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Results for “Muscle Weakness”

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PubMed1984

Glucose-dependent lactate production by homogenates of neuronal tissues prepared from rats treated with 2,4-dithiobiuret, acrylamide, p-bromophenylacetylurea and 2,5-hexanedione.

Chronic treatment of rats with dithiobiuret (DTB) produces a delayed onset muscle weakness and, as suggested by a preliminary study, a distal axonopathy. An inhibition of glycolysis resulting in an energy deficit has been suggested as a possible mechanism of neurotoxin-induced distal axonopathies. To determine whether chronic DTB administration (1 mg/kg/day X 7 days; sacrificed on Day 7) might be associated with a perturbation of glucose metabolism in neuronal tissues, lactate production was measured in brain and spinal cord homogenates prepared from rats which exhibited hindlimb skeletal muscle weakness. Kinetic and statistical analysis showed that glucose-dependent lactate production in these homogenates was not different from that of controls. Lactate production was also determined in brain homogenates prepared from rats intoxicated with acrylamide (50 mg/kg/day X 9 days; sacrificed on Day 9), p-bromophenylacetylurea (200 mg/kg/day X 2 days; sacrificed on Day 14) or 2,5-hexanedione (400 mg/kg/day X 21 days; sacrificed on Day 21). The results indicated that whereas 2,5-hexanedione produced a slight decrease in Vmax, acrylamide and p-bromophenylacetylurea did not cause changes in glucose-dependent lactate production. These findings do not support the suggestion that an inhibition of glycolysis represents a common biochemical lesion associated with neurotoxins which cause delayed onset muscle weakness and distal axonopathy.

Acrylamide↗

PubMedDate not supplied

Prevalence and correction of 25(OH) vitamin D deficiency in peritoneal dialysis patients.

BACKGROUND: Peritoneal dialysis (PD) patients are at risk for 25(OH) vitamin D deficiency due to effluent loss in addition to traditional risk factors. OBJECTIVES: To measure 25(OH) vitamin D deficiency in prevalent PD patients, to evaluate a replacement dose, and to determine the effects of correction. METHODS: 25(OH) vitamin D levels were drawn on prevalent PD patients. Patients deficientin 25(OH) vitamin D were given ergocalciferol, 50000 IU orally once per week for 4 weeks. Patients scored muscle weakness, bone pain, and fatigue on a scale of 0 (none) to 5 (severe). Serum calcium, phosphate, parathyroid hormone (PTH), and 25(OH) vitamin D, and 1,25(OH)2 vitamin D levels were obtained before and after treatment. RESULTS: 25(OH) vitamin D levels were measured in 29 PD patients. Deficiency (<15 ng/mL) was found in 28/29 (97%); 25/29 (86%) had undetectable levels (<7 ng/mL). One course of ergocalciferol corrected the deficiency in all but 1 patient, who required a second course. Scores for muscle weakness and bone pain fell from pre- to posttreatment (p < 0.001). 1,25(OH)2 vitamin D levels rose post ergocalciferol (from 20 to 26 pg/mL, n = 20, p = 0.09). Serum calcium, phosphate, and PTH levels did not change with ergocalciferol. CONCLUSIONS: Most PD patients had marked 25(OH) vitamin D deficiency, which was readily and safely corrected with one course of 50000 IU ergocalciferol, having no effect on serum calcium, phosphorus, or PTH, but complaints of muscle weakness and bone pain decreased. A prospective, placebo-controlled double-blinded study is needed to determine whether replacement of 25(PH) vitamin D is beneficial in PD patients.

Administration, Oral↗

PubMed2003

Spinal accessory neuropathy, droopy shoulder, and thoracic outlet syndrome.

Droopy shoulder has been proposed as a cause of thoracic outlet syndrome. Two patients developed manifestations of neurovascular compression upon arm abduction, associated with unilateral droopy shoulder and trapezius muscle weakness caused by iatrogenic spinal accessory neuropathies following cervical lymph node biopsies. The first patient developed a cold, numb hand with complete axillary artery occlusion when his arm was abducted to 90 degrees. The second patient complained of paresthesias in digits 4 and 5 of the right hand, worsened by elevation of the arm, with nerve conduction findings of right lower trunk plexopathy (low ulnar and medial antebrachial cutaneous sensory nerve action potentials). Spinal accessory nerve grafting (in the first patient) coupled with shoulder strengthening physical exercises in both patients resulted in gradual improvement of symptoms in 2 years. These two cases demonstrate that unilateral droopy shoulder secondary to trapezius muscle weakness may cause compression of the thoracic outlet structures.

