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PubMed2000

Juvenile muscular atrophy of distal upper extremity (Hirayama disease).

This disease is characterized by initially progressive muscular weakness and wasting of the distal upper limb(s) in young people predominantly in men, followed by a spontaneous arrest within several years. This disease has been thought to be separate from motor neuron diseases, yet some authors still consider the illness a variant of motor neuron disease. However, the pathological evidence of ischemic changes in the lower cervical anterior horn should facilitate differentiation of the disorder from degenerative motor neuron disease. Recent radiological investigations proved compressive flattening of the lower cervical cord due to forward displacement of the cervical dural sac and spinal cord induced by neck flexion. These findings suggest that sustained or repeated neck flexion may cause ischemic changes in the cervical anterior horn. Application of a cervical collar to minimize neck flexion prevents progressive muscular weakness in an early stage of the disease.

Arm↗
PubMed2001

Radial nerve entrapment in the upper arm as a cause of lateral arm pain: a report of four cases.

Four patients with no history of trauma presented with lateral arm pain, local tenderness, and a tingling sensation at the distal end of the arm when the radial nerve was percussed in the mid-third of the upper arm (Tinel's sign), but no clinical or subjective signs of muscular weakness. They were treated by decompression of the radial nerve in the fibrous canal proximal to the lateral intermuscular septum. Three of the patients had a complete or pronounced reduction in pain, while the fourth had only a slight improvement. Non-traumatic radial nerve entrapment in the upper arm may be the cause of lateral arm pain without clinical signs of muscular weakness.

Adult↗
PubMed2006

[Neurophysiological study in slow-channel congenital myasthenic syndrome: case report].

The slow-channel syndrome is one of the congenital myasthenic syndromes attributed to inherited kinetic disorders of the ion channel of the acetylcholine receptor of the neuromuscular junction. This is a case report of 25-years-old man with progressive ptosis and limitation of ocular movements since infancy, presented a 6-years history of worse of the external ophthalmoparesis and muscular weakness in the shoulders and hands. The motor nerve conduction studies after a supramaximal single stimulus disclosed a double compound muscle action potential (CMAP) that disappeared after a voluntary contraction of 30 seconds. Repetitive stimulation of facial and spinal accessory nerves showed a CMAP decrement greater than 10% with disappeared of the second potential. The patient received fluoxetine with mild improvement of muscular weakness, but persisted with: ptosis, limitation of ocular movements and repetitive CMAP in the motor nerve conduction study. The characteristic of disease are discussed.

Action Potentials↗
PubMed1981

[Lysinuric protein intolerance: a severe hyperammonemia secondary to l-arginine deficiency (author's transl)]].

Lysinuric protein intolerance is an autosomal recessive disease, due to a defect in intestinal, renal and hepatic dibasic amino acid transport. Two new cases in the same family are reported. The disease appears progressively during the first months of life with failure to thrive, anorexia, vomiting, diarrhea, hepatosplenomegaly, muscular weakness, osteoporosis, anemia, leukothrombocytopenia, hyperammonemia and orotic aciduria after a high-protein intake. Hyperdibasicamino-aciduria was associated with subnormal plasma concentrations of the same aminoacids. Oral l-arginine, l-ornithine, l-lysine, and lysyl-glycine loads confirmed the diagnosis. The supplementation of the diet with l-citrulline resulted in normal levels of blood ammonia. However, hepatosplenomegaly, muscular weakness, osteoporosis remained unchanged and growth was not improved. These may be due to lysine deficiency.

Amino Acid Metabolism, Inborn Errors↗
PubMed1988

Toxicoses in livestock from the hemlocks (Conium and Cicuta spp.).

