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PubMed1976

Intracellular distribution of phosphate in the underfed rat developing weakness and coma following total parenteral nutrition.

Underfed rats infused intravenously with a glucose-amino acid solution at the rate of 390 kcal/kg/day developed a syndrome of muscular weakness, neuropathy, lethargy and precoma or coma associated with severe hypophosphatemia. The movement of phosphate into the cells was studied to determine where it went and into which organic compounds it was incorporated. All but 8% of the labeled phosphate was found in liver, muscle, bone, and carcass residue. Liver cells took up as much phosphate as bone and twice as much as muscle, on weight basis. About 90% of the labeled phosphate entering liver was found in the acid-soluble fraction. The specific activity of liver phosphate increased in the infused underfed rats compared to uninfused underfed rats. Infusion of the underfed rat until signs of the syndrome appeared was associated with a 2.7- to 5-fold increase over the correspondingly infused normal rat in the labeling of glucose-6-phosphate, glucose-1-phosphate, and 6-phosphogluconate. No increase over the infused normal rat was observed in most of the other sugar phosphate compounds nor in the non-sugar phosphate compounds such as phospholipids, nucleic acids or proteins. he changes in sugar phosphates observed in the underfed rats probably reflect the enzymatic atrophy associated with underfeeding and the consequent inability to respond to the huge glucose load.

Animals↗
PubMedDate not supplied

Botulism in foals less than 6 months of age: 30 cases (1989-2002).

Botulism has been recognized as a clinical entity in foals since the 1960s. Also known as "Shaker foal" disease, the toxicoinfectious form of botulism affects foals, with the highest incidence in the United States seen in Kentucky and the mid-Atlantic region. The disease is characterized by progressive muscular weakness caused by the action of botulism neurotoxin at cholinergic neuromuscular junctions. Increased number of episodes and duration of recumbency, muscular trembling, and dysphagia are seen in affected foals. Left untreated, the disease can be rapidly fatal, with death occuring secondary to respiratory muscle paralysis within 24 to 72 hours of the onset of clinical signs. Very mildly affected foals can survive with minimal treatment Despite advances made in treatment of these foals, including administration of botulism antitoxin early in the course of the disease, there is still an impression that the disease carries a high mortality rate. The purpose of this study was to evaluate outcome in 30 foals <6 months of age diagnosed with botulism between 1989 and 2002 at the George D. Widener Large Animal Hospital, New Bolton Center. Two foals were euthanized for economic reasons early in the disease course, and I died while being treated. Survival of treated cases was greater than 96%. Approximately 50% of the cases required oxygen therapy, whereas 30% required mechanical ventilation. All foals, excepting 1 mildly affected foal, received botulism antitoxin. Mean duration of hospitalization was 14 days. With appropriate treatment, foals with botulism have a high survival rate.

Animals↗
PubMed1975

Experimentally induced vitamin E-selenium deficiency in the growing dog.

Eight 5-to 8-week-old Beagle pups were allotted to 4 groups of 2 dogs each. For 55 to 70 days, they were fed either a semisynthetic basal diet (BD) deficient in vitamin E and selenium (Se) (group 1) or the BD supplemented with either 30 IU alpha-tocopherol/kg (group 2), 0.5 ppm Se as selenite (group 3), or 1.0 ppm Se as selenite (group 4). In the dogs fed the BD, clinical signs of vitamin E-Se deficiency developed after 40 to 60 days. These signs were accompanied by increased plasma activity of creatine phosphokinase (CPK) and glutamic oxalacetic transaminase (GOT). The dogs were euthanatized after 10 to 15 days of progressive clinical signs, including muscular weakness, subcutaneous edema, anorexia, depression, dyspnea, and eventual coma. Gross lesions seen at necropsy included ventral subcutaneous edema, generalized skeletal muscular pallor and edema with scattered white longitudinal streaking, prominent brownish yellow discoloration of the intestinal musculature, and a layer of white chalky material at the renal corticomedullary junction. Microscopically, there was evidence of extensive skeletal muscular degeneration and regeneration, focal subendocardial necrosis in the ventricular myocardium, intestinal lipofuscinosis, and renal mineralization. Mean hepatic Se content in the dogs fed the BD was 0.10 ppm (wet weight basis) at necropsy. In the dogs fed the 3 supplemented diets, clinical signs of deficiency did not develop. At necropsy, mild skeletal myopathy was evident histologically in the dogs fed BD and 0.5 ppm Se (group 3) but not in the dogs fed the other supplemented diets. Intestinal lipofuscinosis was found in the dogs fed the 3 supplemented diets but was less severe in the dogs fed the diet supplemented with vitamin E than in those fed diets supplemented with Se.

