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Ovid: Fifty Neurologic Cases from Mayo Clinic

Editors: Noseworthy, John H. Title: Fifty Neurologic Cases from Mayo Clinic, 1st Edition Copyright ©2004 Oxford Unversity Press (Copyright 2004 by Mayo Foundation for Medical Education and Research) > Table of Contents > Case 7: Eight years of pain, 1 year of itch Case 7: Eight years of pain, 1 year of itch CASE 7 History A 55-year-old woman presented with an 8-year history of a pain disorder. At onset, the pain was a sudden, constant burning sensation that involved an area the size of a U.S. $1 coin (about 2.5 cm) in the right groin. She had no aggravating or relieving factors and no allodynia. Three years after the onset of pain, she noted the sudden onset of “an electrical current” sensation involving the medial aspect of the left leg. The burning groin pain fluctuated, and later both sensations improved spontaneously. No functional deficit was apparent. Previous physicians had noted a minor degree of upper motor neuron weakness and left leg hyperreflexia only. Multiple medications and a transcutaneous electrical nerve stimulation unit had failed to help. One year after the spontaneous improvement, the right groin pain recurred in combination with a new symptom of an intense, distressing itching sensation involving the scapular region bilaterally. Multiple medications, including anticonvulsants, antidepressants, and opiate antagonists, failed to help, but a lidocaine transdermal patch controlled the itching. Examination Neurologic examination demonstrated hyperreflexia of the left leg, a left Babinski sign, and hypesthesia to pinprick and thermal stimuli in the right leg. Investigations Magnetic resonance imaging (MRI) was performed. P.26
DIAGNOSIS CASE 7 Central pain disorder: thoracic cavernous angioma
Commentary by Dr. Paola Sandroni MRI demonstrated a 12-mm minimally enhancing intramedullary lesion within the lower aspect of the thoracic cord suggestive of a cavernous angioma (Figure). Itching (or pruritus) is a sensation that generates an urge to scratch the affected area. Itch generally has been considered a form of pain because it can be as distressing as pain. Indeed, itching is conveyed by C fibers, as is pain sensation. No specific itch receptor is known, and the identity of a fiber population specific for itch is still uncertain. This population may be heterogeneous and consist of both itch-specific and polymodal fibers that also convey pain sensation but are exquisitely sensitive to histamine. Intraneural recordings have documented the existence of both fiber types. Exactly where these fibers end peripherally is not known, but most authors think they terminate in both the dermis and epidermis. The overlap of pain and itch peripherally also occurs, at least partly, centrally. Pain has two main pathways (one conveying highly discriminative information and the other conveying more diffuse sensation), but itch appears to have only one pathway. However, it is extremely difficult to study itch in isolation from pain. The scratch reflex, particularly in animals, supports the existence of a powerful integration center at the level of the spinal cord. It is at this level that the pathways for itch and pain likely diverge, as suggested by the opposite effect of opiates (i.e., with opiates, especially when adminstered intrathecally, pain decreases and itch increases). Otherwise, the same neurotransmitters that modulate pain can also modulate itch, particularly serotonin. Although the gate control theory was proposed to explain the modulation of pain sensation, it also applies to itch. The activation of large fibers by scratching is a powerful suppressor of itch. However, activation of thinly myelinated and unmyelinated fibers by cold, heat, and pain also can suppress itch, albeit transiently. Itch and pain almost never coexist in the same area; itch often precedes pain or, less commonly, alternates with it. In a positron emission tomographic study to identify the topographic representation of itch at the level of the cerebral cortex, mainly premotor areas were activated, suggesting that the study documented the basis of the “urge to scratch.” The cingulate cortex also was activated, suggesting the engagement of motivational-emotional and possibly P.27
autonomic systems in a reaction to the unpleasant itching experience. The activation of these systems may explain the curious need to scratch while watching someone else do so. Itch is associated most often with skin conditions, but it is not uncommonly associated with peripheral neuropathies. The few reports of itch caused by a central nervous system lesion included mainly demyelinating disorders or vascular injuries. In these conditions, itching usually is perceived in an area of sensory deficit, suggesting itch has a somatotopic distribution similar to that of the impaired modalities. The treatment of neuropathic itch is similar to that of neuropathic pain and includes such medications as serotonin-modulating agents, anticonvulsants, antidepressants, and capsaicin. Also, antihistamine agents and opiate antagonists (naltrexone) can be effective. The treatment of neuropathic itch with lidocaine has not been reported, although this agent is helpful in non-neuropathic itch. Because a lidocaine patch is effective in treating neuralgic syndromes (particularly postherpetic neuralgia, which also can manifest with intense itching), it would be expected that lidocaine would be helpful in treating neuropathic itch. Although little information is available about the management of central neuropathic itch, one would suspect it would be as challenging to manage as a central pain syndrome. The interesting aspect of the case presented here is the central origin of the symptoms, which usually implicates suppression of inhibitory circuits or spontaneous firing of deafferented neurons (or both). Thus, one would not predict a good response to treatment with a topical peripheral agent. The relief provided by the lidocaine patch suggests that peripheral input is critical in somehow modulating the activity of altered central pathways. P.28

FIGURE. Sagittal T2-weighted image of the thoracic spinal cord showing a peripheral rim of hemosiderin and central zone of increased T2 signal consistent with a cavernous hemangioma. The lesion was enhanced slightly after the administration of gadolinium.

REFERENCE Sandroni P. Central neuropathic itch: a new treatment option? Neurology 2002;59:778-9.

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