S213
Track 2. Clinical Research & Care
P1122 Time Course of Risk Factors for Diabetic Foot Ulceration THOMAS K&iTENBAUER, Susanna Sauseng, Karl Irsigler. L. Boltumwm Institutefor Metabolic Diseases and Nutrition, Hospital L&z, Vienna. Austria
in each group. The results (expressed as mean (SD), * = pt0.05) summarised below:
Intracapillary oxygen saturation (76)
Fluoresceinrisetime(XC) Purpose: Sensory neuropathy and increased plantar pressure are the main risk factors for diabetic foot ulceration. The aim of the study was to analyze prospectively the time course of plantar pressure in type 2 diabetic patients over a mean period of 3.6 years. Methods: Out of an outpatient department, 187 type 2 diabetic patients (31 newly diagnosed type 2 diabetes), without a history of diabetic foot ulceration were recruited. Their mean age was 58.6f8.0 years and their mean HbAlc was 9.6f1.6%. At baseline and during the next 3 years, plantar pressure and peripheral neuropathy were investigated yearly. Mean plantar pressure (MPP) was measured by pedography (Novel, Munich), peripheral neuropathy was assessed by peroneal nerve conduction, clinical foot inspection (signs and symptoms), and vibration perception threshold (VPT) at the great toe. Patients were assigned to 2 subgroups, according to their baseline VPT: with neuropathy (NP): VPT 125volts. n=41, and without NPVPT <25volts, n=l 10. One-hundred fifty-one (81%) subjects completed the study. Results: In general, MPP did increase during the study. The change of MPP in percent at the hallux was for patients with NP +17% (not significant (ns), repeated measures ANOVA) and +2% (ns) in subjects without NP. The respective percentages for other sites were; lesser toes: +38% (p
P1123 Sural Nerve Haemodynamics in Painful and Painless Neuropathy: Clues to the Cause of Pain? SIMON E.M. EATON’, Nigel D. Harris’, Sharaf Ibrahim’, Kirtik A. Pate1 3, Fahid Selmi 4, Solomon Tesfaye ’ , John D. Ward ’ ’ Diabetes Research Unit, ‘Dept. of Medical Physics, 3 Dept. of Surgery, 4 Dept. of Neurosurgery Royal Hallamshire Hospital, Shefield. United Kingdom Morphological analyses of the peripheral nerve have shown no consistent differences that can differentiate between painful and painless neuropathy. Vascular factors and nerve hypoxia are known to be important in the patbogenesis of diabetic neuropathy although their contribution to painful neuropathy has not been fully established. 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
Painful
Painless
74.1(3.3) 24.9(18.1)
67.4(6.5)* 51.0(22.9)*
are
These results indicate that there are distinct differences in sural nerve haemodynamics between painful and painless neuropathy. The significantly higher intracapillary oxygen saturation and faster fluorescein rise time in those with painful symptoms would suggest improved nerve blood flow and less hypoxia in this group. These results would therefore suggest that haemodynamic factors might have an important role in the pathogenesis of neuropathic pain. These findings have implications for the further study and potential treatments of painful diabetic neuropathy.
P1124 Evidence of Spinal Cord Atrophy in Diabetic Peripheral Neuropathy SIMON E.M. EATON’, Nigel D. Harris’, Pam Greenwood3, Iain A. Wtlkinson3, Paul D. Griffiths3, Satyan M. Rajbhandari ‘, Solomon Tesfaye’, John D. Ward’. ‘DiabetesResearch Unit, Royal Hallamshire Hospital, Shefield, United Kingdom: 2 Dept of Medical Physics, Royal Hallamshire Hospital, Shefield, United Kingdom; 3Academic Department of Radiology, University Of Sheffield Diabetic neuropathy (DN) has hitherto been considered to be a disease of the peripheral nerve, involvement of the spinal cord having been largely overlooked. We have assessed the spinal cord in DN using magnetic resonance imaging. TZweighted axial images were taken at three anatomical levels (C4/5, T3/4 and T9/10) in 19 subjects with DN (9 with chronic pain and 10 without), 10 subjects with diabetes and no neuropathy and 10 normal healthy controls. The results for each anatomical level (in mm2) are expressed in the table below (as mean (SD), * = pt0.05, ** = p
c4/5 T3/4 T9llO
COllVOlS
Neuropathy
Non-Neuropathy
99.9 (8.7) 57.3(3.3) 55.0(5.9)
86.9(8.5)** 51.9(6.1)* 53.0(7.2)
92.9(10.7) 56.5(6.7) 54.2(3.0)
Cord cross-sectional area was significantly lower in DN compared to controls at both C4/5 and T3/4. No significant differences were seen at T9/10 or between the painful and painless neuropathy subgroups. Spinal cord atrophy (defined as area less than 2SD below the mean of controls) was found in 9/19 (47%) of neuropathic subjects indicating significant, and potentially irreversible, disease in these subjects. This is the first time that clear involvement of the spinal cord has been demonstrated in diabetic peripheral neuropathy. These results may have implications to both the patbogenesis and treatment of this condition.
P1125 Microcirculatory Responses to Electrical Spinal Cord Stimulation in Painful Diabetic Neuropathy and Other Painful Conditions SIMON E.M. EATON ’ , Nigel D. Harris I, Fahid Selmi ’ , Kirtik A. Pate1 ’ , Ian A. MacFarlane’, John D. Ward’, Solomon Tesfaye’. ‘Diabetes Research Unit, Royal Hallamshire Hospital, Shefield, United Kingdom; 2 Diabetes Centre, Walton Hospital, Liverpool, United Kingdom Electrical spinal cord stimulation (ESCS) has been shown to be effective in reducing pain in a number of conditions, including painful diabetic neuropathy (PDN). ESCS has also been shown to increase microvascular blood flow in peripheral vascular disease. We hypothesised that if nerve hypoxia contributes to pain in PDN, ESCS may relieve the pain by increasing nerve blood flow. We have therefore investigated skin and sural