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DOES LOSS OF MEDIAN NERVE FIBRES INFLUENCE SPONTANEOUS PAIN OCCURRING IN PATIENTS WITH SEVERE CARPAL TUNNEL SYNDROME?
Author(s) -
Buonocore M.,
Bodini A.,
Mazzucchi G.,
Piazzoli S.,
Bagnasco R.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000.00513-7.x
Subject(s) - medicine , carpal tunnel syndrome , median nerve , hypesthesia , neuropathic pain , quantitative sensory testing , nociception , sensory system , anesthesia , peripheral , sensory nerve , carpal tunnel , sensory loss , surgery , neuroscience , psychology , receptor
Following peripheral nerve injury, a variety of mechanisms may generate and maintain pain. Pain mechanisms occurring in entrapment neuropathies are largely unknown. Many studies have related peripheral neuropathic pain to nerve fibre dysfunction. Aim of the study was to test the hypothesis of a possible role played by the loss of nerve fibres in the pathogenesis of pain occurring in patients with severe Carpal Tunnel Syndrome (CTS). Methods: Three consecutive patients (females) with severe monolateral CTS but not spontaneous pain were enrolled. Five females, age‐matched control patients with severe monolateral CTS and spontaneous pain, were also recruited. Severe CTS was confirmed by neurological examination and classified by nerve conduction studies (absence of peripheral sensory and motor evoked potentials). In order to assess small‐diameter fibres the Sympathetic Skin Response (SSR) evoked by auditory, alerting stimuli and recorded from the palm was also bilaterally tested. Results: Patients with and without spontaneous pain demonstrated the same clinical pattern of nerve fibre dysfunction. In particular, all patients had severe hypesthesia (tactile and vibratory) and hypalgesia (pinprick evaluation) over the second and third fingers (palmar surface), with an extension of sensory loss into the palm. Moreover, in all patients, SSR was always bilaterally and symmetrically present. Conclusion: These results failed to indicate a possible role of fibre loss (both large and small) of the median nerve in the pathogenesis of pain occurring in patients with severe CTS. Different pain mechanisms, both neuropathic and nociceptive, may be simultaneously present in any one patient. Studies on a large population of patients are needed.