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PubMed1996

Function of somite and somitocoele cells in the formation of the vertebral motion segment in avian embryos.

We have studied the distribution of thoracic somite and somitocoele-derived cells using homotopical grafting between quail and chicken embryos and reincubation periods of 2-6 days. Serial sections were evaluated with antibodies against quail cells, quail hemangiopoietic cells and desmin. With the exception of neural crest cells in the cranial sclerotome half, all cells of the operated segment are quail cells derived from a single somite. These cells differentiate into sclerotome, myotome and the anlage of the dermis of the back. After longer reincubation periods, the somite-derived quail cells form the neighboring halves of 2 adjacent vertebral bodies and the intervening (disc-homologous) tissue. Resegmentation is furthermore visible in the lamina and the spinous process. Somite cells also form the articular and transverse processes, and the intertransverse muscle including its insertion to the next cranial transverse process. One thoracic somite forms the proximal part of 1 rib. In more distal parts, 1 somite forms the cranial half of 1 rib and the caudal half of the next cranial rib, and the intercostal muscle and part of the connective tissue. Somite-derived quail cells are found in muscle that bridges over 2 segments cranial and caudal from the operated segment. The craniocaudal distribution of endothelial cells is approximately the same. Somitocoele cells that are located centrally in the epithelial somite express the sclerotome-markers Pax-1 and Pax-9. After 2-3 days of reincubation, grafted thoracic somitocoele cells are found mainly in the cranial part of the caudal sclerotome half. They form an area representing the anlagen of the intervertebral disc and the rib. After longer reincubation periods, the grafted quail somitocoele cells form the intervertebral disc-homologous tissue and the proximal part of the rib. In more distal parts of the rib they are located in the cranial half of 1 rib and the caudal half of the next cranial rib. The somitocoele cells also form the surface of the intervertebral joint, and give rise to a small number of endothelial cells that are found up to 1 segment cranial and caudal to the operation site. Our studies show that resegmentation is found in most parts of the vertebra and in the distal ribs. One somite forms the origin and insertion of the segmental muscle. Therefore, the somite can be regarded as the ancestor of the vertebral motion segment. Somitocoele cells are located centrally both in the epithelial somite and in the vertebral motion segment.

Animals↗
PubMed1999

The homeobox gene Msx1 is expressed in a subset of somites, and in muscle progenitor cells migrating into the forelimb.

In myoblast cell cultures, the Msx1 protein is able to repress myogenesis and maintain cells in an undifferentiated and proliferative state. However, there has been no evidence that Msx1 is expressed in muscle or its precursors in vivo. Using mice with the nlacZ gene integrated into the Msx1 locus, we show that the reporter gene is expressed in the lateral dermomyotome of brachial and thoracic somites. Cells from this region will subsequently contribute to forelimb and intercostal muscles. Using Pax3 gene transcripts as a marker of limb muscle progenitor cells as they migrate from the somites, we have defined precisely the somitic origin and timing of cell migration from somites to limb buds in the mouse. Differences in the timing of migration between chick and mouse are discussed. Somites that label for Msx1(nlacZ )transgene expression in the forelimb region partially overlap with those that contribute Pax3-expressing cells to the forelimb. In order to see whether Msx1 is expressed in this migrating population, we have grafted somites from the forelimb level of Msx1(nlacZ )mouse embryos into a chick host embryo. We show that most cells migrating into the wing field express the Msx1(nlacZ )transgene, together with Pax3. In these experiments, Msx1 expression in the somite depends on the axial position of the graft. Wing mesenchyme is capable of inducing Msx1 transcription in somites that normally would not express the gene; chick hindlimb mesenchyme, while permissive for this expression, does not induce it. In the mouse limb bud, the Msx1(nlacZ )transgene is downregulated prior to the activation of the Myf5 gene, an early marker of myogenic differentiation. These observations are consistent with the proposal that Msx1 is involved in the repression of muscle differentiation in the lateral half of the somite and in limb muscle progenitor cells during their migration.

Animals↗
PubMed1998

[An autopsy case of rigid spine syndrome].

We reported an autopsy case of rigid spine syndrome. A 20-year-old woman developed severe respiratory failure despite well-preserved muscle strength in her extremities. Although she had mechanical ventilation during sleep, she had normal arterial blood gas values during daytime. She was found dead in a morning approximately 71/2 years after the onset of the respiratory symptoms. At autopsy, the respiratory diaphragm and intercostal muscles, and the truncal paravertebral and sternocleidomastoid muscles were more significantly affected than the limb muscles. Many corpora amylacea were found in the whole spinal cord, though the significance remains to be elucidated.