The hemlocks, Conium maculatum (poison-hemlock) and Cicuta spp. (waterhemlock), are poisonous plants that cause sizeable losss to the livestock industry. Clinical signs of poisonhemlock toxicosis are similar in all species of livestock and include muscular weakness, incordination, trembling, initial central nervous system stimulation, depression and death from respiratory paralysis. Poison-hemlock also causes skeletal defects in the offspring of cattle, pigs and sheep and cleft palate in pigs when ingested during specific periods of gestation. The primary toxicants in poison-hemlock are coniine and gamma-coniceine. Coniine predominates in mature plants and seed, whereas gamma-coniceine predominates in early growth of the plant. Waterhemlock is the most violently toxic poisonous plant known. The toxicant is cicutoxin, which acts on the central nervous system, causing violent convulsions and death. Clinical signs of poisoning appear within 15 min after ingestion of a lethal dose and include excessive salivation, nervousness, tremors, muscular weakness and convulsive seizures interspersed by intermittent periods of relaxation and a final paralytic seizure resulting in anoxia and death. Elevated activities of lactic dehydrogenase, aspartate aminotransferase and creatine kinase in blood are observed, indicative of muscular damage. Toxicoses from poisonhemlock and waterhemlock generally occur in early spring when both plants emerge before other, more palatable plants begin to grow. All parts of the poison-hemlock plant are toxic. The root or tubers of waterhemlock are toxic; however, experimental evidence concerning the toxicity of other plant parts is inconclusive.

Alkaloids↗
PubMed1986

Severe neonatal centronuclear (myotubular) myopathy: an X-linked recessive disorder.

Prenatal onset and rapidly fatal course of centronuclear myopathy are described in four male newborns including two brothers. Diagnosis was established by muscle biopsy within the first week of life in two and at autopsy in the two other patients: Central nuclei, central aggregation of oxydative enzyme activity in the majority of muscle fibers and type 1 fibre hypotrophy were demonstrated. Prenatal manifestation included polyhydramnios, reduced fetal movements and breech presentation. All four newborns developed respiratory insufficiency requiring artificial ventilation immediately after birth. Severe muscular weakness and hypotonia as well as hardly elicitable grasping, deep tendon reflexes and Moro response were noticed. Additional findings included high arched palate, joint contractures, thin ribs, lung hypoplasia, abundant skin and cryptorchidism. In two families, the pedigree contains other affected males, suggesting X-linked inheritance. Seven female carriers were clinically healthy and one of them showed normal muscle histology. Fourteen previously published neonatal cases of centronuclear myopathy are reviewed and compared with our findings. This severe perinatal form of centronuclear myopathy has to be considered in male fetuses and newborns with polyhydramnios and respiratory failure due to muscular weakness or in infants who died of unexplained postnatal asphyxia. Diagnosis should be established by muscle biopsy.

Genetic Carrier Screening↗
PubMed2004

[Polymyositis induced or associated with lipid-lowering drugs: five cases].

PURPOSE: Rhabdomyolysis and myositis are rare, dose-related complications of statins and fenofibrates. The outcome is favorable as a rule with rapid regression after stopping the responsible drug. Recently, various auto-immune disease with evidence of hypersensitivity to HMG-CoA reductase inhibitors or fibrates drugs have been reported. Less than ten cases of dermatomyositis and polymyositis due to cholesterol-lowering drugs (CLD) have been previously reported. Five more cases polymyositis associated with CLD are reported. METHODS: Symptoms were compatible with diagnosis of polymyositis according to Bohan and Peter and with previous reported criteria for drug-induced myopathy in all cases. None of these patients had previous other connective tissue disorders. RESULTS: Five patients (median age 68 [54-78], female N =4) with CLD treatment (statin N =4, fenofibrates N =1) have developed iatrogenic polymyositis. All of them presented both proximal muscular weakness and increased muscle enzyme levels. One patient had iatrogenic antisynthetase syndrome characterized by mechanic's hand, Raynaud's phenomenon and anti JO1 antibodies. One other had sclerodermic hand oedema. Antinuclear antibodies were positive in 4 cases and muscle biopsy revealed polymyositis infiltrate in 4 cases. CLD treatment was discontinued with partial clinical improvement in 3 cases. Clinical remission was obtained with corticosteroid (N =5) in association with immunosuppresive agents in 3 cases. CONCLUSION: Muscular symptoms in patient with CLD treatment could be the first symptom of a polymyositis revealed or increased by this treatment and must encourage physician with antinuclear antibodies screening especially in case of proximal muscular weakness and increased muscle enzyme levels.

Aged↗
PubMed1990

Osteogenic sarcoma and myasthenia gravis in a dog.

