[Therapy of polyneuropathies].
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Biomedical subjects
Publications and source records attributed to G Reichel.
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UNLABELLED: In extremely unstable (brittle) IDDM patients (n = 11) the metabolic effect of long-term (36 months) CSII proved to be superior to conventional insulin treatment (CIT) (statistical twins, n = 11): HbA1 = 8.6 +/- 0.3 versus 10.4 +/- 0.4, MBG = 5.6 +/- 0.3 versus 8.5 +/- 0.8, M (80)- value = 23.6 +/- 0.6 versus 56.7 +/- 10.2, GCI) = 37.3 +/- 15.6 versus 132 +/- 24.2. In addition, in CSII patients the metabolic control was significantly better than intensified conventional insulin treatment (ICT) before. Retinal morphology improved under CSII in 1 eye, did not change in 10 eyes and deteriorated in 11 eyes. Under CIT retinal findings improved in none, did not change in 16 and deteriorated in 16 eyes. Deteriorations under CSII appeared more frequently during the first than during the second and third year of treatment and seemed to be a consequence of too strict metabolic control and/or too fast decrease of the glycemia at the beginning of CSII. During 36 months of CSII no deterioration but in one case normalization of microproteinuria was observed. Under CIT three cases changed from normal into microproteinuria. Reduced motor nerve conduction velocity (MCV) and/or sensory nerve conduction velocity (SCV) could be normalized in most cases under CSII, but respiratory heart arrhythmia (RHA) at rest could not. Most patients--if highly motivated before starting CSII--remained positively motivated for long-term pump therapy. IN CONCLUSION: Our experiences over three years demonstrate a positive effect of CSII on the metabolism as well as on the course of early stages of microangiopathy and neuropathy. A longer period of observations will be necessary to evaluate this, conclusively.
200 years have gone by since the autonomic disturbance in diabetes mellitus has been described for the first time ever. There is a great deal of information on the close relationship between somatic and visceral symptoms in diabetic polyneuropathy (PNP), so that there should be talked about only of one form of manifestations within the meaning of a distal symmetric somatovisceral PNP. The longer fibres such as the vagal fibres of the viscus, sympathetic fibres of the eye are affected at first and more intensively in the autonomic region same as in the sensory and motor region. Due to the fact that for reasons of fragmentary knowledge pathogenetically substantiated classification of the autonomic disturbances in diabetic PNP is not at hand, such a classification is being made from organotopic and phenomenologic aspects. Frequently, afferent denervation of an organ results in enhancing the effects of an autonomic innervation dysfunction, as for instance in unnoticed hypoglycaemia, in order to modify the symptoms, as for instance in rectal incontinence with unnoticed defecation, or rather to let new symptoms appear, for instance loss of testicular pain. In recent years, appropriate methods of examinations were tested for the clinical routine, permitting to give evidence of autonomic dysfunctions before clinical manifestation. It is still unclear to what extent such subclinical abnormalities are reversible with a more favourable regulation of the metabolic process, for instance with the aid of continuous subcutaneous insulin injections. An impressive symptom of innervation dysfunctions of the cardiovascular system is orthostatic hypertension that may, in exceptional cases, even lead to confinement to bed. The most important pathogenic factor seems to be vascular denervation. A pronounced tachycardia at rest, frequently found in diabetics, is the result of the failure of the vagal autonomic system, and, after additional destruction of the sympathetic fibres, it adjusts itself to a lower level that cannot be changed by reflex mechanisms. Cardialgia absent in the case of myocardial ischemia is a factor of an increased mortality of long-term diabetics. The correlation between vascular denervation and arteriosclerosis or mediasclerosis, respectively, is being under discussion. Denervation on the gastrointestinal tract has an effect on the motility and excretory functions. The innvervation dysfunctions lead to sialadenosis by changing the composition of saliva. In most cases esophageal dysfunction is not perceived by the patient.(ABSTRACT TRUNCATED AT 400 WORDS)
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In recent years there ist a growing interest in autonomic dysfunctions in polyneuropathies. It is reported on four vagal function tests und two tests of the sympathetic system carried out and evaluated. These tests can be conducted without any instrumental application, and permit diagnostic and prognostic statements.
Pseudohypoaldosteronism is a rare syndrome occurring during early infancy, which is mainly characterized by salt-depletion crises. Sodium chloride is lost via the kidneys resulting in a reduced sodium level and raised potassium level in the serum, leading to life-threatening disturbances of water and acid-base concentration. The excessive sodium loss seems to be caused by an unresponsiveness of the renal tubules to endogenous and exogenous mineralocorticoids. The colon, salivary and sweat glands, which are also involved in sodium reabsorption, may likewise be affected by the disease. We describe skin changes in two siblings suffering from pseudohypoaldosteronism, who developed seborrheic dermatitis, folliculitis or miliaria rubra-like lesions during salt-depletion crises. Biochemical analysis revealed a highly increased sodium-chloride concentration in the sweat, saliva, urine and stool of both patients. Destructive inflammatory reactions could be demonstrated histologically within and around the dermal sweat glands, thus indicating the important role of the sweat system in the pathogenesis of skin lesions in pseudohypoaldosteronism.
