TY - JOUR
T1 - A controlled investigation of the cause of chronic idiopathic axonal polyneuropathy
AU - Hughes, R A C
AU - Umapathi, T
AU - Gray, I A
AU - Gregson, N A
AU - Noori, M
AU - Pannala, A S
AU - Proteggente, A
AU - Swan, A V
PY - 2004/8
Y1 - 2004/8
N2 - To investigate the aetiology of chronic idiopathic axonal polyneuropathy (CIAP), 50 consecutive patients were compared with 50 control subjects from the same region. There were 22 patients with painful neuropathy and 28 without pain, 26 with sensory neuropathy and 24 with sensory and motor neuropathy. The typical picture was a gradually progressive sensory or sensory and motor neuropathy. It caused mild or sometimes moderate disability, and. reduced the quality of life. There was no evidence that alcohol, venous insufficiency, arterial disease or antibodies to peripheral nerve antigens played a significant part. There was a possible history of peripheral neuropathy in the first or second-degree relatives of six patients and no controls (P=0.01), and claw toes were present in 12 patients and four controls (P=0.03). Thirty-two per cent of the patients and 14% of the controls had impaired glucose tolerance or fasting hyperglycaemia but, after adjusting for age and sex, the difference was not significant (P=0.45), even in the painful neuropathy subgroup. The mean (SD) fasting insulin concentrations were significantly (P=0.01) higher in the patients [75.9 (44.4) mmol/l] than the controls [47.3 (37.9) mmol/l], and the mean was higher still in the painful neuropathy subgroup [92.2 (37.1) mmol/l] (P
AB - To investigate the aetiology of chronic idiopathic axonal polyneuropathy (CIAP), 50 consecutive patients were compared with 50 control subjects from the same region. There were 22 patients with painful neuropathy and 28 without pain, 26 with sensory neuropathy and 24 with sensory and motor neuropathy. The typical picture was a gradually progressive sensory or sensory and motor neuropathy. It caused mild or sometimes moderate disability, and. reduced the quality of life. There was no evidence that alcohol, venous insufficiency, arterial disease or antibodies to peripheral nerve antigens played a significant part. There was a possible history of peripheral neuropathy in the first or second-degree relatives of six patients and no controls (P=0.01), and claw toes were present in 12 patients and four controls (P=0.03). Thirty-two per cent of the patients and 14% of the controls had impaired glucose tolerance or fasting hyperglycaemia but, after adjusting for age and sex, the difference was not significant (P=0.45), even in the painful neuropathy subgroup. The mean (SD) fasting insulin concentrations were significantly (P=0.01) higher in the patients [75.9 (44.4) mmol/l] than the controls [47.3 (37.9) mmol/l], and the mean was higher still in the painful neuropathy subgroup [92.2 (37.1) mmol/l] (P
UR - http://www.scopus.com/inward/record.url?scp=4043171345&partnerID=8YFLogxK
U2 - 10.1093/brain/awh192
DO - 10.1093/brain/awh192
M3 - Article
SN - 1460-2156
VL - 127
SP - 1723
EP - 1730
JO - Brain
JF - Brain
IS - 8
ER -