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  • 1
    Electronic Resource
    Electronic Resource
    Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study (1996)
    Springer
    Diabetologia 39 (1996), S. 1377-1384 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin-dependent diabetes mellitus ; diabetic neuropathy ; prevalence ; glycaemic control ; microalbuminuria ; impotence ; epidemiology.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The EURODIAB IDDM Complications Study involved the examination of 3250 randomly selected insulin-dependent diabetic patients, from 31 centres in 16 European countries. Part of the examination included an assessment of neurological function including neuropathic symptoms and physical signs, vibration perception threshold, tests of autonomic function and the prevalence of impotence. The prevalence of diabetic neuropathy across Europe was 28 % with no significant geographical differences. Significant correlations were observed between the presence of diabetic peripheral neuropathy with age (p 〈 0.05), duration of diabetes (p 〈 0.001), quality of metabolic control (p 〈 0.001), height (p 〈 0.01), the presence of background or proliferative diabetic retinopathy (p 〈 0.01), cigarette smoking (p 〈 0.001), high-density lipoprotein cholesterol (p 〈 0.001) and the presence of cardiovascular disease (p 〈 0.05), thus confirming previous associations. New associations have been identified from this study – namely with elevated diastolic blood pressure (p 〈 0.05), the presence of severe ketoacidosis (p 〈 0.001), an increase in the levels of fasting triglyceride (p 〈 0.001), and the presence of microalbuminuria (p 〈 0.01). All the data were adjusted for age, duration of diabetes and HbA1c. Although alcohol intake correlated with absence of leg reflexes and autonomic dysfunction, there was no overall association of alcohol consumption and neuropathy. The reported problems of impotence were extremely variable between centres, suggesting many cultural and attitudinal differences in the collection of such information in different European countries. In conclusion, this study has identified previously known and new potential risk factors for the development of diabetic peripheral neuropathy. [Diabetologia (1996) 39: 1377–1384]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050586
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  • 2
    Electronic Resource
    Electronic Resource
    Endoneurial localisation of microvascular damage in human diabetic neuropathy (1993)
    Springer
    Diabetologia 36 (1993), S. 454-459 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; microangiopathy ; peripheral neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty diabetic patients with neuropathy underwent clinical and neurophysiological evaluation together with a detailed morphometric assessment of capillary pathology in endoneurial and epineurial microvascular beds of the sural nerve. Morphological data were compared with ten non-diabetic control subjects. There were no significant differences in control subjects between basement membrane area, endothelial cell area, endothelial cell profile number or luminal area of endoneurial when compared with epineurial capillaries. In contrast, when compared with epineurial capillaries, endoneurial capillaries from diabetic patients demonstrated a significant increase in basement membrane (p〈0.001) and endothelial cell (p〈0.001) area and a significant reduction in luminal area (p〈0.001). There was no significant difference in endothelial cell profile number between endoneurial and epineurial capillaries amongst diabetic patients. Previous studies have demonstrated a good correlation between the degree of microangiopathy and measures of neuropathic severity. In the present study increased endoneurial capillary basement membrane area was significantly related to reduced peroneal nerve conduction velocity (p〈0.001), myelinated fibre density (p〈0.001) and elevated vibration (p〈0.05) and thermal (p〈0.001) perception. Increased endothelial cell area and reduced luminal size were related to a reduced peroneal nerve conduction (p〈0.05, p〈0.01, respectively), reduced myelinated fibre density (p〈0.05, p〈0.01) and elevated thermal perception (p〈0.05, p〈0.001). Epineurial capillary basement membrane, endothelial cell and luminal area failed to relate to measures of neuropathic severity. This study has demonstrated more advanced microangiopathy and a more significant relationship to neuropathic severity in endoneurial compared with epineurial capillaries, thus providing further support for the role of microangiopathy in the pathogenesis of human diabetic neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402283
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  • 3
    Electronic Resource
    Electronic Resource
