Administration Induces TRPM8-Dependent Cold Hyperalgesia". The Journal of ...
Syriatowicz, J. P.; Hu, D.; Walker, J. S.; Tracey, D. J. (1999). "Hyperalgesia due to nerve injury: Role of prostaglandins". ... a compound that sensitizes neurons to mechanical stimuli and mechanical hyperalgesia) which further supports a role for HT ...
... hyperalgesia is believed to involve the activation of cholecystokinin receptors. Stewart-Williams and Podd argue that ... For example, precisely the same inert agents can produce analgesia and hyperalgesia, the first of which, from this definition, ... Verbal suggestion can cause hyperalgesia (increased sensitivity to pain) and allodynia (perception of a tactile stimulus as ... Colloca, Luana; Benedetti, Fabrizio (2007). "Nocebo hyperalgesia: How anxiety is turned into pain". Current Opinion in ...
Nature (2008) 2002: Shin J et al., Bradykinin-12-lipoxygenase-VR1 signaling pathway for inflammatory hyperalgesia. Proc Natl ... 2002). "Bradykinin-12-lipoxygenase-VR1 signaling pathway for inflammatory hyperalgesia". Proc. Natl. Acad. Sci. USA. 99 (15): ...
... increased bradykinin sensitizes somatosensory fibers and thus causes hyperalgesia. Bradykinin may mediate this via pro- ...
"Adenosine receptor subtype-selective antagonists in inflammation and hyperalgesia". Naunyn-Schmiedeberg's Archives of ...
"Neurotrophins and hyperalgesia". Proceedings of the National Academy of Sciences of the United States of America. 96 (14): ...
Opioid-induced hyperalgesia is when exposure to opioids increases the sensation of pain (hyperalgesia) and can even make non- ... Bannister, Kirsty (June 2015). "Opioid-induced hyperalgesia". Current Opinion in Supportive and Palliative Care. 9 (2): 116-121 ... Opioid tolerance should not be confused with opioid-induced hyperalgesia. The symptoms of these two conditions can appear very ...
... medications can cause paradoxical side effects, such as opioid-induced hyperalgesia (severe pain caused by long-term ... Higgins, C.; Smith, B. H.; Matthews, K. (June 2019). "Evidence of opioid-induced hyperalgesia in clinical populations after ... Jensen TS, Finnerup NB (September 2014). "Allodynia and hyperalgesia in neuropathic pain: clinical manifestations and ...
Information about visceral hyperalgesia causes, symptoms, diagnosis and treatment from the experts at Cincinnati Childrens ... Visceral Hyperalgesia What Is Visceral Hyperalgesia? Visceral hyperalgesia is an increased sensitivity to pain in the internal ... How Is Visceral Hyperalgesia Diagnosed?Show There is no specific test to diagnose visceral hyperalgesia. It is generally ... What Causes Visceral Hyperalgesia? Show Increased sensitivity usually starts when something causes irritation to a particular ...
We explore the cause of hyperalgesia. We also examine the various types of the condition and the most effective treatments. ... Other types of hyperalgesia. Another kind of hyperalgesia is opioid-induced hyperalgesia (OIH). OIH occurs when a person ... Primary hyperalgesia. This type of hyperalgesia is when the increased pain occurs in the tissue where the injury took place. An ... Diagnosing hyperalgesia may be difficult for a doctor.. Hyperalgesia can present difficulties for a doctor to treat because a ...
Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues. Opioid-induced hyperalgesia may ... Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management ... Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have ... Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This ...
Hyperalgesia is the second full-length studio album by American alternative rock band Victorian Halls. The album, that contains ... CS1 maint: discouraged parameter (link) "Hyperalgesia by Victorian Halls". iTunes. May 18, 2015. Retrieved June 30, 2017. CS1 ... CS1 maint: discouraged parameter (link) "Victorian Halls released Hyperalgesia @ Bottom Lounge". The Deli Magazine. May 19, ...
Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.. Opioid-induced hyperalgesia ... Hyperalgesia (/ˌhaɪpərælˈdʒiːziə/ or /-siə/; hyper from Greek ὑπέρ (huper, "over"), -algesia from Greek algos, ἄλγος (pain ... Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This ... One unusual cause of focal hyperalgesia is platypus venom.[5]. Long-term opioid (e.g. heroin, morphine) users and those on high ...
Attenuation of thermal nociception and hyperalgesia by VR1 blockers. Carolina García-Martínez, Marc Humet, Rosa Planells-Cases ... Attenuation of thermal nociception and hyperalgesia by VR1 blockers. Carolina García-Martínez, Marc Humet, Rosa Planells-Cases ... Mustard Oil Thermal Hyperalgesia.. Thermal sensitivity of mice was assayed in the hot plate at 52°C. Thereafter, mustard oil ( ... 6 A and B). As expected, mice sensitized with capsaicin showed intense mechanical hyperalgesia in the treated paw (Fig. 6C). ...
Activation of non-neuronal microglia is thought to play a causal role in spinal processing of neuropathic pain. To specifically investigate microglia-mediated effects in a model of neuropathic pain and overcome the methodological limitations of previous approaches exploring microglia function upon nerve injury, we selectively ablated resident microglia by intracerebroventricular ganciclovir infusion into male CD11b-HSVTK-transgenic mice, which was followed by a rapid, complete, and persistent (23 weeks) repopulation of the CNS by peripheral myeloid cells. In repopulated mice that underwent sciatic nerve injury, we observed a normal response to mechanical stimuli, but an absence of thermal hypersensitivity ipsilateral to the injured nerve. Furthermore, we found that neuronal expression of calcitonin gene-related peptide (CGRP), which is a marker of neurons essential for heat responses, was diminished in the dorsal horn of the spinal cord in repopulated mice. These findings identify distinct ...
What is hyperalgesia?. Hyperalgesia is an enhanced pain response. It can result from either injury to part of the body or from ... Primary hyperalgesia occurs at and around the site of the injury. Secondary hyperalgesia occurs when the pain feels as if its ... This leads to the development of hyperalgesia.. Some people experience hyperalgesia following a surgical procedure. This is due ... People with fibromyalgia can also experience hyperalgesia. People with shingles can develop hyperalgesia as well. ...
Vanilloid receptor-1 is essential for inflammatory thermal hyperalgesia Access & Citations. * 1258 Article Accesses. ...
Erythromelalgia(heat hyperalgesia) is in part due to mutations in TTX sensitivity of channel Na 1.7 (Sodium 1.7). Trigeminal ... Knockout IL-1 receptor and reduce hyperalgesia Sodium Channel Dysfunction can contribute to pain. Channel Na 1.3 (Sodium 1.3) ...
Diseases : Hyperalgesia, Hyperglycemia, Neuropathic Pain. Pharmacological Actions : Analgesics, Antioxidants, Bax/Bcl2 Ratio: ... Diseases : Hyperalgesia, Inflammation, Neuropathic Pain. Pharmacological Actions : NF-kappaB Inhibitor, Nitric Oxide Inhibitor ... Diseases : Hyperalgesia, Neuropathic Pain, Rheumatoid Arthritis. Pharmacological Actions : Analgesics, Wnt/β-catenin signaling ... Diseases : Hyperalgesia, Oxidative Stress. Pharmacological Actions : Interleukin-1 beta downregulation, NF-kappaB Inhibitor, ...