Adipose Tissue↗
PubMed1990

50 years ago from the Journal of the Connecticut State Medical Society. 1940. Further studies in the therapy of acute anterior poliomyelitis.

1. Twenty seven consecutive cases of preparalytic infantile paralysis (36.4% of the total admissions) treated with non-specific protein (intramuscular sterile milk), intravenous 50% sucrose and dehydration (restricted intake) are herein reported. There was no paralysis nor mortality in this group. One case developed weakness, which subsequently disappeared entirely before hospital discharge. During a simultaneous period, 47 cases (63.6%) were admitted with either weakness or paralysis. 2. The early administration of this therapy is advocated. 3. The therapy was used in cases presenting muscular weakness and paralysis upon hospital admission with apparent arrest of the process sooner than is usually expected. A rapid recovery was striking in many instances. This was particularly true in the group admitted with weakness only. 73% of these recovered completely and the remaining 27% were improved. In the paralytic group ganglion cell destruction had often completed before hospital admission. In these cases the results would be disappointing with any therapy. 4. Of the 47 cases admitted in the stage of weakness or paralysis, including the bulbar cases, twelve (25.5%) recovered completely, 17 (36.1%) definitely improved, 16 (34%) were unimproved and 2 (4.2%) died. In the entire group (74 cases) there was a mortality of 2.7%, complete recovery in 52.7%, improvement 22.9% and no improvement in 21.6%. 5. Aside from poliomyelitis, we have used the therapy in primary and secondary encephalitis with gratifying results in most cases, which, however, were few in number. 6. Further study on a larger scale would be advantageous in evaluating this therapy, both in poliomyelitis and encephalitis.

Animals↗
PubMed1990

Limb girdle syndromes. Clinical, morphological and electrophysiological studies.

The clinical syndrome of slowly progressive proximal limb and limb girdle muscular weakness and atrophy, or limb girdle syndromes (LGS), has a diverse aetiology. Several of the congenital, mitochondrial and other metabolic myopathies and spinal muscular atrophies are recently recognized causes of LGS. Thus the position of limb girdle muscular dystrophy (LGMD) as a discrete entity in the nosology of muscle disease deserves reappraisal. We have therefore reevaluated our experience of 33 patients in this light. Detailed clinical, electrophysiological, and pathological studies including autopsies in 2 cases, were performed. As a result we are confident that LGMD does exist as a sporadic or autosomal dominant (2 families) or recessive condition (2 families). There are therefore probably at least 2 distinct genotypes. Typical LGMD (18 patients in our series) is characterized by slowly progressive symmetrical proximal upper and lower limb girdle weakness and atrophy, elevation of the serum creatine kinase at some stage, dystrophic or less severe myopathic muscle lesions on biopsy, and myopathic EMG findings. Two minor subgroups of LGMD were identified in our series with similar clinical and laboratory features but distinguishable by the development of either facial (4 patients) or by distal limb muscle involvement (3 patients). A further group of patients with sporadic LGS (5 patients) had slowly progressive proximal symmetrical upper and lower limb-girdle weakness and atrophy with myopathic or neurogenic features on either EMG or muscle biopsy so that the precise characterization was difficult. Two of these patients had distal limb muscle involvement and contractures. One patient had upper limb-girdle muscle atrophy with normal lower limbs. A disorder affecting muscle, nerve or both remains a possibility in these cases.

Adolescent↗
PubMedDate not supplied

[Myopathy of congenital fiber type disproportion. Description of a clinical case].

