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A family with severe X-linked arthrogryposis.

Five males are reported with severe X-linked arthrogryposis. Main findings are marked respiratory insufficiency and feeding problems, multiple contractures, deformities of chest and vertebral column, and typical facies. Most of these findings can be explained by a pronounced prenatal and postnatal muscle weakness. The sole living child has severe psychomotor retardation. Several female carriers show mild features (clubfeet, contractures, hyperkyphosis, and slight muscle weakness). One manifesting carrier is affected more severely (multiple contractures, mental retardation, and various dysmorphic features). Additional investigations including muscle biopsy revealed none of the usual signs of denervation, and pointed to the presence of a degenerative muscle disorder.

Arthrogryposis↗

Upper plexus thoracic outlet syndrome--case report.

A 47-year-old right-handed female became aware of proximal ache and muscle weakness in the right shoulder and elbow in 1997. Atrophy of the right biceps muscle was recognized and the right deltoid, triceps, supraspinatus, and infraspinatus muscles were weak. The Morley test and elevated arm stress test were positive. Neurolysis of the brachial plexus and anterior scalenectomy were performed via a right supraclavicular approach. An abnormal fibromuscular band was identified passing between the upper and middle trunks and constricting the middle trunk. Another scalene muscle anomaly was found passing between the C-5 and C-6 nerve roots and connecting the anterior and middle scalene muscles. These muscles were resected, and thorough neurolysis was performed around all nerves and the trunks. Postoperatively, all symptoms completely resolved and the patient was discharged 5 days after surgery. Thoracic outlet syndrome (TOS) manifests as symptoms of lower cervical nerve involvements with hypesthesia and paresthesia. However, upper plexus TOS manifests as symptoms due to the involvement of the C-5 to C-7 nerve roots, and is relatively rare. Transaxillary first rib resection is performed as the primary operation for TOS, but supraclavicular scalenectomy is effective for upper plexus TOS.

Brachial Plexus↗

Childhood-onset autosomal-dominant limb-girdle muscular dystrophy with cardiac conduction block.

We report childhood-onset autosomal-dominant limb-girdle muscular dystrophy (LGMD) in a Chinese family with complete atrioventricular conduction block in the adult members. Six patients, including 5 men and 1 woman with an age of onset from 3 to 7 years, were affected. The grandfather had exercise intolerance since childhood and complete heart block with pace-maker placement at age 52. Three siblings had proximal muscle weakness and/or wasting since age 5 and heart block in their 40s. Two grandsons at the ages 7 and 3 showed exercise intolerance, and proximal muscle weakness and wasting. Sinus bradycardia was present in the elder grandson. Muscle enzymes were elevated in 3, particularly in childhood. Muscle biopsies from the proband showed myopathic changes with fatty degeneration, whorled fibers, and rimmed vacuoles. In adult patients, muscle magnetic resonance imaging scans disclosed atrophic changes and fatty degeneration in the gluteal, quadriceps, adductors, hamstrings, gastrocnemius, and soleus muscles, while in child probands the early atrophic changes were seen in the gluteal and hamstrings muscles. We conclude that this distinct family is characterized by childhood-onset autosomal-dominant LGMD with heart block and that prevention of sudden death in these patients is important.

Adolescent↗

The role of cytokines, chemokines, and adhesion molecules in the pathogenesis of idiopathic inflammatory myopathies.

Cytokines, chemokines, and adhesion molecules are important mediators in chronic inflammation and in immune regulation. In idiopathic inflammatory myopathies (IIM), increased expression of proinflammatory cytokines particularly interleukin (IL)-1alpha and IL-1beta, tumor necrosis factor (TNF)-alpha and macrophage inflammatory proteins (MIP)-1alpha, as well as of the inhibitory cytokines transforming growth factor (TGF)-beta was observed in muscle. There was no difference in cytokine and chemokine pattern between polymyositis, dermatomyositis, and inclusion body myositis, which could indicate that similar pathogenetic mechanisms are involved in these subsets of myositis. A prominent finding of IL-1alpha expression in endothelial cells, both in patients with active inflammation and in patients with chronic persisting muscle weakness without inflammation, makes this an interesting molecule in understanding the mechanisms for the pathogenesis of muscle weakness. Involvement of the blood vessels in the pathogenesis of myositis was further supported by increased expression of adhesion molecules and by a phenotypical expression of endothelial cells, resembling high endothelium venules in all three subsets of IIM. The molecular studies to date indicate a role of the microvessels in the pathogenesis of IIM not only in DM, as was previously suggested, but also in PM and IBM. The studies also indicate that IL-1alpha could be a target molecule for new therapeutical interventions.

