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PubMedDate not supplied

The otolaryngologic presentation of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis is a progressive dengenerative neuromuscular disease of insidious onset. It involves upper and lower motor neurons and causes both spastic and atrophic muscular symptoms. More than one fourth of patients have complaints relating to the head and neck (bulbar palsy); thus, the otolaryngologist may be the first physician to see them. Predominant symptoms are slurred speech, hoarseness, dysphagia, and dyspnea. Muscular weakness, atrophy, and fasciculation are noted on examination. The course is relentless, and only 20% of patients survive five years after diagnosis.

Adult↗
PubMed1992

Lovastatin/gemfibrozil myopathy: a clinical, histochemical, and ultrastructural study.

Lovastatin has been used with increasing frequency over the past few years to reduce serum cholesterol. The onset of muscle weakness, one of the most serious side effects of long-term treatment with the drug, constitutes a contraindication to the continuation of therapy and commonly occurs in patients who are also receiving gemfibrozil or cyclosporine. We report the clinical and pathologic findings in a patient treated for hypercholesterolemia with lovastatin and gemfibrozil who developed a rapidly progressive necrotizing myopathy. A 57-year-old woman with hyperlipidemia, treated with lovastatin and gemfibrozil, was admitted to the hospital for evaluation of muscular weakness in her legs and neck. Neurologic examination revealed severe proximal muscle weakness involving both upper and lower extremities as well as proximal muscle tenderness and areflexia in the lower limbs. A biopsy of the quadriceps muscle showed multiple foci of mononuclear cell infiltration with myophagocytosis and slight variation in the size and shape of muscle fibers. Electron microscopy of the affected fibers showed accumulations of subsarcolemmal autophagic lysosomes. The patient's condition dramatically improved after discontinuation of lovastatin-gemfibrozil therapy.

Drug Therapy, Combination↗
PubMed1987

Centronuclear myopathy with unusual clinical picture.

The authors describe two cases of familial muscle disease, a mother and her daughter, characterized by centrally placed nuclei and a predominance of hypotrophic type 1 fibers. Clinically the patients exhibited a muscular weakness and atrophy localized mainly distally. Both showed hypertrophy of their calves. The nosological classification of the cases is uncertain; however, both are considered as examples of centronuclear myopathy with unusual clinical features.

Adult↗
PubMed1989

[HTLV-I associated encephalo-myelopathy resembling ALS with concurrence of acute promyelocytic leukemia in a member of the relatives].

A 36 year-old woman beginning with spastic paraparesis at her age of 11 visited us for evaluation of progressive muscular weakness of the distal portions of the upper extremities and difficulty in speaking at her age of 33. The neurological features at the present are as follows; fine horizontal gaze-nystagmus, impaired smooth pursuit ocular movement, highly spastic paraplegia with pes equino-varus necessitating canes and the wheel-chair, highly accentuated PTRs and ATRs associated with positive Babinski's sign, diminished or absent deep reflexes in the upper extremities, moderate muscular wasting with fasciculation on the tongue and distal portions of the upper extremities (rt less than lt). Sensory or cerebellar functions remain normal. No autonomic finding has been manifested. The HTLV-I antibody titers of serum (eg. PA method: x8192 ) and cerebrospinal fluid are highly positive in various methods. That of her mother (no blood-transfusion history) is positive. The provirus genome analysis on peripheral lymphocytes using the Southern blotting method by the cleaving enzyme Psi I was unable to discriminate that of an ATL patient. MRI of the central nervous system revealed higher signal area (short SE) at the C5/6 region and atrophy of C7/8 region. Neither a definite lesion in the lower brain stem, cerebellum nor cerebral hemispheres was identified. The skeletal muscle X-ray CT on the lower extremities revealed the atrophic flexor thighs and the anterior tibial and peroneal muscles. Needle EMG showed the prominent neurogenic changes in the atrophic muscles. Oral prednisolone therapy for four months relieved nystagmus and difficulty in walking, slightly. She, however, discontinued because of its side effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

[Studies on the serum aldolase activity in workers with muscle disorders caused by vibration work].

