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Dietary administration of the growth promoter, clenbuterol, ameliorated denervation-induced atrophy in rat soleus muscles. In acutely denervated muscles the drug inhibited the appearance of atrophy, and in chronically denervated muscles the atrophy was almost fully reversed. Responses in slow twitch oxidative fibres were particularly marked.
We have investigated whether dendritic growth can be induced from sympathetic neurons of aged rats by the application of exogenous nerve growth factor to their target tissues. A previous study showed that significant dendritic atrophy (19%) occurs during aging in the sympathetic neurons innervating the middle cerebral artery and that dendritic atrophy correlated with loss of axon collaterals in the same population of neurons. Using retrograde tracing in conjunction with intracellular injection of fixed tissue and confocal microscopy, we now demonstrate that infusion of nerve growth factor over the peripheral processes of the same neurons from aged rats induces significant dendritic (45%) and cell body (60%) growth. However, not all aspects of the dendritic arborization were affected. Primary dendrites and branch points were not altered by nerve growth factor. In contrast, nerve growth factor induced a significant increase in the number of primary dendrites and branch points (100%) of neurons from young adults. Our results demonstrate that sympathetic neurons undergoing dendritic atrophy during aging can exhibit significant dendritic growth in response to the in vivo infusion of nerve growth factor, although the lack of regenerative response displayed by some parts of the dendritic tree leads us to believe that these neurons also show signs of reduced plasticity.
In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.
We describe two sibs with DIDMOAD-Syndrome, a 19-year-old girl with diabetes mellitus (type I), optic atrophy, inner-ear deafness, and atonia of the urinary tract, and her 5-year-old brother with diabetes mellitus (type I) and optic atrophy. Studies of red blood cell insulin receptors revealed a normal number of receptors per cell and normal affinity to insulin. The syndrome represents an autosomal recessively inherited type of diabetes mellitus, which remains often undiagnozed since most of the symptoms except diabetes mellitus and optic atrophy occur with varying expressivity. An atonia of the efferent urinary tract often with fatal complications is present in 46% of all patients with this syndrome reported in the literature and is unfortunately not included in the acronym DIDMOAD.
Gyrate atrophy of the choroid and retina with hyperornithinaemia (GA), an autosomal recessive disease, affects skeletal muscle in addition to the eye. Muscle biopsy samples show prominent type 2 muscle fibre atrophy. Atrophic fibres also contain accumulations of tubular aggregates in electron microscopy. To evaluate skeletal muscle involvement in detail, the thigh muscles of 7 patients with GA were examined using semi-open conchotome muscle biopsies, computed tomography (CT) and ultralow-field magnetic resonance imaging (MRI) at 0.02 T. In MRI, the T1 and T2 proton relaxation times were measured. Type 2 muscle fibre atrophy was found in all biopsy samples (100%) and tubular aggregates in 6 of the 7 samples studied (87%). The CT density of the muscle tissue was increased in the only child of the study, decreased in 3 elderly subjects, and normal in the remaining 3 patients. Mean T1 relaxation times of the patients were decreased (135 +/- 5 ms) as compared to those of 6 healthy controls (157 +/- 12 ms) (p = 0.002). The T2 relaxation time was slightly increased (40 +/- 3 ms) as compared to the controls (35 +/- 7 ms; not significant, p = 0.3). Our findings suggest that the thigh muscles of the patients with GA universally show changes in CT and MRI studies, but relaxation time measurements gave little additional information on the muscle metabolism.
A study has been performed with the Canon retinographic equipment on 549 eyes belonging to 3 different groups: normal population, ocular hypertension and glaucoma. The study included the evaluation of the optic disk with special attention to the presence of choroidal peripapillary atrophy, and the distribution and defects in the RNFL. A highly significant association was observed between the presence of peripapillary atrophy and the presence of defects in the RNFL, as well as between the intensity of choroidal atrophy and defects in the RNFL. This association was statistically significant in the population of ocular hypertensives (P = 0.0360) but not in the population of eyes considered normal.