Starting from a case they observed and from similar cases of literature, the authors underline the variability of clinical aspects of MDCF which in this case was associated with absence of both motorial acquisitions and skeletal alterations. They underline how their case is characterized by the presence and consistence of musculotendinous retractions and by muscular weakness.

Adolescent↗
PubMed1977

Adult-onset acid maltase deficiency. Case report of an adult with severe respiratory difficulty.

Pompe's disease (acid maltase deficiency) classically affects infants and children, with a few sporadic cases occurring in adults. An adult patient initially have progressive muscular weakness, exertional dyspnea, diaphragmatic paralysis, and objective evidence of restrictive respiratory disease. Muscle biopsy established the diagnosis of acid maltase deficiency. The patient's brother had died at the age of 44 years, after 23 years of a "progressive muscular dystrophy." Acid maltase deficiency should be considered in the differential diagnosis of progressive respiratory insufficiency associated with weakness.

Adult↗
PubMed1983

Two Dutch siblings with congenital muscular dystrophy (Fukuyama type).

Two Dutch siblings are described suffering from muscular weakness, hypotonia, severe joint contractures, mental retardation and epileptic fits. E.M.G. showed a characteristic myopathic pattern. Muscle biopsy revealed changes consistent with congenital muscular dystrophy. On CT marked hypodensities of the cerebral white matter were noticed. These findings are consistent with congenital muscular dystrophy of the Fukuyama type, a peculiar form of congenital muscular dystrophy, extremely rare outside Japan.

Adult↗
PubMed1971

Reappraisal of alcoholic myopathy. Clinical and biopsy study on chronic alcoholics without muscle weakness or wasting.

To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles, we studied 11 chronic alcoholics who had no muscular weakness or wasting. Six patients demonstrated distal hyporeflexic (ankle jerks) sensory neuropathy on clinical examination. Four patients, one of whom was asymptomatic, had slow peroneal motor nerve conduction velocities. Patterns of neuropathy were present in the electromyograms of the proximal muscles of two patients. Muscle biopsy studies with enzyme histochemistry indicated denervation atrophy and myopathic changes in the contralateral quadriceps muscles of eight patients. As denervation atrophy was present, we concluded that these myopathic changes represented the effects of denervation of these muscles. We conclude, therefore, that the proximal subclinical alcoholic myopathy, previously described as primary by ourselves and others, is the result of denervation due to the well-known alcoholic neuropathy.

Adult↗
PubMed2002

Masticatory performance in patients with myasthenia gravis.

Masticatory muscle electromyograms (EMGs) were recorded while patients with bulbar myasthenia gravis chewed artificial food and compared with those of patients with ocular myasthenia gravis, patients in clinical remission who had previously suffered from bulbar myasthenia gravis and healthy individuals. Masticatory performance and EMGs were significantly smaller in the bulbar group. There were no indications of subclinical masticatory muscle weakness in patients with bulbar myasthenia gravis in remission and in patients with ocular myasthenia gravis. Patients with bulbar myasthenia gravis barely compensated for muscular weakness by chewing at a higher percentage of their maximal EMG. These quantitative findings, when combined with subjective reports of masticatory muscle weakness, show that a need to support the jaw is characteristic of patients with bulbar myasthenia gravis who produce low EMG activity.

Adult↗
PubMed1998

Effects of L-carnitine supplementation on muscular symptoms in hemodialyzed patients.

Various muscle symptoms are well recognized among patients on maintenance hemodialysis. Carnitine deficiency may be an important factor of dialysis-associated muscle symptoms, whereas high-dose L-carnitine supplementation may result in unphysiologically high plasma levels of carnitine and carnitine esters. We studied the effect of low-dose L-carnitine treatment (500 mg/d) on muscle symptoms, plasma carnitine fractions, and lipid profiles in 30 periodically dialyzed patients with muscular weakness, fatigue, or cramps/aches. After 12 weeks of L-carnitine treatment, about two-thirds of patients had at least some improvement in muscular symptoms, whereas carnitine fractions were normal or slightly above normal ranges, but lipid profiles showed no demonstrable changes. This study also showed the correlation between plasma-free carnitine deficiency and months on dialysis. These results suggest that prolonged low-dose L-carnitine treatment can improve dialysis-associated muscle symptoms by restoring carnitine tissue levels and washing out acyl moieties.