... Leonardo Yung dos Santos Maciel,1 Kamilla ... C. Huang, Z.-P. Hu, H. Long, Y.-S. Shi, J.-S. Han, and Y. Wan, "Attenuation of mechanical but not thermal hyperalgesia by ... T. Yokoyama, Y. Maeda, K. M. Audette, and K. A. Sluka, "Pregabalin reduces muscle and cutaneous hyperalgesia in two models of ... Y. Zhang, A. Li, J. Xin et al., "Involvement of spinal serotonin receptors in electroacupuncture anti-hyperalgesia in an ...
... was conducted to evaluate the efficacy of oral cryotherapy during oxaliplatin infusions to prevent oral thermal hyperalgesia ( ...
... Anne-Kathrin Bräscher,1 Michael ... K. Świder and P. Bąbel, "The effect of the sex of a model on nocebo hyperalgesia induced by social observational learning," ... B. Colagiuri, V. F. Quinn, and L. Colloca, "Nocebo hyperalgesia, partial reinforcement, and extinction," Journal of Pain, vol. ... E. Vögtle, A. Barke, and B. Kröner-Herwig, "Nocebo hyperalgesia induced by social observational learning," Pain, vol. 154, no. ...
We assessed postoperative pain at rest and with movement along with wound hyperalgesia in a patient ... Wound hyperalgesia was also determined on each side of the horizontal incision with an algometer (8,9). These data are shown in ... Pain and wound hyperalgesia were consistently greater on the "unblocked" side for the 3-wk period of observation. Thus, even ... Prolonged Differential Wound Hyperalgesia After an Interval of Unilateral Epidural Blockade During Lower Abdominal Surgery. ...
... and possibly opioid-induced hyperalgesia (OIH). The purpose of this review is to evaluate the occurrence and significance of ... opioid-induced hyperalgesia (OIH) after acute fentanyl exposure. A … ... Keywords: drug-related side effect; fentanyl; hyperalgesia; opioid; opioid-induced hyperalgesia; pain; tolerance. ... Fentanyl-induced hyperalgesia in acute pain management J Pain Palliat Care Pharmacother. 2015 Jun;29(2):153-60. doi: 10.3109/ ...
Chemical compound and disease context of Hyperalgesia. *Here we present a new model for noradrenaline-sensitive hyperalgesia ... Psychiatry related information on Hyperalgesia. *Both the visceral hyperalgesia and the decrease in somatic pain thresholds ... Hyperalgesia mediated by spinal glutamate or substance P receptor blocked by spinal cyclooxygenase inhibition. Malmberg, A.B., ... Spinal inflammatory hyperalgesia is mediated by prostaglandin E receptors of the EP2 subtype. Reinold, H., Ahmadi, S., Depner, ...
A study published in The Journal of Pain offers hope to those in pain. Researchers examined virtual reality and how it might improve conditioned pain modulation. For those with nerve injuries and other types of pain, VR can improve a dysfunctional pain suppression system. By stimulating the natural.... ...
... this neurotransmitter being associated with hyperalgesia and central sensitization. One of the mechanisms underlying these ... Chronic Monosodium Glutamate Administration Induced Hyperalgesia in Mice by Anca Zanfirescu, Aurelia Nicoleta Cristea, George ... Keywords: monosodium glutamate; hyperalgesia; hot-plate test; formalin test; nitric oxide synthase monosodium glutamate; ... "Chronic Monosodium Glutamate Administration Induced Hyperalgesia in Mice." Nutrients 10, no. 1: 1. ...
Opioid Induced Hyperalgesia (OIH) Modulation With Propranolol. The safety and scientific validity of this study is the ... Opioid Induced Hyperalgesia (OIH) Modulation With Propranolol, in Laparoscopic Abdominal Surgery. Study Start Date :. October ... Opioid Induced Hyperalgesia (OIH) is an entity than has been demonstrated in healthy volunteers and in animal models. Is ... The objective of this work is to evaluate the efficacy of propranolol in the modulation of opioid induced hyperalgesia, with ...
H2 2018Global Markets Directs latest Pharmaceutical and Healthcare disease pipeline guide Hyperalgesia - Pipeline Review, H2 ... 2018, provides an overview of the Hyperalgesia (Central Nervous System). ... Hyperalgesia - Pipeline by Charleston Laboratories Inc, H2 2018. Hyperalgesia - Pipeline by Novartis AG, H2 2018. Hyperalgesia ... Hyperalgesia - Pipeline by Abide Therapeutics Inc, H2 2018. Hyperalgesia - Pipeline by Boehringer Ingelheim GmbH, H2 2018. ...
Pericicatricial hyperalgesia area [ Time Frame: 72 hours after surgery ]. Secondary Outcome Measures: *Pain intensity (rest/ ... Hyperalgesia, postoperative. Local anesthetic, ropivacaine, lidocaine. Colorectal laparoscopic surgery. Pain management after ... Besides hyperalgesia assessment, immediate postoperative and long-term pain, morphine consumption, and endocrin-metabolic ... Hyperalgesia. Pain. Neurologic Manifestations. Nervous System Diseases. Postoperative Complications. Pathologic Processes. ...
Hyperalgesia Opioid-Related Disorders Drug: Acetazolamide Drug: Placebo Oral Tablet Phase 4 ... Administration of Acetazolamide to Prevent Remifentanil Induced Hyperalgesia. The safety and scientific validity of this study ... There is a lot of evidence that suggest that the used of remifentanil is associated with the development of hyperalgesia (a ... Hyperalgesia. Opioid-Related Disorders. Somatosensory Disorders. Sensation Disorders. Neurologic Manifestations. Nervous System ...
... showed a robust response during the perception of secondary hyperalgesia but not primary hyperalgesia (i.e., no mPFC responses ... Secondary hyperalgesia is generally defined as the development of a heightened sensitivity to normal mechanical stimulation in ... Because secondary hyperalgesia pain thresholds were not matched across participants, the pin-prick stimulation used to evoke ... Medial Prefrontal Cortex, Secondary Hyperalgesia, and the Default Mode Network Message Subject (Your Name) has forwarded a page ...
Involvement of vasopressin 3 receptors in chronic psychological stress-induced visceral hyperalgesia in rats.. Bradesi S1, ... These data support a major role for V(3) receptors in repeated psychological stress-induced visceral hyperalgesia and suggest ... Repeated administration of SSR149415 at 1 or 3 mg/kg completely prevented stress-induced visceral hyperalgesia. Similarly, a ... signaling system in the development of stress-induced visceral hyperalgesia in rats. Rats were exposed to a daily 1-h session ...
... indicative of hyperalgesia. The higher the fentanyl dose used, the more pronounced was the fentanyl-induced hyperalgesia. ... Long-lasting hyperalgesia induced by fentanyl in rats: preventive effect of ketamine.. Célèrier E1, Rivat C, Jun Y, Laulin JP, ... and prevented the development of long-lasting hyperalgesia. ...
Fenobam on Heat/Capsaicin Induced Hyperalgesia in Healthy Volunteers. The safety and scientific validity of this study is the ... Hyperalgesia. Somatosensory Disorders. Sensation Disorders. Neurologic Manifestations. Nervous System Diseases. Signs and ... size of the area of hyperalgesia and allodynia around the area sensitized by heat/capsaicin as quantified by cutaneous ... Suppression of the development of cutaneous hyperalgesia and allodynia around the area treated with heat/capsaicin. [ Time ...
