Diffuse Myalgia Research Articles

Extracorporeal Cardiopulmonary Support for Cardiogenic Shock Caused by Pheochromocytoma: A Case Report and Literature Review

Extracorporeal Cardiopulmonary Support for Cardiogenic Shock Caused by Pheochromocytoma: A Case Report and Literature Review

Fibromyalgia, sleep disorder and chronic fatigue syndrome.

Various research studies show that the amalgam of disordered sleep physiology, chronic fatigue, diffuse myalgia, and cognitive and behavioural symptoms constitutes a non-restorative sleep syndrome that may follow a febrile illness, as in the chronic fatigue syndrome. Where rheumatic complaints are prominent such a constellation of disturbed sleep physiology and symptoms also characterizes the fibromyalgia disorder. In contrast to the chronic fatigue syndrome, fibromyalgia is associated with a variety of initiating or perpetuating factors such as psychologically distressing events, primary sleep disorders (e.g. sleep apnoea, periodic limb movement disorder) and inflammatory rheumatic disease, as well as an acute febrile illness. The chronic fatigue syndrome and fibromyalgia have similar disordered sleep physiology, namely an alpha rhythm disturbance (7.5-11 Hz) in the electroencephalogram (EEG) within non-rapid eye movement (NREM) sleep that accompanies increased nocturnal vigilance and light, unrefreshing sleep. Aspects of cytokine and cellular immune functions are shown to be related to the sleep-wake system. The evidence suggests a reciprocal relationship of the immune and sleep-wake systems. Interference either with the immune system (e.g. by a viral agent or by cytokines such as alpha-interferon or interleukin 2) or with the sleeping-waking brain system (e.g. by sleep deprivation) has effects on the other system and will be accompanied by the symptoms of the chronic fatigue syndrome.

Periorbital and facial swelling due to dermatomyositis

A 55-year-old woman presented with a 10-day history of malaise, lethargy and an elevated temperature (up to 39.5°C) accompanied by rigor. She also reported diffuse myalgia, arthralgia and bilateral facial edema. The patient's medical history included a modified mastectomy for invasive breast cancer

Vocal Fold Deposits in Macrophagic Myofasciitis

Macrophagic myofasciitis was first reported in 1998. This disease manifests as diffuse myalgia and chronic fatigue. Its pathophysiology has been traced to the presence of an aluminum adjuvant used in vaccines against hepatitis A and B virus and tetanus toxoid; the adjuvant aggregates at the site of injection. One-third of patients with macrophagic myofasciitis develop autoimmune disease. Vocal fold deposits have been described in autoimmune diseases such as sarcoidosis, systemic lupus erythematosus, multiple sclerosis, rheumatoid arthritis, Sjögren's syndrome, and Hashimoto's thyroiditis. We report what to the best of our knowledge is the first published case of vocal fold deposits in macrophagic myofasciitis.

Infectious myositis

Infectious myositis, an infection of the skeletal muscle(s), is uncommon. This clinical entity may be caused by viral, bacterial, fungal, and parasitic pathogens. Viral etiologies typically cause diffuse myalgias and/or myositis, whereas bacteria and fungi usually lead to a local myositis which may be associated with sites compromised by trauma or surgery and are more common among immunocompromised patients. Localized collections within the muscles are referred to as pyomyositis. Other pyogenic causes of myositis include gas gangrene, group A streptococcal myonecrosis, and other types of non-clostridial myonecrosis. Early recognition and treatment of these conditions are necessary as they may rapidly become life-threatening.

Atypical presentation of macrophagic myofasciitis 10 years post vaccination

Macrophagic myofasciitis (MMF) is an uncommon inflammatory disorder of muscle believed to be due to persistence of vaccine-derived aluminium hydroxide at the site of injection. The condition is characterised by diffuse myalgias, arthralgia and fatigue. We describe a patient with histologically confirmed MMF whose presentation was atypical with left chest and upper limb pain beginning more than 10 years post vaccination. Treatment with steroids led to symptomatic improvement. Although rare, clinicians should consider MMF in cases of atypical myalgia.