Accessory Nerve↗

PubMed1998

Lysosomal glycogen storage disease with normal acid maltase with early fatal outcome.

In a male infant who had cardiomyopathy, generalized muscle weakness and increased serum creatine kinase levels, his muscle biopsy revealed myopathic changes with tiny intracytoplasmic vacuoles containing PAS-positive material and high acid phosphatase activity, but had normal acid maltase activity biochemically. These findings were consistent with those seen in lysosomal glycogen storage disease with normal acid maltase (Danon disease). Sarcolemmal indentations commonly seen in this disease were missing, but a complement membrane attack complex, C5b-9 was positive along the surface membrane of the muscle fibers as seen in X-linked vacuolar myopathy. The patient was on a respirator and died at 27 months of age from pneumonia and hypertrophic cardiomyopathy. Lysosomal glycogen storage disease with normal acid maltase may be manifested at birth with marked skeletal and cardiac involvement leading to death in early infancy.

Biomarkers↗

PubMedDate not supplied

Profiles of neuromuscular diseases. Hereditary motor and sensory neuropathy, types I and II.

Data were collected prospectively for an impairment and disability profile for 86 hereditary motor and sensory neuropathy, types I and II (HMSN) subjects over a 10-yr period. Our data confirm that HMSN is a slowly progressive disorder that has a very heterogeneous phenotypical expression. The disorder was characterized primarily by diffuse muscle weakness with prominent distal atrophy. The mean manual muscle test (MMT) strength grade for all muscle groups combined was 3.9 +/- 0.7 MMT units. There was a slowly progressive decline in strength, only -0.15 MMT units per decade. Distal muscle groups were weaker than proximal muscles, and the decline in strength of the ankle muscles was greater than for the proximal muscles. There was no side dominance. Anthropometric data revealed that distal atrophy may be masked by subcutaneous fat in female subjects. On average, HMSN subjects produced 20-40% less force than normal controls, using quantitative isometric and isokinetic strength measures, even when MMT scores were normal. Pulmonary and cardiac abnormalities were uncommon, as were spine deformity and joint contractures. Only 1 individual had severe restrictive lung disease, and 12 (14%) had a history of significant respiratory complications with no age or disease duration effect. As with the other neuromuscular diseases, maximum expiratory pressure was more affected than forced vital capacity. Fourteen individuals (30%) had abnormal electrocardiograms, and six (7%) had a history of significant cardiovascular complications with no age or disease duration effect. Kyphosis was the major spine deformity. Cardiopulmonary responses to exercise testing were markedly abnormal, showing reduced aerobic capacity. Functional evaluations and timed motor performance tests showed only mild disability in most individuals. With timed motor performance testing muscle weakness translated to impaired motor performance skills. Overall, mean scores on intellectual function and neuropsychologic profiles were normal.

Adult↗

PubMedDate not supplied

Polymyositis and hepatitis concurrent with breast cancer.

OBJECTIVE: To present a rare case of breast cancer associated with both inflammatory muscle disease and liver disease as a paraneoplastic syndrome. CLINICAL PRESENTATION AND INTERVENTION: A woman with breast cancer presented with elevated liver enzymes and progressive proximal muscle weakness. Liver biopsy was consistent with hepatitis and muscle biopsy revealed myositis. The start of corticosteroid therapy was followed by relief of the myopathic symptoms and regression of hepatitis histopathologically. CONCLUSION: A case of polymyositis and hepatitis associated with breast cancer and their flare-up with recurrence of malignancy is presented. In this case, the temporal relation with malignancy following its concurrent remission and relapse suggests a paraneoplastic mechanism.

Autopsy↗

PubMed2001

[A patient of chronic graft-versus-host disease presenting simultaneously with polymyositis and myasthenia gravis].

