Articles: hyperalgesia.
-
Randomized Controlled Trial Clinical Trial
Low-dose lidocaine suppresses experimentally induced hyperalgesia in humans.
The antinociceptive effects of systemically administered local anesthetics have been shown in various conditions, such as neuralgia, polyneuropathy, fibromyalgia, and postoperative pain. The objective of the study was to identify the peripheral mechanisms of action of low-dose local anesthetics in a model of experimental pain. ⋯ Increasing painfulness during sustained pinching has been attributed to excitation and simultaneous sensitization of particular Adelta- and C-nociceptors. This hyperalgesic mechanism seems to be particularly sensitive to low concentrations of lidocaine. These findings confirm clinical experience with lidocaine in pain states dominated by hyperalgesia.
-
Gabapentin (GBP) and S(+)-3-isobutyl-gamma-aminobutyric acid (IBG) are anticonvulsant agents which are effective against many clinical and experimental neuropathic pain states. We examined the efficacy of these agents in a new rat model of secondary mechanical hyperalgesia generated by a mild thermal injury. Under brief halothane anesthesia, an injury was induced by applying one heel to a hot surface (52.5 degreesC) for 45 s. ⋯ Our findings demonstrate a dose-dependent blockade of the mechanical sensitivity caused by a mild thermal injury by both GBP and IBG. Results indicate that IBG is more effective than GBP in this model at doses which do not cause sedation. These observations support the suggested use of these or related gamma-amino acid analogues as an effective treatment for post-operative pain.
-
Tight ligation and transection of the L5 spinal nerve (SNL) gives rise to pain which is dependent upon activity in the sympathetic nervous system. It also results in novel adrenergic sympathetic innervation of the dorsal root ganglion (DRG) with the formation of pericellular axonal basket structures around some DRG neurons. Since the sympathetic sprouting and basket formation may represent an anatomical basis for pain-generating interactions between the sympathetic efferent neurons and sensory afferent neurons, it is of great interest to determine possible chemical mediators of this phenomenon. ⋯ On the other hand, in the IL-6 mice, mechanoallodynia (as assessed with von Frey filaments) was markedly delayed. Sympathetic invasion of the fiber tract and cell layer of the DRG, and the formation of pericellular axonal baskets were all significantly reduced in the IL-6 knockout mice compared to the control strain. These results imply a facilitatory role for IL-6 in pain and sympathetic sprouting induced by nerve injury, and add to the growing list of roles for IL-6 in neuropathological events.
-
Pain assessment and physical examination are the first crucial steps in diagnosis of neuropathic pain disorders because these are still solely diagnosed on clinical grounds. The physical examination should be conducted in such a way that all of the positive sensory phenomena, such as allodynia, hyperalgesia, hyperpathia, summation, and after-sensation are elicited. Other physical examination findings should corroborate the diagnostic impression of neuropathic pain. Specific pain diagnosis should then lead to more specific therapy.
-
Clinical Trial
AMPA/kainate antagonist LY293558 reduces capsaicin-evoked hyperalgesia but not pain in normal skin in humans.
Animal studies suggest that alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-kainate (AMPA-KA) receptors are involved in pain processing. The effects of the competitive AMPA-KA antagonist LY293558 in two types of experimental pain in human volunteers, brief pain sensations in normal skin, and mechanical allodynia-pinprick hyperalgesia were studied after the injection of intradermal capsaicin. ⋯ The authors infer that AMPA-KA receptor blockade reduces the spinal neuron sensitization that mediates capsaicin-evoked pain and allodynia. The low incidence of side effects at effective doses of LY293558 suggests that this class of drugs may prove to be useful in clinical pain states.