Horner Syndrome and Ipsilateral Abduction Deficit Attributed to Giant Cell Arteritis

We recently examined a 77-year-old woman with Horner syndrome and ipsilateral abduction deficit that we attribute to giant cell arteritis (GCA). This combination of findings has not been previously reported in GCA. She had a history of hypertension, hyperlipidemia, atrial fibrillation, congestive heart failure, and colon carcinoma. Six weeks before presentation, she developed bitemporal headaches. She had stopped eating solids as a result of jaw claudication and had lost weight. She had diffuse myalgia and was unable to sleep well because of bilateral scalp tenderness. She noticed binocular horizontal double vision that was worse on left gaze and had experienced numerous episodes of blurring of vision in both eyes. Her family noted drooping of her left upper lid. Neuro-ophthalmic examination revealed a best-corrected visual acuity of 20/40 in both eyes consistent with cataracts. Visual fields and color vision were normal. Left upper lid ptosis of 2 mm was present. In dim light, the right pupil measured 5.5 mm and the left 3.5 mm. In bright light, the right pupil measured 4.5 mm and the left 3 mm. Both pupils reacted briskly to light without afferent defect. Horner syndrome was confirmed by instilling 10% cocaine into both eyes (Fig. 1). (Hydroxyamphetamine was not instilled as a result of its unavailability.) Ocular ductions were full except for reduced abduction of the left eye. There was a 12 prism-diopter esotropia in primary position increasing to 20 on left gaze. The fundus examination was normal.FIG. 1: Left Horner syndrome. After instillation of one drop of a 10% cocaine solution, the right pupil has become dilated and the left pupil has remained small. Left upper lid ptosis is evident.Temporal arterial pulsation was absent and the scalp was tender, but there was no thickening or nodularity. Westergren erythrocyte sedimentation rate (ESR) was 57, C-reactive protein was 4.1, and platelet count was 475,000. MRI of the brain with contrast was normal and magnetic resonance angiography showed an incidental small basilar tip aneurysm. We made a diagnosis of GCA with concurrent Horner syndrome and left lateral rectus paresis. Intravenous methylprednisolone at a dosage of 250 mg per day and 80 mg oral prednisone per day was initiated. She was also started on alendronate, calcium with vitamin D, and ranitidine. Temporal artery biopsy on the left side was consistent with giant cell arteritis (Fig. 2).FIG. 2: Temporal artery biopsy shows inflammatory cells in the vessel wall. Inset shows giant cells (arrows).Within a week of initiation of treatment, she had resolution of diplopia, headaches, and temporal scalp pain. Ptosis and pupillary abnormality remained unchanged. ESR, C-reactive protein, and platelet counts normalized in a week. Prednisone was tapered slowly over 18 months. Horner syndrome resulting from GCA is very rare. Three cases of GCA and Horner syndrome have been reported in the English literature (1-3). Bell et al (1) reported a patient with GCA and Horner syndrome resulting from a brainstem stroke. Askari et al (2) reported a patient with internuclear ophthalmoplegia and Horner syndrome resulting from presumed giant cell arteritis. Bromfield and Slakter (3) reported a patient with GCA with postganglionic Horner syndrome. To our knowledge, no one has reported the combination of Horner syndrome and ipsilateral abduction deficit in GCA. We were unable to perform the hydroxyamphetamine test to confirm the location of the lesion. The absence of brainstem and spinal cord signs and a normal brain MRI argue against a preganglionic location. Hollenhorst et al (4) suggested that paresis of different extraocular muscles at different times is the result of ischemia of the muscles or the nerve and not a brainstem lesion. Barricks et al (5) found extraocular muscle ischemia at autopsy in a patient with bilateral ophthalmoplegia resulting from GCA. Sibony and Lessell (6) reported aberrant regeneration in a patient with pupil-sparing third cranial nerve palsy resulting from GCA and suggested that ophthalmoplegia is neurogenic rather than myogenic. Meadows (7) suggested ischemia of vasa nervorum, whereas Martin (8) suggested ischemia of the extraocular muscles as the likely cause of diplopia in GCA. In our patient, the combination of Horner syndrome and an ipsilateral abduction deficit suggests a cavernous sinus lesion. Within the cavernous sinus, the postganglionic sympathetic fibers travel with the sixth cranial nerve lateral to the internal carotid artery. Bromfield and Slakter (3) proposed that granulomatous inflammation of the internal carotid artery might directly involve the sympathetic fibers. We believe that the sixth cranial nerve in our patient could have been similarly affected. Guruswami Arunagiri, MD Shanmugam Santhi, MD Thomas Harrington, MD Departments of Ophthalmology and Rheumatology, Geisinger Medical Center, Danville, PA

