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PubMed1958

Systemic lupus erythematosus; results of treatment with triamcinolone.

Twenty-nine patients with systemic lupus erythematosus were treated with a new synthetic unsaturated prednisolone derivative, triamcinolone, for as long as 11 months. This hormone is 1.3 times as powerful as prednisone and 4.4 times more potent than hydrocortisone as an anti-inflammatory agent. The average dose for beginning therapy in cases of mild systemic lupus erythematosus was 20.6 mg. a day. The average maintenance dose used to control mild exacerbations of the disease was 26.0 mg. a day. There was no evidence of sodium retention or potassium loss. Sixteen patients had upper gastrointestinal x-ray studies before and during therapy with triamcinolone. There was no evidence of peptic ulceration except in one patient who was receiving 96 mg. a day. Nine patients had gastric analysis with histamine before and during therapy. No significant changes were noted in results of these tests, even in the patient who had an ulcer. No abnormal increase in uropepsin was noted in cases in which this factor was tested. The pattern of clinical improvement closely paralleled that obtained by previous treatment with older steroids. There was a disappearance of all the clinical and laboratory abnormalities produced by the disease, with the exception of long standing renal involvement. A major difference between triamcinolone and other steroids was a tendency to progressive gradual loss of weight, partly owing to fluid loss. Cushingoid appearance produced by other steroid therapy did not disappear. The cutaneous side effects, particularly Cushingoid appearance, hirsutism and striae were more pronounced than with older steroids. The most serious side effect was muscle weakness which appeared in six patients, all women, in from four to thirty-two weeks after starting triamcinolone. The profound muscle weakness, most pronounced in the quadriceps group, gradually cleared after several weeks of therapy with another steroid. Fourteen patients had received prior steroid therapy with all the older anti-inflammatory hormones and seven of them were better controlled and felt better with triamcinolone.

Anti-Inflammatory Agents↗

PubMed1992

Remarkable improvement of activity by CAPD in a hemodialysis patient with a pseudotumor of the craniocervical junction.

Pseudotumor of the craniocervical junction and destructive spondyloarthropathy (DSA) are the most serious forms of dialysis amyloidosis (DAA). Pain and paralysis due to these lesions significantly impair activity of a patients' daily life (ADL). CAPD improved ADL of a 54 year-old male patient complicated with various forms of DAA after 17 years of hemodialysis (HD) treatment. He was first diagnosed as having carpal tunnel syndrome 12 years after initiation of hemodialysis followed by dialysis shoulders(12 years), trigger fingers(12 years), bone cysts(15 years), tendon ruptures(17 years), DSA and a pseudotumor of the craniocervical junction(17 years). Magnetic resonance imaging (MRI) taken in May 1989 revealed a pseudotumor of the craniocervical junction, which was 30 mm in diameter, located in front of partially destroyed C1 and C2. Neck pain and muscle weakness rendered him bed ridden. Six months after switching to CAPD with administration of prednisolone, neck pain disappeared. He recovered the muscle power by physical rehabilitation. At last it became possible for him to perform the CAPD procedure by himself and drive a car to the hospital as an out patient. In such cases of pseudotumors of the craniocervical junction, CAPD is one of the best methods for relieving the pain and muscle weakness.

Activities of Daily Living↗

PubMed1988

Ultrastructural pathology in emetine-induced myopathy.

Progressive myopathy developed in two women who consumed ipecac syrup containing emetine hydrochloride to induce vomiting as part of their anorexia nervosa. Muscle biopsy specimens were characterized by severe disruption of the sarcomeres. The ultrastructural spectrum extended from "Z-band streaming" to the formation of cytoplasmic bodies and also comprised abnormalities of the sarcotubular system, thus suggesting that muscle weakness may be related to both sarcomeric and sarcotubular lesions in this self-inflicted myopathy. It is tempting to suggest that muscle weakness may be correlated with or based on the pathology in sarcomeres and the sarcotubular system. As the myopathy is clinically reversible upon discontinuation of ipecac consumption the morphological findings should also be potentially reversible. Experimentally induced emetine myopathy may, thus, serve as a useful model to study morphological dynamics of sarcomeric lesions, which may be observed separately or simultaneously in a variety of spontaneously occurring human neuromuscular disorders.