... and hyperalgesia (increased pain sensitivity). Clinical and preclinical studies have reported development of hyperalgesia after ... attenuated morphine-induced hyperalgesia. Real-time polymerase chain reaction (RT-PCR) analysis showed that CREB downstream ... attenuated morphine-induced hyperalgesia. Real-time polymerase chain reaction (RT-PCR) analysis showed that CREB downstream ... without interfering with the morphine-induced hyperalgesia. However, i.t. injection of SB20358, a p38 inhibitor and SP660125, a ...
Opioid-induced hyperalgesia (OIH) is most broadly defined as a state of nociceptive sensitization caused by exposure to opioids ... Opioid-induced Hyperalgesia in Humans: Molecular Mechanisms and Clinical Considerations Clin J Pain. Jul-Aug 2008;24(6):479-96. ... Opioid-induced hyperalgesia (OIH) is most broadly defined as a state of nociceptive sensitization caused by exposure to opioids ...
Efficacy of a Polyamine-free Diet Associated or Not With Ketamine on Early and Late Hyperalgesia After Breast Cancer Surgery. ... Efficacy of a Polyamine-free Diet Associated or Not With Ketamine on Early and Late Hyperalgesia After Breast Cancer Surgery ... group as well as pain score, allodynia (Von Frey filaments) and hyperalgesia (algometer).. Chronic pain occurrence (post- ...
  • Amplification in the spinal cord may be another way of producing hyperalgesia. (
  • Another medication is buprenorphine, which can help to reduce the incidence of hyperalgesia by blocking receptors in the brain and spinal cord. (
  • Electroacupuncture suppresses hyperalgesia and spinal Fos expression by activating the descending inhibitory system," Brain Research , vol. 1186, no. 1, pp. 171-179, 2007. (
  • Involvement of spinal serotonin receptors in electroacupuncture anti-hyperalgesia in an inflammatory pain rat model," Neurochemical Research , vol. 36, no. 10, pp. 1785-1792, 2011. (
  • They used brain imaging to characterize the circuits involved in nocebo hyperalgesia within the descending pain pathway from the prefrontal cortex to the spinal cord. (
  • Because nocebo hyperalgesia also modulates activity at the spinal level ( 14 ), we followed this lead and investigated whether nocebo hyperalgesia is mediated through interactions within a cortico-subcortico-spinal network ( 15 ), in analogy to other forms of cognitive pain modulation ( 16 , 17 ). (
  • To document potential mediating effects of the Activator-assisted spinal manipulative therapy (ASMT) on pain and hyperalgesia after acute intervertebral foramen (IVF) inflammation. (
  • Hyperalgesia and Pain following Central Administration of SP(A) Paw withdrawal to radiant heat measured before and after administration of SP peptide to the lumbar spinal cord via an intrathecal cannula in lightly anesthetized animals (IT SP). (
  • This study investigated the role of SAP102 in the formation of hyperalgesia in rats with CIBP SAP102 is present in spinal dorsal horn neurons, but not in astrocytes or microglia. (
  • Increases in PKC gamma expression in trigeminal spinal nucleus is associated with orofacial thermal hyperalgesia in streptozotocin-induced diabetic mice. (
  • The association of cutaneous hyperalgesia with changes in the electrophysiological properties of DRG cells suggests a possible role for intrinsic alterations in the membrane properties of compressed DRG cells in the production and persistence of chronic pain after certain spinal injuries or pathologies of the spine. (
  • The development and maintenance of secondary hyperalgesia depend on complex plastic changes in spinal cord dorsal horn cells after peripheral injury or damage. (
  • Most common chronic non-cancer illnesses causing hyperalgesia are failed back syndrome, degenerative disk disease , disk herniation , spinal stenosis , facet joint disease, fibromyalgia , hip or knee joint arthritis , intercostal neuralgia , post-herpetic neuralgia ( shingles ), diabetic neuropathy and peripheral neuropathy. (
  • Hyperalgesia is caused by irritation of spinal nerve following back surgery. (
  • Scar tissue following surgery often irritates or pinches spinal nerve resulting in hyperalgesia. (
  • Hyperalgesia Caused Due To Pinched Nerve- Scar tissue, disk herniation, disk fragments and entrapped neuropathy causes continuous irritation or pinch of spinal or peripheral nerve, which results in hyperalgesia. (
  • Multiple Sclerosis - Multiple sclerosis causes irritation of spinal nerve and results in wide spread hyperalgesia. (
  • The results suggest that (1) spinal IL-17 is produced by astrocytes and enhances p-NR1 to facilitate inflammatory pain, and 2) EA inhibits hyperalgesia by suppressing IL-17. (
  • A Comparison of the Effects of Burst and Tonic Spinal Cord Stimulation on Hyperalgesia and Physical Activity in an Animal Model of Neuropathic Pain. (
  • The present study therefore investigated under in vivo conditions whether administration of lutein attenuates the inflammation-induced hyperexcitability of trigeminal spinal nucleus caudalis (SpVc) neurons that is associated with mechanical hyperalgesia. (
  • The purpose of this study was to investigate whether 5-HT2A and 5-HT2C receptors in the spinal cord contribute to somatic hyperalgesia induced by orofacial inflammation combined with different modes of stress. (
  • Vera-Portocarrero LP, Zhang ET, King T, Ossipov MH, Vanderah TW, Lai J, Porreca F.Spinal NK-1 receptor expressing neurons mediate opioid-induced hyperalgesia and antinociceptive tolerance via activation of descending pathways // Pain 129: 35- 45, 2007. (
  • Wei F, Dubner R, Ren K. Nucleus reticularis gigantocellularis and nucleus raphe magnus in the brain stem exert opposite effects on behavioral hyperalgesia and spinal Fos protein expression after peripheral inflammation // Pain. (
  • Involvement of vasopressin 3 receptors in chronic psychological stress-induced visceral hyperalgesia in rats. (
  • We used a selective vasopressin 3 (V(3)) receptor antagonist SSR149415 to investigate the involvement of the vasopressin (AVP)/V(3) signaling system in the development of stress-induced visceral hyperalgesia in rats. (
  • Long-lasting hyperalgesia induced by fentanyl in rats: preventive effect of ketamine. (
  • Clinical and preclinical studies have reported development of hyperalgesia after prolonged opioid administration or after a single dose of intrathecal (i.t.) morphine in uninjured rats. (
  • Here, we showed that a single morphine subcutaneous injection induces analgesia followed by a long-lasting delayed hyperalgesia in uninjured and PGE2 sensitized rats. (
  • We have shown recently that opiates produce not only analgesia but also long-lasting hyperalgesia in rats. (
  • Our observation that a small dose of heroin which is ineffective for triggering a delayed hyperalgesia in non-heroin-treated rats induced an enhancement in pain sensitivity for several days after a series of heroin administrations is in agreement with the sensitization hypothesis. (
  • The effectiveness of the opioid receptor antagonist naloxone to precipitate hyperalgesia in rats that had recovered their pre-drug nociceptive value after single or repeated heroin administrations indicates that heroin-deprived rats were in a new biological state associated with a high level balance between opioid-dependent analgesic systems and pronociceptive systems. (
  • Nociceptive somatic stimulation in neonatal rats results in chronic visceral hyperalgesia. (
  • The ability of repeated morphine administration to produce hyperalgesia was studied in rats. (