How Can We Manage Hyperlipidemia and Avoid Rhabdomyolysis in Transplant Patients?

Joseph M Kahwaji, MD, MPH Ryszard R Dudek, MD Case Summary A 25-year-old man with a history of perinuclear antineutrophil cytoplasmic antibodies-associated vasculitis presented to the ambulatory clinic with five days of diffuse myalgias and muscle tenderness. The patient had undergone kidney transplantation three years before presentation and had no post-transplant complications. He was maintained on cyclosporine, prednisone, and mycophenolate mofetil. Simvastatin 20 mg daily was started two months after transplantation for development of post-transplant hyperlipidemia. Three months before presentation, the creatinine concentration was 1.8 mg/dL. Two months before presentation, the simvastatin dosage was increased to 40 mg daily. Results of laboratory studies done at presentation were remarkable for the following: creatine kinase, 25,000 U/L; aspartate aminotransferase, 767 U/L; alanine aminotransferase, 620 U/L; and creatinine, 2.3 mg/dL. Urinalysis revealed 4+ blood and 2+ protein. The cyclosporine concentration, 265 ng/mL, was above the normal range of 100 to 200 ng/mL. A diagnosis of rhabdomyolysis was made on the basis of the symptom of myalgias in the setting of acute renal failure and an elevated creatine kinase concentration. Simvastatin was discontinued, and the patient was instructed to selfhydrate. At one day, five days, and two weeks after initial presentation, follow-up clinical evaluations found that symptoms had eased, and follow-up laboratory studies showed improvement.

G.P.1 08 Phenotype–genotype correlation in two families with muscle phosphofructokinase deficiency

Muscle phosphofructokinase deficiency (PFK) is a relatively rare glycogenosis characterized by mild proximal myopathy associated with compensated hemolytic anaemia and hyperuricemia. We report 2 unrelated families with PFK deficiency. Family 1: A 45-year-old man (pt1) complained of episodic diffuse myalgias, vomiting and dark urines after mild exercise. He had a mild hypertrophic cardiomyopathy. Neurological examination was unremarkable. Family history was negative but his older 12-year-old son showed elevated CK levels (max 600IU/l).