Adult↗
PubMed1981

The interaction between reflex apnoea and bradycardia produced by injecting 5-HT into the nodose ganglion of the cat.

The apnoea, accompanied by bradycardia and hypotension caused by injection of 5-Hydroxytryptamine (5-HT) into the vascularly isolated nodose ganglion is characterised by intense electrical activity in the internal intercostal muscles. No such activity was recorded when apnoea was provoked by electrical stimulation of the central end of the superior laryngeal nerve. The cardiac slowing induced by 5-HT was less marked when the superior laryngeal nerve was concomitantly stimulated with an intensity sufficient to inhibit the internal intercostal activity. When central respiratory drive was depressed by hypocapnic ventilation nodose ganglion-induced bradycardia was comparable to that provoked during electrical stimulation of the superior laryngeal nerve in eupnoea. Unlike chemoreceptor-induced bradycardia the cardiac slowing caused by nodose ganglion stimulation was not reduced by "ramp" inflation of the lungs. The results were similar during hypocapnic depression of the "Respiratory Centre". These findings suggest that: (a) central expiratory activity contributes to the bradycardia induced by nodose ganglion stimulation, and (b) the inhibition of bradycardia by lung expansion occurs before the neural impulses reach the nucleus ambiguus but does not involve the central respiratory neurones.

Animals↗
PubMed1990

Mechanisms of abdominal muscle activation during vomiting.

The possible contribution of spinal reflexes to abdominal muscle activation during vomiting was assessed in decerebrate cats. The activity of these muscles is partly controlled by bulbospinal expiratory neurons in the caudal ventral respiratory group (VRG). In a previous study it was found that the abdominal muscles are still active during vomiting after midsagittal lesion of the axons of these neurons between C1 and the obex (A.D. Miller, L.K. Tan, and I. Suzuki. J. Neurophysiol. 57: 1854-1866, 1987). The present experiments indicate that this postlesion activity was due to spinal stretch reflexes because 1) such midsagittal lesions eliminate abdominal muscle nerve activity during fictive vomiting in paralyzed cats in which there are no abdominal stretch reflexes, 2) the abdominal muscles are activated during vomiting by spinal reflexes after upper thoracic cord transections, and 3) the normal 100-ms delay between diaphragmatic and abdominal activation during vomiting is reduced to approximately 20-25 ms after both types of lesions, which is consistent with postlesion abdominal reflex activation. Our results also suggest that, during normal vomiting, abdominal stretch and tension reflexes have only a minor role if any and abdominal muscle activation is probably mediated primarily or exclusively by expiratory neurons in the caudal ventral respiratory group. However, our finding that phrenic activity is reduced both during vomiting after thoracic transections and during fictive vomiting after paralysis is consistent with a contribution of reflex activity from abdominal and/or intercostal muscles to phrenic discharge during normal vomiting.

Abdominal Muscles↗
PubMed1987

Synaptic vesicle abnormality in familial infantile myasthenia.

In familial infantile myasthenia (FIM) the miniature end-plate potential (MEPP) amplitude is normal in rested muscle, but stimulation in vitro at 10 Hz decreases it abnormally, and neuromuscular transmission fails in a few minutes. In search of a morphologic correlate of the transmission failure, we analyzed the densities and diameters of synaptic vesicles in deep and superficial regions of nerve terminals in external intercostal muscles of three FIM patients and three nonweak controls before and after 10-Hz stimulation for 10 minutes. The densities of superficial or deep synaptic vesicles before or after stimulation in FIM were not significantly different from the corresponding control values. The diameters of superficial and deep synaptic vesicles before stimulation were significantly smaller in the three FIM patients than in the three controls. Stimulation in the FIM patients reduced the MEPP amplitude by 51 to 75%, but increased the vesicle diameter in two patients and did not change the vesicle diameter in one patient. Stimulation in the controls reduced the MEPP amplitude by only 16 to 34%, decreased the vesicle diameter in two, and did not change the vesicle diameter in one. Stimulation after treatment with 1 mg/dl hemicholinium markedly reduced the MEPP amplitude in the controls, had no further effect on the transmission defect in FIM, and had no consistent effect on vesicle diameter in FIM or controls. We conclude that synaptic vesicles are abnormally small in rested muscle in FIM, but vesicle size cannot be reliably correlated with the MEPP amplitude in FIM or controls.

