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PubMed2001

[Foot surgery in Germany. Historical burden or scientific challenge?].

In Germany foot surgery was established in the late nineteenth century. To correct foot deformities due to paralytic disorders, i.e., poliomyelitis, and congenital deformities, different types of tenotomies and arthrodeses were developed to obtain plantigrade weight-bearing and to avoid external orthosis. A description of surgical techniques during the last century is presented in detail. During those years resection arthroplasties for hallux valgus were common, although some authors recommended osteotomies of the first metatarsal as joint-sparing techniques. Nowadays, further knowledge in etiology, pathology, and biomechanics have effected the therapeutic algorithm in hallux valgus. Nevertheless, discussion about this topic has not come to an end. In 1991 the German Foot and Ankle Society (D.A.F.) was founded. Educational courses to improve surgical skills as well as clinical workshops were successfully established. A marked increase in membership and a broad international acceptance confirm these activities.

Foot↗

PubMed2004

Resistance to disuse atrophy in a turtle hindlimb muscle.

The purpose of this study was to characterize the changes in a turtle hindlimb muscle (external gastrocnemius) after exposure to three conditions of disuse: immobilization, tenotomy, and spinalization. Histochemical analysis and measurement of muscle fiber cross-sectional area and weighted cross-sectional area were used to assess the potential conversion of muscle fiber types and changes in fiber size. It was found that unlike its counterpart in mammalian endotherms, the external gastrocnemius muscle of the adult turtle, Trachemys scripta elegans, was remarkably resistant to each model of reduced muscle function. It is suggested that such resistance to disuse is due to intrinsic mechanisms that enable heterothermic mammals and ectothermic vertebrates to tolerate an unfavorable climate and food and water shortages by using hypometabolic states.

Adenosine Triphosphatases↗

PubMed2005

Ponseti technique for the correction of idiopathic clubfeet presenting up to 1 year of age. A preliminary study in children with untreated or complex deformities.

INTRODUCTION: The aim of this study is to evaluate the effectiveness of the Ponseti method in children presenting before 1 year of age with either untreated or complex (initially treated unsuccessfully by other conservative methods) idiopathic clubfeet. PATIENTS AND METHODS: The authors report 134 feet of 92 patients with Dimeglio grade 2, 3, or 4 deformities treated with the Ponseti method. Twenty-four percent of feet were of complex deformities at initial presentation to the authors' clinics. RESULTS: At a mean follow-up of 46 months (range 24-89) we avoided joint release surgery in 97% of feet. Sixty-seven percent required a percutaneous tenotomy of the Achilles tendon. Relapse rate was 31% (41 feet). We treated 2 relapses by restarting the use of orthosis, 17 with re-casting, 18 with anterior tibial tendon transfer following a second relapse, and 4 feet with extensive joint surgery. Compliance with the use of orthosis was identified as the most important risk factor (P<0.0001) for relapses. Previous unsuccessful treatment attempts by other conservative methods did not adversely affect the results unless the cases had iatrogenic deformities. Cases with iatrogenic deformities from previous treatment had a significantly increased risk of non-compliance and relapse. Experience of the treating surgeon and cast complications were also related to relapses. CONCLUSION: Our results show that the Ponseti technique is reproducible and effective in children at least up to 12 months of age. It can also produce good correction in children presenting with complex idiopathic deformities. Therefore, extensive joint releases should not be considered immediately in such cases. The treating surgeon should be meticulous in using the technique and ensure compliance to foot abduction brace in order to avoid recurrences.

Casts, Surgical↗

PubMed1997

The developmental skeletal growth in the rat foot is reduced after denervation.

It has long been known that bone is innervated. In recent years it has been suggested that the local nerves may influence the growth and metabolism of bone by way of neuropeptides. The transient local presence of nerve-containing cartilage canals just before formation of secondary ossification centres in rat knee epiphyses seems to support that view. The purpose of the present study was to see if denervation affects the developmental growth of metatarsal bones in the rat hindfoot. We made sciatic and femoral neurectomies in 7-day-old rat pups and examined the hindfeet at various times after surgery. Immunohistochemical analysis showed that denervation was complete. Radiographic examination revealed that the metatarsal bones were significantly shorter in denervated hindfeet 30 days after denervation (average relative shortening 9.9 +/- 2.3%). Measurements of total foot length showed that denervated feet were subnormally sized already five days postoperatively, before the onset of secondary ossification. The timing of the latter was not affected by denervation. Control rats subjected to tenotomies exhibited normal metatarsal bone lengths. On the basis of these results we suggest that the local nerves may influence the growth of immature bones but do not affect secondary ossification.

Animals↗

PubMed1993

The first successful surgical treatment of mitral stenosis: the 70th anniversary of Elliot Cutler's mitral commissurotomy.

