Hyperalgesia
Nociceptors
Pain Measurement
Carrageenan
Pain
Injections, Spinal
Rats, Sprague-Dawley
Freund's Adjuvant
Neuralgia
Spinal Cord
Ganglia, Spinal
TRPV Cation Channels
Analgesics, Opioid
Touch
Posterior Horn Cells
Morphine
Mustard Plant
Sciatic Neuropathy
Hyperesthesia
Disease Models, Animal
Inflammation
Nociception
Pain, Referred
Spinal Nerves
Sensory Receptor Cells
Drug Tolerance
Visceral Pain
Cyclohexanecarboxylic Acids
Sciatic Nerve
Foot
Edema
Nerve Fibers, Unmyelinated
Reflex, Abdominal
Peripheral Nervous System Diseases
Sensory System Agents
Hindlimb
Analgesics, Non-Narcotic
Receptors, Neurokinin-1
Dose-Response Relationship, Drug
Receptors, N-Methyl-D-Aspartate
Rats, Wistar
Injections, Intradermal
Substance P
Ketamine
Viscera
Dinoprostone
Naloxone
Nerve Growth Factor
Formaldehyde
Trigeminal Caudal Nucleus
Neurokinin-1 Receptor Antagonists
Medulla Oblongata
Mononeuropathies
Amines
Opioid Peptides
Receptors, Opioid, mu
Nerve Compression Syndromes
Facial Pain
Lidocaine
Calcitonin Gene-Related Peptide
Alcoholic Neuropathy
Diabetic Neuropathies
Dizocilpine Maleate
Receptor, PAR-2
Electroacupuncture
Excitatory Amino Acid Antagonists
Dynorphins
Protein Kinase C-epsilon
Receptors, Opioid
Transient Receptor Potential Channels
Acid Sensing Ion Channels
Chronic Pain
Bradykinin
Nociceptive Pain
Analysis of Variance
Anesthetics, Local
Anti-Inflammatory Agents, Non-Steroidal
Trigeminal Nerve Injuries
Minocycline
Amitriptyline
Mice, Inbred C57BL
Receptor, EphB1
Fentanyl
Anesthetics, Dissociative
Skin
Tibial Neuropathy
Neurons
Tachyphylaxis
Receptor, Cannabinoid, CB2
Injections, Subcutaneous
Indomethacin
NAV1.8 Voltage-Gated Sodium Channel
Neuritis
Mice, Knockout
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 condition characterized by an increased sensitivity to pain. It is a type of pain that is caused by an overactive nervous system, which results in a heightened perception of pain in response to a normal or low-intensity stimulus. Hyperalgesia can be caused by a variety of factors, including injury, inflammation, nerve damage, and certain medical conditions such as fibromyalgia, chronic pain syndrome, and multiple sclerosis. It can also be a side effect of certain medications, such as opioids. Symptoms of hyperalgesia may include increased pain sensitivity, a heightened response to touch or pressure, and a reduced ability to tolerate pain. Treatment for hyperalgesia may involve a combination of medications, physical therapy, and other interventions aimed at reducing pain and improving quality of life.
Carrageenan is a type of polysaccharide that is extracted from certain red seaweed species. It is commonly used as a thickener, stabilizer, and emulsifier in a variety of food products, including ice cream, yogurt, and processed meats. In the medical field, carrageenan has been studied for its potential therapeutic effects. Some research suggests that carrageenan may have anti-inflammatory properties and may be useful in the treatment of conditions such as inflammatory bowel disease, arthritis, and cancer. However, more research is needed to fully understand the potential benefits and risks of carrageenan in the medical field.
In the medical field, pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Pain is a complex phenomenon that involves both physical and emotional components, and it can be caused by a variety of factors, including injury, illness, inflammation, and nerve damage. Pain can be acute or chronic, and it can be localized to a specific area of the body or can affect the entire body. Acute pain is typically short-lived and is a normal response to injury or illness. Chronic pain, on the other hand, persists for more than three months and can be caused by a variety of factors, including nerve damage, inflammation, and psychological factors. In the medical field, pain is typically assessed using a pain scale, such as the Visual Analog Scale (VAS), which measures pain intensity on a scale of 0 to 10. Treatment for pain depends on the underlying cause and can include medications, physical therapy, and other interventions.
In the medical field, analgesics are drugs that are used to relieve pain without causing loss of consciousness. They are commonly used to treat a wide range of conditions, including headaches, toothaches, menstrual cramps, and injuries. There are several types of analgesics, including nonsteroidal anti-inflammatory drugs (NSAIDs), opioids, and local anesthetics. NSAIDs, such as aspirin and ibuprofen, work by reducing inflammation and blocking the production of prostaglandins, which are chemicals that cause pain and inflammation. Opioids, such as morphine and oxycodone, work by binding to receptors in the brain and spinal cord, which reduces the perception of pain. Local anesthetics, such as lidocaine, work by numbing a specific area of the body. It is important to note that while analgesics can be effective in relieving pain, they can also have side effects and may not be appropriate for everyone. It is always best to consult with a healthcare provider before taking any medication.
Capsaicin is a chemical compound found in chili peppers that is responsible for their spicy flavor and pungency. In the medical field, capsaicin is used as a topical analgesic, meaning it is applied to the skin to relieve pain. It works by activating sensory nerves called TRPV1 receptors, which are responsible for detecting heat and pain. When capsaicin binds to these receptors, it causes them to fire, which can help to reduce pain signals to the brain. Capsaicin is often used to treat conditions such as arthritis, nerve pain, and migraines. It is available in various forms, including creams, patches, and gels, and is generally considered safe when used as directed. However, some people may experience side effects such as skin irritation, redness, or burning when using capsaicin products.
Freund's Adjuvant is a substance used in medical research and vaccine development to enhance the body's immune response to a vaccine. It is a mixture of heat-killed Mycobacterium tuberculosis and aluminum hydroxide, which is injected into the body along with the vaccine. The adjuvant stimulates the immune system to produce a stronger and more long-lasting immune response to the vaccine, which can help to protect against infection or disease. Freund's Adjuvant is named after its discoverer, Paul Ehrlich's student, Paul Freund.
Neuralgia is a medical condition characterized by pain that is felt along the path of a nerve. It is caused by damage or irritation to the nerve, which can result in a variety of symptoms, including sharp, stabbing, or burning pain, numbness, tingling, and weakness. Neuralgia can affect any nerve in the body, but it is most commonly associated with the trigeminal nerve, which supplies sensation to the face. There are several different types of neuralgia, including trigeminal neuralgia, glossopharyngeal neuralgia, and postherpetic neuralgia. Treatment for neuralgia typically involves medications to manage pain and other symptoms, as well as lifestyle changes and physical therapy. In some cases, surgery may be necessary to treat the underlying cause of the neuralgia.
TRPV cation channels, also known as transient receptor potential vanilloid channels, are a group of ion channels found in the membranes of sensory neurons in the peripheral nervous system. These channels are activated by a variety of stimuli, including heat, capsaicin (the compound that gives chili peppers their heat), and changes in the pH of the extracellular environment. When TRPV channels are activated, they allow positively charged ions, such as sodium and calcium, to flow into the cell. This influx of ions can cause depolarization of the neuron, leading to the generation of an action potential and the transmission of a sensory signal to the central nervous system. TRPV channels play a role in a variety of physiological processes, including pain sensation, thermoregulation, and the detection of certain chemical stimuli. They are also involved in a number of pathological conditions, including inflammatory pain, neurodegenerative diseases, and certain types of cancer. As such, TRPV channels are an important target for the development of new therapeutic agents.
In the medical field, "Analgesics, Opioid" refers to a class of drugs that are used to relieve pain. Opioids are a subclass of analgesics that are derived from the opium poppy or synthesized in the laboratory. Opioids work by binding to specific receptors in the brain and spinal cord, which can reduce the perception of pain and produce feelings of euphoria. They are commonly used to treat moderate to severe pain, such as that caused by surgery, injury, or chronic conditions like cancer. However, opioids can also be addictive and can cause side effects such as drowsiness, nausea, constipation, and respiratory depression. As a result, they are typically prescribed only for short-term use and under close medical supervision.
