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.
Cyclohexanecarboxylic acids are organic compounds consisting of a cyclohexane ring substituted with a carboxylic acid group, typically represented by the structural formula C6H11COOH.
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.
Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.
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.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
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 (i.pl.) 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)

Hyperalgesia is a medical term that describes an increased sensitivity to pain. It occurs when the nervous system, specifically the nociceptors (pain receptors), become excessively sensitive to stimuli. This means that a person experiences pain from a stimulus that normally wouldn't cause pain or experiences pain that is more intense than usual. Hyperalgesia can be a result of various conditions such as nerve damage, inflammation, or certain medications. It's an important symptom to monitor in patients with chronic pain conditions, as it may indicate the development of tolerance or addiction to pain medication.

Pain threshold is a term used in medicine and research to describe the point at which a stimulus begins to be perceived as painful. It is an individual's subjective response and can vary from person to person based on factors such as their pain tolerance, mood, expectations, and cultural background.

The pain threshold is typically determined through a series of tests where gradually increasing levels of stimuli are applied until the individual reports feeling pain. This is often used in research settings to study pain perception and analgesic efficacy. However, it's important to note that the pain threshold should not be confused with pain tolerance, which refers to the maximum level of pain a person can endure.

Nociceptors are specialized peripheral sensory neurons that detect and transmit signals indicating potentially harmful stimuli in the form of pain. They are activated by various noxious stimuli such as extreme temperatures, intense pressure, or chemical irritants. Once activated, nociceptors transmit these signals to the central nervous system (spinal cord and brain) where they are interpreted as painful sensations, leading to protective responses like withdrawing from the harmful stimulus or seeking medical attention. Nociceptors play a crucial role in our perception of pain and help protect the body from further harm.

Pain measurement, in a medical context, refers to the quantification or evaluation of the intensity and/or unpleasantness of a patient's subjective pain experience. This is typically accomplished through the use of standardized self-report measures such as numerical rating scales (NRS), visual analog scales (VAS), or categorical scales (mild, moderate, severe). In some cases, physiological measures like heart rate, blood pressure, and facial expressions may also be used to supplement self-reported pain ratings. The goal of pain measurement is to help healthcare providers better understand the nature and severity of a patient's pain in order to develop an effective treatment plan.

Carriageenans are a family of linear sulfated polysaccharides that are extracted from red edible seaweeds. They have been widely used in the food industry as thickening, gelling, and stabilizing agents. In the medical field, they have been studied for their potential therapeutic applications, such as in the treatment of gastrointestinal disorders and inflammation. However, some studies have suggested that certain types of carriageenans may have negative health effects, including promoting inflammation and damaging the gut lining. Therefore, more research is needed to fully understand their safety and efficacy.

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. It is a complex phenomenon that can result from various stimuli, such as thermal, mechanical, or chemical irritation, and it can be acute or chronic. The perception of pain involves the activation of specialized nerve cells called nociceptors, which transmit signals to the brain via the spinal cord. These signals are then processed in different regions of the brain, leading to the conscious experience of pain. It's important to note that pain is a highly individual and subjective experience, and its perception can vary widely among individuals.

Spinal injections, also known as epidural injections or intrathecal injections, are medical procedures involving the injection of medications directly into the spinal canal. The medication is usually delivered into the space surrounding the spinal cord (the epidural space) or into the cerebrospinal fluid that surrounds and protects the spinal cord (the subarachnoid space).

The medications used in spinal injections can include local anesthetics, steroids, opioids, or a combination of these. The purpose of spinal injections is to provide diagnostic information, therapeutic relief, or both. They are commonly used to treat various conditions affecting the spine, such as radicular pain (pain that radiates down the arms or legs), disc herniation, spinal stenosis, and degenerative disc disease.

Spinal injections can be administered using different techniques, including fluoroscopy-guided injections, computed tomography (CT) scan-guided injections, or with the help of a nerve stimulator. These techniques ensure accurate placement of the medication and minimize the risk of complications.

It is essential to consult a healthcare professional for specific information regarding spinal injections and their potential benefits and risks.

Physical stimulation, in a medical context, refers to the application of external forces or agents to the body or its tissues to elicit a response. This can include various forms of touch, pressure, temperature, vibration, or electrical currents. The purpose of physical stimulation may be therapeutic, as in the case of massage or physical therapy, or diagnostic, as in the use of reflex tests. It is also used in research settings to study physiological responses and mechanisms.

In a broader sense, physical stimulation can also refer to the body's exposure to physical activity or exercise, which can have numerous health benefits, including improving cardiovascular function, increasing muscle strength and flexibility, and reducing the risk of chronic diseases.

Analgesics are a class of drugs that are used to relieve pain. They work by blocking the transmission of pain signals in the nervous system, allowing individuals to manage their pain levels more effectively. There are many different types of analgesics available, including both prescription and over-the-counter options. Some common examples include acetaminophen (Tylenol), ibuprofen (Advil or Motrin), and opioids such as morphine or oxycodone.

The choice of analgesic will depend on several factors, including the type and severity of pain being experienced, any underlying medical conditions, potential drug interactions, and individual patient preferences. It is important to use these medications as directed by a healthcare provider, as misuse or overuse can lead to serious side effects and potential addiction.

In addition to their pain-relieving properties, some analgesics may also have additional benefits such as reducing inflammation (like in the case of nonsteroidal anti-inflammatory drugs or NSAIDs) or causing sedation (as with certain opioids). However, it is essential to weigh these potential benefits against the risks and side effects associated with each medication.

When used appropriately, analgesics can significantly improve a person's quality of life by helping them manage their pain effectively and allowing them to engage in daily activities more comfortably.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Capsaicin is defined in medical terms as the active component of chili peppers (genus Capsicum) that produces a burning sensation when it comes into contact with mucous membranes or skin. It is a potent irritant and is used topically as a counterirritant in some creams and patches to relieve pain. Capsaicin works by depleting substance P, a neurotransmitter that relays pain signals to the brain, from nerve endings.

Here is the medical definition of capsaicin from the Merriam-Webster's Medical Dictionary:

caпсаісіn : an alkaloid (C18H27NO3) that is the active principle of red peppers and is used in topical preparations as a counterirritant and analgesic.

Freund's adjuvant is not a medical condition but a substance used in laboratory research to enhance the body's immune response to an antigen or vaccine. It is named after its developer, Jules T. Freund.

There are two types of Freund's adjuvants: complete and incomplete. Freund's complete adjuvant (FCA) contains killed Mycobacterium tuberculosis bacteria, which causes a strong inflammatory response when injected into the body. This makes it an effective adjuvant for experimental vaccines, as it helps to stimulate the immune system and promote a stronger and longer-lasting immune response.

Freund's incomplete adjuvant (FIA) is similar to FCA but does not contain Mycobacterium tuberculosis. It is less potent than FCA but still useful for boosting the immune response to certain antigens.

It is important to note that Freund's adjuvants are not used in human vaccines due to their potential to cause adverse reactions, including granulomas and other inflammatory responses. They are primarily used in laboratory research with animals.

In a medical context, "hot temperature" is not a standard medical term with a specific definition. However, it is often used in relation to fever, which is a common symptom of illness. A fever is typically defined as a body temperature that is higher than normal, usually above 38°C (100.4°F) for adults and above 37.5-38°C (99.5-101.3°F) for children, depending on the source.

Therefore, when a medical professional talks about "hot temperature," they may be referring to a body temperature that is higher than normal due to fever or other causes. It's important to note that a high environmental temperature can also contribute to an elevated body temperature, so it's essential to consider both the body temperature and the environmental temperature when assessing a patient's condition.

Neuralgia is a type of pain that occurs along the pathway of a nerve, often caused by damage or irritation to the nerve. It is typically described as a sharp, stabbing, burning, or electric-shock like pain that can be severe and debilitating. Neuralgia can affect any nerve in the body, but it most commonly occurs in the facial area (trigeminal neuralgia) or in the nerves related to the spine (postherpetic neuralgia). The pain associated with neuralgia can be intermittent or constant and may be worsened by certain triggers such as touch, temperature changes, or movement. Treatment for neuralgia typically involves medications to manage pain, as well as other therapies such as nerve blocks, surgery, or lifestyle modifications.

The spinal cord is a major part of the nervous system, extending from the brainstem and continuing down to the lower back. It is a slender, tubular bundle of nerve fibers (axons) and support cells (glial cells) that carries signals between the brain and the rest of the body. The spinal cord primarily serves as a conduit for motor information, which travels from the brain to the muscles, and sensory information, which travels from the body to the brain. It also contains neurons that can independently process and respond to information within the spinal cord without direct input from the brain.

The spinal cord is protected by the bony vertebral column (spine) and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each segment corresponds to a specific region of the body and gives rise to pairs of spinal nerves that exit through the intervertebral foramina at each level.

The spinal cord is responsible for several vital functions, including:

1. Reflexes: Simple reflex actions, such as the withdrawal reflex when touching a hot surface, are mediated by the spinal cord without involving the brain.
2. Muscle control: The spinal cord carries motor signals from the brain to the muscles, enabling voluntary movement and muscle tone regulation.
3. Sensory perception: The spinal cord transmits sensory information, such as touch, temperature, pain, and vibration, from the body to the brain for processing and awareness.
4. Autonomic functions: The sympathetic and parasympathetic divisions of the autonomic nervous system originate in the thoracolumbar and sacral regions of the spinal cord, respectively, controlling involuntary physiological responses like heart rate, blood pressure, digestion, and respiration.

Damage to the spinal cord can result in various degrees of paralysis or loss of sensation below the level of injury, depending on the severity and location of the damage.

Spinal ganglia, also known as dorsal root ganglia, are clusters of nerve cell bodies located in the peripheral nervous system. They are situated along the length of the spinal cord and are responsible for transmitting sensory information from the body to the brain. Each spinal ganglion contains numerous neurons, or nerve cells, with long processes called axons that extend into the periphery and innervate various tissues and organs. The cell bodies within the spinal ganglia receive sensory input from these axons and transmit this information to the central nervous system via the dorsal roots of the spinal nerves. This allows the brain to interpret and respond to a wide range of sensory stimuli, including touch, temperature, pain, and proprioception (the sense of the position and movement of one's body).

Transient receptor potential vanilloid (TRPV) cation channels are a subfamily of transient receptor potential (TRP) channels, which are non-selective cation channels that play important roles in various physiological processes such as nociception, thermosensation, and mechanosensation. TRPV channels are activated by a variety of stimuli including temperature, chemical ligands, and mechanical forces.

TRPV channels are composed of six transmembrane domains with intracellular N- and C-termini. The TRPV subfamily includes six members: TRPV1 to TRPV6. Among them, TRPV1 is also known as the vanilloid receptor 1 (VR1) and is activated by capsaicin, the active component of hot chili peppers, as well as noxious heat. TRPV2 is activated by noxious heat and mechanical stimuli, while TRPV3 and TRPV4 are activated by warm temperatures and various chemical ligands. TRPV5 and TRPV6 are primarily involved in calcium transport and are activated by low pH and divalent cations.