In 1923 Elliot Carr Cutler, in conjunction with his cardiology colleague, Samuel Levine, performed a closed transventricular mitral commissurotomy with a tenotomy knife on a 12-year-old patient dying of rheumatic mitral stenosis at the Peter Bent Brigham Hospital. This operation was carried out after several years of experimentation regarding resuscitation of the heart, appropriate incisions, and the pathophysiology of mitral stenosis. The interest in mitral stenosis was rampant at the time because of the huge number of patients suffering from this public health problem. The patient survived and went on to die of pneumonia 4 years postoperatively. Subsequent to this, Cutler performed seven more operations using his new cardiovalvulotome, which was to create controlled mitral regurgitation. Unfortunately, this concept did not promote long-term success and a moratorium for these operations was called in 1929. Nevertheless, this pioneering effort in 1923 was the first successful operation to treat valvular heart disease by a surgical technique.

Child↗

PubMed1986

Training increases the concentration of [3H]ouabain-binding sites in rat skeletal muscle.

Exercise is associated with a net loss of K+ from the working muscles and an increased plasma K+ concentration, indicating that the capacity for intracellular reaccumulation of K+ is exceeded. Training reduces the exercise-induced rise in plasma K+, and an increased plasma [K+] may interfere with physical performance. Since the clearing of K+ from the extracellular space depends on the capacity for active K+ uptake in skeletal muscle, the effects of training and inactivity on the total concentration of (Na+ + K+)-ATPase was determined. Following 6 weeks of swim training, the concentration of [3H]ouabain-binding sites in rat hindlimb muscles was up to 46% (P less than 0.001) higher than in those obtained from age-matched controls. Whereas muscle Na+, K+ contents remained unchanged, the concentration of citrate synthase increased by up to 76% (P less than 0.001). Training induced no change in the [3H]ouabain-binding-site concentration in the diaphragm, but in the heart ventricles, the K+-dependent 3-O-methylfluorescein phosphatase activity increased by 20% (P less than 0.001). Muscle inactivity induced by denervation, plaster immobilisation or tenotomy reduced the [3H]ouabain-binding-site concentration by 20-30% (P less than 0.02-0.001) within 1 week. In conclusion, training leads to a significant and reversible rise in the concentration of (Na+ + K+)-ATPase in muscle cells. This may be of importance for the beneficial effects on physical performance by improving the maximum capacity for K+ clearance.

Animals↗

PubMed1982

The effect of elbow joint afferent discharge on transmission in forelimb flexion reflex pathways to biceps and triceps brachii in decerebrate cats.

The present experiments were performed to investigate the influence of elbow joint afferent discharge on the excitability of reflex arcs mediating flexion withdrawal and crossed extensor reflexes in the forelimb muscles of decerebrate cats. The excitability of flexion withdrawal and crossed extensor reflexes in forelimb muscles was shown to be modulated by elbow joint position. Flexion withdrawal reflexes were most easily elicited when the elbow was extended and crossed extensor reflexes were most easily elicited when the elbow was flexed. This modulation of transmission was not confined to reflex pathways projecting to muscles acting at the elbow but also included pathways to muscles acting at the wrist and shoulder in addition to muscles in the contralateral forelimb. The changing excitability of reflex pathways caused by elbow movement was unaltered by degloving the skin covering the joint and tenotomy of the medial head of triceps and the long head of biceps. However, modulation of reflex excitability by joint movement was totally abolished by local anaesthesia of the joint in an otherwise intact limb. Thus, the present experiments indicate that transmission in forelimb flexion reflex pathways can be powerfully influenced by elbow joint afferent discharge.

Animals↗

PubMed1986

Normal electrical activity is not required for the formation of specific sensory-motor synapses.

These studies sought to determine the role of stretch-evoked electrical activity in muscle sensory axons on the formation of specific monosynaptic connections made by these neurons onto spinal motoneurons. Normal activity was disrupted by tenotomy during the developmental stages that the central connections are made. The pattern of connections was normal, suggesting that normal activity is not required in this system for the formation of specific sensory-motor connections.

Animals↗

PubMed1995

Skeletal muscle contraction modulates carbonic anhydrase phenotype in adult mouse dorsal root ganglion neurons.