Cell Adhesion Molecules↗

[Determination of maximal diaphragm strength in chronic obstructive pulmonary disease: cervical magnetic stimulation versus traditional sniff maneuver].

OBJECTIVE: Magnetic stimulation of the diaphragm allows its strength to be assessed. The clinical applications of this technique are becoming more widespread given that the patient's cooperation is not required. The aim of the present study was to compare this inhalation technique with traditional voluntary forced inspiration (sniff test) in a group of patients with chronic obstructive pulmonary disease (COPD). PATIENTS AND METHODS: Sixteen men with moderate-to-severe COPD were studied (mean [SD] forced expiratory volume in 1 second, 35% [15%] of the reference value). For all patients, the maximal transdiaphragmatic pressure (a measure of the contractility of the muscle) was determined at peak inspiration and during cervical magnetic stimulation. RESULTS: A moderate correlation between measurements with the 2 techniques was observed. The value obtained with stimulation was approximately 20% of that obtained with the sniff maneuver (22 [7] cm H2O vs 97 [27] cm H2O, respectively). The stimulation technique yielded an intraindividual coefficient of variability of 12% (7%) and an interindividual one of 33% (6%). Very similar values for these coefficients were obtained with the sniff maneuver. Qualitative analysis of the stimulation technique showed it to have a high sensitivity (89%) for diagnosing muscle weakness, with few false negatives. In contrast, specificity was very low (43%), and false positives for muscle weakness were relatively common. The overall effectiveness of the prediction was acceptable (69%). CONCLUSIONS: Cervical magnetic stimulation appears to be a good clinical option for ruling out diaphragm weakness. It is particularly indicated in patients with limited capacity for understanding instructions or those unable to cooperate.

Aged↗

Interferon gamma (IFN-gamma) is necessary for the genesis of acetylcholine receptor-induced clinical experimental autoimmune myasthenia gravis in mice.

Experimental autoimmune myasthenia gravis (EAMG) is an animal model of human myasthenia gravis (MG). In mice, EAMG is induced by immunization with Torpedo californica acetylcholine receptor (AChR) in complete Freund's adjuvant (CFA). However, the role of cytokines in the pathogenesis of EAMG is not clear. Because EAMG is an antibody-mediated disease, it is of the prevailing notion that Th2 but not Th1 cytokines play a role in the pathogenesis of this disease. To test the hypothesis that the Th1 cytokine, interferon (IFN)-gamma, plays a role in the development of EAMG, we immunized IFN-gamma knockout (IFN-gko) (-/-) mice and wild-type (WT) (+/+) mice of H-2(b) haplotype with AChR in CFA. We observed that AChR-primed lymph node cells from IFN-gko mice proliferated normally to AChR and to its dominant pathogenic alpha146-162 sequence when compared with these cells from the WT mice. However, the IFN-gko mice had no signs of muscle weakness and remained resistant to clinical EAMG at a time when the WT mice exhibited severe muscle weakness and some died. The resistance of IFN-gko mice was associated with greatly reduced levels of circulating anti-AChR antibody levels compared with those in the WT mice. Comparatively, immune sera from IFN-gko mice showed a dramatic reduction in mouse AChR-specific IgG1 and IgG2a antibodies. However, keyhole limpet hemocyanin (KLH)-priming of IFN-gko mice readily elicited both T cell and antibody responses, suggesting that IFN-gamma regulates the humoral immune response distinctly to self (AChR) versus foreign (KLH) antigens. We conclude that IFN-gamma is required for the generation of a pathogenic anti-AChR humoral immune response and for conferring susceptibility of mice to clinical EAMG.

Animals↗

Combined spinal and epidural analgesia in a parturient with severe myasthenia gravis.

BACKGROUND AND OBJECTIVES: A 27-year-old woman with a history of myasthenia gravis presented for vaginal delivery. METHODS: A combined spinal epidural was initiated with 7.5 microg intrathecal sufentanil at the time of first request for analgesia followed by 140 mg epidural lidocaine prior to spontaneous vaginal delivery. RESULTS: The patient had a pain-free spontaneous vaginal delivery uncomplicated by muscle weakness. CONCLUSION: Combined spinal and epidural anesthesia using intrathecal opioids initially provides labor analgesia with minimal muscle weakness in the parturient with myasthenia gravis.

Adult↗

Muscle and joint elastic properties during elbow flexion in Duchenne muscular dystrophy.

