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At least 199 records · Page 11Linked to original sources
PubMed1992

[Chronic myelomonocytic leukemia associated with translocation 1;7, marked platelet aggregation and cryofibrinogenemia: a case report].

A 64-year-old male was admitted in September 1989 with complaints of fever and muscular weakness in the extremities. A peripheral blood examination on admission revealed WBC 10,300/microliters (monocytes 32%), RBC 195 x 10(4)/microliters, Hb 7.9 g/dl, Plt 12.8 x 10(4)/microliters with trilineage dysplasia. Bone marrow biopsy was normoplastic marrow with 25.7% of monocytes including immature blasts. Cytochemical analysis of the monocytes showed positive for peroxidase and dual esterase staining. Chromosomal analysis of peripheral blood revealed 46, XY, -7, +der(1) t(1;7)(p11;p11). A diagnosis of chronic myelomonocytic leukemia was made. Hemostatic studies revealed cryofibrinogenemia, marked platelet aggregation on blood smear, hyperfibrinogenemia and a marked increase in maximal amplitude of thrombelastogram. Treatment with prednisolone and VP16, resulted in a reduction of peripheral monocytes and a disappearance of cryofibrinogen, marked platelet aggregation and a decrease in muscular weakness. Nine months after diagnosis he died of DIC, pneumonia, lung abscess and sepsis.

Chromosomes, Human, Pair 1↗
PubMed1989

[A case report of quadriparesis due to compression of the medulla oblongata by the elongated left vertebral artery].

A patient, 30-year-old man, was admitted to Shinshu University Hospital with gait disturbance and numbness of both arms and legs in June 1985. General physical findings were normal except for facial asymmetry, i.e. mild right facial hemiatrophy. Blood pressure was normal and there were no signs of arteriosclerosis. Neurological examination revealed marked bilateral pyramidal tract signs, muscular weakness of all extremities predominant of the right side, spastic gait and sensory disturbance with impairment of pin prick and light touch sensation in the second and third trigeminal nerve regions and extremities of the left side, and mild loss of vibratory sense and numbness in all extremities. X-ray examination of the cervical spine and the myelogram of the spinal canal were normal. CT scan of the brain performed 3 hours after the myelography showed that the left vertebral artery extended from the left side of the medulla oblongata to the midline and distorted it by compression. MRI confirmed the findings of the CT scan. Vertebral angiography disclosed that the elongated left vertebral artery crossed the ventral aspect of the medulla oblongata. Compression of the medulla oblongata by the vertebral artery was diagnosed and neurovascular decompression was performed. About one month after the operation his spastic gait and muscular weakness were slightly improved, but these symptoms progressed thereafter. One year after operation his spastic gait was more marked than preoperatively. In many cases with dolichoectatic intracranial arteries, hypertension and arteriosclerosis have been reported to be usually associated with this condition. In other opinions dolichoectasia has been suggested to be a congenital disease, because such vessels are occasionally present in children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Neuromuscular function and organotin compounds.