Adult↗
PubMed1991

[Reconstruction of anterior chest wall defect with ceramic bone grafts--a case of localized malignant mesothelioma].

The reconstruction of an anterior chest wall defect was performed on a 61-year-old male after resecting a localized malignant mesothelioma. The tumor was resected with body of the sternum, the anterior portion of the bilateral second, third and fourth ribs, muscles, subcutaneous tissue and skin. The defect was 12.5 cm x 9.5 cm in size. The reconstruction of the defect was made with Marlex mesh, two ceramic bone grafts and a latissimus dorsi musculocutaneous flap. Double Marlex mesh was sewn under the edges of the ribs and the intercostal muscles of the defect by interrupted sutures. In order to fit the ceramic bone graft to the defect transversely, two pieces of ceramic bones (Iliac crest spacers) were selected from various sizes. They were connected by a stainless steel wire through the holes which were originally made at the edge for fixation, and the connected portion was covered with methyl methacrylate. Two ceramic bone grafts were fixed to each of the stumps of the bilateral third and fourth ribs by monofilament threads. A musculocutaneous pedicle flap made from the right latissimus dorsi covered the operative filed. There were no postoperative wound infection and no extrusion of the prostheses seven months after the operation.

Biocompatible Materials↗
PubMed1983

In vitro degradation of leucine in muscle, adipose tissue, liver, and kidney of fed and starved sheep.

In vitro rates of conversion of [1-14C]leucine to 4-methyl-2-oxo[1-14C]pentanoate and of oxidation of [1-14C] and [U-14C]leucine were measured for tissues from fed and starved (5 days) sheep. Slices of liver and kidney and preparations of adipose tissue and of fibre bundles of external intercostal muscle (EIC) were used. Skeletal muscle is likely the major site of leucine catabolism in sheep although adipose tissue is capable of substantial metabolism. Muscle and adipose tissue from fed sheep released 17 and 5% of the [1-14C]leucine transaminated as 4-methyl-2-oxo-[1-14C]pentanoate and upon starvation the proportions were increased (P less than 0.001) to 46 and 32%. Starvation reduced (P less than 0.01) leucine catabolism in all tissues except the kidney. The pattern of leucine catabolism in EIC muscle changed from extensive oxidation in the fed state to being limited essentially to transamination and decarboxylation in the starved state.

Adipose Tissue↗
PubMed1995

Multiple defects and perinatal death in mice deficient in follistatin.

Follistatin, an activin-binding protein and activin antagonist in vitro, can bind to heparan sulphate proteoglycans and may function in vivo to present activins to their receptors. In the mouse, follistatin messenger RNA is first detected in the deciduum (on embryonic day 5.5), and later in the developing hindbrain, somites, vibrissae, teeth, epidermis and muscle. In Xenopus laevis, overexpression of follistatin leads to induction of neural tissue. Here we use loss-of-function mutant mice to investigate the function of follistatin in mammals. We find that follistatin-deficient mice are retarded in their growth, have decreased mass of the diaphragm and intercostal muscles, shiny taut skin, skeletal defects of the hard palate and the thirteenth pair of ribs, their whisker and tooth development is abnormal, they fail to breathe, and die within hours of birth. These defects are more widespread than those seen in activin-deficient mutant mice, indicating that follistatin may modulate the actions of several members of the transforming growth factor-beta family.

Animals↗
PubMed1995

Respiratory muscle activity and oxygenation during sleep in patients with muscle weakness.