TRPV channels play important roles in pain sensation, neurogenic inflammation, and temperature perception. Dysfunction of these channels has been implicated in various pathological conditions such as chronic pain, inflammatory diseases, and cancer. Therefore, TRPV channels are considered promising targets for the development of novel therapeutics for these conditions.

Analgesics, opioid are a class of drugs used for the treatment of pain. They work by binding to specific receptors in the brain and spinal cord, blocking the transmission of pain signals to the brain. Opioids can be synthetic or natural, and include drugs such as morphine, codeine, oxycodone, hydrocodone, hydromorphone, fentanyl, and methadone. They are often used for moderate to severe pain, such as that resulting from injury, surgery, or chronic conditions like cancer. However, opioids can also produce euphoria, physical dependence, and addiction, so they are tightly regulated and carry a risk of misuse.

I'm sorry for any confusion, but "touch" is not a term that has a specific medical definition in the context you've provided. In a general sense, touch refers to the ability to perceive things through physically contacting them, which is a function of our nervous system. However, it's not a term used to describe a specific medical condition, diagnosis, treatment, or procedure. If you have any more specific context or question in mind, I'd be happy to try and help further!

Posterior horn cells refer to the neurons located in the posterior (or dorsal) horn of the gray matter in the spinal cord. These cells are primarily responsible for receiving and processing sensory information from peripheral nerves, particularly related to touch, pressure, pain, and temperature. The axons of these cells form the ascending tracts that carry this information to the brain for further processing. It's worth noting that damage to posterior horn cells can result in various sensory deficits, such as those seen in certain neurological conditions.

Morphine is a potent opioid analgesic (pain reliever) derived from the opium poppy. It works by binding to opioid receptors in the brain and spinal cord, blocking the transmission of pain signals and reducing the perception of pain. Morphine is used to treat moderate to severe pain, including pain associated with cancer, myocardial infarction, and other conditions. It can also be used as a sedative and cough suppressant.

Morphine has a high potential for abuse and dependence, and its use should be closely monitored by healthcare professionals. Common side effects of morphine include drowsiness, respiratory depression, constipation, nausea, and vomiting. Overdose can result in respiratory failure, coma, and death.

I'm sorry for any confusion, but "Mustard Plant" is not a term typically used in medical definitions. Mustard plants are actually a type of crop plant from the Brassicaceae family, which also includes vegetables like broccoli and cabbage. The seeds from these plants are often ground to make mustard condiments and spices. If you're looking for information related to potential medicinal uses or health effects of mustard plants or their derivatives, I would be happy to help with that.

Sciatic neuropathy is a condition that results from damage or injury to the sciatic nerve, which is the largest nerve in the human body. The sciatic nerve originates from the lower spine (lumbar and sacral regions) and travels down through the buttocks, hips, and legs to the feet.

Sciatic neuropathy can cause various symptoms, including pain, numbness, tingling, weakness, or difficulty moving the affected leg or foot. The pain associated with sciatic neuropathy is often described as sharp, shooting, or burning and may worsen with movement, coughing, or sneezing.

The causes of sciatic neuropathy include compression or irritation of the nerve due to conditions such as herniated discs, spinal stenosis, bone spurs, tumors, or piriformis syndrome. Trauma or injury to the lower back, hip, or buttocks can also cause sciatic neuropathy.

Diagnosing sciatic neuropathy typically involves a physical examination and medical history, as well as imaging tests such as X-rays, MRI, or CT scans to visualize the spine and surrounding structures. Treatment options may include pain management, physical therapy, steroid injections, or surgery, depending on the severity and underlying cause of the condition.

Hyperesthesia is a medical term that refers to an increased sensitivity to sensory stimuli, including touch, pain, temperature, or sound. It can affect various parts of the body and can be a symptom of several different conditions, such as nerve damage, multiple sclerosis, or complex regional pain syndrome. Hyperesthesia can cause discomfort, pain, or even intense pain in response to light touch or other stimuli that would not normally cause such a reaction. Treatment for hyperesthesia depends on the underlying cause and may include medications, physical therapy, or other interventions.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Inflammation is a complex biological response of tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is characterized by the following signs: rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). The process involves the activation of the immune system, recruitment of white blood cells, and release of inflammatory mediators, which contribute to the elimination of the injurious stimuli and initiation of the healing process. However, uncontrolled or chronic inflammation can also lead to tissue damage and diseases.

'Animal behavior' refers to the actions or responses of animals to various stimuli, including their interactions with the environment and other individuals. It is the study of the actions of animals, whether they are instinctual, learned, or a combination of both. Animal behavior includes communication, mating, foraging, predator avoidance, and social organization, among other things. The scientific study of animal behavior is called ethology. This field seeks to understand the evolutionary basis for behaviors as well as their physiological and psychological mechanisms.

Nociception is the neural process of encoding and processing noxious stimuli, which can result in the perception of pain. It involves the activation of specialized nerve endings called nociceptors, located throughout the body, that detect potentially harmful stimuli such as extreme temperatures, intense pressure, or tissue damage caused by chemicals released during inflammation. Once activated, nociceptors transmit signals through sensory neurons to the spinal cord and then to the brain, where they are interpreted as painful experiences.

It is important to note that while nociception is necessary for pain perception, it does not always lead to conscious awareness of pain. Factors such as attention, emotion, and context can influence whether or not nociceptive signals are experienced as painful.

Referred pain is a type of pain that is felt in a part of the body other than its actual source. This occurs because the brain incorrectly interprets nerve signals from damaged tissues or organs. In the case of referred pain, the brain misinterprets the location of the pain signal and attributes it to a different area of the body.

Referred pain is often described as a dull, aching sensation rather than a sharp, stabbing pain. It can be difficult to diagnose because the source of the pain may not be immediately apparent. Common examples of referred pain include:

* Heart attack pain that is felt in the left arm or jaw
* Gallbladder pain that is felt in the right shoulder blade
* Kidney stones that cause pain in the lower back and abdomen
* Appendicitis that causes pain in the lower right quadrant of the abdomen, but can sometimes be referred to the lower left quadrant in pregnant women or those with a longer colon.

Referred pain is thought to occur because the nerves carrying pain signals from different parts of the body converge on the same neurons in the spinal cord before traveling to the brain. If these neurons are stimulated by pain signals from multiple sources, the brain may have difficulty distinguishing between them and may interpret the pain as coming from a single location.

Spinal nerves are the bundles of nerve fibers that transmit signals between the spinal cord and the rest of the body. There are 31 pairs of spinal nerves in the human body, which can be divided into five regions: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each spinal nerve carries both sensory information (such as touch, temperature, and pain) from the periphery to the spinal cord, and motor information (such as muscle control) from the spinal cord to the muscles and other structures in the body. Spinal nerves also contain autonomic fibers that regulate involuntary functions such as heart rate, digestion, and blood pressure.

Sensory receptor cells are specialized structures that convert physical stimuli from our environment into electrical signals, which are then transmitted to the brain for interpretation. These receptors can be found in various tissues throughout the body and are responsible for detecting sensations such as touch, pressure, temperature, taste, and smell. They can be classified into two main types: exteroceptors, which respond to stimuli from the external environment, and interoceptors, which react to internal conditions within the body. Examples of sensory receptor cells include hair cells in the inner ear, photoreceptors in the eye, and taste buds on the tongue.

Drug tolerance is a medical concept that refers to the decreased response to a drug following its repeated use, requiring higher doses to achieve the same effect. This occurs because the body adapts to the presence of the drug, leading to changes in the function or expression of targets that the drug acts upon, such as receptors or enzymes. Tolerance can develop to various types of drugs, including opioids, benzodiazepines, and alcohol, and it is often associated with physical dependence and addiction. It's important to note that tolerance is different from resistance, which refers to the ability of a pathogen to survive or grow in the presence of a drug, such as antibiotics.

Visceral pain is a type of pain that originates from the internal organs (viscera) such as the stomach, intestines, liver, or heart. It's often described as diffuse, dull, and hard to localize, unlike somatic pain which arises from the skin, muscles, or bones and is usually easier to pinpoint.

Visceral pain may be caused by various conditions like inflammation, infection, ischemia (reduced blood supply), distention or stretching of the organ walls, or direct damage to the organs. The sensation of visceral pain can be modulated and referred to other areas of the body due to the complex interactions in the nervous system, making it sometimes challenging to diagnose the exact source of the pain.

Cyclohexanecarboxylic acids are a type of organic compound that consists of a cyclohexane ring, which is a six-carbon saturated hydrocarbon, substituted with a carboxylic acid group (-COOH). This group contains a carbon atom double bonded to an oxygen atom and single bonded to a hydroxyl group (-OH).

The cyclohexane ring can be in various forms, including the chair, boat, or twist-boat conformations, depending on the orientation of its constituent atoms. The carboxylic acid group can ionize to form a carboxylate anion, which is negatively charged and has a deprotonated hydroxyl group.

Cyclohexanecarboxylic acids have various applications in industry and research, including as intermediates in the synthesis of other chemicals, solvents, and pharmaceuticals. They can also be found naturally in some plants and microorganisms.

The sciatic nerve is the largest and longest nerve in the human body, running from the lower back through the buttocks and down the legs to the feet. It is formed by the union of the ventral rami (branches) of the L4 to S3 spinal nerves. The sciatic nerve provides motor and sensory innervation to various muscles and skin areas in the lower limbs, including the hamstrings, calf muscles, and the sole of the foot. Sciatic nerve disorders or injuries can result in symptoms such as pain, numbness, tingling, or weakness in the lower back, hips, legs, and feet, known as sciatica.

In medical terms, the foot is the part of the lower limb that is distal to the leg and below the ankle, extending from the tarsus to the toes. It is primarily responsible for supporting body weight and facilitating movement through push-off during walking or running. The foot is a complex structure made up of 26 bones, 33 joints, and numerous muscles, tendons, ligaments, and nerves that work together to provide stability, balance, and flexibility. It can be divided into three main parts: the hindfoot, which contains the talus and calcaneus (heel) bones; the midfoot, which includes the navicular, cuboid, and cuneiform bones; and the forefoot, which consists of the metatarsals and phalanges that form the toes.

Edema is the medical term for swelling caused by excess fluid accumulation in the body tissues. It can affect any part of the body, but it's most commonly noticed in the hands, feet, ankles, and legs. Edema can be a symptom of various underlying medical conditions, such as heart failure, kidney disease, liver disease, or venous insufficiency.

The swelling occurs when the capillaries leak fluid into the surrounding tissues, causing them to become swollen and puffy. The excess fluid can also collect in the cavities of the body, leading to conditions such as pleural effusion (fluid around the lungs) or ascites (fluid in the abdominal cavity).

The severity of edema can vary from mild to severe, and it may be accompanied by other symptoms such as skin discoloration, stiffness, and pain. Treatment for edema depends on the underlying cause and may include medications, lifestyle changes, or medical procedures.

Unmyelinated nerve fibers, also known as unmyelinated axons or non-myelinated fibers, are nerve cells that lack a myelin sheath. Myelin is a fatty, insulating substance that surrounds the axon of many nerve cells and helps to increase the speed of electrical impulses traveling along the nerve fiber.

