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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the short-term effect of oral pulsed high-dose dexamethasone for myositis we treated eight newly diagnosed patients with three 28-day cycles of oral dexamethasone. Primary outcome measures were muscle strength, pain, and serum creatine kinase activity. Six patients responded. Side effects were mild. At follow-up five responders were still in remission, without medication. Pulsed high-dose dexamethasone seems beneficial in myositis. A larger, prednisone-controlled trial is justified to analyze long-term efficacy.
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PMID:Oral pulsed high-dose dexamethasone for myositis. 1075 Nov 11

Thyroid eye disease is the most common cause of unilateral and bilateral proptosis in adults. It occurs most frequently in women aged 30 to 50 years. Clinical features include eyelid retraction, periorbital edema, conjunctival injection and chemosis, proptosis, extraocular muscle restriction, exposure keratopathy, and optic nerve compromise. Thyroid eye disease differs from idiopathic orbital myositis in that the latter is characterized by a more acute onset, more severe pain, and a rapid response to systemic corticosteroid therapy. Echography and computed tomography in thyroid eye disease reveal enlarged extraocular muscle bellies with relative sparing of the tendons. Despite evidence of an immune-mediated cause, the precise pathophysiologic mechanisms of thyroid eye disease remain unknown.
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PMID:Thyroid eye disease. 1075 12

A 46-year-old man who had been suffering from palmoplantar pustulosis (PPP) for 3 years had anterior chest pain and left temporal pain from six months after the onset of his disease. A bone scan revealed abnormal uptake at the sternoclavicular joint and left temporal region. The head CT and MRI gave the diagnosis of temporal osteomyelitis with meningitis and myositis. His headache continued even after tonsillectomy and was effectively treated with cyclosporine A (3 mg/kg/day). Oral cyclosporine A was beneficial for the osteomyelitis and skin lesions. Sterile lytic bone lesions occurring most often at the sternocostoclavicular joint have been associated with PPP. However, there have been no reports of a PPP patient with temporal osteomyelytic involvement.
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PMID:Palmoplantar pustulosis with pustulotic arthroosteitis involving temporal osteomyelitis and meningitis. 1082 92

Skeletal muscle can be the site of inflammatory diseases that lead to muscle weakness, pain, and increased myogenic serum enzymes. Most of these inflammatory myopathies are idiopathic. In some cases inflammatory myopathies are due to infectious agents. We describe the pathological aspects of muscle biopsies of 2 Brazilian siblings who acquired toxoplasmosis at the same time and in similar conditions. One developed a tetraplegia that was confirmed to be due to inflammatory myositis due to toxoplasma. The other developed myocarditis, with heart failure, without skeletal muscle weakness. In both cases many toxoplasma organisms were observed in the muscle biopsies, but in case 1 only was there an inflammatory myopathy with myofiber necrosis; the inflammatory cells were predominantly macrophages with some CD4+ cells and rare CD20+ cells. In case 1, expression of CD54 was observed in many inflammatory cells as well in endothelial cells, but only in endothelial cells in case 2. After treatment with clindamycin and corticosteroids both cases had only partial improvement, case 1 with a residual muscle weakness and case 2 with residual cardiac insufficiency (requiring digoxin). These cases show that the presence of the parasite in myofibers is not enough to induce an inflammatory myositis with muscle cell necrosis. This suggests that immunological disturbances may contribute to the development of inflammatory myositis due to toxoplasma.
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PMID:Skeletal muscle pathology in 2 siblings infected with Toxoplasma gondii. 1085 91

We report a 38-year-old man who had three episodes of pain and swelling in the right calf from the age of 27 years. On each episode, pain worsened gradually, lasted for a few months and subsided spontaneously. Venography performed at the first episode was reported to be unremarkable. At the third episode, physical examinations showed tender and hard muscles in the right calf without findings of knee arthritis. The right calf pain became stronger when standing than when lying and on the ankle dorsiflexion. Laboratory examinations showed leukocytosis, a slightly elevated level of CRP, and normal CK levels. MRI showed diffuse high intensities in the right soleus and the lateral head of right gastrocnemius on T2-weighted images, where CT showed slightly low densities. To rule out focal myositis, the right soleus was biopsied. The muscle specimen showed perimysial and endomysial edema, dilatation of venules and capillaries, and focal mononuclear cell infiltration in the venule wall. Intermyofibrillar networks were well preserved. There were no necrotic or regenerating fibers, nor sarcolemmal expression of HLA-ABC. On electron microscopy, the processes of fibroblasts in the endomysium were swollen. This case illustrated muscle edema caused by local venous congestion possibly due to venulitis of unknown cause.
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PMID:[A case of unilateral recurrent calf myalgia with muscle edema due to venous congestion]. 1118 11