ACUTE TUBULAR NECROSIS DUE TO RHABDOMYOLYSIS RESULTING FROM INFLUENZA A INFECTION

To the Editor: An 82-year-old man was hospitalized with delirium at the University Hospital La Milétrie in February 2005. His medical history included giant cell arteritis diagnosed 9 years before and still treated with corticosteroids (prednisolone 4 mg/d). Treatment with fentanyl (25-μg patch) and codeine (up to 2,400 mg/d) was started because of refractory sciatic pain. His medications also included paroxetine (20 mg/d), bromazepam (6 mg twice daily), and zopiclone (7.5 mg/d). The clinical examination revealed disorientation and back pain without any other abnormalities. Laboratory data were normal, and his serum creatinine level was 8.9 mg/dL. The delirium resolved after the codeine, hypnotic agents, and antidepressant drug were discontinued, but 1 week after admission, the patient presented with a influenzalike syndrome: fever (38.2°C), rhinorrhea, and diffuse myalgias. He had been vaccinated against influenza 4 months earlier. Despite the vaccination, a nasopharyngeal swab confirmed infection with influenza (A/H3N2 virus). A routine laboratory examination revealed acute renal failure; his creatinine serum level was 7 mg/dL, associated with rhabdomyolysis with an elevated serum level of creatine phosphokinase (CPK) (13,212 UI/L) (normal<120) and high myoglobin (5,260 μg/L) (normal <90). Urinalysis disclosed proteinuria (0.5 g/d) and microhematuria. Renal echography was normal. Acute tubular necrosis was suspected. Because of pulmonary edema, the patient was transferred to the Department of Nephrology for dialysis. After hemodialysis, the patient recovered slowly, and his creatinine serum level decreased to 2.9 mg/dL 1 week later and 1.1 mg/dL 1 month later. The patient was discharged from the hospital to his home. A case of severe rhabdomyolysis after influenza is reported. Muscular weakness and pain were the main symptoms, although in 50% of cases of rhabdomyolysis, patients do not complain of myalgia.1 Up to 40% of patients with rhabdomyolysis develop acute renal failure. Hypovolemia and the direct nephrotoxic effects of components of myoglobin explain the renal failure.2 The initial development of delirium might have enhanced the risk of dehydration in this patient because of poor fluid intake. Rhabdomyolysis represents muscle necrosis due to increased intracellular calcium and obstruction of the tubules by myoglobin.3 CPK appears to be the most sensitive marker for muscle necrosis.4 A peak CPK value of 230,600 UI/L has been reported after a viral illness.5 Influenza is the most common infectious precipitant of rhabdomyolysis and has been reported in 25 of 59 cases in a review of the literature.6 A direct viral invasion can precipitate rhabdomyolysis. Early and aggressive intravenous fluid therapy usually is recommended to prevent acute renal failure. Alkalinization of the urine might protect against precipitation of myoglobin. The current results also highlight the need to improve vaccination rates against influenza in healthcare professionals, because this elderly patient, despite a previous vaccination, became infected while in the hospital. Financial Disclosure: No financial support for any authors Author Contributions: Pradère and Paccalin: acquisition of subjects and/or data, and preparation of manuscript. Planchard, Plouzeau, Merlet-Chicoine, and Valéro: preparation of manuscript. Sponsor's Role: No sponsor.

A 59-year-old woman with fever, cough, and eosinophilia

HISTORY OF PRESENT ILLNESS The patient is a 59-year-old woman with a history of asthma diagnosed 10 years ago and chronic sinusitis who presented for evaluation of a 1-month history of intermittent fevers with temperatures to 101.5°F, cough productive of white phlegm, and diffuse myalgias. One day before admission, the patient developed dyspnea at rest that did not respond to inhaled albuterol at home. The fevers and cough persisted despite a 2-week course of levofloxacin. Six years before the current hospital admission, the patient was admitted to an outside hospital with similar complaints and erythematous, scaly lesions on the extensor surfaces of her metacarpophalangeal and elbow joints bilaterally. Her inpatient workup included blood tests, chest computed tomography (CT), fiberoptic bronchoscopy, and transesophageal echocardiography. The patient had never been hospitalized for an asthma exacerbation, but she had required 2 emergency department visits for increased asthma symptoms. She had also been treated with oral corticosteroids more than 20 times for asthma exacerbations while concurrently being prescribed inhaled corticosteroids. However, the patient admitted to being noncompliant with both inhaled corticosteroid therapy and physician appointments for management of her asthma. During the previous asthma exacerbations that required treatment with oral corticosteroids, the patient denied having fevers, myalgias, or anorexia. On review of systems, the patient complained of fatigue, anorexia, and a 15-lb weight loss during the past 2 months. There was no history of hemoptysis. She had noted intermittent watery diarrhea and reflux symptoms for 1 year.