In unmyelinated nerve fibers, the axons are surrounded by a thin layer of Schwann cell processes called the endoneurium, but there is no continuous myelin sheath. Instead, the axons are packed closely together in bundles, with several axons lying within the same Schwann cell.

Unmyelinated nerve fibers tend to be smaller in diameter than myelinated fibers and conduct electrical impulses more slowly. They are commonly found in the autonomic nervous system, which controls involuntary functions such as heart rate, blood pressure, and digestion, as well as in sensory nerves that transmit pain and temperature signals.

An abdominal reflex is a withdrawal response that occurs when the skin in the lower abdomen is stimulated, leading to contraction of the muscles in the same side of the abdomen. This reflex is mediated by the T10-L1 spinal cord segments and is typically tested during a physical examination to assess the integrity of the nervous system. A decreased or absent abdominal reflex may indicate damage to the peripheral nerves, spinal cord, or brain.

Peripheral Nervous System (PNS) diseases, also known as Peripheral Neuropathies, refer to conditions that affect the functioning of the peripheral nervous system, which includes all the nerves outside the brain and spinal cord. These nerves transmit signals between the central nervous system (CNS) and the rest of the body, controlling sensations, movements, and automatic functions such as heart rate and digestion.

PNS diseases can be caused by various factors, including genetics, infections, toxins, metabolic disorders, trauma, or autoimmune conditions. The symptoms of PNS diseases depend on the type and extent of nerve damage but often include:

1. Numbness, tingling, or pain in the hands and feet
2. Muscle weakness or cramps
3. Loss of reflexes
4. Decreased sensation to touch, temperature, or vibration
5. Coordination problems and difficulty with balance
6. Sexual dysfunction
7. Digestive issues, such as constipation or diarrhea
8. Dizziness or fainting due to changes in blood pressure

Examples of PNS diseases include Guillain-Barre syndrome, Charcot-Marie-Tooth disease, diabetic neuropathy, and peripheral nerve injuries. Treatment for these conditions varies depending on the underlying cause but may involve medications, physical therapy, lifestyle changes, or surgery.

Analgesia is defined as the absence or relief of pain in a patient, achieved through various medical means. It is derived from the Greek word "an-" meaning without and "algein" meaning to feel pain. Analgesics are medications that are used to reduce pain without causing loss of consciousness, and they work by blocking the transmission of pain signals to the brain.

Examples of analgesics include over-the-counter medications such as acetaminophen (Tylenol) and nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen (Advil, Motrin) and naproxen (Aleve). Prescription opioid painkillers, such as oxycodone (OxyContin, Percocet) and hydrocodone (Vicodin), are also used for pain relief but carry a higher risk of addiction and abuse.

Analgesia can also be achieved through non-pharmacological means, such as through nerve blocks, spinal cord stimulation, acupuncture, and other complementary therapies. The choice of analgesic therapy depends on the type and severity of pain, as well as the patient's medical history and individual needs.

Afferent neurons, also known as sensory neurons, are a type of nerve cell that conducts impulses or signals from peripheral receptors towards the central nervous system (CNS), which includes the brain and spinal cord. These neurons are responsible for transmitting sensory information such as touch, temperature, pain, sound, and light to the CNS for processing and interpretation. Afferent neurons have specialized receptor endings that detect changes in the environment and convert them into electrical signals, which are then transmitted to the CNS via synapses with other neurons. Once the signals reach the CNS, they are processed and integrated with other information to produce a response or reaction to the stimulus.

I'm sorry for any confusion, but "Sensory System Agents" is not a widely recognized or established medical term. Sensory systems refer to the parts of the nervous system that process and transmit information about the world around us, including the senses of sight, hearing, touch, taste, and smell. However, there are no specific "agents" that are generally recognized as being solely dedicated to affecting these systems in a medical context.

If you're referring to specific pharmaceutical agents or drugs that affect sensory systems, these would be more accurately described using terms related to the specific system (like "ophthalmic agents" for vision, or "anesthetics" for touch/pain) and the specific drug class or mechanism of action.

If you have a more specific context in mind, I'd be happy to try to provide a more targeted answer!

A hindlimb, also known as a posterior limb, is one of the pair of extremities that are located distally to the trunk in tetrapods (four-legged vertebrates) and include mammals, birds, reptiles, and amphibians. In humans and other primates, hindlimbs are equivalent to the lower limbs, which consist of the thigh, leg, foot, and toes.

The primary function of hindlimbs is locomotion, allowing animals to move from one place to another. However, they also play a role in other activities such as balance, support, and communication. In humans, the hindlimbs are responsible for weight-bearing, standing, walking, running, and jumping.

In medical terminology, the term "hindlimb" is not commonly used to describe human anatomy. Instead, healthcare professionals use terms like lower limbs or lower extremities to refer to the same region of the body. However, in comparative anatomy and veterinary medicine, the term hindlimb is still widely used to describe the corresponding structures in non-human animals.

Analgesics, non-narcotic are a class of medications used to relieve pain that do not contain narcotics or opioids. They work by blocking the transmission of pain signals in the nervous system or by reducing inflammation and swelling. Examples of non-narcotic analgesics include acetaminophen (Tylenol), ibuprofen (Advil, Motrin), naproxen (Aleve), and aspirin. These medications are often used to treat mild to moderate pain, such as headaches, menstrual cramps, muscle aches, and arthritis symptoms. They can be obtained over-the-counter or by prescription, depending on the dosage and formulation. It is important to follow the recommended dosages and usage instructions carefully to avoid adverse effects.

Visceral afferents are specialized nerve fibers that carry sensory information from the internal organs (viscera) to the central nervous system. These afferent neurons detect and transmit information about various visceral stimuli, such as pain, temperature, touch, pressure, chemical changes, and the state of organ distension or fullness. The information they relay helps regulate physiological functions, including digestion, respiration, and cardiovascular activity, and contributes to the perception of bodily sensations and visceral pain. Visceral afferents are an essential component of the autonomic nervous system and have their cell bodies located in the dorsal root ganglia or nodose ganglia.

Neurokinin-1 (NK-1) receptors are a type of G protein-coupled receptor that bind to the neuropeptide substance P, which is a member of the tachykinin family. These receptors are widely distributed in the central and peripheral nervous systems and play important roles in various physiological functions, including pain transmission, neuroinflammation, and emesis (vomiting).

NK-1 receptors are activated by substance P, which binds to the receptor's extracellular domain and triggers a signaling cascade that leads to the activation of various intracellular signaling pathways. This activation can ultimately result in the modulation of neuronal excitability, neurotransmitter release, and gene expression.

In addition to their role in normal physiological processes, NK-1 receptors have also been implicated in a number of pathological conditions, including pain, inflammation, and neurodegenerative disorders. As such, NK-1 receptor antagonists have been developed as potential therapeutic agents for the treatment of these conditions.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

N-Methyl-D-Aspartate (NMDA) receptors are a type of ionotropic glutamate receptor, which are found in the membranes of excitatory neurons in the central nervous system. They play a crucial role in synaptic plasticity, learning, and memory processes. NMDA receptors are ligand-gated channels that are permeable to calcium ions (Ca2+) and other cations.

NMDA receptors are composed of four subunits, which can be a combination of NR1, NR2A-D, and NR3A-B subunits. The binding of the neurotransmitter glutamate to the NR2 subunit and glycine to the NR1 subunit leads to the opening of the ion channel and the influx of Ca2+ ions.

NMDA receptors have a unique property in that they require both agonist binding and membrane depolarization for full activation, making them sensitive to changes in the electrical activity of the neuron. This property allows NMDA receptors to act as coincidence detectors, playing a critical role in synaptic plasticity and learning.

Abnormal functioning of NMDA receptors has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and chronic pain. Therefore, NMDA receptors are a common target for drug development in the treatment of these conditions.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

An "injection, intradermal" refers to a type of injection where a small quantity of a substance is introduced into the layer of skin between the epidermis and dermis, using a thin gauge needle. This technique is often used for diagnostic or research purposes, such as conducting allergy tests or administering immunizations in a way that stimulates a strong immune response. The injection site typically produces a small, raised bump (wheal) that disappears within a few hours. It's important to note that intradermal injections should be performed by trained medical professionals to minimize the risk of complications.

Substance P is an undecapeptide neurotransmitter and neuromodulator, belonging to the tachykinin family of peptides. It is widely distributed in the central and peripheral nervous systems and is primarily found in sensory neurons. Substance P plays a crucial role in pain transmission, inflammation, and various autonomic functions. It exerts its effects by binding to neurokinin 1 (NK-1) receptors, which are expressed on the surface of target cells. Apart from nociception and inflammation, Substance P is also involved in regulating emotional behaviors, smooth muscle contraction, and fluid balance.

**Ketamine** is a dissociative anesthetic medication primarily used for starting and maintaining anesthesia. It can lead to a state of altered perception, hallucinations, sedation, and memory loss. Ketamine is also used as a pain reliever in patients with chronic pain conditions and during certain medical procedures due to its strong analgesic properties.

It is available as a generic drug and is also sold under various brand names, such as Ketalar, Ketanest, and Ketamine HCl. It can be administered intravenously, intramuscularly, orally, or as a nasal spray.

In addition to its medical uses, ketamine has been increasingly used off-label for the treatment of mood disorders like depression, anxiety, and post-traumatic stress disorder (PTSD), owing to its rapid antidepressant effects. However, more research is needed to fully understand its long-term benefits and risks in these applications.

It's important to note that ketamine can be abused recreationally due to its dissociative and hallucinogenic effects, which may lead to addiction and severe psychological distress. Therefore, it should only be used under the supervision of a medical professional.

Viscera is a medical term that refers to the internal organs of the body, specifically those contained within the chest and abdominal cavities. These include the heart, lungs, liver, pancreas, spleen, kidneys, and intestines. In some contexts, it may also refer to the reproductive organs. The term viscera is often used in anatomical or surgical descriptions, and is derived from the Latin word "viscus," meaning "an internal organ."

Narcotic antagonists are a class of medications that block the effects of opioids, a type of narcotic pain reliever, by binding to opioid receptors in the brain and blocking the activation of these receptors by opioids. This results in the prevention or reversal of opioid-induced effects such as respiratory depression, sedation, and euphoria. Narcotic antagonists are used for a variety of medical purposes, including the treatment of opioid overdose, the management of opioid dependence, and the prevention of opioid-induced side effects in certain clinical situations. Examples of narcotic antagonists include naloxone, naltrexone, and methylnaltrexone.

Dinoprostone is a prostaglandin E2 analog used in medical practice for the induction of labor and ripening of the cervix in pregnant women. It is available in various forms, including vaginal suppositories, gel, and tablets. Dinoprostone works by stimulating the contraction of uterine muscles and promoting cervical dilation, which helps in facilitating a successful delivery.

It's important to note that dinoprostone should only be administered under the supervision of a healthcare professional, as its use is associated with certain risks and side effects, including uterine hyperstimulation, fetal distress, and maternal infection. The dosage and duration of treatment are carefully monitored to minimize these risks and ensure the safety of both the mother and the baby.

Naloxone is a medication used to reverse the effects of opioids, both illicit and prescription. It works by blocking the action of opioids on the brain and restoring breathing in cases where opioids have caused depressed respirations. Common brand names for naloxone include Narcan and Evzio.

