• T Rudolph and E Farbu.
• Department of Neurology, Stavanger University Hospital, Stavanger, Norway. ruth@sus.no
• Eur. J. Neurol. 2007 Jun 1;14(6):603-8.

AbstractThe aim of this study was to evaluate the causes, prevalences, clinical manifestations of hospital-referred polyneuropathies, and evaluate neurophysiological findings in idiopathic polyneuropathy. From 2000 to 2005, 226 patients with polyneuropathy were examined. Polyneuropathy was diagnosed when symptoms, clinical- and neurophysiological findings were compatible with affection of at least two peripheral nerves. They were classified in symptomatic and idiopathic polyneuropathy after investigation. Clinical manifestations were evaluated for diabetes- (DPN), inflammatory- (INPN), hereditary- (HPN) and idiopathic polyneuropathy (IDPN). Neurophysiological findings were investigated in IDPN. 72% had a symptomatic polyneuropathy. Most frequent causes were diabetes mellitus (18%), inflammation, (16%) and hereditary (14%). Most common prevalences per 100,000 were as follows: IDPN, 21; DPN, 13 and HPN, 11. Predominating clinical manifestations were: sensory and motor in INPN, HPN and IPN; sensory in DPN. Pain was more present in IDPN and DPN than in others. In IDPN axonal demyelinating affection was present in 20%. Symptomatic polyneuropathy was common and diabetes mellitus, inflammation and hereditary were frequent causes. In IDPN, DPN, HPN and INPN different clinical patterns were found. Additionally, in IDPN axonal demyelinating affection was more frequent than previously reported.

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