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PubMed2001

Cardiac damage in pediatric carbon monoxide poisoning.

BACKGROUND: Cardiovascular disorders including myocardial ischemia and heart failure have been described in both laboratory animals and humans following carbon monoxide poisoning. Carbon monoxide cardiotoxicity may be clinically occult and often remains undiagnosed because of the lack of overt symptoms and specific ischemic changes in the electrocardiogram. Routine myocardial necrosis markers have low diagnostic efficiency, particularly in patients with concomitant skeletal muscle necrosis or multiple organ failure complicating carbon monoxide poisoning. Carbon monoxide-induced cardiotoxicity has been investigated rarely in children. CASE REPORT: This paper describes carbon monoxide poisoning in a 12-year-old child who suffered from occult cardiac damage despite mild symptoms and low carboxy hemoglobin concentrations. Myocardial and mitral valve dysfunctions were observed, suggesting an ischemia-like syndrome. Cardiac damage was completely reversible within 1 month. CONCLUSION: This case report supports that a prolonged carbon monoxide exposure can cause cardiac damage in children even in the absence of specific symptoms, cerebral failure and high carboxyhemoglobin concentrations.

Carbon Monoxide Poisoning↗

PubMed2000

Cardiac involvement in primary myopathies.

Simultaneous or temporarily staggered affection of both the skeletal as well as the cardiac muscle (cardiac involvement, CI) is a frequent finding in primary myopathies (MPs). CI leads to impulse generation defects, impulse conduction defects, thickened myocardium, left ventriculalr hypertrabeculation, dilatation of the cardiac cavities, secondary valve insufficiency, reduction of coronary vasodilative reserve, intracardial thrombus formation, and heart failure with systolic and diastolic dysfunction. CI has been found in Duchenne muscular dystrophy (MD), Becker MD, Emery-Dreifuss MD, facioscapulohumeral MD, sarcoglycanopathies, myotubular congenital MD, myotonic dystrophies type 1 and 2, proximal myotonic myopathy, myoadenylate deaminase deficiency, glycogenosis type II, III, IV, VII and IX, carnitine deficiency, mitochondriopathy, desmin MP, nemaline MP, central core disease, multicore MP, congenital fiber-type disproportion MP, Barth syndrome, McLeod syndrome and Bethlem MP. Patients with any of the above-mentioned myopathies should be cardiologically investigated as soon as their diagnosis is established, since sufficient cardiac therapy improves CI in MPs and since management of these patients is influenced by the degree of CI.

Cardiomyopathies↗

PubMed2006

Strength deficits in primary focal hand dystonia.

Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co-contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output.

Adult↗

PubMed1997

[The peripheral pharmacology of erection].

The peripheral control of local mechanisms of erection and detumescence has now been more clearly elucidated. This knowledge has been acquired as a result of the recent development of pharmacological research designed to study the regulation of erectile smooth muscle tone. Smooth muscle fibres of the corpora cavernosa and arteries supplying the penis relax in response to a reduction of intracellular calcium. This relaxation allows both an increase of the blood flow to the penis and opening of sinusoid spaces. Cyclic nucleotides, cAMP and cGMP, are intracellular messengers of the mediators acting on smooth muscle fibres and regulating these intracellular calcium movements. Gap-junctions, greatly facilitating rapid ion exchanges between smooth muscle fibres, make erectile tissue a real functional syncytium. Nonadrenergic, noncholinergic neurotransmitters, mainly nitric oxide (NO), are synthesized by parasympathetic neurons present in cavernous nerves and act directly on smooth muscle fibres. NO increases the intracellular cGMP concentration. Other proerectile mediators, such as acetylcholine, CGRP or substance P, act via endothelial cells by promoting the synthesis and release of NO by these cells. In contrast, neurotransmitters of the sympathetic nervous system, norepinephrine and neuropeptide Y, and endothelin, secreted by endothelial tissues, induce contraction of cavernous smooth muscle fibres, thereby opposing erection. Oxygenation of the cavernous tissue is also an important factor in the regulation of local mechanisms of erection. Poor oxygenation prevents the synthesis of cGMP and predisposes to cavernous fibrosis due to increased synthesis of collagen via TGF beta. A better understanding of the peripheral pharmacology of erection opens the way to new pathophysiological and therapeutic prospects in the broad symptomatic context of erectile dysfunction.