We report a patient of polymyositis and myasthenia gravis as manifestations of chronic graft-versus-hot disease (GVHD). A 48-year-old man was diagnosed as having chronic myelogenous leukemia at the age of 42 years, and had bone marrow transplantation (BMT) two years after the onset of the disease. Since he suffered from mild liver dysfunction and cutaneous involvement manifesting chronic GVHD, he was placed on prednisolone and cyclophosphamide. As his condition improved, the prednisolone was gradually tapered. Forty-one months after the BMT, the patient developed muscle pain and muscle weakness. A diagnosis of polymyositis was made from muscle biopsy and laboratory findings. An increase in the prednisolone dose was effective but a few weeks later the patient noticed ptosis and recurrence of muscle weakness. A tensilon test and anti-acetylcholine receptor antibody produced positive results, leading to a diagnosis of myasthenia gravis. Only one case of polymyositis and myasthenia gravis as manifestations of chronic GVHD has been reported, and in our patient both symptoms appeared almost at the same time. Although neuromuscular symptoms as a manifestation of chronic GVHD are rare, all patients receiving BMT should be carefully followed up neurologically to detect neuromuscular complications.

Bone Marrow Transplantation↗

PubMed1983

Natural history of potassium-deficiency myopathy in the dog: role of adrenocorticosteroid in rhabdomyolysis.

Potassium deficiency occurs in several conditions and is reported to cause muscle weakness and rhabdomyolysis. The mechanisms by which potassium deficiency cause muscle disease remain unknown, but the primary purpose of the present study was to determine whether abnormal muscle glycogen metabolism causes muscle weakness, as suggested by previous work. We monitored the natural history of potassium deficiency in two groups of dogs, one of which also received deoxycorticosterone acetate (DOCA), an agent commonly used in other studies to accelerate potassium loss. Group I dogs on potassium-free diet alone showed a 41% decrease in muscle potassium, no change in serum CO2, creatine kinase (CK), or muscle phosphorylase activity and only mild histopathologic abnormalities before death, after 198 +/- 42 days on the diet (mean +/- S.D.). In contrast, group II dogs on the same diet plus DOCA developed clinically similar severe weakness and died more rapidly than group I, 37 +/- 7 days (p less than 0.03). DOCA dogs showed a more rapid decrease in muscle potassium to the same level as group I, a 37% increase in serum CO2, an increase in serum CK to 1060 to 2775 IU/ml, a 23% decrease in muscle phosphorylase activity, and severe muscle histopathology, including rhabdomyolysis. Neither group showed any change in body weight, electromyogram (EMG), muscle glycogen concentration, glycogen synthetase activity, serum or muscle magnesium or phosphorus, or serum T3 or T4. In conclusion, dietary potassium deficiency in dogs causes severe weakness and death without causing rhabdomyolysis or abnormal muscle glycogen metabolism. Adding DOCA to the potassium-free diet creates a different model characterized by rapid clinical deterioration and rhabdomyolysis.

Animals↗

PubMedDate not supplied

Low grip strength, impaired tongue force and hyperactivity induced by overexpression of neurotrophin-3 in mouse skeletal muscle.

Transgenic mice overexpressing neurotrophin-3 (NT-3) in skeletal muscle (mlc/NT-3 mice) develop abnormal muscle spindles in skeletal muscle and display abnormal motor function in the form of gait and locomotive disturbances. The purpose of this work was to characterize the functional consequences of NT-3 overexpression in skeletal muscle with further behavioral assessments that permitted inferences about muscle weakness in the tongue or forelimbs as well as potential central nervous system (CNS) abnormalities compared to wild-type controls. Wild-type (n=12) and mlc/NT-3 (n=12) male mice were tested in five procedures (in chronological order): lick dynamics, locomotor activity, grid ataxia, go-no-go discrimination procedure, and grip strength. Relative to wild-type mice, the mlc/NT-3 mice exhibited lower tongue force, hyperactivity, slowed limb retrieval in the grid ataxia test, similar discrimination performance, and lower grip strength. Overall, the data suggest that chronically elevated levels of NT-3 in mouse skeletal muscle cause muscle weakness in the mlc/NT-3 mice. Surprisingly, mlc/NT-3 mice also exhibited significant hyperactivity, suggesting that NT-3 overexpression in the periphery may have caused abnormalities in the CNS that are related to the cortical processing of proprioceptive afferent information.

