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The mechanisms responsible for hypoventilation during rapid-eye-movement (REM) sleep in patients with diaphragmatic weakness are not clear. Therefore, we studied the effects of unilateral (UDP) and bilateral (BDP) diaphragmatic paralysis on ventilation during wakefulness (W), slow-wave sleep (SWS), and REM sleep. Studies were performed in 3 trained dogs in which small silicone cuffs had been implanted surgically around the phrenic nerves. Reversible diaphragmatic paralysis was induced during wakefulness or sleep by bathing the phrenic nerves in local anesthetic injected through a catheter attached to the phrenic cuffs. The UDP reduced abdominal expansion and increased rib cage expansion, but had no effect on minute volume of ventilation (VI) or end-tidal PCO2 (PACO2). The BDP produced marked abdominal paradox, but did not reduce VI during W or SWS and had no effect on tidal volume or respiratory frequency. In contrast, during REM sleep, VI was decreased by an average of 21% mainly because of a fall in tidal volume, and PACO2 increased by 2.4 mm Hg compared with that during the intact state. Furthermore, addition of extra dead space to the breathing circuit, which was well tolerated in intact dogs, led to a progressive increase in PACO2 during BDP and to arousal from sleep. The findings indicate that acute BDP does not impair ventilation during quiet W or SWS, but reduces ventilation during REM sleep, supporting the concept that during REM sleep maintenance of ventilation is critically dependent on diaphragmatic compensation for intercostal and accessory muscle inhibition.
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PMID:Effect of acute diaphragm paralysis on ventilation in awake and sleeping dogs. 363 36

The influence of tonic inspiratory muscle activity on the relaxation characteristics of the chest wall, rib cage (RC), and abdominal wall (ABW) has been investigated in four highly trained subjects. Chest wall shape and volume were estimated with magnetometers. Pleural pressure (Pes) and abdominal pressure were measured with esophageal and gastric balloons, respectively. Subjects were seated reclining 30 degrees from upright, and respiratory muscle weakness was produced by pancuronium bromide until RC inspiratory capacity was decreased to 60% of control. Only minor changes were observed for Konno-Mead relaxation characteristics (RC vs. ABW) between control and paralysis. Similarly, although RC relaxation curves (RC vs. Pes) during paralysis were significantly different from control (P less than 0.05), the changes were small and not consistent. The differences between paralysis-induced changes in resting end-expiratory position of the chest wall and helium-dilution functional residual capacity (FRC) suggested changes in volume of blood within the chest wall. We conclude that 1) although tonic inspiratory activity of chest wall muscles exists, it does not significantly affect the chest wall relaxation characteristics in trained subjects; 2) submaximal paralysis produced by pancuronium bromide is likely to modify either spinal attitude or the distribution of blood between extremities and the thorax; these effects may account for the changes in FRC in other studies.
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PMID:Effects of paralysis with pancuronium on chest wall statics in awake humans. 399 28

Static and dynamic lung volumes, maximum respiratory pressures and lung compliance and resistance were registered in 54 subjects with hemiplegia or hemiparesis after stroke. These measures of ventilatory function were related to the degree of motor impairment and to the interval between stroke and investigation. In general ventilatory function, particularly parameters depending upon expiratory force, was restricted. This was most pronounced in subjects with severe hemiplegia while those with hemiparesis had only small changes. Since dynamic lung volumes (corrected for volume loss), lung compliance and resistance were all normal, it is evident that intrinsic lung function was unaffected. Inspiratory capacity - but no other measured variables of respiratory function - was lower six months after the stroke than earlier. It is suggested that expiratory muscle dys-coordination and weakness caused expiratory dysfunction while the less pronounced inspiratory restriction may be caused by muscular dysfunction and, as time goes by, by rib cage contracture.
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PMID:Restrictive ventilatory dysfunction in stroke: its relation to locomotor function. 658 33