Patients with respiratory muscle weakness show nocturnal hypoventilation, with oxygen desaturation particularly during rapid eye movement (REM) sleep, but evidence in individuals with isolated bilateral diaphragmatic paresis (BDP) is conflicting. The effect of sleep on relative activity of the different respiratory muscles of such patients and, consequently, the precise mechanisms causing desaturation have not been clarified. We have studied eight patients, four with generalized muscle weakness and four with isolated BDP during nocturnal sleep with measurements including oxygen saturation and surface electromyographic (EMG) activity of various respiratory muscle groups. Nocturnal oxygenation correlated inversely with postural fall in vital capacity, an index of diaphragmatic strength. During REM sleep, hypopnoea and desaturation occurred particularly during periods of rapid eye movements (phasic REM sleep). In most subjects, such events were "central" in type and associated with marked suppression of intercostal muscle activity, but two subjects had recurrent desaturation due to "obstructive" hypopnoea and/or apnoea. Expiratory activity of the external oblique muscle was present whilst awake and during non-rapid eye movement (NREM) sleep in seven of the eight subjects in the semirecumbent posture. This probably represents an "accessory inspiratory" effect, which aids passive caudal diaphragmatic motion as the abdominal muscles relax at the onset of inspiration. Expiratory abdominal muscle activity was suppressed in phasic REM sleep, suggesting that loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea. We conclude that, in patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Electromyography↗
PubMed1996

Human chest wall function during epidural anesthesia.

BACKGROUND: Although epidural anesthesia (EA) can significantly disrupt the function of the respiratory system, data concerning its effects on respiratory muscle activity and the resulting motion of the chest wall are scarce. This study aimed to determine the effects of lumbar EA on human chest wall function during quiet breathing. METHODS: Six persons were studied while awake and during mid-thoracic (approximately a T6 sensory level) and high (approximately a T1 sensory level) lumbar EA produced by either 2% lidocaine (two persons) or 1.5% etidocaine (four persons) with 1:200,000 epinephrine. Respiratory muscle activity was measured using fine-wire electromyography electrodes. Chest wall configuration during high EA was determined using images of the thorax obtained by three-dimensional, fast computed tomography. The functional residual capacity was measured using a nitrogen dilution technique. RESULTS: High EA abolished activity in the parasternal intercostal muscles of every participant but one, whereas the mean phasic activity of the scalene muscles was unchanged. High EA significantly decreased the inspiratory volume displacement of the rib cage compared with intact breathing but did not have a significant effect on diaphragm displacement. Therefore, high EA decreased the percentage contribution of rib cage expansion to inspiratory increases in thoracic volume (delta Vth) (from 27 +/- 2 [MSE] to 10 +/- 11% of delta Vth). Paradoxic rib cage motion during inspiration (i.e., a net inward motion during inspiration) developed in only one participant. High EA substantially increased the functional residual capacity (by 295 +/- 89 ml), with a significant net caudad motion of the end expiratory position of the diaphragm. In addition, high EA significantly decreased the volume of liquid in the thorax at end expiration in five of the six participants, a factor that also contributed to the increase in functional residual capacity in these persons. CONCLUSIONS: Rib cage expansion continues to contribute to tidal volume during high EA in most subjects, even when most of the muscles of the rib cage are paralyzed; the mean phasic electrical activity of unblocked respiratory muscles such as scalenes does not increase in response to rib cage muscle paralysis produced by EA; and high EA increases the functional residual capacity, an increase produced in most participants by a caudad motion of the diaphragm and a decrease in intrathoracic blood volume.

Adult↗
PubMed1999

Insulin acts in hypokalemic periodic paralysis by reducing inward rectifier K+ current.

OBJECTIVE: To define how insulin acts in hypokalemic periodic paralysis (HypoPP). BACKGROUND: HypoPP results from point mutations of the skeletal muscle L-type Ca2+ channel. Attacks of flaccid paralysis are associated with hypokalemia and triggered by insulin. A persistent inward current causes depolarization-induced paralysis. The relationships of the Ca2+ channel mutations to the persistent inward current and how insulin triggers paralytic attacks are not yet known. METHODS: Intercostal muscle fibers from HypoPP and normal subjects were studied in vitro at 37 degrees C using two electrodes to determine action potential thresholds and a three-electrode voltage clamp to study membrane currents. RESULTS: HypoPP fibers were depolarized in bathing solution with 4 mM K+. Reducing K+ from 4.0 mM to 2.5 or 1.0 mM depolarized HypoPP fibers but hyperpolarized normal fibers. Adding 12 mU/mL of insulin to bathing fluids increased the depolarization of HypoPP fibers and increased the hyperpolarization of normal fibers. Depolarized HypoPP had increased action potential thresholds. The fraction of excitable muscle fibers decreased with increasing fiber depolarization. Blocking Na+ channels or L-type Ca2+ channels did not prevent depolarization induced by hypokalemia or by insulin. Insulin reduced the conductance of the inward rectifier K+ channel for outward-flowing currents. CONCLUSIONS: Insulin potentiates depolarization of hypokalemic periodic paralysis (HypoPP) fibers by reducing inward rectifier K+ conductance. The Ca2+ mutations in HypoPP indirectly derange membrane excitability by altering the function of other membrane channels.