Morphine is a powerful opioid medication that is used to relieve severe pain. It is derived from the opium poppy and is one of the most potent naturally occurring opioids. Morphine works by binding to specific receptors in the brain and spinal cord, which can reduce the perception of pain and produce feelings of euphoria. It is often prescribed for patients who are experiencing severe pain, such as those with cancer or after surgery. Morphine can be administered in a variety of ways, including orally, intravenously, or through injection. It can also be used in combination with other medications to enhance its pain-relieving effects. However, morphine can also be highly addictive and can lead to dependence and withdrawal symptoms if used for an extended period of time. It is important for patients to use morphine only as directed by their healthcare provider and to avoid taking more than the recommended dose.
Sciatic neuropathy is a condition that occurs when there is damage or compression of the sciatic nerve, which is the largest nerve in the human body. The sciatic nerve runs from the lower back down the back of each leg, and it is responsible for controlling movement and sensation in the lower extremities. There are several potential causes of sciatic neuropathy, including injury, infection, compression by a herniated disk or other spinal condition, and certain medical conditions such as diabetes or multiple sclerosis. Symptoms of sciatic neuropathy can include pain, numbness, tingling, weakness, and muscle spasms in the lower back, buttocks, and legs. Treatment for sciatic neuropathy depends on the underlying cause and the severity of the symptoms. In some cases, conservative treatments such as physical therapy, pain medication, and lifestyle changes may be effective. In more severe cases, surgery may be necessary to relieve pressure on the nerve or repair damage.
Hyperesthesia is a medical condition characterized by an increased sensitivity or over-responsiveness to stimuli. It can refer to an increased sensitivity to touch, pressure, temperature, pain, or other types of sensory input. Hyperesthesia can be a symptom of various medical conditions, including nerve damage, inflammation, or infection. It can also be caused by certain medications or substances, such as alcohol or certain drugs. In some cases, hyperesthesia may be a harmless condition that resolves on its own. However, in other cases, it may be a sign of a more serious underlying health issue that requires medical attention. Treatment for hyperesthesia depends on the underlying cause and may include medications, physical therapy, or other interventions.
In the medical field, "Disease Models, Animal" refers to the use of animals to study and understand human diseases. These models are created by introducing a disease or condition into an animal, either naturally or through experimental manipulation, in order to study its progression, symptoms, and potential treatments. Animal models are used in medical research because they allow scientists to study diseases in a controlled environment and to test potential treatments before they are tested in humans. They can also provide insights into the underlying mechanisms of a disease and help to identify new therapeutic targets. There are many different types of animal models used in medical research, including mice, rats, rabbits, dogs, and monkeys. Each type of animal has its own advantages and disadvantages, and the choice of model depends on the specific disease being studied and the research question being addressed.
Inflammation is a complex biological response of the body to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective mechanism that helps to eliminate the cause of injury, remove damaged tissue, and initiate the healing process. Inflammation involves the activation of immune cells, such as white blood cells, and the release of chemical mediators, such as cytokines and prostaglandins. This leads to the characteristic signs and symptoms of inflammation, including redness, heat, swelling, pain, and loss of function. Inflammation can be acute or chronic. Acute inflammation is a short-term response that lasts for a few days to a few weeks and is usually beneficial. Chronic inflammation, on the other hand, is a prolonged response that lasts for months or years and can be harmful if it persists. Chronic inflammation is associated with many diseases, including cancer, cardiovascular disease, and autoimmune disorders.
In the medical field, "Behavior, Animal" refers to the study of the actions, responses, and interactions of animals, including humans, with their environment. This field encompasses a wide range of topics, including animal behavior in the wild, animal behavior in captivity, animal behavior in domestic settings, and animal behavior in laboratory settings. Animal behaviorists study a variety of behaviors, including social behavior, mating behavior, feeding behavior, communication behavior, and aggression. They use a variety of research methods, including observational studies, experiments, and surveys, to understand the underlying mechanisms that drive animal behavior. Animal behavior research has important applications in fields such as conservation biology, animal welfare, and veterinary medicine. For example, understanding animal behavior can help conservationists develop effective strategies for protecting endangered species, and it can help veterinarians develop more effective treatments for behavioral disorders in animals.
In the medical field, "Pain, Referred" refers to a type of pain that is felt in a location other than the site of the actual injury or disease. This type of pain is caused by irritation or compression of nerves or other structures that transmit pain signals to the brain. For example, if a person has a kidney stone, they may experience pain in their lower back or abdomen, even though the stone is located in their kidney. This is because the nerves that transmit pain signals from the kidney also pass through the lower back and abdomen, causing pain to be felt in those areas. Referred pain can be caused by a variety of conditions, including muscle strains, joint injuries, digestive disorders, and certain types of cancer. It is important for healthcare providers to accurately diagnose the underlying cause of referred pain in order to provide appropriate treatment.
Visceral pain is a type of pain that originates from the internal organs, such as the stomach, intestines, liver, pancreas, bladder, and reproductive organs. Unlike somatic pain, which is felt in the muscles, bones, and skin, visceral pain is often described as a deep, dull ache or pressure that can be difficult to localize. Visceral pain can be acute or chronic, and it can be caused by a variety of conditions, including inflammation, infection, injury, or disease. Some common causes of visceral pain include gastritis, peptic ulcers, inflammatory bowel disease, kidney stones, and appendicitis. In the medical field, visceral pain is typically assessed and treated by a team of healthcare professionals, including primary care physicians, gastroenterologists, and surgeons. Treatment options may include medications to manage pain and inflammation, lifestyle changes, and in some cases, surgery.
Cyclohexanecarboxylic acids are a class of organic compounds that contain a six-membered ring of carbon atoms with a carboxylic acid group (-COOH) attached to one of the carbon atoms. They are commonly used in the pharmaceutical industry as intermediates in the synthesis of various drugs and as starting materials for the preparation of other organic compounds. In the medical field, cyclohexanecarboxylic acids and their derivatives have been studied for their potential therapeutic effects, including anti-inflammatory, analgesic, and anti-cancer activities. However, more research is needed to fully understand their potential medical applications.
Edema is a medical condition characterized by the accumulation of excess fluid in the body's tissues. It can occur in any part of the body, but is most commonly seen in the feet, ankles, legs, and hands. Edema can be caused by a variety of factors, including heart failure, kidney disease, liver disease, hormonal imbalances, pregnancy, and certain medications. It can also be a symptom of other medical conditions, such as cancer or lymphedema. Edema can be diagnosed through physical examination and medical imaging, and treatment depends on the underlying cause.
Peripheral nervous system diseases refer to disorders that affect the peripheral nerves, which are the nerves that carry signals from the brain and spinal cord to the rest of the body. These diseases can affect the nerves themselves or the tissues surrounding them, and can result in a range of symptoms, including pain, numbness, weakness, and tingling. Some examples of peripheral nervous system diseases include: 1. Charcot-Marie-Tooth disease: A group of inherited disorders that affect the nerves in the hands and feet, causing weakness, numbness, and loss of sensation. 2. Guillain-Barre syndrome: A rare autoimmune disorder in which the body's immune system attacks the peripheral nerves, causing weakness and paralysis. 3. Peripheral neuropathy: A general term for any disorder that affects the peripheral nerves, which can be caused by a variety of factors, including diabetes, alcoholism, and exposure to certain toxins. 4. Multiple sclerosis: An autoimmune disorder that affects the central nervous system, including the brain and spinal cord, but can also affect the peripheral nerves, causing symptoms such as numbness and weakness. 5. Amyotrophic lateral sclerosis (ALS): A progressive neurodegenerative disorder that affects the nerves controlling muscle movement, leading to weakness and paralysis. Treatment for peripheral nervous system diseases depends on the specific disorder and its underlying cause. In some cases, medications or physical therapy may be used to manage symptoms, while in other cases, surgery or other interventions may be necessary.