Naloxone is an opioid antagonist, meaning that it binds to opioid receptors in the body without activating them, effectively blocking the effects of opioids already present at these sites. It has no effect in people who have not taken opioids and does not reverse the effects of other sedatives or substances.

Naloxone can be administered via intranasal, intramuscular, intravenous, or subcutaneous routes. The onset of action varies depending on the route of administration but generally ranges from 1 to 5 minutes when given intravenously and up to 10-15 minutes with other methods.

The duration of naloxone's effects is usually shorter than that of most opioids, so multiple doses or a continuous infusion may be necessary in severe cases to maintain reversal of opioid toxicity. Naloxone has been used successfully in emergency situations to treat opioid overdoses and has saved many lives.

It is important to note that naloxone does not reverse the effects of other substances or address the underlying causes of addiction, so it should be used as part of a comprehensive treatment plan for individuals struggling with opioid use disorders.

Nerve Growth Factor (NGF) is a small secreted protein that is involved in the growth, maintenance, and survival of certain neurons (nerve cells). It was the first neurotrophin to be discovered and is essential for the development and function of the nervous system. NGF binds to specific receptors on the surface of nerve cells and helps to promote their differentiation, axonal growth, and synaptic plasticity. Additionally, NGF has been implicated in various physiological processes such as inflammation, immune response, and wound healing. Deficiencies or excesses of NGF have been linked to several neurological disorders, including Alzheimer's disease, Parkinson's disease, and pain conditions.

Formaldehyde is a colorless, pungent, and volatile chemical compound with the formula CH2O. It is a naturally occurring substance that is found in certain fruits like apples and vegetables, as well as in animals. However, the majority of formaldehyde used in industry is synthetically produced.

In the medical field, formaldehyde is commonly used as a preservative for biological specimens such as organs, tissues, and cells. It works by killing bacteria and inhibiting the decaying process. Formaldehyde is also used in the production of various industrial products, including adhesives, resins, textiles, and paper products.

However, formaldehyde can be harmful to human health if inhaled or ingested in large quantities. It can cause irritation to the eyes, nose, throat, and skin, and prolonged exposure has been linked to respiratory problems and cancer. Therefore, it is essential to handle formaldehyde with care and use appropriate safety measures when working with this chemical compound.

The Trigeminal Caudal Nucleus, also known as the nucleus of the spinal trigeminal tract or spinal trigeminal nucleus, is a component of the trigeminal nerve sensory nuclear complex located in the brainstem. It is responsible for receiving and processing pain and temperature information from the face and head, particularly from the areas innervated by the ophthalmic (V1) and maxillary (V2) divisions of the trigeminal nerve. The neurons within this nucleus then project to other brainstem regions and ultimately to the thalamus, which relays this information to the cerebral cortex for conscious perception.

Neurokinin-1 (NK-1) receptor antagonists are a class of drugs that block the action of substance P, a neuropeptide involved in pain transmission and inflammation. These drugs work by binding to NK-1 receptors found on nerve cells, preventing substance P from activating them and transmitting pain signals. NK-1 receptor antagonists have been studied for their potential use in treating various conditions associated with pain and inflammation, such as migraine headaches, depression, and irritable bowel syndrome. Some examples of NK-1 receptor antagonists include aprepitant, fosaprepitant, and rolapitant.

The medulla oblongata is a part of the brainstem that is located in the posterior portion of the brainstem and continues with the spinal cord. It plays a vital role in controlling several critical bodily functions, such as breathing, heart rate, and blood pressure. The medulla oblongata also contains nerve pathways that transmit sensory information from the body to the brain and motor commands from the brain to the muscles. Additionally, it is responsible for reflexes such as vomiting, swallowing, coughing, and sneezing.

Peripheral nerve injuries refer to damage or trauma to the peripheral nerves, which are the nerves outside the brain and spinal cord. These nerves transmit information between the central nervous system (CNS) and the rest of the body, including sensory, motor, and autonomic functions. Peripheral nerve injuries can result in various symptoms, depending on the type and severity of the injury, such as numbness, tingling, weakness, or paralysis in the affected area.

Peripheral nerve injuries are classified into three main categories based on the degree of damage:

1. Neuropraxia: This is the mildest form of nerve injury, where the nerve remains intact but its function is disrupted due to a local conduction block. The nerve fiber is damaged, but the supporting structures remain intact. Recovery usually occurs within 6-12 weeks without any residual deficits.
2. Axonotmesis: In this type of injury, there is damage to both the axons and the supporting structures (endoneurium, perineurium). The nerve fibers are disrupted, but the connective tissue sheaths remain intact. Recovery can take several months or even up to a year, and it may be incomplete, with some residual deficits possible.
3. Neurotmesis: This is the most severe form of nerve injury, where there is complete disruption of the nerve fibers and supporting structures (endoneurium, perineurium, epineurium). Recovery is unlikely without surgical intervention, which may involve nerve grafting or repair.

Peripheral nerve injuries can be caused by various factors, including trauma, compression, stretching, lacerations, or chemical exposure. Treatment options depend on the type and severity of the injury and may include conservative management, such as physical therapy and pain management, or surgical intervention for more severe cases.

Mononeuropathy is a medical condition that refers to damage or dysfunction affecting a single peripheral nerve, outside of the brain and spinal cord. This can result in weakness, numbness, or pain in the area served by that specific nerve. Mononeuropathies can occur due to various reasons such as trauma, compression, infection, or systemic diseases like diabetes. The symptoms and severity may vary depending on the type and location of the affected nerve.

Amines are organic compounds that contain a basic nitrogen atom with a lone pair of electrons. They are derived from ammonia (NH3) by replacing one or more hydrogen atoms with alkyl or aryl groups. The nomenclature of amines follows the substitutive type, where the parent compound is named as an aliphatic or aromatic hydrocarbon, and the functional group "amine" is designated as a suffix or prefix.

Amines are classified into three types based on the number of carbon atoms attached to the nitrogen atom:

1. Primary (1°) amines: One alkyl or aryl group is attached to the nitrogen atom.
2. Secondary (2°) amines: Two alkyl or aryl groups are attached to the nitrogen atom.
3. Tertiary (3°) amines: Three alkyl or aryl groups are attached to the nitrogen atom.

Quaternary ammonium salts have four organic groups attached to the nitrogen atom and a positive charge, with anions balancing the charge.

Amines have a wide range of applications in the chemical industry, including pharmaceuticals, dyes, polymers, and solvents. They also play a significant role in biological systems as neurotransmitters, hormones, and cell membrane components.

Opioid peptides are naturally occurring short chains of amino acids in the body that bind to opioid receptors in the brain, spinal cord, and gut, acting in a similar way to opiate drugs like morphine or heroin. They play crucial roles in pain regulation, reward systems, and addictive behaviors. Some examples of opioid peptides include endorphins, enkephalins, and dynorphins. These substances are released in response to stress, physical exertion, or injury and help modulate the perception of pain and produce feelings of pleasure or euphoria.

Opioid mu receptors, also known as mu-opioid receptors (MORs), are a type of G protein-coupled receptor that binds to opioids, a class of chemicals that include both natural and synthetic painkillers. These receptors are found in the brain, spinal cord, and gastrointestinal tract, and play a key role in mediating the effects of opioid drugs such as morphine, heroin, and oxycodone.

MORs are involved in pain modulation, reward processing, respiratory depression, and physical dependence. Activation of MORs can lead to feelings of euphoria, decreased perception of pain, and slowed breathing. Prolonged activation of these receptors can also result in tolerance, where higher doses of the drug are required to achieve the same effect, and dependence, where withdrawal symptoms occur when the drug is discontinued.

MORs have three main subtypes: MOR-1, MOR-2, and MOR-3, with MOR-1 being the most widely studied and clinically relevant. Selective agonists for MOR-1, such as fentanyl and sufentanil, are commonly used in anesthesia and pain management. However, the abuse potential and risk of overdose associated with these drugs make them a significant public health concern.

Piperidines are not a medical term per se, but they are a class of organic compounds that have important applications in the pharmaceutical industry. Medically relevant piperidines include various drugs such as some antihistamines, antidepressants, and muscle relaxants.

A piperidine is a heterocyclic amine with a six-membered ring containing five carbon atoms and one nitrogen atom. The structure can be described as a cyclic secondary amine. Piperidines are found in some natural alkaloids, such as those derived from the pepper plant (Piper nigrum), which gives piperidines their name.

In a medical context, it is more common to encounter specific drugs that belong to the class of piperidines rather than the term itself.

Nerve compression syndromes refer to a group of conditions characterized by the pressure or irritation of a peripheral nerve, causing various symptoms such as pain, numbness, tingling, and weakness in the affected area. This compression can occur due to several reasons, including injury, repetitive motion, bone spurs, tumors, or swelling. Common examples of nerve compression syndromes include carpal tunnel syndrome, cubital tunnel syndrome, radial nerve compression, and ulnar nerve entrapment at the wrist or elbow. Treatment options may include physical therapy, splinting, medications, injections, or surgery, depending on the severity and underlying cause of the condition.

Postoperative pain is defined as the pain or discomfort experienced by patients following a surgical procedure. It can vary in intensity and duration depending on the type of surgery performed, individual pain tolerance, and other factors. The pain may be caused by tissue trauma, inflammation, or nerve damage resulting from the surgical intervention. Proper assessment and management of postoperative pain is essential to promote recovery, prevent complications, and improve patient satisfaction.

Facial pain is a condition characterized by discomfort or pain felt in any part of the face. It can result from various causes, including nerve damage or irritation, injuries, infections, dental problems, migraines, or sinus congestion. The pain can range from mild to severe and may be sharp, dull, constant, or intermittent. In some cases, facial pain can also be associated with other symptoms such as headaches, redness, swelling, or changes in sensation. Accurate diagnosis and treatment of the underlying cause are essential for effective management of facial pain.

Lidocaine is a type of local anesthetic that numbs painful areas and is used to prevent pain during certain medical procedures. It works by blocking the nerves that transmit pain signals to the brain. In addition to its use as an anesthetic, lidocaine can also be used to treat irregular heart rates and relieve itching caused by allergic reactions or skin conditions such as eczema.

Lidocaine is available in various forms, including creams, gels, ointments, sprays, solutions, and injectable preparations. It can be applied directly to the skin or mucous membranes, or it can be administered by injection into a muscle or vein. The specific dosage and method of administration will depend on the reason for its use and the individual patient's medical history and current health status.

Like all medications, lidocaine can have side effects, including allergic reactions, numbness that lasts too long, and in rare cases, heart problems or seizures. It is important to follow the instructions of a healthcare provider carefully when using lidocaine to minimize the risk of adverse effects.

Calcitonin gene-related peptide (CGRP) is a neurotransmitter and vasodilator peptide that is widely distributed in the nervous system. It is encoded by the calcitonin gene, which also encodes calcitonin and catestatin. CGRP is produced and released by sensory nerves and plays important roles in pain transmission, modulation of inflammation, and regulation of blood flow.

