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Results for “Muscular weakness”

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At least 163 records · Page 9Linked to original sources
PubMed1997

[An adult case of dermatomyositis complicated with cecum perforation and panniculitis].

The case of dermatomyositis complicated with cecum perforation and panniculitis occurred in a 62-year-old woman was reported. She was admitted to Keio University Hospital with a history of proximal muscular weakness, and dysphagia. Physical examination showed erythema over the face and shoulder. Serum level of muscle enzymes was remarkably increased. The diagnosis of dermatomyositis was made based on proximal muscular weakness, elevated serum level of muscle enzymes and myogenic change of electromyocardiogram. The treatment with 60 mg/day of prednisolone was started, and was a good response. However, 7 months later the disease became active again when the amount of prednisolone was reduced to 13 mg/day. Subsequently she complained of abdominal pain on the right lower quadrant. The surgical findings included peritonitis due to the perforation of the cecum and multiple ulcers of the cecum. After operation, azathioprine was added. Four years and 9 months later, she noticed skin erythema with ulceration and subcutaneous nodule. Skin biopsy indicated the findings of the panniculitis with membrano-cystic lesion. It was thought that both cecum perforation and panniculitis were caused by angiopathy which was often seen in childhood dermatomyositis.

Cecal Diseases↗
PubMed2002

Sarcoidosis in two patients with chronic hepatitis C treated with interferon, ribavirin and amantadine.

We report two patients with chronic hepatitis C, both nonresponders to a previous course of interferon (IFN), who developed or suffered an exacerbation of sarcoidosis while under treatment with IFN-alpha2a, ribavirin and amantadine. Patient 1: symptoms appeared after week 4 and treatment was withdrawn at month 9 due to severe weight loss, marked dyspnea, muscular weakness, dryness of mouth and facial paralysis. Stage III pulmonary sarcoidosis and polyneuropathy were confirmed. The patient had become steroid dependent and nine months after cessation of the treatment dyspnea and muscular weakness still persisted. She achieved a complete sustained response of hepatitis C. Patient 2: presented with a previous diagnosis of granulomatous hepatitis with chronic active hepatitis C and chronic dermatitis. The treatment exacerbated a cutaneous sarcoidosis. Furthermore, hiliar adenopathies consistent with stage I sarcoidosis became evident. Sarcoidosis responded to corticosteroids, but elevated transaminases and hepatitis C viraemia resisted. Hence, the combination of amantadine with ribavirin and IFN can develop or exacerbate subclinical sarcoidosis. A synergistic effect of these three drugs is suggested.

Adult↗
PubMed1985

Diaphragmatic paralysis due to spinal muscular atrophy. An unrecognised cause of respiratory failure in infancy?

An unusual form of spinal muscular atrophy presenting with respiratory failure was observed in four infants from two families. In one, whose death was attributed to pneumonia, the diagnosis was inferred retrospectively after two siblings died from an identical illness and were shown to have diaphragmatic paralysis and the typical electrophysiological and histological features of spinal muscular atrophy. Other signs of skeletal muscular weakness were absent or inconspicuous. The fourth, unrelated infant presented in an identical way but has survived for over a year on a ventilator. Two months after the onset of respiratory paralysis, more extensive skeletal muscular weakness was seen. Other infants, dying of unexplained respiratory illness, may have this disorder and some may be included in the miscellany of disorders that constitute the sudden infant death syndrome.

Female↗
PubMed1993

[Radicular paralysis with reference to lumbar root compression syndromes. Incidence, extent and follow-up in a neurosurgical patient sample].

This is a retrospective study of 170 patients which were operated on for lumbar intervertebral disc herniation. The mean follow-up was 8 weeks. All patients showed muscular weakness before operation. Incidence, severity, and natural history of motor deficit following lumbar discectomy are reported. Moreover it was of special interest to analyze the effect of sex, age, severity and duration of muscular weakness, and timing of surgery on changes in radicular function.

Adult↗
PubMed2006

[Four siblings with becker muscular dystrophy (BMD) manifesting severe mental retardation].