In the medical field, analgesia refers to the relief of pain without loss of consciousness. It is a common medical intervention used to manage pain caused by various conditions, such as surgery, injury, illness, or chronic conditions. There are different types of analgesia, including: 1. Local analgesia: This type of analgesia involves the use of numbing agents to block pain signals in a specific area of the body, such as during a dental procedure or surgery. 2. Systemic analgesia: This type of analgesia involves the use of medications that are absorbed into the bloodstream and affect the entire body to relieve pain. Examples include opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetaminophen. 3. Neuromodulation: This type of analgesia involves the use of electrical or magnetic stimulation to alter the way the nervous system processes pain signals. Analgesia is an important part of pain management and can help improve a patient's quality of life by reducing pain and discomfort. However, it is important to use analgesia appropriately and with caution, as it can also have side effects and risks, such as addiction, respiratory depression, and constipation.
In the medical field, "Analgesics, Non-Narcotic" refers to a class of drugs that are used to relieve pain without causing addiction or other harmful side effects associated with narcotic painkillers. These drugs work by blocking the transmission of pain signals from the body to the brain. Examples of non-narcotic analgesics include acetaminophen (Tylenol), aspirin, ibuprofen (Advil, Motrin), and naproxen (Aleve). These drugs are commonly used to treat mild to moderate pain, such as headaches, muscle aches, and menstrual cramps. They are generally considered safe and effective when used as directed, but can cause side effects such as stomach upset, nausea, and dizziness. It is important to note that non-narcotic analgesics may not be effective for severe pain or pain that is chronic in nature. In these cases, stronger painkillers, such as opioids, may be necessary. However, the use of opioids carries a higher risk of addiction and other harmful side effects, so they are typically reserved for cases where other pain management options have been exhausted.
Receptors, Neurokinin-1 (NK1 receptors) are a type of G protein-coupled receptor found on the surface of certain cells in the body, including nerve cells (neurons) and immune cells. These receptors are activated by a group of signaling molecules called neurokinins, which are released by nerve cells in response to various stimuli, such as injury, stress, or inflammation. NK1 receptors play a role in a number of physiological processes, including pain perception, inflammation, and regulation of the immune system. They are also involved in the development of certain diseases, such as chronic pain, asthma, and irritable bowel syndrome. In the medical field, NK1 receptors are targeted by drugs used to treat a variety of conditions, including pain, nausea, and inflammation. One example of a drug that targets NK1 receptors is aprepitant, which is used to prevent nausea and vomiting caused by chemotherapy. Other drugs that target NK1 receptors include telaprevir and maraviroc, which are used to treat hepatitis C and HIV, respectively.
Receptors, N-Methyl-D-Aspartate (NMDA) are a type of ionotropic glutamate receptor found in the central nervous system. They are named after the agonist N-methyl-D-aspartate (NMDA), which binds to and activates these receptors. NMDA receptors are important for a variety of physiological processes, including learning and memory, synaptic plasticity, and neuroprotection. They are also involved in various neurological and psychiatric disorders, such as schizophrenia, depression, and addiction. NMDA receptors are heteromeric complexes composed of two subunits, NR1 and NR2, which can be differentially expressed in various brain regions and cell types. The NR2 subunit determines the pharmacological properties and functional profile of the receptor, while the NR1 subunit is essential for receptor function. Activation of NMDA receptors requires the binding of both glutamate and a co-agonist, such as glycine or d-serine, as well as the depolarization of the postsynaptic membrane. This leads to the opening of a cation-permeable channel that allows the influx of calcium ions, which can trigger various intracellular signaling pathways and modulate gene expression. In summary, NMDA receptors are a type of glutamate receptor that play a crucial role in various physiological and pathological processes in the central nervous system.
Substance P is a neuropeptide that is involved in the transmission of pain signals in the nervous system. It is a small protein that is produced by sensory neurons in the peripheral nervous system and is released into the spinal cord and brain when these neurons are activated by noxious stimuli such as injury or inflammation. Substance P acts on specific receptors on nerve cells in the spinal cord and brain, triggering the release of other neurotransmitters and hormones that contribute to the perception of pain. It is also involved in other physiological processes, such as regulating blood pressure and heart rate. In the medical field, substance P is often studied in the context of pain management and the development of new pain medications. It is also used as a diagnostic tool in certain conditions, such as inflammatory bowel disease and irritable bowel syndrome, where it may be present in higher levels in the body.
Ketamine is a medication that is primarily used as an anesthetic for surgical procedures and to treat severe pain. It is a synthetic drug that belongs to a class of medications called dissociative anesthetics, which work by altering the patient's perception of reality and creating a dissociative state. Ketamine is also sometimes used off-label for other medical conditions, such as depression, anxiety, and chronic pain. It is administered intravenously or intramuscularly and can produce a range of effects, including sedation, analgesia, and dissociation. While ketamine can be effective for certain medical conditions, it can also have side effects, including nausea, vomiting, hallucinations, and changes in blood pressure and heart rate. It is important for healthcare providers to carefully monitor patients who receive ketamine and to adjust the dosage as needed to minimize the risk of adverse effects.
Dinoprostone is a synthetic prostaglandin E1 (PGE1) medication that is used in the medical field to induce labor in pregnant women who are past their due date or who are at risk of complications during delivery. It is typically administered vaginally as a gel or tablet, and works by stimulating the muscles of the uterus to contract and push the baby out of the womb. Dinoprostone is also sometimes used to treat certain conditions that can cause bleeding in the uterus, such as uterine fibroids or abnormal bleeding during pregnancy. It is generally considered safe and effective for use in pregnant women, but like all medications, it can cause side effects in some people. These may include cramping, bleeding, and uterine contractions.
Naloxone is a medication used to reverse the effects of opioid overdose. It works by binding to opioid receptors in the brain and body, blocking the effects of opioids and causing the person to breathe normally again. Naloxone is often administered as an injection, but it can also be administered nasally or intravenously. It is commonly used in emergency medical settings to treat opioid overdose, but it can also be used in non-emergency situations, such as in the management of chronic pain or opioid addiction.
Nerve Growth Factor (NGF) is a protein that plays a crucial role in the development and maintenance of the nervous system. It is produced by various cells, including neurons, glial cells, and some immune cells. NGF is involved in the survival, growth, and differentiation of neurons, particularly sensory neurons in the peripheral nervous system. It also plays a role in the development of the sympathetic nervous system and the enteric nervous system. In addition to its role in the nervous system, NGF has been shown to have anti-inflammatory and neuroprotective effects, and it has been studied for its potential therapeutic applications in various neurological disorders, including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. NGF is also involved in the development and progression of cancer, and it has been shown to promote the growth and survival of some cancer cells. As a result, it has been targeted as a potential therapeutic target in cancer treatment.
Formaldehyde is a colorless, flammable gas with a pungent, suffocating odor. It is commonly used in the medical field as a preservative for tissues, organs, and other biological samples. Formaldehyde is also used as an antiseptic and disinfectant, and it is sometimes used to treat certain medical conditions, such as leprosy and psoriasis. In the medical field, formaldehyde is typically used in concentrations of 1-4%, and it is applied to the tissue or organ to be preserved. The formaldehyde causes the cells in the tissue to become rigid and hard, which helps to preserve the tissue and prevent decay. Formaldehyde is also used to disinfect medical equipment and surfaces, and it is sometimes used to treat wounds and skin conditions. While formaldehyde is effective at preserving tissue and disinfecting surfaces, it can also be harmful if it is inhaled or absorbed through the skin. Exposure to high concentrations of formaldehyde can cause irritation of the eyes, nose, and throat, as well as coughing, wheezing, and shortness of breath. Long-term exposure to formaldehyde has been linked to certain types of cancer, including nasopharyngeal cancer and sinonasal cancer.
Peripheral nerve injuries refer to damage or trauma to the nerves that are located outside of the brain and spinal cord. These nerves are responsible for transmitting signals between the central nervous system and the rest of the body, allowing us to feel sensations, move our muscles, and control our organs. Peripheral nerve injuries can occur as a result of a variety of factors, including trauma, compression, infection, or disease. Symptoms of peripheral nerve injuries can vary depending on the location and severity of the injury, but may include numbness, tingling, weakness, or loss of sensation in the affected area. Treatment for peripheral nerve injuries depends on the cause and severity of the injury. In some cases, conservative treatments such as physical therapy or medication may be sufficient to manage symptoms and promote healing. In more severe cases, surgery may be necessary to repair or replace damaged nerve tissue.
