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Tactile pain

Eguchi, N., el at (1999). Lack of tactile pain (allodynia) in lipocalin-type... [Pg.379]

AN EMOTIONS MODEL OF THE HUMAN ETHOGRAM 3.1. Tactile Pain and Tactile Pleasure... [Pg.32]

Eguchi N, Minami T, Shirafuji N, Kanaoka Y, Tanaka T, Nagata A, et al. Lack of tactile pain (allodynia) in lipocalin-type prostaglandin D synthase-deficient mice. Proc Natl Acad Sci USA 1999 96 726-730. [Pg.416]

Flavor has been defined as a memory and an experience (1). These definitions have always included as part of the explanation at least two phenomena, ie, taste and smell (2). It is suggested that in defining flavor too much emphasis is put on the olfactory (smell) and gustatory (taste) aspects (3), and that vision, hearing, and tactile senses also contribute to the total flavor impression. Flavor is viewed as a division between physical sense, eg, appearance, texture, and consistency, and chemical sense, ie, smell, taste, and feeling (4). The Society of Flavor Chemists, Inc, defines flavor as "the sum total of those characteristics of any material taken in the mouth, perceived principally by the senses of taste and smell and also the general senses of pain and tactile receptors in the mouth, as perceived by the brain" (5). [Pg.10]

Flavor. The sensation produced by a material taken into the mouth, perceived principally by the senses of taste and smell, but also by the common chemical sense produced by pain, tactile, and temperature receptors in the mouth. [Pg.19]

The sensation of pain, following injury or disease, in response to a previously non-noxious stimulus is termed allodynia . Tactile allodynia is caused by... [Pg.64]

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. [Pg.459]

AM1241 (360) exhibited high affinity and selectivity for CB2 [it (CBi) = 280 nM, (CB2) = 3.4 nM]. (360) Dose dependently inhibited experimental neuropathic pain in a spinal nerve ligation-induced tactile and thermal hypersensitivity model [224]. Other indole derivatives bearing sulfonamide moieties on the side chain, such as compound (361), were disclosed [225]. Though 67 derivatives including pyridyl and other heteroaromatics instead of the indole core were listed, no specific biological data were shown. [Pg.266]

A highly complex network of arteries, arterioles, and capillaries penetrates the dermis from below and extends up to the surface of, but not actually into, the epidermis. A matching venous system siphons the blood and returns it to the central circulation. Blood flow through the vasculature is linked to the production and movement of lymph through a complementary dermal lymphatic system. The dermis is laced with tactile, thermal, and pain sensors. [Pg.195]

Primary sensory neurons sense pain and convey it to the spinal cord. Nociceptors have unmyelinated (C fiber) or thinly myelinated (AS) axons, while the low-threshold Ap-fiber mechanoreceptors involved in tactile and proprioceptive perception have large myelinated sensory neurons (Table 57-1). The peripheral terminals of primary sensory neurons convert changes in the environment into neuronal activity by transducing mechanical (Ch. 51), thermal or chemical stimuli into ion fluxes across their... [Pg.928]

Features of central sensitization are pain in response to normally innocuous tactile stimuli, and the spread of pain sensitivity beyond the site of tissue injury. Central sensitization plays a major role in acute post-traumatic pain, and also in migraine, neuropathic pain (see below) and some diffuse chronic pain syndromes, such as fibromyalgia and irritable bowel syndrome. In these conditions, which have no detectable peripheral trigger, an autonomous central sensitization may be the pathology, increasing the gain in neuronal activity in the CNS and thereby producing abnormal responses to normal inputs. [Pg.933]

Ectopic activity in C fibers elicits central sensitization in the dorsal horn, contributing to the generation of tactile allodynia, a prominent feature of neuropathic pain. [Pg.936]

Equilibrium changes, vision disorders, pain disorders, tactile disorders, auditory disorders... [Pg.185]

Anaesthesia Loss of feehng or sensation. Although the term is used for loss of tactile sensibihty, or of any of the other senses, it is apphed espedally to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU]... [Pg.74]

Compounds with moderate p-affinities are very potent in a variety of pain models in mice and rats. In addition to antinociceptive efficacy in models of acute pain (tail flick, writhing) these compounds inhibit acute and persistent inflammatory pain (Randall Selitto, formalin test). Furthermore, they show strong inhibition of acute visceral pain (colorectal distension) and of tactile and cold allodynia in models of neuropathic pain (spinal nerve ligation (Chung), chronic constriction injury (Bennett)). The data suggest these compounds to be potential candidates for the management of clinical pain indications. Somatic and visceral pain with and without inflammatory conditions as well as neuropathic pain might be addressed with this approach. [Pg.361]

Nerve injury, followed by pain related behaviour, is induced by loose ligation of the ischiatic nerve of one hind paw of the rat. 3-4 weeks after ligation, neuropathic pain-like behaviour is seen as increased sensitivity towards heat and pressure stimuli (hyperalgesia). Also pain reactions toward non-noxious tactile (mechanical allodynia) or cold stimuli (cold allodynia) can be observed. Mechanical allodynia is tested with von Frey hairs and cold allodynia by putting the animals on metal plate cooled to 4 °C. The number of paw liftings is counted (Bennett and Xie, Pain 1988, 33, 87-107). [Pg.579]

Chung model of neuropathic pain Nerve injury in rats is induced by a tight ligation of the root of the spinal nerve at L5-L6. Animals show hyperalgesia and allodynia similar to the Bennet model. Tactile allodynia, measured with von Frey hairs, is the most reliable parameter of pain intensity in this model (Kim and Chung, Pain 1992, 50, 355-363). [Pg.580]

Olfactory, visual, auditory, vestibular and tactile functioning and pain and temperature sensitivity should all be tested. Not only the presence or absence of sensory functioning, but also the range of sensitivity should be investigated. For instance, not only the capacity to hear is Important, but also the range of frequencies that can be detected. There are tests for most aspects of sensory capacity, several of vhich can be used in their present form in young rat pups (see e.g. refs. 109, 136, 177, 182, 186, 188). [Pg.300]

Morita, K., Kitayama, T., Morioka, N., and Dohi, T. (2008). Glycinergic mediation of tactile allodynia induced by platelet-activating factor (PAF) through glutamate-NO-cyclic GMP signalling in spinal cord in mice. Pain 138, 525—536. [Pg.217]

While a single administration had no effect on pain behavior measured by sensitivity to mechanical stimulation (Fig. 1A), repeated treatment with linalool, 1 h before L5 ligation and then daily for 7 days, attenuated tactile allodynia reaching statistical significance at day 7 (Fig. IB). A prolonged treatment with linalool for up to 14 consecutive days showed similar results and did not ameliorate further hypersensitivity induced by SNL (data not shown). This suggests that... [Pg.231]

Liu, C. N., Wall, R D., Ben-Dor, E., Michaelis, M., Amir, R., and Devor, M. (2000). Tactile allodynia in the absence of C-fiber activation Altered firing properties of DRG neurons following spinal nerve injury. Pain 85, 503-521. [Pg.234]

Other chemical sensations associated with the trigeminal ganglion include temperature sensations such as the coolness (35) associated with menthol and the heat associated with capsaisin. Oral sensations elicited by chemical solutions also include tactile sensations such as smooth, dry, or powdery, and such disagreeable sensations as pain. Some of these sensations may represent different degrees of activation of a single system or the activation of several separate systems. [Pg.16]


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See also in sourсe #XX -- [ Pg.31 ]




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