Sonographic assessment of nerve blood flow in diabetic neuropathy

2019 ◽  
Vol 37 (2) ◽  
pp. 343-349
Author(s):  
A. A. Borire ◽  
T. Issar ◽  
N. C. Kwai ◽  
L. H. Visser ◽  
N. G. Simon ◽  
...  
Diabetes Care ◽  
1995 ◽  
Vol 18 (8) ◽  
pp. 1160-1167 ◽  
Author(s):  
M. Nagamatsu ◽  
K. K. Nickander ◽  
J. D. Schmelzer ◽  
A. Raya ◽  
D. A. Wittrock ◽  
...  

2016 ◽  
Vol 02 (01) ◽  
pp. E13-E18 ◽  
Author(s):  
L. Risch ◽  
M. Cassel ◽  
J. Messerschmidt ◽  
K. Intziegianni ◽  
K. Fröhlich ◽  
...  

2015 ◽  
Vol 56 (12) ◽  
pp. 7286 ◽  
Author(s):  
Grant Cull ◽  
Reinhard Told ◽  
Claude F. Burgoyne ◽  
Simon Thompson ◽  
Brad Fortune ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Katherine E. Wilson ◽  
Jimmy Tat ◽  
Peter J. Keir

Purpose. The purpose of this study was to assess nerve hypervascularization using high resolution ultrasonography to determine the effects of wrist posture and fingertip force on median nerve blood flow at the wrist in healthy participants and those experiencing carpal tunnel syndrome (CTS) symptoms. Methods. The median nerves of nine healthy participants and nine participants experiencing symptoms of CTS were evaluated using optimized ultrasonography in five wrist postures with and without a middle digit fingertip press (0, 6 N). Results. Both wrist posture and fingertip force had significant main effects on mean peak blood flow velocity. Blood flow velocity with a neutral wrist (2.87 cm/s) was significantly lower than flexed 30° (3.37 cm/s), flexed 15° (3.27 cm/s), and extended 30° (3.29 cm/s). Similarly, median nerve blood flow velocity was lower without force (2.81 cm/s) than with force (3.56 cm/s). A significant difference was not found between groups. Discussion. Vascular changes associated with CTS may be acutely induced by nonneutral wrist postures and fingertip force. This study represents an early evaluation of intraneural blood flow as a measure of nerve hypervascularization in response to occupational risk factors and advances our understanding of the vascular phenomena associated with peripheral nerve compression.


1994 ◽  
Vol 266 (6) ◽  
pp. E980-E985 ◽  
Author(s):  
M. Kihara ◽  
P. J. Zollman ◽  
I. L. Smithson ◽  
T. D. Lagerlund ◽  
P. A. Low

Insulin administration can cause or worsen experimental and human diabetic neuropathy ("insulin neuritis"). In this study, we tested the hypothesis that insulin administration impairs tissue oxygenation. We infused insulin under nonhypoglycemic conditions and evaluated its effect on endoneurial oxygen tension, nerve blood flow, and the oxyhemoglobin dissociation curve of peripheral nerve in normal and diabetic rats. Intravenous insulin infusion resulted in a dose-dependent reduction in endoneurial oxygen tension in normal nerves (from 26% at 0.04 U/kg insulin to 55% at 32 U/kg). The nerves of rats with streptozotocin-induced diabetes were resistant, but with control of hyperglycemia this susceptibility to the endoneurial hypoxic effect of insulin returned. The reduction in endoneurial oxygen tension regressed with glycosylated hemoglobin (Y = 53.8-2.7X, where Y = %reduction in endoneurial oxygen tension and X = HbA1; r = 0.87; P = < 0.001). Diabetes or insulin administration resulted in only minimal and physiologically insignificant alterations in the oxygen dissociation curve and 2,3-diphosphoglycerate of sciatic nerve. Instead, insulin administration resulted in a reduction in nerve nutritive blood flow and an increase in arteriovenous shunt flow. When the latter was eliminated by the closure of arteriovenous shunts (infusion of 5-hydroxytryptamine), endoneurial oxygen reverted to normal. These findings indicate a deleterious vasoactive effect of insulin and may explain the development of insulin neuritis.


Diabetologia ◽  
1984 ◽  
Vol 27 (6) ◽  
pp. 563-567 ◽  
Author(s):  
A. G. Archer ◽  
V. C. Roberts ◽  
P. J. Watkins

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