Mononeuropathy is a type of peripheral neuropathy that affects a single nerve. It is characterized by symptoms such as pain, numbness, weakness, and tingling in the affected area. Mononeuropathy can be caused by a variety of factors, including injury, compression, infection, or autoimmune disorders. Treatment for mononeuropathy depends on the underlying cause and may include medications, physical therapy, or surgery.
In the medical field, amines are organic compounds that contain a nitrogen atom bonded to one or more carbon atoms. They are often used as drugs, either as medications or as intermediates in the synthesis of other drugs. Amines can be classified into several categories based on their chemical structure and properties. Some common types of amines include primary amines, secondary amines, and tertiary amines. Primary amines have one nitrogen atom bonded to one hydrogen atom and two carbon atoms. Examples of primary amines include histamine, which is involved in allergic reactions, and dopamine, which plays a role in the regulation of movement and mood. Secondary amines have one nitrogen atom bonded to two hydrogen atoms and one carbon atom. Examples of secondary amines include epinephrine, which is used to treat severe allergic reactions and asthma, and norepinephrine, which is involved in the regulation of blood pressure and heart rate. Tertiary amines have one nitrogen atom bonded to three carbon atoms. Examples of tertiary amines include trimethoprim, which is used to treat bacterial infections, and procainamide, which is used to treat certain types of heart arrhythmias. Amines can also be classified based on their physical properties, such as their solubility in water and their ability to form salts with acids. Some amines are water-soluble and can be used as electrolytes in intravenous solutions, while others are insoluble and are used as local anesthetics.
Opioid peptides are a class of naturally occurring peptides that bind to opioid receptors in the brain and body, producing a range of effects, including analgesia (pain relief), sedation, and euphoria. These peptides are found in various parts of the body, including the brain, spinal cord, and gastrointestinal tract, and are involved in a variety of physiological processes, including pain modulation, stress response, and regulation of appetite and breathing. The most well-known opioid peptides are the endogenous opioids, which include endorphins, enkephalins, and dynorphins. These peptides are synthesized from larger precursor molecules and are released into the body in response to various stimuli, such as physical activity, stress, or injury. Opioid peptides are also used in medicine as analgesics, particularly for the treatment of severe pain. Synthetic opioid peptides, such as fentanyl and sufentanil, are often used in anesthesia and intensive care settings, while natural opioid peptides, such as morphine and codeine, are used in pain management. However, the use of opioid peptides can also lead to dependence and addiction, particularly when used for prolonged periods or in high doses.
Receptors, Opioid, mu (OPRM1) are a type of protein found on the surface of nerve cells in the brain and throughout the body. These receptors are activated by opioid drugs, such as morphine, heroin, and oxycodone, as well as endogenous opioid peptides, such as endorphins and enkephalins. The mu-opioid receptors play a key role in the body's response to pain, as well as in regulating mood, reward, and stress. They are also involved in the development of addiction to opioid drugs. Mutations in the OPRM1 gene can affect the function of mu-opioid receptors and may be associated with altered responses to opioid drugs and an increased risk of addiction.
Piperidines are a class of organic compounds that contain a six-membered ring with nitrogen atoms at positions 1 and 4. They are commonly used in the pharmaceutical industry as a building block for the synthesis of a wide range of drugs, including analgesics, anti-inflammatory agents, and antihistamines. Piperidines are also found in natural products, such as alkaloids, and have been used in traditional medicine for their various therapeutic effects. In the medical field, piperidines are often used as a starting point for the development of new drugs, as they can be easily modified to produce a wide range of pharmacological activities.
Nerve compression syndromes are a group of conditions that occur when a nerve is compressed or pinched, leading to pain, numbness, weakness, or other symptoms. These conditions can affect any nerve in the body, but are most commonly seen in the neck, back, and extremities. There are several types of nerve compression syndromes, including carpal tunnel syndrome, cubital tunnel syndrome, radial tunnel syndrome, tarsal tunnel syndrome, and sciatica. These conditions can be caused by a variety of factors, including repetitive motions, poor posture, injury, or underlying medical conditions such as arthritis or diabetes. Treatment for nerve compression syndromes typically involves addressing the underlying cause of the compression, such as through physical therapy, medication, or surgery. In some cases, lifestyle changes such as improving posture or modifying work habits may also be recommended to prevent further compression of the affected nerve.
Pain, Postoperative refers to the discomfort or pain experienced by a patient after undergoing surgery. It is a common and expected complication of surgery, and can range from mild to severe. Postoperative pain can be caused by a variety of factors, including tissue damage, inflammation, and nerve stimulation. It is typically managed with a combination of pain medications, such as opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), and local anesthetics, as well as other treatments such as physical therapy, ice packs, and relaxation techniques. Proper management of postoperative pain is important for promoting healing, reducing the risk of complications, and improving the patient's overall comfort and quality of life.
Facial pain is a medical condition characterized by discomfort or pain in the face, head, or neck. It can be acute or chronic and can be caused by a variety of factors, including injury, infection, inflammation, or nerve damage. There are several types of facial pain, including: 1. Migraine: A type of headache that is often accompanied by other symptoms such as nausea, vomiting, and sensitivity to light and sound. 2. Trigeminal neuralgia: A condition that causes intense, stabbing pain in the face, often triggered by simple activities such as chewing or talking. 3. Temporomandibular joint disorder (TMD): A condition that affects the joint that connects the jaw to the skull, causing pain, stiffness, and difficulty chewing. 4. Cluster headache: A type of headache that occurs in clusters, typically lasting several weeks or months, and is accompanied by symptoms such as redness and watering of the eye. 5. Atypical facial pain: A condition characterized by chronic, non-throbbing pain in the face that is not caused by a specific underlying condition. Treatment for facial pain depends on the underlying cause and can include medications, physical therapy, nerve blocks, and surgery. It is important to seek medical attention if you are experiencing facial pain, as it can be a sign of a more serious underlying condition.
Lidocaine is a local anesthetic medication that is commonly used to numb a specific area of the body during medical procedures or surgeries. It works by blocking the transmission of pain signals from the nerves to the brain. Lidocaine is available in various forms, including topical creams, gels, ointments, and injections. It is also used to treat certain types of abnormal heart rhythms, such as atrial fibrillation, and to relieve symptoms of neuropathy, a condition in which the nerves are damaged or diseased. Lidocaine is generally considered safe when used as directed, but it can cause side effects such as dizziness, nausea, and allergic reactions in some people.
Calcitonin Gene-Related Peptide (CGRP) is a neuropeptide that is primarily produced by the C cells of the thyroid gland and by certain sensory neurons in the peripheral nervous system. It is also found in high concentrations in the trigeminal ganglion, which is the main sensory ganglion of the face. CGRP plays a role in the regulation of various physiological processes, including vasodilation, pain perception, and inflammation. It is also involved in the pathophysiology of migraine headaches, where it is thought to contribute to the dilation of blood vessels in the brain and the release of other inflammatory molecules. In the medical field, CGRP is used as a diagnostic marker for certain conditions, such as medullary thyroid cancer, and as a target for the development of new treatments for migraine headaches and other conditions. It is also being studied as a potential therapeutic agent for a variety of other conditions, including chronic pain, osteoporosis, and inflammatory bowel disease.
Alcoholic neuropathy is a type of nerve damage that occurs as a result of long-term and excessive alcohol consumption. It is a common complication of chronic alcoholism and can affect any part of the body, but it most commonly affects the peripheral nerves, which are the nerves that are located outside of the brain and spinal cord. The symptoms of alcoholic neuropathy can vary depending on which nerves are affected, but they may include numbness, tingling, burning sensations, weakness, and loss of coordination. In severe cases, alcoholic neuropathy can lead to muscle wasting, difficulty walking, and loss of bladder or bowel control. Alcoholic neuropathy is caused by a combination of factors, including the toxic effects of alcohol on the nerves, vitamin deficiencies, and poor nutrition. It is typically diagnosed through a combination of physical examination, nerve conduction studies, and blood tests to measure vitamin levels. Treatment for alcoholic neuropathy typically involves stopping or reducing alcohol consumption, as well as addressing any underlying vitamin deficiencies and providing supportive care to manage symptoms. In some cases, medications may be prescribed to help manage pain or other symptoms.
