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)

The importance of the combination of electromyographic examination and the Tensilon test in the diagnosis of Myasthenia gravis pseudoparalytica of the eye muscles is discussed. After intravenous injection of Tensilon in ocular myasthenia, an activity increase is found in the electromyogram, even when the motor effect on the diseased muscle is not recognisable. Myopathies and peripheral neurogenic paresis do not respond to Tensilon.
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PMID:[Electromyography of eye muscles in myasthenia gravis]. 739 81

We present a mother and 2 children with congenital myopathy whose clinical signs were facial paresis in all three, and mild involvement of the lower extremities in the mother and one son. All three presented skeletal abnormalities, hypertelorism, arched palate, retraction of the Achilles tendon or short neck. Symptoms were not progressive and muscle biopsies showed central cores and nemaline rods in the mother and only nemaline rods in the 2 sons. The mother also suffered carpal tunnel syndrome, as had other members of the family as the result of autosomal dominant inheritance.
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PMID:[Congenital myopathy with cores and nemaline rods in one family]. 775 14

We studied a family with late-onset (fifth or sixth decade) or asymptomatic hereditary myopathy of the anterior tibial muscle. The occurrence of the disease in two successive generations pointed out an autosomal dominant pattern of inheritance. The initial symptom was uni- or bilateral foot drop resembling peroneal paresis. Surprisingly many of the diagnosed patients were asymptomatic and considered themselves healthy whether there was any foot drop or not. The anterior tibial muscles were atrophic in patients with foot drop but the long toe extensors were usually and the short ones were always spared. Apparently the toe extensors could relieve the foot drop symptom. As shown by computed tomography there was often an early uni- or bilateral involvement of the semimembranosus muscle in males. The proband showed also a late involvement of the femoral biceps and the minor gluteal muscles. The muscles of the upper extremity were spared. The anterior tibial muscles had a characteristic myopathic alteration with rimmed vacuoles in histopathological study. This picture was most evident in latent cases without atrophy of the anterior tibial muscle, but with distinctly abnormal EMG of that muscle. Non-affected muscles showed only slight non-specific histopathological changes. We suggest that this disease is a new mild variety of autosomal dominant distal myopathy with rimmed vacuoles.
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PMID:Late onset foot-drop muscular dystrophy with rimmed vacuoles. 780 61

We present five patients with distal weakness in the lower extremities with onset in adolescence. Paresis tended to occur in the gastrocnemia in 3 patients and was accompanied by marked elevation of CPK (> 10 times higher than normal). Muscle biopsies showed signs of dystrophy. The clinical picture for these patients was consistent with the diagnosis of recessive distal myopathy (Miyoshi's form). The differential sign in the other 2 cases was greater involvement of the anteroexternal leg muscles and the presence of rimmed vacuoles similar to those characteristic of Nonaka's vacuolar distal myopathy.
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PMID:[Recessive distal myopathies. Five cases]. 789 6

This study investigated the potential value of eccentric (ECC) and concentric (CONC) isokinetic testing for quantifying motor deficit in patients with spastic paresis secondary to motor neuron disease. We hypothesized that, at a moderately fast (120 degrees s-1) angular velocity, spastic patients would demonstrate different ECC-CONC torque relationships from healthy controls or patients with non-spastic neuromuscular disorders. Eleven patients with motor neuron disease having clinical evidence of spasticity, and 11 disease-control patients (with non-spastic disorders, e.g. lower motor neuron disease or myopathy) underwent isokinetic testing. One healthy subject was matched to each of the 22 patients. The average torque generated during maximal voluntary ECC and CONC knee flexion (KF) and extension (KE) was measured using an isokinetic dynamometer (Kin-Com). Reliability was established (all ICC > or = 0.97) for patient torque measurements. Relative strength (% of control subject torque) in spastic patients was significantly higher for ECC than for CONC actions in both KF and KE; conversely, in non-spastic disease-control patients relative strength was not affected by the type of muscle action. The ECC/CONC average torque ratios for KE and KF at 120 degrees s-1 were significantly greater in spastic patients than controls, but did not differ from controls in non-spastic patients. In spastic patients the ECC-CONC imbalances were related to ambulatory dysfunction. In four spastic patients followed with serial testing, the disproportion between ECC and CONC voluntary capacity persisted over time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Eccentric and concentric muscle performance in patients with spastic paresis secondary to motor neuron disease. A preliminary report. 801 93

