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PubMed1986

Antagonism of dithiobiuret toxicity in rats.

Daily administration of dithiobiuret (DTB, 1 mg/kg X 6 days, ip) produced delayed onset muscle weakness in rats as indicated by failure in a treadmill test. In nerve-muscle preparations from DTB-intoxicated rats neuromuscular toxicity was manifested as contractile fatigue during tetanic nerve stimulation. As muscle weakness developed, feed intake decreased and the animals lost body weight. Water intake was not altered during this time, but urine output was increased concomitant with the development of muscle weakness and resulted in a state of negative water balance. Daily administration of d-penicillamine (d-PEN) antagonized DTB-induced treadmill failure in a dose-dependent fashion. A daily dose of d-PEN (1 mMol/kg, ip) that completely antagonized treadmill failure also antagonized the contractile fatigue, reduced feed intake, weight loss and negative water balance caused by DTB administration. In rats already intoxicated with DTB, initiating daily d-PEN treatment or discontinuing further DTB administration, caused the animals to recover normal treadmill performance after a latent period of five days. A single dose of d-PEN (1 mMol/kg, iv) was not effective in reversing treadmill failure or contractile fatigue in rats already intoxicated with DTB. Thus, continuous daily administration of d-PEN was necessary for it to be effective. A single dose of d-PEN (1 m Mol/kg, ip) administered one hr after [14C]-DTB (1 mg/kg, ip) did not affect the plasma and tissue concentrations of DTB-derived radioactivity or their corresponding elimination kinetics. Cumulative urinary and fecal excretion of DTB-derived radioactivity were also unaffected by d-PEN administration as were the relative proportions of DTB and two of its metabolites, monothiobiuret and thiuret, in urine. Other agents that produced dose-dependent antagonism of DTB toxicity were diethyldithiocarbamate, disulfiram, cysteamine and 2,2'-dipyridyl. Considering the chemical and biological properties of DTB and its antagonists, a mechanism of antagonism involving an alteration of the thiol-disulfide and/or divalent metal cation status of motor axon terminals is postulated.

2,2'-Dipyridyl↗

PubMed1989

[A case of progressive myopathy with tubular aggregates].

Tubular aggregates (TA) are unusual intramuscular structures stained basophilic on hematoxilin and eosin (HE) staining and red on modified Gomori trichrome (GT) staining. The structures are said to be originated from sarcoplasmic reticulum and are collections of tubules with double membranes on electron microscopic studies. The TA are usually seen in biopsy muscles from patients with muscle pain and cramps but without muscle weakness, periodic paralysis or alcoholic myopathy. In addition, there are five reports on families with progressive myopathy and tubular aggregates in the literature. We presented here a 48-year-old postman without any family history, who had had progressive muscle weakness for 17 years. He had never noticed pain or cramps in his muscles, not taken any particular medicine, and not had regular alcoholic beverages. There was no ptosis, facial weakness, masticatory muscle weakness or dysphagia. Muscle wasting, started from the proximal part of four extremities had progressed to the distal part of them. He could not walk on heels or toes and walked with waddling gait. He stood up with Gowers' maneuver. Serum GOT, GPT and CK were elevated. EMG showed myogenic pattern and MCV was normal. The muscle biopsies were performed; the first one taken from quadriceps femoris muscle at 42 years old showed myopathic changes including marked variation in fiber sizes, with scattered necrotic fiber splitting and TA in type 2B fibers. The second biopsy from biceps brachii muscle at the age of 48 years, showed densely proliferated fibrous tissues, marked variation fiber sizes and scattered split fibers. The TA were rarely seen and type 2B fibers were decreased in number.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗

PubMed2002

Respiratory muscle evaluation of the patient with neuromuscular disease.