Adult↗

PubMed1986

Clinical and genetic studies of muscular dystrophy in young girls.

During the years 1971-81, we treated 7 girls with clinical features suggestive of Duchenne dystrophy. Muscle weakness developed at 1.5 or at 5-8 years and progressed rapidly. Two girls were in wheel-chairs in their teens. Muscle atrophy began in the proximal parts of the lower extremities and pseudohypertrophy of the calf occurred in all patients. Serum creatine phosphokinase (CPK) activity was moderately to highly elevated in all cases and EMG showed a moderate to marked myopathic pattern. Chromosomal studies showed normal finding in the five examined. Mental retardation (IQ 37-73) was present in four. Consanguinity was present in 3 out of the 7 cases. Two mothers showed elevated levels of CPK and myopathic patterns on EMG. In addition, one mother had slight muscle weakness at the age of 42 and another had prominent pseudohypertrophy of the calf. Sex-linked recessive inheritance might be considered here, because carriers of autosomal recessive type never showed elevated levels of CPK or mild myopathic symptoms. The other five of our seven might be cases of autosomal recessive inheritance, because the mothers had normal serum CPK levels and in 2 families there was a consanguinity.

Adolescent↗

PubMed2006

Asymmetrical bilateral paresis of the superior oblique muscle.

BACKGROUND: To review the preoperative signs of bilateral superior oblique paresis and to analyze their presence. METHODS: The proposed preoperative signs of bilateral superior oblique (SO) muscle paresis were separated into "certain signs" and "suspicious signs." The signs were analyzed for accuracy using case examples and statistics. RESULTS: A strong preoperative sign of bilateral SO muscle paresis was reversal of the hypertropia in the ipsilateral (and/or ipsi-supralateral) position and/or in the contralateral head tilt position. In such cases, the addition of a light contralateral weakening procedure to the operation aimed at the elimination of the hypertropia caused by the more affected SO muscle prevented development of the clinical picture of a contralateral SO muscle paresis. A suggestive preoperative sign of bilateral SO muscle weakness was marked reduction of the hypertropia in the ipsilateral (and ipsi-supralateral) position, as well as in the contralateral head tilt position. In these cases, a contralateral inferior oblique muscle weakening was deferred until after motility could be reassessed postoperatively. An additional sign of possible bilateral SO muscle weakness was the presence of a large V pattern. CONCLUSIONS: When planning surgery for apparent unilateral SO muscle paresis, the surgeon should be aware of the often subtle preoperative signs of bilateral SO muscle paresis. Early diagnosis allows the surgeon to avoid the reversal of the clinical picture or to advise the patient of the possibility of a bilateral problem.

Eye Movements↗

PubMed1992

[A case of motor neuron disease with IgM gammopathy which showed anti-cerebrum antibody].

A patient, 50-year-old female, developed progressive weakness of lower extremities, and gait disturbance for 2 years. Neurological examination revealed hyperreflexia with pathological reflex, fasciculation in the limbs and tongue, muscle weakness and atrophy in distal limbs, but no sensory disturbance. Needle EMG showed neurogenic findings compatible with motor neuron disease (MND). Laboratory data showed polyclonal IgM hyperimmunoglobulinemia, positive several autoimmune antibodies including antisingle strand DNA antibody (Ab), ENAab, SS-A ab and RA. There were no antibodies for gangliosides and Myelin-associated glycoprotein (MAG), but positive antibody for 54KD protein of cerebral gray and white matter. The clinical manifestations including gait disturbance and muscle weakness, and serum IgM level were moderately improved by plasmapheresis which is considered important for consideration of causes of MND.

Autoantibodies↗

PubMed2001

Maximal respiratory pressures in myasthenia gravis. Relation to single fiber electromyography.

