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PubMed1992

Epidemiology of the post-polio syndrome.

A late-onset syndrome, consisting of muscle weakness, muscle pain, and unaccustomed fatigue, has been reported with increasing frequency among former poliomyelitis patients. A population-based cohort of poliomyelitis patients from Allegheny County, Pennsylvania, was traced and surveyed to estimate the prevalence and incidence and to identify determinants of the post-polio syndrome. A questionnaire validated in clinical examinations of 40 cohort members was used in the survey. The prevalence of the post-polio syndrome was 28.5% of all paralytic cases (95% confidence interval 24.4-32.6). The risk of post-polio syndrome was significantly higher among patients who sustained substantial permanent impairment after polio and among females. The incidence did not vary with age at acute onset, acute severity, or level of physical activity after recovery. The strongest determinant of post-polio syndrome onset was the length of the interval following the acute illness, with incidence peaking at 30-34 years. Of all cases of post-polio syndrome, 79% reported no major change in impairment status since onset. This study demonstrates that poliomyelitis patients are not equally susceptible to post-polio syndrome within the interval of 30-40 years after the original illness. For syndrome cases, the onset was associated with new neuromuscular symptoms and functional changes but not with major new impairment.

Acute Disease↗

PubMed1994

Disability in poliomyelitis sequelae.

Patients who have been affected by poliomyelitis may develop new symptoms such as muscle weakness, muscle atrophy, muscle or joint pain, and unexplained fatigue several decades after the onset of their poliomyelitis (post-polio syndrome [PPS]). We report on the results of our study of 59 patients with poliomyelitis using a number of instruments for disability assessment, including a 4- to 5-year follow-up. The main impact of disability for most patients is in mobility-related activities. Dependence in personal activities of daily living is fairly rare, whereas dependence and difficulties in instrumental activities of daily living (eg, cooking, transportation, cleaning, shopping) are more common and also more severe in persons with PPS. Mental health, emotional reactions and social activity, interaction, and isolation are usually less affected, although considerable coping problems may occur, especially in persons with PPS who have new health problems and increasing disabilities. Examples of disabilities, intervention measures, and coping processes are given with case reports. The importance of a broad and interdisciplinary approach is emphasized, in which impairment as well as disability aspects should be considered in treatment and intervention programs.

Activities of Daily Living↗

PubMed1988

Congenital fiber type disproportion in an adult: a morphometric and microchemical study.

A 20-year-old man with marfanoid habitus had a history of congenital hypotonia and muscle weakness. Muscle biopsy showed extreme fiber type disproportion. There was total absence of Type 2B fibers. The severely hypertrophic Type 2A fibers showed twice the normal concentration of creatine phosphate at rest. These advanced morphometric, histochemical and biochemical changes may be interpreted as compensatory phenomena, which may explain the patient's pronounced functional improvement with advancing age.

Adenosine Triphosphatases↗

PubMed1975

Granulomatous myopathy: its relationship to sarcoidosis and polymyositis.

In three cases of generalized muscle weakness, muscle biopsy revealed well-defined, non-caseating epithelioid granulomata with giant cells. In one of these patients there was, in addition, a high serum CPK and histological evidence of widespread muscle cell degeneration and regeneration, apparently unrelated to the granulomatous process. In a re-examination of the histopathology of these cases, using biopsy material from a fourth case of proven sarcoidosis as a standard, it was concluded that there are no special features of the granulomatous/giant cell process which permit the separation of the case of presumed polymyositis. However, it appeared that granulomata per se do not exert a significant ill effect on surrounding muscle cells, and that evidence of widespread degeneration of muscle cells is the important point of distinction.

Adult↗

PubMed1980

Hypoparathyroidism and elevated muscle enzymes.

We studied a patient with hypocalcemia and increased serum activity of sarcoplasmic enzymes. Idiopathic hypoparathyroidism was established by history, low serum parathyroid hormone content, and marked responsiveness of urinary cyclic AMP and phosphate to parathyroid hormone. Muscle-associated isoenzymes of creatine phosphokinase and lactic dehydrogenase were increased, but there was no concomitant muscle weakness. Muscle biopsy was normal by morphologic and histochemical examination. The patient was treated with calcium and vitamin D. As the calcium rose, there were corresponding decreases in the serum activities of creatine phosphokinase and lactic dehydrogenase, with correlation coefficients of -0.88 and -0.64, respectively (p less than 0.01).

Adult↗

PubMed1991

Hypercapnic respiratory failure due to L-tryptophan-induced eosinophilic polymyositis.

