[The origin of myelinated nerve fibers of the peribronchial plexus].
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Children with neuroblastoma whose opsomyoclonus recurs or persists after initial surgery should be carefully evaluated for tumor. If no tumor is detectable, therapy with ACTH should be considered in patients whose symptomatology is severe enough to compromise normal development.
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Fast axonal transport is altered in nerves from amyotrophic lateral sclerosis (ALS) patients. Microtubules are involved in axonal transport. We analyzed the possibility of an involvement of microtubule modifications underlying the alterations in transport using biochemical and morphologic analysis of intercostal nerves from ALS and control patients. In intercostal nerves displaying no morphologic signs of acute neuronal degeneration, two-dimensional gels showed modifications of the group of beta tubulins and abnormal spots of proteins, some appearing to be closely related to tau proteins. These results suggest that microtubule proteins are modified in ALS before ultrastructural axonal degeneration, but the significance of these abnormalities remains hypothetical.
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The influence of vascularized intercostal nerve detachment on axonal regeneration and skeletal muscle recovery was examined in two experiments using two mongrel dogs. Experiment 1: The influence of detachment of the vascularized intercostal nerve on axonal regeneration and interfascicular blood flow was examined. Detachment of the intercostal nerve without accompanying blood vessels resulted in a marked decrease in blood flow and axonal degeneration at the distal 60% of the total length of the intercostal nerve. In contrast, no significant axonal degeneration was observed in the intercostal nerve that remained vascularized. Experiment 2: The condition of the biceps brachii muscles was continuously studied up to 9 months after intercostal nerve transfer. 1) Nine months after the intercostal nerve transfer, the regeneration of the biceps brachii as estimated by the wet weight was better at the vascularized side than at the unvascularized side. 2) Histochemical analysis on the biceps brachii revealed that type 1 fiber was predominant over type 2 fiber at six months post-transfer, whereas both type 1 and type 2 fiber were equally present at one month after transfer.
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Shoulder girdle compression syndroms appear intermittently and according to body carriage. Very seldom they are caused by neck ribs, mostly by a costoclavicular narrowness. Important for the symptoms is the nerval plexus compression, for diagnostic reasons the blood vessel compression. Essential are provocating tests, subclavia phonogramms and in doubtful cases, angiography. Oszillo- and sonography often fail, EMG and nerval conductive measurement are only of differential diagnostik importance. In all together 120 healthy persons compression was shown phonographically, phlebographically and manometrically in 58--88%. Only the symptomatic and distinct compression are abnormal. Physiotherapy should be applied, only operative decompression is a causal treatment. The transaxilar resection of the first rib with scalenotomy and eventually also resection of a neck rib is by fat better than any other method. This is a report of 112 operated patients.
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The progress of the functional conversion in cases where the 3rd and 4th intercostal nerves were crossed to the musculocutaneous nerve to regain elbow flexion after a total avulsion type of brachial plexus injury was followed up by means of the electromyogram, goniogram and spirogram in 25 patients. The joint position sense was further studied. It was found that in the early stage of reinnervation, spontaneous activity which synchronized with respiration was found in the biceps brachii muscles, but this involuntary element disappeared gradually and followed this the volitional control and endurance improved and became quite satisfactory within several years. It was observed that skin sensation played an important role in judging joint position.
In anesthetized cats, the somato-sympathetic reflex was recorded in T3 white ramus and in the lower cardiac nerve during stimulation of intercostal nerves of the T3 and T5 segments. The amplitude of the early response in the preganglionic nerve was considerably higher than the amplitude of the late response, while the reverse was true for the postganglionic nerve. After transection of the spinal cord in the C4-5 level, the late responses were observed both in the lower cardiac nerve and in T3 white ramus. The late response seems to be realisable by the spinal structures. Active role of sympathetic ganglion in transmission of impulses from the spinal cord to effectors, was noted.
The present study investigated the contributions of vagal and nonvagal sensory nerve fibers on neurogenic inflammation in rat bronchial airways. A surgical procedure was developed via the rat mediastinum ventral intercostal space to prepare an intercostal opening without causing pneumothorax for performing stellate ganglionectomy alone, thoracic vagus nerve section alone, and stellatectomy plus thoracic vagotomy, and for injecting capsaicin (2 microl, 10 mg/ml) and 6-hydroxydopamine (2 microl, 50 mg/ml) into the ganglion. One week later in our procedure, we investigated if neurogenic inflammation induced by an intravenous injection of capsaicin (300 nmol/ml/kg) and innervation density of substance P-immunoreactive sensory axons could be decreased after chronic denervation in the rat lower airways. The major findings were that surgical removal of the right stellate ganglion and local capsaicin application resulted in a significant attenuation of neurogenic plasma extravasation in the right bronchial tree evoked by systemic capsaicin application. Reduction of neurogenic plasma extravasation was totally abolished by combined stellatectomy and thoracic vagotomy. The number of substance P-containing axons was also greatly decreased following these surgical and capsaicin treatments. It is concluded that sensory nerve fibers from both vagal source and nonvagal (spinal) source, which associated with the stellate ganglion, contributed significantly to neurogenic inflammation in the bronchial airways with a slightly higher contribution from the vagus nerve.
The aim of the present study was to analyze changes in the enkephalin immunoreactivity of sympathetic prevertebral ganglia coeliac plexus and inferior mesenteric ganglion) and intestinal tract (myenteric plexus and external muscle layers) in cats 2 days after left thoracic splanchnic nerve ligation, using radioimmunoassay and immunohistochemical techniques. Specific polyclonal antibodies directed against methionine- and leucine-enkephalin were used. The nerve ligation led to a considerable increase in the enkephalin immunoreactivity in the cranial part of the ligated nerves. This finding confirms the presence, in the cat, of an enkephalin output originating from thoracic spinal structures which are probably enkephalin-containing preganglionic neurons. In prevertebral ganglia the nerve ligation induced a marked decrease in the enkephalin immunoreactivity, which was probably due to the interruption of thoracic enkephalin efferents projecting towards both the coeliac plexus and the inferior mesenteric ganglion. In the digestive tract, the nerve ligation depressed the methionine-enkephalin immunoreactivity only in the gastro-duodenal region, and had no effect on the ileo-colonic region. The results of the present study add to the growing evidence that the sympathetic nervous system is involved in regulating the enteric enkephalinergic innervation, which is probably involved in controlling the intestinal motility.
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To determine whether the gut or liver releases galanin during sympathetic neural activation, we performed bilateral thoracic splanchnic nerve stimulation (BTSNS) in halothane-anesthetized dogs. Using experimentally determined galanin extraction rates of 60% for gut and no extraction by liver, calculations demonstrated a minor increase in gut spillover during BTSNS (delta = +4.8 +/- 1.8 pmol/min), whereas liver spillover of galanin-like immunoreactivity (GLIR) increased markedly (delta = +27.9 +/- 9.5 pmol/min). To confirm the finding of liver galanin release, GLIR was measured in femoral artery, portal vein, and hepatic vein during hepatic nerve stimulation (HNS). GLIR spillover from gut was not increased by HNS (delta = +1.9 +/- 6.3 pmol/min). In contrast, liver GLIR spillover was greatly increased during HNS (delta = +53.3 +/- 16.4 pmol/min). Extracts of canine liver contained 2.7 +/- 0.4 pmol GLIR/g tissue. We conclude that, despite the known significant galanin content of the gut, little galanin is released from this organ during sympathetic activation. In contrast, the liver, heretofore not described to contain galanin, contains and releases significant amounts of the peptide during sympathetic activation.