cutaneous manifestations of neurological diseases- review of neuro-pathophysiology and diseases...

© 2005 European Society of Veterinary Dermatology 137 Veterinary Dermatology 2005, 16 , 137–146 BlackwellPublishing,Ltd. Review Cutaneous manifestations of neur ological diseases: re vie w of neuro-pathophysiology and diseases causing pruritus KIRSTEN GNIRS* and PASCAL PRÉLAUD† *3 rue du D auphiné, F-94100 Saint Maur des Fossés, France †17 rue Fernet, F-94700 Maisons-Alfort, France ( Received 16 June 2004; accepted 10 January 2004) Abstract Pruritus does not always originate from stimulation to the skin associated with primary der matolog- ical disorders. It may be caused by neurological or behavioural disorders . The essential role of the nervous system in the control (enhancement and inhibition) of pruritus and its pathophysiology are presented. In order to allow differentia tion between dermatological and neurological disorders, inherited or acquired peripheral neuropathies and central nervous disorders (Arnold–Chiari syndrome, seizure-related disorders, central nervous system tumours) that may induce itch are discussed. INTRODUCTION The majority of pruritic skin diseases in dogs and cats are caused by ectoparasitic infestations, bacterial and fungal infec tion or hypersensitivit ies. How ever , pruritus does not alwa ys originate from external stimulation to the skin, but can be caused by neurologi cal or behavioural disorders. The essential role of the peripheral and central nervous system in the control (enhancement and inhibition) of pruritus has been described. 1,2 The goal of this paper is to review the basic pathoph ys- iology of pruritus, predomina ntly that of neurological origin. It is hoped that this information will be useful in the clinical setting, allowing differentiation of patients with skin disease due to neurological causes from those with primary dermatological disorders . P athophysio logy of pruritus Pruritus or itching is defined c linically as an unpleasant sensation that causes an animal to rub, lick, chew, or scratch at its skin. 3 It is a physiological self-protectiv e mechanism and, similar to other cutaneous sensations such as pain, touch, perception of vibration, cold or heat, it helps to defend the skin against harm from the environment. Additionally, pruritus is a major sign of skin and some systemic diseases. Pruritus can be local- ized (acral lick dermatitis), regional (pedal pruritus) or generalized. Pruritus can be evok ed in the skin directly by mechanical and thermal s timuli or indirectly through chemical mediators. It may also occur as a result of peripheral nerve disease or be generated from the spinal cord or brain, independent of peripheral stimulation. Pruritus is not a disease, but a sign of an under- lying dermatological condition or neuro-psycholo gical disorder . Establishing what initiates the pruritus in an individual case requires evalua tion of multiple internal and external factors 4 that vary from condition to condition and animal to animal. 5 Pruritus vs. pain Pruritus and pain are both defined as signs resulting from an unpleasant sensation. Pain and itch are trans- mitted predominantly through slow-conducting, unmye- linated C-fibres. 6 One theory for pruritus was that it is a subliminal version of pain (intensity theory). Accord- ingly, weak noxious stimuli would cause minor activation of nociceptors, which would be felt as itch, whereas stronger noxious stimuli would activate nociceptors more intensely and provoke pain. 6 However, recent studies have clearly shown that there is a distinct neuronal pathway for itch, functionally separate from the pain pathway. Primary afferent nerve fibres that carry histamine-induced itch have been found in humans 7 and, more recen tly, spinal neu rones have been identified that respond specifically to histamine. 8 The combination of dedicated peripheral and central neurones, with a unique response pattern to pruritogenic mediators and anatomically distinct projections to the thalamus, provides the basis for a specific neuronal pathway for itch. Unfortunately, it has not yet been possible to morphologicall y differentiate neurones that mediate itch from those that mediate pain. However, there are complex interactions between pain and itch. There is not a complete distinction between pruritic and pain-producing (algogenic) substances in the activation of pruriceptors and nociceptors. The inhibition of itch by pain is well known and can explain the antipruritic effect of scratching. The opposite effect also exists and has clinical implications: inhibition of pain processing (e.g. by spinal opioids) can generate itch. 3 Conversely, blockade of spinal opioid receptors Correspondence: Kirsten Gnirs, 3 rue du Dauphiné, F-94100 Saint Maur des Fossés, France , E-mail: kgnirs@hotmail .com

cutaneous manifestations of neurological diseases- review of neuro-pathophysiology and diseases...

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