Acetylcholine↗

PubMed1997

Antibodies against striated muscle, connective tissue and nuclear antigens in patients with thyroid-associated ophthalmopathy: should Graves' disease be considered a collagen disorder?

The identity and subcellular localization of the principal extraocular muscle (EOM) antigens and prevalences of the corresponding serum autoantibodies in thyroid-associated ophthalmopathy (TAO) need to be clarified. We have used porcine eye muscle tissue, which expresses all autoantigens identified in human tissue, as substrate in an indirect immunofluorescence assay. Several different patterns of antibody binding to EOM tissue antigens were observed with sera from patients with TAO namely, membrane, cytoplasmic, interstitial (endomysial) and nuclear. Overall, sera from 75% of patients with TAO contained one or more antibodies reactive with EOM, compared to 32% of patients with Graves' hyperthyroidism, 38% with Hashimoto's thyroiditis, and 16% of normals. All sera which reacted with EOM membrane or cytoplasmic antigens also reacted with the same antigen(s) in other skeletal muscle, but not in the other tissues tested. Sera from 31% of patients with TAO, but only 7% of those with Hashimoto's thyroiditis, and no patient with Graves' hyperthyroidism without evident ophthalmopathy, contained antinuclear antibodies (ANA). The most common nuclear fluorescence pattern was the finely speckled type typically associated with anti-Sm or anti-RNP antibodies. Significant positive correlations in patients with TAO were found between (i) EOM dysfunction and ANA (ii) eye disease of < 1 yr duration and EOM membrane-reactive antibodies and (iii) eye disease of < 1 yr duration and interstitial (endomysial) tissue-reactive antibodies. Although patients with Graves' disease do not usually exhibit other signs or immunologic features of a generalized collagen disorder, the finding of high prevalences of ANA and anti-striated muscle antibodies and, less often, anti-connective tissue antibodies in patients with ophthalmopathy, is consistent with it being a collagen-like disorder of the striated muscle, connective tissue and the thyroid. The reason why the inflammatory process is mainly limited to these tissues is unclear although cross reaction of ANA with tissue specific proteins or increased expression of muscle and connective tissue antigens in the orbit and skin, are possibilities.

Adult↗

PubMed2005

A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle.

Obesity and type 2 diabetes have been associated with a high-fat diet (HFD) and reduced mitochondrial mass and function. We hypothesized a HFD may affect expression of genes involved in mitochondrial function and biogenesis. To test this hypothesis, we fed 10 insulin-sensitive males an isoenergetic HFD for 3 days with muscle biopsies before and after intervention. Oligonucleotide microarray analysis revealed 297 genes were differentially regulated by the HFD (Bonferonni adjusted P < 0.001). Six genes involved in oxidative phosphorylation (OXPHOS) decreased. Four were members of mitochondrial complex I: NDUFB3, NDUFB5, NDUFS1, and NDUFV1; one was SDHB in complex II and a mitochondrial carrier protein SLC25A12. Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1) alpha and PGC1beta mRNA were decreased by -20%, P < 0.01, and -25%, P < 0.01, respectively. In a separate experiment, we fed C57Bl/6J mice a HFD for 3 weeks and found that the same OXPHOS and PGC1 mRNAs were downregulated by approximately 90%, cytochrome C and PGC1alpha protein by approximately 40%. Combined, these results suggest a mechanism whereby HFD downregulates genes necessary for OXPHOS and mitochondrial biogenesis. These changes mimic those observed in diabetes and insulin resistance and, if sustained, may result in mitochondrial dysfunction in the prediabetic/insulin-resistant state.

Adult↗

PubMed1999

Functional analysis of troponin I regulatory domains in the intact myofilament of adult single cardiac myocytes.