A 33-year-old man with BMD manifesting severe mental retardation is reported. This patient has mild pseudohypertrophy in his calf muscles and showed an elevation of creatine kinase (CK) level in the serum (2215 IU/L). He was diagnosed as autistic at the age of three. His intellectual level was estimated to be two years old in social intelligence and four months old in speech ability at the age of 33. However his muscle strength remains within the normal range. All of his three siblings have similar symptoms, such as severe mental retardation and elevated CK level in the serum (1735-3641 IU/L) and lack apparent muscular weakness. Gene analyses by multiplex PCR and Southern blotting showed all of the siblings had the deletion of exon 4 in the dystrophin gene. Pathological findings of a muscle biopsy specimen showed a mild irregular dystrophin stain of the muscle surface membrane. This is a rare familial case of Becker muscular dystrophy manifesting severe mental retardation with scarce muscular weakness.

Adult↗
PubMed1985

Potentially fatal cardiac dysrhythmia and hyperkalemic periodic paralysis.

An 11-year-old boy was evaluated for mild periodic muscular weakness exacerbated on separate occasions by disopyramide phosphate and procainamide. He and his mother both had bidirectional ventricular tachydysrhythmia (BVT), short stature, microcephaly, and clinodactyly. The mother, but not the child, had lingual myotonia. The two antiarrhythmic drugs worsened the muscular weakness without benefiting the cardiac dysrhythmia. Potassium loading produced skeletal muscle weakness and transient conversion of the BVT to normal sinus rhythm. Hypokalemia aggravated the BVT without causing weakness. Acetazolamide had no effect. The patient suffered a nonfatal cardiac arrest after several days of increased carbohydrate intake. Imipramine controlled the dysrhythmia without inducing weakness. Periodic paralysis should be considered as the diagnosis in children with BVT, a potentially fatal condition.

Arrhythmias, Cardiac↗
PubMed1991

[Advanced stage of giant axonal neuropathy].

A woman has appeared normal during her neonatal and childhood period except for a short stature. Her parents were healthy and non-consanguineous. At the age of 8, she noticed difficulty in climbing stairs and had tendency to fall. In her 13th year, she developed marked scoliosis and genu valgum. Physical examination at 14 years of age revealed a gentle and shy child of short stature with brown-black kinky hair. Neurological examinations revealed progressive mental retardation, optic nerve atrophy, moderate and coarse nystagmus on lateral and vertical gaze, atrophic tongue with fasciculations, slow and scanning speech, distal muscular weaknesses with diffuse atrophies in the four extremities and sensory deficiencies in all modalities with a glove-stocking type distribution. At the age of 15, she was unable to walk without a wheelchair. During the course she showed slowly progressive muscular weakness, ataxia and decreasing sensation especially in the lower extremities. She died of infection of the respiratory and urinary tracts at the age of 25. Pathologically the abnormalities in the biopsied and autopsied sural nerve were characterized by an advanced stage of nerve fiber degeneration without giant axons. The phrenic nerve obtained at autopsy at 1 to 10 cm from axon terminal revealed the presence of several large focal axonal swelling of 15-20 microns in diameter. On the other hand, sections of the phrenic nerve at 15 cm from axon terminal displayed a mild to moderate reduction in the number of myelinated fibers without giant axons. The difference of pathological findings among these specimens seems to depend on the time as well as the site of the examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Cardiologic evaluation in a family with Emery-Dreifuss muscular dystrophy].