Pharyngeal constrictor paresis (PHCP) is sometimes found in videoradiography of the swallowing act in patients complaining of dysphagia. Ten patients with PHCP and 10 dysphagic, age- and sex-matched controls with normal videoradiography were neurologically evaluated and examined with magnetic resonance imaging (MRI) of the brain and brainstem in order to learn the pathogenetic process behind PHCP. The study revealed 8 PHCP patients and 1 dysphagic control with abnormal clinical neurological findings such as myopathy, cerebrovascular disease, or extrapyramidal disease. The neurological examination revealed considerable information of prognostic and therapeutic value in PHCP patients. The MRI was abnormal in 7 PHCP patients and 4 dysphagic controls. However, the findings in MRI were nonspecific but the examination was found to be valuable in selected cases. It is concluded that PHCP is an indicator of neurological disease and accordingly, such patients should be examined by a neurologist to establish the cause of the disease.
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PMID:Pharyngeal constrictor paresis: an indicator of neurologic disease? 835 45

Monensin was given via gavage to 5- and 6-week-old broad-breasted white turkeys. The birds were allotted into four groups--three groups given monensin and one group of controls--in two experimental trials. Treated turkeys in Trial 1 received one dose of monensin per day for 4 days at 4.7 mg monensin/kg body weight, 8.8 mg/kg, or 17.6 mg/kg. Treated turkeys in Trial 2 received one dose of monensin per day for 5 days at 1.93 mg/kg, 4.7 mg/kg, or 8.8 mg/kg. Turkeys receiving the lowest dose showed no clinical signs of myopathy. Birds receiving 4.7 mg monensin/kg developed ataxia after the third dose and rear limb paresis and paralysis after the fifth dose. Turkeys receiving 8.8 mg/kg were ataxic after the second dose and paretic or paralyzed after the fourth dose. Turkeys receiving 17.6 mg/kg were ataxic 3 hours after the first dose and paretic or paralyzed 8 hours after the first dose. Histologically, a necrotizing skeletal myopathy was present in the muscles of the rear limbs. A dose-related response was observed in the percentage of myofibers damaged in birds that survived until the end of the trials. Intrafiber edema and vacuolation were observed in histologic sections from myocardium of turkeys from the two highest dose groups.
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PMID:Skeletal myopathy produced with experimental dosing of turkeys with monensin. 845 87

Pharmacologic administration of sedatives is used routinely in the care of the critically ill to enhance patient comfort and optimize care. Long-term administration of NMB drugs is far less frequent but often occurs in patients with greater organ dysfunction. The experience of several authors using NMB drugs in the ICU is summarized in Table 5. Both classes of drugs have potential untoward effects. Some are readily predictable; others are not. NMB drugs enjoy a long record of safe, effective use during the perioperative period, but certain issues linger in defining appropriate administration to critically ill patients. Major concerns focus on the appropriate drug selection and delivery, monitoring, and neuromuscular recovery of patients who receive NMB drugs for longer than 24 hours. The development of myopathy and paresis has been increasingly recognized after prolonged use of NMB drugs in the ICU. Further investigation needs to fully characterize this process, identify those at risk, and outline a mechanism to prevent or limit the injury. Prolonged weakness may occur secondary to changes in the basic pharmacology and elimination of NMB drugs in ICU patients. Pathophysiologic changes in the nerve, muscle, or neuromuscular junction may also play a role in the development of some cases of prolonged weakness or myopathy after discontinuation of NMB drugs. Concerns about the potential for direct or indirect toxicity of NMB drugs to skeletal muscle and in the CNS remain. Resolution of these issues will improve the selection and optimal administration of sedative and NMB drugs in the ICU setting.
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PMID:Complications associated with sedative and neuromuscular blocking drugs in critically ill patients. 853 89