Recently carbonic anhydrase (CA) activity was demonstrated in adult mammalian proprioceptive neurons of the lumbar dorsal root ganglion (DRG). To assess if neuron-target interactions govern the neuronal CA phenotype, we examined how various experimental procedures which modify the interactions of these neurons with their central and peripheral targets, affect mouse L5 lumbar DRG CA activity. In normal mice and under central disconnection, carbonic anhydrase activity was detected in 30% of neurons. One day after sciatic nerve transaction the percentage of CA-positive neurons decreased to around 50% of that in controls, although both the total number of neurons per ganglion and glial CA content were unchanged. The pattern of CA activity then remained stable until at least 30 days post-operative. All experimental procedures used to block muscle contraction, including ventral rhizotomy, tenotomy, local application to the nerve of both tetrodotoxin and lidocaine or intramuscular injection of the botulinum toxin, produced a significant decrease in neuronal CA staining. Moreover, axonal transport block by vinblastine induced a decrease in CA-positive neurons. These results show that functional neuron-muscle interactions independent of DRG-spinal Cord influences contribute to the regulation of CA activity in lumbar DRG neurons. This modulation could be under the control of unidentified activity-dependent molecular mechanism involving stimuli through the skeletal muscle contraction, inducing in turn, the synthesis of a CA-regulating factor(s) retrogradely transported to the neuronal cell body and/or nuclei.

Animals↗

PubMed1991

Neural influence on the expression of acetylcholinesterase molecular forms in fast and slow rabbit skeletal muscles.

With the aim of investigating the roles of motor innervation and activity on muscle characteristics, we studied the molecular forms of acetylcholinesterase (AChE) in fast-twitch (semimembranosus accessorius; SMa) and slow-twitch (semimembranosus proprius; SMp) muscles of the rabbit. We have shown that SMa and SMp express different patterns and tissue distribution of AChE forms and that the effect of long denervation varies with age. Three principal findings concerning expression of AChE molecular forms emerge from these studies. (1) The activity of AChE and the pattern of its molecular forms are particularly altered in adult denervated SMa and SMp muscles. AChE activity increases by 10-fold in both muscles, but asymmetric forms disappear in SMa and increase by 20-fold in SMp muscles. A similar alteration of AChE is found after tenotomy of these muscles, showing that the effect of denervation may be partly due to suppression of muscle activity. (2) The different changes occurring in the composition of AChE molecular forms in adult denervated SMa and SMp muscles are consistent with fluorescent staining with anti-AChE monoclonal antibodies and with DBA or VVA lectins, which bind to AChE asymmetric, collagen-tailed forms. These lectins poorly stain denervated SMa muscle surfaces but intensely stain neuromuscular junctions and extrasynaptic areas in denervated SMp muscle. (3) In contrast with the adult, denervation of 1-day-old muscles does not markedly modify the total amount of AChE or the proportions of its molecular forms, despite dramatic effects on muscle structure. These results are supported by studies of labeling with fluorescent DBA: the lectin only slightly stains the muscle fiber surface of denervated 15-day-old SMp muscle. Taken together, these data show that denervated muscles escape physiological regulation, producing increased levels of AChE with highly variable cellular distribution and patterns of molecular forms, depending on the age of operation and on the type of muscle.

Acetylcholinesterase↗

PubMed1983

The multiple molecular forms of acetylcholinesterase in "motor end-plate disease" in the mouse (medJ and med allelic forms): sensitivity of the 10 S form to partial or total loss of muscle activity.

Motor end-plate disease in the mouse is a mutation, lethal at the time of weaning. Two alleles exist, med and medJ, with medJ/medJ surviving slightly longer. The multiple molecular forms of acetylcholinesterase show an abnormal developmental pattern during the course of the disease. A decrease in the 10 S AChE proportion to total AChE activity is the major change in gastrocnemius muscle. Similar AChE changes occur after total short-term denervation, tenotomy, and in other genetic diseases. Thus it appears that AChE is modified in med/med muscle as the result of a partial or total loss of muscle activity.

Acetylcholinesterase↗

PubMed1989

Work overload induced changes in fast and slow skeletal muscle myosin heavy chain gene expression.

Work induced hypertrophy of the slow postural soleus and the fast phasic plantaris muscles was produced by tenotomy of the synergistic gastrocnemius muscle. Increases in weight of both muscles were associated with proportionately even larger increases in total RNA and mRNA levels. Alterations in levels of specific myosin heavy chain (MHC) isoform mRNAs were measured using the slot blot procedure with radioactively labelled oligonucleotides as probes. Type 1 MHC gene expression was unaffected in both muscles by work overload, whereas type 2a was deinduced in the soleus and type 2b was deinduced in the plantaris. The neonatal MHC gene was transiently reinduced in the plantaris.

Animals↗

PubMed1979

Fracture of an ossified Achilles tendon.

A case of rupture of an ossified Achilles tendon is described. It is suggested that the management of this condition is surgical. Previously undescribed histological appearances demonstrate osteogenic potential. The significance of subcutaneous Achilles tenotomy is discussed.