Administration, Oral↗
PubMed1994

The first case of polymyositis associated with interferon therapy.

A 54-year-old man with renal cell carcinoma was treated with interferon (IFN)-gamma for 3 weeks soon after nephrectomy. Three months later he received IFN-alpha therapy for 8 weeks due to chronic active hepatitis C. He subsequently contracted polymyositis (PM): proximal muscle weakness, an elevation of muscle enzymes, myogenic patterns on the electromyograph and histologically specific findings in biopsied muscle specimens. After discontinuation of IFN his muscular weakness gradually recovered.

Carcinoma, Renal Cell↗
PubMed2005

[Juvenile dermatomyositis in 12 years old girl].

We would like to present a selected case of 12-aged girl, with recognition of dermatomyositis (DM). At the age of 11 in the normally developing child, erythematous-oedematous changes have appeared on the face, particularly intensified in the vicinity of the orbital cavities (so called: pseudoglasses), as well as erythema and teleangiectasis on the dorsum of hands and small-sized diarthroidal joints (the Gottron's symptom). Subsequently, lower physical efficiency and distinctly weakness in the child's extremities occurred. In EMG (quadriceps muscle of the thigh) myogenous traits have been proven. Neurological examination revealed as follows: muscular weakness (adynamia), mainly lower limbs (grade 3 in the Lovett's scale, along with decreased loss of muscles tone), lack of the periosteal reflex near lower limbs, positive Gower's symptom and increased anterior spinal curvature. In the biochemical examinations accelerated erythrocyte sedimentation rate (ESR), and a rise of activity in muscles enzymes were stated. In the child's blood serum, we disclosed antinuclear antibodies ANA (type of granular luminescence, titre 160), to be rather evident to presence of autoimmunological process. During examinations of the musculocutaneus specimen, DM-markers have been detected. Capillaroscopy proved specific presence of numerous vessels, multiple capillary tubes, individual gemmated vessels and completely invisible dermatomyositous border. Patient was treated with per os sterid--Encorton at the initial dose of 2 mg/day, every other day during the lapse of 6 weeks to reach the normal CPK-activity, and consequently clinical picture under "on-line" surveillance, gradually reducing a specific medicine up to maintenance dose through 18 months. At present, the patient is subjected to check-up and monitoring by Neurological Outpatient and Rehabilitain Clinic for Children.

Antibodies, Antinuclear↗
PubMed2001

Lung function in children with Duchenne's muscular dystrophy.

Duchenne's muscular dystrophy (DMD), characterized by gradually developing muscular weakness, leads to respiratory symptoms and reduced lung function. We aimed to assess lung function in 25 patients with DMD in relationship to age and muscular function. The 25 boys, mean age 13 years, comprized patients in southern Norway with DMD, taking part in an epidemiological follow-up study. None had chronic respiratory disease. Lung function was measured by maximum expiratory flow-volume loops and whole body plethysmography, and repeated after 1 year (n= 14). Lung function was reduced compared to predicted values for healthy children. Forced expiratory volume in 1 sec (FEV1)% predicted and forced vital capacity (FVC)% predicted correlated (significantly) inversely to age. FEV1 and FVC decreased annually 5.61 and 4.2% of predicted, respectively. Absolute values of FVC (litres) and FEV1 (1 sec(-1)) increased until mean age 14 years, decreasing thereafter. Values in % predicted decreased steadily throughout the age range (6-19 years). Lung function correlated closely to upper limb muscle function.

Adolescent↗
PubMed2005

[A case of asymmetric demyelinating neuropathy in a patient with chronic graft-versus-host disease].