A 24-year-old man presenting with fever, rash, and myalgias subsequently developed hypercapnic respiratory failure and severe limb muscle weakness. Muscle biopsy revealed eosinophilic myositis, due to the ingestion of large quantities of L-tryptophan as a dietary supplement. Complete recovery occurred with corticosteroid administration. Significant involvement of the respiratory muscles can be a predominant feature of this newly described disease entity.

Adult↗

PubMed2004

Stem cell therapy for muscular dystrophy.

Muscular dystrophy is a heterogeneous group of neuromuscular disorders that manifests as progressive muscle weakness, muscle wasting and, in many cases, death. Although there has been enormous progress in the molecular understanding of muscular dystrophy, there is still no cure. There are, however, several different therapeutic options under investigation, including adult-derived stem cell transplantation. Encouraging and pioneering experiments in mouse models for Duchenne's muscular dystrophy (DMD) demonstrated that myoblasts could be transplanted into dystrophic muscle; these myoblasts repaired a small proportion of damaged myofibres. Subsequent work has been devoted to optimisation of this technique. In doing so, a number of adult-derived stem cells have been isolated, characterised and used in promising animal transplantation experiments. Further research is ongoing, and is clearly necessary to make this therapy a viable treatment option for patients with muscular dystrophy.

Animals↗

PubMedDate not supplied

Inflammatory myopathies in childhood: correlation between nailfold capillaroscopy findings and clinical and laboratory data.

OBJECTIVE: Nailfold capillaroscopy is an important tool for the diagnosis and follow-up of patients with rheumatic diseases, in particular dermatomyositis and scleroderma. A relationship has been observed in adults between improved capillaroscopic findings and reduced disease activity. Our aim was to correlate disease activity (clinical and laboratory data) and nailfold capillaroscopy findings in 18 patients with inflammatory myopathies. METHODS: This prospective study included 13 juvenile dermatomyositis patients (Bohan and Peter criteria) (mean age of 8.8 years) and five patients with overlap syndrome (mean age of 15.7 years). We evaluated disease activity (skin abnormalities and muscle weakness, muscle enzymes and acute phase reactants) and its correlation with nailfold capillaroscopy findings (dilatation of isolated loops, dropout of surrounding vessels and giant capillary loops). We used a microscope with special light and magnification of 10 to 16X. RESULTS: Eighteen patients underwent a total of 26 capillaroscopic examinations, seven of them on two or more occasions (13 were performed during the active disease phase and 13 during remission). Twelve of the 13 examinations performed during the active phase exhibited scleroderma pattern and 8 of the 13 examinations performed during remission were normal. Therefore, in 20 of the 26 examinations clinical and laboratory data and nailfold capillaroscopy findings correlated (p = 0.01). CONCLUSIONS: Nailfold capillaroscopy is a non-invasive examination that offers satisfactory correlation with disease activity and could be a useful tool for the diagnosis and follow-up of inflammatory myopathies.

Adolescent↗

PubMed2000

Mechanisms for neuronal degeneration in amyotrophic lateral sclerosis and in models of motor neuron death (Review).

Amyotrophic lateral sclerosis (ALS), also referred to as motor neurone disease, is a fatal neurological disease that is characterized clinically by progressive muscle weakness, muscle atrophy, and eventual paralysis. The neuropathology of ALS is primary degeneration of upper (motor cortical) and lower (brainstem and spinal) motor neurons. The amyotrophy refers to the neurogenic atrophy of affected muscle groups, and the lateral sclerosis refers to the hardening of the lateral white matter funiculus in spinal cord (corresponding to degeneration of the corticospinal tract) found at autopsy. Because the mechanisms for the motor neuron degeneration in ALS are not understood, this disease has no precisely known causes and no effective treatments. Very recent studies have identified that the degeneration of motor neurons in ALS is a form of apoptotic cell death that may occur by an abnormal programmed cell death (PCD) mechanism. In order to treat ALS effectively, we need to understand the mechanisms for motor neuron apoptosis more completely. Future studies need to further identify the signals for PCD activation in neurons as they relate to the pathogenesis of ALS and to clarify the molecular pathways leading to motor neuron apoptosis in animal and cell culture model systems. These studies should lead to a better understanding of motor neuron death and to the design of new therapeutic experiments critical for the future treatment of ALS.

Amyotrophic Lateral Sclerosis↗

PubMed1999

Amyotrophic lateral sclerosis: Lou Gehrig's disease.