Afferent Pathways↗

PubMed1991

Correlation of histopathological and clinical findings in neuromuscular diseases.

Our file comprises bioptic and necroptic materials of skeletal muscles: progressive spinal muscle atrophy of adults 16, amyotrophic lateral sclerosis 12, infantile progressive spinal amyotrophy Werdnig-Hoffmann 9, chronic progressive amyotrophy Oppenheim 6, syringomyelia and syringobulbia 3, conditions after spinal cord accidents. Diagnosis was difficult because one time the neurological marks were at the head and other time the muscular ones. In the clinical picture there was muscle weakness and atrophy, the spontaneous and palpation painfulness was missing. Muscle weakness und its intensity did not correspond to the degree of muscle atrophies. The discrepancies of electromyographic and histopathologic pictures are explained by occurrence of so-called concomitant myopathies, which arise most probably from the disorders of histioceptive-proprioceptive system.

Electromyography↗

PubMed2006

Evaluation of patients with paramyotonia at 23Na MR imaging during cold-induced weakness.

PURPOSE: To prospectively examine whether sodium 23 (23Na) magnetic resonance (MR) imaging can be used to visualize acute intracellular Na+ accumulation and the effects of specific therapy in patients with paramyotonia congenita (PC). MATERIALS AND METHODS: Ethics committee approval and informed consent were obtained. Sixteen patients (four women, 12 men; mean age, 46.7 years +/- 16.7 [standard deviation]) with confirmed PC and 10 healthy volunteers (three women, seven men; mean age, 26.6 years +/- 3) were examined by using a 1.5-T MR system with a 16.8-MHz surface coil. 23Na MR imaging was performed before and after local cooling of the nondominant lower leg and exercising, with experimentally induced weakness scored by a neurologist. The 23Na MR examination was repeated in 13 patients and all volunteers after 3 days and, additionally, in seven patients after 4 days of oral administration of mexiletine, which blocks Na+ channels. The 23Na MR protocol comprised two-dimensional (2D) fast low-angle shot (FLASH), 2D radial, and free induction decay (FID) sequences. The FID data were fitted to a biexponential decay curve to evaluate the slow and fast components of the T2 relaxation time. Fast and slow components were assigned to intra- and extracellular Na+ concentrations, respectively. Radial and FLASH MR images were evaluated by means of a region-of-interest analysis by using 0.3% saline solution for reference. T1- and T2-weighted MR imaging were also performed. Data were analyzed by using a parametric t test. RESULTS: After exercising, all patients developed considerable weakness exclusively in the cooled lower leg; no weakness was observed in volunteers. In patients, all 23Na MR images showed a significant increase in 23Na signal intensity in the cooled lower leg (P < .001) in comparison with nonsignificant findings in volunteers. After treatment with mexiletine, cooling and exercise induced almost no muscle weakness and no changes in 23Na MR signal intensity in patients. CONCLUSION: 23Na MR imaging enables visualization of muscular Na+ accumulation associated with muscle weakness in patients with PC, and effects of specific therapy can be detected.

Adult↗

PubMed2005

An adolescent with pharyngeal-cervical-brachial variant of Guillain-Barré syndrome after cytomegalovirus infection.

A 15-year-old Japanese girl developed bulbar palsy and upper limb-dominant muscle weakness 2 weeks after the onset of an upper respiratory tract infection due to cytomegalovirus (CMV). Her symptoms resembled that seen in the pharyngeal-cervical-brachial variant (PCB) of Guillain-Barré syndrome (GBS). Although bulbar palsy usually continues for several months in PCB, her bulbar palsy was very mild and improved rapidly before intravenous immunoglobulin therapy was instituted. Serum anti-GT1a IgG antibody titer was elevated at the acute phase of the disease and gradually decreased. The bulbar palsy-dominant GBS is thought to relate to anti-GT1a antibody and Campylobacter jejuni infection in adult patients. Our Case report suggests that CMV can also induce the production of anti-GT1a antibody, thereby resulting in PCB. When one sees acute onset bulbar palsy and limb muscle weakness, the possibility of PCB, even in children, should be considered, thus compelling the need for serum anti-ganglioside antibody measurement.

