Abductor hallucis release in congenital metatarsus varus

Summary Adduction of the forefoot diagnosed in the young child generally corrects spontaneously. Resistant forefoot adduction is usually combined with a degree of supination of the forefoot and described as congenital metatarsus varus.In true congenital metatarsus varus there is a contraction or shortening of the abductor hallucis muscle and tendon which is considered to be the primary deforming factor.In the early severe or resistant deformity correction can be achieved by either division of the tendon with release of its capsular attachment, or, in the more severe deformity, by complete release of the abductor hallucis muscle from its extensive attachment to bone and soft tissues.

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Résumé L'adduction de l'avant-pied découverte chez l'enfant jeune se corrige spontanément en règle générale. Dans le cas contraire, elle s'associe habituellement à un certain degré de supination de l'avant-pied et elle est alors décrite comme metatarsus varus congénital.Dans le véritable metatarsus varus congénital il existe une rétraction ou une brièveté du tendon et du muscle abducteur du 1 ^er orteil que l'on considère comme le facteur déterminant de la déformation.Dans les cas de déformation d'emblée sévère ou persistante, la correction peut être obtenue soit par section du tendon et de son insertion sur la capsule, soit, dans les cas les plus graves, par désinsertion complète du muscle abducteur du 1 ^er orteil, tant au niveau de l'os que des parties molles.

     

Survival of nerve and Schwann cells in allografts after cyclosporin A treatment

Because nerve and Schwann cells in allografts are rejected by normal rats, we investigated whether or not these neurological cells would survive if rats were treated with the new immunosuppressive drug, Cyclosporin A. Untreated rats rejected nerve and Schwann cells in allografts of ganglia or nerve. On the other hand, nerve and Schwann cells survived in allografts in Cyclosporin A-treated rats even after drug therapy was terminated. These results indicate that Cyclosporin A may be of value if allogenic nerve or Schwann cells are needed to aid in the repair of injured nerve tissue.     

Differential effects of vecuronium on the thumb and the big toe muscles evaluated by acceleration measurement

To clarify the differential effects of vecuronium on the thumb and on the big toe, train-of-four (TOF) stimuli were applied to the ulnar nerve at the wrist and the tibial nerve at the ankle in anesthetized patients using two acceleration transducers. Ten adult patients, aged 21–55 years, were studied. Anesthesia was induced by an intravenous injection of thiopental, and vecuronium 0.1 mg·kg⁻¹ was used for paralysis. Anesthesia was maintained with nitrous oxide (66%)-oxygen-sevoflurane (1 MAC). The duration of time to the maximal twitch depression on the thumb and the big toe was 136.5±32.5 s and 183.0±40.1 s (P<0.05), respectively. The time to 25% recovery of the twitch height on the thumb and the big toe was 48.1±17.3 min and 39.1±11.6 min, respectively; the time to 50% recovery of twitch height on the thumb and the big toe was 54.1±16.1 min and 40.0±9.2 min (P<0.05), respectively. When paralysis was reversed at 25% of TOF ratio on the thumb, the value of the TOF ratio on the big toe was 58.5±18.2% (P<0.01).     

Cytoarchitecture of diabetic myopathy during the pathogenesis of the disease: Fast versus slow muscle