CGRP exists as two forms, α-CGRP and β-CGRP, which differ slightly in their amino acid sequences but have similar biological activities. α-CGRP is found primarily in the central and peripheral nervous systems, while β-CGRP is expressed mainly in the gastrointestinal tract.

CGRP exerts its effects by binding to specific G protein-coupled receptors, which are widely distributed in various tissues, including blood vessels, smooth muscles, and sensory neurons. Activation of CGRP receptors leads to increased intracellular cyclic AMP levels, activation of protein kinase A, and subsequent relaxation of vascular smooth muscle, resulting in vasodilation.

CGRP has been implicated in several clinical conditions, including migraine, cluster headache, and inflammatory pain. Inhibition of CGRP signaling has emerged as a promising therapeutic strategy for the treatment of these disorders.

Alcoholic neuropathy is a type of nerve damage that occurs due to excessive alcohol consumption. It's caused by the toxic effects of alcohol and its byproducts on nerves throughout the body, particularly in the peripheral nervous system. The condition typically develops over time, with symptoms becoming more severe as alcohol abuse continues.

The symptoms of alcoholic neuropathy can vary widely depending on which nerves are affected. However, common symptoms include:

1. Numbness or tingling in the arms and legs
2. Muscle weakness and cramps
3. Loss of reflexes
4. Difficulty with balance and coordination
5. Pain or burning sensations in the extremities
6. Heat intolerance
7. Bladder and bowel dysfunction
8. Sexual dysfunction

Treatment for alcoholic neuropathy typically involves addressing the underlying alcohol abuse, as well as managing symptoms with medications and physical therapy. In severe cases, hospitalization may be necessary to monitor and manage complications. It's important to note that abstaining from alcohol is the only way to prevent further nerve damage and improve symptoms over time.

Diabetic neuropathies refer to a group of nerve disorders that are caused by diabetes. High blood sugar levels can injure nerves throughout the body, but diabetic neuropathies most commonly affect the nerves in the legs and feet.

There are four main types of diabetic neuropathies:

1. Peripheral neuropathy: This is the most common type of diabetic neuropathy. It affects the nerves in the legs and feet, causing symptoms such as numbness, tingling, burning, or shooting pain.
2. Autonomic neuropathy: This type of neuropathy affects the autonomic nerves, which control involuntary functions such as heart rate, blood pressure, digestion, and bladder function. Symptoms may include dizziness, fainting, digestive problems, sexual dysfunction, and difficulty regulating body temperature.
3. Proximal neuropathy: Also known as diabetic amyotrophy, this type of neuropathy affects the nerves in the hips, thighs, or buttocks, causing weakness, pain, and difficulty walking.
4. Focal neuropathy: This type of neuropathy affects a single nerve or group of nerves, causing symptoms such as weakness, numbness, or pain in the affected area. Focal neuropathies can occur anywhere in the body, but they are most common in the head, torso, and legs.

The risk of developing diabetic neuropathies increases with the duration of diabetes and poor blood sugar control. Other factors that may contribute to the development of diabetic neuropathies include genetics, age, smoking, and alcohol consumption.

Dizocilpine maleate is a chemical compound that is commonly known as an N-methyl-D-aspartate (NMDA) receptor antagonist. It is primarily used in research settings to study the role of NMDA receptors in various physiological processes, including learning and memory.

The chemical formula for dizocilpine maleate is C16H24Cl2N2O4·C4H4O4. The compound is a white crystalline powder that is soluble in water and alcohol. It has potent psychoactive effects and has been investigated as a potential treatment for various neurological and psychiatric disorders, although it has not been approved for clinical use.

Dizocilpine maleate works by blocking the action of glutamate, a neurotransmitter that plays a key role in learning and memory, at NMDA receptors in the brain. By doing so, it can alter various cognitive processes and has been shown to have anticonvulsant, analgesic, and neuroprotective effects in animal studies. However, its use is associated with significant side effects, including hallucinations, delusions, and memory impairment, which have limited its development as a therapeutic agent.

Proteinase-activated receptor 2 (PAR-2) is a type of G protein-coupled receptor that is widely expressed in various tissues, including the respiratory and gastrointestinal tracts, skin, and nervous system. PAR-2 can be activated by serine proteases such as trypsin, mast cell tryptase, and thrombin, which cleave the N-terminal extracellular domain of the receptor to expose a tethered ligand that binds to and activates the receptor.

Once activated, PAR-2 signaling can lead to a variety of cellular responses, including inflammation, pain, and altered ion channel activity. PAR-2 has been implicated in several physiological and pathophysiological processes, such as airway hyperresponsiveness, asthma, cough, gastrointestinal motility disorders, and skin disorders.

In summary, PAR-2 is a type of receptor that can be activated by serine proteases, leading to various cellular responses and involvement in several disease processes.

Electroacupuncture is a form of acupuncture where a small electric current is passed between pairs of acupuncture needles. This technique is used to stimulate the acupoints more strongly and consistently than with manual acupuncture. The intensity of the electrical impulses can be adjusted depending on the patient's comfort level and the desired therapeutic effect. Electroacupuncture is often used to treat conditions such as chronic pain, muscle spasms, and paralysis. It may also be used in the treatment of addiction, weight loss, and stroke rehabilitation.

Myalgia is a medical term that refers to muscle pain or inflammation in the soft tissues of the body. The pain can be acute, occurring suddenly and lasting for a few days, or chronic, persisting over a longer period of time. Myalgia can affect any muscle in the body, but it is most commonly experienced in the neck, back, and extremities.

The causes of myalgia are varied and can include injury, overuse, infection, inflammation, or neurological conditions. Common causes of myalgia include fibromyalgia, polymyositis, dermatomyositis, and infections such as influenza or Lyme disease.

Treatment for myalgia depends on the underlying cause of the muscle pain. Rest, physical therapy, stretching exercises, and over-the-counter pain relievers may be sufficient for mild cases of myalgia. In more severe cases, prescription medications, injections, or other therapies may be necessary to manage the pain and address any underlying medical conditions.

Excitatory amino acid antagonists are a class of drugs that block the action of excitatory neurotransmitters, particularly glutamate and aspartate, in the brain. These drugs work by binding to and blocking the receptors for these neurotransmitters, thereby reducing their ability to stimulate neurons and produce an excitatory response.

Excitatory amino acid antagonists have been studied for their potential therapeutic benefits in a variety of neurological conditions, including stroke, epilepsy, traumatic brain injury, and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, their use is limited by the fact that blocking excitatory neurotransmission can also have negative effects on cognitive function and memory.

There are several types of excitatory amino acid receptors, including N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors. Different excitatory amino acid antagonists may target one or more of these receptor subtypes, depending on their specific mechanism of action.

Examples of excitatory amino acid antagonists include ketamine, memantine, and dextromethorphan. These drugs have been used in clinical practice for various indications, such as anesthesia, sedation, and treatment of neurological disorders. However, their use must be carefully monitored due to potential side effects and risks associated with blocking excitatory neurotransmission.

Dynorphins are a type of opioid peptide that is naturally produced in the body. They bind to specific receptors in the brain, known as kappa-opioid receptors, and play a role in modulating pain perception, emotional response, and reward processing. Dynorphins are derived from a larger precursor protein called prodynorphin and are found throughout the nervous system, including in the spinal cord, brainstem, and limbic system. They have been implicated in various physiological processes, as well as in the development of certain neurological and psychiatric disorders, such as chronic pain, depression, and substance use disorders.

Protein Kinase C-epsilon (PKCε) is a serine-threonine protein kinase that belongs to the family of Protein Kinase C (PKC) enzymes. These enzymes play crucial roles in various cellular processes, including signal transduction, cell survival, differentiation, and apoptosis.

PKCε is specifically involved in regulating several signaling pathways related to inflammation, proliferation, and carcinogenesis. It can be activated by different stimuli such as diacylglycerol (DAG) and phorbol esters, which lead to its translocation from the cytosol to the plasma membrane, where it phosphorylates and modulates the activity of various target proteins.

Abnormal regulation or expression of PKCε has been implicated in several diseases, including cancer, cardiovascular diseases, and neurodegenerative disorders. Therefore, PKCε is considered a potential therapeutic target for these conditions, and inhibitors of this enzyme are being developed and tested in preclinical and clinical studies.

Opioid receptors are a type of G protein-coupled receptor (GPCR) found in the cell membranes of certain neurons in the central and peripheral nervous system. They bind to opioids, which are chemicals that can block pain signals and produce a sense of well-being. There are four main types of opioid receptors: mu, delta, kappa, and nociceptin. These receptors play a role in the regulation of pain, reward, addiction, and other physiological functions. Activation of opioid receptors can lead to both therapeutic effects (such as pain relief) and adverse effects (such as respiratory depression and constipation).

Transient receptor potential (TRP) channels are a type of ion channel proteins that are widely expressed in various tissues and cells, including the sensory neurons, epithelial cells, and immune cells. They are named after the transient receptor potential mutant flies, which have defects in light-induced electrical responses due to mutations in TRP channels.

TRP channels are polymodal signal integrators that can be activated by a diverse range of physical and chemical stimuli, such as temperature, pressure, touch, osmolarity, pH, and various endogenous and exogenous ligands. Once activated, TRP channels allow the flow of cations, including calcium (Ca2+), sodium (Na+), and magnesium (Mg2+) ions, across the cell membrane.

TRP channels play critical roles in various physiological processes, such as sensory perception, neurotransmission, muscle contraction, cell proliferation, differentiation, migration, and apoptosis. Dysfunction of TRP channels has been implicated in a variety of pathological conditions, including pain, inflammation, neurodegenerative diseases, cardiovascular diseases, metabolic disorders, and cancer.

There are six subfamilies of TRP channels, based on their sequence homology and functional properties: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPP (polycystin), and TRPML (mucolipin). Each subfamily contains several members with distinct activation mechanisms, ion selectivity, and tissue distribution.

In summary, Transient Receptor Potential Channels are a group of polymodal cation channels that play critical roles in various physiological processes and are implicated in many pathological conditions.

Acid-sensing ion channels (ASICs) are a type of ion channel protein found in nerve cells (neurons) that are activated by acidic environments. They are composed of homomeric or heteromeric combinations of six different subunits, designated ASIC1a, ASIC1b, ASIC2a, ASIC2b, ASIC3, and ASIC4. These channels play important roles in various physiological processes, including pH homeostasis, nociception (pain perception), and mechanosensation (the ability to sense mechanical stimuli).

ASICs are permeable to both sodium (Na+) and calcium (Ca2+) ions. When the extracellular pH decreases, the channels open, allowing Na+ and Ca2+ ions to flow into the neuron. This influx of cations can depolarize the neuronal membrane, leading to the generation of action potentials and neurotransmitter release.

In the context of pain perception, ASICs are activated by the acidic environment in damaged tissues or ischemic conditions, contributing to the sensation of pain. In addition, some ASIC subunits have been implicated in synaptic plasticity, learning, and memory processes. Dysregulation of ASIC function has been associated with various pathological conditions, including neuropathic pain, ischemia, epilepsy, and neurodegenerative diseases.