A 47-year-old man, who suffered from acute lymphocytic leukemia at 45 years old and was treated with hematopoietic stem cell transplantation at 46 years old after the induction of complete remission by the standard chemotherapy, developed the symptoms of chronic graft-versus-host disease (cGVHD) such as dry eyes, dry mouth, skin thickening, skin scaling, skin pigmentation and impaired liver function. He was admitted to our hospital because of the acute development of diplopia and weakness of his left upper extremity accompanying with the exacerbation of other symptoms of cGVHD. Neurological examinations revealed the right abducens nerve palsy and asymmetric muscular weakness of the extremities; the proximal part of the left upper extremity and the distal part of the right upper extremity were markedly involved. Neurophysiological studies including magnetic motor root stimulation revealed demyelinating neuropathy specifically involving the motor nerves. On the basis of these findings, a diagnosis of peripheral neuropathy associated with cGVHD was made. Nighteen reports are available on peripheral neuropathy in cGVHD patients, but to date little is known about the pathophysiology of this condition. Most of those patients have been diagnosed as having symmetric demyelinating polyneuropathy, such as Guillain-Barré syndrome or chronic inflammatory demyelinating polyneuropathy. In this study, contrary to previous reports, the asymmetric involvement of motor nerves is noteworthy. Accumulation and further analyses of the cases like the present case are necessary to elucidate the pathogenesis of peripheral neuropathy in cGVHD.

Chronic Disease↗
PubMed1995

[Muscular involvement in the course of AIDS. Anatomo-clinical study of 17 cases].

We report 17 patients seropositive for the human immunodeficiency virus, with muscle tissue involvement in different stages of the disease. Some patients are treated with azidothymidine (AZT). Others have no opportunistic infections. In all cases, there are some muscular symptoms such as progressive symetric and proximal muscular weakness with myalgias, elevated serum muscle enzymes, abnormal electromyogramma and very often a peripheral neuropathy. The muscle biopsy reveals the following features: rarely a focal muscular opportunistic infection in advanced stage of the disease is observed; a polymyositis is quite often the first clinical manifestation of the disease; a myopathy with mitochondrial involvement is observed in some of the AZT treated patients; some cachectic, under nourrished, bedridden patients present a type II muscle fiber atrophy. We conclude that a muscle biopsy could help us in our therapeutic planning directing us to a corticotherapy in the polymyositis, mitochondriopathies and wasting syndrome. Interruption alone of AZT or associated with a treatment by carnitine could allow remission of the muscular pathology.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Proposed model of botulinum toxin-induced muscle weakness in the rabbit.

Osteoarthritic patients show only a weak association between radiographic signs of joint disease and joint pain and disability. Conversely, muscle weakness is one of the earliest and most common symptoms of patients with osteoarthritis (OA). However, while many experimental models of osteoarthritis include a component of muscular weakness, no model has isolated this factor satisfactorily. Therefore, the purpose of this study was to develop and validate an experimental animal model of muscle weakness for future use in the study of OA. Botulinum Type-A toxin (BTX-A) was uni-laterally injected into the quadriceps musculature of New Zealand white rabbits (3.5 units/kg). Isometric knee extensor torque at a range of knee angles and stimulation frequencies, and quadriceps muscle mass, were quantified for control animals, and at one- and six-months post-repeated injections, in both, the experimental and the contralateral hindlimb. Ground reaction forces were measured in all animals while hopping across two force platforms. Isometric knee extension torque and quadriceps muscle mass was systematically decreased in the experimental hindlimb. Vertical ground reaction forces in the push off phase of hopping were also decreased in the experimental compared to control hindlimbs. We conclude that BTX-A injection into the rabbit musculature creates functional and absolute muscle weakness in a reproducible manner. Therefore, this model may be used to systematically study the possible effects of muscle weakness on joint degeneration, either as an isolated intervention, or in combination with other interventions (anterior cruciate ligament transection, meniscectomy) known to create knee joint degeneration.

Animals↗
PubMed1980

A progressive, familial myopathy of the pietrain pig: the clinical syndrome.

A familial progressive muscular weakness is described in a herd of pietrain pigs. The onset of disease was at two to three weeks of age taking the form of a muscular tremor when the piglets were standing. An impaired gait followed and by 12 weeks of age the pigs had become permanently recumbent. The observed incidence of the syndrome and the breeding data available were consistent with an autosomal recessive inheritance of the condition.

Animals↗