Fibromyalgia and Diffuse Myalgia

Chronic pain is one of the most common complaints encountered by primary care clinicians. Often, patients present not with well localized pain but with diffuse and nonspecific myalgias. Fibromyalgia is the most common etiology for this type of pain. In community-based studies, 2% [1] and 1.2% to 6.2% of school-age children screened positive for fibromyalgia [2–4]. Women and girls are at higher risk than males, and risk increases with age, peaking between 55 and 79 years [1,5]. Persons suffering from fibromyalgia most commonly complain of widespread pain. The pain is usually bilateral and is usually worse in the neck and trunk [6]. Additional symptoms include fatigue, waking unrefreshed, morning stiffness, paresthesias, and headaches [6–12]. Compared with patients with other rheumatologic conditions, persons with fibromyalgia more often suffer from comorbid conditions [13], including chronic fatigue syndrome, migraine headaches, irritable bowel syndrome, irritable bladder symptoms, temporomandibular joint syndrome, myofascial pain syndrome, restless leg syndrome, and affective disorders [13–15]. Fibromyalgia can cause significant morbidity [1,16,17]. Patients with fibromyalgia require an average of 2.7 drugs at any time for fibromyalgiarelated symptoms and have an average of 10 outpatient visits per year, with one hospitalization every 3 years [13]. Fibromyalgia has been associated with higher rates of osteoporosis [18]. Patients with fibromyalgia have higher rates of surgery, including hysterectomies, appendectomies, back/ neck surgery, and carpal tunnel surgery, compared with patients with other

Clear as Mud

A previously healthy 17-year-old boy presented to his primary care physician, reporting four days of low back pain, a temperature as high as 40°C, headache, diffuse myalgias, and vomiting. He lived in the central Midwest and was about to begin his senior year in high school.

Statines et troubles musculaires : comparaison des notifications par les patients et les professionnels de santé

Background and methodsStatin- and especially cerivastatin-induced muscle effects reported by patients and doctors to the Limoges centre of pharmacovigilance during the years 2000 and 2001 were compared. In both instances, only reports with complaints of muscle pain or modification of creatine phospokinase (CPK) values and cases with one statin or one statin-fibrate association were selected. ResultsIn the reports of 28 patients (21 involving cerivastatin), 80 % of the patients complained of diffuse myalgia. The dose was normal. The CPK value (six cases) was 1.7±0.9 N (upper limit of normal) [1–3.2 N]. Thirteen medical reports were received at the pharmacovigilance centre during the years 2000 and 2001: eight myalgias and five increases in CPK without muscle pain (9±9 N [1–20 N]). No common cases were identified among patients’ and doctors’ reports. Doctors tended to declare more severe effects, not necessarily associated with clinical signs. Patients’ reports were at times inaccurate. ConclusionBefore including patients’ reports in the present pharmacovigilance database, a thorough reconsideration is necessary.

Esomeprazole-Induced Central Fever with Severe Myalgia

To report a case of central fever associated with severe myalgia following esomeprazole. A 64-year-old man presented with intense cephalalgia; severe, diffuse myalgia; and fever (>40 degrees C) after esomeprazole initiation for treatment of gastritis. Five hours after ingestion of the first esomeprazole pill (40 mg), the patient developed fever associated with cephalalgia and myalgia. This condition lasted about 40 hours and disappeared spontaneously. Symptoms partially responded to acetaminophen. Four days later, the patient received a second dose of esomeprazole 40 mg. Subsequently, 4 hours later, fever (>40 degrees C), headache, and difficulty in the movement of all parts of the body recurred. Neurologic examination was negative except for a minor state of disorientation. All reflexes were normal or slightly decreased. No skin lesions or breathing difficulty was noted. Routine blood tests were normal. Again, symptoms resolved spontaneously about 40 hours later. The temporal connection between esomeprazole intake and the onset of fever suggests a probable causal link, as confirmed by the Naranjo probability scale. However, the pathogenic mechanism remains unclear. Considering that esomeprazole is able to cross the blood-brain barrier, its peak serum concentration is reached 90-180 minutes after oral administration, and its serum half-life is approximately 2 hours, we assume that the appearance of fever with accompanying neurologic and muscular symptoms might result from the drug interference with the hypothalamic regulatory center of body temperature. Hyperpyrexia of central origin associated with intense cephalalgia and myalgia may occur as an adverse effect of esomeprazole therapy.