The stethograph is an air-filled tube strapped to the chest. It was popular in the early part of the century as a means of detecting rib cage motion. When a second stethograph is strapped to the abdomen and coupled to an x-y recorded, a 'loop' is generated which characterizes the thoracoabdominal motion during inspiration. Inspiratory muscle weakness or dysynchrony can be reliably and economically evaluated with this technique. Visualizing thoracoabdominal motion on an x-y recorded provides a useful means of instructing patients during breathing retraining.
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PMID:Douglas revisited. A stethographic method for visualizing thoracoabdominal motion. 708 91

The effect of 6-hydroxydopamine (6-OHDA) injected into the cerebral ventricles on behaviour of singly- and group-housed cats was investigated. 6-OHDA in doses of 0.5, 1 and 2 mg was administered every morning for 5 to 8 days. In small doses 6-OHDA in singly- and group-housed cats evoked motor phenomena such as tremor, ataxia, rigidity, weakness and sometimes clonic-tonic convulsions. Occasionally restlessness, irritability and rage were observed. Large doses of 6-OHDA in group-housed cats, after a short latent period (2-3 days) produced aggression which intensified on subsequent injections, and thereafter, on repeated administrations, no longer occurred. The aggression consisted of restlessness, irritability, anger, rage, apprehension, threat, attack, fighting, flight and crying. Of autonomic phenomena mydriasis, dyspnea and sometimes piloerection were observed. The aggression was initiated by the most restless cat, or by disturbing the animals, such as by moving the cage. When 6-OHDA no longer produced aggressive behaviour, motor changes such as tremor, ataxia, rigidity, walking on broad base, weakness with adynamia and clonic-tonic convulsions developed. These latter symptoms were produced by large doses of 6-OHDA in singly-housed cats. In these animals spontaneous signs of aggressive behaviour usually were not observed, although if handled they showed rage, snarling and hissing. When singly-housed cats were kept in the same cage with group-housed animals, the singly-housed cats usually became aggressive. It appears that hyperactivity induced aggression in 6-OHDA-treated cats.
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PMID:6-hydroxydopamine and aggression in cats. 719 85

The conventional wheelchair sling seat provides little or no support to the spine of a child with myopathy or neurogenic muscular weakness. As the spinal muscles become weaker scoliosis may develop with associated deformity, pain and restriction of cardio-respiratory function. If muscle weakness is severe, the resultant fully developed deformity is virtually impossible to treat. Slowing the rate of increase of the deformity is, therefore, the most hopeful avenue of attack. This work addresses the hypothesis that custom moulded seating can increase sitting comfort and slow the rate of progression of spinal curvature in children with paralytic scoliosis, and further, that a range of standard or modular seats can achieve these goals at less cost. Previous work on this problem has ranged from simply padding the armrest, in order to distribute force over the rib cage, through to custom moulded seating. Our initial experience with custom moulding, using the bean bag evacuation and consolidation technique, produced several comfortable seats although the technique was labour intensive and therefore costly. This led us to attempt to develop a method of providing comfortable seating that would help control spinal deformity at reasonable cost. This paper describes the design of a standardized seating system for school age children with myopathy or neurogenic muscular weakness. Preliminary results indicate that this technique may have advantages over alternative methods of treatment. The radiological study is continuing.
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PMID:Modular seating for paralytic scoliosis: design and initial experience. 732 72

Pregnancy often poses a risk to patients with neuromuscular and skeletal disorders when these affect the respiratory muscles or the rib cage. The outlook is determined both by the severity of the underlying condition and the physiological changes during pregnancy. Patients with a vital capacity of less than 1 to 1.5 litres, hypercapnia, severe scoliosis, diaphragm weakness or pulmonary hypertension before pregnancy are particularly at risk. Pregnancy may adversely affect the conducting airways, respiratory pump and gas exchange in the lungs. Close monitoring of high risk patients during pregnancy is required and either a termination of pregnancy or mechanical respiratory support may be indicated if ventilatory or cardiac failure develops.
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PMID:Pregnancy in neuromuscular and skeletal disorders. 808 20