Troponin I is the putative molecular switch for Ca(2+)-activated contraction within the myofilament of striated muscles. To gain insight into functional troponin I domain(s) in the context of the intact myofilament, adenovirus-mediated gene transfer was used to replace endogenous cardiac troponin I within the myofilaments of adult cardiac myocytes with the slow skeletal isoform or a chimera of the slow skeletal and cardiac isoforms. Efficient expression and myofilament incorporation were observed in myocytes with each exogenous troponin I protein without detected changes in the stoichiometry of other contractile proteins and/or sarcomere architecture. Contractile function studies in single, permeabilized myocytes expressing exogenous troponin I provided support for the presence of a Ca(2+)-sensitive regulatory domain in the carboxyl terminus of troponin I and a second, newly defined Ca(2+)-sensitive domain residing in the amino terminus of troponin I. Additional experiments demonstrated that the isoform-specific, acidic pH-induced contractile dysfunction in myocytes appears to lie in the carboxyl terminus of troponin I. Functional results obtained from adult cardiac myocytes expressing the chimera or isoforms of troponin I now define multiple troponin I regulatory domains operating in the intact myofilament and provide new insight into the Ca(2+)-sensitive properties of troponin I during contraction.

Actin Cytoskeleton↗

PubMed1998

mtDNA depletion and impairment of mitochondrial function in a case of a multisystem disorder including severe myopathy.

The ratio of mtDNA and a nuclear reference gene was estimated by Southern blotting in the skeletal muscle DNA of a 3-year-old girl who suffered from congenital brain damage, focal epilepsy, hepatomegaly, malabsorption syndrome and severe myopathy. The signal ratio of mtDNA versus 18S rDNA was 22% of the mean value obtained from controls. No major deletions or insertions were found and the MERRF, MELAS and NARP mutations were ruled out. Mitochondrial DNA-encoded enzyme activities and mitochondrial respiration were reduced. The analysis of the NAD(P)H and flavoprotein redox states of intact fibres revealed the presence of mitochondrial dysfunction. In tissue sections a moderate elevation of type I and type II fibre diameter variation was detected, aberrant NADH- and succinate dehydrogenase staining and some ragged red fibres. This suggested that a mitochondrial disorder caused by a decrease in the amount of intact wild-type mtDNA was responsible for the severe myopathy.

Abnormalities, Multiple↗

PubMed2005

Transcriptional coactivator PGC-1 alpha controls the energy state and contractile function of cardiac muscle.

Skeletal and cardiac muscle depend on high turnover of ATP made by mitochondria in order to contract efficiently. The transcriptional coactivator PGC-1alpha has been shown to function as a major regulator of mitochondrial biogenesis and respiration in both skeletal and cardiac muscle, but this has been based only on gain-of-function studies. Using genetic knockout mice, we show here that, while PGC-1alpha KO mice appear to retain normal mitochondrial volume in both muscle beds, expression of genes of oxidative phosphorylation is markedly blunted. Hearts from these mice have reduced mitochondrial enzymatic activities and decreased levels of ATP. Importantly, isolated hearts lacking PGC-1alpha have a diminished ability to increase work output in response to chemical or electrical stimulation. As mice lacking PGC-1alpha age, cardiac dysfunction becomes evident in vivo. These data indicate that PGC-1alpha is vital for the heart to meet increased demands for ATP and work in response to physiological stimuli.

Animals↗

PubMed2004

Fenofibrate impairs rat mitochondrial function by inhibition of respiratory complex I.

Fibrates are used for the treatment of dyslipidemia and known to affect mitochondrial function in vitro. To better understand the mechanisms underlying their mitochondrial effects, fibrate actions on complex I of the respiratory chain and cell respiration were studied in vitro. In homogenates of rat skeletal muscle, fenofibrate, and to a lesser extent clofibrate, reduced the activity of complex I (10, 30, and 100 microM fenofibrate: -41 +/- 7%, -70 +/- 2%, and -78 +/- 4%; 100 microM clofibrate: -27 +/- 7%; p < 0.005 each). Inhibition of complex I by fenofibrate (100 microM) was confirmed by reduced state 3 respiration of isolated mitochondria consuming glutamate + malate as substrates for complex I (-33 +/- 4%; p < 0.0005), but not of such consuming succinate as substrate for complex II (-8 +/- 4%; NS). In isolated rat muscle, 24-h fenofibrate exposure (25, 50, and 100 microM) decreased CO(2) production from palmitate (-15 +/- 7%, -23 +/- 8%, and -22 +/- 7%; p < 0.05 each) and increased lactate release (+15 +/- 5%, +14 +/- 5%, and + 17 +/- 6%; p < 0.02 each) indicating impaired cell respiration. Ciprofibrate and gemfibrocil (but not bezafibrate) impaired cell respiration without any inhibition of complex I. Our findings support the notion that individual fibrates induce mitochondrial dysfunction via different molecular mechanisms and show that fenofibrate predominantly acts by inhibition of complex I of the respiratory chain.

