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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Itch sensation can be inhibited by simultaneously applied cutaneous pain at the same skin site via a central mechanism. Deep muscle pain is often associated with sensory changes in the corresponding dermatome. We investigated whether experimentally induced muscle pain has any influence on histamine-induced itch and vice versa in a double blind placebo-controlled study. Experiments were performed in 18 healthy subjects. In nine individuals control iontophoresis of histamine into the forearm produced a distinct itch sensation. Another nine individuals participated in an additional experiment in which histamine and saline were iontophoresed on the forearm in a randomized double-blinded two-way crossover design after intramuscular injection of capsaicin into the ipsilateral brachioradial muscle. Capsaicin-induced muscle pain reduced itch sensation significantly. In contrast, capsaicin-induced muscle pain increased significantly after cutaneous histamine application compared to muscle pain after iontophoresis of saline (placebo). These novel data indicate that muscle pain inhibits itch and histamine increases muscle pain. A bi-directional interaction between cutaneous histamine-sensitive afferents and nociceptive muscle afferents via central mechanisms is suggested.
Eur J Pain 2004 Jun
PMID:Interaction between histamine-induced itch and experimental muscle pain. 1510 68

We compared itch sensations and axon reflex flare induced by transcutaneous electrical (0.08-8 ms, 2-200 Hz) and chemical (histamine iontophoresis; 100 microC) stimulation. Stimuli were applied to non-lesional volar wrist skin in 20 healthy human subjects and 10 patients with atopic dermatitis. Intensity of evoked itch and pain sensations were rated on a numerical rating scale (NRS) of 0 (no sensation) to 10 (the maximum sensation imaginable). The axon reflex erythema was measured by laser Doppler imager and areas of alloknesis (itch evoked by light brushing) and hyperknesis (itch evoked by pricking) were assessed psychophysically. Electrical stimulation was most effective for stimulus durations >or=2 ms and frequencies >or=50 Hz. It evoked pure itch as threshold sensation in 80% of the subjects that was perceived with a delay of approximately 1 s. Itch intensities of up to 7/10 were not accompanied by an axon reflex flare. In contrast, histamine provoked a massive increase of axon reflex erythema and maximum itch ratings of 3.1+/-0.2. The extention of alloknesis areas (2.3+/-0.5 cm) evoked by electrical stimulation clearly exceeded those induced by histamine (0.7+/-0.3 cm). Healthy subjects and patients with atopic dermatitis did not differ significantly in their response to either stimulation. We conclude that C-fiber activation underlies the electrically evoked itch sensation. The low electrical thresholds and the absence of an axon reflex flare suggest that these fibers are not identical with the previously described mechano-insensitive histamine responsive C fibers, but represent a separate peripheral neuronal system for the induction of itch.
Pain 2005 Jan
PMID:Electrically evoked itch in humans. 1562 75

To our knowledge there are no studies evaluating the prevalence and characteristics of itch, pain, and burning sensation among patients with mild to moderate chronic venous insufficiency or assessing the impact of these symptoms on quality of life. In this report 100 patients met the inclusion criteria. Patients who suffered from itch were also assessed with the use of a validated questionnaire and a modified Skindex-16 questionnaire. We found that the prevalence of itch was 66%. Concomitant itch and burning sensation as well as itch and pain were noted in 47% and 44% of the patients, respectively. No correlation was noted between the severity of these symptoms and the degree of venous insufficiency. Itch had a negative impact on quality of life. A limitation of this study is that the participants, who were primarily hospital employees, are more likely to develop these symptoms. Therefore this study does not reflect the true prevalence of these symptoms in the general population. This study found that itch, pain, and burning sensation are common symptoms of mild to moderate chronic venous insufficiency with a significant impact on quality of life.
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PMID:Itch, pain, and burning sensation are common symptoms in mild to moderate chronic venous insufficiency with an impact on quality of life. 1611 63