1. Maximal voluntary contraction (MVC), series elastic stiffness and total joint stiffness during elbow flexion were investigated in healthy boys and in boys with Duchenne muscular dystrophy (DMD) in order to assess changes in mechanical properties induced by the disease. 2. Two methods were used to perform stiffness measurements: (i) the application of sinusoidal perturbations to the joint during flexion efforts, allowing the calculation of total joint stiffness; (ii) the use of quick-release movements of the elbow, which had previously been maintained in isometric contraction, allowing the calculation of series elastic stiffness. In each case, stiffness was linearly related to torque, leading to the calculation of a normalized stiffness index as the slope of this stiffness-torque relationship. 3. As expected, mean MVC was found to be much higher for healthy boys (20.02 +/- 5.20 N m) than for DMD patients (3.09 +/- 2.44 N m). Furthermore, the results showed that it was possible to characterize healthy and DMD children by virtue of the mechanical properties measured. Mean series elastic stiffness index was higher for DMD children (142.55 +/- 136.58 rad(-1)) than for healthy subjects (4.39 +/- 2.53 rad(-1)). The same holds for mean total joint stiffness index: 43.68 +/- 67.58 rad(-1) for DMD children and 2.26 +/- 0.70 rad(-1) for healthy subjects. In addition, increases in stiffness were more marked in DMD patients exhibiting high levels of muscle weakness. 4. These changes are interpreted in terms of the adaptation of the properties of the muscles and joint involved, i.e. muscle fibres, tendons, peri- and intra-articular structures.

Adolescent↗

Coenzyme Q10 deficiency and isolated myopathy.

Three unrelated, sporadic patients with muscle coenzyme Q10 (CoQ10) deficiency presented at 32, 29, and 6 years of age with proximal muscle weakness and elevated serum creatine kinase (CK) and lactate levels, but without myoglobinuria, ataxia, or seizures. Muscle biopsy showed lipid storage myopathy, combined deficiency of respiratory chain complexes I and III, and CoQ10 levels below 50% of normal. Oral high-dose CoQ10 supplementation improved muscle strength dramatically and normalized serum CK.

Adult↗

[A case of mixed connective tissue disease successfully treated for hemophagocytic syndrome with intermittent intravenous injection of cyclophosphamide].

A 52 year-old woman noticed general fatigue, polyarthralgia, and muscle weakness of lower extremities in October 2001. In December, she felt difficulty in walking due to muscle weakness. In January 2002, she admitted another hospital because of dyspnea on exertion and edema of lower extremities. Laboratory test revealed leukocytopenia, the elevation of creatine kinase and positive anti-U1-RNP antibodies. Her chest computed tomography (CT) showed severe interstitial pneumonia. Cardiac echogram revealed that she had pericardial effusion and pulmonary hypertension. Then she was transferred to Keio University Hospital and she was diagnosed as having mixed connective tissue disease (MCTD) manifestating myositis, interstitial pneumonia, pulmonary hypertension and pericarditis. Prednisolone (PSL) 60mg daily following to methylprednisolone (mPSL) pulse therapy was begun and her symptoms were gradually improved. In middle of February, she complained of high fever over 39.0 degrees C. Bacterial culture tests were negative and laboratory data indicated pancytopenia and a high level of serum ferritin. Bone marrow aspiration revealed hemophagocytosis in bone marrow specimens and she was diagnosed as having hemophagocytic syndrome associated with MCTD. mPSL pulse therapy was not effective and intermittent cyclophosphamide pulse therapy (IV-CY) was performed resulting in improvement of the symptoms. This case suggested the effectiveness of IV-CY therapy in patients with corticosteroid-resistant HPS associated with connective tissue diseases.

Cyclophosphamide↗

Familial amyotrophic lateral sclerosis with posterior column degeneration and basophilic inclusion bodies: a clinical, genetic and pathological study.

We report an autopsy case of familial amyotrophic lateral sclerosis (FALS). The patient was a Japanese woman with hereditary burden. Family history revealed 12 patients with FALS over four generations. She developed muscle weakness of the proximal part of the upper extremities at age 42, followed by dysarthria, dysphagia, muscle weakness and atrophy in the lower extremities, spasticity, hyperreflexia and Babinski's sign. At age 44, she needed ventilatory support. At age 45, she died of bronchopneumonia. The total duration of the disease was three years and one month. Genetic study showed the absence of a mutation in the Cu/Zn superoxide dismutase-1 gene. Neuropathological examination revealed not only neuronal loss in the upper and lower motor neuron and Clarke's column, but also degeneration of the pyramidal tracts, middle root zone of the posterior column and posterior spinocerebellar tract. Bunina bodies and Lewy body-like inclusion bodies were absent. A few basophilic inclusion bodies were present in the neurons of the brain stem and anterior horn of the lumbar cord. Based on these clinical, genetic and pathological findings with a review of the literature, we concluded that our case was the first reported case of FALS with posterior column involvement and basophilic inclusion bodies.