  • Furthermore, when exposed to inflammatory insults or known mediators, naked mole-rats do not display thermal hyperalgesia.Nevertheless, the activation of capsaicin-sensitive sensory neurons in naked mole-rats does not produce pain-related behavior.The pain biology of the naked mole-rat is unique among mammals, thus the study of pain mechanisms in this unusual species can provide major insights into what constitutes 'normal' mammalian nociception. (
  • Furthermore, when exposed to inflammatory insults or known mediators, naked mole-rats do not display thermal hyperalgesia. (
  • In contrast, naked mole-rats do display nocifensive behaviors in the formalin test and show mechanical hyperalgesia after inflammation. (
  • Naked mole-rats also display hyperalgesia following intrathecal SP injection albeit only at higher doses (100 μM, n = 6 animals per dose). (
  • In rats injected with complete Freund's adjuvant (CFA), which induces inflammatory heat hyperalgesia, DRG neurons showed an increase in LIMK activity and in the phosphorylation and thus inhibition of the LIMK substrate cofilin, an actin-severing protein. (
  • Extended access to nicotine leads to a CRF1 receptor dependent increase in anxiety-like behavior and hyperalgesia in rats. (
  • Enhanced excitability of sensory neurons in rats with cutaneous hyperalgesia produced by chronic compression of the dorsal root ganglion. (
  • Postoperatively, the threshold force applied by punctate stimulation of the plantar surface of the hind paw decreased significantly on the foot ipsilateral to the CCD (mechanical hyperalgesia) but changed little on the contralateral foot or on either foot for control rats. (
  • Based on our studies using a model of intermittent sound stress in rats, we have suggested that sound stress-induced enhancement of immune mediator hyperalgesia requires activity in both neuroendocrine stress axes: the sympathoadrenal (via release of epinephrine) and hypothalamic pituitary adrenal (HPA) (via release of corticosterone) 12 . (
  • We found that two structurally dissimilar but equally potent sEH inhibitors can be delivered through the transdermal route and that sEH inhibitors effectively attenuate thermal hyperalgesia and mechanical allodynia in rats treated with LPS. (
  • In carrageenan-induced paw inflammation, pretreatment of rats with 2B5 substantially prevented the development of tissue edema and hyperalgesia in affected paws. (
  • Thermal hyperalgesia and mechanical allodynia were determined by the shortened latency of foot withdrawal to radiant heat and von Frey filament stimulation to the hind paw, respectively. (
  • 13 Also, it is possible to use periincisional mechanical allodynia and hyperalgesia as objective measures of opioid-induced hyperalgesia in clinical settings. (
  • Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues. (
  • Various studies of humans and animals have demonstrated that primary or secondary hyperalgesia can develop in response to both chronic and acute exposure to opioids. (
  • Doctors usually divide hyperalgesia into primary and secondary categories. (
  • There are two types of hyperalgesia - primary and secondary. (
  • Secondary hyperalgesia occurs when the pain feels as if it's spreading to a non-injured site of the body. (
  • Also, as a secondary outcome, in a group than will not receive the study drug, we will evaluate the temporal changes in opioid induced hyperalgesia, by pain sensitivity measured in the postoperative hours 2, 4 and 24. (
  • This fMRI study observed that the mPFC is specifically active during pain perception resulting from secondary hyperalgesia, which arises from traumatized tissue. (
  • Secondary hyperalgesia is generally defined as the development of a heightened sensitivity to normal mechanical stimulation in uninjured skin surrounding an injury. (
  • It is well established that the mechanisms generating secondary hyperalgesia lie within the CNS as opposed to the peripheral mechanisms responsible for inducing primary hyperalgesia, i.e., hypersensitivity at the site of trauma ( Maihöfner and Handwerker, 2005 ). (
  • The authors of this study used a balanced design that used electrical stimulation to induce trauma, normally benign pin pricks to assess hyperalgesia, and subsequent intravenous application of lidocaine, a potent analgesic, to block perception of secondary hyperalgesia in normal participants undergoing fMRI scanning. (
  • Under these conditions, the mPFC (as well as the posterior cingulate, another major hub of the DMN) showed a robust response during the perception of secondary hyperalgesia but not primary hyperalgesia (i.e., no mPFC responses were detected during pin-prick stimulation at the site of the electrical trauma). (
  • Moreover, a significant negative correlation was found between the magnitude of mPFC (but not posterior cingulate) BOLD response and the size of secondary hyperalgesia response under placebo. (
  • That is, individuals with high levels of mPFC during periods of evoked secondary hyperalgesia pain had a smaller surface area of uninjured responsive skin during psychophysical testing and individuals with low levels of mPFC activity had a larger area of responsive skin. (
  • A secondary hyperalgesia is one in which the pain sensitivity occurs in surrounding undamaged tissues. (
  • This component of mechanical hyperalgesia persisted for at least 30 min and was present in the skin exposed to the irritants (primary hyperalgesia) as well as in a zone of untreated skin surrounding the injury (secondary hyperalgesia) measuring 38 ± 4 cm 2 after capsaicin. (
  • Recently, we showed that knee joint manipulation decreases secondary mechanical hyperalgesia in the paw induced by injection of capsaicin into the ankle joint in rat (Sluka and Wright, 2001). (
  • Thermal thresholds for cold and hot sensation and for pain (by limit method) were evaluated at the site of skin incision (primary-) and distantly (secondary hyperalgesia). (
  • Conclusions: Compared with placebo, DM enabled reduction of postoperative analgesics consumption, improved well-being, and reduced sedation, pain intensity and primary and secondary thermal hyperalgesia. (
  • Mechanical hyperalgesia surrounding the wound in postoperative patients shares the same central neuronal mechanism as heat-induced secondary hyperalgesia and confirms a degree of central sensitization. (
  • Central sensitization is expressed behaviorally as secondary hyperalgesia and contributes to prolonged postoperative pain. (
  • In humans, NMDA-receptor antagonism decreases secondary hyperalgesia subsequent to experimentally-induced pain. (
  • Burns D, Hill L, Essandoh M, Jarzembowski TM, Schuler HG, Janicki PK, Effect of valdecoxib pretreatment on pain and secondary hyperalgesia: a randomized controlled trial in healthy volunteers [ISRCTN05282752, NCT00260325]. (
  • Assess age differences in the intensity and course of secondary hyperalgesia after surgery. (
  • Raja, S. N., Campbell, J. N., and Meyer, R. A., "Evidence for Different Mechanisms of Primary and Secondary Hyperalgesia Following Heat Injury to the Glabrous Skin" // Brain 107, 1179-1188 (1984). (
  • The focal form is typically associated with injury, and is divided into two subtypes: Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues. (
  • Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues. (
  • While placebo hypoalgesia refers to decreased pain sensitivity due to an inert treatment (e.g., sham procedure and inert substance), its counterpart nocebo hyperalgesia is defined as increased pain sensitivity attributable to an inert treatment [ 2 ]. (
  • The use of morphine, the standard opioid drug, is limited by its undesirable effects, such as tolerance, physical dependence, and hyperalgesia (increased pain sensitivity). (