This review presents clinically relevant issues regarding the assessment of respiratory muscles in individuals with neuromuscular disorders, and discusses the advantages and disadvantages of methods generally available to the clinician. Vital capacity (VC) and total lung capacity (TLC) are routinely measured in pulmonary function laboratories and are typically reduced in the context of severe respiratory muscle weakness, but the sensitivity and specificity of these measures are limited. Better measures of respiratory muscle weakness are maximal static inspiratory and expiratory pressures (PI max and PE max). PI max is reduced even with mild or moderate degrees of inspiratory muscle weakness, but low values also may be related to submaximal effort. To circumvent this problem, pressures can be measured using simpler maneuvers such as a maximal sniff. Specific tests of diaphragm function such as measurements of maximal transdiaphragmatic pressure are invasive and not routinely available to the clinician. Recently, noninvasive methods that specifically assess diaphragm function, such as diaphragm ultrasound of the zone of apposition and magnetic or electrophrenic nerve stimulation, have shown promise as new techniques for clinical use.

Journal Article↗

PubMed2002

Outcome in juvenile dermatomyositis.

The clinical features, outcome and complications of juvenile dermatomyositis were studied in a tertiary care hospital by retrospective analysis of case records. Nineteen patients were treated over an 11-year period. Median age at diagnosis was 12 years (2.5-16 years). Median duration of disease prior to diagnosis was 12 months (2-96 months). Proximal muscle weakness was seen in all 19 cases, neck muscle weakness in 14, pharyngeal muscle involvement in 5 and respiratory muscle involvement in 3 cases. Heliotrope rash was seen in 9 and Gottrons rash in 8 patients. Myocarditis and GI bleed were seen in 1 each while interstitial lung disease was seen in 2 patients. All except one patient received prednisolone. Methotrexate was used in 13 and azathioprine in 3 patients. Eight patients are in complete remission (CR), 8 partial remission and 2 patients had no response. Complications were calcinosis in 5, contractures in 2, TB in 4 and pyogenic infections in 4 patients. Juvenile dermatomyositis needs to be recognised early and treated aggressively to improve outcome.

Adolescent↗

PubMed1990

[Pathophysiology of respiratory insufficiency in neuromuscular diseases].

In end stage neuromuscular disease respiratory muscle fatigue can lead to respiratory failure. There is no close correlation between the degree of peripheral muscle weakness and the weakness of the respiratory muscles. Early in the disease the maximum in- and expiratory pressures can be abnormal even though the results of spirometry are normal. Progressive weakness of the respiratory muscles results in a decrease in vital capacity and eventually in alveolar hypoventilation, especially during sleep. General muscle weakness and fatigue may be the reasons why sleep hypoventilation is often overlooked in its early stages. Dyspnea may be a early symptom but it is not unusual that alveolar hypoventilation remains undetected until complications ensue (Cor pulmonale, polycythemia, altered alertness).