Adult↗

[Physiopathology of respiratory muscles].

Different factors can have deleterious effect the inspiratory muscles: increased intrinsic mechanical loading of the inspiratory muscles, functional inspiratory muscle weakness, increased ventilatory demand related to capacity... These muscle changes influence exercise tolerance and contribute to dyspnea.

Dyspnea↗

[A case of deletion of the short arm of chromosome 18 associated with chronic polymyositis].

A case of deletion of the short arm of chromosome 18 (18p- syndrome) associated with chronic polymyositis is described. The patient was a 37-year-old woman, who had psychomotor retardation in her early childhood. She started to notice a difficulty in raising both arms at 14 years of age and furthermore, she developed a gait disturbance due to weakness of the proximal muscles of the lower extremities from 34 years of age. Her parents were first cousins. On physical examination, she showed many dysmorphic features, such as short stature, round face, hypertelorism, low nasal bridge, small chin, high arched palate, abnormal dentition, short and webbed neck, and broad chest. Neurological examination revealed a low intelligence (IQ 47), severe proximal muscle weakness with moderate proximal muscle atrophy in all extremities, a waddling gait, and decreased or absent deep tendon reflexes of all extremities except for bilateral ankle jerks. Serum creatine kinase and myoglobin levels were slightly elevated. Needle EMG study showed fibrillation potentials at rest and polyphasic and low amplitude motor unit potentials of short duration on volitional activity in the affected muscles. Muscle biopsy demonstrated a variation in fiber size, necrotic fibers and mononuclear cell infiltration. These findings were compatible with those of chronic polymyositis. In addition, cytogenetic findings revealed 46.XX.18p- karyotype, although her parents had no chromosome abnormality. She had no immunological abnormality except for a positive rheumatoid factor and elevation of CD4/CD8 ratio on lymphocyte subset analysis in peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Inclusion body myositis: clinical and histopathological features of 36 patients.

Thirty-six patients (15 females, 21 males) with inclusion body myositis (IBM) were studied. The diagnosis was established according to clinical and histopathological criteria. Clinical features were insidious onset of slowly progressive muscle weakness and wasting with depressed or absent tendon reflexes especially in the lower limbs. The pattern of muscle weakness was variable. The majority of patients (58%) showed proximal and symmetrical weakness usually most prominent in the legs. Isolated distal (6%) and asymmetrical weakness (19%) was less frequently observed. Myalgia occurred in 42% of the patients. The age at onset of symptoms ranged from 20 to 73 years (mean 47 years). Serum creatine kinase levels were normal (11%) or mildly elevated (89%). Needle electromyography revealed myopathic features in about 80% of the patients, and results of nerve conduction studies were normal in most of the cases. The predominant histopathological findings were numerous muscle fibers with rimmed vacuoles (100% of the patients), groups of atrophic fibers (92%), and inflammatory infiltrates (89%). The inflammatory infiltrates were located predominantly at endomysial sites and were composed mainly of T8 cells. Electron microscopy showed characteristic intracytoplasmic filamentous inclusions in all 36 cases. Immunosuppressive treatment in 16 patients failed to prevent disease progression in all but one patient with an associated Sjögren's syndrome. It is concluded that the consistent combination of typical histopathological findings and characteristic clinical features offers a firm basis for the diagnosis of IBM. IBM should be suspected in any adult patient presenting with clinical signs of a chronic polymyositis unresponsive to immunosuppressive therapy. The etiology and pathogenesis of IBM remain to be established.

Adult↗

[Pravastatin-associated polymyositis, a case report].

A 69 year old man complained of general myalgia, arthralgia and muscle weakness in two weeks after he started to take 10 mg per day pravastatin. Symptoms progressed at least for 3 months after withdrawal of the medication. The muscle weakness was more in distal upper extremities and the iliopsoas muscle. Serum CK was 943IU/L. The anti-nuclear and Jo-1 antibody were positive. EMG examinations disclosed fibrillation potentials at rest and myopathic discharges by a voluntary contractor. Symptoms as well as serum CK values improved promptly by treatment with prednisolone. From these clinical and laboratory results, it was speculated that this patient suffered from subacute polymyositis, although pathological studies were not performed. Because of continuing hypercholesterolemia, the patient was retreated with atorvastatin, presenting similar, but less serious symptoms. So far, three cases of statin-associated polymyositis or dermatomyositis were reported. Statins could influence the immune system, but it is still unsettled if statins cause autoimmune polymyositis. This problem warrants further study.