In 145 patients suffering from type-I-diabetes with or without signs or symptoms of polyneuropathy basal and glucose-glucagon-induced secretion of insulin was determined. Patients without remaining insulin secretion exhibited somewhat more often polyneuropathies, slowing of nerve conduction, or reduced respiratory heart arrhythmia. If diabetes lasts for more than 10 years, insulin secretion ist reduced to such a low level that its may not have any significant preventive capability with respect to polyneuropathy.
The distal latencies, motor and sensory nerve conduction velocities, and respiratory heart arrhythmia (RHA) were measured in 14 patients with type I diabetes but without clinical signs of polyneuropathy. The electroneurographic parameters tended to improve as the HbA1 value decreased. The RHA was not affected.
10 labile insulin-dependent diabetic patients treated with CSII were followed up for 6 to 16 months under conditions of everyday life. The mean blood glucose (MBG), glycosylated haemoglobin (HbA1), motor nerve conduction velocity (MCV), and respiratory heart arrhythmia at rest (RHA) were investigated. A significant improvement of metabolic control was observed (MBG 8.03 +/- 1.40 vs 5.18 +/- 0.87 mmol/l, p less than 0.01; HbA1 10.7 +/- 1.3 vs 8.7 +/- 1.6%, p less than 0.05) in comparison with the control values under intensified conventional therapy. MCV increased gradually but the average RHA remained unchanged. The psychological examination employing a questionnaire reflects that all patients selected were highly motivated and that their positive attitudes were further stabilized during pump treatment. An average of three mild hypoglycaemic episodes occurred per month per patient; these were no more than under intensified conventional treatment. Other minor clinical and technical complications occurred at a total frequency of one per month per patient and did not achieve therapeutical relevance.
The application of an isolated punctiform stimulation with a needle electrode using the opposite large-surface electrode as an anode makes it possible to study the whole peripheral nerve including the nerve root after its exit from the spinal canal electroneurographically. This method enables the determination of nerve conduction speeds even over short nerve distances in a more exact way. The simultaneous stimulation of nearby nervous structures, which is frequently observed when surface electrodes are used, can be avoided.
Two arm and two leg nerves in each of a group of healthy subjects were stimulated electrically and the muscle action potentials were taken from the corresponding regions by surface electrodes. Volumetrically conducted potentials appeared in almost all cases, and other nerves were stimulated at the same time in many cases. The resultant errors in the calculation of the speed of pulse transmission are considerable. The use of a concentric needle electrode is recommended for recording evoked muscle action potentials.
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A report is given on experience gained during the electroneurographic examination of 800 diabetics of all ages and on the results of respiratory heart arrhythmia measurement on 215 diabetics. It is proposed that diabetic nervous disturbances should be divided into the following groups: 1--early diabetic and subclinical disturbances, 2--somatovisceral polyneuropathy in type I diabetics, 3--polyneuropathy in type II diabetics, 4--mononeuropathy, mononeuropathy multiplex and proximal amyotrophy. The disturbances in group 1 can be reversed by metabolic control. Only the PNP in group 2 shows a firm statistical correlation to duration of diabetes mellitus and to microangiopathy. This appears to be a dying back neuropathy, probably caused by the chronically catabolic metabolic situation.
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Electromyographical and electroneurographical examinations are indicated in the forefield of the surgical treatment for radicular syndromes, traumatic plexus and nerve lesions as well as compression or bottle-neck syndromes. The electrophysiological findings point out the neurogenic nature of the disturbance. They furthermore furnish statements with respect to the localisation, the extent, the kind and the prognosis of the lesions. The electromyographical and electroneurographical examination programme is determined by the anatomical innervation conditions and the questions that are of clinical interest. In case of radicular syndromes it is mainly the localisation with respect to the height of the root lesions that is of interest. In plexus lesions, the question regarding the reinnervation chance is usually to the fore. In primary nerve lesions, the question whether there is a partial or total nerve separation is above all of interest. In secondary nerve lesions and the bottle-neck syndromes it is usually necessary to determine the exact site of the lesions and the extent of the chronic compression damage. In this paper, these aspects ae discussed on the basis of the more important clinical pictures and practical hints for diagnosis and therapy are given.