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Sural Nerve Haemodynamics In Painful And Painless Neuropathy: Clues To The Cause Of Pain?
Author(s) -
Eaton Sem,
Ibrahim S,
Harris Nd,
Selmi F,
Patel Ka,
Tesfaye S,
Ward Jd
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.1529-8027.2000abstracts-21.x
Subject(s) - medicine , sural nerve , anesthesia , diabetic neuropathy , hemodynamics , neuropathic pain , polyneuropathy , pathogenesis , peripheral neuropathy , diabetes mellitus , surgery , endocrinology
Despite extensive research the cause of painful diabetic neuropathy remains elusive. Vascular factors and nerve hypoxia are known to be important in the pathogenesis of diabetic neuropathy although their contribution to painful neuropathy has not been fully determined. Using a combination of microlightguide spectrophotometry and fluorescein angiography we have recently confirmed that sural nerve intracapillary oxygen saturation and blood flow are reduced in diabetic neuropathy. We have applied these techniques to examine differences between painful and painless diabetic neuropathy by comparing 11 patients with pain to 8 patients without. There were no significant differences in neurophysiological parameters in each group. Intracapillary oxygen saturation (%HbO 2 ) was significantly higher in those subjects with painful symptoms compared to those without (median values 73.8% vs 67.7%, p < 0.05). Fluorescein rise time (FRT) was also significantly faster in those with painful neuropathy (18.3 vs 53.6 seconds, p < 0.05). These results indicate that there are distinct differences in sural nerve haemodynamics between painful and painless neuropathy. The higher %HbO 2 and faster FRT suggest the nerve is not hypoxic in painful neuropathy. These results would suggest that haemodynamic factors might have an important role in the pathogenesis of neuropathic pain.