Electrophysiological studies in diabetic neuropathy
01 Aug 1970-Journal of Neurology, Neurosurgery, and Psychiatry (BMJ Publishing Group Ltd)-Vol. 33, Iss: 4, pp 442-452
TL;DR: Evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes is supported.
Abstract: In 30 patients with diabetic neuropathy sensory potentials in the median nerve, motor conduction in the lateral popliteal and median nerves, and electromyographic findings in distal and proximal muscles were compared with the severity of symptoms and signs. All patients had abnormalities in at least one of the electrophysiological parameters. The sensory potentials were the most sensitive indicator of subclinical involvement; abnormalities were found in 24 patients, 12 of whom had no sensory symptoms or signs and five of whom had no other clinical or electrophysiological evidence of neuropathy in the upper extremities. This indicates that sensory nerve fibres may be affected before motor. The next most sensitive parameter was the presence of fibrillation potentials, found in more than half the distal muscles examined. Slowing in motor conduction in the lateral popliteal nerve was the only electrophysiological change correlated to the severity of the neuropathy, and no other electrophysiological parameter was correlated to the duration or the severity of the neuropathy or the diabetes. An onset of neuropathy before or simultaneously with the manifestations of the diabetes, as well as the frequent occurrence of asymptomatic changes in sensory conduction, support the evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes. Of three patients with clinical signs or symptoms of a diabetic amyotrophy, two had asymptomatic electrophysiological abnormalities in distal nerves and muscles, consistent with widespread involvement of the peripheral nerves. The third patient had electromyographic changes in the medial vastus muscles suggestive of a myopathy. Motor and sensory conduction in distal and proximal nerves were normal.
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TL;DR: Although antioxidants are being used for other chronic diseases, controlled clinical trials are warranted to investigate potential beneficial effects of antioxidants in the development of retinopathy in diabetic patients.
Abstract: Oxygen metabolism is essential for sustaining aerobic life, and normal cellular homeostasis works on a fine balance between the formation and elimination of reactive oxygen species (ROS). Oxidative stress, a cytopathic consequence of excessive production of ROS and the suppression of ROS removal by antioxidant defense system, is implicated in the development of many diseases, including Alzheimer's disease, and diabetes and its complications. Retinopathy, a debilitating microvascular complication of diabetes, is the leading cause of acquired blindness in developed countries. Many diabetes-induced metabolic abnormalities are implicated in its development, and appear to be influenced by elevated oxidative stress; however the exact mechanism of its development remains elusive. Increased superoxide concentration is considered as a causal link between elevated glucose and the other metabolic abnormalities important in the pathogenesis of diabetic complications. Animal studies have shown that antioxidants have beneficial effects on the development of retinopathy, but the results from very limited clinical trials are somewhat ambiguous. Although antioxidants are being used for other chronic diseases, controlled clinical trials are warranted to investigate potential beneficial effects of antioxidants in the development of retinopathy in diabetic patients.
631 citations
TL;DR: Staging approaches to staging severity of neuropathy should be developed and used in expressing abnormality and minimal criteria for the diagnosis of diabetic polyneuropathy have been proposed and validated tests to assess neuropathic symptoms and sensory deficits have been developed.
Abstract: The reported prevalence of diabetic polyneuropathy varies from 5 to 80%. This unsatisfactory state may relate to evaluation of different patient groups, different minimal criteria for the diagnosis of neuropathy, and different degrees of surveillance. To made matters worse, patients with polyneuropathy tend to be equated ignoring differences in severity. To remedy this situation, four recommendations are made: (1) population-based patients should be studied, (2) nerve conduction should be used to set minimal criteria for neuropathy because the test is objective, sensitive, and repeatable, (3) validated tests of symptoms and deficits should also be used because clinical manifestations of neuropathy cannot be accurately inferred from electrophysiologic measurements, and (4) approaches to staging severity of neuropathy should be developed and used in expressing abnormality. To this end minimal criteria for the diagnosis of diabetic polyneuropathy have been proposed, and validated tests to assess neuropathic symptoms and sensory deficits have been developed. In this report we also propose a staging approach utilizing nerve conduction and neurologic history and examination and validated tests of neuropathic symptoms and deficits.
545 citations
TL;DR: Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symmetrical sensory-motor polyneuropathy, and three with multiple mononeuropathy.
Abstract: Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symmetrical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.
362 citations
TL;DR: The performance characteristics of several criteria for the diagnosis of sensorimotor polyneuropathy in healthy subject‐ and diabetic subject cohorts are provided and staged and continuous approaches to estimate severity of DSPN are outlined.