Recently, vibrating tools such as chain saws, pneumatic hammers, rock drills, riveters, and grinders have been widely introduced in various industries in order to increase efficiency and to reduce the burden of labor. The disease due to hand-arm vibration often causes serious damages to the operator's body, more particularly of the circulatory, peripheral nervous, osteo-articular and muscular systems. Many kinds of examinations such as roentgenography, electromyography, and sthenometry have been used to diagnose the damage to the musculoskeletal systems. Among these, the measurement of muscular strength, evaluated by grip and pinch strength, is widely used in mass examinations of vibration hazards but this is not always effective in precise recognition of the decrease in muscular strength. In the present study, therefore, in order to diagnose the severity of muscle disorders objectively, serum activities of aldolase (ALD), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), which are called "muscle enzymes," were determined in 260 chain saw operators aged 40 to 59 years. The same tests were performed for 46 healthy subjects (controls) of a similar age-range, who had a very short experience handling bush cleaners. All chain saw operators were classified into four groups according to the total chain saw operating time (TOT): 1) 58 operators with up to 2,500 hours' experience, 2) 70 with 2,500-5,000 hours' experience, 3) 74 with 5,000-10,000 hours' experience, and 4) 58 with over 10,000 hours' experience. The relationships were investigated in their enzyme activities on the one hand, and their TOT, muscular strength and numbness and pain symptoms related to muscle disorders of the upper extremities on the other hand. The following results were obtained: 1) Serum ALD and LDH activities in chain saw operators increased in proportion to the decrease in muscular strength. The activity of ALD showed a tendency to increase with increased TOT. The ALD activity in the group with over 5,000 hours' experience was significantly higher than that in the control group. However, no relationships were observed between CPK, LDH activities and TOT. 2) In chain saw operators with numbness and pain symptoms, ALD activity in the group with 2,500 hours' experience was significantly higher than that in the control group. However, no obvious relationships were found between CPK, LDH activities and numbness and pain symptoms. 3) In chain saw operators with muscular weakness in addition to numbness and pain symptoms, ALD activity in the group with over 2,500 hours' experience was significantly higher than that in the control group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

[A clinical, histochemical and ultrastructural study of mitochondrial myopathy].

Among 189 consecutive cases with neuromyopathies, abnormalities of mitochondria in the muscles were seen in 5 cases. Ragged rad fibers (Rrf) were found with muscle biopsy with the use of staining of Gomory Trichrome. The ultrastructural abnormalities as revealed under the electron microscope in the mitochondria were as follows: 1. the mitochondria contained a lot of paracrystalline inclusion; 2. they were composed of lamellae; and 3., the mitochondria also showed dense spherical inclusions with abundant glycogen-rich sarcoplasm. The clinical manifestations of these patients consisted of: 1. muscular atrophy of various degrees. 2. muscular weakness of the proximal parts of the limbs, and 3. ptosis and ophthalmoplegia (in three cases). Three of the patients were treated with coenzyme Q10 with improvement of some of the symptoms and signs.

Adult↗
PubMed1992

Case-of-the-month: autosomal recessive myotonia congenita: marked muscle weakness in a 16-year-old boy.

A 16-year-old boy had a 10-year history of stiffness in leg muscles. There was marked weakness of neck flexors, shoulder abductors, and ankle dorsiflexors, with hypertrophy of most muscle groups and both action and percussion myotonia. The parents were normal. Motor unit potential mean duration was reduced in the weakest muscle (tibialis anterior), and a biopsy of the same muscle showed only minimal abnormalities. Exercise and repetitive stimulation (30 Hz) of the tibialis anterior disclosed a decline in the compound muscle action potential that appeared to correlate with the muscular weakness.

Adolescent↗
PubMedDate not supplied

Familial facioscapulohumeral muscular dystrophy: phenotypic diversity and genetic abnormality.

We report two cases showing facioscapulohumeral muscular dystrophy (FSHD) with phenotypic diversity but the same genetic abnormality detected by a p13E-11 probe. The proband, a 26-year-old woman, showed an early onset, tortuosity of retinal arterioles and respiratory failure. The 53-year-old mother of the proband had limb-girdle (L-G) type muscular weakness with very mild facial involvement. Muscle biopsy showed perivascular cell infiltration in both patients. These cases suggest that the phenotypic diversity ranges from L-G type weakness to severe respiratory failure in FSHD family.

Adult↗
PubMed1994

Dilated cardiomyopathy and the dystrophin gene: an illustrated review.

