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PubMed1991

Discharge behaviour of feline gamma-motoneurones following induction of an artificial myositis.

The study was undertaken to test the widely held hypothesis that a painful lesion of the skeleto-motor system leads to an increase in the neuromuscular component of muscle tone by activating gamma-motoneurones in the affected region. In chloralose-anaesthetized cats, artificial myositis was induced in the lateral gastrocnemius-soleus (LGS) muscle and several hours later the impulse activity was recorded from single gamma-motoaxons supplying the medial gastrocnemius (MG) muscle. Under the conditions of the study, the majority of the fusimotor neurones had a resting activity and could be readily excited by natural stimuli. In contrast to the assumptions of the working hypothesis, the gamma-motoneurones in the myositis animals were not activated but showed a strong inhibition; both resting activity and excitability by electrical and natural stimuli were decreased. Additional recordings from fusimotor neurones of a flexor muscle (tibialis anterior, TA) demonstrated that in the preparation used, the behaviour of the flexor gamma-motoneurones was different from extensor ones in that the former usually had no resting activity and did not respond to natural stimuli. The only discernible effect of a myositis of the LGS muscle on the TA gamma-motoneurones was a decrease in their electrical reflex threshold. The results of the study do not support the assumption that a painful muscle lesion is followed by an activation of the gamma-loop that leads to an increase in muscle tone. Instead, the data may offer an explanation for the weakness and--in chronic cases--the reflex atrophy of lesioned muscles.

Acoustic Stimulation↗
PubMed1988

Focal myositis in the hand.

Focal myositis is a rare, benign, pseudotumor of skeletal muscle that is usually seen as a steadily enlarging soft tissue tumor in an otherwise healthy patient. Focal involvement of muscle with severe myopathic and inflammatory changes characterize the histology. The natural course of this disorder is spontaneous regression. We report the case of a 7-year-old girl with focal myositis of the index lumbrical muscle. This is the first reported incidence of focal myositis that involves muscle of the hand.

Child↗
PubMedDate not supplied

Infantile myositis: a case diagnosed in the neonatal period.

Infantile myositis is an inflammatory myopathy occurring in children under one year of age. This condition is extremely rare in the neonatal period and may be confused with other causes of generalized weakness. Creatine kinase activity is usually markedly elevated and electromyography demonstrates low amplitude, polyphasic motor unit activity. Muscle biopsy, necessary for diagnosis, documents characteristic findings of perifascicular atrophy and the presence of perivascular inflammatory cells. The diagnosis should be followed by corticosteroid treatment. The patient presented is the youngest biopsy-proved case of infantile myositis. In this report, his symptoms and clinical course are compared with those of previously described patients. The role of infectious agents and the immune state in the etiology of infantile myositis is considered.

Biopsy↗
PubMed1995

[Myositis ossificans progressiva].

BACKGROUND: Myositis ossificans progressiva is a rare progressive disease of connective tissue with a poor prognosis. CASE REPORT: A 16 year-old girl suffered from lameness of her right leg associated with inguinal swelling. Progressive aggravation of pain with extension of swelling to the posterior part of her thigh required an X-ray examination which showed hip dysplasia and calcifications around the hip. Angiography was normal; a diagnosis of hematoma was suggested by scannography and bone scintigraphy, but biopsy showed features of nodular fasciitis. The association of progressive ectopic ossification to malformation of the big toe led to diagnosis of myositis ossificans progressiva. CONCLUSIONS: Congenital malformations, most commonly of big toes and thumbs, are important for distinguishing myositis ossificans progressiva from other diseases of muscle.

Adolescent↗
PubMed2004

HLA typing in focal myositis.

It is still controversial if idiopathic focal myositis is a part of systemic polymyositis. We present here four patients, including identical twins, with focal myositis accompanied by the same HLA typings. Gradually developing unilateral calf muscle pain was an initial symptom in all patients. Neither muscular weakness nor creatine kinase (CK) elevation was observed, while minimal inflammatory findings such as erythrocyte sedimentation rate (ESR) increase appeared in serum. Magnetic resonance imaging (MRI) revealed localized abnormalities of calf muscles. Biopsy specimen was characterized by perimysial and endomysial inflammatory infiltration consisted of T cells and macrophages and rare necrotic fibers. Corticosteroid administrations ameliorated their symptoms and signs, though recurrence occurred along with decreasing doses. HLA typings common to all patients were A2, B62, Cw3, and DQ3, whereas HLA-D DNA typings were DQB1 *0303 for two patients, and DQB1*0302 for three patients. These findings suggest that at least some focal myositis may be a new disease unit, with a common genetic background but not a part of systemic polymyositis.

Adult↗
PubMed2004

External ophthalmoplegia due to ocular myositis in a patient with ophthalmic herpes zoster.

External ocular muscle palsies in patients with ophthalmic zoster are traditionally interpreted as diseases of III, IV or VI cranial nerves. Orbital myositis associated with zoster ophthalmicus has been diagnosed only rarely. We describe a patient with ophthalmic zoster and external ophthalmoplegia due to ocular myositis demonstrated by MR imaging. Treatment with acyclovir and cortisone resulted in a rapid improvement of the ophthalmoplegia. In ophthalmic herpes zoster associated with external ocular muscle palsies, ocular myositis is an important differential diagnosis to inflammatory involvement of the cranial nerves III, IV, and VI.