  • Because the NMDA receptor antagonist dizocilpine maleate (MK-801) prevented both heroin-induced long-lasting enhancement in pain sensitivity and naloxone-precipitated hyperalgesia, these findings further suggest that tolerance, sensitization, and one withdrawal symptom, hyperalgesia, are issued from a neuroadaptive process in which NMDA systems play a critical role. (
  • A primary hyperalgesia is a type of hyperalgesia in which the pain sensitivity occurs directly in the damaged tissues. (
  • None of this, however, has anything to do with OIH, which is a distinct condition whereby exposure to exogenous opioids results in decreased pain tolerance/increased pain sensitivity - hyperalgesia. (
  • Paradoxical morphine-induced hyperalgesia (MIH) is a form of nociceptive sensitization in which subjects exposed to morphine treatment develop a paradoxical increased pain sensitivity or exacerbate pre-existing pain 1 , 2 . (
  • A pressure algometer and standardized monofilaments or weighted pinprick stimuli are used for assessing pressure and punctate allodynia and hyperalgesia and a thermal tester is used for thermal testing. (
  • The chief symptom of hyperalgesia is an increasingly extreme reaction to painful stimuli without any new injuries or worsening of a medical condition. (
  • Summary The principle finding of the present study is that there are two types of mechanical hyperalgesia developing in human hairy skin following injurious stimuli. (
  • Mechanical hyperalgesia comprises a dynamic component (brush-evoked pain, allodynia) signalled by large myelinated afferents and a static component (hyperalgesia to pressure stimuli) signalled by unmyelinated afferents. (
  • Both substances evoked burning pain and hyperalgesia to mechanical stimuli. (
  • In all mammals, tissue inflammation leads to pain and behavioral sensitization to thermal and mechanical stimuli called hyperalgesia. (
  • We found that the LIM motif-containing protein kinases (LIMKs), which regulate actin dynamics, promoted the development of inflammatory hyperalgesia (excessive sensitivity to painful stimuli). (
  • However, experimental studies report that opioids may also elicit hyperalgesia (increased sensitivity to noxious stimuli) and allodynia (nociceptive responses to innocuous stimulation). (
  • The immediate postoperative period is associated with spontaneous pain and hyperalgesia, i.e., increased pain response (both intensity and duration) to normally painful stimuli following tissue injury or damage. (
  • Hyperalgesia is increased feeling of pain after painful stimuli and allodynia is increased feeling of pain following non-painful stimuli like touch or pressure over skin. (
  • Opioid induced hyperalgesia (OIH) is escalation of sensation of residual pain following both noxious and non-noxious stimuli. (
  • We tested the hypotheses that PGE 2 -G is increased in DRGs of HbSS-BERK mice and sensitizes nociceptors (sensory neurons that respond to noxious stimuli), and that blocking its synthesis would decrease hyperalgesia in HbSS-BERK mice. (
  • Zanfirescu A, Cristea AN, Nitulescu GM, Velescu BS, Gradinaru D. Chronic Monosodium Glutamate Administration Induced Hyperalgesia in Mice. (
  • Furthermore, analyses of mice lacking VR1 have shown that VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia ( 20 , 21 ). (
  • Note that very low doses of SP lead to thermal hyperalgesia in mice (1 μM). (
  • Given the paramount role of NF-κB in inflammation, we investigated the regulation and function of IKKε in models of inflammatory hyperalgesia in mice. (
  • However, in inflammatory pain models, IKKε-deficient mice exhibited a significantly reduced nociceptive behavior in comparison with wild type mice, indicating that IKKε contributed to the development of inflammatory hyperalgesia. (
  • With hyperglycemia and body weight loss, STZ mice exhibited orofacial thermal hyperalgesia, along with increased PKCγ expression in Sp5C. (
  • Insulin treatment at the early stage of diabetes could alleviate the orofacial thermal hyperalgesia and impaired increased PKCγ in Sp5C in diabetic mice. (
  • Furthermore, in monosodium iodoacetate-induced osteoarthritis in mice, it was found that morin at 25 and 50 mg/kg, significantly reduced the heat hyperalgesia and increased the spontaneous motility in mice on days 7, 14, and 21. (
  • Pioglitazone attenuates tactile allodynia and thermal hyperalgesia in mice subjected to peripheral nerve injury. (
  • While studying the influence of transient receptor potential vanilloid 1 (TRPV1) on DPN in the STZ-induced diabetic mouse model, we found that a proportion of STZ-treated mice was nondiabetic but still exhibited hyperalgesia. (
  • Peripheral alpha4beta2 nicotinic acetylcholine receptor signalling attenuates tactile allodynia and thermal hyperalgesia after nerve injury in mice. (
  • We used CCK(2) receptor deficient (CCK(2) (-/-)) mice and assessed their mechanical sensitivity using Von Frey filaments, as well as the development and time course of mechanical hyperalgesia in a model of neuropathic pain. (
  • Next, we found that CCK(2) (-/-) mice did not develop mechanical hyperalgesia in the Bennett's neuropathic pain model. (
  • In the Berkley transgenic murine model of SCD, HbSS-BERK mice express only human hemoglobin S. These mice share many features of SCD patients, including persistent inflammation and hyperalgesia. (
  • Systemic administration of R-flurbiprofen preferentially reduced production of PGE 2 -G over that of PGE 2 in DRGs, decreased mechanical and thermal hyperalgesia, and decreased sensitization of nociceptors in HbSS-BERK mice. (
  • The same dose of R-flurbiprofen had no behavioral effect in HbAA-BERK mice (the transgenic control), but local injection of PGE 2 -G into the hind paw of HbAA-BERK mice produced sensitization of nociceptors and hyperalgesia. (
  • Systemic administration of R-flurbiprofen preferentially reduced production of PGE2-G over that of PGE2 in DRGs, decreased mechanical and thermal hyperalgesia, and decreased sensitization of nociceptors in HbSS-BERK mice. (
  • The effect of fluoxetine on thermal hyperalgesia in STZ-induced diabetic mice: possible involvement of 5-HT1/2 receptors', Iranian Journal of Pharmaceutical Research , Volume 3(Supplement 1), pp. 108-108. (
  • Diabetic mice exhibited a significant hyperalgesia as compared to control mice. (
  • Inhibition of ACC, but not somatosensory cortex reverses hyperalgesia in primary and bystander mice. (
  • OBJECTIVE Morbid obesity may be accompanied by diabetes and painful diabetic neuropathy, a poorly understood condition that is manifested by mechanical or thermal allodynia and hyperalgesia. (
  • A common complication of diabetes is peripheral diabetic neuropathy (PDN), which is often marked by mechanical and thermal allodynia and hyperalgesia and cannot yet be treated effectively because of the lack of knowledge of its pathophysiology ( 2 , 3 ). (
  • Therefore, we tested the hypothesis that relatively large intraoperative doses of remifentanil provoke postoperative hyperalgesia as indicated by periincisional allodynia and hyperalgesia and that small-dose ketamine prevents hyperalgesia. (
  • Hyperalgesia is similar to other sorts of pain associated with nerve irritation or damage such as allodynia and neuropathic pain, and consequently may respond to standard treatment for these conditions, using various drugs such as SSRI or tricyclic antidepressants, Nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, gabapentin or pregabalin, NMDA antagonists, or atypical opioids such as tramadol. (
  • Hyperalgesia is considered a form of neuropathic pain. (
  • 11,14 Furthermore, depletion of monocytes/macrophages ameliorates hyperalgesia in chemically induced peritonitis (acid-induced writhing) 15 and in neuropathic pain models. (