Comparison of Intravenous Pamidronate to Standard Therapy for Osteoporosis

Bisphosphonates are potent therapies for osteoporosis, but some patients cannot tolerate oral forms. Our study sought to examine the effectiveness and safety of intravenous pamidronate as an alternate osteoporotic therapy in these patients. We conducted a retrospective study of 26 patients treated with intermittent, intravenous pamidronate (30 mg every 3 months) and 52 matched controls treated with standard therapy, all with osteoporosis. Primary outcome was response to therapy, defined as either stabilization or increase in bone mineral density. Secondary outcomes were patient safety and tolerability. At an average of 16.1 months of follow up, 64% of pamidronate-treated patients responded to therapy at the lumbar spine, 65% at the femoral neck, and 63% at the trochanter. These response rates were not significantly different than those of the standard care group in which 69% were receiving oral bisphosphonates. Adverse events were uncommon and included mild, diffuse myalgias and flu-like symptoms. Intravenous pamidronate is a well-tolerated osteoporosis therapy that has an effect on bone density comparable to standard therapy in patients unable to take oral bisphosphonates.

Succinylcholine Myalgia and Fasciculation: All the Facts

How best to prevent the muscle fasciculations and diffuse myalgia associated with succinylcholine? These investigators performed a formal meta-analysis of randomized, controlled trials of pretreatment agents; the analysis was limited to agents that were evaluated in at least three trials. Of 161 studies identified, 52 met all criteria for inclusion. Forty-three trials evaluated both fasciculation and myalgia, 6 evaluated myalgia alone, and 3 evaluated fasciculation alone; the studies included 5318 …

Sindbis viruses and other alphaviruses as cause of human arthritic disease

Amongst the arthritis-causing arboviruses, i.e. those spread by insects, the alphavirus group is of special interest. These viruses occasionally cause vast outbreaks, such as O'nyong-nyong in Africa in 1959. In Fennoscandia, Sindbis-related Ockelbo, Pogosta, or Karelian fever viruses have been found to cause significant morbidity. The major symptoms in addition to joint inflammation are fever, fatigue, headache and rash. The joint symptoms may persist for weeks, even months. The diagnosis is based on the clinical picture and serology. The causative viruses are closely related but not identical. It appears that at least in Finland the Pogosta disease is more common than thought, and the symptoms may often be overlooked. Several factors related to the viruses, their hosts, and global environmental changes may affect the spread of these viruses. All over the world arbovirus-caused diseases have increased, because of global changes.

Clinical quiz: A pediatric case presenting with fever and diffuse myalgia

Familial Mediterranean fever (FMF) is a multisystem disease characterized by recurrent polyserositis episodes seen in certain ethnic groups. In recent years the clinical picture of FMF has been expanded and severe myalgia is a frequently recognized component of the syndrome. Protracted febrile myalgia syndrome (PFMS), characterized by severe paralyzing myalgia, high fever, abdominal pain, diarrhea, arthritis/arthralgia, and transient vasculitic rashes mimicking Henoch-Schonlein purpura, was first described in patients with FMF in 1994. We describe an 11-year-old Turkish girl with a second attack of PFMS before being diagnosed as having FMF, emphasizing the importance of myalgia for the diagnosis of FMF even in the absence of other symptoms.

Nosocomial Transmission of Dengue

Nosocomial Transmission of Dengue