A 70-year old man with acute intermittent porphyria had acute transient bibrachial paresis with moderate contracture of the involved muscles, which showed electrical silence in a conventional electromyographic investigation with surface electrodes placed over the contracted muscle belly (filter: 20 Hz-2 Hz, amplifier 50 microV). Slow finger movements were still possible and showed typical muscle-action potentials. This electroclinical correlation points to myopathic localized dysfunction, perhaps similar to rare case reports with patients having metabolic myopathy of McArdle's type.
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PMID:[Acute intermittent porphyria with transient paresis and contracture. Evidence for initial myopathic dysfunction?]. 955 64

The protozoan parasite Toxoplasma gondii is a serious cause of fetal mortality in sheep and goats. Oocysts, the parasite stage responsible for initiating infection, are produced following a primary infection in cats. A primary infection in pregnant sheep and goats can establish a placental and fetal infection which may result in fetal death and resorption, abortion or stillbirth. Diagnosis is aided by the clinical picture, the presence of characteristic small white necrotic foci in placental cotyledons, the possible presence of a mummified fetus and on fetal serology and histopathology. Development of the polymerase chain reaction (PCR) specific for T. gondii may also provide a valuable diagnostic tool. Measures to control abortion include improved management of farm cats, fodder and water. Vaccination of sheep with the live vaccine is an effective preventive measure and the use of decoquinate in feed may be useful in some situations. Neospora caninum is related to T. gondii and while its asexual life cycle is similar to that of the latter it is currently not known whether it has a similar sexual life cycle in a definitive host. Neospora is an important cause of fetal loss in cattle and parallels that of T. gondii infection in sheep and goats. While it does not appear to cause frequent losses in these latter animals, experimental infection is readily induced in them and if initiated during pregnancy provides a very good model of the bovine infection. Furthermore clinical signs and pathological lesions in sheep and goats are similar to those induced in them by T. gondii, although there are subtle histopathological differences. These changes will aid possible diagnosis as will specific serological tests such as the indirect immunofluorescent antibody test and the enzyme linked immunosorbent assay and the PCR. Sarcocystis, which exists as numerous species, undergoes a coccidian-like life cycle with each having a distinctive definitive (usually carnivore) host which excretes sporocysts into the environment. Clinical sarcocystiosis is much less commonly diagnosed than toxoplasmosis and neither is it normally associated with fetal infection or abortion in either sheep or goats. However, infection is extremely common throughout the world and follows ingestion of food or water contaminated with sporocysts. Clinical signs, when seen, include fever, anaemia, inappetance and weight loss or reduced weight gain. Central nervous signs (hind limb weakness, ataxia, paresis), acute myopathy and death may occur. Diagnosis is difficult as infection is so common and clinical signs absent, mild or non-specific. Serology may be useful in some situations and histopathology/immunohistochemistry is valuable for confirming the cause of death. Control relies on preventing contamination of pasture and water with faeces of dogs, foxes and cats or by controlling access of young susceptible stock to contaminated land. Relatively little is known of the immunity induced by infection with Sarcocystis spp. but research indicates that protective immunity does develop and that cell-mediated mechanisms are probably important. It is likely that sarcocystiosis is underdiagnosed as a problem and that better diagnostic methods are needed to show the true extent of the losses caused. Neosporosis on the other hand would appear not to be so common in sheep and goats. The value of experimental infections in these animals may be to provide a comparative model of the infection in cattle in the same way that our understanding of toxoplasmosis in sheep provides a superior model of human toxoplasmosis.
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PMID:Protozoan infections (Toxoplasma gondii, Neospora caninum and Sarcocystis spp.) in sheep and goats: recent advances. 968 43


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