  • Neuropathic pain causes hyperalgesia. (
  • Neuropathic pain is described as hyperalgesia and allodynia. (
  • The cause of hyperalgesia pain is neuropathic pain. (
  • Initial back pain is nociceptive pain and become neuropathic pain when symptoms of hyperalgesia become predominant. (
  • Hyperalgesia induced by opioid is different than hyperalgesia caused by neuropathic pain. (
  • In this study, we evaluated the possible beneficial effect of chronic pelargonidin (PG) treatment on hyperalgesia in streptozotocin (STZ)-diabetic neuropathic rat. (
  • Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management. (
  • Opioid-induced hyperalgesia (OIH) is most broadly defined as a state of nociceptive sensitization caused by exposure to opioids. (
  • Hyperalgesia from opioids is caused by a number of biological factors in the body. (
  • Experimental evidence suggests that opioid tolerance and opioid-induced hyperalgesia might limit the clinical utility of opioids in controlling chronic pain. (
  • The use of opioids is commonly associated with opioid tolerance (OT) and opioid-induced hyperalgesia (OIH), which limit efficacy and compromise safety. (
  • You may feel hyperalgesia induced by opioids. (
  • Erythromelalgia(heat hyperalgesia) is in part due to mutations in TTX sensitivity of channel Na 1.7 (Sodium 1.7). (
  • Manipulations that reduced LIMK activity or abundance, prevented the phosphorylation of cofilin, or disrupted actin filaments in DRG neurons attenuated CFA-induced heat hyperalgesia. (
  • It is noteworthy that these compounds eliminated pain and neurogenic inflammation evoked by intradermal injection of capsaicin into the animal hindpaw, as well as the thermal hyperalgesia induced by tissue irritation with nitrogen mustard. (
  • 1) ASMT applied on L5, L6, or L5 and L6 spinous process significantly reduced the severity and duration of thermal and mechanical hyperalgesia produced by the IVF inflammation. (
  • These studies show that ASMT can significantly reduce the severity and shorten the duration of pain and hyperalgesia caused by lumbar IVF inflammation. (
  • 11,12 In carrageenan-induced inflammation, the infiltrate is mostly formed by monocytes/macrophages at the time of the highest intensity of hyperalgesia. (
  • Selective neutralization of prostaglandin E2 blocks inflammation, hyperalgesia, and interleukin 6 production in vivo. (
  • These results indicate that PGE2 plays a major role in tissue edema, hyperalgesia, and IL-6 production at sites of inflammation, and they suggest that selective pharmacologic modulation of PGE2 synthesis or activity may provide a useful means of mitigating the symptoms of inflammatory disease. (
  • A dose-response study of topical allyl-isothiocyanate (mustard oil) as human surrogate model of pain, hyperalgesia, and neurogenic inflammation. (
  • Chronic pathological conditions such as tissue inflammation can change the properties of somatic sensory pathways, leading to hyperalgesia [ 4 ]. (
  • Opioid-induced hyperalgesia may develop as a result of long-term opioid use in the treatment of chronic pain. (
  • Long-term opioid (e.g. heroin, morphine) users and those on high-dose opioid medications for the treatment of chronic pain, may experience hyperalgesia and experience pain out of proportion to physical findings, which is a common cause for loss of efficacy of these medications over time. (
  • These data support a major role for V(3) receptors in repeated psychological stress-induced visceral hyperalgesia and suggest that pharmacological manipulation of the AVP/V(3) pathway might represent an attractive alternative to the CRF/CRF(1) pathway for the treatment of chronic stress-related gastrointestinal disorders. (
  • Opioid treatments of chronic pain followed by opioid withdrawals may lead to hyperalgesia. (
  • It was found that chronic morphine administration produced hyperalgesia between 60 and 120 minutes after the drug. (
  • It purports to "demystify" opioid-induced hyperalgesia (OIH) but in fact its thrust seems more oriented toward defending the practice of chronic opioid therapy (COT) and downplaying the significance of OIH in the non-surgical setting. (
  • Mechanical and thermal hyperalgesia and ectopic neuronal discharge after chronic compression of dors. (
  • We have recently demonstrated, in a model of chronic widespread pain, that prolonged enhancement of immune mediator hyperalgesia, induced by unpredictable sound stress, requires a contribution of both the sympathoadrenal (epinephrine) and the hypothalamic-pituitary adrenal (corticosterone) neuroendocrine stress axes. (
  • Neuroimmune activation and neuroinflammation in chronic pain and opioid tolerance/hyperalgesia. (
  • What Are The Different Causes Of Hyperalgesia Associated With Chronic Pain? (
  • Endogenous glutamate plays a significant role in nociceptive processing, this neurotransmitter being associated with hyperalgesia and central sensitization. (
  • There is a lot of evidence that suggest that the used of remifentanil is associated with the development of hyperalgesia (a reduction of nociceptive thresholds). (
  • Fentanyl administration exhibited a biphasic time-dependent effect: first, an early response (for 2-5 h) associated with a marked increase in nociceptive threshold (analgesia), and second, a later response associated with sustained lowering of the nociceptive threshold (5 days for the longest effect) below the basal value (30% of decrease for the maximal effect) indicative of hyperalgesia. (
  • Peripheral inflammatory hyperalgesia depends on the sensitization of primary nociceptive neurons. (
  • Monocytes/macrophages have also been linked to the development of hyperalgesia because they produce nociceptive mediators such as tumor necrosis factor α and interleukins 1 and 6. (
  • Morphine-induced hyperalgesia (MIH) is a severe adverse effect accompanying repeated morphine treatment, causing a paradoxical decrease in nociceptive threshold. (
  • Inflammatory Diseases that Can Cause Hyperalgesia- Joint pain, arthritis , and joint injury causes nociceptive pain and if not adequately treated results in hyperalgesia. (
  • however, its effect on nociceptive neuron-associated hyperalgesia remains to be determined. (
  • These results together suggest that administration of lutein attenuates inflammatory hyperalgesia associated with hyperexcitability of nociceptive SpVc WDR neurons via inhibition of the peripheral Cox-2 signaling cascade. (
  • Hyperalgesia occurs when these receptors become more sensitive. (
  • NMDA receptor antagonists help to block the overly sensitized pain receptors in people with hyperalgesia. (
  • These findings indicate that SAP102 can anchor NMDA receptors to affect hyperalgesia formation in bone cancer pain. (
  • These findings demonstrate that the model of short access to nicotine self-administration has limited validity for tobacco dependence, highlight the translational relevance of the model of extended-intermittent access to nicotine self-administration for tobacco dependence and demonstrate that activation of CRF1 receptors is required for the emergence of abstinence-induced anxiety-like behavior, hyperalgesia and excessive nicotine intake. (
  • Bradykinin receptors antagonists and nitric oxide synthase inhibitors in vincristine and streptozotocin induced hyperalgesia in chemotherapy and diabetic neuropathy rat model. (
  • The results of this paper confirm that inhibition of bradykinin receptors and inducible NO synthase but not neuronal NO synthase activity reduces diabetic hyperalgesia. (
  • The prolonged opioid treatment often causes physiological changes in pain receptors and synapses resulting in hyperalgesia. (