Itch is one of the alarm sensations that human beings have phylogenetically evolved for a defense purpose. Many theories and evidences regarding the biological, pathophysiological, and clinical aspects have been given, but an update on the neuroanatomy paths and consequent treatments is required. Some chemicals that are released after skin injury and facilitate the inflammatory process can induce itch or pain or basically lead to a sensitization of the nociceptor response. In clinical practice, the present authors note a continuum of sensations from touch to pain, among which many metaesthetic sensations can be described, even if the patients themselves cannot precisely define them. The specificity of itch neurons is therefore based on their spinal connections to the itch pathway rather than on unique peripheral receptors. The ambiguity of "itch unit" discharge to pruritics and algogens may be solved by the central inhibition of itch by pain: it is common knowledge that scratching relieves itching. Conversely, centrally acting pain-inhibiting opioids enhance itch by disinhibition. The relation between itch and pain is interesting in its clinical and physiopathological aspects in order to select appropriate treatment.
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PMID:Itch, pain, and metaesthetic sensation. 1629 2

Itch features considerable interindividual variability in humans, and initial studies using animal models have demonstrated a likely role of genetic factors in mediating such variability. In an attempt to systematically study genetic mediation of itch in the mouse such that gene identification by linkage mapping might be achieved, we examined scratching behavior induced by histamine and chloroquine in mice of 11 inbred mouse strains. Multiple chloroquine drug doses were used, revealing the existence of inverted-U dose-response relationships in every strain, allowing us to determine strain-dependent peak scratching behavior over the entire dose range. Peak chloroquine-induced scratching varied by 2.5-fold in this set of strains; scratching behavior shows moderate heritability in the mouse. The present data also reveal, for the first time, significant sex differences in pruritogen-induced scratching behavior, with female mice scratching an average of 23% more than males. Finally, a comparison of the strain means obtained here with previously collected data using nociceptive assays revealed a suggestive negative genetic correlation between chloroquine-induced itch and thermal pain, such that strains sensitive to pain are resistant to itch and vice versa. This finding may have implications both for our understanding of itch pathophysiology and for the identification of itch-related genes.
Pain 2006 Sep
PMID:Influence of genotype, dose and sex on pruritogen-induced scratching behavior in the mouse. 1679 23

Histamine, substance P, serotonin and bradykinin were applied by iontophoresis to lesional and visually non-lesional skin of 14 patients with atopic dermatitis, and normal skin of 15 healthy volunteers. Itch could be evoked by light stroking of skin with a cotton swab (alloknesis) in all lesional skin sites, but not in non-lesional or normal skin. Substances were applied in the same skin area before and 3 h after administration of placebo or antihistamine (olopatadine hydrochloride: H1-receptor-blocker). Intensities of itch and pain sensation and areas of flare and wheal were measured. All the substances induced significantly more intense itch in lesional skin than in non-lesional skin of patients. Even bradykinin, which evoked only weak itch and pain of similar intensities in non-lesional skin of patients and in healthy volunteers, induced intense itch in lesional skin, while the simultaneously increased pain did not suppress the itch sensation, indicating central sensitization. Histamine- and substance P-induced itch was almost completely suppressed by antihistamines, whereas bradykinin- and serotonin-induced itch was not. This suggests that substance P is a histamine-dependent pruritogen also in lesional skin under sensitized conditions but that bradykinin and serotonin are histamine-independent pruritogens in lesional skin. It is concluded that serotonin and bradykinin, classic endogenous algogens, can turn into potent histamine-independent pruritogens in lesional skin of atopic dermatitis.
Pain 2006 Dec 15
PMID:Bradykinin is a potent pruritogen in atopic dermatitis: a switch from pain to itch. 1684 20