Animals↗

PubMed2004

Combined transplantation of skeletal myoblasts and mesenchymal cells (cocultivation) in ventricular dysfunction after myocardial infarction.

OBJECTIVE: Cell therapy in the myocardium has been mainly performed with satisfactory results using 2 cell types: skeletal myoblasts (myogenic) and mesenchymal cells (angiogenic). This study assessed the combined transplantation of those 2 cell types (SMM) into infarcted rats. METHODS: Myocardial infarction was induced by ligature of the left coronary artery in 26 Wistar rats. After one week, the animals underwent echocardiography for assessing ejection fraction (EF%) and left ventricular end-diastolic and systolic volumes (EDV, ESV, mL). After 2 days, the animals were reoperated on and divided into 2 groups: 1) control (n = 10), which received 0.15 mL of culture medium; and 2) SMM (n = 16), which received 7.5x10(6) heterologous skeletal myoblasts and mesenchymal cells in the infarcted region. The cells were obtained from puncture of the iliac crest and biopsy of skeletal muscle, and were cultured in vitro. After one month, the animals underwent a new echocardiography. RESULTS: No significant difference in EF, EDV, and ESV was observed between the 2 groups on baseline echocardiographic values. One month after transplantation, the following was observed: a reduction in EF in the control group (29.31 +/- 5.6% to 23.54 +/- 6.51%; P = 0.048); and an increase in EF in the SMM group (24.03 +/- 8.68% to 31.77 +/- 9.06%; P = 0.011). The presence of neovascularization and muscle fibers was identified in the regions of myocardial fibrosis in the SMM group. CONCLUSION: Cocultivation of skeletal myoblasts and mesenchymal cells is functionally effective.

Animals↗

PubMed1997

[Coma-associated neuropathy].

To evaluate signs of peripheral nerve dysfunction, over a period of 31 months all patients treated for more than 14 days in our intensive care unit (ICU) had clinical and electrophysiological examination. The results of 78 patients were analysed: 53 had diseases of the central nervous system, 25 suffered from general cerebral hypoxia, mainly after cardiopulmonary reanimation. 54 showed bilateral signs of denervation activity, additionally 10 patients had fibrillation potentials unilateral to their spastic hemiparesis. 19 patients had denervation potentials only in proximal muscles of the upper limbs. Generalized denervation activity developed mainly after septic organ failure. On the other hand 35 patients showed denervation potentials already between day 14 and 21, suggesting an affection of peripheral nerve function in the first week of ICU treatment. Time course, pattern of distribution and frequency of electrophysiological abnormalities are not generally consistent with alterations of nutrition, metabolism or hypoxia in the course of ICU treatment. Clinical signs of peripheral nerve dysfunction were present in 40% of the patients showing denervation in the EMG.

Adolescent↗

PubMed1993

Skeletal muscle bioenergetics in myotonic dystrophy.

Skeletal muscle function of 15 patients with myotonic dystrophy (dystrophia myotonica, DM) was investigated using 31P magnetic resonance spectroscopy to evaluate bioenergetics and intracellular pH at rest and during exercise and recovery. Results from DM patients, normal controls and mitochondrial myopathy patients were compared in order to assess the possible contribution of abnormal mitochondrial metabolism to muscle dysfunction in DM. In resting DM muscle, intracellular pH (pHi) was normal, but there were significant elevations in the concentration ratios of Pi/ATP, phosphomonoesters/ATP and phosphodiesters/ATP. In patients with the most severe exercise intolerance the phosphocreatine/ATP ratio was also reduced. Resting muscle of 11 mitochondrial myopathy patients showed similar changes to those of the most exercise-intolerant DM patients. In exercising DM muscle, energy stores were rapidly depleted as in mitochondrial myopathy. Muscle acidified in all subjects, but in DM the decrease in pHi was less than in normal muscle. Recovery half-times for phosphocreatine, Pi and ADP were normal in DM but slow in mitochondrial myopathy. The initial rate of phosphocreatine repletion after exercise was rapid in DM, consistent with high [ADP], but slow in mitochondrial myopathy in spite of elevated [ADP]. Because recovery is an oxidative process, we conclude that there was no decrease in the oxidative capacity of the muscles in this group of DM patients. In the subjects in whom it could be measured, the rate of recovery of intracellular pH was greater in the 3 DM patients (0.14, 0.15 and 0.16 U/min) than in the 7 normal controls (0.08-0.12 U/min, mean 0.10). The results do not rule out a minor abnormality in glycogenolysis, but they suggest that the failure to acidify normally during exercise is probably due to rapid proton efflux.