Mammalian exposure to toxic levels of the trialkyltin compounds, triethyltin (TET) and trimethyltin, results in pathological manifestations largely restricted to the nervous system. The remarkable features of TET toxicity are cerebral edema and muscular weakness. Rats exposed orally to TET (10-30mg TET Br/l of drinking water) progress through an increasingly compromised state beginning with mild ataxia and hindlimb weakness after one week, spastic paresis of the hindlimbs by two weeks; and hindlimb paraplegia and sensory changes by 3 weeks. Histopathological studies of chronic TET-exposed rats report minimal ultrastructural damage to distal peripheral nerves, myelin, and muscle. Chromatolytic reactions are observed in some alpha motor neurons; intramyelinic vacuolization in the ventral roots and horn is substantial by 3 weeks. Myelin vacuolization and degeneration are observed to a lesser extent in the dorsal roots of the spinal cord. Wet weights and myofiber diameters of EDL and soleus muscles are reduced during chronic TET intoxication, but no histopathology is evident using light microscopy. Conduction of compound action potentials in vivo along distal sensory fibers, ventral roots and distal motor fibers (in sciatic n.) is normal in 3 week TET rats as compared to control; however, nerve conduction velocity is decreased in the segment of the H-reflex arc involving the dorsal roots. Earlier studies by Stoner and coworkers led to suggestions that the neuromuscular junction may be preferentially affected by TET and could contribute, in part, to the symptoms of muscular weakness. In support of this hypothesis preliminary studies from our laboratory and others indicate that neurotransmission is functionally depressed at the myoneural junction following chronic TET treatment in vivo or when applied in vitro to isolated muscle preparations. Stimulated, but not unstimulated, release of acetylcholine from the vascular perfused rat phrenic nerve-hemidiaphragm preparation is decreased by TET especially at higher stimulation rates (20 Hz). In vitro administration of TET Br (10(-6)M) results in an irreversible decrease in the amplitude of evoked endplate potentials; chronic in vivo exposure to TET causes a decrease in the resting membrane potential of soleus muscle (in situ recordings) and provokes a peculiar post-stimulus (200Hz bursts) elevation of spontaneous miniature endplate potentials in isolated cut diaphragm preparations.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed2003

[Two cases of rheumatoid arthritis developed after polymyositis].

We report two cases of rheumatoid arthritis (RA) who later had developed after polymyositis (PM). The first patient was 64-year old male who experienced muscular weakness of the four limbs in proximity 10 years ago. He was diagnosed as PM because of the elevated serum CK and the myogenic pattern of EMG, and his symptoms were improved by treatment with corticosteroid. He started to complain polyarthralgia 2 years ago, followed by interstitial pneumonia, pleuritis and skin ulcer. He was admitted because of exacerbated polyarthralgia, multiple subcutaneous nodules, skin eruption and fever. The level of serum CK was within normal range but CRP was elevated and CH 50 was decreased. The laboratory examination showed positive cryoglobulin and high titer of rheumatoid factor, but anti-Jo 1 antibody was negative. The hand X-ray showed bone erosions in bilateral wrist joints. Skin biopsy revealed leukocytoclastic vasculitis. Based on these findings, he was diagnosed as malignant RA. He was successfully treated with methylprednisolone pulse therapy, cyclophosphamide and prostaglandin E 1. The second patient was 77-year old male with pneumoconiosis who experienced muscular weakness of the four limbs in proximity 4 years ago. He was diagnosed as PM based on his clinical and laboratory findings and was treated with temporary corticosteroid. He started to have polyarthralgia last year, and he was admitted because of increasing arthralgia after the treatment of pulmonary tuberculosis. The level of serum CK was slightly elevated due to hypothyroidism, and CRP was highly elevated. Rheumatoid factor and cryoglobulin were positive, but anti-Jo 1 antibody was negative. The hand X-ray showed bone erosions in bilateral wrist joints. Crystals of pyrophosphate calcium was observed in knee joints. He was diagnosed as RA associate with pseudogout. His symptoms were relieved with corticosteroid, salazosulfapyridine and anti-tuberculous therapy. These two cases had altered their clinical features from PM to definite RA, and both had pulmonary complications. Previous reports described the cases of RA followed by PM, most of which were induced by such drugs as D-penicillamine, but the cases of PM who later had developed RA are extremely unusual. The overlapped cases of RA and PM tend to highly associate with pulmonary lesions.

Aged↗
PubMed2005

[Diabetes mellitus and massive lower leg edema without heart failure].