Adolescent↗

PubMed2000

Distal myopathy in nephropathic cystinosis.

In long-standing nephropathic cystinosis complications are observed in various organs. Distal myopathy was first described in detail in 1994. The prevalence was calculated to be 24%. We studied seven patients with nephropathic cystinosis with neurophysiological techniques. Only two patients complained of a distal muscle weakness but all showed signs of myopathy on electromyography, which was more pronounced in the distal muscles. Motor and sensory nerve conduction parameters were within normal ranges. One patient with the juvenile form of nephropathic cystinosis also had myopathy. We conclude that distal myopathy can be detected in nephropathic cystinosis even in the absence of clinically overt muscle weakness. Cystine-depleting therapy with cysteamine is recommended for all patients with cystinosis, even after renal transplantation, and the effect on the myopathy should be studied.

Adolescent↗

PubMed2001

The outbreak of West Nile virus infection in the New York City area in 1999.

BACKGROUND: In late August 1999, an unusual cluster of cases of meningoencephalitis associated with muscle weakness was reported to the New York City Department of Health. The initial epidemiologic and environmental investigations suggested an arboviral cause. METHODS: Active surveillance was implemented to identify patients hospitalized with viral encephalitis and meningitis. Cerebrospinal fluid, serum, and tissue specimens from patients with suspected cases underwent serologic and viral testing for evidence of arboviral infection. RESULTS: Outbreak surveillance identified 59 patients who were hospitalized with West Nile virus infection in the New York City area during August and September of 1999. The median age of these patients was 71 years (range, 5 to 95). The overall attack rate of clinical West Nile virus infection was at least 6.5 cases per million population, and it increased sharply with age. Most of the patients (63 percent) had clinical signs of encephalitis; seven patients died (12 percent). Muscle weakness was documented in 27 percent of the patients and flaccid paralysis in 10 percent; in all of the latter, nerve conduction studies indicated an axonal polyneuropathy in 14 percent. An age of 75 years or older was an independent risk factor for death (relative risk adjusted for the presence or absence of diabetes mellitus, 8.5; 95 percent confidence interval, 1.2 to 59.1), as was the presence of diabetes mellitus (age-adjusted relative risk, 5.1; 95 percent confidence interval, 1.5 to 17.3). CONCLUSIONS: This outbreak of West Nile meningoencephalitis in the New York City metropolitan area represents the first time this virus has been detected in the Western Hemisphere. Given the subsequent rapid spread of the virus, physicians along the eastern seaboard of the United States should consider West Nile virus infection in the differential diagnosis of encephalitis and viral meningitis during the summer months, especially in older patients and in those with muscle weakness.

Adolescent↗

PubMed1989

[Detection of immune complexes in the sera and around the muscle fibers in a case of myasthenia gravis and polymyositis].

A case of myasthenia gravis accompanied with polymyositis and malignant thymoma, detected immune complexes in the sera and around the muscle fibers, was described. A 37-year-old woman was admitted to Shinshu University Hospital in September, 1987 because of dyspnea, dysphagia and muscle weakness. She first noticed her right blepharoptosis 3 weeks before admission. Weakness of all four limbs and myalgia of lower extremities were noticed one week later. These symptoms got worse and nocturnal dyspnea, dysphagia and easy fatigability at mastication appeared. On admission, she looked ill and neurological examination revealed left blepharoptosis, bilateral facial weakness, weakness of all four limbs, more prominent in proximal muscles and tenderness of lower extremities. Edrophonium test was positive, improving her muscle weakness. Laboratory examination revealed the elevated serum levels of CK, the increased titre of circulating immune complexes and high titres of acetylcholine receptor antibodies and anti-skeletal muscle antibodies. Electromyographic study showed myogenic pattern and Harvey-Masland test revealed waning at low frequency stimulation. Muscle biopsy showed marked perivascular infiltration of lymphocytes, accompanied by phagocytosis and interstitial fibrosis. IgG deposits were shown around the muscle fibers exclusively around the infiltrates of mononuclear cells. Granular deposits of C3 were also shown specifically around the muscle fibers exclusively around the infiltrates of mononuclear cells. Thymectomy was performed on September 21, 1987. Invasion of thymoma, predominantly lymphocytic type, to right lung and pericardium was observed histologically. After thymectomy, she got better. Immunological data and immunohistochemical examination of the present case suggest that in the case of myasthenia gravis accompanied with polymyositis and malignant thymoma, immune complexes may play a primary role on the pathogenesis of myositis.