Orbital myositis is a rare disorder considered as a subgroup of inflammatory orbital pseudotumors. The pathophysiology is still unknown. Patients typically present with orbital pain exacerbated by eye movement and diplopia. Response to steroids is dramatic. We report a case of idiopathic myositis of the right inferior muscle, which recovered after steroid therapy.
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PMID:[Idiopathic orbital myositis]. 1139 17

Orbital myositis is an inflammatory disorder of the orbital muscles causing orbital pain and restriction of eye movements. Although rare in children, it is most frequently seen after orbital trauma or as a post-infectious process. We describe a child with chronic relapsing psoriasis, juvenile psoriatic arthritis and relapsing bilateral orbital myositis.
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PMID:Psoriasis, psoriatic arthropathy and relapsing orbital myositis. 1142 74

Orbital myositis is an uncommon subgroup of the nonspecific orbital inflammatory syndromes (previously termed orbital pseudotumor) and presents with eyelid swelling and redness, conjunctival chemosis, pain, proptosis, and diplopia. The disease is to date of unknown origin; autoimmune processes are suspected for the etiology. In the case of an otherwise healthy young male patient (age 28 years), the coexistence of chronic sinusitis primarily led to the diagnosis of sinugen orbital cellulitis. Despite antibiotic drug administration and surgical drainage of the paranasal sinuses the symptoms persisted. A second computed tomography revealed fusiform, inflammatory enlargement of the m. rectus lateralis. This muscle showed a restrictive paresis so that initially the m. rectus medialis was suspected to be paretic. The patient responded dramatically to administration of prednisolone within 2 days. The differential diagnosis between a sinugen orbital complication and orbital myositis is significant because corticosteroids are contraindicated for orbital cellulitis whereas they remain the therapy of choice for orbital myositis.
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PMID:[Ocular myositis. A rare differential diagnosis of sinus-induced orbital complications]. 1154 88

The authors report a rare case of pseudomalignant myositis ossificans occurring during childhood. A female aged 10 years with no previous history of trauma came to their observation with findings of pain and progressive swelling in the gluteal region. The severity of the clinical findings and the absence of characteristic ossification in the x-rays obtained at the onset of the disease suggested that neoplastic pathology be excluded. Diagnosis (bone scan, CT scan, MRI, angiography, biopsy) and the progression of the disease, until its complete clinical resolution, are discussed in light of a review of the literature (44 cases of pseudomalignant myositis ossificans during pediatric age). All of the elements that may be of help in diagnosis and capable of avoiding surgical procedures that are either untimely or improper are emphasized.
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PMID:Pseudomalignant myositis ossificans in children. Description of a case and review of the literature. 1156 21