ANAMNESIS AND CLINICAL FINDINGS: The 47-year-old male patient was admitted to the hospital because of newly diagnosed diabetes and elevated liver function tests (gamma glutamyl transferase 303 U/l). On admission the patient reported a reduction of appetite, which had increased during the past 2 weeks, fatigue, muscular weakness, polyuria and polydypsia. On physical examination the patient was moderately overweight, the blood pressure was normal. There were leg edema, which had not responded to previous treatment. There were no additional signs of right heart failure. INVESTIGATIONS: On admission there were hypokalemia and increased parameters of cholestasis. Cortilsol concentration was elevated (1744 microg/l). Hypokalemia which was refractory to treatment raised the differential diagnosis of Conn's syndrome or ectopic secretion of ACTH, although these conditions are frequently associated with arterial hypertension. Cushing's syndrome was finally diagnosed despite of the lack of classical symptoms. Underlying reason was an adenocarcinoma of the pancreas with ectopic secretion of ACTH. TREATMENT AND COURSE: Therapy was targeted to control the excessive secretion of cortisol. A treatment attempt with subcutaneous somatostatin and the adrenal enzyme inhibitor ketoconazole failed to control increased cortisol secretion. Bilateral surgical adrenalectomy was performed because of the patient's progressively deteriorating clinical condition. The patient developed a lethal septic shock after surgery, most likely due to the cortisol-induced immunosuppression. CONCLUSION: 1. In patients presenting with muscular weakness, leg oedema refractory to treatment, hypokalemia and hyperglycemia hypercortisolism should be ruled out even in the absence of typical clinical signs. 2. Massive hypercortisolism (as present in ectopic ACTH secretion) is not necessarily associated with arterial hypertension.

Adenocarcinoma↗
PubMed1999

Experience of social support in rehabilitation: a phenomenological study.

The progressive muscular weakness brought on by muscular dystrophy causes the sufferer many problems in everyday life. Earlier studies in Sweden have shown that adults with hereditary muscular dystrophy often have difficulty in gaining access to rehabilitation. For this reason a special rehabilitation programme was drawn up and carried out, extending over a period of 18 months. The purpose of the study is to describe the participants' experience of social support in connection with the programme. Thirty-seven participants (21 women and 16 men) were interviewed. The analytical method was phenomenological, incorporating validation by independent judges. Nine overall themes emerged from the interviews: psychosocial support, meeting other people with muscular dystrophy, knowledge and learning, adjustment in daily life, coping with illness-related problems, adjustment at work, management of physical disability, medical examination and treatment, and involvement of relatives. The results indicate that the participants encountered staff with a sense of commitment and felt themselves to be 'seen and confirmed'. From the discussions and the contact with others in the same situation there arises a sense of affinity and a better understanding of one's own situation. There was appreciation of the education about the disease, its hereditary aspect, technical aids, grants and physical training. Hardly any of the participants spoke of knowing such things before. In conclusion there was approval of the received support, and recognition that persons with muscular dystrophy should be given access to recurrent rehabilitation.

Activities of Daily Living↗
PubMed2006

Frequency of dystrophic muscle abnormalities in chronic progressive external ophthalmoplegia: analysis of 86 patients.

BACKGROUND: There are few reports describing the coexistence of dystrophic features with those typical of mitochondrial myopathies in muscle biopsy. A recent study suggested that dystrophic features are frequent in patients with chronic progressive external ophthalmoplegia (CPEO) with a high mutation load, but the actual frequency of these abnormalities in CPEO remains undetermined. OBJECTIVE: To review the occurrence of dystrophic abnormalities in a large series of patients with CPEO to assess the frequency of such abnormalities and to verify whether they are correlated with specific mitochondrial DNA (mtDNA) mutations. METHODS: Retrospective survey of case series (86 patients with CPEO). RESULTS: Only three cases with dystrophic abnormalities were found: two with a large scale mtDNA deletion and one with the A3251G mutation. All three patients showed predominantly proximal muscular weakness resembling limb girdle muscular dystrophy. CONCLUSIONS: Dystrophic abnormalities are rare in CPEO and are not correlated with a specific molecular defect.

Adult↗
PubMedDate not supplied

[Myopathy and hypothyroidism].

Muscular disturbances in hypothyroid children are: generalized muscular weakness of proximal predominance, muscular hypotonicity, pseudohypertrophy (of gastrocnemius muscles chiefly), slow relaxation stage of osteotendinous reflexes, rise of muscular enzymes (CPK andaldolase), unspecific electromyographic changes and histopathologic disturbances comprised by persistent decrease of fibers type II. All these changes are reversible with thyroglobulin therapy; therefore they exert no influence on the prognosis of hypothyroid patients.