A child is reported with Behcet's disease who presented with skin and joint manifestations, oral ulcers, brainstem syndrome and neurogenic muscular atrophy. The neurogenic muscular atrophy was confirmed by electrophysiologic, histologic and histochemical studies. Electron microscopy of muscle showed a vasculopathy. The possible etiology of the muscle lesions is discussed. The relevant literature on muscle and peripheral nerve involvement in Behcet's disease is reviewed. It is proposed that neuromyopathy be added to the neurological manifestations of Behcet's disease. To our knowledge, this is the first case of neurogenic atrophy reported in Behcet's disease.
Computerized tomography was performed in 31 patients presenting clinical signs of cerebellar degeneration. CT abnormalities consistent with cerebellar atrophy were found in all cases but one. Specific patterns of abnormality were found in olivo-ponto-cerebellar degeneration and in alcoholic atrophy. The CT findings in spino-cerebellar degeneration were varied, ranging from severe diffuse cerebellar atrophy to normality, possibly according to age and duration of symptoms.
19 biopsies of polymyositis patients were compared with 19 matched controls. The presence of smaller fibres in the periphery of the fascicles has been analyzed quantitatively using a perifascicular atrophy factor. The thinner fibres are multiplied by a factor from 1-4, considering their significance for the diagnosis of fibre atrophy. The value obtained with this method from centrally located fibres as related to the value from peripherally located ones is called the perifascicular atrophy factor. If this is less than -300 a myopathy of the group of the polymyositis/dermatomyositis can be assumed. 47 per cent of dermatomyositis biopsies and none of the controls were below this range
The pathogenesis of the hepatic atrophy that accompanies hepatolithiasis was investigated pathomorphologically using a canine model. Two groups were evaluated: infected and noninfected. In the infected group, inflammation in Glisson's capsule caused by cholangitis involved the portal vein at the region of the large bile duct. At this region, the periportal fibrosis ratio was significantly greater in the infected group than in the noninfected group both at 1 and 3 months. At the regions of the septal and interlobular bile ducts, the caliber ratio of the portal vein in the two experimental groups was less than in the normal liver both at 1 and 3 months. At both regions, the caliber ratio of the portal vein in the infected group was less than in the noninfected group at 3 months. The rate of atrophy was significantly greater in the infected group than in the noninfected group at 3 months. These results suggest that disturbance of the portal venous blood flow attributed to cholangitis of the large bile ducts is one of the most important factors leading to hepatic atrophy in hepatolithiasis.
Angiotensin-converting enzyme (ACE) as a part of the renin angiotensin system (RES) regulates blood pressure and fluid and electrolyte homeostasis, and the enzyme is considered to have a function in reproduction. Reduced enzyme activities have been observed in atrophied testes as a results of zinc and pituitary deficiencies. Vitamin A deficiency causes atrophy of testes. The present study was conducted on three groups of male, 3-wk-old, Wistar rats. After 54 d of the experimental period, testicular weights of the vitamin A-deficient rats (A- group, allowed free access to vitamin A- deficient diet) was significantly lower than its pair-fed, PF (given restricted amount control diet) and A+ (allowed free access to control diet) groups. Zinc concentrations and both soluble and particulate ACE activities in the testes of vitamin A- deficient rats (A- group) were significantly lower than the other two groups. No significant differences were observed regarding zinc concentration, particulate ACE, and total ACE activities in the testes of PF and A+ groups. Vitamin A deficiency did not significantly affect the enzyme activity in the lung. From the observations of the present study, we speculate that testicular atrophy in vitamin A deficiency may have resulted from lower zinc concentration and decreased ACE activity in that organ.