OBJECTIVES: The respiratory muscle weakness was evaluated in mild forms of myasthenia gravis (MG) and was compared with single fiber electromyography results (SFEMG) in the extensor digitorum communis muscle. MATERIAL AND METHODS: We assessed 61 treated MG patients without clinical respiratory involvement (13 ocular forms, 28 form IIa and 20 form IIb patients) by maximal respiratory pressure (MRP) to ascertain whether they were consistent with SFEMG results. RESULTS: Maximal expiratory pressure (MEP) and maximal inspiratory pressure (MIP) were reduced below the lower limit for healthy subjects in 85% and 77% of ocular patients; in 93% and 89% of form IIa, respectively; and in 95% of form IIb. The highest percentage of MEP and MIP reduction showed a positive correlation with increased jitter (r=0.45, P<0.001; r=0.27; P<0.05 respectively) and impulse blocking (r=0.35, P<0.01; r=0.28, P<0.05 respectively). CONCLUSION: We consider MRP measure useful for assessing respiratory muscle weakness in MG patients with subclinical respiratory involvement.

Adult↗

PubMed2005

[Collagenopathy (Ullrich congenital muscular dystrophy, Bethlem myopathy)].

Collagenopathies with collagen VI mutations include Ullrich congenital muscular dystrophy (Ullrich's disease) and Bethlem myopathy. Patients with Ullrich's disease have generalized muscle weakness, multiple contractures of the proximal joints and hyperextensibility of the distal joints. Bethlem myopathy is characterized by the combination of proximal muscle weakness and contractures of finger, elbow, and ankle joints. We found for the first time a deficiency of collagen VI in Ullrich's disease. Furthermore, we found an abnormality of cell adhesion and abnormal regeneration or maturation in Ullrich's disease. Mutations in the genes COL6A1, COL6A2, COL6A3 are associated with Ullrich's disease and Bethlem myopathy. Bethlem myopathy is inherited in an autosomal dominant manner and Ullrich's disease usually in an autosomal recessive manner. Recently, de novo dominant mutations are reported in Ullrich's disease. We evaluated the role of nonsense-mediated mRNA decay (NMD) in Ullrich's disease that has a frameshift mutation with a premature termination codon in the COL6A2 gene causing the loss of collagen VI. The pharmacological block of NMD caused upregulation of the mutant collagen VI and partially functional extracellular matrix formation. Our results suggest that NMD inhibitors can be used as a therapeutic tool to rescue some human genetic diseases exacerbated by NMD.

Collagen Type VI↗

PubMed1984

Excretion of porphyrins and porphyrin precursors during neuromuscular paralysis produced by dithiobiuret.

Urinary excretion of porphyrin precursors delta-aminolevulinic acid (ALA) and porphobilinogen (PBG) and total porphyrins was measured during intoxication of rats with 2,4-dithiobiuret (DTB), a chemical which produces delayed-onset neuromuscular weakness, in an attempt to ascertain whether or not DTB poisoning in the rat would serve as an animal model of the neurologic symptoms of acute intermittent porphyria. Daily administration of DTB (1 mg/kg/day, i.p.) produced flaccid skeletal muscle weakness first detected after 4 to 5 days of treatment. Onset of skeletal muscle weakness was associated with a significant increase in urinary excretion of ALA. The excretion of PBG and total porphyrin was also increased; however, the increase was not significant. The increase in porphyrins and porphyrin precursors was due to increased urine output which coincided with the onset of neuromuscular weakness; urinary concentrations of ALA, PBG, and porphyrins were not increased by DTB. Measurements of free-erythrocyte protoporphyrin, taken after 7 days of DTB treatment, indicated a significant elevation of free erythrocyte protoporphyrin concentration. The pattern of alterations in the heme precursors associated with DTB-induced paralysis in rats is quite different from that observed in humans afflicted with acute intermittent porphyria. Therefore, we conclude that DTB-induced paralysis in the rat does not represent an accurate animal model of acute intermittent porphyria.

Aminolevulinic Acid↗

PubMedDate not supplied

Familial amyloidotic polyneuropathy in Hokkaido: a case report.