Acyclovir↗
PubMed2005

[Intramuscular vascular malformations as a differential diagnosis of focal myositis].

INTRODUCTION: Focal myositis constitutes an original and rare pathological entity, characterized by a localized inflammation within skeletal muscle, presenting as a soft tissue painful tumefaction. Diagnosis requires histological confirmation because of its non-specific clinical feature and the numerous differential diagnoses. EXEGESIS: We report a 27 year-old man who presented with suggestive symptoms of focal myositis. MR imaging and echography were compatible with this diagnosis but also demonstrated the existence of a vascular component within the tumefaction. The diagnosis of a benign vascular malformation with intramuscular development was made by a surgically guided biopsy. CONCLUSION: Vascular malformations are histologically heterogeneous with extremely variable clinical expressions. When they develop within skeletal muscle, they may mimic focal myositis. Hence, their diagnosis has to be evoked before performing muscle biopsy, because of the potential hemorrhagic risk.

Adult↗
PubMed2004

Tacrolimus-associated myositis: a case report in a renal transplant patient.

A 55-year-old Caucasian man who had received a second kidney graft in July 1993, was switched from cyclosporine to tacrolimus in June 2000 due to deterioration of renal function. Thereafter, he began to complain of muscle cramps in both quadriceps with an increased CPK and EMG findings of polyneuropathy. A muscle biopsy demonstrated acute myositis. Prednisone was administered with amelioration of the patient's symptoms, but with persistently increased CPK and myoglobin levels. In February 2001, mycophenolate mofetil was introduced and tacrolimus tapered to 3 mg daily to seek a toxic role of this immunosuppressant, since there was no other cause of myositis. A sudden decrease in CPK was observed, but the complete normalization took place only after its withdrawal in September 2002. This case represents a tacrolimus-associated myositis.

Electromyography↗
PubMed1990

Orbital myositis with Lyme disease.

We examined, treated, and followed up for nine years a 5-year-old girl with active Lyme disease and orbital myositis. Clinically, the patient demonstrated typical symptoms for each of the major stages of Lyme disease, including fever, erythema chronicum migrans, aseptic meningitis, Bell's palsy, and arthritis. She subsequently developed clinical and computed tomographic evidence of orbital myositis. Although orbital myositis is generally considered to be an idiopathic inflammation, our findings suggest that in certain patients it may be a manifestation of Lyme disease.

Arthritis↗
PubMed1983

Acute and subacute orbital myositis.

Of 12 consecutive patients (nine women and three men ranging in age from 18 to 70 years) with orbital myositis, four had histories of ocular or systemic autoimmune disease. Five patients treated within two weeks of developing acute orbital pain and extraocular muscle dysfunction were classified as having acute myositis. They responded to corticosteroids within 72 hours although three had single recurrences during six- to 16-month follow-up periods. No patients were heterotropic or proptotic at the final examination. Seven patients with less severe or atypical symptoms who had delays of two or more months between onset and treatment were classified as having subacute myositis. All had recurrences with five having two or more. Three required supplemental radiation therapy during seven- to 20-month follow-up periods. At the final examinations, six patients had motility defects and one had proptosis, indicating that delays in treatment may lead to recurrences, extraocular muscle dysfunction, and proptosis.

Acute Disease↗
PubMed2000

Myositis ossificans of the chest wall simulating malignant neoplasm.

Myositis ossificans originating from the chest wall is extremely rare. We report a case of myositis ossificans occurring in a young woman with progressive painful swelling in the chest wall. Preoperative examination suggested a malignant neoplasm originating from soft tissue. Although rare, myositis ossificans is one of the potential causes of painful swelling in the chest wall, and can be mistaken for a malignant neoplasm.

Adolescent↗
PubMed2002

Proliferative myositis: a rare pseudosarcoma of the chest wall.

Proliferative myositis is a rare, inflammatory tumor that is often misdiagnosed as sarcoma. The clinical course of proliferative myositis is benign, and local recurrence after simple excision is uncommon. Typically, the lesion presents in the extremities or the head and neck. We present an unusual case of proliferative myositis with involvement of the anterior chest wall.

Diagnosis, Differential↗
PubMed2005

[Parkinson's disease, progressive lumbar kyphosis and focal paraspinal myositis].

INTRODUCTION: The camptocormia (bent spine) is characterized by a severe forward flexion of the thoracolumbar spine which disappears in the supine position. Clinical case. We describe a typical case observed in a parkinsonian patient. The MRI, electromyogram and biopsy of the paraspinal muscles revealed a typical myositis pattern. DISCUSSION: This case, the sixth published to our knowledge, confirms that focal myositis is associated with the camptocormia in Parkinson's disease. Typically it is observed in male subjects, appearing 4 to 6 years after the onset of Parkinson's disease, in fluctuating patients treated by an association of L-Dopa and agonist. It appears quickly and becomes the most important symptom. Antiparkinsonian drugs are useless. CONCLUSION: This exceptional picture raises original pathophysiological and therapeutic questions. Systematic studies should be performed in order to detail the pathophysiological link between these 3 entities: Parkinson's disease, focal myositis and camptocormia.