  • 1 Activation of glial cells results in a pro-inflammatory state of pain receptors, which results in magnification of pain impulses expressing hyperalgesia. (
  • Ketamine pretreatment, which had no analgesic effect on its own, enhanced the earlier response (analgesia) and prevented the development of long-lasting hyperalgesia. (
  • This type of hyperalgesia is when the increased pain occurs in the tissue where the injury took place. (
  • It is in regard to this type of hyperalgesia that homoeopathy can provide adequate and effective treatment for the affected person. (
  • Different types of hyperalgesia exist, and doctors have a variety of theories regarding why people experience hyperalgesia. (
  • Some types of hyperalgesia may result in severe pain caused by the slightest body movement or the stimulation of a proprioceptor (bones, muscles, ligaments, joints). (
  • But there also are other types of hyperalgesia that affect organs like the stomach, liver, kidneys and even the intestines. (
  • The objective of this work is to evaluate the efficacy of propranolol in the modulation of opioid induced hyperalgesia, with lower postoperative requirements of analgesia rescue. (
  • Preemptive hyperalgesia, not analgesia? (
  • The i.t injection of extracellular signal-regulated kinase (ERK) inhibitor blocked morphine-induced analgesia, without interfering with the morphine-induced hyperalgesia. (
  • However, whether a single systemic administration of an intermediate opioid dose (i.e., a dose that induces analgesia without compromising the overall activity, such as, locomotion or respiratory functions) induces hyperalgesia is still controversial. (
  • 1-5 In some, opioid-induced hyperalgesia was observed to follow analgesia and lasted long after opioid exposure ended. (
  • Nocebo hyperalgesia has received sparse experimental attention compared to placebo analgesia. (
  • The parallel fluctuation of brush-evoked and burning background pain therefore suggest that on-going activity from nociceptors is required to maintain a central state that permits dynamic mechanical hyperalgesia to be expressed in humans. (
  • Furthermore, varenicline (0.1 and 0.5 mg/kg) reversed nicotine withdrawal signs such as hyperalgesia and somatic signs and withdrawal-induced aversion in a dose-related manner. (
  • There were significantly negative correlations between serum PEP activity and severity of pressure hyperalgesia and the non-somatic, cognitive symptoms of the Hamilton Depression Rating Scale. (
  • In contrast, hyperalgesia in muscle is caused by somatic efferents in this view. (
  • Among the potential mechanisms leading to opioid-induced hyperalgesia and antinociceptive tolerance, N -methyl-d-aspartate (NMDA) pain-facilitator processes seem to play a key role. (
  • 14,15 Experimental studies performed in animals and volunteers have shown that NMDA receptor antagonists such as ketamine inhibit central sensitization and prevent opioid-induced hyperalgesia. (
  • In animal models of pain, NMDA agonists induce central sensitization and hyperalgesia whereas antagonists decrease or prevent hyperalgesia. (
  • Our primary aim is to determine whether perioperative NMDA-receptor antagonism has differential effects on postoperative pain, hyperalgesia and morbidity in younger and older patients. (
  • In this review, we focus on the contribution of conditioning in the induction of placebo hypoalgesia and nocebo hyperalgesia and present accumulating evidence that conditioning independent from explicit expectation can cause these effects. (
  • After giving a brief overview over current evidence and models on the development of placebo hypoalgesia and nocebo hyperalgesia including conditioning and expectation approaches, we will turn to studies that stress the significance of conditioning and demonstrate that conditioning effects might have been misunderstood and/or underestimated. (
  • Labeling an inert treatment as expensive medication led to stronger nocebo hyperalgesia than labeling it as cheap medication. (
  • In particular, activity in the prefrontal cortex mediated the effect of value on nocebo hyperalgesia. (
  • The aim of the present study was to investigate if personality traits and fear of pain could predict experimental nocebo hyperalgesia. (
  • The results from the present study suggest that dispositional fear of pain might be a useful predictor for nocebo hyperalgesia and emotional states concomitant with expectations of increased pain. (
  • Our goal is to demonstrate that healthy volunteers treated with fenobam will develop a significantly reduced area of cutaneous hyperalgesia compared to volunteers treated with placebo, after exposure to the heat/capsaicin model of cutaneous sensitization. (
  • A Double Blind, Randomized, Placebo Controlled, Crossover Study to Investigate the Anti-hyperalgesic Efficacy of a Single Dose of Fenobam on Heat/Capsaicin Induced Cutaneous Hyperalgesia in Adult Healthy Volunteers. (
  • Suppression of the development of cutaneous hyperalgesia and allodynia around the area treated with heat/capsaicin. (
  • Hardy JD, Wolff HG, Goodell H. Experimental evidence on the nature of cutaneous hyperalgesia. (
  • Some people experience hyperalgesia following a surgical procedure. (
  • People with fibromyalgia can also experience hyperalgesia. (
  • This lidocaine-induced sensitization might contribute to postoperative hyperalgesia. (
  • Since the manipulation is proximal to the injured joint, these data suggest that central neural mechanisms mediate the reduction in hyperalgesia. (
  • SEVERAL peripheral endogenous antinociceptive mechanisms are involved in counteracting inflammatory hyperalgesia. (
  • Previous studies demonstrated that electroacupuncture (EA) alleviates hyperalgesia, but the mechanisms remained unclear. (
  • Two predominant theories exist for the explanation of hyperalgesia one based upon central mechanisms and one by peripheral. (
  • According to this theory, referred pain with hyperalgesia is mainly caused by central mechanisms. (
  • Models and Mechanisms of Hyperalgesia and Allodynia // Physiolo. (
  • A new animal model for assessing mechanisms and management of muscle hyperalgesia // Pain 85: 333-343, 2000. (
  • What Is Visceral Hyperalgesia? (
  • Visceral hyperalgesia is an increased sensitivity to pain in the internal organs of the body, like the stomach, pancreas or intestines. (
  • What Are Symptoms of Visceral Hyperalgesia? (
  • How Is Visceral Hyperalgesia Diagnosed? (
  • There is no specific test to diagnose visceral hyperalgesia. (
  • Widespread hyperalgesia in irritable bowel syndrome is dynamically maintained by tonic visceral impulse input and placebo/nocebo factors. (
  • Repeated administration of SSR149415 at 1 or 3 mg/kg completely prevented stress-induced visceral hyperalgesia. (
  • Primary hyperalgesia occurs at and around the site of the injury. (
  • When the ability to perceive light touch had been abolished, there was also no touch-evoked pain, indicating that this component of mechanical hyperalgesia is mediated by large-diameter primary afferents. (
  • Importantly, at this stage of the block, when only unmyelinated primary afferents conducted, neither spontaneous pain, nor hyperalgesia to heat, nor the lowered pressure pain threshold had changed significantly. (
  • Ketamine has been shown to have some effectiveness in managing hyperalgesia. (
  • 17 However, we did not study the action of ketamine and specially the effects of ketamine on remifentanil-induced hyperalgesia in the postoperative setting, which have yet to be evaluated. (
  • The aim of this prospective, randomized, placebo-controlled study was to compare the effects of ketamine and paracetamol on preventing remifentanil induced hyperalgesia. (