Adolescent↗
PubMed1993

[A case of non-Fukuyama type congenital muscular dystrophy with progression in early adulthood, ocular involvement, and sensorineural deafness].

Congenital muscular dystrophy (CMD) is a concept applied to infants showing muscular weakness and hypotonia at birth, with myopathic changes which are histopathologically similar to those of muscular dystrophy. Patients with Fukuyama-type CMD (FCMD), characterized by progressive muscular dystrophy, mental retardation and occasionally, convulsions, are more frequently seen in Japan than those with non-Fukuyama type CMD (NFCMD). FCMD has been regarded as a distinct clinical and pathological entity, although the nosologic status of CMD is still controversial. A 24-year-old man had exhibited hypotonia and weakness at birth and delay in early development. During childhood, his muscular weakness improved, and he rode a bicycle and enjoyed skiing. However, his strength began to deteriorate at the age of 19 years. Neurological examination on admission revealed prominent muscular wasting and weakness, predominantly in the proximal limbs. He had ocular involvement (corneal opacity and slow saccades), sensorineural deafness, and a high-arched palate, saddle nose and funnel chest as anomalous conditions. Serum CK was moderately elevated and EMG showed myogenic patterns. A muscle biopsy specimen of the left biceps brachii was dystrophic, showing increased variation in fiber size with fibrous tissue proliferation, an increased number of centralized nuclei, fiber splitting and degenerating/regenerating fibers. Those findings were compatible with those seen in NFCMD. In Japan, only one patient with NFCMD who was followed to adulthood has been reported. This patient's symptoms progressed very slowly. The present patient's course of illness was stable during childhood but progressive in early adulthood. It suggests heterogeneous clinical expression of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Elevated plasma levels of transforming growth factor beta1 in patients with muscular dystrophy.

The progression of muscular weakness of patients suffering from muscular dystrophies directly correlates with the progressive loss of myofibers, accompanied by fibrosis. Since transforming growth factor beta1 (TGF-beta1) promotes tissue fibrosis, we measured the plasma TGF-beta1 level in patients with various muscular dystrophies in order to determine whether the level is elevated in patients with muscular dystrophy and if the level reflects the severity of tissue fibrosis. The plasma TGF-beta1 level was significantly elevated in patients with Duchenne muscular dystrophy and congenital muscular dystrophy (CMD), but not in those with Becker muscular dystrophy. Growth factors related to muscle fiber regeneration and fibrosis might be a key factor in the progression of muscular dystrophy and could be a target for therapeutic studies.

Adolescent↗
PubMed1990

[Hypothyroid myopathy. Clinico-pathologic study of 20 cases].

20 patients afflicted with primary hypothyroidism were studied in order to evaluate the association of clinical or sub-clinical myopathy, detected by neurophysiological (electromyography) (EMG) or neuropathological methods (muscular biopsy with enzymatic study). 70% of the patients had muscular weakness (moderate in 30% and severe in 40%) of the scapular and pelvic muscles. 60% of the patients had muscular cramps. There was no myodema nor muscular atrophy or hypertrophy. Seric CPK was high in 70% of the cases. EMG was myopathic in 65%. All cases with weakness registered EMG alterations. The histological findings were import findings were important. The enzymatic techniques showed alterations of the fiber subtypes in 90% of the cases. The type I fibers had sarcolemmal and mitochondrial accumules in 85% and 70% had areas without oxidative activity, similar to "core". In this study, we did not find any correlation between the evolution time of hypothyroidism, hormonal levels, CPK increase, and muscular weakness. The EMG was myopathic in cases with severe weakness, however, in patients with moderate weakness it could also prove abnormal. There was no correlation between the electric myopathic pattern, CPK levels and thyroid hormones.

Adult↗
PubMedDate not supplied

Late postpoliomyelitis muscular atrophy: clinical, virologic, and immunologic studies.