Adenosine Diphosphate↗

PubMed2005

Correlation between a patient-derived functional questionnaire and abnormal neuromuscular transmission in Myasthenia Gravis patients.

OBJECTIVE: To correlate the patient-derived physical function score, as measured by the disease specific Myasthenia Gravis Questionnaire (MGQ), and the score obtained with commonly used generic 36-item questionnaire, the Short-Form health survey (SF-36), with the degree of abnormal neuromuscular transmission measured by Single-Fibre EMG (SFEMG) and repetitive nerve stimulation (RNS) in Myasthenia Gravis (MG) patients. METHODS: SFEMG and RNS were performed in the deltoid muscle and SFEMG was also performed in the orbicularis oculi muscle in 45 MG patients. The patients were asked to fill out the MGQ, which has been translated and validated into Swedish, and the SF-36. The sum of MGQ items generates a global MGQ score. Items are also divided into 3 muscle specific domains: generalized, bulbar and ocular. RESULTS: The global MGQ score and generalized domain score of MGQ were strongly correlated with the degree of abnormal neuromuscular transmission, as measured by SFEMG in the deltoid muscle. Scores from ocular and bulbar domains of MGQ were not related to neurophysiological findings. Physical composite scores of SF-36 correlated significantly with the abnormal SFEMG findings in the deltoid. CONCLUSIONS: The degree of disturbed neuromuscular transmission in a proximal limb muscle correlates with a patient's subjective experience of generalized myasthenic dysfunction. SIGNIFICANCE: The observed correlation adds a new dimension to neurophysiological examinations in patients with MG.

Adult↗

PubMed2005

Leg dysfunctions in a hatched chick model of spina bifida aperta.

We created chicks with spina bifida aperta (SBA) by incising the roof plate of the neural tube of embryos at Hamburger and Hamilton stage 18 or 19. Incision over the length of three somites caused spina bifida occulta (SBO)-like malformation in 47% of the hatchlings. Incision over the length of five and seven somites caused SBA-like malformation in 100% of the hatchlings. The SBO chicks exhibited no symptoms, whereas the SBA chicks exhibited paralysis of a leg muscle and imbalance between an agonist and an antagonist leg muscles. Lesions in these SBA chicks were located in the spinal segments that give rise to motor neurons that innervated the dysfunctional muscles. Histological analysis revealed that there were fewer small spinal neurons (interneurons) at the site of the lesion in SBA chicks than in the normal chicks and that there was no such difference in the number of the large spinal neurons (motor neurons). Leg dysfunctions in this model of SBA may be attributable to the smaller number of interneurons in the spinal segments that contain motor neurons that innervate the dysfunctional muscle. This model may facilitate studies of the pathological mechanisms that lead to leg dysfunctions in SBA chicks.

Animals↗

PubMed2001

Inter-segment foot motion and ground reaction forces over the stance phase of walking.