Emery-Dreifuss muscular dystrophy is an X-linked recessive condition characterized by mild muscular weakness predominantly in a humero-peroneal distribution with variable facial involvement. Onset is in childhood with slow progression of weakness. The disease is often associated with cardiac involvement, mainly with bradyarrhythmias which might be responsible for sudden death. The most striking finding derived from the literature is the high incidence of sudden death; in the 7 large families described, out of the 79 reported patients 32 died suddenly at a young age (between 25 and 56 years). We performed a cardiologic evaluation of 11 subjects of a large italian family with affected males in four generations: 5 affected males (3 adults and 2 boys), 3 carriers and 3 healthy relatives (2 females and 1 male). Supraventricular arrhythmias were documented either in the dystrophic males or in the carriers. There was no correlation between the severity of cardiac rhythm abnormality and the severity of muscular weakness in the affected males, 3 of whom required pacemaker insertion. All the carriers were free of muscular involvement, but showed arrhythmias of variable degree, in one case requiring pacemaker insertion. In conclusion our data indicate an extremely high incidence of bradyarrhythmias, sometimes serious, in patients with Emery-Dreifuss muscular dystrophy. Holter monitoring is therefore mandatory and electrophysiological study is sometime necessary. Because of the high risk of sudden death in adult patients, we recommend permanent pacemaker implantation even in asymptomatic subjects, as soon as bradyarrhythmias are detected.

Adolescent↗
PubMed1991

[Acetylcholine receptor antibody titer, sensitivity to curare electromyogram and disease severity in myasthenia gravis].

All of 39 rabbits immunized with acetylcholine receptors invariably formed anti-AChR Abs and some of them developed muscular weakness or flaccid paralysis. Pharmacological, physiological and ultrastructural studies indicated that the pathology of experimental autoimmune myasthenia gravis in rabbits resembled that of human myasthenia gravis. The titer of anti-AChR Abs correlated poorly with disease severity and did not simply predicted the muscular weakness. The results ruled out the possibility that antigenic modulation of AChR was sufficient to account for the induction of myasthenia gravis. There was a close relationship between the sensitivity to curare and disease severity, but only part of immunized animals appeared electromyogram change. This led us to conclude that serum anti-AChR concentration would not be the single pathological factor in myasthenia gravis and disease severity may correlate with amount of normal AChR.

Animals↗
PubMed1991

Pathogenetic mechanisms of fetal akinesia deformation sequence and oligohydramnios sequence.

This article briefly reviews the participation of fetal compression, muscular weakness, and fetal akinesia in the genesis of the anomalies found in fetal akinesia deformation sequence (FADS) and oligohydramnios sequence (OS). Both sequences share phenotypic manifestations, such as arthrogryposis, short umbilical cord, and lung hypoplasia, in relation to decreased intrauterine fetal motility. Other characteristic manifestations found in OS, such as Potter face, and redundant skin, are produced by fetal compression. On the other hand, growth retardation, craniofacial anomalies, micrognathia, long bone hypoplasia, and polyhydramnios found in FADS could be related to intrauterine muscular weakness.

Abnormalities, Multiple↗
PubMed1993

[A case of X-linked recessive bulbospinal muscular atrophy with demyelinating neuropathy and hypertrophy of the calves].

We report a 53-year-old man of X-BSMA with neuropathy. The patient developed slowly progressive muscular weakness and wasting over a 2-year period with an accompanying numbness in the finger tip. He can run normally but not so fast. When he was aged 52-year old, difficulty in running progressed. General physical examination revealed nothing particular except for hypertension and gynecomastia. He showed muscular weakness and atrophy in the tongue, shoulder girdle, and upper and lower limbs. Calf muscle hypertrophies were prominent on both sides. The tendon reflexes were absent. Slight sensory impairment for vibration and pin-prick was present distally in all limbs. Autonomic nerve dysfunction was not observed. Hyperglycemia, elevated HbA1c and elevated serum CK (1,242 IU/l) were seen. The computed tomographic analyses on skeletal muscle showed hypertrophic changes in the calf muscles with a few fatty infiltrations. Electromyography showed a systemic neurogenic pattern. Motor nerve conduction velocities were slightly delayed in the lower limits. Sensory nerve action potentials were not elicited in all nerves tested. Sural nerve biopsy disclosed marked reduction of myelinated fibres for that of large diameter with thin myelin. Teased fibre studies showed a definite increase in the incidence of fibres with segmental demyelination and remyelination. In electron microscopic examination, typical or atypical onion bulb formation was observed on individual fibres. Axonal changes were minimum. We believe that segmental demyelination observed in this patient is not secondary to axonal damage. We, also, investigated AR gene abnormality by polymerase chain reaction (PCR) in this patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Demyelinating Diseases↗
PubMed2005

Acute barium nitrate intoxication treated by hemodialysis.