Humans↗

PubMed2007

Multisystem Proteinopathy

CLINICAL CHARACTERISTICS: Multisystem proteinopathy (MSP) is a genetically heterogeneous, multisystem degenerative disorder characterized by adult-onset proximal and distal muscle weakness (clinically resembling a limb-girdle muscular dystrophy syndrome), early-onset Paget disease of bone (PDB), and premature frontotemporal dementia (FTD). Muscle weakness progresses to involve other limb and respiratory muscles. PDB involves focal areas of increased bone turnover that typically lead to spine and/or hip pain and localized enlargement and deformity of the long bones; pathologic fractures occur on occasion. Early stages of FTD are characterized by dysnomia, dyscalculia, comprehension deficits, and paraphasic errors, with minimal impairment of episodic memory; later stages are characterized by inability to speak, auditory comprehension deficits for even one-step commands, alexia, and agraphia. Mean age at diagnosis for muscle disease is 43 years, PDB is 41 years, and FTD is 56 years. Dilated cardiomyopathy, amyotrophic lateral sclerosis, and Parkinson disease are now known to be part of the spectrum of findings associated with MSP. DIAGNOSIS/TESTING: The diagnosis of MSP is established in a proband with typical clinical findings and a heterozygous pathogenic variant in VCP, HNRNPA1, HNRNPA2B1, or SQSTM1 identified by molecular genetic testing. MANAGEMENT: Treatment of manifestations: Weight control to avoid obesity; physical therapy and stretching exercises to promote mobility and prevent contractures; occupational therapy and mechanical aids (canes, walkers, orthotics, wheelchairs) as needed for ambulation/mobility; surgical intervention for foot deformity and scoliosis as needed; respiratory aids when indicated; assisted living arrangements for muscle weakness and/or dementia; bisphosphonates to relieve pain and disability from PDB; social and emotional support; education regarding safety precautions. Surveillance: Echocardiogram and electrocardiogram with repeat cardiac evaluation every two to three years or earlier if symptomatic; annual pulmonary function studies; sleep studies as clinically indicated; annual alkaline phosphatase measurement; skeletal imaging as indicated for evaluation of PDB; neurologic and neuropsychological assessment every two to three years or more frequently as needed; multidisciplinary monitoring for respiratory, cardiac, musculoskeletal, and cognitive decline. GENETIC COUNSELING: MSP is inherited in an autosomal dominant manner. Most individuals diagnosed with MSP have an affected parent. Estimates based largely on VCP-MSP suggest that approximately 5% of individuals have a de novo pathogenic variant. Each child of an individual with MSP has a 50% chance of inheriting the MSP-related pathogenic variant. Marked intrafamilial variability may be observed among heterozygous family members, including differences in age at onset, severity, rate of progression, and the specific combination of manifestations. Once the MSP-related pathogenic variant has been identified in an affected family member, predictive testing for at-risk family members and prenatal/preimplantation genetic testing are possible.

Inclusion Body Myopathy with Early-Onset Paget Dis↗

PubMed1998

Decompensated cor pulmonaleas the first manifestation of adult-onset myopathy.

A 46-year-old white female was admitted for decompensated cor pulmonale (CP). It had not interfered with her daily activities and she had not experienced shortness of breath, fatigue or muscle weakness prior to the onset of right heart failure. A thorough investigation revealed severe generalized muscle weakness with restrictive chest bellows disease and secondary CP (mean pressure in the pulmonary artery 60 mm Hg). After having refused respiratory support the patient died a few days after admission. The muscle biopsy was consistent with adult-onset acid-maltase deficiency. This is a rare case of metabolic myopathy presenting as decompensated CP without previous symptoms of muscle weakness. This condition can easily be treated with nocturnal ventilatory support, improving the quality and length of life.

Diagnosis, Differential↗

PubMed2000

The expanding clinical and genetic spectrum of the myotonic dystrophies.

Core features of the dominantly inherited myotonic dystrophies are myotonia, muscle weakness and cataract. Classic myotonic dystrophy (Steinert's disease) has been defined as a genetic entity by the underlying CTG repeat expansion on chromosome 19q13.3 (= DM1 locus). Later on, another disorder similar to but different from myotonic dystrophy was described as proximal myotonic myopathy (PROMM). The majority of PROMM families have been linked to a recently discovered locus on chromosome 3q21 (= DM2 locus).--This article analyses the clinical features of 70 patients from 14 German PROMM families linked to the 3q locus. In contrast to Steinert's disease, these patients did not reveal mental deficiency; no congenital type was found; weakness was mainly located in the proximal leg muscles; clinical myotonia was very mild and sometimes absent; episodes of pain occurred. In the majority of patients, the disorder seems to be more benign compared to Steinert's disease. However, life threatening cardiac involvement is possible; rarely, muscle weakness may progress until the patient is bedridden.--Some families with a PROMM-like phenotype do not link to the locus on 3q. The group of the myotonic dystrophies will get new members in the future.

Adult↗

PubMed1993

[Myopathy and polyneuropathy caused by colchicine].