A 7-year-old Saint Bernard developed muscular weakness 1 year after right forelimb amputation and adjuvant cisplatin chemotherapy for osteogenic sarcoma. Clinical and laboratory findings supported a diagnosis of myasthenia gravis, and the dog had clinical improvement in response to prednisone treatment. Two additional dogs with myasthenia gravis and osteogenic sarcoma were identified by review of the medical records of the University of California Veterinary Medical Teaching Hospital. Findings indicated that myasthenia gravis or other neuromuscular transmission disorders may be associated with muscular weakness in dogs with osteogenic sarcoma.

Animals↗
PubMed2001

Laryngopharyngeal sensory deficits as a predictor of aspiration.

OBJECTIVE: This study evaluates whether patients with severe sensory deficits in the hypopharynx are at increased risk for aspiration and determines the relationship between pharyngeal muscular weakness and hypopharyngeal sensory deficits. STUDY DESIGN AND SETTING: Forty patients with dysphagia who underwent flexible endoscopic evaluation of swallowing with sensory testing were prospectively divided into 2 groups. One group included patients with severe sensory deficits determined by an absent laryngeal adductor reflex and the other with normal sensitivity. Subjects were given liquid and puree consistencies and were evaluated for aspiration as well as pharyngeal muscle contraction. RESULTS: The differences in incidence of aspiration and pharyngeal muscular weakness between the 2 groups were significant (P < 0.001 Fisher's exact test). CONCLUSION: There is a strong association between motor function deficits and hypopharyngeal sensory deficits. SIGNIFICANCE: The association of sensory loss and motor deficits together with the use of flexible endoscopic evaluation of swallowing with sensory testing can predict those patients who are at highest risk for aspiration.

Adult↗
PubMed1997

The effect of priming with vecuronium and rocuronium on young and elderly patients.

UNLABELLED: The priming principle consists of administering a subparalyzing dose of nondepolarizing neuromuscular blocking drug 3-6 min before giving a second dose for tracheal intubation. This study was performed to observe the effects of priming doses of vecuronium and rocuronium on pulmonary function tests and muscular weaknesses in young (25-35 yr of age) and elderly (65-73 yr of age) patients. Ten young and 10 elderly patients were each placed in vecuronium and rocuronium groups. Oxygen saturation and train-of-four (TOF) ratio were determined, and pulmonary function tests were performed. Then 20% of the 95% effective dose (ED95) of the muscle relaxants was given intravenously. All tests were performed again 4 min after vecuronium and 3 min after rocuronium. Other signs of muscular weaknesses were also recorded. Elderly patients showed more signs of muscle weakness in both groups. The TOF ratio was 0.77 and 0.79 in the elderly rocuronium and vecuronium groups, respectively, and 0.89 and 0.90 in the young rocuronium and vecuronium groups, respectively. Dynamic spirometry revealed decreases in forced expiratory volume in 1 s and forced vital capacity in both groups, and no significant changes in peak expiratory flow rate. The expiratory reserve volume was reduced more in the elderly groups. Oxygen saturation decreased in both groups. We conclude that oxygen saturation, pulmonary function, and muscle strength decrease more in the elderly than in their younger counterparts from priming doses of vecuronium or rocuronium. IMPLICATIONS: The priming principle consists of giving a subparalyzing dose of muscle relaxant 3-6 min before giving a second dose for tracheal intubation. We found that priming doses of vecuronium and rocuronium produced greater decreases in oxygen saturation and pulmonary function in the elderly (aged 65-73 yr) than their younger (aged 25-35 yr) counterparts. Priming may not be a safe approach in elderly patients.

Adult↗
PubMed1999

Short stature in Duchenne muscular dystrophy: a study of 34 patients.