Diabetic patients exhibit varying degrees of peripheral neuropathy. One of the sequelae of the neuropathy is muscle weakness in the lower limbs, described either as diabetic amyotrophy if the weakness affects the proximal musculature, or motor neuropathy if it affects the distal musculature. The weakness is thought to be related to metabolic disturbances of the disease and changes in the peripheral nerve. In animal models of diabetes, degeneration of myofibers and imyoneural junctions has been noted in both fast (extensor digitorum longus, EDL), and slow (soleus, SOL) muscles. However, observations of changes in skeletal muscle during the pathogenesis of the disease have not been made in either human or animal models of diabetes. It is the purpose of this study to compare the time course in the pathogenesis of diabetic myopathy in these two different types of muscles. Soleus and EDL muscles from 6, 14, and 24+-week-old C57BL/KsJ-db/db and db/+ female mice (N = 12/group) were fixed in situ, processed using standard electron microscopic procedures, and analyzed under the electron microscope. Although both muscles exhibited signs of degeneration, disruption of the mitochondria, and excessive lipid stores, the initial onset and the extent of the myopathy were delayed in soleus. In addition, fewer myofibers in the soleus muscle exhibited signs of denervation and reinnervation. Therefore, diabetic myopathy is progressive during the pathogenesis of the disease but SOL appears to be more resistant to progression of the disease. © 1994 Wiley-Liss, Inc.     

Transplantation of extensor carpi radialis longus muscle in normal and dystrophic chicks

The etiology of avian muscular dystrophy was examined by a cross-transplantation technique. Care was taken for the transplants to regenerate and develop under neural influence, by using the small extensor carpi radialis longus (ECRL) muscle. The ECRL muscles were exchanged between normal and dystrophic chicks 2 to 3 days ex ovo, and the muscle weight, number of muscle fibers, muscle fiber size, and contractile properties of the transplanted muscles were observed 60 to 65 days after operation when the tissue reconstitution was virtually complete. The results obtained for the physiologic, anatomic, and histologic parameters strongly suggested that there exists some failure in the host environment of the dystrophic chicken. The analyses of the histologic parameters suggested that a genetic disorder may also reside in the muscle tissue itself. The myotonic nature of the muscle membrane, however, probably does not contribute significantly to the abnormal behavior of dystrophic chickens. The importance of some neurogenic abnormalities in avian muscular dystrophy is discussed in relation to the results reported by other investigators.     

Development and growth of extensor carpi radialis longus muscle in normal and dystrophic chickens

The development and growth of the skeletal muscles in normal and dystrophic chickens were studied to obtain a clue to the mechanism of dystrophic pathogenesis. A relatively small and isolated muscle--the extensor carpi radialis longus (ECRL) muscle--was utilized to analyze quantitatively the histologic and physiologic parameters. Both normal and dystrophic chickens attained qualitatively the same parameters, but there were some quantitative differences. The first disorder to appear in the dystrophic muscle was a substantial retardation of muscle cell proliferation in the early postnatal development, and the fiber loss was fully compensated by hypertrophy of the remaining cells. The succeeding abnormalities in the dystrophic muscle, e.g., reduction of efficiency in the tension output per unit area, were interpreted as compensating reactions. Therefore, it is likely that the dystrophic lesions in avian muscular dystrophy are caused by retardation of muscle cell proliferation in the early postnatal period. Possible mechanisms for the retardation are discussed in terms of the nerve--muscle trophic interactions which could be greatly intensified in the early postnatal period.     

Effect of nerve extract on number of acetylcholine receptors in denervated muscles of rats

We have shown elsewhere that injection of an extract of peripheral nerves reduces the atrophy of denervated muscle fibers in vivo. Denervated muscle fibers exhibit supersensitivity to acetylcholine owing to the production of extrajunctional acetylcholine receptors. We sought to determine whether or not injection of nerve extract can influence the numbers of acetylcholine receptors in normal, immobilized, or denervated extensor digitorum longus muscles of rats. The receptors were assayed by measuring the binding of ¹²⁵I-α-bungarotoxin. Normally innervated muscles injected with nerve extract exhibited slightly increased binding of the toxin, but this was due to the injections per se. Immobilization caused a small, transient increase in binding of α-bungarotoxin, whereas denervated muscles bound considerably more toxin than innervated controls. The nerve extract did not reduce or prevent the increase in acetylcholine receptors caused by denervation but instead caused an even greater increase. We concluded that the neurotrophic factor extracted from peripheral nerve that is responsible for the maintenance of the sizes of the fibers probably does not down-regulate extrajunctional acetylcholine receptors. The limitation of acetylcholine receptors to the end-plate regions is probably effected by a different mechanism which has yet to be elucidated.     

