![]() ![]() Even the most distal PNS lesion can affect the spinal cord and then the brain to cause NI. ![]() Lesions anywhere in the PNS appear capable of causing NI, whether distally (axonopathy) or centered on the sensory ganglion (e.g., shingles) or the proximal nerve roots. ![]() Lesions that primarily affect motor neurons, amyotrophic lateral sclerosis, for instance, are not associated with NI. Many patients present with pain alone, or pain plus itch, but some report only itch, for unknown reasons. Neuropathic itch is caused by the same type of neurological injuries and diseases that cause neuropathic pain as well. Neuropathological study shows clearly that injury to specific neurons is necessary to produce itch, namely, to the subset of sensory small fibers that encode itch signals, which includes C-fiber and A-delta primary afferents with various transduction patterns ( Chapter 9). Peripheral nervous system (PNS) lesions appear to be the most common causes of NI, most likely because these are more common than injuries to the well-protected central nervous system (CNS). For instance, applying 7T magnetic resonance imaging (MRI) to the spinal cord of a patient with NI after cavernous hemangioma (see below) suggested the hypothesis that his late-onset central itch might be triggered by delayed white matter degeneration ( Cohen-Adad et al. Better visualization of white matter tracts is particularly relevant for network disorders such as NI. As imaging methods advance, it should improve our understanding of the pathways and mechanisms of NI. A stroke, tumor, or multiple sclerosis plaque in the same brain region will generate similar signs and symptoms. As always, the cause of the lesion is less important than its location. Studying patients has demonstrated that NI is caused by lesions that specifically affect itch neurons, just as other neurological symptoms reflect the functions of the specific neurons damaged. The relevant methods include localization by neurological examination, imaging ( Chapter 24), and rarely, anatomical or surgical pathology. Regarding pruritus, the causal pathologies are even less defined than for neuropathic pain, so the author favors the less restrictive IFSI definition of neuropathic itch that permits “disorders” as well as “diseases” of the nervous system.Īs is typical in neurology, discovering the anatomical pathways for normal itch sensation has been aided by studying patients with neurological diseases or injuries that caused their itch. The requirement for a structural abnormality is problematic because in many patients, the causal lesions can often be hard to localize, meaning that they therefore no longer qualify as having neuropathic pain ( Jensen et al. 212) that defined neuropathic pain more broadly, specifically as “pain initiated or caused by a primary lesion or dysfunction in the nervous system.” In the 2012 version, “dysfunction” has been removed and a lesion or disease affecting the nervous system is now required. This replaces the definition in the IASP’s Classification of Chronic Pain ( Merskey and Bogduk 1994, p. From the neurological perspective, NI is primarily a modality-specific sensory hallucination, and the literature on other types of sensory hallucinations, e.g., tinnitus, the Charles Bonnet syndrome, phantom pain (recently reviewed in Sacks ) can help inform understanding.Īt the time of this writing, pain specialists are digesting 2012 revisions by the International Association for the Study of Pain (IASP) to their definition of neuropathic pain, which restricts it to “pain caused by a lesion or disease of the somatosensory system” ( ). nerve damage, nerve compression, nerve irritation” ( Ständer et al. Etiology Category III (NI) is defined as “arising from diseases or disorders of the central or peripheral nervous system, e.g. The International Forum for the Study of Itch (IFSI) recognizes four types of itch causality-dermatologic, systemic, neurologic, and psychiatric ( Ständer et al. At a practical level, NI can only be diagnosed after dermatological and systemic causes have been excluded, so dermatological evaluation should usually precede referral to a neurologist. In other words, there is uncoupling of the stimulus-response curve for itch sensation since dysfunction or disease of itch-signaling neurons is causing them to fire without cause. NI is thus defined as perception of itch in the absence of pruritogenic stimuli (formerly known to dermatologists as pruritus sine materia). The epistemology of neuropathic itch (NI) is based on that of neuropathic pain, which has so far worked well, no doubt because most peripheral itch neurons are a subset of peripheral pain neurons. ![]()
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