In Duchenne muscular dystrophy (DMD), short stature is a feature of unknown cause. This cross-sectional study of 34 male patients (mean age 8.0 y, age range 1.2-13.7 y) was conducted to examine the relationship between auxological parameters, markers of growth and the extent of muscular weakness. Weight and length at birth (SDS +/- SD; 0.0 +/- 1.2; 0.2 +/- 1.5) and target height SDS (-0.2 +/- 0.7) were normal. Height (HT) SDS (-1.0 +/- 1.1) was lower than the normal population (p < 0.001) and did not correlate with age. Body mass index SDS (-0.1 +/- 1.6) was normal. Tests of insulin-like growth factor-I SDS (-0.6 +/- 1.2) and insulin-like growth factor binding protein-3 SDS (0.1 +/- 1.3) ruled out a severe derangement in the GH-IGF-axis. The carboxy-terminal propeptide of type I procollagen (PICP) SDS (0.6 +/- 1.5) was normal, but bone-specific alkaline phosphatase (BAP) SDS (-1.7 +/- 0.8) was low (p <0.001). HT SDS did not correlate with BAP SDS. The Vignos scale, a grading of muscular function (score: 0 = unaffected; 11 = confined to bed) (median (range): 3 (0-9)) correlated strongly with age (r = 0.77, p < 0.0001), but did not correlate with HT SDS, PICP SDS or BAP SDS. In conclusion, DMD patients are significantly shorter than the normal population, though the HT SDS does not change with age. Growth hormone deficiency does not seem to be the cause of short stature in DMD. Significantly low BAP levels are probably the result of the reduced muscle mass, which leads to a lower biomechanical load on the bone and thus a reduction in bone turnover. The short stature observed in our study is unlikely to be the result of muscular weakness.

Adolescent↗
PubMedDate not supplied

[Glycogenosis type II, infantile variant. Report of a case and review of the literature].

A case of glycogenosis type II infantile onset (Pompe's disease) is presented, and the literature is reviewed in order to establish the basis of the diagnostic suspect. We studied an 8-month old female with muscular weakness--and cardiac failure. The chest X-ray: cardiomegaly; electrocardiogram: PR interval of 0.06 seconds, gigant QRS complexes, biventricular hypertrophy, and the echocardiogram and cineangiography: left ventricle hypertrophy and hypokinesia. The patient died because of refractory heart failure. Histochemical examination demonstrated excessive intracellular accumulation of glycogen. Also, in the muscle, the kidneys and the liver we did not find any alpha 1,4 glucosidase. Then, the diagnosis of glycogenosis type II infantile onset was established. Finally, we conclude that this disease should be suspected in every infant with muscular weakness, cardiac failure, cardiomegaly, electrocardiogram with shortness of PR interval, gigant QRS complexes and biventricular hypertrophy, and that needs to be confirmed by muscle biopsy. At the moment, there has not been reported any case of Pompe's disease in the Mexican literature.

Echocardiography↗
PubMed1981

Modular seating for paralytic scoliosis: design and initial experience.

The conventional wheelchair sling seat provides little or no support to the spine of a child with myopathy or neurogenic muscular weakness. As the spinal muscles become weaker scoliosis may develop with associated deformity, pain and restriction of cardio-respiratory function. If muscle weakness is severe, the resultant fully developed deformity is virtually impossible to treat. Slowing the rate of increase of the deformity is, therefore, the most hopeful avenue of attack. This work addresses the hypothesis that custom moulded seating can increase sitting comfort and slow the rate of progression of spinal curvature in children with paralytic scoliosis, and further, that a range of standard or modular seats can achieve these goals at less cost. Previous work on this problem has ranged from simply padding the armrest, in order to distribute force over the rib cage, through to custom moulded seating. Our initial experience with custom moulding, using the bean bag evacuation and consolidation technique, produced several comfortable seats although the technique was labour intensive and therefore costly. This led us to attempt to develop a method of providing comfortable seating that would help control spinal deformity at reasonable cost. This paper describes the design of a standardized seating system for school age children with myopathy or neurogenic muscular weakness. Preliminary results indicate that this technique may have advantages over alternative methods of treatment. The radiological study is continuing.

Child↗
PubMed1980

[2 cases of congenital adrenocortical unresponsiveness to ACTH (author's transl)].

Congenital adrenocortical unresponsiveness to ACTH is characterized by hyperpigmentation, muscular weakness, and episodes of hypoglycemia, with lethargy or coma and convulsion, and without signs or symptoms of salt wasting. Endocrinological evaluation reveals low levels of serum and urinary glucocorticoids, elevated levels of plasma ACTH and unresponsiveness to exogenous ACTH. On the other hand, aldosterone secretion or excretion is normal and is elevated during a low sodium diet. We reported on two patients with this syndrome. Case A, a 4 year-old-girl, showed skin hyperpigmentation, hypoglycemia, convulsion and coma. She was tall wlth a marked advance of bone age. Case B, a 4 year-old-boy, showed skin hyperpigmentation, fatigability and muscular weakness. Both of them revealed low urinary excretion of THE, THF, cortolone, and beta-cortolone and low levels of plasma cortisol. The levels of urinary glucocorticoids and plasma cortisol did not respond to ACTH administration. During a low sodium diet, urinary aldosterone excretion was elevated, urinary sodium excretion ws decreased, and the patients were able to conserve sodium normally. We also summerized other reported cases and discussed the etiology of this syndrome.

