Nerve morphology in experimental diabetes.
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Biomedical subjects
Publications and source records attributed to J Jakobsen.
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A case of atraumatic rupture of the spleen is described. The underlying disease was found to be periarteritis nodosa. Involvement of the spleen is common in this disease, but to our knowledge atraumatic rupture of this organ in a patient with histologic verified periarteritis nodosa has not previously been reported. In the present case the splenic rupture was the incident which led to the diagnosis. A possible mechanism of the rupture is proposed.
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The aim of the present study was to investigate whether heart rate variation as obtained simply from an electrocardiographic registration is influenced in subjects given antidepressive medication. The mean difference between consecutive R-R intervals (MCD) was reduced in patients (n = 23) treated with various doses of tri- or tetracyclic antidepressants [7.7 (1.8-32.3) ms in patients versus 24.8 (7.0-87.7) ms in controls]. Among those receiving 1.67 mg tricyclic antidepressant or more per kilogram body wt (n = 12) MCD was further reduced [5.0 (2.1-12.0) ms] with no overlapping of values as compared to controls (n = 9). In a subgroup of patients treated with clomipramine the MCD was related inversely to the dosage (R = 0.78, P less than 0.02). In an additional group of seven patients, MCD was reduced following a few days of treatment with antidepressants as compared to pretreatment values (P less than 0.02), indicating that the reduction is a result of therapy and not a concomitant of the affective state. We suggest that measurements of heart rate variation could be a useful tool to measure anticholinergic effects of antidepressants.
Population data on complete and removable partial prosthodontics in Iowa indicated the following. Denture wearers tend to be persons in the older age groups. The percentage of edentulous persons was lower than that reported nationally in 1971. Of every 1,000 persons, 156 were wearing dentures in one or both arches. Of every 1,000 persons, 53 needed a repair, reline, or replacement of an existing denture. Of every 1,000 persons, 70 needed a denture but were not wearing one. Persons of lower income and education were less likely to seek dental care but had the greatest need for treatment. Persons of lower income and education were at higher risk of having some form of mucosal lesions. The public will be unlikely to make use of dental services to prevent or treat lesions or to service a prosthesis unless they are specifically educated to do so.
A case of congenital oculomotor paralysis demonstrating retraction of the upper lid and constriction of the pupil in response to eye movements is described. The pupil was found to be unresponsive to light, but to contract promptly on attempted ocular movements which involved motor neurons of the third nerve. As demonstrated by infrared pupillography, the duration of the constriction phase was found to be remarkably long. Also, very little hippus was noted during constriction. The findings are explained on basis of the 'misdirection' hypothesis according to which regenerating nerve fibres find a wrong path in the peripheral part of the damaged nerve.
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Recent studies on the distribution of labeled endogenous proteins in the experimental neuropathies induced by streoptozotocin diabetes, galactose feeding, zinc pyridinethione, 2,5-hexanedione, acrylamide, and p-bromophenylacetylurea (BPAU) have demonstrated an impaired build up of retrogradely transported material derived from the more distal parts of peripheral nerve. In BPAU neuropathy the transport abnormality is strongly related to the degree of muscle weakness; following treatment with acrylamide the extent of the impairment is dose related. In both toxic conditions the transport abnormality is present well in advance of the first clinical signs of neuropathy. We therefore suggest that changes in retrograde axonal transport play an initial and important role in the development of many axonopathies.
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The effect of retrograde axonal transport of doses of acrylamide ranging from 50 to 500 mg/kg was studied in sensory nerve of rats. Accumulation of trichloroacetic acid-phosphotungstic acid-insoluble label was measured in a collection segment distal to a double ligature placed on the sciatic nerve at intervals 9-15 h and 9-24 h following injection into the dorsal root ganglion of the fifth lumbar root of [35S]methionine and [3H]fucose. After a dose of 100 mg/kg of acrylamide no neurological signs of neuropathy had yet appeared, but retrograde buildup of protein label was significantly reduced for the long interval (2.20 +/- 0.49 arbitrary units (AU) (mean +/- SD) versus 2.81 +/- 0.57 AU in controls, 2p = 0.034). No abnormality of the short interval appeared before a dose of 500 mg/kg was reached. The retrograde transport abnormality was dose-related (r = -0.85, n = 28, and 2p = 1.2 x 10(-8)), as was the degree of neuropathy evaluated by "blind" neurological scoring (r = 0.88, n = 14, and 2p = 2.8 x 10(-5)). After a dose of 500 mg/kg, when the rats were severely disabled with almost total incoordination of the hindlegs, the retrograde accumulation of the long interval was profoundly depressed (1.08 +/- 0.28 AU versus 2.81 +/- 0.57 AU in controls, 2p = 1.2 x 10(-7)). Similar changes were seen in accumulation of glycoprotein label. After the rats had recovered for 4-10 weeks neurological signs of neuropathy had disappeared and the transport abnormality had improved. To test the specificity of acrylamide on the retrograde transport defect N-hydroxymethylacrylamide and methylene-bisacrylamide, which do not induce neuropathy, were studied. None of these related compounds influenced the transport. These observations imply that in acrylamide intoxication a defect in the amount of material carried by retrograde axonal transport rather than in "turnaround" time or in transport velocity is present, that the transport abnormality precedes the development of neuropathy, and that it is related to the degree of the neurological disability. We suggest that the retention of protein in the distal axons in the functional counterpart of the well-known accumulation of vesicular organelles in the preterminals.
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The effect of sustained insulin-induced hypoglycemia on peripheral nerve function and structure was examined in rats. After a period of hypoglycemia (less than 2.5 mmol/L) of at least 72 h, axonal degeneration and reduction of the maximal amplitude of the evoked muscle action potential occurred, the two abnormalities being correlated negatively (r = -0.99, 2P = 0.00097). One of five rats developed paresis of both hindlegs as well as nerve damage and perikaryal alterations of lower motor neurons.
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