OBJECTIVE: To compare the magnitude and patterns of motion of the rearfoot segment relative to the leg, forefoot segment relative to the rearfoot, height change in the medial longitudinal arch and ground reaction forces of normal adult males during the stance phase of walking. BACKGROUND: Knowledge of normal motion of the rearfoot and forefoot segments and of the arch during stance phase is important in clinical management. METHODS: Motion data were obtained from surface markers, and force data from a force plate, from the right limb of participants while walking at a self-selected pace. RESULTS: Stance phase range of motion across sagittal, frontal and transverse planes was 12 degrees, 4 degrees and 10 degrees for the forefoot, compared to 22 degrees, 8 degrees and 10 degrees for the rearfoot. Most motion occurred at the beginning and end of stance phase when support was via only the rearfoot or forefoot, and when forces were maximal. Arch height decreased from heel contact and increased after heel rise to its maximum at toe-off. CONCLUSIONS: The extent of forefoot segment motion confirms the significance of midfoot joints to normal foot function. Between foot flat and heel rise, the forefoot pattern of motion is indicative of foot stability. Typical foot motion does not obey descriptions of triplanar motion such as 'pronation' and 'supination'. RELEVANCE: Typical stance phase foot motion has been described according to a forefoot:rearfoot model and rearfoot:leg model of motion, together with profiles of medial longitudinal arch height and ground reaction forces. This information can be applied in the management of foot dysfunction and should stimulate research into midfoot motion and overall control of the foot.

Adult↗

PubMed2001

Psychological and physiological factors associated with tilt table testing for neurally mediated syncopal syndromes.

This study investigated psychological and physiological factors in two groups of patients who had tilt table testing for autonomic dysfunction. The first group of 61 patients completed assessments of depression, anxiety, and symptom effects on lifestyle. The 25 patients identified as tilt positive were younger (30.5 years) and had higher mean depression scores (7.6) compared to the tilt-negative response group (n = 36); the latter averaged 40 years of age and had mean depression scores of 4.6. These differences were statistically significant. Women testing tilt positive were significantly more depressed than tilt-negative women (P = 0.02). More severe depressive symptoms were associated with lower blood pressure (BP) (P < 0.05). A second group of 52 patients was monitored during tilt for BP, heart rate (HR), skin temperature (TEMP), skin conductance level (SCL), and forehead muscle tension (EMG). Twenty-seven tested positive and 23 were negative. There were statistically significant group differences in systolic BP and diastolic BP (P < 0.05). There was a significant interaction between tilt status (positive or negative) and time (P = 0.03) in HR. TEMP increased 2 degrees over time in both groups (P < 0.05). The decrease in SCL from 13.7 to 10.4 mu omega in the tilt-positive response group compared to the slight increase in the tilt-negative group was significantly different (P < 0.05). Identification of psychological factors correlated with BP and physiological changes that accompany decreases in BP in tilt-positive response patients could guide management of patients with autonomic dysfunction.

Adult↗

PubMed2006

[Magnetic resonance analysis of the subscapularis muscle after open anterior shoulder stabilization].

PURPOSE: Analysis of the magnetic resonance imaging of the subscapularis musculotendinous unit (SSC) after primary and revision open shoulder stabilization and their correlation with the clinical function. MATERIALS AND METHODS: In a retrospective cohort study, 13 patients (mean age of group A: 36.5 years) after primary and 12 (mean age of group B: 34.2 years) after revision open stabilization underwent postoperative MRI of the shoulder. The digital data was analyzed with respect to the vertical und transverse diameters (V[slashed circle], T[slashed circle]) in a defined image slice. A signal intensity analysis was performed (infraspinatus/subscapularis signal-to-noise ratio = ISP/SSC SNR). The clinical examination included the SSC tests and signs and the Constant and Rowe score. Twelve healthy volunteers (group C) served as the control. RESULTS: From group C to group B, the mean V[slashed circle] of the SSC decreased significantly (p < 0.05) as did the mean T[slashed circle] of the cranial part of the SSC muscle (= crSSC) (p < 0.05). The mean T[slashed circle] of the caudal part of the SSC muscle (= caSSC) did not differ significantly between all groups (p > 0.05). The ISP-SSC SNR was significantly lower (p < 0.05) in the crSSC of groups A und B than in group C. In the caSSC, the SNR increased in groups A and B. In 53.8 % of group A and 92.3 % of group B, clinical signs of SSC insufficiency were found. There was no significant difference between the Constant and the Rowe score in both groups (p > 0.05). Complete tendon ruptures were not observed in any case. CONCLUSIONS: MRI enables semi-quantitative analysis of the postoperative changes of the subscapularis muscle. The decrease of the ISP/SSC SNR points to a fatty degeneration in the crSSC. The results provide indications of the causes of the clinical dysfunction of the subscapularis musculotendinous unit after open shoulder stabilization.

Adult↗