Seventeen relatively young patients, ages 31-65 years (average, 45) with prior poliomyelitis, who after a number of years of stability had experienced new neuromuscular symptoms, were studied. Seven patients had deterioration of functional capacity and then stabilization without new muscular weakness. The other 10 had late postpoliomyelitis muscular atrophy (late PPMA ) characterized by focal progressive muscle weakness, wasting, fasciculations, and muscle pains affecting previously spared muscles or muscles previously affected but recovered. Four patients with late PPMA had lymphorrhages or lymphocytic infiltrates in their biopsied muscle; three of three patients had oligoclonal IgG bands in their spinal fluid, and five had variable peripheral T lymphocyte-subset ratios. In one patient with late PPMA , antibodies to poliovirus were specifically elevated in the cerebrospinal fluid. Our findings indicate that new motor-neuron disease can occur in patients with prior poliomyelitis and that immunopathologic mechanisms may play a role.

Adult↗
PubMed2000

Metabolic abnormalities associated with skeletal myopathy in severe anorexia nervosa.

The aim of this study was to characterize the metabolic disturbance associated with the skeletal myopathy resulting from extreme weight loss in anorexia nervosa. Muscle function was examined in eight female patients with severe (40%) weight loss due to anorexia nervosa and histologically confirmed myopathy. A wide range of biochemical and hematologic investigations were carried out, including serum enzymes and the response of plasma lactate to ischemic exercise of forearm muscles. All patients showed proximal muscular weakness. A diminished lactate response to ischemic exercise was a consistent finding, and a reduction of serum carnosinase activity was also found. There were no other consistent biochemical or hematologic abnormalities apart from lymphopenia of no clinical consequence. These findings contribute to our understanding of severe protein-energy malnutrition on the musculoskeletal system. The resulting disorder is a metabolic myopathy from which the patients recover rapidly as their nutrition improves. Although the patients admitted to a variety of abnormal eating behaviors, no correlation was found between a specific type of abnormal eating behavior and subsequent biochemical abnormalities. Reinstating appropriate eating behavior will treat the myopathy.

Adolescent↗
PubMed1978

A clinical and genetic study of spinal muscular atrophy of adult onset: the autosomal recessive form as a discrete disease entity.

A clinical and genetic study of spinal muscular atrophy (SMA) of adult onset is reported. A genetic analysis of all cases of SMA occurring over a ten-year period in North-east England (48 index cases) has shown that chronic proximal SMA of adult onset is a distinct clinical and genetic entity, and is not a variant of the more common and relatively benign late juvenile cases. Nine cases of SMA of adult onset have been studied, occurring in 6 families. The median age of clinical onset was 35 years and the mean age at initial medical presentation was 37 years. The sex ratio was 5:4 (males:females). The condition is relatively benign and there is no evidence to date that life expectancy is shortened; there is usually no premonitory evidence of muscular weakness in early adult life. The muscular involvement is relatively symmetrical and the distal musculature is well preserved; clinical progression of the disease is interrupted by periods of apparent arrest. No patient was able to walk completely unaided twenty years after the initial clinical onset; the median age of patients in the study was 61 years but only one was confined to a wheelchair. In the early stages the recessive form of familial motor neuron disease must be excluded. A segregation analysis of sibs born after index cases was undertaken (segregation ratio of 0.20). This finding is consistent with autosomal recessive inheritance with an extended period during which the disease might initially present. The presence of new dominant mutations cannot be excluded, but is unlikely to account for more than 10% of cases. The carrier rate in the English population is estimated to be 1 in 300, with a gene frequency q = 0.00165. Prevalence is 0.32 per 100,000 in the general population. Empirical risks for genetic counselling are presented.

Adolescent↗
PubMed1997

Molecular analysis of the androgen receptor gene in Kennedy's disease. Report of two families and review of the literature.