    Exercise-induced conduction velocity increment: a marker of impaired peripheral nerve blood flow in diabetic neuropathy (1992)
    Springer
    Diabetologia 35 (1992), S. 155-159 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; nerve blood flow ; sural nerve ; sural sensory conduction velocity ; temperature ; exercise
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Severe microvascular disease exists at the stage of clinical diabetic neuropathy. A non-invasive test that will identify those diabetic subjects who will eventually develop neuropathy is essential for early intervention. Sural sensory conduction velocity was recorded (x 3) in 12 non-neuropathic diabetic subjects, 15 diabetic subjects with established neuropathy and 16 age-matched normal control subjects, before and after exercise to 80% age/sex predicted maximum heart rate. Fixed sural electrodes were used. Subcutaneous temperature was recorded by a needle thermocouple placed near the sural nerve. Sural sensory conduction velocity increased significantly after exercise in normal subjects (p〈0.01, mean increase 5.07 m/s) and non-neuropathic diabetic subjects (p〈0.02, mean increase 3.99 m/s) but not in neuropathic subjects (mean increase 0.99 m/s). Subcutaneous temperature rose significantly in normal subjects (p〈0.01, mean increase 2.07°C) and non-neuropathic diabetic subjects (p〈0.001, mean increase 2.52 °C) but not in neuropathic subjects (mean increase 0.15 °C). However, sural sensory conduction velocity increased by 1.2 m · s−1. °C−1 following direct warming of the limb in six neuropathic subjects which was comparable to that of normal and non-neuropathic subjects (1.49 and 1.48 m · s−1. °C−1). The impairment of exercise conduction increment in diabetic neuropathy suggests impaired nerve blood flow in diabetic neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402548
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  • 4
    Electronic Resource
    Electronic Resource
    Endothelial dysfunction and diabetic angiopathy (1994)
    Springer
    Diabetologia 37 (1994), S. 1167-1168 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418383
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  • 5
    Electronic Resource
    Electronic Resource
    Vascular factors in diabetic neuropathy (1994)
    Springer
    Diabetologia 37 (1994), S. 847-854 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; microangiopathy ; nerve ; hypoxia ; blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Despite considerable research we still do not have a comprehensive explanation for the pathogenesis of diabetic neuropathy. Although chronic hyperglycaemia is almost certainly involved, it is not known whether the primary pathology is metabolic, microvascular, or an interaction between the two. Hyperglycaemia-induced polyol pathway hyperactivity associated with nerve sorbitol accumulation and myo-inositol depletion may play a part in the genesis of diabetic neuropathy. The case for microvascular disease in diabetic neuropathy is now strong. Fibre loss in human sural nerve is multifocal, suggesting ischaemia. The degree of vessel disease has been related to the severity of neuropathy. People with chronic obstructive pulmonary disease develop the so called “hypoxic neuropathy” in which similar microvascular changes occur as in diabetic neuropathy. In rats with experimental diabetic neuropathy nerve blood flow is reduced and oxygen supplementation or vasodilator treatment improved the deterioration in conduction velocity and nerve blood flow. Similarly, in human diabetic neuropathy, there is impaired nerve blood flow, epineurial arterio-venous shunting and a reduction in sural nerve oxygen tension. At what stage during the development of nerve damage these changes occur is yet to be determined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400938
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  • 6
    Electronic Resource
    Electronic Resource
    Impaired blood flow and arterio-venous shunting in human diabetic neuropathy: a novel technique of nerve photography and fluorescein angiography (1993)
    Springer
    Diabetologia 36 (1993), S. 1266-1274 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; sural nerve ; nerve blood flow ; epineurial vessel photography ; fluorescein angiography ; arterio-venous shunting ; vasa nervorum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary New techniques of sural nerve photography and fluorescein angiography which are able to provide an index of nerve blood flow have been developed. Under local anaesthetic, 3 cm of sural nerve was exposed at the ankle using an operating microscope. Without disturbing the epineurium, vessels were identified and photographed at a standard magnification (× 30). These were independently graded by an ophthalmologist not otherwise involved with the study. Fluorescein angiography was then carried out on the exposed nerve. The fluorescein appearance time and