A 54-year-old man began to feel numbness in his hands at the age of 42 (1975). His condition became progressively worse accompanied by muscle weakness of the lower limbs and glove and stocking paresthesia of the extremities. The patient was admitted to our hospital on March 23, 1987. Neurological examination revealed distal dominant muscle weakness, sensory disturbance and areflexia. Electrocardiogram and ultrasound-cardiogram strongly suggested cardiomyopathy. A biopsy of the rectal wall and the cardiac muscle revealed amyloid deposits. The patient, his elder brother and one of his daughters had abnormal serum transthyretin (TTR, a protein referred as prealbumin). Therefore, the diagnosis of familial amyloidotic polyneuropathy (FAP) was confirmed. The patients's brother and daughter mentioned above, however, had no abnormal findings on physical examination and they were thus considered to be asymptomatic carriers. There may be more cases of asymptomatic carriers, if examination of abnormal TTR is more frequently analyzed.

Amyloidosis↗

PubMed1996

Severe dystrophinopathy in a patient with congenital hypotonia.

We studied a 2-year-old child with congenital hypotonia and proximal muscle weakness. There was no family history of neuromuscular disease. The child also had hypospadia. The central nervous system was apparently not involved. Muscle biopsy showed a dystrophic pattern and dystrophin was absent as shown by immunofluorescence and by Western blot. Vinculin and spectrin were also reduced, while merosin was normal in muscle fibers. This observation suggests that congenital hypotonia may be associated with a severe form of dystrophinopathy.

Abnormalities, Multiple↗

PubMed2005

Hyperkalemia-induced residual neuromuscular blockade: a case report.

Muscle relaxants are routinely administered during anesthesia. The residual effects of nondepolarizing muscle relaxants must be reversed by the anesthesia provider prior to extubation of the trachea to ensure that patients can safely protect their own airways and maintain adequate ventilation. Many factors can potentiate the effects of muscle relaxants, and each of these factors must be taken into consideration when postoperative muscle weakness is encountered. Only after the cause of residual neuromuscular weakness is discerned can the appropriate treatment be determined. This article describes the anesthetic management of a patient who experienced postoperative residual muscle weakness secondary to unsuspected hyperkalemia. A discussion of potassium's role in membrane excitability and factors that must be considered in the differential diagnosis of residual neuromuscular weakness is included.

Aged, 80 and over↗

PubMed2003

A locus on chromosome 15q for a dominantly inherited nemaline myopathy with core-like lesions.

Nemaline myopathy is a congenital neuromuscular disorder characterized by muscle weakness and the presence of nemaline rods. Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1). In addition, mutations in the ryanodine receptor gene (RYR1) have been associated with core-rod myopathy. Here we report linkage in two unrelated families, with a variant of nemaline myopathy, with associated core-like lesions. The clinical phenotype consists of muscle weakness in addition to a peculiar kind of muscle slowness. A genome-wide scan revealed a locus for nemaline myopathy with core-like lesions on chromosome 15q21-q23 for both families. Combining the two families gave a two-point LOD score of 10.65 for D15S993. The alpha-tropomyosin-1 gene (TPM1) located within this region is the strongest candidate gene. However, no mutations were found in the protein-coding region of TPM1, although small deletions or mutations in an intron cannot be excluded. The critical region contains few other candidate genes coding for muscle proteins and several genes of unknown function, and has not yet been sequenced completely. The novel phenotype of nemaline myopathy in the two presented families corresponds to an also novel, as yet uncharacterized, genotype.

Adolescent↗

PubMed2002

Divergent abnormal muscle relaxation by hypertrophic cardiomyopathy and nemaline myopathy mutant tropomyosins.

Mutations in tropomyosin (Tm) have been linked to distinct inherited diseases of cardiac and skeletal muscle, hypertrophic cardiomyopathy (HCM), and nemaline myopathy (NM). How HCM and NM mutations in nearly identical Tm proteins produce the vastly divergent clinical phenotypes of heightened, prolonged cardiac muscle contraction in HCM and skeletal muscle weakness in NM is currently unknown. We report here a direct comparison of the effects of HCM (A63V) and NM (M9R) mutant Tm on membrane-intact myocyte contractile function as assessed by adenoviral gene transfer to fully differentiated cardiac muscle cells. Wild-type, and mutant HCM, and mutant NM proteins were expressed at similar levels in myocytes and incorporated into sarcomeres. Interestingly, HCM mutant Tm produced significantly longer contractions by slowing relaxation, whereas NM mutant Tm produced the opposite effect of accelerated muscle relaxation. We propose slowed relaxation caused by HCM mutant Tm can directly contribute to diastolic dysfunction seen in HCM even without secondary cardiac remodeling. Conversely, hastening of relaxation by NM mutant Tm may shift the force-frequency relationship in skeletal muscle and contribute to muscle weakness seen in NM. Together, these results implicate divergent, abnormal "turning off" of muscle contraction as a cellular basis for the differential pathogenesis of mutant Tm-associated HCM and NM.