Adult↗
PubMed1982

Electrophysiology of neuromuscular junction disease: an appreciation of the contributions of Edward H. Lambert.

As the muscle fiber action potential is "all or none" and is not of constant voltage recorded in volume from remote electrodes, there are serious limitations on assessment of the "safety factor" for neuromuscular transmission by stimulus-response recording from surface electrodes, or by single fiber EMG. Lambert's use of biopsied intercostal muscle with microelectrode recording of spontaneous and evoked end-plate potentials has permitted more accurate analysis of transmission disorders. His personal and collaborative studies on experimental myasthenia gravis, congenital myasthenic syndromes, amyotrophic lateral sclerosis, and the Lambert-Eaton myasthenic syndrome are reviewed. It is suggested that studies of acetylcholine receptor agonists require reevaluation as indicating inadequacies of present models.

Carcinoma, Bronchogenic↗
PubMed1984

Development of basal lamina in synaptic and extrasynaptic portions of embryonic rat muscle.

Each vertebrate skeletal muscle fiber is ensheathed by a basal lamina (BL) which passes through the synaptic cleft of the neuromuscular junction. In the adult, the synaptic portion of the BL is both functionally and chemically specialized. We have used an immunofluorescence method to compare the development of synaptic and extrasynaptic portions of BL in embryonic rat intercostal muscles. Immunohistochemical staining of adult muscle fibers with monoclonal and serum antibodies defines "synaptic" antigens (including acetylcholinesterase) that are concentrated in synaptic BL, "extrasynaptic" antigens that are concentrated in extrasynaptic regions, and "shared" antigens (including collagen IV, fibronectin, laminin, and a heparan sulfate proteoglycan) that are present in both synaptic and extrasynaptic BL ( Sanes and Chiu , 1983). Synapses appear on newly formed myotubes on embryonic Day 14 (E14; birth is on E22 ). Patches of BL that contain shared and extrasynaptic antigens are present on myotube surfaces by E15, and BL forms a continuous sheath by E17. Shared antigens are present at but not confined to synaptic areas by E15. Two synaptic antigens appear in synaptic areas a day later, and are not detectable extrasynaptically . At least one extrasynaptic antigen is present at immature synapses, and lost or masked by E19 . Thus synaptic BL is not assembled as a unit; rather, components are added, lost, or modified as synaptogenesis proceeds.

Acetylcholinesterase↗
PubMed2005

Inheritance of recurrent exertional rhabdomyolysis in thoroughbreds.

OBJECTIVE: To develop a diagnostic test for recurrent exertional rhabdomyolysis (RER) in Thoroughbreds that relied on in vitro contracture of muscle biopsy specimens and determine whether the inheritance pattern of RER diagnosed on the basis of this contracture test was consistent with an autosomal dominant trait. DESIGN: Clinical trial. ANIMALS: 8 adult horses with RER and 16 control adult horses for development of the contracture test; 23 foals for inheritance of RER. PROCEDURE: External intercostal muscle biopsy specimens from the 24 adult horses were tested for contracture in response to halothane and caffeine, and criteria for a positive test result were determined. These criteria were then applied to results for the 23 foals to determine whether they had RER. Simple segregation analysis was performed to determine whether results were consistent with a dominant pattern of inheritance. RESULTS: Results of the contracture test were positive for 5 of the 12 colts and 4 of the 11 fillies. Results of segregation analysis were consistent with an auto-. somal dominant pattern of inheritance. Two sires with RER produced colts with RER, supporting the hypothesis that RER had an autosomal, rather than an X-linked, inheritance pattern. In addition, in 1 instance, an unaffected colt was produced by 2 affected parents, which was not consistent with a recessive mode of inheritance. CONCLUSIONS AND CLINICAL RELEVANCE: Although the expression of the RER trait is influenced by sex, temperament, and diet, among other factors, results from the in vitro muscle contracture test and this breeding trial suggest that RER in Thoroughbreds can be modeled as a genetic trait with an autosomal dominant pattern of inheritance.