Aged↗

Reducing body myopathy with cytoplasmic bodies and rigid spine syndrome: a mixed congenital myopathy.

At the age of five years a male child started to develop a progressive rigid spine, torsion scoliosis, and flexion contractures of his elbows, knees, hips, and ankles owing to severe proximal and distal muscle weakness. He had three muscle biopsies from three different muscles at ages 7, 11, and 14 years, respectively. Myopathologically, these muscle tissues contained numerous inclusions which, at the ultrastructural level, turned out to be reducing bodies and cytoplasmic bodies, often in close spatial proximity. Similar histological inclusions, although not further identified by histochemistry and electron microscopy, were seen in his maternal grandmother's biopsied muscle tissue who had developed weakness of the legs and hands after the age of 50 years. The patient's parents were healthy, but the mother's quadriceps muscle showed an increased spectrum of muscle fibre diameters. Our patient, thus, had a neuromuscular disorder, perhaps familial, presenting as a mixed congenital myopathy, i.e., reducing body myopathy with cytoplasmic bodies, of which the morphological lesions could be consistently documented over several years in his different limb muscles. While other mixed congenital myopathies had shown cores and rods, both related to sarcomeres and thus possibly morphogenetically related, cytoplasmic bodies thought to be related to Z-bands and reducing bodies dissimilar to any muscle fibre constituent do not share any common denominator. Therefore, we suggest that this neuromuscular disorder may be a unique mixed congenital myopathy, either sporadic or genetic. In the latter case, the transmission pattern suggested X-linked recessive inheritance, but an autosomal-dominant transmission with variable penetrance could not be ruled out.

Adult↗

[A case of facioscapulohumeral muscular dystrophy with sensorineural hearing loss and retinal angioma].

We report a sporadic case of 12 years old boy with facioscapulohumeral dystrophy (FSHD), sensorineural hearing loss and exudative angioma of bilateral retina. His hearing loss was noted at 9 years, followed by muscle weakness of his right upper extremity at 11 years. Complete neurological examination at 12 years revealed FSH type distribution of muscle weakness with high serum CK level (330 U/L), moderate sensorineural hearing loss and exudative angiomas of bilateral retina. The biopsy from biceps brachii muscle showed advanced dystrophic changes with a dense inflammatory cell infiltration predominating on perivascular distribution and type II fiber predominance. The features of infiltrating lymphocytic surface antigen seen in this case were compatible with those of FSHD rather than those of polymyositis. In the literature, the association of FSHD with hearing loss and retinal vessel abnormalities has been documented on 15 cases as an unusual form of FSHD. However, it has otherwise been noted that the associations of FSHD and hearing loss or retinal vessel abnormalities are unequivocally frequent, Whenever special attention has been made. Morphological examination with light and electron microscopies on the muscle specimen in this patient did not demonstrate any recognizable abnormality such as arterio-venous shunt or thickening of vessel wall basal lamina. However, it cannot be completely excluded that exudation around the abnormal vessel wall in the muscle may play an initial role in the pathogenesis of FSHD. Further morphological survey on vessel abnormalities may be necessary in the FSHD muscle.

Child↗

Corticosteroid-induced myopathy of the respiratory muscles.

Corticosteroids may cause myopathy of both skeletal and respiratory muscles. This is of specific clinical importance in patients with chronic obstructive pulmonary disease (COPD), who already have impaired respiratory muscle function. After treatment with fluorinated steroids, side-effects occur more frequently and are worse compared to treatment with non-fluorinated steroids. Acute myopathy and atrophy are caused by short-term high-dose corticosteroid administration, resulting in rhabdomyolysis, diffuse muscle weakness and severe dyspnoea. In contrast, chronic myopathy occurs after prolonged treatment with corticosteroids, and results in proximal muscle weakness and type IIb fibre atrophy. The pathophysiology of steroid myopathy is unknown, but reduction in protein synthesis and increased glycogen accumulation may play a major role. Animal models have demonstrated weakening of the diaphragm and a decrease in body and diaphragm mass after corticosteroid administration. In humans, a reduction in respiratory and peripheral muscle strength, an elevation of urinary creatine excretion and selective type IIb fibre atrophy may be observed. Treatment of corticosteroid-induced myopathy consists of tapering the dose of steroids or switching to non-fluorinated steroids.

Adrenal Cortex Hormones↗