Itch is the major symptom of many allergic or inflammatory skin diseases; yet it is still difficult to measure objectively. Human studies on the physiology and pathophysiology of the itch sensation (e.g. functional magnetic resonance imaging studies) have been hampered by the lack of an efferent and manageable "on-off" stimulus. Here, a short-term temperature-modulated human histamine itch model is presented. In nine healthy right-handed male volunteers (age 29+/-2.6 years), 1% histamine dihydrochloride was used in the skin prick model as standard itch stimulus on the right forearm with subsequent thermal modulation of the target skin area using a Medoc TSA II NeuroSensory Analyzer thermode. Modulation occurred in rapid alternating order from 32 degrees C (neutral) to 25 degrees C (slight cold) and vice versa; each temperature block lasted 20 seconds. Subjective itch ratings were recorded using a computerized visual analog scale (VAS) and - for qualitative assessment - the Eppendorf Itch Questionnaire (EIQ). All subjects reported localized itch sensations without pain; mean VAS itch intensity was 50.6+/-3.5% during the 25 degrees C blocks and 33.8+/-3.9% during the 32 degrees C blocks (P<0.0001). Also, mean EIQ ratings were significantly higher related to the 25 degrees C blocks. In spite of the common knowledge that intensive cold can inhibit itch sensation, a reproducible, significant enhancement of histamine-induced itch by short-term moderate temperature decrease could be shown. This effect might be explained by peripheral and central adaptation processes triggered by alternating afferent activity patterns and might be used - owing to its "on/off" characteristics-in future itch physiology studies such as functional magnetic resonance imaging.
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PMID:Short-term alternating temperature enhances histamine-induced itch: a biphasic stimulus model. 1700 77

Itch and pain, like other sensations, serve as physiological self-protective mechanisms. However, in many clinical conditions, unrelieved itch and pain have potentially devastating effects on body functions. Thus, these two sensations present maladaptive phenomena. In this review, we present the neurophysiologic mechanisms of pruritus and pain, including their mutual interactions, but the accent is on causes, consequences and assessment of pruritus and pain in cancer patients. Understanding the mechanisms of pain and itch may optimize pain control in cancer patients amd enhance their quality of life.
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PMID:Neurophysiologic approach to pruritus and pain in cancer patients. 1731 63

Itch (pruritus) is a sensory phenomenon characterized by a (usually) negative affective component and the initiation of a special behavioral act, i.e. scratching. Older studies predominantly have interpreted itch as a type of pain. Recent neurophysiological findings, however, have provided compelling evidence that itch (although it indeed has intimate connections to pain) rather needs to be understood as a separate sensory modality. Therefore, a novel pruriceptive system has been proposed, within which itch-inducing peripheral mediators (pruritogens), itch-selective receptors (pruriceptors), sensory afferents and spinal cord neurons, and defined, itch-processing central nervous system regions display complex, layered responses to itch. In this review, we begin with a current overview on the neurophysiology of pruritus, and distinguish it from that of pain. We then focus on the functional characteristics of the large family of transient receptor potential (TRP) channels in skin-coupled sensory mechanisms, including itch and pain. In particular, we argue that - due to their expression patterns, activation mechanisms, regulatory roles, and pharmacological sensitivities - certain thermosensitive TRP channels are key players in pruritus pathogenesis. We close by proposing a novel, TRP-centered concept of pruritus pathogenesis and sketch important future experimental directions towards the therapeutic targeting of TRP channels in the clinical management of itch.
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PMID:TRP channels as novel players in the pathogenesis and therapy of itch. 1746 67

Functional brain imaging studies on itch usually use histamine as a stimulus and, in consequence, have to cope with the highly variable time course of this particular itch sensation. In this study, we describe a novel method of histamine application. To provoke itch, a mixture of histamine and codeine was applied through intradermally positioned microdialysis fiber. The itch was terminated by lidocaine application through the same fiber. During one fMRI session, this procedure was repeated four times in four different microdialysis fibers, including one placebo control. Itch ratings of the subjects were correlated with blood-oxygen-level-dependent (BOLD) effects. In a subsequent experiment performed in the same fMRI session, heat pain was provoked in the right forearm with a Peltier thermode. During both experiments, activation clusters were found in brain areas that have been described previously to be frequently activated in response to painful stimuli. This includes prefrontal areas, supplementary motor areas (SMA), premotor cortex, anterior insula, anterior midcingulate cortex, S1, S2, thalamus, basal ganglia, and cerebellum. In general, itch stimulation entailed more activation clusters, in particular on the contralateral brain side. Only on itch, but not on heat pain, negative BOLD signals were found in the subgenual anterior cingulate cortex and the amygdala. The latter results may be associated with the itch induced urge to scratch. Amygdala deactivation may be related to the preparation of scratching by aiming to dissolve the otherwise aversive effects of the noxious scratch stimuli. These negative BOLD effects may also be attributed to the stressful character of itch stimulation.
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PMID:Itch induced by a novel method leads to limbic deactivations a functional MRI study. 1771 98


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