A forty-six year old man with chronic renal failure and a toxic chronic liver disease developed progressive muscle weakness after a long trial with colchicine. Physical exam revealed muscle weakness and proximal muscle atrophy with hyporeflexia. Serum levels of creatine kinase were high and signs of myopathy and axonal and demyelinating polyneuropathy was evidenced in electrophysiological studies. Muscle biopsy disclosed a vacuolar myopathy, disruption of myofibers and dilatation of sarcoplasmic reticulum. The clinical pictures was attributed to a toxic myopathy and polyneuropathy due to colchicine, thus this treatment was discontinued. Four week later, the patient was symptom free, the levels of seric creatine kinase were normal and a new muscle biopsy was normal, with disappearance of previous histological findings.

Colchicine↗

PubMed1986

Acid maltase deficiency in an adult. Evidence for improvement in respiratory function with high-protein dietary therapy.

Acid maltase deficiency (AMD) in the adult is associated with progressive ventilatory muscle weakness and death from respiratory failure, but effective therapy is not available at present. Because recent evidence suggests that muscle catabolism may contribute to muscle weakness in AMD, we treated a 55-yr-old man with AMD and severe ventilatory muscle weakness with a high-protein (1.6 g/kg), weight-reducing diet for 27 months. High-protein dietary therapy was associated with striking improvement in respiratory function, including measures of ventilatory muscle strength and endurance. We suggest that high-protein dietary therapy may be useful in adults with AMD and respiratory insufficiency.

Adult↗

PubMed1997

[A case of Ki-1 lymphoma-associated eosinophilic polymyositis].

We report on a patient of Ki-1 lymphoma-associated hypereosinophilic syndrome and eosinophilic polymyositis. A 22-year-old male was admitted to a hospital because of anterior chest pain, when he had a white cell count of 12,000 with 33% of eosinophils. He first noticed muscle weakness in the right shoulder at age 23 years. At the age of 25, he experienced marked muscle weakness in his arms and neck, which brought him to our hospital. Neurological examination on admission revealed moderate muscle atrophy and weakness in the neck flexors and both upper extremities, and marked muscle hypertrophy in the sternocleidomastoideus and trapezius muscles. Laboratory studies showed a white blood cell count of 17,700 with 56% of eosinophils. His serum creatine kinase (CK) level was elevated to 347 units. A muscle biopsy specimen showing active myositis infiltrated by eosinophils confirmed the diagnosis of eosinophilic myositis. Although eosinophilia and serum CK activity decreased markedly with corticosteroid treatment, his muscle weakness was unchanged. At the age of 27 years, lymphadenopathy developed. Immunocytochemical examination on a biopsied neck lymph node indicated Ki-1 lymphoma with positive Ki-1, CD45 and epithelial membrane antibodies. In spite of chemotherapy and local irradiation treatment, he died four months after the emergence of Ki-1 lymphoma. We discussed the relationship between hypereosinophilic syndrome, eosinophilic polymyositis and Ki-1 lymphoma on pathogenetic mechanism.

Adult↗

PubMed2004

Unusual muscle disease in HIV infected patients.

Two patients presented with proximal muscle weakness, a normal or minor elevation of creatine phosphokinase (CPK) and normal findings on electromyography. Muscle biopsy in one patient revealed CD8+ polymyositis, and in the other showed ddI induced myopathy. These cases illustrate the importance of muscle biopsy in identifying the underlying pathology in HIV infected patients with muscle weakness and little or no abnormality in laboratory investigations.

Anti-HIV Agents↗

PubMed1990

[Pindolol-induced rhabdomyolysis in sarcoid myopathy].