Adrenocorticotropic Hormone↗
PubMed1984

Antigenic modulation of junctional acetylcholine receptor is not sufficient to account for the development of myasthenia gravis in receptor immunized mice.

Myasthenia gravis (MG) is a disease thought to result from an autoimmune response against the nicotinic acetylcholine receptor of the neuromuscular junction. Although there is little doubt that the muscular weakness characteristic of MG can be attributed to an antibody-mediated reduction in the density of AChR, the mechanism responsible for this reduction remains uncertain. In the present studies we have used a mouse model of MG, termed experimental myasthenia gravis (EMG), to test the possibility that antigenic modulation of AChR may be the principle mechanism whereby this reduction in AChR density is achieved. We found that immunization of mice with AChR, on average, leads to a twofold increase in the rate of junctional AChR degradation. Because this effect occurred to the same extent in mice that developed severe paralysis and in those that gave no indication of muscular weakness, the role of antigenic modulation as a major pathologic mechanism in MG is questioned.

Animals↗
PubMed1975

[Familial case of myotonia with muscular hypertrophy, weakness corrected by effort and atrophy of type II fibers].

A 35 years old man has a non progressive muscle disease which appeared when he was 6. Clinically, there is a slight muscle hypertrophy, an important spontaneous myotonia and a curious muscle weakness, quite marked on the first efforts, but disappearing entirely after a few muscle contractions. The E.M.G. is normal but for the myotonic reaction. Muscle biopsy shows a selective atrophy of type II fibers. The disease is a genetic one, a sister and a brother of our patient having noticed the same symptom. The place of this disease among the congenital myotonias is discussed.

Adult↗
PubMed1995

Use of cement for attachment in Neocalceostomoides brisbanensis, a calceostomatine monogenean from the gill chamber of the blue catfish, Arius graeffei.

The thin, weakly muscular, disc-shaped haptor of the calceostomatine monogenean Neocalceostomoides brisbanensis is attached to surfaces in the gill chamber of its catfish host by cement. It is unlikely that any suction is generated (there are no muscular loculi) and the hooks are reduced in size. Two distinctive secretions are associated with the haptor: a finely granular secretion from glandular tissue within the haptor and anterior to it, which enters the dorsal haptor tegument near the periphery of the disc and spreads throughout the ventral haptor tegument; a coarser secretion produced in the peduncle and posterior region of the body, which finds its way to gland openings near the hamuli via centrally situated large and small haptor reservoirs. It seems most likely that the tegumentary secretion is the cement, but other possibilities are discussed. It is suggested that the increasing importance of cement for haptor attachment in calceostomatines has led to the development of a weakly muscular, foliaceous haptor and a progressive reduction of the hooks.

Animals↗
PubMed2001

"Adult" form of muscular carnitine palmitoyltransferase II deficiency: manifestation in a 2-year-old child.

UNLABELLED: We describe a 6-year-old girl admitted with acute muscular weakness and pain which made her unable to walk. Her parents reported a 4-year history of similar episodes which occurred once or twice a year and always resolved spontaneously. Laboratory investigations showed elevated serum creatine kinase which peaked at day 2 of the attack with 18,600 U/l. Carnitine palmitoyltransferase-II deficiency was suspected based on the determination of serum acylcarnitines by tandem mass spectrometry which showed a characteristic elevation of long-chain C16 and C18:1 acylcarnitines. The diagnosis was confirmed by impaired in-vitro palmitate oxidation in blood and the detection of a homozygous substitution S113L in the carnitine palmitoyltransferase-II gene. CONCLUSION: Carnitine palmitoyltransferase-II deficiency should be included in the differential diagnosis of isolated muscular weakness even when manifesting in early childhood.

Age of Onset↗