We investigated the effect of beraprost sodium (BPS), a new prostacyclin analog, and dizocilpine (MK-801) on repeated ischemia-induced cerebral atrophy and chronic cortical neuronal loss in gerbils. The left common carotid artery of gerbils was repeatedly occluded (for 10, 7, 7, and 7 min) at intervals of 24 h. The thickness of the cerebral cortex of the ischemic hemisphere diminished with increasing time of reperfusion after an ischemic insult. The animals were given BPS (1-100 micrograms/kg, po) or MK-801 (3-300 micrograms/kg, sc) after the first ischemic insult, and then twice daily for 4 wk. Increases in the amount of neuronal loss and acidophilic neurons, and progressive atrophy were observed with increasing time of reperfusion in the cerebral cortex of the ischemic hemisphere. Cortical sections revealed no astrocytes positive for glial fibrillary acidic protein (GFAP), whereas the hippocampal CA1 area showed neuronal loss accompanied by GFAP-positive astrocytes. In control animals at 4 wk survival, the area ratio (area of ischemic cortex/area of opposite cortex) and the cortical neurons ratio (number of neurons in ischemic cortex/number of neurons in opposite cortex) were 89.8 +/- 3.0% and 74.6 +/- 3.4%, respectively. BPS was found to inhibit atrophy and chronic cortical neuronal loss in the ischemic hemisphere in a dose-dependent manner, whereas MK-801 showed no inhibitory effects at any dose tested. These results may suggest that the nature of neuronal degeneration differs between the cortical and hippocampal areas, that cortical neuronal degeneration might not involve glutamate pathways with NMDA receptors in this model, and that prostacyclin could play an essential role in prevention of ischemia-induced progressive neuronal loss.
Pancreatic vasculature was studied in rats treated with a dietary copper-deficient regimen to assess and characterize changes in the exocrine angioarchitecture of the gland. The deficient state is known to induce progressive acinar degeneration, atrophy, and subsequent replacement with noninflammatory lipomatosis. This study was carried out since little information exists regarding changes in the vasculature that accompany acute glandular necrosis. Corrosion casts produced from Mercox injected deficient rats were studied using scanning electron microscopy and compared to injected preparations studied by light microscopy. Results show that with initial atrophy of degenerative acini (6-8 wk), pancreatic lobules decreased in size and the volume of the vascular bed reduced. From wk 8 onward, the accumulation of fat cells expanded the configuration of lobules to more normal dimensions. Although vascular interconnectivity within lobules remained reduced, its basic angioarchitecture remained intact and served to vascularize fat cells in lieu of acini. No acute angiopathic changes indicative of vascular disorganization were found. These observations support the hypothesis that the vasculature of the atrophied pancreas, although modified in regions of the gland most severely targeted by acinar necrosis, remains intact and its basic structural features preserved. Preliminary evidence also supports the observation that preservation of the basic elements of lobular angioarchitecture may form the basis for subsequent regeneration of acinar tissue in the reversed deficient state.
PURPOSE: To determine the usefulness of quantitative measurement of bone atrophy in the diagnosis and the long-term follow-up of patients with complex regional pain syndrome (CRPS). The bone-sparing effect of a 5-hydroxytriptamine (5-HT2) antagonist was also studied. METHODS: Bone mass was measured by computerized micro-densitometry at the middle position of the second metacarpal. The effect of repeated stellate ganglion blocks (SGBs) three times per week with mepivacaine (n = 11), administration of a 5-HT2 antagonist (sarpogrelate hydrochloride, 300 mg a day po) (n = 12), and combined therapy (n = 10) were compared by micro-densitometry and conventional visual analogue scale (VAS) for analgesia after three months of treatment. RESULTS: In CRPS patients, metacarpal index (cortical bone thickness), maximum bone density (cortical bone density), minimum bone density (trabecular bone density), and average bone density were reduced on the affected side (14.1%, 12.1%, 25.0% and 19.3% respectively). The rate of reduction in bone mass correlated with the duration of the disease (P < 0.05). Therapy with the 5-HT2 receptor antagonist (with or without repeated SGBs) decreased pain intensity (from 6.10 to 3.81 with SGB, from 6.30 to 2.91 without SGB, respectively; P < 0.01) and bone atrophy evaluated by micro-densitometry (P < 0.05). In contrast, repeated SGBs alone reduced pain intensity (from 6.30 to 2.91; P < 0.01) but did not ameliorate bone atrophy. CONCLUSION: Bone micro-densitometry is useful in the assessment and follow-up of CRPS and for evaluation of treatment. The 5-HT2 antagonist, sarpogrelate hydrochloride, is a promising treatment for CRPS patients.