Multicore myopathy is a rare congenital myopathy that can cause progressive weakness, but it has not been recognized previously to have respiratory consequences. This study describes two patients who developed respiratory failure because of respiratory muscle weakness. Both patients had low vital capacities without evidence of airway obstruction, and CO2 retention. Physical examination found that neck accessory muscles and abdominal muscles were very weak. In inspiration the abdomen expanded, but the rib cage contracted. Detailed studies were done in one patient with magnetometers, esophageal and gastric pressures, flow and volume, and electromyograms of abdominal and neck accessory muscles. Peak static inspiratory and expiratory pressures were 28 and 30 cm H2O, respectively, and maximal transdiaphragmatic pressure was 28 cm H2O. Vital capacity was reduced to 44% of predicted. Lung compliance was normal. In spontaneous breathing while supine, rib-cage diameters decreased while gastric pressure increased in inspiration, suggesting the weak diaphragm was the main muscle of respiration. EMG recordings showed no evidence of recruitment of the wasted neck accessory muscles (sternocleidomastoid and scalene), whereas electromyograph plus mechanics measurements gave evidence of abdominal muscle use in the sitting but not the supine posture. More limited studies in the second patient gave similar results. Multicore disease in these two patients thus caused marked weakness of all respiratory muscles, affected the intercostal-accessory group more than the diaphragm, and led to respiratory failure.
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PMID:The respiratory muscles in multicore myopathy. 831 4

Respiratory muscle weakness is the primary cause of respiratory dysfunction in neuromuscular disease (NMD), but structural abnormalities of the chest wall also play a role. In adults with NMD, restrictive lung disease is in part caused by reduced chest wall compliance (C(W)), believed to reflect stiffening of connective tissue resulting from chronically reduced chest wall motion in the presence of respiratory muscle weakness. We hypothesized that chronic limitation of chest wall motion in young children with NMD leads to structural underdevelopment of the chest wall, and results in increased, rather than decreased, C(W). In 18 subjects with NMD, ranging from 3 mo to 3.8 yr of age, we compared C(W) with values obtained in children without NMD. A modification of the Mead-Whittenberger technique was used, with respiratory muscle relaxation provided by brief manual ventilation. Respiratory system compliance (Crs) and lung compliance (C(L)) were calculated from airway opening pressure, transpulmonary pressure, and tidal volume. C(W) was calculated as 1/C(W) = 1/Crs - 1/C(L) during manual ventilation. C(W)/kg was higher in subjects with NMD than in controls, at 5.2 +/- 2.8 (mean +/- SD) versus 2.4 +/- 0.8 ml/cm H2O (p < 0.001). In subjects who had normal lung compliance values during spontaneous breathing (C(Lspont)), C(W)/C(Lspont) was significantly greater in subjects with NMD (5.5 +/- 3.2) than in controls (1.9 +/- 1.0) (p < 0.001). By predisposing to rib cage deformation and reduced end-expiratory lung volume, abnormally high C(W) in infants and young children with NMD may contribute to respiratory dysfunction.
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PMID:Chest wall compliance in infants and children with neuromuscular disease. 888 5

A possible protective effect of a novel free radical scavenger, OPC-14117, on the progressive motor neuron death in wobbler mice was examined. Clinical parameters such as mortality, body weight, motor activity as a rolling number of circular cage, and forelimb muscle power as grasping on a rolling column, an angle of slipping down from slope, and hanging ability on a flat plate were compared every 4 weeks from 4 to 36 weeks of age among mice groups treated with vehicle or daily oral administration of OPC-14117 of 10 or 30 mg/kg body weight. The treatment with OPC-14117 dose dependently improved the clinical parameters such as mortality, motor activity, and forelimb weakness. Pathological analysis showed that a diffuse neurogenic change in the forelimb muscle was improved at 36 weeks of age in the drug treated mice with a marked preservation of motor neurons in the spinal cord. Treatment of the mice with the drug reduced age-dependent increase of lipid peroxides in the spinal cord in vivo, and a supplement of the drug to the homogenate of spinal cord in vitro ameliorated the formations of lipid peroxides generated by an exogenous addition of ascorbate or xanthine/xanthine oxidase. These results suggest that OPC-14117 has a protective effect on the motor neuron death probably as a free radical scavenger, resulting in an improvement of clinical symptoms in wobbler mice.
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PMID:Protective effect of a novel free radical scavenger, OPC-14117, on wobbler mouse motor neuron disease. 908 82


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