[On a comparative analysis of trophic disorders caused by denervation or single local irradiation of an intact or a denervated extremity of the rabbit].
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1. Calcium current (ICa) activation was studied in denervated extensor digitorum longus muscle fibres of the rat. Denervation was performed by surgically removing 6-8 mm of the sciatic nerve at the sciatic notch. Controls were normal fibres from non-operated rats. Electrical recordings were carried out using the double Vaseline-gap technique. 2. Current-voltage (I-V) curves showed that the ICa amplitude increased during the first 4-6 days after denervation and subsequently decreased during the second week. Between days 4 and 6 after denervation, the peak ICa amplitude (at 0 mV) was -5.9 +/- 0.5 microA/microF (mean +/- S.E.M.) as compared with -4.8 +/- 0.3 microA/microF in normal fibres. Between days 14 and 15 after denervation, the ICa amplitude was -2.9 +/- 0.4 microA/microF. 3. The time constant of ICa activation (tau a) was significantly increased by denervation. At 0 mV, tau a in normal fibres was 44.8 +/- 1.4 ms. Between 4 and 6 days after denervation tau a was 58.1 +/- 4.8 ms, and between 14 and 15 days after denervation, 55.8 +/- 3.8 ms. 4. The time constant of deactivation (tau d) decreased after denervation. At -10 mV, the tau d in normal fibres was 103.4 +/- 14 ms. The value decreased to 74.5 +/- 8.6 and 74.0 +/- 17 ms between days 4 and 6 and days 14 and 15 of denervation respectively. 5. Charge movement (Qon) was reduced progressively without major changes in the steepness (k) and position on the voltage axis of the Qon-Vm relationship. The fitted parameters under control were Qmax = 15.4 nC/microF, mid-point potential Vq1/2 = -25.2 mV and k = 11.9 mV. Between days 14 and 15 of denervation, the values for Qmax, Vq1/2 and k were 6.7 nC/microF, -36.8 mV and 11.3 mV respectively. 6. Calcium permeability (PCa) in normal and denervated fibres at stages during denervation was calculated according to the Hodgkin-Huxley model. At 0 mV PCa was 1.24 x 10(-5) cm/s in normal fibres, and 7.43 x 10(-6) cm/s after 2 weeks of denervation. 7. The m infinity-Vm relationship was shifted to more positive potentials after denervation without significant changes in the steepness factor k. The V1/2 value in normal fibres was -4.4 mV, and 5.8 mV after two weeks of denervation. 8. The ICa sensitivity to nifedipine was not modified in the different groups of denervated fibres studied. With 10 microM-nifedipine, the 1-(ICa in nifedipine/ICa control) relationships were 0.74 +/- 0.03 in normal fibres and 0.76 +/- 0.12, 14 days after denervation.
PURPOSE: We reviewed the MR appearance of motor denervation of the third (mandibular) division of the trigeminal nerve (V3) and of the hypoglossal nerve. METHOD: Six cases of tumor of the head and neck with motor denervation were retrospectively evaluated. These comprised two patients with V3 denervation, three patients with hypoglossal nerve denervation, and one patient with both V3 and hypoglossal denervation. The observation was conducted for 6 to 44 months after onset. In denervated muscles, changes in signal intensity in T(1)- and T(2)-weighted images, degree of contrast enhancement, and volume of muscle were estimated during the follow-up period. RESULTS: In all cases of V3 denervation, the muscles showed no change in signal intensity in the T(1)-weighted images up to three months after onset. In two cases of hypoglossal denervation, the tongues appeared ipsilaterally hyperintense in the T(1)-weighted images within the first three months. In one case with V3 denervation and two cases with hypoglossal denervation, denervated muscles appeared hyperintense in the T(2)-weighted images up to three months after onset. At three months after denervation, the signal intensities of all motor-denervated areas increased in both T(1)- and T(2)-weighted images. Postcontrast T(1)-weighted images obtained within the first three months displayed contrast enhancement of all denervated muscles. In three cases of V3 denervation, the volumes of the affected muscles were reduced after the first three months. In three cases of hypoglossal denervation, the ipsilateral volume of the tongue decreased at three months after onset. CONCLUSION: Up to three months after onset, the denervated muscles appeared hyperintense in the T(2)-weighted images and contrast enhancement in postcontrast T(1)-weighted images before fatty infiltration and volume loss were apparent. Familiarity with the MR appearance of denervated muscles accompanying tumors of the head and neck is important to avoid confusion with inflammatory or neoplastic processes.