A 72-year-old man suddenly developed severe muscle weakness following the treatment with pindolol (Calvisken) for three days. Neurological examination on admission disclosed marked proximal muscle weakness with absent deep tendon reflexes. Laboratory data showed significant increase of serum CK, aldolase and myoglobin. Electromyography revealed both neurogenic and myogenic changes in all muscle tested. Skeletal muscle CT showed patchy low density areas in muscles of thigh and leg, especially in the hamstrings. Femoral muscle biopsy demonstrated a granulomatous nodule with multinucleated giant cells in the degenerated muscle fibers showing small-grouped atrophy. By Mb-PAP staining, Mb-negative fibers were randomly distributed among normally stained ones. Leu 1, 3a, 4, HLA-DR positive cells were found adjacent to the granuloma by immunoperoxidase staining. After immediate withdrawal of pindolol and treatment with steroid, he recovered muscle strength and enzyme activities were normalized in a week. Beta blockers have been known to induce muscle cramps or pain and moderate elevation of serum muscle enzymes. However, severe muscle weakness with highly elevated enzyme activities leading to rhabdomyolysis as noticed in the present case was rarely reported in the literature. Underlying sarcoid myopathy might be suspected to exaggerate this unusual case of pindolol-induced rhabdomyolysis. A careful use of pindolol is emphasized.

Aged↗

PubMed2000

Classical and amyopathic dermatomyositis seen at the National Skin Centre of Singapore: a 3-year retrospective review of their clinical characteristics and association with malignancy.

INTRODUCTION: Dermatomyositis is a condition well-known to medical physicians, especially rheumatologists and dermatologists. Classically, patients present with typical cutaneous features and proximal muscle weakness. Amyopathic dermatomyositis has been reported in recent literature where patients present with skin changes without muscle involvement. MATERIALS AND METHODS: We reviewed 28 patients diagnosed with dermatomyositis at the National Skin Centre over a 3-year period from 1996 to 1998 to assess the prevalence of this amyopathic variant in our local population and its association with malignancy. RESULTS: Out of the 28 patients, 13 (46.4%) had no clinical or laboratory evidence of myositis at presentation. Nine patients (32.1%) had clinical muscle weakness and 6 patients (21.4%) had laboratory evidence of myositis. Malignancies were detected in 12 patients (42.8%), half of which were nasopharyngeal carcinomas. There was no significant difference in the prevalence of malignancy between those with detectable muscle weakness (33.3%) and those without (47.4%). However, there was a significant higher prevalence of malignancy in those with clinical and laboratory evidence of myositis (66.6%) than those without (15.4%). CONCLUSION: We conclude that amyopathic dermatomyositis is a common presentation in our population and may have a lower risk of malignancy than the classical variant. Screening for malignancy, especially nasopharyngeal carcinoma, is recommended for all dermatomyositis patients.

Adolescent↗

PubMed2000

[Osteomalacia in immigrants: therapeutic management of two cases].

BACKGROUND: Vitamin D deficiency in immigrant adults eventually leads to an osteomalacia syndrome with its characteristic clinical features of bone pain, muscle weakness and difficulty in walking (waddling gait). CASE REPORT: We report on 2 female immigrants from Ethiopia and Eritrea who developed the typical clinical signs of osteomalacia such as generalized bone pain and muscle weakness. Also in osteomalacia there is a significant decrease in bone density but more relevant for diagnosis are low serum levels of 25-OH-vitamin D and as radiological features pseudofractures (Looser's zones). Bone biopsy definitely proves the diagnosis. Simple treatment with vitamin D and calcium is highly effective. CONCLUSION: Since there is an increasing number of immigrants into northern European countries osteomalacia should always be taken into consideration if such patients develop skeletal pain syndrome and muscle weakness.

Adult↗

PubMed1987

Temporal analysis of dithiobiuret neurotoxicity in rats and assessment of potential nonneural causes.