Amyotrophic lateral sclerosis (ALS), commonly called Lou Gehrig's disease, is a progressive neuromuscular condition characterized by weakness, muscle wasting, fasciculations and increased reflexes. Approximately 30,000 Americans currently have the disease. The annual incidence rate is one to two cases per 100,000. The disease is most commonly diagnosed in middle age and affects more men than women. It usually presents with problems in dexterity or gait resulting from muscle weakness. Difficulty in speaking or swallowing is the initial symptom in the bulbar form of the disease. Over a period of months or years, patients with ALS develop severe, progressive muscular weakness and other symptoms caused by loss of function in both upper and lower motor neurons. Sphincter control, sensory function, intellectual abilities and skin integrity are preserved. Patients become completely disabled, often requiring ventilatory support and gastrostomy. Death usually occurs within five years of diagnosis and is attributed to respiratory failure or cachexia. The etiology of the disease is unknown. Current research is focused on abnormalities of neuronal cell metabolism involving glutamate and the role of potential neurotoxins and neurotrophic factors. New drugs are being developed based on these theories. Current management involves aggressive, individualized alleviation of symptoms and complications.

Amyotrophic Lateral Sclerosis↗

PubMed2000

Survey of the late consequences of polio in Edinburgh and the Lothians.

OBJECTIVE: This study aimed to identify the nature and frequency of new symptoms and associated disabilities experienced by people who suffered poliomyelitis many years ago, and their access to hospital services. DESIGN: Postal survey regarding symptoms, disability (Office of Population Censuses & Surveys (OPCS) disability questionnaire), and experience of services. SUBJECTS & SETTING: People known to the British Polio Fellowship and the regional rehabilitation service who had previously had polio and were resident in Edinburgh and the Lothians. RESULTS: The study population of 125 people had a median age of 59 years, and 60% were female. The most common symptoms, present in over 60%, were: cold intolerance, fatigue, increased and new muscle weakness, muscle and joint pain, and sleep disturbance. Motor disabilities, particularly of lower limbs, were prominent. Patient contact with hospital services in the preceding five years was: clinic (62%); physiotherapy (46%); occupational therapy (29%); speech therapy (2%); wheelchair service (42%); orthotics (40%). CONCLUSIONS: New problems are sufficiently frequent and severe to warrant a more detailed study to quantify the health care requirements of the post-polio population.

Adult↗

PubMed1992

Dystrophin test in differential diagnosis of childhood muscular dystrophies.

Two cases of childhood muscular dystrophy are described. One of them had clinical features suggestive of Emery-Dreifuss muscular dystrophy and the other with some features of Prader-Willi syndrome, besides proximal muscle weakness. Muscle biopsy from both cases revealed a clear abnormality of dystrophin, and were diagnosed as having Duchenne muscular dystrophy (DMD) by immunofluorescence examination; that is, absent dystrophin at the membrane of the muscle fibers. The clinical spectrum of DMD-related myopathies and the importance of dystrophin testing in childhood muscular dystrophies is discussed.

Biopsy↗

PubMed2003

[Two distinct types of neuropathy associated with Sjögren's syndrome developed in one patient. The importance of the selection of an appropriate therapeutic regimen].

A 62-year-old woman was admitted to our hospital because of muscle weakness and sensory disturbance in extremities. She showed weakness, muscle atrophy and sensory abnormality in four limbs with patchy distribution, suggesting involvement of multiple peripheral nerve trunks. Serum titers of anti-SS-A, SS-B, and antinuclear antibody were elevated. Sural nerve biopsy showed recanalization and lymphocytic infiltration in the epineural small vessels, suggesting the presence of vasculitis. She was diagnosed as having vasculitic neuropathy complicated with Sjögren's syndrome. Methylprednisolone pulse therapy followed by oral prednisolone was started and these symptoms gradually improved in one month. At age 63, she felt dysesthesia in the right lower limb and this sensory abnormality spreaded to upper limbs. Two years later, she was admitted again due to clumsiness of hands and gait disturbance. Neurological examination showed decreased vibration and position sense of lower limbs and limb ataxia in addition to dysesthesia. Electrophysiological studies demonstrated significant decrease in amplitude of sensory nerve action potentials and delayed somatosensory evoked potentials after N13, indicating impairment of dorsal root ganglions. She was treated with intravenous immunoglobulin (400 mg/kg, total 15 g/day) for 5 days. One week later, sensory ataxia was improved. It has been known that Sjögren's syndrome is often complicate with various types of neuropathies including vasculitic neuropathy and sensory neuropathy. Our patient developed these two different types of neuropathies which were dramatically improved after two different therapeutic regimens; indicating the importance to select a suitable treatment regimen in accordance with the mechanism of neuropathy associated with Sjögren's syndrome.

Adrenal Cortex Hormones↗

PubMed1991

[Delayed manifestation of mitochondrial myopathy--complex I and IV deficiency of the mitochondrial respiratory chain with progressive paresis].