Very little is known regarding structural and functional responses of the vascular bed of skeletal muscle to denervation and about the role of microcirculatory changes in the pathogenesis of post-denervation muscle atrophy. The purpose of the present study was to investigate the changes of the anatomical pattern of vascularization of the extensor digitorum longus muscle in WI/HicksCar rats 1, 2, 4, 7, 12, and 18 months following denervation of the limb. We found that the number of capillaries related to the number of muscle fibers, i.e. the capillary-to-fiber ratio (CFR), decreased by 88%, from 1.55 +/- 0.35 to 0.19 +/- 0.04, during the first 7 months after denervation and then slightly declined at a much lower rate during the next 11 months of observation to 10% of the CFR in normal muscle. Between months 2 and 4 after denervation, the CRF decreased by 2.4 times, from 58% to 24% of the control value. The loss of capillaries during the first 4 months following nerve transection was nearly linear and progressed with an average decrement of 4.16% per week. Electron microscopy demonstrated progressive degeneration of capillaries following nerve transection. In muscle cells close to degenerating capillaries, the loss of subsarcolemmal and intermyofibrillar mitochondria, local disassembly of myofibrils and other manifestations of progressive atrophy were frequently observed. The levels of devascularization and the degree of degenerative changes varied greatly within different topographical areas, resulting in significant heterogeneity of intercapillary distances and local capillary densities within each sample of denervated muscle. Perivascular and interstitial fibrosis that rapidly developed after denervation resulted in the spatial separation of blood vessels from muscle cells and their embedment in a dense lattice of collagen. As a result of this process, diffusion distances between capillaries and the surfaces of muscle fibers increased 10-400 times. Eighteen months after denervation most of the capillaries were heavily cushioned with collagen, and on the average 40% of the muscle cells were completely avascular. Devascularization of the tissue was accompanied by degeneration and death of muscle cells that had become embedded in a dense lattice of collagen. Immunofluorescent staining for the vascular isoform of alpha-actin revealed preservation of major blood vessels and a greater variability in thickness of their medial layer. Hyperplastic growth of the medial layer in some blood vessels resulted in narrowing of their lumens. By the end of month 7 after denervation, large deposits of collagen around arterioles often exceeded their diameters. Identification of oxidative muscle fibers after immunostaining for slow-twitch myosin, as well as using ultrastructural criteria, has shown that after 2 months of denervation oxidative muscle fibers were less susceptible to atrophy than glycolytic fibers. The lower rate of atrophy of type I muscle fibers at early stages of denervation may be explained by their initially better vascularization in normal muscle and their higher capacity to retain capillaries shortly after denervation. Thus, degeneration and loss of capillaries after denervation occurs more rapidly than the loss of muscle fibers, which results in progressive decrease of the CFR in denervated muscle. The change of capillary number in denervated muscle is biphasic: the phase of a rapid decrease of the CFR during the first 7 months after nerve transection is followed by the phase of stabilization. The presence of areas completely devoid of capillaries in denervated muscle and the virtual absence of such areas in normal muscle indicate the development of foci of regional hypoxia during long-term denervation. The anatomical pattern of muscle microvascularization changes dramatically after nerve transection. Each muscle fiber in normal muscle directly contacts on average 3-5 capillaries. (ABSTRACT TRUNCATED)
PURPOSE: To illustrate and describe the appearance of both long-standing and relatively recently occurring motor denervation of the hypoglossal nerve and of the third (mandibular) division of the trigeminal nerve (V3), with emphasis on findings particular to MR imaging. METHODS: Findings from 11 patients with V3 denervation and from seven patients with hypoglossal denervation resulting from a variety of abnormalities were reviewed retrospectively. The motor denervation appearance and functional compromise of the affected musculature are described in terms of the chronicity of the denervation process. RESULTS: The appearance of V3 and hypoglossal motor denervation varies with the chronicity of the process. Long-standing denervation results in extensive fatty replacement and a decrease in the size of the affected musculature. Relatively recently occurring denervation results in abnormal contrast enhancement and edemalike signal changes in the denervated musculature. Fatty replacement was observed acutely in hypoglossal denervation but did not manifest until the subacute stage in V3 denervation. Increased volume of the denervated musculature may also accompany acute denervation signal changes. CONCLUSION: V3 and hypoglossal denervation have a variable appearance depending on the chronicity of the process. Recognition of MR imaging patterns of denervation may allow earlier diagnosis of a denervating lesion and may help to distinguish denervation from similar-appearing processes, such as infection or neoplasia.