  • It was shown that ketamine and paracetamol were both effective in preventing remifentanil induced hyperalgesia. (
  • Yalcin N, Uzun ST, Reisli R, Borazan H, Otelcioglu S. A Comparison of Ketamine and Paracetamol for Preventing Remifentanil Induced Hyperalgesia in Patients Undergoing Total Abdominal Hysterectomy. (
  • The purpose of this review is to evaluate the occurrence and significance of opioid-induced hyperalgesia (OIH) after acute fentanyl exposure. (
  • A literature search was conducted from October 1995 through January 2015 using MEDLINE, Embase, and Scopus with the terms hyperalgesia, fentanyl, pronociceptive, acute tolerance, and acute. (
  • Hyperalgesia has been described following remifentanil and morphine use, but the question remains about the associated risk with acute fentanyl exposure. (
  • Hyperalgesia should be considered in patients with uncontrolled pain despite escalating fentanyl doses, since the possibility of fentanyl-induced OIH exists in the acute setting. (
  • Acute administration of remifentanil may lead to opioid-induced hyperalgesia (OIH). (
  • The same applies to all innervated parts of the body, on which manifestations of hyperalgesia are particularly acute, even without applying pressure on the painful area or stimulating it in any way whatsoever. (
  • Therefore, here we investigated whether activation of P2X7R by ATP and the subsequent release of IL-1β in DRG participate in peripheral inflammatory hyperalgesia. (
  • This evidence places the SGC as an active player in the establishment of peripheral inflammatory hyperalgesia and highlights the importance of the events in DRG for the treatment of inflammatory diseases. (
  • Peripheral Neuropathy most often causes hyperalgesia in late stages. (
  • Hyperalgesia is an increased sensitivity to pain that may be caused by damage to nocicpetors or peripheral nerves. (
  • As it can be difficult to distinguish from tolerance, opioid-induced hyperalgesia is often compensated for by escalating the dose of opioid, potentially worsening the problem by further increasing sensitivity to pain. (
  • Hyperalgesia is a condition where a person develops an increased sensitivity to pain. (
  • The key symptom of hyperalgesia is feeling increased sensitivity to pain without additional injury or worsening of another condition. (
  • Hyperalgesia is a condition in which you experience an enhanced sensitivity to pain. (
  • Hyperalgesia pertains to the excessive sensitivity to pain . (
  • There is accumulating evidence that opioid therapy might not only be associated with the development of tolerance but also with an increased sensitivity to pain, a condition referred to as opioid-induced hyperalgesia (OIH). (
  • Two trials oppose whereas four trials support the occurrence of fentanyl-induced hyperalgesia. (
  • The higher the fentanyl dose used, the more pronounced was the fentanyl-induced hyperalgesia. (
  • studied opioid-induced hyperalgesia (OIH) and reported that opioid administration, but not trauma-induced nerve injury, augmented PRL and decreased PRLR-L in female animals, promoting the activation of PRLR-S and the development of OIH. (
  • These molecules attenuated in vivo thermal nociception and hyperalgesia, and suppressed capsaicin-evoked pain. (
  • The virus treatment alone did not alter thermal thresholds (first three data points), but in contrast to naive animals, topical capsaicin leads to thermal hyperalgesia (shortened latencies) in the virus-treated paw. (
  • Measurement of heat/cold pain threshold and area of heat/capsaicin-induced hyperalgesia. (
  • Here, we show that both magnitude and duration of heroin-induced delayed hyperalgesia increase with intermittent heroin administrations, leading to an apparent decrease in the analgesic effectiveness of a given heroin dose. (
  • 3,5 Opioid-induced processes that underlie hyperalgesia decrease antinociception and contribute to opioid tolerance. (
  • According to some authors, hyperalgesia and related phenomena at skin level are induced by sympathetic efferents, because an experimental, local anesthetic block of the sympathetic ganglia led to disappearance or marked decrease of referred pain, hyperalgesia, and dermographic skin alterations. (
  • Opioid-induced hyperalgesia is a phenomenon defined by increasing pain after opioid exposure with the worsening of pain occurring when opioid doses are increased. (
  • 7 Moreover, delayed hyperalgesia develops from short-acting opioid exposure, 8-10 and relatively large intraoperative opioid doses are associated with greater postoperative opioid consumption and higher pain scores. (
  • However, as with other forms of nerve dysfunction associated pain, treatment of hyperalgesia can be clinically challenging, and finding a suitable drug or drug combination that is effective for a particular patient may require trial and error. (
  • The use of a transcutaneous electrical nerve stimulation device has been shown to alleviate hyperalgesia. (
  • Although there are many potential causes associated with hyperalgesia, the condition is thought to be the result of changes to nerve pathways, which cause a person's nerves to have an overactive response to pain. (
  • There are several nerve or "pain" pathways in the body where signals can start to miscommunicate with each other, resulting in hyperalgesia. (
  • Hyperalgesia can develop due to tissue or nerve injury as part of a surgery or procedure. (
  • Based on the differences in quality of sensations, in spatial and temporal profiles and in susceptibility to differential nerve blocks, we conclude that irritant chemicals induce a dynamic and static component of mechanical hyperalgesia signalled by large-diameter or unmyelinated fibres, respectively. (
  • Hyperalgesia Caused Due To Trigeminal Neuralgia - Trigeminal neuralgia causes hyperalgesia spread over all three branches of trigeminal nerve or one of the three branches of trigeminal nerve. (
  • Shingles or Post-Herpetic Neuralgia - Hyperalgesia pain is along the nerve, which is affected by viral infection. (
  • In general, hyperalgesia is the result of increased nerve sensitivity caused by an injury, although it could also be caused by a sensitivity to heat. (
  • For most people with hyperalgesia, this is usually the preferred choice. (
  • Fibromyalgia patients with severe pressure hyperalgesia had significantly lower PEP activity than normal controls and fibromyalgia patients with less severe hyperalgesia. (
  • Stress markedly exacerbates pain in diseases such as fibromyalgia and rheumatoid arthritis 1 - 4 , 8 , and we have hypothesized that stress causes generalized hyperalgesia by enhancing pronociceptive effects of immune mediators (e.g. cytokines and prostaglandins). (
  • In streptozotocin-induced hyperalgesia, inducible NO synthase participates in pronociceptive activity of bradykinin, whereas in vincristine-induced hyperalgesia bradykinin seemed to activate neuronal NO synthase pathway. (
  • Prolonged Differential Wound Hyperalgesia After an Interval. (
  • We assessed postoperative pain at rest and with movement along with wound hyperalgesia in a patient who had undergone lower abdominal surgery under general anesthesia with a unilateral epidural block that persisted throughout surgery and in whom the epidural catheter was replaced immediately afterward. (
  • Pain and wound hyperalgesia were consistently greater on the "unblocked" side for the 3-wk period of observation. (
  • After establishment, adrenal medullectomy abolished the enhancement of epinephrine-induced cutaneous and muscle hyperalgesia. (
  • PGE 2 -G is known to produce hyperalgesia. (