intensity of fluorescence were quantified, using computer analysis of digitised images. Thirteen subjects with chronic sensory motor neuropathy, five non-neuropathic diabetic and nine normal control subjects were studied. The mean epineurial vessel pathology score of the neuropathic group was significantly higher than the combined normal control and non-neuropathic diabetic groups (p 〈0.01). Direct epineurial arteriovenous shunting was observed in six neuropathic and one non-neuropathic diabetic patients and not in any of the normal control subjects. The nerve fluorescein appearance time was significantly delayed in subjects with chronic sensory motor neuropathy (51.5 ± 12 s) compared to both normal (34.7 ± 9 s, p 〈0.01) and non-neuropathic diabetic subjects (33.4 ± 11 s, p 〈0.025). The mean intensity of fluorescence at 96, 252 and 576 s, was significantly lower in subjects with chronic sensory motor neuropathy compared with both of the other groups (p 〈0.05). The epineurial vessel pathology score was significantly related to reduced sural (p 〈0.01) and peroneal (p 〈0.001) nerve conduction velocities, elevated vibration (p 〈0.01) and thermal (p 〈0.001) perception and the severity of retinopathy (p 〈0.002). The fluorescein appearance time was significantly related to reduced sural sensory (p 〈0.02) conduction velocity, elevated vibration (p 〈0.01) perception and epineurial vessel (p 〈0.002) pathology score, but it failed to relate to peroneal motor (p = 0.06) conduction velocity, thermal (p = 0.1) perception and the severity of retinopathy (p = 0.3). Intensity of fluorescence was significantly related to fluorescein appearance time (at 96 s, p 〈0.001; at 576 s, p 〈0.05) but did not relate to measures of neuropathic severity. These techniques have enabled us to observe that epineurial vessel anatomy is abnormal and that nerve blood flow is impaired in subjects with chronic sensory motor neuropathy. In addition epineurial arterio-venous shunting may be a feature of diabetic neuropathy. These techniques may further be applied to study nerve blood flow in early diabetic neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400804
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  • 7
    Electronic Resource
    Electronic Resource
    Vascular factors in diabetic neuropathy (1994)
    Springer
    Diabetologia 37 (1994), S. 847-854 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetic neuropathy ; microangiopathy ; nerve ; hypoxia ; blood flow.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Despite considerable research we still do not have a comprehensive explanation for the pathogenesis of diabetic neuropathy. Although chronic hyperglycaemia is almost certainly involved, it is not known whether the primary pathology is metabolic, microvascular, or an interaction between the two. Hyperglycaemia-induced polyol pathway hyperactivity associated with nerve sorbitol accumulation and myo-inositol depletion may play a part in the genesis of diabetic neuropathy. The case for microvascular disease in diabetic neuropathy is now strong. Fibre loss in human sural nerve is multifocal, suggesting ischaemia. The degree of vessel disease has been related to the severity of neuropathy. People with chronic obstructive pulmonary disease develop the so called “hypoxic neuropathy” in which similar microvascular changes occur as in diabetic neuropathy. In rats with experimental diabetic neuropathy nerve blood flow is reduced and oxygen supplementation or vasodilator treatment improved the deterioration in conduction velocity and nerve blood flow. Similarly, in human diabetic neuropathy, there is impaired nerve blood flow, epineurial arterio-venous shunting and a reduction in sural nerve oxygen tension. At what stage during the development of nerve damage these changes occur is yet to be determined. [Diabetologia (1994) 37: 847–854]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400938
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Arterio-venous shunting and proliferating new vessels in acute painful neuropathy of rapid glycaemic control (insulin neuritis) (1996)
    Springer
    Diabetologia 39 (1996), S. 329-335 
    Details
    ISSN: 1432-0428
