[The difficulties of rigidity determination with the Schioetz tonometer].
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Laminectomy is the accepted treatment for spinal canal stenosis in cases where conservative treatment has failed. Opinions diverge on the resulting clinical instability and the necessity of instrumented stabilization. The present biomechanical study was performed to determine the functional impairment following laminectomy and the stabilizing effect of flexible and rigid devices. This was the first time that the effects of agonist and antagonist intersegmental lumbar muscle forces acting on intact, unstable and instrumentally stabilized functional spinal units have been investigated. Six human cadaveric lumbar spines were tested in a spine tester. The coactivation of agonist and antagonist muscle forces resulted in increased stability under the load conditions of bending and rotation; a slight increase in the range of motion was noted during flexion. The functional impairment following laminectomy was corrected by ligamentoplasty and by means of muscle forces. Ligamentoplasty appears to be an alternative to decompression with spondylodesis, especially in patients with well-developed muscles.
Malignant hyperthermia (MH) is a chemically induced, genetic myopathy characterized by metabolic and respiratory acidosis, arrhythmias, hyperpyrexia, and muscular rigidity usually occurring during or within 24 hours postanesthesia. It is initiated by some anesthetic drugs, muscle relaxants, and possibly by catecholamines produced by stress. The incidence of the disease is 1:15,000 in populations who have received a general anesthetic. A recently developed platelet bioassay test allows for rapid identification of the susceptible individual, while medication with dantrolene sodium can usually prevent or reverse the syndrome.
The syntheses and antinociceptive activities of all three isomeric 1-[2-(pyridyl)ethyl]-4-(propionanilido)-piperidine isosteres (11a-c) of fentanyl (1) are described. The 2- (11a), 3- (11b) and 4-pyridyl (11c) isomers exhibited 10, 2 and 0.2 times the antinociceptive activity of fentanyl, respectively. The ED50 values for 11a, 11b, 11c and fentanyl in the rat 4% NaCl-induced writhing test were 0.00023, 0.00085, 0.0087 and 0.0021 mg/kg sc, respectively. The 3-pyridyl (11b) and 4-pyridyl (11c) compounds were further elaborated to the 6-phenyl-1,6-dihydropyridine (12), C-2 H, Me, n-Bu and Ph 1,2-dihydropyridine (13a-d) analogues having a phenoxycarbonyl substituent on the dihydropyridine ring nitrogen. The most active compound in this series was 1-(2-[3-(1-phenoxycarbonyl-6-phenyl-1,6-dihydropyridyl)ethyl ])-4- (propionanilido)piperidine (12), which provided a 58% inhibition of writhing at a dose of 0.4 mg/kg sc. 1-(2-[4-(1-phenoxycarbonyl-1,2-dihydropyridyl)ethyl])-4- (propionanilido)piperidine (13a) exhibited an ED50 of 1.3 mg/kg sc, indicating a decrease in antinociceptive activity of about a 100 fold relative to the parent 4-pyridyl compound (11c). The dihydropyridine analogues 12 and 13 exhibit substantial antinociceptive activity relative to meperidine (ED50 = 0.6 mg/kg sc). The muscular rigidity effect induced by the pyridine compounds (11a-c) at a dose of 4 mg/kg sc, was not illicited by the dihydropyridine analogues at the same dose, or at a high dose of 40 mg/kg sc (13a). Compounds 12 and 13 may therefore be useful lead compounds for the development of more useful 4-anilidopiperidines if the antinociceptive activity can be dissociated from the muscular rigidity effect.
The parkinsonian syndromes include idiopathic Parkinson's disease, parkinsonian syndromes secondary to several known causative agents, and parkinsonian syndromes associated with more widespread CNS lesions and extensive neurologic deficits. They constitute movement disorders with a similar constellation of symptoms: rigidity, tremor, bradykinesia, gait impairment, and postural instability. All of the parkinsonian syndromes are associated with excess morbidity and mortality from respiratory causes, and all can produce the pattern of pulmonary function impairment consistent with neuromuscular disease. In addition, the parkinsonian syndromes can produce upper airway obstruction and abnormalities of ventilatory control, both of which can be life-threatening in those with MSA. The medications used to treat these disorders can also produce respiratory disease. A syndrome of L-dopa-induced respiratory dysfunction has been described, which may be a heterogeneic disorder of choreiform movements of the respiratory muscles, rigidity-akinesis of the respiratory muscles, or abnormal central control of ventilation, all related to the drug. In addition, the ergot-derived dopamine agonists can cause pleural and pulmonary fibrosis.
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