Animals↗

PubMed1997

Tongue involvement in a patient with granulomatous myositis.

A 64-year-old woman had difficulty swallowing and talking, weakness of the tongue, and progressive muscle weakness that was proven to be caused by a granulomatous myopathy. This case resembled a motor neuron disease, indicating that granulomatous myopathy should be considered in patients with similar presentations, since it is a treatable condition with a more benign prognosis.

Anti-Inflammatory Agents↗

PubMed2006

[Cause and treatment of dysuria post trans-urethral resection of prostate].

OBJECTIVE: To evaluate the cause and treatment of dysuria post trans-urethral resection of prostate (TURP). METHODS: The clinical data and the treatment of 22 cases of dysuria post TURP were analyzed retrospectively. RESULTS: All cases including 3 cases of glandular and extraneous material residual, 5 cases of urethrostenosis, 7 cases of bladder neck contracture, and 7 cases of detrusor muscle weakness, were cured after the treatment. CONCLUSION: The main causes of dysuria post TURP were glandular residual, urethrostenosis, bladder neck contracture, and detrusor muscle weakness. Correct preoperative diagnosis and treatment during/post operation are the key to the prevention of dysuria post TURP.

Aged↗

PubMedDate not supplied

Tizanidine in the management of spasticity and musculoskeletal complaints in the palliative care population.

Spasticity and other muscle symptoms in the palliative care patient can contribute to suffering, significantly detracting from overall quality of life. Current therapy primarily includes use of centrally acting muscle relaxants, which are beneficial in treating some symptoms, but frequently have extensive side effects, such as sedation and muscle weakness. Tizanidine, a central alpha 2 adrenergic agonist, has been shown in clinical studies to be as effective as other commonly used antispastic agents, but without debilitating muscle weakness. Tizanidine can cause sedation, which is minimized by dose titration. When taken at night, patients report improvement in getting to sleep and little drowsiness or "hangover sensation" upon waking. Tizanidine is potentially helpful to many palliative care patients with chronic muscle pain and sleep disturbances.

Clonidine↗

PubMed2000

Physical therapy in the treatment of fibromyalgia.

Fibromyalgia (FM) is a syndrome of unknown etiology characterized by chronic wide spread pain, increased tenderness to palpation and additional symptoms such as disturbed sleep, stiffness, fatigue and psychological distress. While medication mainly focus on pain reduction, physical therapy is aimed at disease consequences such as pain, fatigue, deconditioning, muscle weakness and sleep disturbances and other disease consequences. We systematically reviewed current treatment options in the treatment of fibromyalgia. Based on evidence from randomized controlled trials cardiovascular fitness training importantly improves cardiovascular fitness, both subjective and objective measures of pain as well as subjective energy and work capacity and physical and social activities. Based on anecdotal evidence or small observational studies physiotherapy may reduce overloading of the muscle system, improve postural fatigue and positioning, and condition weak muscles. Modalities and whole body cryotherapy may reduce localized as well as generalized pain in short term. Trigger point injection may reduce pain originating from concomitant trigger points in selected FM patient. Massage may reduce muscle tension and may be prescribed as a adjunct with other therapeutic interventions. Acupuncture may reduce pain and increase pain threshold. Biofeedback may positively influence subjective and objective disease measures. TENS may reduce localized musculoskeletal pain in fibromyalgia. While there seems to be no single best treatment option, physical therapy seem to reduce disease consequences. Accordingly a multidisciplinary approach combining these therapies in a well balanced program may be the most promising strategy and is currently recommended in the treatment of fibromyalgia.

Acupuncture Therapy↗