Diabetic neuropathy is a type of nerve damage that can occur as a complication of diabetes. It is caused by damage to the nerves that control movement, sensation, and other functions in the body. There are several types of diabetic neuropathy, including: 1. Peripheral neuropathy: This is the most common type of diabetic neuropathy and affects the nerves in the extremities, such as the hands, feet, and legs. It can cause numbness, tingling, pain, and weakness in the affected areas. 2. Autonomic neuropathy: This type of neuropathy affects the nerves that control automatic bodily functions, such as heart rate, digestion, and blood pressure. It can cause symptoms such as dizziness, fainting, and gastrointestinal problems. 3. Proximal neuropathy: This type of neuropathy affects the nerves in the arms and legs, causing weakness and muscle wasting in the affected areas. 4. Mononeuropathy: This is a type of neuropathy that affects a single nerve, causing symptoms such as pain, numbness, and weakness in the affected area. Diabetic neuropathy can be a serious complication of diabetes and can lead to a range of problems, including foot ulcers, infections, and even amputations. It is important for people with diabetes to manage their blood sugar levels and to see their healthcare provider regularly for monitoring and treatment.
Dizocilpine maleate, also known as dizocilpine or dizocilpine dibromide, is a drug that belongs to a class of compounds called N-methyl-D-aspartate (NMDA) receptor antagonists. It is used in scientific research to study the effects of NMDA receptor antagonists on the brain and nervous system. In the medical field, dizocilpine maleate has been studied for its potential therapeutic effects in a variety of neurological and psychiatric conditions, including Parkinson's disease, Huntington's disease, and schizophrenia. However, it has not been approved for use in humans by regulatory agencies such as the US Food and Drug Administration (FDA) due to concerns about its safety and efficacy. Dizocilpine maleate is a potent and selective NMDA receptor antagonist that blocks the action of glutamate, a neurotransmitter that plays a key role in learning, memory, and other cognitive functions. It is believed that by blocking NMDA receptors, dizocilpine maleate can reduce the overactivity of neurons in the brain that is thought to contribute to the symptoms of certain neurological and psychiatric conditions. However, dizocilpine maleate has also been associated with a range of side effects, including cognitive impairment, psychosis, and motor dysfunction. As a result, its use in humans is limited and is typically only conducted in controlled clinical trials under the supervision of a qualified healthcare professional.
Receptor, PAR-2 is a protein that acts as a receptor for a family of proteases called protease-activated receptors (PARs). PAR-2 is expressed on various cells in the body, including immune cells, endothelial cells, and smooth muscle cells. Activation of PAR-2 by proteases, such as trypsin or thrombin, leads to a cascade of intracellular signaling events that can result in a variety of physiological responses, including inflammation, pain, and angiogenesis. PAR-2 has been implicated in a number of diseases, including inflammatory bowel disease, cancer, and cardiovascular disease, and is therefore a potential target for therapeutic intervention.
Myalgia is a medical term that refers to muscle pain or discomfort. It can be a symptom of a variety of medical conditions, including muscle strains, injuries, infections, and autoimmune disorders. Myalgia can also be a side effect of certain medications or medical treatments. The pain associated with myalgia can range from mild to severe and can affect one or more muscles in the body. Treatment for myalgia depends on the underlying cause and may include medication, physical therapy, or other interventions.
Dynorphins are a group of endogenous opioid peptides that are synthesized in the central nervous system. They are similar in structure to the endorphins, but have different effects on the body. Dynorphins are primarily involved in the regulation of pain, reward, and stress responses. They bind to opioid receptors in the brain and spinal cord, and can produce analgesic, sedative, and mood-altering effects. Dynorphins are also involved in the development of addiction and withdrawal symptoms, and have been implicated in the pathophysiology of a number of psychiatric disorders, including depression and anxiety.
Protein Kinase C-epsilon (PKC-epsilon) is a type of protein kinase enzyme that plays a role in various cellular processes, including cell growth, differentiation, and apoptosis. It is a member of the Protein Kinase C (PKC) family of enzymes, which are involved in the regulation of cell signaling pathways. PKC-epsilon is activated by the binding of diacylglycerol (DAG) and calcium ions, which are produced by the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) by phospholipase C (PLC). Once activated, PKC-epsilon phosphorylates various substrates, including other proteins, lipids, and nucleotides, leading to changes in cellular behavior. In the medical field, PKC-epsilon has been implicated in various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. For example, PKC-epsilon has been shown to play a role in the development and progression of breast cancer, and its inhibition has been proposed as a potential therapeutic strategy for this disease. Additionally, PKC-epsilon has been implicated in the regulation of blood pressure and the development of hypertension, as well as in the pathogenesis of Alzheimer's disease and other neurodegenerative disorders.
Receptors, Opioid are specialized proteins found on the surface of cells in the body that bind to opioid drugs, such as morphine, heroin, and oxycodone. These receptors are part of the body's natural pain-relieving system and are involved in regulating pain, mood, and reward. When opioid drugs bind to these receptors, they can produce a range of effects, including pain relief, sedation, and euphoria. However, long-term use of opioid drugs can lead to dependence and addiction, as the body becomes accustomed to the presence of the drug and requires more of it to achieve the same effect.
Transient Receptor Potential (TRP) channels are a family of non-selective cation channels that are widely expressed in various tissues and cell types throughout the body. These channels are activated by a wide range of stimuli, including changes in temperature, pH, osmolarity, and mechanical forces. TRP channels play important roles in various physiological processes, including sensory perception, pain transmission, and regulation of cell proliferation and differentiation. They are also involved in various pathological conditions, such as inflammation, neurodegeneration, and cancer. In the medical field, TRP channels are of great interest as potential therapeutic targets for a variety of diseases. For example, TRP channels have been implicated in the pathogenesis of chronic pain, and drugs that modulate TRP channel activity are being developed as potential analgesics. Additionally, TRP channels have been shown to play a role in the development and progression of various cancers, and targeting these channels may provide new strategies for cancer treatment.
Acid Sensing Ion Channels (ASICs) are a family of ion channels that are activated by protons (hydrogen ions) and are found in the nervous system, including neurons and sensory cells. These channels are involved in a variety of physiological processes, including the detection of changes in pH and the regulation of synaptic transmission. ASICs are expressed in a number of different types of neurons, including sensory neurons that detect touch, pain, and temperature, as well as neurons in the brain and spinal cord. They are also found in sensory cells in the inner ear, which are responsible for detecting sound and balance. When protons bind to ASICs, they cause the channel to open and allow ions to flow across the cell membrane. This can lead to changes in the electrical activity of the neuron and can trigger the release of neurotransmitters, which are chemical messengers that transmit signals between neurons. ASICs play an important role in a number of physiological processes, including the detection of changes in pH, the regulation of synaptic transmission, and the modulation of pain and other sensory signals. They are also involved in a number of pathological conditions, including chronic pain, multiple sclerosis, and stroke.
Chronic pain is a type of pain that persists for more than 12 weeks and is not relieved by standard medical treatments. It can be caused by a variety of factors, including injury, illness, or underlying medical conditions. Chronic pain can be severe and can significantly impact a person's quality of life, leading to physical and emotional distress, as well as social isolation and disability. Treatment for chronic pain typically involves a combination of medications, physical therapy, and other interventions, and may require the involvement of a multidisciplinary team of healthcare professionals.
Bradykinin is a peptide hormone that plays a role in the regulation of blood pressure, inflammation, and pain. It is produced in the body by the breakdown of larger proteins called kinins, which are released from blood vessels and other tissues in response to injury or inflammation. Bradykinin acts on various types of cells in the body, including blood vessels, smooth muscle cells, and nerve cells, to cause a range of physiological effects. In the blood vessels, bradykinin causes them to dilate, or widen, which can lead to a drop in blood pressure. It also increases the permeability of blood vessels, allowing fluid and other substances to leak out and cause swelling. In addition to its effects on blood vessels, bradykinin is also involved in the body's inflammatory response. It stimulates the release of other inflammatory mediators, such as prostaglandins and leukotrienes, which can cause redness, swelling, and pain. Overall, bradykinin plays an important role in the body's response to injury and inflammation, and its activity is tightly regulated by various enzymes and other factors in the body.