    Keywords: Insulin neuritis ; diabetic neuropathy ; sural nerve ; nerve blood flow ; arterio-venous shunting ; nerve ; hypoxia ; new vessel formation ; fluorescein angiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin neuritis, or painful neuropathy following rapid improvement in glycaemic control, is well recognised but its aetiology is unclear. An understanding of the processes involved in the genesis of acute painful neuropathy of rapid glycaemic control may give an insight into the early pathogenetic factors leading to diabetic nerve damage in general. We have identified five subjects with insulin neuritis including one who developed severe autonomic neuropathy following treatment with insulin. Subjects underwent: 1) assessment of neuropathic symptom and deficit scores; 2) quantitative sensory and electro-physiological studies and 3) sural nerve epineurial vessel photography and fluorescein angiography in vivo. The sural nerve photographs were independently graded by an ophthalmologist. All subjects with insulin neuritis presented with severe sensory symptoms but clinical examination and electrophysiological tests were normal except in the subject with the severe autonomic neuropathy in whom all the tests were abnormal. On nerve photography, there was an abundance of epineurial nutrient vessels although these showed severe abnormalities including arteriolar attenuation, tortuosity and arterio-venous shunting in all subjects. Proliferating neural ‘new vessels’ which bear striking similarities to those found in the retina and that were more leaky to fluorescein than normal vessels, were observed in three subjects. Venous distension and/or tortuosity was also observed in three subjects and this was most marked in the subject with severe autonomic neuropathy. This study shows that epineurial nutrient vessel anatomy is abnormal in subjects with acute painful neuropathy of rapid glycaemic control, a condition previously thought to be purely metabolic in origin. The presence of epineurial arterio-venous shunting and a fine network of vessels resembling the new vessels of the retina, may lead to a ‘steal’ effect rendering the endoneurium ischaemic. This process may be important in the genesis of neuropathic pain, and further supports the importance of vascular factors in the pathogenesis of diabetic neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418349
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Arterio-venous shunting and proliferating new vessels in acute painful neuropathy of rapid glycaemic control (insulin neuritis) (1996)
    Springer
    Diabetologia 39 (1996), S. 329-335 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin neuritis ; diabetic neuropathy ; sural nerve ; nerve blood flow ; arterio-venous shunting ; nerve ; hypoxia ; new vessel formation ; fluorescein angiography.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin neuritis, or painful neuropathy following rapid improvement in glycaemic control, is well recognised but its aetiology is unclear. An understanding of the processes involved in the genesis of acute painful neuropathy of rapid glycaemic control may give an insight into the early pathogenetic factors leading to diabetic nerve damage in general. We have identified five subjects with insulin neuritis including one who developed severe autonomic neuropathy following treatment with insulin. Subjects underwent: 1) assessment of neuropathic symptom and deficit scores; 2) quantitative sensory and electrophysiological studies and 3) sural nerve epineurial vessel photography and fluorescein angiography in vivo. The sural nerve photographs were independently graded by an ophthalmologist. All subjects with insulin neuritis presented with severe sensory symptoms but clinical examination and electrophysiological tests were normal except in the subject with the severe autonomic neuropathy in whom all the tests were abnormal. On nerve photography, there was an abundance of epineurial nutrient vessels although these showed severe abnormalities including arteriolar attenuation, tortuosity and arterio-venous shunting in all subjects. Proliferating neural ’new vessels' which bear striking similarities to those found in the retina and that were more leaky to fluorescein than normal vessels, were observed in three subjects. Venous distension and/or tortuosity was also observed in three subjects and this was most marked in the subject with severe autonomic neuropathy. This study shows that epineurial nutrient vessel anatomy is abnormal in subjects with acute painful neuropathy of rapid glycaemic control, a condition previously thought to be purely metabolic in origin. The presence of epineurial arterio-venous shunting and a fine network of vessels resembling the new vessels of the retina, may lead to a ’steal' effect rendering the endoneurium ischaemic. This process may be important in the genesis of neuropathic pain, and further supports the importance of vascular factors in the pathogenesis of diabetic neuropathy. [Diabetologia (1996) 39: 329–335]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418349
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    Paper (German National Licenses)
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  • 10
    Electronic Resource
    Electronic Resource
    Transperineurial Capillary Abnormalities in the Sural Nerve of Patients with Diabetic Neuropathy
    Amsterdam : Elsevier
    Microvascular Research 48 (1994), S. 236-245 
    Details
    ISSN: 0026-2862
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/mvre.1994.1051
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