Chronic pain is defined as pain that persists or recurs for a period of 3 months or longer, beyond the normal healing time for an injury or illness. It can be continuous or intermittent and range from mild to severe. Chronic pain can have various causes, such as nerve damage, musculoskeletal conditions, or chronic diseases like cancer. It can significantly impact a person's quality of life, causing limitations in mobility, sleep disturbances, mood changes, and decreased overall well-being. Effective management of chronic pain often involves a multidisciplinary approach, including medications, physical therapy, psychological interventions, and complementary therapies.

Bradykinin is a naturally occurring peptide in the human body, consisting of nine amino acids. It is a potent vasodilator and increases the permeability of blood vessels, causing a local inflammatory response. Bradykinin is formed from the breakdown of certain proteins, such as kininogen, by enzymes called kininases or proteases, including kallikrein. It plays a role in several physiological processes, including pain transmission, blood pressure regulation, and the immune response. In some pathological conditions, such as hereditary angioedema, bradykinin levels can increase excessively, leading to symptoms like swelling, redness, and pain.

Reaction time, in the context of medicine and physiology, refers to the time period between the presentation of a stimulus and the subsequent initiation of a response. This complex process involves the central nervous system, particularly the brain, which perceives the stimulus, processes it, and then sends signals to the appropriate muscles or glands to react.

There are different types of reaction times, including simple reaction time (responding to a single, expected stimulus) and choice reaction time (choosing an appropriate response from multiple possibilities). These measures can be used in clinical settings to assess various aspects of neurological function, such as cognitive processing speed, motor control, and alertness.

However, it is important to note that reaction times can be influenced by several factors, including age, fatigue, attention, and the use of certain medications or substances.

Nociceptive pain is a type of pain that results from the activation of nociceptors, which are specialized sensory receptors located in various tissues throughout the body. These receptors detect potentially harmful stimuli such as extreme temperatures, pressure, or chemical irritants and transmit signals to the brain, which interprets them as painful sensations.

Nociceptive pain can be further classified into two categories:

1. Somatic nociceptive pain: This type of pain arises from the activation of nociceptors in the skin, muscles, bones, and joints. It is often described as sharp, aching, or throbbing and may be localized to a specific area of the body.
2. Visceral nociceptive pain: This type of pain arises from the activation of nociceptors in the internal organs, such as the lungs, heart, and digestive system. It is often described as deep, cramping, or aching and may be more diffuse and difficult to localize.

Examples of conditions that can cause nociceptive pain include injuries, arthritis, cancer, and infections. Effective management of nociceptive pain typically involves a multimodal approach that includes pharmacologic interventions, such as non-opioid analgesics, opioids, and adjuvant medications, as well as non-pharmacologic therapies, such as physical therapy, acupuncture, and cognitive-behavioral therapy.

Rhizotomy is a surgical procedure where the root(s) of a nerve are cut. It is often used to treat chronic pain, spasticity, or other neurological symptoms that have not responded to other treatments. In some cases, only a portion of the nerve root may be severed (selective rhizotomy), while in others the entire root may be cut (root transaction). The specific nerves targeted during a rhizotomy depend on the individual patient's condition and symptoms.

This procedure is typically performed by a neurosurgeon, and it can be done through an open surgical approach or using minimally invasive techniques such as endoscopic or percutaneous approaches. After the surgery, patients may require physical therapy to help regain strength and mobility in the affected area. Potential risks of rhizotomy include numbness, weakness, and loss of reflexes in the areas served by the severed nerves.

Analysis of Variance (ANOVA) is a statistical technique used to compare the means of two or more groups and determine whether there are any significant differences between them. It is a way to analyze the variance in a dataset to determine whether the variability between groups is greater than the variability within groups, which can indicate that the groups are significantly different from one another.

ANOVA is based on the concept of partitioning the total variance in a dataset into two components: variance due to differences between group means (also known as "between-group variance") and variance due to differences within each group (also known as "within-group variance"). By comparing these two sources of variance, ANOVA can help researchers determine whether any observed differences between groups are statistically significant, or whether they could have occurred by chance.

ANOVA is a widely used technique in many areas of research, including biology, psychology, engineering, and business. It is often used to compare the means of two or more experimental groups, such as a treatment group and a control group, to determine whether the treatment had a significant effect. ANOVA can also be used to compare the means of different populations or subgroups within a population, to identify any differences that may exist between them.

Local anesthetics are a type of medication that is used to block the sensation of pain in a specific area of the body. They work by temporarily numbing the nerves in that area, preventing them from transmitting pain signals to the brain. Local anesthetics can be administered through various routes, including topical application (such as creams or gels), injection (such as into the skin or tissues), or regional nerve blocks (such as epidural or spinal anesthesia).

Some common examples of local anesthetics include lidocaine, prilocaine, bupivacaine, and ropivacaine. These medications can be used for a variety of medical procedures, ranging from minor surgeries (such as dental work or skin biopsies) to more major surgeries (such as joint replacements or hernia repairs).

Local anesthetics are generally considered safe when used appropriately, but they can have side effects and potential complications. These may include allergic reactions, toxicity (if too much is administered), and nerve damage (if the medication is injected into a nerve). It's important to follow your healthcare provider's instructions carefully when using local anesthetics, and to report any unusual symptoms or side effects promptly.

Non-steroidal anti-inflammatory agents (NSAIDs) are a class of medications that reduce pain, inflammation, and fever. They work by inhibiting the activity of cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins, chemicals that contribute to inflammation and cause blood vessels to dilate and become more permeable, leading to symptoms such as pain, redness, warmth, and swelling.

NSAIDs are commonly used to treat a variety of conditions, including arthritis, muscle strains and sprains, menstrual cramps, headaches, and fever. Some examples of NSAIDs include aspirin, ibuprofen, naproxen, and celecoxib.

While NSAIDs are generally safe and effective when used as directed, they can have side effects, particularly when taken in large doses or for long periods of time. Common side effects include stomach ulcers, gastrointestinal bleeding, and increased risk of heart attack and stroke. It is important to follow the recommended dosage and consult with a healthcare provider if you have any concerns about using NSAIDs.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Trigeminal nerve injuries refer to damages or traumas affecting the trigeminal nerve, also known as the fifth cranial nerve. This nerve is responsible for sensations in the face and motor functions such as biting and chewing. Trigeminal nerve injuries can result in various symptoms depending on the severity and location of the injury, including:

1. Loss or reduction of sensation in the face, lips, gums, teeth, or tongue.
2. Pain, often described as burning, aching, or stabbing, in the affected areas.
3. Numbness or tingling sensations.
4. Difficulty with biting, chewing, or performing other motor functions.
5. Impaired taste sensation.
6. Headaches or migraines.
7. Eye dryness or excessive tearing.

Trigeminal nerve injuries can occur due to various reasons, such as trauma during facial surgeries, accidents, tumors, infections, or neurological conditions like multiple sclerosis. Treatment options depend on the cause and severity of the injury and may include medication, physical therapy, surgical intervention, or pain management strategies.

Minocycline is an antibiotic medication that belongs to the tetracycline class. Medically, it is defined as a semisynthetic derivative of tetracycline and has a broader spectrum of activity compared to other tetracyclines. It is bacteriostatic, meaning it inhibits bacterial growth rather than killing them outright.

Minocycline is commonly used to treat various infections caused by susceptible bacteria, including acne, respiratory infections, urinary tract infections, skin and soft tissue infections, and sexually transmitted diseases. Additionally, it has been found to have anti-inflammatory properties and is being investigated for its potential use in treating neurological disorders such as multiple sclerosis and Alzheimer's disease.

As with all antibiotics, minocycline should be taken under the guidance of a healthcare professional, and its usage should be based on the results of bacterial culture and sensitivity testing to ensure its effectiveness against the specific bacteria causing the infection.

Hyperesthesia is a medical term that refers to an increased sensitivity to sensory stimuli, including touch, pain, or temperature. It can affect various parts of the body and can be caused by different conditions, such as nerve damage, multiple sclerosis, or complex regional pain syndrome. Hyperesthesia can manifest as a heightened awareness of sensations, which can be painful or uncomfortable, and may interfere with daily activities. It is essential to consult a healthcare professional for an accurate diagnosis and appropriate treatment if experiencing symptoms of hyperesthesia.

Amitriptyline is a type of medication known as a tricyclic antidepressant (TCA). It is primarily used to treat depression, but it also has other therapeutic uses such as managing chronic pain, migraine prevention, and treating anxiety disorders. Amitriptyline works by increasing the levels of certain neurotransmitters (chemical messengers) in the brain, such as serotonin and norepinephrine, which help to regulate mood and alleviate pain.

The medication is available in various forms, including tablets and liquid solutions, and it is typically taken orally. The dosage of amitriptyline may vary depending on the individual's age, medical condition, and response to treatment. It is essential to follow the prescribing physician's instructions carefully when taking this medication.

Common side effects of amitriptyline include drowsiness, dry mouth, blurred vision, constipation, and weight gain. In some cases, it may cause more severe side effects such as orthostatic hypotension (low blood pressure upon standing), cardiac arrhythmias, and seizures. It is crucial to inform the healthcare provider of any pre-existing medical conditions or current medications before starting amitriptyline therapy, as these factors can influence its safety and efficacy.

Amitriptyline has a well-established history in clinical practice, but it may not be suitable for everyone due to its potential side effects and drug interactions. Therefore, it is essential to consult with a healthcare professional before using this medication.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

The lumbosacral region is the lower part of the back where the lumbar spine (five vertebrae in the lower back) connects with the sacrum (a triangular bone at the base of the spine). This region is subject to various conditions such as sprains, strains, herniated discs, and degenerative disorders that can cause pain and discomfort. It's also a common site for surgical intervention when non-surgical treatments fail to provide relief.

EphB1 is a type of receptor tyrosine kinase (RTK) that belongs to the Eph family of receptors. It is a single-pass transmembrane protein that contains an extracellular domain with a binding site for its ligand, ephrin-Bs, and an intracellular domain with tyrosine kinase activity.

EphB1 receptors are primarily expressed in the nervous system, where they play important roles in various developmental processes, including axon guidance, neuronal migration, and synaptic plasticity. They also have been implicated in tumorigenesis and cancer progression, as well as in the regulation of immune responses.

The binding of ephrin-Bs to EphB1 receptors triggers a variety of intracellular signaling pathways that can lead to both forward and reverse signaling. Forward signaling occurs when the activated EphB1 receptor phosphorylates downstream effector proteins, leading to changes in cell behavior such as repulsion or adhesion. Reverse signaling occurs when ephrin-Bs, which are also transmembrane proteins, activate their own intracellular signaling pathways upon binding to EphB1 receptors.

Overall, the EphB1 receptor is a crucial component of the Eph/ephrin signaling system that plays important roles in various biological processes and has potential implications for disease treatment and diagnosis.

Fentanyl is a potent synthetic opioid analgesic, which is similar to morphine but is 50 to 100 times more potent. It is a schedule II prescription drug, typically used to treat patients with severe pain or to manage pain after surgery. It works by binding to the body's opioid receptors, which are found in the brain, spinal cord, and other areas of the body.