Nociceptive pain is a type of pain that is caused by the activation of nerve fibers called nociceptors. Nociceptors are specialized sensory receptors that are sensitive to stimuli such as heat, cold, pressure, and chemical irritants. When these stimuli are detected by nociceptors, they send signals to the spinal cord and brain, which are interpreted as pain. Nociceptive pain is the most common type of pain and can be caused by a variety of factors, including injury, inflammation, infection, and tissue damage. It is often described as sharp, stabbing, or burning and can be localized to a specific area of the body. Treatment for nociceptive pain typically involves addressing the underlying cause of the pain, such as treating an injury or infection. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids may also be used to manage pain. In some cases, physical therapy or other forms of rehabilitation may be recommended to help reduce pain and improve function.
Analysis of Variance (ANOVA) is a statistical method used to compare the means of three or more groups. In the medical field, ANOVA can be used to compare the effectiveness of different treatments, interventions, or medications on a particular outcome or variable of interest. For example, a researcher may want to compare the effectiveness of three different medications for treating a particular disease. They could use ANOVA to compare the mean response (e.g., improvement in symptoms) between the three groups of patients who received each medication. If the results show a significant difference between the groups, it would suggest that one medication is more effective than the others. ANOVA can also be used to compare the means of different groups of patients based on a categorical variable, such as age, gender, or race. For example, a researcher may want to compare the mean blood pressure of patients in different age groups. They could use ANOVA to compare the mean blood pressure between the different age groups and determine if there are significant differences. Overall, ANOVA is a powerful statistical tool that can be used to compare the means of different groups in the medical field, helping researchers to identify which treatments or interventions are most effective and to better understand the factors that influence health outcomes.
Anesthetics, Local are medications that are used to numb a specific area of the body, such as a tooth or a surgical site, to reduce pain and discomfort during a procedure. These medications work by blocking the transmission of pain signals from the nerves in the affected area to the brain. Local anesthetics are typically administered by injection, cream, or spray, and their effects can last for several hours. There are several types of local anesthetics, including lidocaine, benzocaine, and novocaine, each with its own specific properties and uses. Local anesthetics are commonly used in dentistry, surgery, and other medical procedures where a patient needs to be numbed for a specific area of the body.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a class of medications that are commonly used to relieve pain, reduce inflammation, and lower fever. They work by inhibiting the production of prostaglandins, which are chemicals that cause inflammation, pain, and fever. NSAIDs are available over-the-counter (OTC) or by prescription and are used to treat a variety of conditions, including headaches, menstrual cramps, arthritis, and muscle pain. Some common examples of NSAIDs include aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve), and celecoxib (Celebrex). While NSAIDs are generally safe and effective when used as directed, they can also have side effects, including stomach pain, nausea, diarrhea, and increased risk of bleeding. Long-term use of high doses of NSAIDs can also increase the risk of serious side effects, such as stomach ulcers, kidney damage, and heart attack or stroke. Therefore, it is important to use NSAIDs only as directed by a healthcare provider and to be aware of any potential side effects.
Trigeminal nerve injuries refer to any damage or dysfunction of the trigeminal nerve, which is the largest and most complex cranial nerve in the human body. The trigeminal nerve is responsible for sensation and motor function in the face, including the eyes, nose, mouth, and teeth. Trigeminal nerve injuries can occur as a result of various factors, including trauma, tumors, infections, and degenerative diseases. Symptoms of trigeminal nerve injuries may include facial pain, numbness, tingling, weakness, and difficulty with facial expression or chewing. Treatment for trigeminal nerve injuries depends on the underlying cause and severity of the injury. In some cases, conservative treatments such as medication, physical therapy, or nerve blocks may be effective. In more severe cases, surgery may be necessary to repair or replace damaged nerve tissue.
Minocycline is a type of antibiotic medication that belongs to the tetracycline family. It is commonly used to treat a variety of bacterial infections, including acne, respiratory infections, urinary tract infections, and skin infections. Minocycline works by inhibiting the growth of bacteria, which helps to reduce the severity and duration of the infection. Minocycline is available in both oral and intravenous forms, and it is typically taken once or twice a day, depending on the specific infection being treated. It is important to follow the dosage instructions provided by your healthcare provider and to complete the full course of treatment, even if you start to feel better before the medication is finished. Like all medications, minocycline can cause side effects. Common side effects include nausea, vomiting, diarrhea, headache, and dizziness. More serious side effects are rare, but can include allergic reactions, liver damage, and photosensitivity (increased sensitivity to sunlight). If you experience any side effects while taking minocycline, you should contact your healthcare provider right away.
Hypesthesia is a medical term that refers to an abnormal sensitivity or increased perception of touch, pressure, temperature, or pain in a specific area of the body. It is often described as a feeling of pins and needles, burning, tingling, or numbness. Hypesthesia can be caused by a variety of factors, including nerve damage, injury, inflammation, or compression. It can also be a symptom of certain medical conditions, such as multiple sclerosis, diabetes, or peripheral neuropathy. In the medical field, hypesthesia is typically evaluated and treated by a neurologist or other healthcare provider who specializes in the diagnosis and management of neurological disorders. Treatment options may include medication, physical therapy, or surgery, depending on the underlying cause of the hypesthesia.
Amitriptyline is a tricyclic antidepressant medication that is primarily used to treat depression, anxiety, and chronic pain. It works by increasing the levels of certain neurotransmitters in the brain, such as serotonin and norepinephrine, which can help to improve mood and reduce pain. Amitriptyline is available in both immediate-release and extended-release forms, and it is typically taken orally. It can also be used to treat other conditions, such as insomnia, migraines, and irritable bowel syndrome. However, like all medications, amitriptyline can have side effects. Common side effects include dry mouth, blurred vision, dizziness, constipation, and weight gain. More serious side effects can include increased heart rate, high blood pressure, and serotonin syndrome, which is a potentially life-threatening condition that can occur when serotonin levels in the brain become too high. It is important to note that amitriptyline should only be taken under the guidance of a healthcare professional, as it can interact with other medications and may not be suitable for everyone.
EphB1 is a type of receptor protein that plays a role in cell signaling and communication. It is a member of the Eph receptor family, which is involved in the development and maintenance of the nervous system, as well as in processes such as cell migration, axon guidance, and angiogenesis. EphB1 receptors are found on the surface of cells and bind to specific ligands, which are proteins that interact with the receptor to trigger a signaling cascade within the cell. This signaling cascade can lead to a variety of cellular responses, including changes in gene expression, cell proliferation, and cell migration. EphB1 receptors have been implicated in a number of diseases and conditions, including cancer, cardiovascular disease, and neurological disorders. For example, studies have shown that EphB1 signaling may play a role in the development and progression of certain types of cancer, such as breast cancer and glioblastoma. In addition, EphB1 signaling has been shown to be involved in the development of blood vessels, which may be relevant to conditions such as angiogenesis and cardiovascular disease.
Fentanyl is a synthetic opioid pain medication that is approximately 100 times more potent than morphine. It is used to treat severe pain, such as that caused by cancer or after surgery. Fentanyl is available in a variety of forms, including tablets, lozenges, patches, and injections. It is also sometimes used in combination with other medications, such as hydromorphone or oxycodone, to increase their effectiveness. Fentanyl can be highly addictive and can cause respiratory depression, which can be life-threatening. It is important to use fentanyl only under the guidance of a healthcare professional and to follow their instructions carefully.