We describe a 53-year-old patient with a progressive mitochondrial myopathy of late-onset, restricted to skeletal muscle only without external ophthalmoplegia. The myopathy developed at the age of 46 years initially with exercise intolerance and subsequently progressive permanent muscle weakness. Muscle biopsy revealed severe myopathic changes, ragged red fibers, and a marked multifocal cytochrome-c-oxidase deficiency. Biochemical analysis showed a deficiency of complexes I and IV of the mitochondrial respiratory chain. Genetic analysis of mitochondrial DNA revealed no deletions. Mitochondrial myopathies restricted to skeletal muscle have to be considered in the differential diagnosis of late-onset progressive myopathies.

Biopsy↗

PubMed1988

[McArdle disease: differential diagnosis of the increase in creatine kinase induced by the exercise test].

In a Turkish couple presenting atypical precordial pain, muscle pain and a massive increase of creatine kinase during and one day after bicycle ergometry, suspicion of McArdle's disease was confirmed by a pathologic ischemic forearm worktest, a pathologic serial stimulation test and by pathologic glycogen content with lack of myophosphorylase activity on histochemical examination of thigh muscle tissue. Characteristic signs of McArdle's disease such as muscle weakness, muscle pain and muscle swelling, especially after exertion, were detected only after specific questioning of the patients. McArdle's disease was also detected by phosphor nuclear resonance in the two male children. Frequent consanguinity in the small isolated mountain village where the family originated explains why all four members of two generations are affected by the autosomal recessive disease.

Adult↗

PubMed1980

Congenital non-progressive myopathy, associated with scoliosis--clinical, histological, histochemical and electron microscopic studies of seven cases.

Five cases of central core disease, one case of multicore disease and one case of non-specific myopathy, all of which were associated with scoliosis, were studied in regard to clinical features, histology, histochemistry and electron microscopy. The characteristic clinical features were non-progression, delayed motor development and proximal muscle weakness. Muscle biopsy was the most important diagnostic procedure. Routine histology might not reveal core regions where oxydative enzymatic activity was decreased or was absent in the muscle fibers, but histochemistry disclosed clearly single or multiple core regions. Electron microscopy showed a structured or unstructured core in central core disease. Scoliosis was commonly associated and was very similar to idiopathic scoliosis. Some curves did not progress while others progressed and did not cease progression with maturation. Surgical correction and stabilization was carried out on two cases without complication. The importance of recognition of these myopathies was emphasized.

Adolescent↗

PubMed1995

Classification criteria for polymyositis and dermatomyositis.

OBJECTIVE: The establishment of classification criteria for polymyositis (PM) and dermatomyositis (DM). METHODS: Questionnaires inquiring about patients with DM, PM, systemic lupus erythematosus, progressive systemic sclerosis and noninflammatory neuromuscular diseases were distributed to the main medical institutes in Japan. Data were collected and analyzed by computer. RESULTS: Among skin lesions of DM, heliotrope rash, Gottron's sign and erythema or purpura on the extensor surfaces of the extremity joints were shown to be distinguishing criteria. In both DM and PM, proximal muscle weakness, muscle grasping and spontaneous pain, nondestructive arthritis or arthralgia, elevated CK or aldolase level, presence of systemic inflammatory signs, myogenic changes on EMG, positive and anti Jo-1 antibody and pathologic findings compatible with inflammatory myositis were distinguishing criteria items. CONCLUSION: When a patient satisfies one of 3 skin lesion items and at least 4 other items, he or she shall be classified as having DM, sensitivity 94.1%. When a patient satisfies at least 4 items other than skin lesion items, he or she shall be classified as having PM, sensitivity 98.9%. Specificity of DM and PM is 95.2%.

Dermatomyositis↗

PubMed1993

Progressive nemaline rod myopathy in a woman coinfected with HIV-1 and HTLV-2.

Nemaline-rod myopathy was recently reported in eight young males infected with human immune deficiency virus type 1 (HIV-1). A 41-year-old woman had a 2-year history of progressive proximal-muscle weakness. Muscle biopsy demonstrated the presence of nemaline rods, predominantly in type 1 fibers. She was coinfected with HIV-1 and HTLV-2, as evidenced by positive polymerase chain reaction and serology. There was no lymphopenia or CD4 lymphopenia, despite an abnormal T-cell subset ratio, high CD8 count, skin anergy, and depressed in vitro response to mitogens. This case raises the possibility that dual infection may play a role in the pathogenesis of the rare nemaline-rod myopathies of HIV-infected patients.

Adult↗