To evaluate the hypothesis that depressed neuromuscular transmission causes dithiobiuret (DTB)-induced muscle weakness in rats, the temporal development of impaired treadmill performance and deficits in the nerve-elicited muscle contractions were compared during daily treatment with the toxicant (DTB, 1 mg/kg/day X 6 days). Diminished treadmill test performance after 4 days of treatment marked the initial detection of impaired motor function. At this time fading (loss of tension during tetanus) of gastrocnemius contractions elicited in response to 100-Hz sciatic nerve stimulation occurred in DTB-treated rats but not in controls. After 5 and 6 days of treatment, treadmill failure became complete, tetanic fade worsened dramatically, and peak contractile tension measured during trains of nerve stimulation (10-250 Hz) decreased progressively. Appearing by Day 6 were marked body weight loss, dehydration, hypothermia, and a depression in serum concentrations of thyroid hormones. Total oxygen content of the blood was not reduced at any time during treatment, and serum concentrations of glucose, sodium, potassium, calcium, chloride, and phosphorus in DTB-treated rats on Day 6 were similar to those of control animals. Therefore, hypoxia, hypoglycemia, or a serum electrolyte imbalance do not initiate or modulate the neuromuscular toxicity. Light microscopic evaluation of liver, kidney, lung, thyroid, and other organs in intoxicated rats was unremarkable and in skeletal muscles and selected sites of brain, spinal cord, and sciatic nerve no morphologically significant lesions were observed. Even when DTB-intoxicated rats were maintained in a state of flaccid muscle weakness for 5 continuous days, peripheral nerve lesions proximal to the intramuscular nerves were not detected. Thus, depressed neuromuscular transmission appears to be the primary cause of the flaccid muscle weakness and no evidence was obtained that nonneural effects of DTB initiate or modulate this effect.

Animals↗

PubMed2001

Quadriceps concentric and eccentric exercise 2: differences in muscle strength, fatigue and EMG activity in eccentrically-exercised sore and non-sore muscles.

The purpose of this study was to determine whether the previously reported muscle weakness and increases in EMG and EMG/force ratio after eccentric exercise were related to ensuing soreness or simply to the exercise mode. Delayed-onset muscle soreness, maximal voluntary force and the surface electromyogram (EMG) of the quadriceps were studied in 10 healthy male subjects following 20 min of bench-stepping with a constant leading leg. Prior to stepping and at 0, 0.25, 0.50, 0.75, 1, 3, 24 and 48 h afterwards the subjects performed a 30 s isometric maximal voluntary contraction (MVC) of the extensors of each leg during which the isometric force and the root mean square voltage of the surface EMG (rms EMG) were recorded. Muscle soreness was recorded prior to and at 0, 0.75, 3, 24 and 48 h after the stepping task by means of a force probe. No soreness was experienced in the concentrically exercised muscles, but in the eccentrically exercised muscles 5 subjects were not sore and 5 experienced soreness after 24 h, increasing to 48 h. There were no significant differences between sore and non-sore muscles in muscle weakness, fatigue during 30 s, the EMG amplitudes or the EMG/force ratios during peak force and the 30 s MVC (p >0.05). Muscle weakness following eccentric exercise was related to the exercise mode and was independent of subsequent soreness. Both weakness and soreness may be related to muscle damage, but involve different mechanisms.

Adult↗

PubMed1991

[Nemaline myopathy with type 2 fiber predominance; a case report].

A 4-year-old boy was admitted to our hospital because of dyspnea and muscle-weakness. His developmental milestones were delayed. His face was long with opened mouth. He spoke with nasal voice. He had proximally dominant muscle weakness and his deep tendon reflexes were absent. Laboratory examination revealed normal serum creatine kinase level and a myopathic EMG pattern. Blood gas analysis revealed metabolic acidosis with PH 7.35, PCO2 55.4 mmHg, PO2 62.4 mmHg, BE 3.0, probably from the metabolic acidosis by respiratory muscle weakness. In the biopsied left biceps brachii muscle, there were scattered fibers with nemaline bodies and abnormal fiber type distribution; type 1, 2 A, 2 B and 2 C fibers comprised 7%, 70%, 21% and 2% respectively. Small type 1 fibers and type 1 fiber predominance are the characteristic and common histochemical findings in nemaline myopathy. Accordingly, type 2 fiber predominance in the present patient is a unique, rare phenomenon. The finding might result from a preferential loss of type 1 motoneurons or muscle fiber type transformation from type 1 to type 2 fibers due to a certain abnormal neuronal influence on developing muscles.

Child, Preschool↗