Achilles Tendon↗

PubMed1990

Calpains (intracellular calcium-activated cysteine proteinases): structure-activity relationships and involvement in normal and abnormal cellular metabolism.

1. Calpains (calcium-activated cysteine proteinases) have evolved by gene fusion events involving calmodulin-like genes, cysteine proteinase genes and other sequences of unknown origin. 2. The enzymes are composed of two non-identical subunits, each of which contains functional calcium-binding sequences. 3. Calpains are inhibited by the endogenous protein inhibitor, calpastatin and some calmodulin antagonists are also inhibitors of calpain. A number of synthetic proteinase inhibitors also inhibit calpains. 4. Calpains can be activated by phospholipids, an endogenous protein activator and some amino acid derivatives. 5. Various protein substrates for calpains have been recognized in vitro, but the identity of in situ substrates remains unclear. 6. Proposals have been made for calpain function, including involvement in signal transduction, platelet activation, cell fusion, mitosis and cytoskeleton and contractile protein turnover. 7. Calpain and calpastatin expression is altered in a number of abnormal states including muscular dystrophy, muscle denervation and tenotomy, hypertension and platelet abnormalities.

Animals↗

PubMed1975

Nerve supply and experimental myotonia in rats.

20, 25-Diazacholesterol does not induce myotonia in denervated mammalian skeletal muscle, and cordotomy also renders the muscles resistant to the induction of myotonia. Denervation of muscle already rendered myotonic, has no effect on the intensity of the phenomenon. Finally, tenotomy and posterior rhizotomy leave the myotonic activity in the "deafferentated" muscles unchanged. These findings are discussed in relation to "trophic" influences of the motor pathways on the postsynaptic structures of skeletal muscle.

Action Potentials↗

PubMed1980

Mechanisms of muscular hypertrophy.

The effects of synergist tenotomy have been studied on rat soleus muscles after denervation and after interference with sciatic axoplasmic flow with colchicine. The results suggest that neural, as well as muscular, factors cause compensatory hypertrophy (CH) of soleus. The myogenic factor may be mild depolarization of the muscle membranes by passive stretch, as a result of which Ca++ ions enter and stimulate metabolism.

Animals↗

PubMed1983

Compensatory hypertrophy of the soleus in tumor-bearing rats.

Compensatory hypertrophy of the rat soleus was compared between normal rats (N) and rats bearing a non-metastasizing mammary tumor (TB). Two weeks after the tumor inoculation, introduced subcutaneously on the midline of the upper back, the two groups of rats underwent unilateral tenotomy of the plantaris and gastrocnemius muscles to induce functional overload or compensatory hypertrophy of the soleus. One week later, the body weight (BW), wet muscle weights (MW), percent of Type I (slow-twitch) and Type II (fast-twitch) muscle fibers and contractile parameters of the isometric twitch (Pt) and tetanic (Po) tensions were evaluated. The TB animals did not show any signs of cancer cachexia. The sham-operated control soleus muscles of the two groups were similar in wet MW, maximum isometric Pt and Po. The latent period (LP), the contraction time (CT), the half relaxation time (HRT) and the number of Type I (slow-twitch) fibers were increased significantly. The hypertrophied muscles in the N and TB rats showed significant declines in the maximum isometric Pt, compared to their respective controls. These data suggest that the compensatory hypertrophy of muscle is expressed similarly in both the normal and tumor-bearing rats but that it interferes with the generation of isometric twitch tension in the muscle.

Adaptation, Physiological↗

PubMed1984

Core myofibers and related alterations induced in rats' soleus muscle by immobilization in shortened position.

Experimental induction of core myofibers by tenotomy or local tetanus suggests that mechanical factors such as muscle tension loss, shortening or immobilization may play a role in core fiber formation. To test this hypothesis, we investigated the morphologic alterations induced in soleus (SOL) and extensor digitorum longus (EDL) muscles following immobilization of rats' hindlimb in various positions. The SOL and EDL muscles were immobilized in either shortened or lengthened state by applying wire-meshed plaster cast for 1, 2 and 3 weeks. The muscles were dissected out, measured, weighed and examined by histochemistry and electron microscopy. Gross atrophy was noted in all muscles but was greatest in shortened SOL. The SOL atrophy was diffuse and associated with relative increase in type 2 fibers. In EDL, the atrophy selectively involved fibers with low oxidative enzyme activity. Core myofibers were seen mainly in shortened SOL and consisted of myofibrillar derangement, loss of myofilaments and streaming of Z bands. The preferential involvement of shortened SOL (tonic, fatigue-resistant, slow-twitch muscle) suggests that the functional length, loss of tension subsequent to shortening and intrinsic biochemical properties of the muscle are important in core fiber formation.

Animals↗