Neurophysiological and neurochemical basis of modern pruritus treatment

被引:79
作者
Staender, Sonja [1 ]
Weisshaar, Elke [2 ]
Luger, Thomas A. [1 ]
机构
[1] Univ Munster, Dept Dermatol, Clin Neurodermatol, D-48149 Munster, Germany
[2] Heidelberg Univ, Dept Social Med, Heidelberg, Germany
关键词
central nervous system; itch; neuroreceptors; pruritus; therapy;
D O I
10.1111/j.1600-0625.2007.00664.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 [皮肤病与性病学];
摘要
Chronic pruritus of any origin is a frequent discomfort in daily medical practice, and its therapy is challenging. Frequently, the underlying origin may not be identified and symptomatic therapy is necessary. Conventional treatment modalities such as antihistamines often lack efficacy, and hence new therapeutic strategies are necessary. The neuronal mechanisms underlying chronic pruritus have been partly identified during the past years and offer new therapeutic strategies. For example, mast cell degranulation, activation of neuroreceptors on sensory nerve fibres and neurogenic inflammation have been identified to be involved in induction and chronification of the symptom. Accordingly, controlling neuroreceptors such as cannabinoid receptors by agonists or antagonists showed high antipruritic efficacy. Pruritus is transmitted to the central nervous system by specialized nerve fibres and sensory receptors. It has been demonstrated that pruritus and pain have their own neuronal pathways with broad interactions. Accordingly, classical analgesics for neuropathic pain (gabapentin, antidepressants) also exhibit antipruritic efficacy upon clinical use. In summary, these recent developments show that highlighting the basis of pruritus offers modern neurophysiological and neurochemical therapeutic models and the possibility to treat patients with refractory itching of different origin.
引用
收藏
页码:161 / 169
页数:9
相关论文
共 85 条
[1]
Induction of CB1 cannabinoid receptor by inflammation in primary afferent neurons facilitates antihyperalgesic effect of peripheral CB1 agonist [J].
Amaya, Fumimasa ;
Shimosato, Goshun ;
Kawasaki, Yasuhiko ;
Hashimoto, Satoru ;
Tanaka, Yoshifumi ;
Ji, Ru-Rong ;
Tanaka, Masaki .
PAIN, 2006, 124 (1-2) :175-183
[2]
Inhibitory effect of loratadine on leukotriene B4 production by neutrophils either alone or during interaction with human airway epithelial cells [J].
Amsellem, C ;
Czarlewski, I ;
Lagarde, M ;
Pachéco, Y .
PULMONARY PHARMACOLOGY & THERAPEUTICS, 1998, 11 (04) :245-252
[3]
Inhibitory effects of azelastine on substance P-induced itch-associated response in mice [J].
Andoh, T ;
Kuraishi, Y .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2002, 436 (03) :235-239
[4]
Intradermal leukotriene B4, but not prostaglandin E2, induces itch-associated responses in mice [J].
Andoh, T ;
Kuraishi, Y .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1998, 353 (01) :93-96
[5]
Spinothalamic lamina I neurons selectively sensitive to histamine: a central neural pathway for itch [J].
Andrew, D ;
Craig, AD .
NATURE NEUROSCIENCE, 2001, 4 (01) :72-77
[6]
Involvement of histamine H4 and H1 receptors in scratching induced by histamine receptor agonists in BalbC mice [J].
Bell, JK ;
McQueen, DS ;
Rees, JL .
BRITISH JOURNAL OF PHARMACOLOGY, 2004, 142 (02) :374-380
[7]
Pregabalin pharmacology and its relevance to clinical practice [J].
Ben-Menachem, E .
EPILEPSIA, 2004, 45 :13-18
[8]
Oral nalmefene therapy reduces scratching activity due to the pruritus of cholestasis: A controlled study [J].
Bergasa, NV ;
Alling, DW ;
Talbot, TL ;
Wells, MC ;
Jones, EA .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1999, 41 (03) :431-434
[9]
Bernet D, 2002, BULL EUR ASSN FISH P, V22, P229
[10]
EFFECTS OF MENTHOL AND COLD ON HISTAMINE-INDUCED ITCH AND SKIN REACTIONS IN MAN [J].
BROMM, B ;
SCHAREIN, E ;
DARSOW, U ;
RING, J .
NEUROSCIENCE LETTERS, 1995, 187 (03) :157-160