Disease Progression↗
PubMed1975

Pseudomalignant myositis ossificans. A pathological study of eight cases.

Eight cases of pseudomalignant myositis ossificans are presented. There was a male predominance and four patients were under 20 years of age. There was no history of trauma, but there was evidence of mild local or general inflammation with positive roentgenograms in two cases. Histologically there was active fibroblastic proliferation, appearing to develop essentially in fibrin deposits with metaplasia leading to the formation of an unusual osteoid. The newly formed mass was surrounded by bone and compressed the surrounding muscle fibers, which were either atrophic or trapped therein. The histological criteria distinguishing this disorder from other forms of myositis ossificans are discussed, and comparisons are drawn with nodular fascitis and proliferative myositis. An association with the latter was observed in one case. This nontumourous growth must be distinguished from osteogenic sarcoma of soft tissue. The differential diagnosis is based on careful histological criteria, which must be supported by clinical and radiological data.

Adolescent↗
PubMed1992

Characterization of bone forming cells in posttraumatic myositis ossificans by lectins.

Lectins were used to characterize bone forming cells in posttraumatic myositis ossificans. The lectins applied were as follows: Arachis hypogaea (PNA): specific for beta-D-galactose (1,3)N-acetyl-D-galactosamine (Gal-1,3 GalNac), Canavalia ensiformis (Con A): specific for alpha-D-glucose (D-Glc) and alpha-D-mannose (D-Man) and Wheat germ (WGA): specific for N-acetyl(1,4)D-glucosamine (Glc-NaC) and neuraminic acid. The development of myositis ossificans was characterized by the appearance of a WGA binding cell population. The lectin-binding sites appeared as a cluster in the supranuclear cytoplasm, corresponding to the Golgi-complex. However, the WGA lectin-binding sites disappeared in the mature form of myositis ossificans. We assume that these lectin binding cells may be the bone marrow derived precursors of myofibroblast-like cells which are responsible for bone formation within the damaged muscle.

Adolescent↗
PubMed1987

[Electromyographic aspects of inclusion body myositis. Macro-electromyographic study].

Histological and electrophysiological features in cases of inclusion body myositis are often difficult to interpret, suggesting either a "myogenic" or a "neurogenic" disorder. One case of inclusion body myositis is described. Conventional needle electromyography recording was interpreted as "neurogenic": abundant fibrillation potentials and positive sharp waves, reduced interference pattern, polyphasic-high amplitude-long duration motor unit potentials. Macro-EMG was performed in quadriceps muscle. Fibre density was normal and median value of the amplitude of macro motor unit potentials was increased, suggesting a larger size of motor units. Morphologic and electrophysiologic features indicate compensatory and regeneration mechanisms resulting in an increase of motor unit during the course of inclusion body myositis. This can explain atypical electromyographic and morphologic data in this disease.

Adult↗
PubMed1987

Myositis ossificans after total hip replacement and perioperative muscle ischemia.

It has been suggested that muscle ischemia could contribute to myositis ossificans and that the ischemia could result from prolonged retraction during surgery. Biopsy specimens of the gluteus medius muscle were taken at the beginning and the end of 30 primary total hip arthroplasties and the intracellular lactate and phosphocreatine (PCr) measured. Postoperative myositis ossificans was classified according to Brooker after 1 year, and the surface of the heterotopic bone projected above the greater trochanter in an anteroposterior roentgenogram was measured by planimetry. The findings suggest that muscle ischemia is not an important cause of myositis ossificans after hip arthroplasty, but elevated levels of lactate and lowered levels of intracellular PCr may occur as nonspecific responses to tissue trauma that through other mechanisms may lead to ossification.

Aged↗
PubMed2002

Animal models of myositis.

Current animal models of human myositis include spontaneous, induced, and transgenic models. Although it is clear that none of these models possesses all the features of the human diseases, they may provide insight into the pathophysiologic mechanisms, and possibly the therapy, of inflammatory muscle disease. Because the human IIMs are phenotypically heterogeneous, but may be divided into more homogeneous subgroups based upon clinical or serologic features, it is possible that different pathogeneses are involved in different subgroups. It is unlikely that any single model would reproduce all features of the human disease. It may be possible, however, to gain insight into some subgroups of the human disease if certain animal models faithfully reproduce one or more subtypes or aspects of the IIMs. Because immunogenetic risk factors, and exposure to certain environmental agents important in triggering myositis in genetically susceptible persons, may be necessary components for human disease induction, transgenic approaches to humanizing murine immune systems and a better understanding of environmental risk factors will be productive avenues for future research. Additional investigations into the molecular basis of the human myositis syndromes and the pathogenesis of the spontaneous, induced, and transgenic animal models should ultimately allow for better understanding and therapy of these diseases.

Animals↗