The present article concentrates on mechanisms that lead to the excitation of nociceptors in soft tissues and nociceptive neurones in the spinal dorsal horn. These mechanisms may contribute to the so-called unspecific low back pain. Properties of nociceptors in soft tissues: A nociceptive ending in soft tissue contains a multitude of receptor molecules in its membrane. The molecular receptors include binding sites for algesic substances that are released during painful stimulation or pathologic alterations of the tissue: bradykinin (BK), serotonin (5-HT), prostaglandin E2 (PG E2), adenosine triphosphate (ATP) and protons (H(+)). The excitation and sensitisation of nociceptors by these substances can be explained by the binding of the substances to the receptor molecules in the membrane of the receptive ending and ensuing opening of ion channels or activation of metabolic cascades. Purinergic receptor molecules in the membrane of nociceptors are activated by ATP. These receptors may be of particular importance for deep somatic pain, because ATP is present in large amounts in muscle tissue and is released during muscle damage. ATP-sensitive nociceptors appear to be distinct from nociceptors that can be excited by protons. The conduction of nociceptive information from muscle to the spinal cord is partly carried by unmyelinated fibres that possess tetrodotoxin-resistant (TTX-r) Na(+)-channels. Therefore, a drug that specifically blocks TTX-r Na(+)-channels would be a new attractive tool in the treatment of patients with deep somatic pain. Chronic muscle lesions such as a myositis have been shown to be associated with a higher innervation density of the tissue with free nerve endings that contain the neuropeptide substance P (SP). Many of these endings are likely to be nociceptors. Since a painful stimulus that acts on a muscle with increased nociceptor density will excite more nociceptors and elicit more pain, the increase in nociceptor density constitutes a peripheral mechanism for hyperalgesia. In muscle free nerve endings - many of which are nociceptive - the neuropeptides SP, calcitonin gene-related peptide (CGRP) and somatostatin have been shown to be present. These substances are released from the receptive endings in muscle when they are stimulated. SP and CGRP have a strong effect on blood vessels and induce local vasodilatation and oedema. The local oedema in the vicinity of the nociceptor is associated with the release of BK from plasma proteins, which increases the excitability of the nerve ending (see below). Thus, a local vicious cycle forms that may contribute to the formation of trigger points. Sensitisation of nociceptors and peripheral hyperalgesia: Nociceptors are easily sensitised, i.e. following a conditioning stimulus they are more sensitive to the unconditioned stimulus. In animals and humans, the responses to injections of BK can be increased by 5-HT or PG E2. The responses of muscle nociceptors to mechanical stimuli are likewise enhanced after administration of BK. During overuse, ischemia or inflammation of soft tissues, the tissue concentrations of BK, PG E2, and 5-HT are elevated and sensitise muscle nociceptors. A sensitised nociceptor is excited and elicits pain when innocuous mechanical stimuli act on the muscle, e.g. during contractions or stretch. Therefore, in chronically altered soft tissues, weak everyday stimuli are likely to cause pain. Mechanisms at the spinal level: In experiments on rats in which a myositis of the gastrocnemius-soleus (GS) muscle was induced experimentally, the effects of a peripheral painful lesion on the discharge behaviour of sensory dorsal horn neurones were studied. One of the main effects of the myositis was an expansion of the input (target) region of the muscle nerve, i.e. the population of dorsal horn neurones responding to an electrical standard stimulus applied to the GS muscle nerve grew larger. One reason for the myositis-induced expansion of the input region is hyperexcitability of the neurones caused by the release of SP and glutamate from the spinal terminals of muscle afferents with ensuing activation of NMDA channels in dorsal horn neurones (central sensitisation). The central sensitisation is of clinical importance because it can explain the hyperalgesia and spread of pain in patients. In contrast to excitability, the resting activity of dorsal horn neurones - which is likely to induce spontaneous pain in patients - does not appear to depend on the release of SP and glutamate but on the concentration of nitric oxide (NO) in the spinal cord. A pharmacological block of the NO synthesis led to a significant increase in background activity without affecting the excitability of the dorsal horn neurones. Such an increase in background activity was observed exclusively in nociceptive neurones, i.e. a local lack of NO in the spinal cord induces spontaneous pain. According to data from animal experiments, a decrease in the spinal NO concentration occurs as a sequel of a chronic muscle lesion; therefore, a lack of NO is a probable factor for the induction of chronic spontaneous pain. Normally, lesion-induced pain subsides and does not develop into chronic pain. The mechanisms governing the return to normal neuronal behaviour after a peripheral lesion are not well studied. Probably, the activation of inhibitory mechanisms, e.g. increased spinal synthesis of GABA or elevated activity of the descending antinociceptive system contribute to the restoration of normal function. The final step in the transition from acute to chronic pain are structural changes that perpetuate the functional changes. In the rat myositis model, an increase in the number of synapses on the surface of NO-snythesizing cells was present 8 h following induction of the myositis. These data show that structural changes appear quite early in the development of a painful disorder. A novel hypothesis for the development of chronic pain states that a strong nociceptive input to the spinal cord leads to cell death predominantly in inhibitory interneurones. Most of these interneurones are assumed to be tonically active; when their number decreases, the nociceptive neurones are chronically disinhibited and elicit continuous pain also in the absence of a noxious stimulus.
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PMID:[Pathophysiology of low back pain and the transition to the chronic state - experimental data and new concepts]. 1179 44


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