Anesthetics, Inhalation↗
PubMed1988

Respiratory muscle response to load and glycogen content in type I and II fibers.

To study the relation between the response of respiratory muscle to inspiratory loads and glycogen content, we subjected unanesthetized sheep to moderate and severe inspiratory flow resistive (IFR) loads. Only severe IFR loads eventually led to a decrease in transdiaphragmatic pressure (Pdi) and a concomitant rise in PaCO2. Respiratory and nonrespiratory skeletal muscle samples were obtained at necropsy. Glycogen content was determined biochemically in muscle homogenates. Frozen sections were stained with periodic acid-Schiff (PAS) for glycogen and fibers were typed using myosin ATPase stain. Fibers were categorized as full, intermediate, or devoid of glycogen by a subjective scoring system of PAS staining intensity. We found that glycogen content decreased in the costal and crural diaphragm and in the intercostal muscles as the duration of moderate IFR loaded breathing was increased. With severe loads glycogen content decreased significantly, reaching about 40 and 22% of control levels in the costal and crural diaphragm, respectively (P less than 0.01). In addition, with severe IFR loads, a statistically significant proportion of both type I and type II muscle fibers was depleted of glycogen when compared with that of controls (P less than 0.05), but more type II fibers were depleted than type I fibers (50 vs 23%). These data indicate that in sheep subjected to IFR loads: (1) glycogen content in the respiratory muscles decreases as the severity and duration of loaded breathing increases and (2) respiratory muscle fatigue occurs at a time when considerable glycogen is still present in type I fibers in the diaphragm.

Airway Resistance↗
PubMed1989

Synaptic effects of intercostal tendon organs on membrane potentials of medullary respiratory neurons.

1. Stimulation of intercostal muscle tendon organs or their afferent fibers reduces medullary inspiratory neuron activity, decreases motor output to inspiratory muscles, and increases the activity of expiratory laryngeal motoneurons. The present study examines the synaptic mechanisms underlying these changes to obtain information about medullary neurons that participate in the afferent limb of this reflex pathway. 2. Membrane potentials of medullary respiratory neurons were recorded in decerebrate paralyzed cats. Postsynaptic potentials (PSPs) elicited in these neurons by intercostal nerve stimulation (INS) were compared before and after intracellular iontophoresis of chloride ions. After chloride injection, the normal hyperpolarization caused by inhibitory (I) PSPs is "reversed" to depolarization. 3. In inspiratory neurons, reversal of IPSPs by chloride injection also reversed hyperpolarization produced by INS when applied during any portion of the respiratory cycle. This observation suggests that increased chloride conductance of the postsynaptic membrane mediated the inhibition. Further, it is very likely that the last-order interneuron in the afferent pathway must be excited by INS and alter inspiratory neuron activity via an inhibitory synapse. The linear relationship between the amplitude of the INS induced PSP and membrane potential of inspiratory neurons provided evidence that neurons in the afferent pathway are not respiratory modulated. 4. The membranes of expiratory vagal motoneurons and post-inspiratory neurons were depolarized by INS during all portions of the respiratory cycle before IPSP reversal. Reversal of IPSPs affected neither this depolarization of expiratory vagal motoneurons during stage I and II expiration nor that of post-inspiratory neurons during stage I expiration. Thus this depolarization probably resulted from synaptic excitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed2006

Recurrence in skeletal muscle from squamous cell carcinoma of the uterine cervix: a case report and review of the literature.

BACKGROUND: The occurrence of skeletal muscle metastases is a very rare event. Only two cases of late skeletal muscle recurrence from cervical cancer have been documented until now. CASE PRESENTATION: A 38-year old patient, submitted to radical hysterectomy and pelvic lymphadenectomy for a squamous FIGO stage IB1 cervical carcinoma, presented after 76 months with a palpable, and painless swelling on the left hemithorax. MRI showed a nodule located in the context of the intercostal muscles. Pathology revealed the presence of metastasis of squamous cell carcinoma of similar morphology as the primary. On the basis of FDG-PET findings, which excluded other sites of disease, surgical excision of the lesion was performed. The patient was triaged to chemotherapy plus external radiotherapy. CONCLUSION: A case of skeletal muscle recurrence from cervical cancer after a very long interval from primary diagnosis is reported. Muscular pain or weakness, or just a palpable mass in a patient with a history of cancer has always to raise the suspicion of muscle metastasis.

Adult↗