AIMS/HYPOTHESIS: Although clear peripheral nerve pathological abnormalities have been demonstrated in diabetic peripheral neuropathy (DPN), there is little information with regard to brain involvement. Our aim was to use in vivo proton magnetic resonance specroscopy (H-MRS) in patients with DPN in order to assess the neuro-chemical status of the thalamus, which acts as the gateway to the brain for somatosensory information. METHODS: Participants included 18 type 1 diabetic men (eight without DPN, ten with DPN) and six non-diabetic healthy volunteers, who all underwent detailed clinical and neurophysiological assessments yielding a Neuropathy Composite Score (NCS) derived from Neuropathy Impairment Score of the Lower Limbs plus seven tests of nerve function prior to investigation via a single-voxel H-MRS technique, which was used to sample ventral posterior thalamic parenchyma. Spectroscopic resonances including those due to N-acetyl aspartate (NAA) were assessed at both short and long echo-time, providing putative indicators of neuronal function and integrity, respectively. RESULTS: At long echo-time we observed significantly lower NAA:creatine (p = 0.04) and NAA:choline (p = 0.02) ratios in DPN patients than in the other groups. No group differences were detected at short echo-time. We found a significant positive association between both sural amplitude (rho = 0.61, p = 0.004) and nerve conduction velocity (r = 0.58, p = 0.006) and NAA:creatine signal among participants with diabetes. Vibration detection threshold (rho = -0.70, p = 0.004) was significantly related to NAA:choline ratio. Heart rate variability with deep breathing (rho = -0.46, p = 0.05) and NCS (rho = -0.53, p = 0.03) were significantly related to NAA:creatine ratio. CONCLUSIONS/ INTERPRETATION: The significantly lower NAA:creatine ratio in DPN is suggestive of thalamic neuronal dysfunction, while the lack of difference in short echo-time between the groups does not suggest neuronal loss. Taken together with the observed correlations between NAA and neurophysiological assessments, these findings provide evidence for thalamic neuronal involvement in DPN.
AIMS/HYPOTHESIS: Although clear peripheral nerve pathological abnormalities have been demonstrated in diabetic peripheral neuropathy (DPN), there is little information with regard to brain involvement. Our aim was to use in vivo proton magnetic resonance specroscopy (H-MRS) in patients with DPN in order to assess the neuro-chemical status of the thalamus, which acts as the gateway to the brain for somatosensory information. METHODS:Participants included 18 type 1 diabeticmen (eight without DPN, ten with DPN) and six non-diabetic healthy volunteers, who all underwent detailed clinical and neurophysiological assessments yielding a Neuropathy Composite Score (NCS) derived from Neuropathy Impairment Score of the Lower Limbs plus seven tests of nerve function prior to investigation via a single-voxel H-MRS technique, which was used to sample ventral posterior thalamic parenchyma. Spectroscopic resonances including those due to N-acetyl aspartate (NAA) were assessed at both short and long echo-time, providing putative indicators of neuronal function and integrity, respectively. RESULTS: At long echo-time we observed significantly lower NAA:creatine (p = 0.04) and NAA:choline (p = 0.02) ratios in DPNpatients than in the other groups. No group differences were detected at short echo-time. We found a significant positive association between both sural amplitude (rho = 0.61, p = 0.004) and nerve conduction velocity (r = 0.58, p = 0.006) and NAA:creatine signal among participants with diabetes. Vibration detection threshold (rho = -0.70, p = 0.004) was significantly related to NAA:choline ratio. Heart rate variability with deep breathing (rho = -0.46, p = 0.05) and NCS (rho = -0.53, p = 0.03) were significantly related to NAA:creatine ratio. CONCLUSIONS/ INTERPRETATION: The significantly lower NAA:creatine ratio in DPN is suggestive of thalamic neuronal dysfunction, while the lack of difference in short echo-time between the groups does not suggest neuronal loss. Taken together with the observed correlations between NAA and neurophysiological assessments, these findings provide evidence for thalamic neuronal involvement in DPN.
Authors: I D Wilkinson; S Lunn; K A Miszkiel; R F Miller; M N Paley; I Williams; R J Chinn; M A Hall-Craggs; S P Newman; B E Kendall; M J Harrison Journal: J Neurol Neurosurg Psychiatry Date: 1997-10 Impact factor: 10.154
Authors: I D Wilkinson; M N Paley; M A Hall-Craggs; R J Chinn; W K Chong; B J Sweeney; B E Kendall; R F Miller; S P Newman; M J Harrison Journal: Magn Reson Imaging Date: 1996 Impact factor: 2.546
Authors: Lijun Qiu; Xiangliang Tan; Mengchen Zou; Binchang Lao; Yikai Xu; Yaoming Xue; Fang Gao; Ying Cao Journal: Nan Fang Yi Ke Da Xue Xue Bao Date: 2018-12-30
Authors: Myria Petrou; Rodica Pop-Busui; Bradley R Foerster; Richard A Edden; Brian C Callaghan; Steve E Harte; Richard E Harris; Daniel J Clauw; Eva L Feldman Journal: Acad Radiol Date: 2012-05 Impact factor: 3.173
Authors: Silvia Mangia; Anjali F Kumar; Amir A Moheet; Rachel J Roberts; Lynn E Eberly; Elizabeth R Seaquist; Ivan Tkáč Journal: J Cereb Blood Flow Metab Date: 2013-02-13 Impact factor: 6.200