Cardiomyopathy is often found in patients with Duchenne and Becker muscular dystrophy, which are X linked muscle diseases caused by mutations in the dystrophin gene. Dystrophin defects present in many different ways and cases of mild Becker muscular dystrophy have been described in which cardiomyopathy was severe. Female carriers of Duchenne muscular dystrophy can develop symptomatic skeletal myopathy alone or combined with dilated cardiomyopathy. They can also develop dilated cardiomyopathy alone. X linked dilated cardiomyopathy has been found in association with dystrophin defects. The relation between the molecular defects and the cardiac phenotypes has not yet been established. New mutations in the dystrophin gene are common and such mutations cause one third of the cases with Duchenne and Becker muscular dystrophy. This means that sporadic cases of cardiomyopathy caused by dystrophin defects are likely. This paper reports such a case in a boy of 14 who died of dilated cardiomyopathy. Before the cardiac investigation, which was performed one month before he died, he had not complained of muscular weakness. He had minor signs of limb girdle myopathy and slightly increased concentrations of serum creatine kinase. He was found to have an unusual deletion in the dystrophin gene.

Adolescent↗
PubMed2004

Dysferlinopathy associated with rigid spine syndrome.

Dysferlinopathy and rigid spine syndrome occurring in a 50-year-old man is reported. The patient noticed stiffness of knee and ankle joints, which gradually extended to neck, wrist and elbow joints leading to difficulty in anterior flexion. Muscular weakness and wasting of the lower extremities had developed since age 40, accompanied by a limitation of anterior bending of the spine. Elevated serum CK was noticed. Muscle CT revealed atrophy with moderate fatty replacement of muscles in the neck, shoulder and pelvic girdle, and marked replacement in the para-vertebral muscles, posterior compartment of hamstrings and calf muscles. Electromyography showed a typical myogenic pattern, and muscle biopsy disclosed dystrophic changes, compatible with limb-girdle muscular dystrophy 2B. Loss of dysferlin expression was verified by immunohistochemistry, which was confirmed by a mini-multiplex Western blotting system. Gene analyses of the dysferlin gene disclosed compound heterozygotes for frameshift (G3016 + 1A) and a missense mutation (G3370T). This study might propose some clues to resolve the combination of musular dystrophies and rigid spine syndrome.

Dysferlin↗
PubMed2001

Muscular effects in late polio.

New or increased muscular weakness, fatigue and muscle and joint pain with neuropathic electromyography (EMG) changes in a person with a confirmed history of polio constitute the cardinal symptoms of the post-polio syndrome. Unusual tiredness or fatigue is a common complaint in late polio subjects as is intolerance to cold. Fatigue in polio subjects can have several explanations: emotional fatigue, central nervous system fatigue, 'general' fatigue and/or neuromuscular fatigue. Some studies indicate central fatigue, but it is unclear how often and to which degree there will be a central muscular fatigue. Polio patients are known to be deconditioned (reduced function because of low activity level), and aerobic power is reduced. Defects in the neuromuscular transmission may be present but are not seen in all post-polio subjects with reduction in force and increased fatigability. The fatigue experienced by late polio patients is most likely an augmented peripheral muscle fatigue. Possible explanations may be an imperfection in the sarcoplasmatic reticulum with altered calcium release mechanisms (activation) or in sliding filament function (contractile properties). This may be a secondary effect to the enlarged muscle fibres. However, the prolonged subjective feeling of fatigue reported despite unchanged maximal voluntary contraction (MVC) remains unexplained.

Electromyography↗
PubMed1975

Remediable neuromuscular disorders.

Generalized muscular weakness may develop from a variety of causes, and in many cases is reversible with appropriate treatment of the underlying disorder.

Adult↗
PubMed1988

Velopharyngeal incompetence as the presenting symptom of myotonic dystrophy.

Velopharyngeal incompetence has previously been described in the late stages of myotonic dystrophy. However, we have seen three cases in which velopharyngeal incompetence was the presenting symptom. Despite different ethnic backgrounds, the patients shared a similar appearance, all three had the characteristic "myopathic facies," mandibulomaxillary disproportion, muscular weakness, and positive family history. Identifying a progressive neuromuscular disorder as the cause of velopharyngeal incompetence has important treatment and prognostic implications. Based on the experience described in this report, we feel that the velopharyngeal incompetence of the myotonic patient might best be managed nonsurgically.

Adolescent↗
PubMed2004

Spinal cord neuropathology in human West Nile virus infection.