A 22-year-old male was admitted to hospital with diarrhea and vomiting, cardiac arrhythmias, severe hypokalemia and gradual onset of muscular weakness. A potassium infusion was started, but for several hours serum potassium remained low. Evidence of toxic ingestion was initially lacking. When it became clear -- after a considerable delay -- that the patient had ingested barium nitrate, hemodialysis was started. This resulted in rapid clinical improvement with correction of hypokalemia and restored muscular function. Intoxication with barium causes hypokalemia, arrhythmias, muscular weakness and paralysis, often requiring respiratory support. This patient presented with symptoms typical of severe barium intoxication, non-responsive to potassium supplementation. There are few published reports on the use of hemodialysis in barium poisoning. This case confirms the possible benefit of hemodialysis in severe cases, where potassium supplementation alone is insufficient.

Adult↗
PubMed2002

[A case of allopurinol-induced muscular damage in a chronic renal failure patient].

A 73-year-old woman with chronic renal failure developed generalized muscular weakness and pain 6 days after the start of allopurinol treatment(200 mg/day). Routine laboratory tests revealed elevated levels of serum creatine kinase, and the patient was clinically diagnosed as rhabdomyolysis, due probably to severe myositis. A high level of serum oxipurinol, the chief active metabolite of allopurinol, was also revealed. The muscular weakness was relieved in seven weeks with intermittent hemodiafiltration.

Aged↗
PubMed1989

[A family of hereditary motor and sensory neuropathy with spastic paraplegia (HMSN type V)].

Three siblings with hereditary motor and sensory neuropathy with spastic paraplegia (HMN V) were described. Their grandfather was suspected to have the similar symptoms. Their parents were normal and not consanguineous. The first case was a 54-year-old woman. She has suffered from difficulty in walking since the age of 10 years. Distal muscular weakness and wasting began at 20 years old. She was admitted to our hospital for investigation in 1988. Results of examination of the brain, cranial nerve, and cerebellar function were normal. The deep reflexes were hyperactive in the arm and knee, while absent at the ankle. Babinski's sign was definitely positive. Muscular weakness and wasting were noted in intrinsic hand muscles and in those below her knees. There were pes cavus and hammer toes, and the gait was spastic. Mild sensory disturbance was noted in distal limbs. The conduction velocity of motor nerve fibers of her limbs was below normal and that of sensory nerve fibers normal. Muscle biopsy of biceps brachii revealed neurogenic changes. Sural nerve biopsy showed decreased number of myelinated fibers of large diameter and formation of small oinion-bulb. The second and third cases were her brothers and proven to have the similar condition, but their onset of illness were earlier and their affections were more severe. A few cases of HMSN V with nerve biopsy findings have so far been reported and the family presented here is the first report in Japan.

Biopsy↗
PubMed1983

Calcium and vitamin-D metabolism in nephrotic syndrome.

A child with long-standing steroid resistant minimal-change nephrotic syndrome developed mild muscular weakness. Laboratory studies demonstrated reduction in both protein-bound and ionized calcium concentrations which were accompanied by high serum PTH and low urinary calcium excretion. These findings were related to the marked sustained reduction in the serum concentrations of 25-hydroxyvitamin-D3 and 1,25-dihydroxyvitamin-D3. Relief of the muscular weakness and normalization of serum ionized calcium and PTH were realized with oral administration of 1,25-dihydroxyvitamin-D3 at 0.25 mcg per day. These beneficial effects persisted for over one year of follow-up.

Calcifediol↗
PubMed2001

Effects of limb elevation and increased intramuscular pressure on human tibialis anterior muscle blood flow.