Blood-brain barrier disturbance and reconstitution after spinal cord hemisection in the rat

Electrophysiologic characteristics and ultrastructural features of single muscle fibers of the dystrophic mouse (C57BL/6J-dy^2J) at various stages of disease were investigated and comparison with those of normal muscle. Resting membrane potentials of the extensor digitorum longus muscle fibers from both normal and dystrophic young mice (to 3 weeks) were between ?90 and ?40 mV. With advancing ages to 7 to 9 weeks, the membrane potentials of normal fibers increased and tended to be within a narrow range around the mean value (?74 mV), whereas those of dystrophic fibers remained at the same value as at 3 weeks (?63 mV), with large deviations. The twitch tension of single fibers induced by direct stimulation was drastically reduced in dystrophic muscle, approximately from one-half to one-third of what it had been in normal fibers. Three-dimensional structures of the T-system in normal muscle observed under a conventional electron microscope revealed the formation of a dense network of tubules along the A-I boundaries of the myofibrils. In dystrophic muscle, the network was poorly developed and the tubules looked disrupted, although the arrangement of myofilaments was preserved relatively well even in the advanced stages. It seems likely that the drastic reduction of contractile force in dystrophic muscle is due to the defect of the internal membrane system, rather than the degeneration of contractile elements.     

Intracellular activity of potassium in normal and dystrophic skeletal muscle from C57BL/6J mice

Potassium-sensitive intracellular microelectrodes were used in vitro to investigate the cause of the depolarization of the resting membrane seen in dystrophic skeletal muscle fibers. In dystrophic fibers the membrane potential (E_m) was found to agree closely with the potassium equilibrium potential (E_K), calculated from measurements of intra- and extracellular potassium activity (a_K), whereas the E_m of normal fibers was depolarized with respect to E_K. However, when (a_K)_o was varied the value of E_m in normal and dystrophic fibers did not conform to that predicted from the Nernst equation. Calculations showed that a relatively high membrane permeability to Na could only partly explain the differences. Na loading of fibers indicated that dystrophic fibers may have a greater electrogenic capacity despite a reported decrease in membrane ATPase activity. It was concluded that measurement of the intracellular activities of Na and Cl as well as K is necessary before the depolarization of dystrophic fibers may be fully described. The changes observed were in agreement with the hypothesis that there is a general membrane disorder associated with muscular dystrophy.     

Motor unit categorization on basis of contractile properties: An experimental analysis of the composition of the cat's m. peroneus longus

Summary Recordings were made of isometric contractions of single motor units of the cat's m. peroneus longus (PerL). The units were activated by stimulation of dissected filaments of ventral roots. In accordance with the general principles introduced by Burke et al. (1973), the 80 isolated PerL units were classified into three or four type-categories according to their contractile speed and endurance. Three currently used varieties of a fatigue index were calculated and found to give equivalent results. Units with a high, intermediate and low resistance to fatigue were responsible for about 22.5, 25.4 and 52.1% respectively of the total muscle force. Two alternative methods for fast/slow categorization were compared: (i) classifying all units as slow that failed to show a sag in partly fused contractions (sagcriterion, Burke et al. 1973) and (ii) classifying all units as slow that had a more prolonged twitch contraction time than that of fatigue-sensitive units (FF vs. S-criterion). The relative contribution of slow units to total muscle force was about 2.8 times as great (14 versus 5%) for a classification by the FF vs. S-criterion than for a subdivision according to sagging behaviour. When compared to equivalent data from previously published studies of feline hindlimb muscles, peroneus longus was found to resemble gastrocnemius medialis in relative motor unit composition. The maximum force of individual PerL units was, however, on average 50% of that reported for corresponding types of gastrocnemius units.