Anesthetics, Dissociative are a class of drugs that are used to induce a state of unconsciousness and amnesia during medical procedures. They are also known as general anesthetics because they affect the entire central nervous system, including the brain and spinal cord. Dissociative anesthetics work by binding to specific receptors in the brain, which disrupts the normal functioning of the brain and leads to a loss of consciousness. They are often used in combination with other anesthetics to provide a more complete and effective anesthetic effect. Examples of dissociative anesthetics include ketamine, propofol, and etomidate. These drugs are commonly used in surgical procedures, as well as in emergency situations where a rapid induction of anesthesia is required. It is important to note that dissociative anesthetics can have side effects, including nausea, vomiting, dizziness, and confusion. They can also cause respiratory depression, which can be life-threatening if not properly monitored. As with any anesthetic, the use of dissociative anesthetics should be carefully considered and monitored by a qualified healthcare professional.
Tibial neuropathy is a medical condition that refers to damage or dysfunction of the tibial nerve, which is the largest nerve in the lower leg. The tibial nerve runs down the back of the leg and supplies sensation and muscle control to the foot and ankle. There are several causes of tibial neuropathy, including injury, compression, or disease. Some common causes include diabetes, trauma, and certain medications. Symptoms of tibial neuropathy may include pain, numbness, tingling, weakness, and difficulty walking or standing. Diagnosis of tibial neuropathy typically involves a physical examination and imaging tests such as an MRI or nerve conduction studies. Treatment options may include medication, physical therapy, and in some cases, surgery. It is important to seek medical attention if you suspect you may have tibial neuropathy, as early diagnosis and treatment can help prevent further nerve damage and improve symptoms.
The term "Receptor, Cannabinoid, CB2" refers to a specific type of protein found on the surface of certain cells in the body. These proteins, called CB2 receptors, are part of the endocannabinoid system, which plays a role in regulating a variety of physiological processes, including pain, inflammation, and immune function. CB2 receptors are primarily found in the immune system, although they are also present in other tissues, such as the brain, spinal cord, and peripheral nervous system. Activation of CB2 receptors can have a range of effects on the body, depending on the specific circumstances and the cells involved. Cannabinoids are a class of compounds that interact with CB2 receptors, including endogenous cannabinoids (which are produced by the body) and exogenous cannabinoids (which are derived from plants or other sources). Some cannabinoids, such as THC (tetrahydrocannabinol), are psychoactive and can produce the "high" associated with marijuana use. Other cannabinoids, such as cannabidiol (CBD), are non-psychoactive and have been studied for their potential therapeutic effects. In the medical field, CB2 receptors and their interactions with cannabinoids are being investigated for their potential role in treating a variety of conditions, including chronic pain, inflammation, and certain types of cancer. However, more research is needed to fully understand the mechanisms by which CB2 receptors and cannabinoids exert their effects, and to determine the optimal dosages and treatment regimens for these compounds.
Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) that is commonly used to relieve pain, reduce inflammation, and lower fever. It works by blocking the production of prostaglandins, which are chemicals that cause pain, inflammation, and fever. Indomethacin is available in various forms, including tablets, capsules, and suppositories. It is often prescribed for conditions such as arthritis, menstrual cramps, and headaches. It can also be used to treat gout, kidney stones, and other inflammatory conditions. However, indomethacin can have side effects, including stomach pain, nausea, vomiting, and diarrhea. It can also increase the risk of bleeding and ulcers in the stomach and intestines. Therefore, it is important to use indomethacin only as directed by a healthcare provider and to report any side effects immediately.
NAV1.8 Voltage-Gated Sodium Channel is a type of ion channel that is responsible for generating action potentials in sensory neurons, including nociceptors (pain-sensing neurons) and mechanoreceptors (touch-sensing neurons). It is the primary voltage-gated sodium channel expressed in these neurons and plays a crucial role in the transmission of sensory information to the central nervous system. The channel is activated by changes in membrane potential and allows the influx of sodium ions into the cell, leading to depolarization and the generation of an action potential. Mutations in the gene encoding for NAV1.8 have been linked to several neurological disorders, including inherited forms of pain and insensitivity to pain.
Neuritis is a medical condition that refers to inflammation or damage to one or more nerves. It can affect any part of the nervous system, including the brain, spinal cord, and peripheral nerves. Neuritis can be caused by a variety of factors, including infections, autoimmune disorders, toxins, and injuries. Symptoms of neuritis can vary depending on the location and severity of the inflammation, but may include pain, numbness, tingling, weakness, and muscle spasms. In some cases, neuritis can lead to permanent nerve damage or even paralysis. Treatment for neuritis depends on the underlying cause and severity of the condition. In some cases, medications such as anti-inflammatory drugs or corticosteroids may be used to reduce inflammation and relieve symptoms. Physical therapy or other forms of rehabilitation may also be recommended to help restore function and mobility. In severe cases, surgery may be necessary to repair or remove damaged nerves.
Tolmetin is a nonsteroidal anti-inflammatory drug (NSAID) that is used to relieve pain, reduce inflammation, and lower fever. It is commonly prescribed for conditions such as arthritis, menstrual cramps, and headaches. Tolmetin works by inhibiting the production of prostaglandins, which are chemicals that cause inflammation and pain. It is available in both oral and topical forms, and is usually taken by mouth. Tolmetin can cause side effects such as stomach pain, nausea, and diarrhea, and may increase the risk of bleeding and ulcers in the stomach and intestines. It is important to follow the dosage instructions provided by your healthcare provider and to inform them of any other medications you are taking before starting tolmetin.
Hyperalgesia
Hyperalgesia (album)
Opioid-induced hyperalgesia
Complex regional pain syndrome
Ketamine
Opioid
Rostral ventromedial medulla
Victorian Halls
Allodynia
Nociceptor
Chronic pain
Nav1.8
Bernhard Landwehrmeyer
SIB-1757
Sérgio Henrique Ferreira
Failed back syndrome
Algophobia
Opioid rotation
Hemopressin
Oxymorphazone
Analgesic
Plerixafor
Μ-opioid receptor
Functional gastrointestinal disorder
RQ-00203078
Dorsal root ganglion
Nocebo
Glutamate receptor
Dihydrocodeine
Oh Uhtaek
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Mechanical hyperalgesia2
- This enhanced responsiveness to nociceptive input of the central nervous system primarily manifests as an increased sensitivity to painful mechanical pinprick stimuli extending beyond the site of injury (secondary mechanical hyperalgesia) and is thought to be a key mechanism in the development of chronic pain, such as persistent post-operative pain. (iasp-pain.org)
- Despite the growing number of publications , it is unclear whether these athletes have mechanical hyperalgesia associated with pain , which could alter the treatment options undertaken. (bvsalud.org)
Opioid-induced hype1
- A new warning is being added about opioid-induced hyperalgesia (OIH) for both IR and ER/LA opioid pain medicines. (medlineplus.gov)
Allodynia and hyperalgesia3
- Allodynia and hyperalgesia are almost always present. (bmj.com)
- manifestations of allodynia and hyperalgesia are commonly present in chronic painful temporomandibular disorder. (bvsalud.org)
- This study aimed to analyze clinical parameters suggestive of central sensitization (pressure pain threshold, allodynia, and hyperalgesia) in women with chronic painful temporomandibular disorder before and after a mindfulness-based intervention, through a before-and-after intervention study, longitudinal, uncontrolled. (bvsalud.org)
Analgesia2
Edema1
- Both complex regional pain syndrome (CRPS) I and II have a hallmark of allodynia, severe hyperalgesia, edema , skin changes, and abnormal alterations in sudomotor and vasomotor function. (medicinenet.com)
Symptom1
- The main symptom of visceral hyperalgesia is pain. (cvs.com)
Pain3
- Some people can become more sensitive to pain (hyperalgesia). (www.nhs.uk)
