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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of muscle weakness with hypertension is presented. The patient had symptoms of depression. Diagnosis of hyperaldosteronism was suspected because of a low serum potassium and confirmed by discovery of an adrenal adenoma. The role of hypokalemia in mental disturbances is reviewed. Emphasis is placed on possible metabolic etiologies when mood changes, muscle paresis and hypertension coexist.
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PMID:Hyperaldosteronism (Conn's disease) presenting as depression. 46 62

The use of electromyography (EMG) as a diagnostic aid for equine hyperkalemic periodic paresis (EHPP) was investigated in seven affected and seven control horses. Affected horses were confirmed positive for EHPP either by elevated serum potassium concentration with clinical signs of myotonia, or by inducing hyperkalemia and clinical signs using oral potassium chloride challenge. All horses were asymptomatic at the time EMG was performed, using bipolar fine wire needle electrodes. The myopotentials were recorded on magnetic tape and displayed on paper charts for analysis. Insertional and resting activity were recorded from the right supraspinatus, triceps, extensor carpi radialis and gluteal muscles in standing horses. Myotonic discharges were seen in six of seven affected horses but not in any of the controls. All seven affected horses and two control horses had prolonged insertional activity. Five out of seven affected horses and one control horse displayed spontaneous motor unit discharges unrelated to recording electrode movement. Myoelectrical potentials containing closely timed muscle potentials, i.e. doublets, were found in all affected horses, with four of seven affected horses also showing triplets. These potentials were not observed in any of the controls. No obvious difference in activity was observed among the four muscle sites tested. It is concluded that EMG is a safe and useful tool for diagnosing EHPP in horses not currently displaying clinical signs. Myotonic discharges and doublets appear to be the most diagnostically significant electromyographic abnormalities in EHPP affected horses.
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PMID:Use of electromyography for the diagnosis of equine hyperkalemic periodic paresis. 224 82

A weaner ration containing carbadox at concentrations of 331 to 363 mg/kg was accidentally fed to suckling and weaned pigs in an 84 sow herd. Discarded ration was fed to 36 sows. One hundred and sixty five weaner pigs died in a 10 week period with clinical signs including refusal to eat, ill thrift, the passing of hard pelleted faeces, posterior paresis and death in seven to nine days. The surviving weaners did not thrive and some males showed poor testicular development. Sows and suckling pigs that consumed the ration also failed to thrive as did the progeny of affected sows. The main pathological finding was obliteration of the zona glomerulosa of the adrenal cortex. Increased potassium and decreased sodium concentrations in serum were the most notable and consistent biochemical findings.
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PMID:Accidental carbadox overdosage in pigs in an Irish weaner-producing herd. 271 36

For ten years, severe physical exercise in a 24 year old male patient had been an almost constant trigger of frequent attacks of pareses which were mostly accompanied by complete tetraplegia and once by the occurrence of cardiac arrest with atrial fibrillation. During the attack, the serum potassium concentration fell to 1.2 mmol/l, whereas the intraleukocytic potassium concentration rose from 136 mmol/l to 149 mmol/l. The catecholamine excretion in the urine was raised during the first 24 hours after admission as an emergency (189 micrograms noradrenalin and 54 micrograms adrenalin). After intravenous adrenalin infusion (0.01-0.1 microgram/kg X min) during the symptom-free interval, there was a major fall of the serum potassium concentration from 3.9 mmol/l to 3.1 mmol/l. This was not accompanied by a raised insulin excretion and could be prevented by prior administration of the nonselective beta blocker propranolol. On the basis of these results, the patient was treated prophylactically with three times 40 mg/d p.o. propranolol. Pareses requiring treatment no longer occurred under this therapy.
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PMID:[Severe periodic hypokalemic paralysis. Prevention using beta-receptor blockade]. 288 27

High mortality in two flocks of 1900 turkey breeder hens accidentally fed 280 g monensin/ton of complete feed is described. Mortality attributed to the poisoning was 76% in flock 1 and 18% in flock 2. Clinically, turkeys were found dead, exhibited respiratory distress with wings extended laterally, had fine tremors, or showed posterior paresis and inability to rise. The most striking finding at necropsy was the almost complete absence of gross lesions. Some turkeys had severely congested lungs; however, many did not. A few birds had pale streaks within the adductor muscles of the legs. Microscopic lesions included myofiber degeneration and necrosis of skeletal and myocardial muscle. Serum phosphorus, lactate dehydrogenase, and creatine phosphokinase were markedly elevated, whereas potassium, chloride, and calcium values were lowered.
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PMID:Monensin toxicity in turkey breeder hens. 293 Apr