Adult↗

PubMed1982

Ipecac-induced myopathy simulating dermatomyositis.

We studied a young woman with an eating disorder. To induce vomiting, she took syrup of ipecac daily for 2 years, and then developed insidious, progressive muscle weakness. Skin findings were similar to those of dermatomyositis. Muscle biopsy, however, was similar to experimental emetine myopathy and lacked inflammatory features. Upon cessation of ipecac abuse, strength returned. We believe that this patient had ipecac-induced muscle weakness.

Adult↗

PubMed1993

Vacuolar myopathy sparing the quadriceps.

Twenty-two Jewish patients, belonging to 15 families, 11 of them from Iran and three possibly of Iranian stock, suffered from progressive muscle weakness and wasting. The initial symptom was usually distal leg muscle weakness, appearing in the third or fourth decade and insidiously involving the proximal muscles and to a lesser extent the upper limbs. The quadriceps muscle was consistently spared even in advanced cases. Computerized tomography (CT) scans of muscles demonstrated variable wasting and fatty replacement of limb and axial muscles, while the vastus lateralis muscle retained its normal CT appearance. The typical light microscopy features of the affected muscles were: presence of vacuoles within muscle fibres, internal nuclei, longitudinal fibre splitting and, in severely affected muscles, endomysial fibrosis without, inflammation or fibre necrosis. Electron microscopy suggested that the vacuoles were autophagic. Cytoplasmic and intranuclear inclusions were rare. While electromyography (EMG) revealed presence of spontaneous activity, however, analysis of muscle action potentials, turns-amplitude ratio, macro-EMG and single fibre EMG suggested a primary myopathic disorder. Consanguinity in seven families, the parents being first cousins, and the presence of additional affected siblings of both sexes may suggest an autosomal recessive trait. The presence of this disorder in Iranian Jews may indicate that this is a distinct myopathic entity.

Action Potentials↗

PubMed1989

[A nosological study of a patient showing ataxia & lower motor neuron involvement].

A sporadic case of spinocerebellar degeneration with prominent involvement of the motor system has recently been encountered. A 54-year-old man without family history noticed speech disturbance at the age of 46 and weakness in his right hand the following year. The muscle weakness and atrophy were slowly progressive and made walk impossible at the age of 50, when his dysphagia increased. At the age of 54, he was admitted to our hospital when neurological findings revealed marked amyotrophy of general skeletal muscle and tongue with fasciculation. Deep tendon reflexes were decreased. Cerebellar ataxia was impossible to evaluate because of profound muscle weakness. And sensory disturbance was suspected in the distal portion of the lower extremities. CT scan revealed progressive atrophy of the brain stem and cerebellum. The patient died at the age of 54 due to CO2 narcosis. The clinical course was 8 years. A summary of the pathological findings was as follows: 1) Marked neuronal loss of the anterior horn of the spinal cord and motor cranial nerve nuclei except for oculomotor nuclei, with mild degeneration of pyramidal tract below lumbosacral level. 2) Degeneration of cerebellipetal system, spinocerebellar tract, Clarke's column and the middle root zone and cerebellifugal system, dentate nucleus, superior cerebellar peduncles, and red nucleus. 3) Mild degeneration of pontine nuclei, inferior olivary nuclei, pontine transverse fibers, the middle and inferior cerebellar peduncles, cerebellar white matter and Purkinje cells as in OPCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyotrophic Lateral Sclerosis↗