The effects of limb elevation and increased intramuscular pressure (IMP) on blood flow in the tibialis anterior muscle and leg neuromuscular function were studied in eight healthy subjects. Muscle blood flow (MBF) was measured by photoplethysmography using a custom-designed probe. IMP was elevated bilaterally by vein obstruction (60-65 mmHg) lasting 30 min induced by a thigh tourniquet of casted legs. Skin sensibility of the feet and the amplitude and area of the compound muscle action potentials from the extensor digitorum brevis muscle were evaluated. The subject kept one leg elevated 32 cm above heart level and the contralateral leg at heart level. All recordings were made before, during and after vein obstruction. IMP increased to 40 mmHg in the vein-obstructed casted legs. Perfusion pressure decreased from [mean (SD)] 42 (5.8) mmHg to 17 (6.4) mmHg in the elevated leg and from 65 (9.9) mmHg to 43 (8.4) mmHg in the non-elevated leg. MBF decreased by 50% in the elevated leg and by 42% in the non-elevated leg. Subjects experienced sensory dysfunction and muscular weakness in the elevated leg. In conclusion, increased IMP, induced by venous obstruction of a casted leg, reduced perfusion pressure and MBF, and resulted in a diminished amplitude and area of the compound muscle action potentials. Limb elevation above heart level combined with venous stasis of a casted leg further reduced perfusion pressure and MBF, and induced sensory dysfunction and muscular weakness.

Action Potentials↗
PubMed2004

[The clinical features of myasthenia gravis affecting nonskeleton muscles].

OBJECTIVE: To propose a method for diagnosis and differential diagnosis of myasthenia gravis (MG) with heart and liver injury, anisocoria, dysacusis, impatience etc. METHODS: (1) Before and after administering cholinesterase inhibitor and immune therapy, 55 patients with MG were re-examined for heart and liver and followed up. (2) 1 mg neostigmine was injected to the MG patients with anisocoria and dysacusis, the symptoms were observed and brainstem auditory evoked potential was performed before and after 30 minutes and 2 hours. RESULTS: With the relaxation of muscular weakness and fatigability distinctive of MG, other special symptoms will improve and no further special therapy is needed. CONCLUSIONS: MG is an autoimmune disease mediated by auto-antibodies that attack the acetylcholine receptors not only at the skeletal muscle, but also at many other organs such as heart, liver, hearing apparatus pupillary sphincters and genitals. With the relaxation of muscular weakness, these symptoms will improve. The effect of administering cholinesterase inhibitors is the key point of differential diagnosis.

Adolescent↗
PubMedDate not supplied

[Pediatric Guillain-Barré syndrome. Experience in the Neuropediatrics Unit of a Portuguese hospital].

INTRODUCTION: Guillain-Barré syndrome (GBS) is an acute inflammatory ascending polyradiculoneuropathy. Autoimmune mechanisms play a role in the demyelinating process. Clinically, progressive symmetric loss of motor strength, areflexia, sensitive and autonomic manifestations are observed. Albuminocytological dissociation and electrophysiological signs of demyelination are frequently found. It is the most common cause of acute flaccid paralysis in children. PATIENTS AND METHODS: Retrospective review of all children with GBS admitted to Garcia de Orta Hospital in a 10 year period (1994-2003). RESULTS: 17 children (18 months to 14 years) were admitted during this period. Respiratory or gastrointestinal prodrome was identified in 15 children, with positive serologic studies in six. The main clinical manifestations were disturbances of gait, progressive muscular weakness, sensitive manifestations (pain, paresthesias) and osteotendinous areflexia. 13 children had albuminocytological dissociation and acute demyelinating neuropathy was identified in 12.64% of children were treated with immunoglobulins (2 g/kg). Clinical evolution was favourable in 16 cases, with a death secondary to autonomic dysfunction. CONCLUSIONS: Clinical presentation may be unspecific, particularly in young patients, with pain as a primary complaint, preceding muscular weakness and areflexia. Increased cerebrospinal protein and abnormal electrodiagnostic studies may be absent in the early course of GBS. Immunoglobulin therapy was efficacious and well-tolerated.

Adolescent↗