Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used automatic decomposition electromyography (ADEMG) to study 41 muscles in 29 patients with well-defined peripheral and central motor disorders. In motor neuron diseases motor unit action potentials (MUAPs) showed increased amplitudes, firing rates and firing variability. Relatively large MUAPs sometimes were not identified by the computer program if they lacked sufficient high-frequency signal content, or were too variable in shape. In myopathies the MUAPs showed reduced amplitudes, durations and turns, and sometimes dramatic increases in firing rates. Also, the mean number of MUAPs per recording site was often increased, indicating excessive recruitment. In polymyositis (the best studied myopathy) the nature and magnitude of the MUAP shape and firing abnormalities were usually similar at different levels of contractile force, suggesting that motor units are affected without regard to recruitment order. In upper motor neuron paresis (multiple sclerosis), the shape properties of the MUAPs were normal, but mean firing rates were reduced, and firing variability increased. These findings confirm many of the traditional criteria for distinguishing neurogenic from myopathic disease electrophysiologically at the level of the individual MUAP. In addition, they demonstrate the potential diagnostic sensitivity of MUAP firing rate measurements for detecting neuromuscular dysfunction, and for differentiating between some cases of central and peripheral paresis, but not for distinguishing peripheral neurogenic from myopathic weakness, since firing rates tend to increase in both. Increased firing rate variability may be a marker of central or peripheral neurogenic weakness.
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PMID:Motor unit firing rates and firing rate variability in the detection of neuromuscular disorders. 247 26

Neospora caninum infection was diagnosed in 5 young dogs from 2 litters with a common parentage. The pups were born healthy, but developed hind limb paresis 5 to 8 weeks after birth. The predominant lesions were polyradiculoneuritis and granulomatous polymyositis. Neospora caninum was seen microscopically in sections of naturally infected pups, and was isolated in cell cultures, mice, and dogs inoculated with infected canine tissues. Antibodies to N caninum were detected in sera of infected dogs by indirect fluorescent antibody test.
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PMID:Neonatal Neospora caninum infection in dogs: isolation of the causative agent and experimental transmission. 314 21

Experimental inoculation of newborn NMRI mice with Echo virus, type 9, strain A. Barty *ECHO 9 virus AB) resulted in diffuse polymyositis 4 days later. The disease, after a delay of 1 day, increased in intensity and was accompanied by a rapid, progressive paresis leading to death 7-11 days following infection. As early as 24-48 h after inoculation, we detected initial ultrastructural degenerative changes, characterized by segmental dilation fo the sarcoplasmic reticulum. Disruption and breakage of myofibrils followed, and lead to the formation of increasing numbers of contraction bands. Ultimately, virus-mediated nuclear and other organellar injury resulted in muscle fiber necrosis. In addition, we observed some substructural cellular events related to virus propagation. Beginning on the 4th day after infection, pronounced proliferation of the sarcoplasmic-reticulum membranes became evident in perinuclear and subsarcolemmal areas in the mature muscle fibers, myoblasts, and post-fused myotubes of mice inoculated within 18 h after birth. These cytological alterations were not noted in the myoblasts and myotubes of NMRI mice injected with virus 2 or 4 days after birth.
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PMID:Ultrastructural degenerative changes of age-dependent ECHO 9 virus-induced polymyositis in infant mice. 611 16

Newborn mice of different strains (including NMRI) infected with 2-5 x 10(6) pfu of echovirus type 9 strain A. Barty developed progressive flaccid paralysis five days after inoculation, followed by death. Suckling mice injected with the same infective dose two, four, or six days after birth disclosed at most transient paresis and survived. Infectivity titrations revealed in all groups a similar rate of virus multiplication exceeding 10(8) 50% tissue culture infective doses per mouse four days after virus inoculation. Histologically, polymyositis resulting in muscle fiber necrosis was seen. The percentage of damaged muscle tissue declined with increasing age of the experimental groups. It is concluded that in order for paralysis to occur, at least 50% of skeletal muscle tissue must be destroyed by virus-induced lesions before the sixth day of life. Electron microscopy demonstrated additional age-dependent, virus-mediated disturbances of postnatal muscle growth. Reparative events in destroyed muscle fibers seemed to be unaffected in all age groups.
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PMID:Age dependence of paralysis induced by echovirus type 9 in infant mice. 685 75

The clinical and pathological findings in 2 sibling Bloodhound pups with spastic paresis of the pelvic limbs due to toxoplasmosis are described. Macropathology consisted of bilateral atrophy of the musculature of the affected limbs. Histopathology revealed meningo-encephalitis involving the cerebellum and medulla oblongata, diffuse meningomyelitis, radiculoneuritis of the lumbar spinal nerves and polymyositis and atrophy of skeletal muscle. Epizootological investigations failed to determine the source of the infection. Dissemination of the infection by a route other than the haematogenous pathway is considered and discussed.
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PMID:Spastic paresis in two littermate pups caused by Toxoplasma gondii. 731 Jul 96

Polymyositis is characterized by inflammatory process in muscles and muscle weakness is the main clinical sign of the disease. We report a case of a 65-years old woman suffering from polymyositis with flaccid paraparesis. Forms of polymyositis where only proximal muscles of lower extremities are involved are very rare, so it may cause diagnostic mistakes. Because of that, it is very important to pay a special attention when making the diagnose of paresis.
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PMID:[A case of polymyositis with flaccid paraparesis]. 1110 84

Mixed connective tissue disease (MCTD) is a chronic autoimmune disease, which has a broad range of clinical manifestations shared by systemic lupus erythematosus, systemic sclerosis, polymyositis/dermatomyositis, and rheumatoid arthritis. MCTD is featured with high serum titers of anti-ribonucleoprotein antibodies and multiple system involvement. Its spinal cord involvement mainly manifests as transverse myelopathy (TM) and longitudinal extensive transverse myelopathy (LETM). Myelopathy in MCTD is extremely rare, and is usually characterized by serious neurological complications, such as paralysis or muscular paresis, sensory impairment, and smooth muscle dysfunction. Progressive clinical manifestations combined with laboratory examinations and magnetic resonance imaging examinations play important roles in the diagnosis of this disease. In order to prevent permanent neurological damage to the spinal cord, plasmapheresis and intravenous immunoglobulin can be performed in patients at the early disease stage. Early high-dose corticosteroids combined with cyclophosphamide, followed by low doses of immunosuppressors, can improve the long-term prognosis of patients. There are only nine global cases reported on MCTD associated with myelopathy at present. The death rate and disability rate of myelopathy in MCTD are extremely high. In this review, the pathomechanisms, clinical manifestations, auxiliary examination, diagnosis, differential diagnosis, treatment, and prognosis of myelopathy in MCTD were systematically elucidated.
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PMID:Myelopathy associated with mixed connective tissue disease: clinical manifestation, diagnosis, treatment, and prognosis. 3111 2