Muscular atrophy is a symptom characterized by the loss of normal muscle mass. It is caused by a decline in the total number of muscle cells, or by a substantial decline in the substance of individual muscle cells. It has been associated with a preceding muscle weakness. Muscular atrophy occurs late in the course of a disease. Due to the limited ability of muscle cells to regenerate, it is frequently irreversible. Hence the aim is to detect the early stages of muscular decline and to prevent outright muscular atrophy. To achieve this it is necessary to be aware of the large number of diseases that can induce this in order to ensure timely referral to a specialist.
Leucopenia and diarrhoea are the main side effects observed after the use of mycophenolate mofetil (MMF) in renal-transplant patients. The mechanism of diarrhoea remains unknown. We report on four cases presenting with severe diarrhoea, which appeared, respectively, at 4, 10, 24, and 66 months after MMF therapy had been started. All patients presented with weight loss and biological signs of malabsorption syndrome. Oesophago-gastroduodenoscopy revealed duodenal villous atrophy, which was confirmed by pathology examination. Anti-endomysium antibodies were negative. In all patients, diarrhoea disappeared within 1 month of MMF withdrawal without a gluten-free diet. A control oesophago-gastroduodenoscopy was performed in one patient 6 months later and was considered normal. None of the patients showed evidence of cytomegalovirus in enterocytes or cytomegalovirus-positive viraemia. In conclusion, villous atrophy induced by MMF might be one of the mechanisms of diarrhoea. It is mandatory to differentiate coeliac disease from MMF-induced villous atrophy because, in the latter case, a gluten-free diet is not required.
The purpose of this study was to investigate the atrophic pattern of the muscle groups and their individual muscles in the thigh after meniscal lesions and arthroscopic partial menisectomy. A total of 32 individuals (17 men and 15 women) who underwent arthroscopic knee surgery participated in this study. Their operated and non-operated thighs were scanned by magnetic resonance imaging to determine the volume of the quadriceps (QF), hamstring (HM), and adductors (AD). Compared with the non-operated limb, the volume of the QF was significantly lower in the operated limb; however, no significant difference was observed in the HM and AD. The volume of individual muscles of the QF, i.e. the rectus femoris (RF), vastus lateralis (VL), vastus intermedius (VI), and vastus medialis (VM), in the operated limb was significantly lower than the volume of those in the non-operated limb (P<0.01, all). Although the relative change in the VM was significantly higher than that of the RF (P<0.05), specific atrophy was not found among four individual muscles in the QF. We concluded that meniscal lesions and partial menisectomy induce atrophy in the QF only in the thigh, and that no specific atrophy, e.g. VM, seemed to occur within the individual muscles in the QF.
We describe an MRI technique for quantifying optic nerve atrophy resulting from a single episode of unilateral optic neuritis. We imaged 17 patients, with a median time since onset of optic neuritis of 21 months (range 3-81 months), using a coronal-oblique fat-saturated short-echo fast fluid-attenuated inversion-recovery (sTE fFLAIR) sequence. The mean cross-sectional area of the intraorbital portion of the optic nerves was calculated by a blinded observer from five consecutive 3 mm slices from the orbital apex forwards using a semiautomated contouring technique and compared with data from 16 controls. The mean optic nerve area was 11.2 mm2 in the affected eye of the patients, 12.9 mm2 in the contralateral eye (P = 0.006 compared to the affected eye) and 12.8 mm2 in controls (P = 0.03 compared to the affected eyes). There was a significant negative correlation between disease duration and the size of the affected optic nerve (r = -0.59, P = 0.012). The measurement coefficient of variation was 4.8%. The sTE fFLAIR sequence enables measurement of optic nerve area with sufficient reproducibility to show optic nerve atrophy following a single episode of unilateral optic neuritis. The correlation of increasing optic nerve atrophy with disease duration would be consistent with ongoing axonal loss in a persistently demyelinated lesion, or Wallerian degeneration following axonal damage during the acute inflammatory phase.