Fentanyl can be administered in several forms, including transdermal patches, lozenges, injectable solutions, and tablets that dissolve in the mouth. Illegally manufactured and distributed fentanyl has also become a major public health concern, as it is often mixed with other drugs such as heroin, cocaine, and counterfeit pills, leading to an increase in overdose deaths.

Like all opioids, fentanyl carries a risk of dependence, addiction, and overdose, especially when used outside of medical supervision or in combination with other central nervous system depressants such as alcohol or benzodiazepines. It is important to use fentanyl only as directed by a healthcare provider and to be aware of the potential risks associated with its use.

Dissociative anesthetics are a class of drugs that produce a state of altered consciousness, characterized by a sense of detachment or dissociation from the environment and oneself. These drugs work by disrupting the normal communication between the brain's thalamus and cortex, which can lead to changes in perception, thinking, and emotion.

Some examples of dissociative anesthetics include ketamine, phencyclidine (PCP), and dextromethorphan (DXM). These drugs can produce a range of effects, including sedation, analgesia, amnesia, and hallucinations. At high doses, they can cause profound dissociative states, in which individuals may feel as though they are outside their own bodies or that the world around them is not real.

Dissociative anesthetics are used medically for a variety of purposes, including as general anesthetics during surgery, as sedatives for diagnostic procedures, and as treatments for chronic pain and depression. However, they also have a high potential for abuse and can produce significant negative health effects when taken recreationally.

In medical terms, the skin is the largest organ of the human body. It consists of two main layers: the epidermis (outer layer) and dermis (inner layer), as well as accessory structures like hair follicles, sweat glands, and oil glands. The skin plays a crucial role in protecting us from external factors such as bacteria, viruses, and environmental hazards, while also regulating body temperature and enabling the sense of touch.

Tibial neuropathy refers to damage or dysfunction of the tibial nerve, which is one of the major nerves in the leg. The tibial nerve provides motor and sensory innervation to the lower leg, ankle, and foot muscles, as well as the skin on the sole of the foot.

Tibial neuropathy can result from various causes, including trauma, compression, diabetes, or other systemic diseases that affect the nerves. The symptoms of tibial neuropathy may include pain, numbness, tingling, or weakness in the affected leg and foot. In severe cases, it can lead to muscle wasting and difficulty walking.

The diagnosis of tibial neuropathy typically involves a thorough physical examination, including a neurological assessment, as well as electrical testing of nerve function (nerve conduction studies and electromyography). Treatment depends on the underlying cause but may include medication, physical therapy, or surgery in some cases.

Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.

Tachyphylaxis is a medical term that refers to the rapid and temporary loss of response to a drug after its repeated administration, especially when administered in quick succession. This occurs due to the decreased sensitivity or responsiveness of the body's receptors to the drug, resulting in a reduced therapeutic effect over time.

In simpler terms, tachyphylaxis is when the body becomes quickly desensitized to a medication after taking it multiple times in a short period, causing the drug to become less effective or ineffective at achieving the desired outcome. This phenomenon can occur with various medications, including those used for treating pain, allergies, and psychiatric conditions.

It's important to note that tachyphylaxis should not be confused with tolerance, which is a similar but distinct concept where the body gradually becomes less responsive to a drug after prolonged use over time.

A cannabinoid receptor CB2 is a G-protein coupled receptor that is primarily found in the immune system and cells associated with the immune system. They are expressed on the cell surface and are activated by endocannabinoids, plant-derived cannabinoids (phytocannabinoids) like those found in marijuana, and synthetic cannabinoids.

CB2 receptors are involved in a variety of physiological processes including inflammation, pain perception, and immune function. They have been shown to play a role in modulating the release of cytokines, which are signaling molecules that mediate and regulate immunity and inflammation. CB2 receptors may also be found in the brain, although at much lower levels than CB1 receptors.

CB2 receptor agonists have been studied as potential treatments for a variety of conditions including pain management, neuroinflammation, and autoimmune disorders. However, more research is needed to fully understand their therapeutic potential and any associated risks.

Subcutaneous injection is a route of administration where a medication or vaccine is delivered into the subcutaneous tissue, which lies between the skin and the muscle. This layer contains small blood vessels, nerves, and connective tissues that help to absorb the medication slowly and steadily over a period of time. Subcutaneous injections are typically administered using a short needle, at an angle of 45-90 degrees, and the dose is injected slowly to minimize discomfort and ensure proper absorption. Common sites for subcutaneous injections include the abdomen, thigh, or upper arm. Examples of medications that may be given via subcutaneous injection include insulin, heparin, and some vaccines.

Indomethacin is a non-steroidal anti-inflammatory drug (NSAID) that is commonly used to reduce pain, inflammation, and fever. It works by inhibiting the activity of certain enzymes in the body, including cyclooxygenase (COX), which plays a role in producing prostaglandins, chemicals involved in the inflammatory response.

Indomethacin is available in various forms, such as capsules, suppositories, and injectable solutions, and is used to treat a wide range of conditions, including rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, gout, and bursitis. It may also be used to relieve pain and reduce fever in other conditions, such as dental procedures or after surgery.

Like all NSAIDs, indomethacin can have side effects, including stomach ulcers, bleeding, and kidney damage, especially when taken at high doses or for long periods of time. It may also increase the risk of heart attack and stroke. Therefore, it is important to use indomethacin only as directed by a healthcare provider and to report any unusual symptoms or side effects promptly.

NAV1.8 (SCN10A) voltage-gated sodium channel is a type of ion channel found in excitable cells such as neurons and some types of immune cells. These channels play a crucial role in the generation and transmission of electrical signals in the form of action potentials. The NAV1.8 subtype, specifically, is primarily expressed in peripheral nervous system tissues, including sensory neurons responsible for pain perception.

NAV1.8 voltage-gated sodium channels are composed of four homologous domains (I-IV), each containing six transmembrane segments (S1-S6). The S4 segment in each domain functions as a voltage sensor, moving in response to changes in the membrane potential. When the membrane potential becomes more positive (depolarized), the S4 segment moves outward, which opens the channel and allows sodium ions (Na+) to flow into the cell. This influx of Na+ ions further depolarizes the membrane, leading to the rapid upstroke of the action potential.

The NAV1.8 channels are known for their unique biophysical properties, including slow activation and inactivation kinetics, as well as relative resistance to tetrodotoxin (TTX), a neurotoxin that blocks most voltage-gated sodium channels. These characteristics make NAV1.8 channels particularly important for generating and maintaining the electrical excitability of nociceptive neurons, which are responsible for transmitting pain signals from the periphery to the central nervous system.

Mutations in the SCN10A gene, which encodes the NAV1.8 channel, have been associated with various pain-related disorders, such as inherited erythromelalgia and small fiber neuropathies, highlighting their significance in pain physiology and pathophysiology.

Neuritis is a general term that refers to inflammation of a nerve or nerves, often causing pain, loss of function, and/or sensory changes. It can affect any part of the nervous system, including the peripheral nerves (those outside the brain and spinal cord) or the cranial nerves (those that serve the head and neck). Neuritis may result from various causes, such as infections, autoimmune disorders, trauma, toxins, or metabolic conditions. The specific symptoms and treatment depend on the underlying cause and the affected nerve(s).

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Tolmetin is a non-steroidal anti-inflammatory drug (NSAID) that is used to relieve pain, inflammation, and fever. It works by inhibiting the production of prostaglandins, which are hormone-like substances that cause pain and inflammation in the body. Tolmetin is available in immediate-release and sustained-release forms, and it is typically prescribed to treat conditions such as osteoarthritis, rheumatoid arthritis, and juvenile rheumatoid arthritis.

The medical definition of Tolmetin can be found in various pharmaceutical and medical references, including the Merck Manual, the American Hospital Formulary Service (AHFS) Drug Information, and the National Library of Medicine's MedlinePlus. According to these sources, the chemical name for Tolmetin is (3R,5S)-3-(4-methylbenzoyl)-5-(3-methoxy-4-hydroxyphenyl)-1H-indole-2-one, and its molecular formula is C19H16NO3.

Tolmetin has a number of potential side effects, including stomach pain, nausea, vomiting, diarrhea, gas, dizziness, and headache. It can also increase the risk of serious gastrointestinal side effects, such as bleeding, ulcers, and perforations in the stomach or intestines, especially in people who are over the age of 65 or have a history of stomach ulcers or other gastrointestinal problems. Tolmetin can also increase the risk of heart attack, stroke, and other cardiovascular events, particularly in people who take it for a long time or at high doses.

Tolmetin is available only by prescription, and it should be taken exactly as directed by a healthcare provider. It is important to follow the instructions on the label carefully and to talk to a doctor or pharmacist if there are any questions about how to take Tolmetin or what the potential side effects may be.