CONTEXT: During the 1999 New York City West Nile virus (WNV) outbreak, 4 patients with profound muscle weakness, attributed to Guillain-Barré syndrome, were autopsied. These cases were the first deaths caused by WNV, a flavivirus, to be reported in the United States. The patients' brains had signs of mild viral encephalitis; spinal cords were not examined. During the 2002 national epidemic, several patients in Mississippi had acute flaccid paralysis. Electrophysiologic studies localized the lesions to the anterior horn cells in the spinal gray matter. Four of 193 infected patients in Mississippi died and were autopsied. All 4 experienced muscular weakness and respiratory failure that required intubation. Postmortem examinations focused on the spinal cord. OBJECTIVE: To emphasize apparent tropism of WNV for the ventral gray matter of the spinal cord. DESIGN: Cerebral hemispheres, basal ganglia, diencephalon, brainstem, cerebellum, and spinal cord sections were stained with hematoxylin-eosin and incubated with antibodies to T cells, B cells, and macrophages/microglial cells. RESULTS: We identified neuronophagia, neuronal disappearance, perivascular chronic inflammation, and microglial proliferation in the ventral horns of the spinal cord, especially in the cervical and lumbar segments. Loss of ganglionic neurons, nodules of Nageotte, and perivascular lymphocyte aggregates were found in dorsal root and sympathetic ganglia. Severity of cellular reaction was proportional to the interval length between patient presentation and death. CONCLUSION: West Nile virus caused poliomyelitis. Injury to spinal and sympathetic ganglia mirrored the damage to the spinal gray matter. The disappearance of sympathetic neurons could lead to the autonomic instability observed in some WNV patients, including labile vital signs, hypotension, and potentially lethal cardiac arrhythmias.

Aged↗
PubMed2005

[Multiple sclerosis and physical activities].

INTRODUCTION: Multiple sclerosis (MS) is a neurological disease of the central nervous system that most often affects young people. It is characterized by various debilitating symptoms. The aim of this study was to assess physical activities in patients with MS and how these affect their quality of life. METHODS: Forty-five patients were questioned about their physical activities. The following were taken into account: the characteristics of MS within each patient, the level of disease severity (EDSS score) and the quality of life (on the SEP-59 questionnaire). RESULTS: Fifteen patients had to give up a physical activity because of their illness but more so due to ataxia, fatigue and muscular weakness. Fifteen patients take part in a physical activity, the principal motivation being for their personal well-being. The mean EDSS was 4.2. Answers on the SEP-59 revealed found that patients with MS who took part in a physical activity had significantly better well-being in general. DISCUSSION AND CONCLUSION: Physical activities seem to improve the quality of life of patients with MS who, in general, already have a poor quality of life in relation to the general population. Knowing that muscular function is improved through exercise in patients with an EDSS less than 6, it would seem advantageous for them to take part in a regular physical activity.

Adolescent↗
PubMed1999

Autosomal dominant limb-girdle muscular dystrophy with ankle joint contracture.

We herein describe a Japanese family suffering from autosomal dominant limb-girdle muscular dystrophy showing a later onset and a predilection for males. All patients developed a plantar flexion contracture of the ankles when no distal muscular weakness was evident. The serum creatine kinase activity was remarkably elevated to 55 times the normal value. These clinical features suggest a novel phenotype.

Adult↗
PubMed1970

Necrosis of muscle with carcinoma: myositis or myopathy?

A man aged 59 years developed a rapidly progressive muscular weakness which within a few weeks involved almost the entire musculature. A carcinoma of the stomach was discovered at necropsy. The skeletal muscles showed widespread necrosis with minimal inflammatory reaction. The findings are compared with those in a woman of 51 with Hashimoto's thyroiditis who developed a slowly progressive weakness of her trunk muscles which after some months began to involve the limbs. Post-mortem examination revealed typical polymyositis with massive inflammatory infiltration and limited necrosis of muscle. We conclude that these two types of muscle disease are morphologically, and probably pathogenetically, different.

Biopsy↗
PubMed1992

Quadriceps myositis.

A young woman with slowly progressive muscular weakness and atrophy localized in both thighs is reported. Laboratory, electromyographic and histological findings suggested that the patient suffered from chronic myositis with a background of autoimmune disorder. Quadriceps myositis is a rare condition. The previously reported cases of this disease in the literature are reviewed.

Adult↗