- CBD gummies may help if you suffer from hyperalgesia (oversensitivity to pain) (3). (cfah.org)
- Hyperalgesia, allodynia, and pressure pain threshold were tested at trigeminal and extra-trigeminal points before and after the intervention as well as the application of the questionnaire to measure the level of mindfulness (Mindful Attention Awareness Scale). (bvsalud.org)
Stimuli1
- HFS induced an increased sensitivity to mechanical pinprick stimuli at both forearms, directly (T1) and 20 min (T2) after HFS, confirming the successful induction of secondary hyperalgesia at both forearms. (iasp-pain.org)
SKIN1
- While participants performed a somatosensory detection task that required focusing attention towards one of the forearms, secondary hyperalgesia was induced at both forearms using bilateral and simultaneous high-frequency electrical stimulation (HFS) of the skin. (iasp-pain.org)
Muscle1
- 25. Sluka KA, Rasmussen LA. Fatiguing exercise enhances hyperalgesia to muscle inflammation. (bvsalud.org)
Central1
- The focus of spatial attention during the induction of central sensitization can modulate the subsequent development of secondary hyperalgesia. (iasp-pain.org)
Health1
- Available at: https://www.cincinnatichildrens.org/health/v/visceral-hyperalgesia. (cvs.com)
Heat hyperalgesia1
- σ1 receptor knockout (σ1-KO) mice did not develop cold allodynia and showed significantly less mechanical allodynia, although they developed heat hyperalgesia after SNI. (ugr.es)
Visceral hyperalgesia1
- We use a rat model of stress induced visceral hyperalgesia to examine the relationship the microbiome and host gene expression. (nih.gov)
Secondary Hyperalgesia4
- Secondary Hyperalgesia: Increased pain sensitivity beyond the injury site. (keydifference.in)
- Background and Objectives Ketamine is an N -methyl-D-aspartate (NMDA) receptor antagonist, and has been proven effective in alleviating secondary hyperalgesia in human subjects when injected intravenously. (bmj.com)
- The aim of this study was to investigate the effects of oral administration of ketamine on secondary hyperalgesia evoked by standardized tissue injury. (bmj.com)
- Conclusion Oral ketamine 0.5 or 1.0 mg/kg has no effect on secondary hyperalgesia or thermal or mechanical pain thresholds in human volunteers. (bmj.com)
Response to non-painful stimuli1
- This manifests as an increased sensitivity to painful stimuli ( hyperalgesia ) or pain sensation in response to non-painful stimuli ( allodynia ). (wikipedia.org)
Opioid7
- NATIONAL HARBOR, MD - Opioid-induced hyperalgesia is among the most pressing concerns in the national discussion of opioid addiction, underscored by the US Food and Drug Administration's (FDA) call for clinical trials to better understand the risks, but the issue is mired in more complexities and confusion than many may even realize, an expert says. (medscape.com)
- In a very preliminary effort to better understand the measures of pain to predict opioid-induced hyperalgesia, Dr Harden and his colleagues compared pain test responses among patients with chronic low back pain, including 10 who were receiving medium- to high-dose opioids (45 to 424 morphine milligram equivalency conversion) and 10 who were not taking opioids. (medscape.com)
- Maybe this is not an iatrogenic (opioid) hyperalgesia but 'natural' hyperalgesia that occurs in chronic pain. (medscape.com)
- To discuss the phenomenon of opioid induced hyperalgesia (OIH) and investigate the data and clinical recommendations available on this topic. (nih.gov)
- Opioid induced hyperalgesia: clinical implications for the pain practitioner. (nih.gov)
- Complications of long-term opioid therapy for management of chronic pain: the paradox of opioid-induced hyperalgesia. (nih.gov)
- Opioid-induced hyperalgesia (OIH): a real clinical problem or just an experimental phenomenon? (nih.gov)
Thermal3
- Since TRPV1 agonists such as LPA 18∶1, 9- and 13-HODE, 5- and 12-HETE were elevated in the skin, they may contribute to thermal hyperalgesia and mechanical allodynia during UVB-induced inflammatory pain. (ox.ac.uk)
- Combination of Rheum ribes and metformin against diabetes, thermal hyperalgesia, and tactile allodynia. (greenmedinfo.com)
- Using tail flick, hot plate latencies, and von Frey paw withdrawal thresholds, thermal hyperalgesia and tactile allodynia were assessed. (greenmedinfo.com)
Mechanical2
- Despite the growing number of publications , it is unclear whether these athletes have mechanical hyperalgesia associated with pain , which could alter the treatment options undertaken. (bvsalud.org)
- Activation of cyclin-dependent 5 mediates orofacial mechanical hyperalgesia. (nih.gov)
Inflammatory3
- Hyperalgesia, which includes both acute and inflammatory processes, is characterized as an increased sensitivity to pain [5]. (nih.gov)
- Synthesis of lipid mediators during UVB-induced inflammatory hyperalgesia in rats and mice. (ox.ac.uk)
- Padhy B.M. and V.L.Kumar ( 2005) Inhibition of Calotropis procera latex-induced inflammatory hyperalgesia by oxytocin and melatonin Mediators Inflamm. (science20.com)
Sensitivity to painful1
- Hyperalgesia, in essence, is an increase in the sensitivity to painful sensations, which causes the sensations to feel more severe and intense than they would in an individual who is not suffering from the condition. (keydifference.in)
Peripheral sensitization1
- A look at the potential mechanisms of hyperalgesia leads to a host of possibilities, including peripheral sensitization, central sensitization, disinhibition, or possibly sympathetic nervous system involvement. (medscape.com)
Painful2
- Hyperalgesia is a neurologic condition that is characterized by an exaggerated more intense sense of pain reaction to normally painful stimuli or those which typically trigger moderate discomfort. (keydifference.in)
- Consequently, the combination's potent inhibitory effect on α-glucosidase and serum insulin elevation might be responsible for its hypoglycemic potential, whereas its antioxidant effects might be responsible for the amelioration of painful hyperalgesia and allodynia, suggesting that the combination has better antidiabetic and antinociceptive effects and fewer side effects than treatment with MTF alone. (greenmedinfo.com)
Antagonist1
- Furthermore, treatment with a CGRP antagonist ameliorated the pain hyperalgesia in NPFFR2-Tg mice, returning the pain threshold to a control level. (tmu.edu.tw)
Rats1
- In an attempt to broaden the therapeutic application of a novel neuromodulatory compound identified in the traditional seizure models, the ETSP has examined the efficacy of the most promising and/or novel investigational ASD s in several models of nociception, including the partial sciatic nerve ligation model of chronic allodynia in rats (Test 23) and the formalin test model of hyperalgesia in mice (Test 22). (nih.gov)
Chronic pain2
- The early findings appear to support, however, the assertion that hyperalgesia (central sensitization) in many cases may be part of the natural progression of chronic pain. (medscape.com)
- Hyperalgesia can manifest in a variety of circumstances, including acute pain or chronic pain conditions or due to some medical treatment. (keydifference.in)
Mice1
- We found the expression levels of NPFF and NPFFR2 were increased in the lumbar dorsal horn of animals with CFA- and carrageenan-induced inflammation and both NPFFR2 over-expressing transgenic (NPFFR2-Tg) and NPFFR2 agonist-treated mice displayed hyperalgesia. (tmu.edu.tw)
Sensitization1
- LE cell sensitization has effects, resembling hyperalgesia and allodynia, that compensate for loss of sensory function during injury and help protect against subsequent threats. (jneurosci.org)
Investigate1
- Here, we investigate whether temporal suggestions modulate the timing of nocebo hyperalgesia in an experimental model of sustained pain. (unimib.it)
Activation1
- Together, these results demonstrate that NPFFR2 activation modulates pain transmission by up-regulating the pain mediator CGRP, leading to hyperalgesia. (tmu.edu.tw)
Effect2
- The people on opioids in fact had lower pain on this single test, and one interpretation of that would be that they're getting an analgesic effect from the opioids, not hyperalgesia," Dr Harden said. (medscape.com)
- 0.001), showing that hyperalgesia was only present in the group that expected the effect of the cream to set in early. (unimib.it)
Injury1
- Primary Hyperalgesia: Increased pain sensitivity at the site of injury. (keydifference.in)
Content1
- BackgroundThe direction and the magnitude of verbal suggestions have been shown to be strong modulators of nocebo hyperalgesia, while little attention has been given to the role of their temporal content. (unimib.it)
Determine2
- The one certainly, however, is that much more research needs to be done concerning the hyperalgesia phenomena in order to determine, for instance, how to prevent it, Dr Harden said. (medscape.com)
- Being able to determine if a patient suffering from hyperalgesia or allodynia can help medical professionals to make an accurate diagnosis. (keydifference.in)