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 ...
"Victorian Halls released Hyperalgesia @ Bottom Lounge". The Deli Magazine. May 19, 2015. Retrieved June 30, 2017. "Hyperalgesia ... Hyperalgesia is the second full-length studio album by American alternative rock band Victorian Halls. The album, that contains ...
... (OIH) or opioid-induced abnormal pain sensitivity, also called paradoxical hyperalgesia, is an ... Opioid-induced hyperalgesia has also been criticized as overdiagnosed among chronic pain patients, due to poor differential ... Ketamine, an NMDA antagonist, has been shown to prevent the extended use of opioid in post-operative hyperalgesia when it is ... Although tolerance and opioid-induced hyperalgesia both result in a similar need for dose escalation to receive the same level ...
Pöyhiä R, Vainio A (January 2006). "Topically administered ketamine reduces capsaicin-evoked mechanical hyperalgesia". The ... and hyperalgesia. Symptoms may change over time, and they can vary from person to person. The more dynamic symptoms (especially ... Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or temperature sensation and/or deep somatic ... mechanical hyperalgesia) and showed a "significantly increased activation" of not just the S1 cortex (contralateral), S2 ( ...
Mao J (19 April 2016). Opioid-Induced Hyperalgesia. CRC Press. pp. 127-. ISBN 978-1-4200-8900-4. Archived from the original on ... 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 ...
Hyperalgesia Opioid-induced hyperalgesia (OIH) has been evident in patients after chronic opioid exposure. Adverse effects of ... 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 ...
It is different from hyperalgesia, an exaggerated response from a normally painful stimulus. The term comes from Ancient Greek ... Coutaux A, Adam F, Willer JC, Le Bars D (2005). "Hyperalgesia and allodynia: peripheral mechanisms". Joint Bone Spine. 72 (5): ...
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 ...
"Effects of Pregabalin on Mechanical Hyperalgesia". ClinicalTrials.gov. United States National Library of Medicine. 4 April 2007 ...
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 with this problem probably have hyperalgesia. The Fear of Pain Questionnaire (currently the FPQ-III), a mental health ...
Opioid-induced hyperalgesia Kraychete, DC; Sakata, RK (July 2012). "Use and rotation of opioids in chronic non-oncologic pain ...
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. ...
Opioid-induced hyperalgesia is when exposure to opioids increases the sensation of pain (hyperalgesia) and can even make non- ... Opioid tolerance should not be confused with opioid-induced hyperalgesia. The symptoms of these two conditions can appear very ... Oxford University Press, 2004). Bannister K (June 2015). "Opioid-induced hyperalgesia: where are we now?". Current Opinion in ...
"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 ...
DuPen A, Shen D, Ersek M (September 2007). "Mechanisms of opioid-induced tolerance and hyperalgesia". Pain Management Nursing. ...
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 ...
Hyperalgesia is directly involved with spinal NMDA receptors. Administered NMDA antagonists in a clinical setting produce ...
"Opioid-Induced Hyperalgesia: How Opioids Can Increase Pain". Hospital for Special Surgery. Retrieved 5 September 2022. " ...
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): ...
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 when you have an increased sensitivity to pain. Learn about the causes, symptoms, and treatment options for ... This can cause hyperalgesia.‌. If you take opioids or opioid painkillers, you can develop opioid-induced hyperalgesia. Although ... Primary hyperalgesia, which is extreme pain around your injured body part. *Secondary hyperalgesia, which is when the pain ... There are different kinds of hyperalgesia:‌. Opioid-induced hyperalgesia. This refers to the increased pain sensitivity you ...
... completely blocked hyperalgesia. When injected intrathecally (i.t.), kainic acid itself failed to induce hyperalgesia and AMPA/ ... induces a persistent hyperalgesia in the mouse and rat by. Giovengo SL, Kitto KF, Kurtz HJ, Velazquez RA, Larson AA. Department ... Together these data suggest that a persistent hyperalgesia results from the transient activation of AMPA/KA receptors that are ... Intraperitoneal (i.p.) injection of kainic acid induced a persistent thermal hyperalgesia, when tested using the hot plate ( ...
... Nature. 2000 May 11;405(6783):183-7. doi: 10.1038/ ... their ability to develop carrageenan-induced thermal hyperalgesia was completely absent. We conclude that VR1 is required for ...
After ruling out a worsening of the underlying condition, healthcare professionals should include opioid-induced hyperalgesia ... Read this clinical commentary to learn more about recognizing and managing opioid-induced hyperalgesia. ... After ruling out a worsening of the underlying condition, healthcare professionals should include opioid-induced hyperalgesia ... Read this clinical commentary to learn more about recognizing and managing opioid-induced hyperalgesia. ...
Intra-CeA CRF infusion mimicked stress-induced hyperalgesia. Avoiders exhibited thermal hyperalgesia that was reversed by ... These data suggest that rats with high stress reactivity exhibit hyperalgesia that is mediated by CRF-CRFR1 signaling in CeA. ... We hypothesized that CRF-CRFR1 signaling in central amygdala (CeA) mediates stress-induced hyperalgesia in rats with high ... Finally, intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the anti-hyperalgesic ...
PKA/AKAP/VR-1 Module: A Common Link of Gs-Mediated Signaling to Thermal Hyperalgesia. Parvinder Kaur Rathee, Carsten Distler, ... We conclude that the PKA/AKAP/VR-1 module represents the molecular target of Gs-coupled receptors to cause thermal hyperalgesia ... A number of inflammatory mediators that cause inflammatory pain and hyperalgesia exert their effect via Gs-coupled membrane ... Thus, the PKA/AKAP/VR-1 module presents as the molecular correlate of Gs-mediated inflammatory hyperalgesia. ...
"HYPERALGESIA OF PERIPHERAL NEURITIS" J Clin Invest. 1945 Jul;24(4):503-12. doi: 10.1172/JCI101629. ...
Effect of Peritumoral Bupivacaine on Primary and Distal Hyperalgesia in Cancer-Induced Bone Pain. Publication Type : Journal ... However, bupivacaine failed to reverse distal hyperalgesia in 14 day-PTI rats. ATF3 and GFAP expression were much enhanced in ... HomePublicationsEffect of Peritumoral Bupivacaine on Primary and Distal Hyperalgesia in Cancer-Induced Bone Pain ... Sahadev Shankarappa, "Effect of Peritumoral Bupivacaine on Primary and Distal Hyperalgesia in Cancer-Induced Bone Pain.", J ...
Coexistence of chronic hyperalgesia and multilevel neuroinflammatory responses after experimental SCI: a systematic approach to ...
The results indicated dose-related effects of methanolic extract on paw edema, hyperalgesia and serum IL-6 level reduction in ... Inflammatory symptoms such as hyperalgesia and paw edema in CFA-injected rats paw were measured by radiant heat and ... Zaringhalam J, Manaheji H, Mghsoodi N, Farokhi B, Mirzaiee V . Spinal mu-opioid receptor expression and hyperalgesia with ... Achillea santolina reduces serum interlukin-6 level and hyperalgesia during complete Freund9 s adjuvant-induced inflammation in ...
Visceral hyperalgesia is a higher awareness of organs working normally inside the body. A person may notice normal intestinal ... The main symptom of visceral hyperalgesia is pain. The type of pain can differ from person to person. It may be dull and achy, ... It is not clear why visceral hyperalgesia happens. It often starts after an infection, illness, or injury. ... Visceral hyperalgesia. Cincinnati Childrens hospital website. Available at: https://www.cincinnatichildrens.org/health/v/ ...
Visceral hyperalgesia. Visceral hyperalgesia is the second part of the traditional three-part complex that characterizes ... visceral hyperalgesia, and psychopathology. [8] More recently, it is believed that components of the gut microbiota potentially ...
A condition known as opiate induced hyperalgesia may develop from long-term opioid use which heightens an individuals ... Treating Opiate-Induced Hyperalgesia. If you or a loved one is experiencing heightened levels of pain even though opioids are ... Hyperalgesia is a condition that pairs with tolerance of opiates, causing an increased sensitivity to pain. Patients who once ... Opiate-induced hyperalgesia is a condition that develops after long-term opiate use for chronic pain conditions or recreational ...
Opioid-induced hyperalgesia may develop as a result of long-term opioid use in the treatment of chronic pain.[2] Various ... Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This ... Hyperalgesia is similar to other sorts of pain associated with nerve irritation or damage such as allodynia and neuropathic ... Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have ...
Classic method for measuring paw hyperalgesia in rats and mice paws according to the paw pressure method of Randall Selitto. ... Neuropathic Pain, Hyperalgesia, Inflammation, Joint Pain (Arthritis)*Addiction and Reward, Social Behaviour and Autism*Motor ...
Hyperalgesia and Allodynia: Cases of hyperalgesia and allodynia have been ‎reported with opioid therapy of any duration [see ... Opioid-Induced Hyperalgesia and Allodynia Opioid-Induced Hyperalgesia (OIH) occurs when an opioid analgesic ‎paradoxically ... Opioid-Induced Hyperalgesia and Allodynia [see WARNINGS]‎. The most frequent adverse reaction in 1066 patients treated in ... Hyperalgesia and Allodynia Inform patients and caregivers not to increase opioid dosage without first ‎consulting a clinician. ...
However, areas 3 and 4 (PRP-treated areas) had smaller Von Frey g values than areas 1 and 2. There was no hyperalgesia in the ... Repeated PRP Injections Cause Hypersensitivity and Hyperalgesia in Rats. Oct 3rd, 2019 ... All four areas of the backs of the experimental rats developed hyperalgesia. ... caused hyperalgesia in rats when compared to saline injections. ...
WATKINS LR; WIERTELAK EP; GOEHLER LE; MOONEYHEIBERGER K; MARTINEZ J; FURNESS L; SMITH KP; MAIER SF ...
We show how it is used with a novel electrode for pain and secondary hyperalgesia ... or alternatively to evoke secondary hyperalgesia. This type of hyperalgesia can last for several hours and may be used to ... High-frequency electrical stimulation of the human skin induces heterotopical mechanical hyperalgesia, heat hyperalgesia, and ... In this article, we discuss the DS7A, its role in studies of pain and secondary hyperalgesia and present a novel stimulation ...
Opioid-induced hyperalgesia (OIH) is one of the major problems associated with prolonged use of opioids for the treatment of ... We found that curcumin administered intrathecally or orally significantly attenuated hyperalgesia in mice with morphine-induced ...
p , 0.05 compared with control (ANOVA); n = 4. g, Spinal injection of IL-1β, TNFα, and IL-6 (10 ng) induces heat hyperalgesia ... a-f, Induction of CREB phosphorylation and heat hyperalgesia by PICs. a-d, pCREB immunostaining in the superficial dorsal horn ... Injection of all three PICs (10 ng) into spinal cord CSF induced marked heat hyperalgesia, as shown by a decrease in PWLs (Fig ... However, the overall effect of sIL-6R is pronociceptive, because it induced pCREB at 30 min and heat hyperalgesia at 30-120 min ...
Hyperalgesia. *Hyperalgesia is an increased sensitivity to pain.. *It can be difficult to distinguish from tolerance, since the ... Hyperalgesia can occur relatively quickly or over time through chronic opioid use. ...
Neither expectancy nor fear ratings predicted placebo analgesia or nocebo hyperalgesia. It appears that a hidden conditioning ... and fear in placebo analgesia and nocebo hyperalgesia. A total of 42 healthy volunteers were randomly assigned to three groups ...
Hyperalgesia, Pain and Nitric Oxide. Pain, as a sensation, is notoriously difficult to define in scientific terms, mostly due ... LTP mediated hyperalgesia occurs with the contribution of projection neurons in lamina I expressing the neurokinin 1 (NK1) ... The ensuing hyperalgesia and allodynia warns the animal to the need to protect the affected region on the periphery. NO is ... Hyperalgesia: Heightened sensitivity to pain caused by injury to peripheral tissues or neural elements. It can be elicited by ...
These studies contribute to our understanding of how advanced age and sex alter morphine anti-hyperalgesia and enhance our ... Fullerton, Evan, "The Impact Of Advanced Age On Morphine Anti-Hyperalgesia And The Role Of Mu Opioid Receptor Signaling In The ... The Impact Of Advanced Age On Morphine Anti-Hyperalgesia And The Role Of Mu Opioid Receptor Signaling In The Periaqueductal ... These studies contribute to our understanding of how advanced age and sex alter morphine anti-hyperalgesia and enhance our ...
Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult. BMC ... Dive into the research topics of Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after ... Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult. / ... Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult. In ...
externally administered thermal hyperalgesia: A parametric fMRI study. / Mohr, C.; Leyendecker, S.; Helmchen, C. in: European ... externally administered thermal hyperalgesia: A parametric fMRI study. C. Mohr, S. Leyendecker, C. Helmchen*. * ... externally administered thermal hyperalgesia: A parametric fMRI study. European Journal of Neuroscience, 27(3), 739-749. https ... externally administered thermal hyperalgesia: A parametric fMRI study, European Journal of Neuroscience, Jg. 27, Nr. 3, S. 739 ...
Exploring Opioid-Induced Hyperalgesia: When the Cure Becomes the Cause. Announcement This article will help you understand more ...
Hyperalgesia. In contrast to opioid tolerance, opioid-induced hyperalgesia (OIH) occurs when a patient who has been taking ... Hyperalgesia. -. +. Observed more commonly with opioid-induced neurotoxicity. May be more common with morphine and ... Hyperalgesia connotes increased sensations of pain out of proportion to what is usually experienced. ... Richebe P, Cahana A, Rivat C: Tolerance and opioid-induced hyperalgesia. Is a divorce imminent? Pain 153 (8): 1547-8, 2012.[ ...

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