Pain response

Abbadie C (2005) Chemokines, chemokine receptors and pain. Trends Immunol 26 529-534 Abbadie C, Lindia JA, Cumiskey AM, Peterson LB, Mudgett JS, Bayne EK, DeMartino JA, MacIntyre DE, Forrest MJ (2003) Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2. Proc Natl Acad Sci USA 100 7947-7952 Ahn DK, Lee KR, Lee HJ, Kim SK, Choi HS, Lim EJ, Park JS (2005) Intracistemal administration of chemokines facditated formalin-induced behavioral responses in the orofacial area of freely moving rats. Brain Res Bull 66 50-58... 

Another intriguing observation is that the female sex-hormone 17/i-estradiol (28) could dramatically potentiate capsaicin responses, whereas the male hormone testosterone had marginal inhibitory activity. Sex differences in pain responses have long been known, with women being more sensitive to capsaicin-induced pain than men [94]. The differential modulation of capsaicin responses by female and male hormones might provide a rationale to explain this observation. 

Hyperalgesia An increased pain response to a stimulus that normally causes pain. 

In addition to stability effects, pH adjustment can influence comfort, safety, and activity of the product. Comfort can be described as the subjective response of the patient after instillation of the product in the cul-de-sac (i.e., whether it may cause a pain response such as stinging or burning). Eye irritation is normally accompanied by an increase in tear fluid secretion (a defense mechanism) to aid in the restoration of normal physiological conditions. Accordingly in addition to the discomfort encountered, products that produce irritation will tend to be flushed from the eye, and hence a more rapid loss of medication may occur with a probable reduction in the therapeutic response [15]. 

When the placebo cream had not been applied, the researchers found activation in areas of the brain that they identified as the pain matrix . But when the same pain stimuli were administered with the placebo cream, activation in these pain-responsive regions of the brain was reduced, and the more pain relief the subjects reported, the greater the reduction of activation in the pain matrix. This told Wager that people actually do experience less pain when given placebo analgesics, and this change in experience is accompanied by changes in brain activity. 

An injured area is typically more sensitive to subsequent stimuli. As a result, painful stimuli, or even normally nonpainful stimuli, may cause an excessive pain response. An increase in the sensitivity of nociceptors is referred to as primary hyperalgesia. A classic example of hyperalgesia is a bum. Even light touch of a burned area may be painful. 

Endogenous opioids and opioid receptors inhibit pain responses 932 CLINICAL PAIN 932... 

Neuropathic pain is often chronic, not well described, and not easily treated with conventional analgesics. There may be exaggerated painful responses to normally noxious stimuli (hyperalgesia) or painful responses to normally nonnoxious stimuli (allodynia). 

Individualization of therapy is essential, and continuous assessment of pain response, side effects, and behavior is required. 

Burstein SH, Hull K, Hunter SA, Latham V. (1988). Cannabinoids and pain responses a possible role for prostaglandins. FASEB J. 2(14) 3022-26. 

Pain response to cold water Opioid analgesic... 

The peptide, melatonin, has been implicated in autism. Excess melatonin is thought to decrease learning, memory, attention, emotionality, motivation and pain responses (reviewed Chamberlain Herman, 1990)—all behaviours that are abnormal in autism. Melatonin, released from the pineal gland, is implicated in controlling serotonin and POMC (proopiomelanocortin) peptides, such as beta-endorphin, and an elevation may contribute to, or cause, the serotonin and opioid abnormalities (Chamberlain Herman, 1990). 

Be alert to the onset of pain because the drug is less effective if a full pain response recurs before the next dose... 

Xiao, W. H. and Bennett, G. J. Magnesium suppresses neuropathic pain responses in rats via a spinal site of action, Brain Res. 1994, 666, 168-172. 

Pharmacological investigations have proven J-113397 to be the most potent ORL1 antagonist known today (Ozaki et al., 2000a, b Bigoni et al., 2000 Ichikawa et al., 2001). J-113397 is reported to be active in the formalin test, but inactive against pain responses to thermal and mechanical stimuli (Okuda et al., 2000). 

In 2000 Hamilton et al. reported that ATP in human skin elicits a dose-related pain response which is potentiated under conditions of hyperalgesia. The authors used iontophoresis to deliver ATP to the forearm skin of volunteers who rated the magnitude of the evoked pain on a visual analog scale. ATP consistently produced a modest burning pain, which began within 20 s. of starting iontophoresis and was maintained for several minutes. Persistent iontophoresis of ATP led to desensitization... 

It must be mentioned, however, that intrathechal administration of IB-MECA does not exhibit an antinociceptive profile in acute nociception as assessed in the early phase pain response of the formalin test, but it does depress the late phase of... 

IP pgi2 Gs, inc cAMP - Inc thrombosis, dec pain responses to chemical stimuli... 

One compound that is not an NSAID but is often lumped into this group is acetaminophen (Tylenol, A.154) (Figure A.43). Acetaminophen is both an analgesic and suppresses fever but has no effect on inflammation and blood clotting. Acetaminophen also has less impact on the stomach lining than NSAIDs. Acetaminophen is believed to act both by COX inhibition as well as other pain response pathways. Unlike NSAIDs, acetaminophen acts on cannabinoid receptors. 

M, Noda T, Tanabe T (2000) Altered pain responses in mice lacking alpha IE subunit of the voltage-dependent Ca2+ channel. Proc Natl Acad Sci U S A 97 6132-7... 

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