We have performed a molecular analysis of the androgen receptor gene in two families with suspected Kennedy's disease (spinal and bulbar muscular atrophy, SBMA) with the aim of making a firm diagnosis of the disease. The 2 patients studied were sporadic cases. Both presented clinical signs compatible with the diagnosis of SBMA: limb and facial muscular weakness of adult onset progressing toward muscular atrophy. Clinical signs of partial androgen insensitivity syndrome usually observed in SBMA were present only in patient 2. Enzymatic amplification of the CAG repeat region of exon 1 of the androgen receptor gene was performed on genomic DNA. PCR products were submitted to agarose or acrylamide electrophoresis for size evaluation. Precise determination of the CAG number was performed by direct sequencing of purified amplification products. Androgen receptor gene analysis was also performed in 2 sisters of patient 1 and in the mother, sisters and daughter of patient 2. Androgen receptor-binding activity was also determined on cultured genital skin fibroblasts of patient 1. Analysis of PCR products showed in both patients a single band that was much larger in size than the control. The expansion of the CAG repeat number was confirmed by direct sequencing: the exact number of CAG was 47 in patient 1 and 42 in patient 2 (n = 12-32). The 2 studied sisters of patient 1 did not present the abnormal fragment, demonstrating they are not carriers for the disease. Conversely, the mother, sisters and daughter of patient 2 presented both normal and mutated alleles. The migration of the labelled PCR products on a sequencing gel revealed a meiotic instability of expanded CAG repeat in family 2. Moreover, patient 1 had a decreased androgen-binding capacity on cultured genital skin fibroblasts. In both families, analysis of the androgen receptor gene permitted us to diagnose SBMA in the patients and to establish the carrier status in siblings. These results correspond to the literature data and confirm the usefulness of CAG repeat evaluation in the diagnosis of Kennedy's disease. They highlight the relationship between the androgen receptor and motoneuron growth, development and regeneration.

Base Sequence↗
PubMed2006

EFNS guideline on diagnosis and management of post-polio syndrome. Report of an EFNS task force.

Post-polio syndrome (PPS) is characterized by new or increased muscular weakness, atrophy, muscle pain and fatigue several years after acute polio. The aim of the article is to prepare diagnostic criteria for PPS, and to evaluate the existing evidence for therapeutic interventions. The Medline, EMBASE and ISI databases were searched. Consensus in the group was reached after discussion by e-mail. We recommend Halstead's definition of PPS from 1991 as diagnostic criteria. Supervised, aerobic muscular training, both isokinetic and isometric, is a safe and effective way to prevent further decline for patients with moderate weakness (Level B). Muscular training can also improve muscular fatigue, muscle weakness and pain. Training in a warm climate and non-swimming water exercises are particularly useful (Level B). Respiratory muscle training can improve pulmonary function. Recognition of respiratory impairment and early introduction of non-invasive ventilatory aids prevent or delay further respiratory decline and the need for invasive respiratory aid (Level C). Group training, regular follow-up and patient education are useful for the patients' mental status and well-being. Weight loss, adjustment and introduction of properly fitted assistive devices should be considered (good practice points). A small number of controlled studies of potential-specific treatments for PPS have been completed, but no definitive therapeutic effect has been reported for the agents evaluated (pyridostigmine, corticosteroids, amantadine). Future randomized trials should particularly address the treatment of pain, which is commonly reported by PPS patients. There is also a need for studies evaluating the long-term effects of muscular training.

Advisory Committees↗
PubMed2003

[Muscle weakness].

A 31-year old cook suffered from episodes with muscular weakness since 3 weeks. These episodes resolved, at times, spontaneously and completely after a few hours. The weakness affected mainly the muscles of trunk and proximal extremities. Investigation of the patient revealed flaccid tetraparesis with diminished tendon reflexes, however, cranial muscles were not affected. Mental function and sensibility were intact. These findings were consistent with hypopotassemic periodic paralysis rather than a neurological or psychiatric disease. Serum potassium was determined as 1.8 mmol/l. Moreover, the patient suffered from atrial fibrillation. Grave's disease could be identified as the underlying cause of hypopotasemic periodic paralysis and atrial fibrillation. Further manifestations of primary hyperthyroidism were nervousness, diarrhea and weight loss of 5 kg observed during the previous months. The symptoms resolved under treatment with potassium, betablocker and thyrostatic agents. The patient was treated with warfarin because of atrial fibrillation and finally underwent electroconversion.

Adrenergic beta-Antagonists↗