The case of a 42-year-old man is reported, who on four occasions developed a hypokalaemic periodic paralysis after an intramuscular injection of "Ambene". The detailed examination of this patient shows, that it is the primary, autosomal dominant inherited form of hypokalaemic periodic paralysis, and not the secondary form, which is caused by a renal or gastrointestinal loss of potassium. Clinical and electrophysiological, as well as histopathological and electron microscopic findings are presented, showing the typical vacuolar myopathy with submicroscopic tubular structures. In the literature there is evidence for an increased sensitivity of the muscle membrane to insulin with an increased potassium-shift inside the cell in hypokalaemic periodic paralysis. "Ambene" is a combination, which contains amongst other substances dexamethasone and the local anaesthetic drug lidocain. In the present case the paresis was possibly caused by a combined effect of dexamethasone with a consequent hyperglycaemia and lidocain with a change in the excitability of the muscle membrane. The pathophysiological mechanism of hypokalaemic periodic paralysis is discussed in terms of the release by the combination of these two drugs. It has not previously been reported that "Ambene" can provoke a hypokalaemic periodic paralysis. This is a severe side effect because of the resulting cardiac and respiratory problems.
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PMID:[Hypokalemic periodic paralysis provoked by "Ambene"]. 293 67

The concentrations of sodium, potassium, calcium, magnesium, phosphorus, sulphur and chlorine, in the skeletal muscle fibres of cows with parturient paresis, downer cows, normally calving cows and unmated heifers were determined by means of an X-ray microanalysis technique. The most consistent finding was an increase in the concentration of chlorine in the muscle samples from the downer cows. There were no other significant differences between the concentrations of these elements in samples from the different groups of cows, but the calcium concentration was higher in the muscle samples collected one month after parturition than in the samples collected close to parturition.
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PMID:Concentrations of sodium, potassium, calcium, magnesium and chlorine in the muscle cells of downer cows and cows with parturient paresis. 797 93

Increasing weakness occurring over several days, involving the upper and lower limbs, and progressing to symmetrical paresis is a clinical presentation that raises many diagnostic issues. When faced with these circumstances most clinicians opt for a range of neurological possibilities. However, metabolic possibilities are equally important and are eminently treatable. There are a variety of reasons why potassium depletion presents as paralysis in Aboriginal Australians. The cause may not be apparent, although careful questioning may unearth clues that can lead to a diagnosis. Once the potassium level has been measured in the blood the diagnosis becomes obvious, but until that time the presentation can be confusing. Early serum potassium measurement is recommended with this clinical picture.
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PMID:Hypokalaemic paralysis in remote aboriginal communities. 876 84

A severely hypocalcaemic, hypomagnesaemic lactating bitch exhibited clinical signs of pulmonary oedema, paresis, dementia, gastrointestinal ileus and urinary bladder atony. The total calcium, ionised calcium and magnesium levels were extremely low. The clinical picture was very different from the one typically encountered in canine lactation tetany, and instead resembled bovine postparturient paresis. Muscle tremors, rigidity and seizures were not part of the acute clinical picture, but rather atony, weakness and paresis. General muscle dysfunction probably resulted from the extremely low ionised calcium levels in combination with very low levels of magnesium and possibly potassium. Heart failure and atony of the urinary bladder and intestines were probably a result of the severe hypocalcaemia. The alteration in calcium to magnesium ratio may have depressed neuromuscular transmission, leading to paresis and atony. The unusual electrocardiogram possibly also resulted from abnormal magnesium and calcium cation levels.
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PMID:Paresis and unusual electrocardiographic signs in a severely hypomagnesaemic, hypocalcaemic lactating bitch. 967 8

The analysis of 36 case records of patients with peritonitis (n = 12) and intestinal obstruction (n = 24) is presented. Nasogastrointestinal intubation of the small bowel was used in combined treatment. The aims, indications and contraindications for the intubation are formulated. Bacteriologic and biochemical parameters of bowel content were studied. It was established that the quantity of enterobacteria and unfermenting gram-negative bacteria was increased in intestinal paresis, the alkaline phosphatase, amylase, bilirubin, transaminase, a potassium content were increased as well. For the tube to function from the first hours after its introduction it should be periodically properly washed with sodium hypochlorite in concentration 300 mg/l.
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PMID:[Small intestine intubation for treatment of patients with peritonitis and intestinal obstruction]. 1035 70


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