Abstract: Prior to a joint meeting of the Neurodiab Association and International Symposium on Diabetic Neuropathy held in Toronto, Ontario, Canada, 13-18 October 2009, Solomon Tesfaye, Sheffield, UK, convened a panel of neuromuscular experts to provide an update on polyneuropathies associated with diabetes (Toronto Consensus Panels on DPNs, 2009). Herein, we provide definitions of typical and atypical diabetic polyneuropathies (DPNs), diagnostic criteria, and approaches to diagnose sensorimotor polyneuropathy as well as to estimate severity. Diabetic sensorimotor polyneuropathy (DSPN), or typical DPN, usually develops on long-standing hyperglycaemia, consequent metabolic derangements and microvessel alterations. It is frequently associated with microvessel retinal and kidney disease-but other causes must be excluded. By contrast, atypical DPNs are intercurrent painful and autonomic small-fibre polyneuropathies. Recognizing that there is a need to detect and estimate severity of DSPN validly and reproducibly, we define subclinical DSPN using nerve conduction criteria and define possible, probable, and confirmed clinical levels of DSPN. For conduct of epidemiologic surveys and randomized controlled trials, it is necessary to pre-specify which attributes of nerve conduction are to be used, the criterion for diagnosis, reference values, correction for applicable variables, and the specific criterion for DSPN. Herein, we provide the performance characteristics of several criteria for the diagnosis of sensorimotor polyneuropathy in healthy subject- and diabetic subject cohorts. Also outlined here are staged and continuous approaches to estimate severity of DSPN.
359 citations
TL;DR: Reproducibility of tests used to characterize and quantitate severity of neuropathy was found high r1 with small confidence intervals for the Neurologic Disability Score (NDS); weakness subset of NDS (W-NDS) and vibratory and cooling detection thresholds (using computer-assisted sensory examination [CASE] IV).
Abstract: A cross-sectional survey and subsequent longitudinal study among diabetic residents of Rochester, MN- The Rochester Diabetic Neuropathy Study (RDNS)-is population-based and uses quantitative, validated, and unique end points to detect, classify, and stage neuropathy. Nondiabetic persons, drawn from the same population, serve as controls. For patients 10 to 70 years old, the RDNS cohort is representative of diabetics living in Rochester, MN. We assessed reproducibility of tests used to characterize and quantitate severity of neuropathy in 20 diabetic subjects without neuropathy and with varying severities of neuropathy. Using intraclass correlation coefficient (r 1 ) as a measure of test reproducibility, we found high r 1 (usually 0.9 or better) with small confidence intervals for the Neurologic Disability Score (NDS); weakness subset of NDS (W-NDS); vibratory and cooling detection thresholds (using computer-assisted sensory examination [CASE] IV); compound muscle action potentials; sensory nerve action potentials; and motor nerve conduction velocities. There was good agreement among three trained observors for NDS and the W-NDS.
293 citations
References
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Book•
01 Jan 1925
TL;DR: The prime object of as discussed by the authors is to put into the hands of research workers, and especially of biologists, the means of applying statistical tests accurately to numerical data accumulated in their own laboratories or available in the literature.
Abstract: The prime object of this book is to put into the hands of research workers, and especially of biologists, the means of applying statistical tests accurately to numerical data accumulated in their own laboratories or available in the literature.
11,308 citations
1,416 citations
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270 citations
"Electrophysiological studies in dia..." refers background in this paper
...These studies concerned patients with or without diabetic neuropathy (Lawrence and Locke, 1961; Mulder et al., 1961; Skillman et al., 1961; Fagerberg et al., 1963; Mayer, 1963; Gamstorp, 1964; Eeg- Olofsson and Petersen, 1966) and mixed groups (Gregersen, 1964, 1967)....
[...]
...…average slowing in motor conduction along the median and ulnar nerves has been reported to be as severe as in the lateral popliteal nerve, both in patients with and without clinical signs of neuropathy (Mulder et al., 1961; Lawrence and Locke, 1962; Mayer, 1963; Gamstorp, 1964; Gregersen, 1967)....
[...]
TL;DR: The chapter attempts to describe the expected diversed underlying pathological alterations in patients with diabetes mellitus and to relate the changes to the clinical syndromes.
Abstract: The chapter attempts to describe the expected diversed underlying pathological alterations in patients with diabetes mellitus and to relate the changes to the clinical syndromes.
Keywords:
perikaryal;
nerve fiber;
horn cell;
ganglia;
tissue;
vascular
256 citations