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)

Four patients without symptoms of episodic hyperkalemic weakness from two families with paramyotonia congenita (Eulenburg) are described. 1. Maximum voluntary muscle contraction of the upper and lower arm was studied under isometric conditions at different temperatures. If the temperature was lowered stepwise, distinct paresis occured at 32--31 degrees C which increased with the amount of muscular effort. The upper arm muscles, however, developed weakness gradually after cooling. 2. During cooling of the resting muscle, the EMG showed dense spontaneous activity of the fibrillary type, which decreased again at about 30 degrees C. It can be assumed that in paramyotonia congenita cooling produces muscle cell membrane depolarization which at a critical level causes the firing of action potentials and finally muscular paresis. 3. Increasing muscular stiffness can be interpreted as abnormally slow muscular relaxation after isometric contraction. In the forearm muscles the time to 3/4 relaxation after cooling was about six times normal, in the upper arm muscles only two times normal. As an additional parameter the mechanical resistance to passive stretching of a muscle has been studied. This passive muscular tension increased simultaneously with the onset of weakness. 4. The close relation between weakness and stiffness suggest that both symptoms are caused by the same basic defect which is probably located in the sarcolemma. It is suggested that a defect of the sodium channel causes a cooling-dependent increase in sodium conductance. Raised intracellular sodium causes in the first place membrane depolarization, and in the second place depression of calcium reuptake through competition by sodium for calcium binding sites. This would explain muscle stiffness and delayed relaxation as well.
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PMID:Influence of temperature on isometric contraction and passive muscular tension in paramyotonia congenita (Eulenburg). 9 68

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
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PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

Cows fed a balanced diet with the required amounts of calcium and phosphorus developed acute hypocalcemia and hypophosphatemia shortly after parturition, even in the presence of the a responsive parathyroid gland, when bone resorption was selectively inhibited by the prepartal administration of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP). When serum total and ionized calcium levels declined below 6.0 and 1.0 mg/100 ml, respectively, cows developed clinical signs similar to naturally occurring parturient paresis. The plasma immunoreactive parathroid hormone levels were similar prepartum, at parturition, and 1 day postpartum in cows administered EHDP as in control cows. Parathyroid chief cells were predominately in the actively synthesizing phase of the secretory cycle with a prominent Golgi apparatus and lamellar arrays of rough endoplasmic reticulum. Many chief cells were degranulated of mature secretory gransules. Calcitonin activity in thyroid extracts, determined by bioassay, and the numbers of secretory granules in thyroid C-cells were similar in both groups of cows. EDTA infusion after 60 days of the experiment demonstrated that the immediately available calcium reserves were reduced in EHDP-treated cows. The serum calcium remained significantly lower and did not return to preinfusion levels by 24 hours. Serum calcium in control cows returned to within the normal range by 6 hours after EDTA infusion. The urinary excretion of hydroxyproline was consistently reduced prepartum and following EDTA infusion in cows receiving EHDP. The experimental induction of parturient of parturient hypocalcemia by the prepartal administration of EHDP provides a valuable model for studies to investigate the mechanisms in bone responsible for the development of severe hypocalcemia that occurs in response to the increased calcium demand imposed by parturition and the initiation of lactation.
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PMID:Experimental parturient hypocalcemia in cows following prepartal chemical inhibition of bone resportion. 18 Aug 13

The prophylactic effect in parturient paresis of an intramuscular injection of 10 million i.u. vitamin D3 one week prior to the expected calving date, was investigated in 84 cows which had previously suffered from parturient paresis. Clinical observations in connection with the development of parturient paresis after injection of vitamin D3 were compared with corresponding observations made on cows within the same population at the previous calving when no vitamin D3 was administered. The incidence of clinical parturient paresis in cows given vitamin D3 was 44.3 per cent. There were no significant differences in the incidence of parturient paresis in cows injected with vitamin D3 during the periods less than 2, 2--4, 5--8 and greater than 8 days before parturition. Average plasma calcium levels (mg/100 ml) before first calcium treatment, results of treatment, and the incidence of retained placenta in vitamin D3 injected cows did not differ significantly from corresponding data for cows with clinical parturient paresis which had not been given vitamin D3 before calving. It is concluded that vitamin D3 does not have any prophylactic effect in parturient paresis in cows in Eastern Norway.
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PMID:The prophylactic use of vitamin D3 in parturient paresis in the cow in a practice district in eastern Norway. A retrospective investigation. 20 8

A synthetic biologically active derivative of vitamin D (350 microgram of 1alpha-hydroxycholecalciferol [1alpha(OH)CC]) was injected into 2 nonlactating 7-year-old Israeli-Friesian cows. Plasma calcium values increased after 24 hours, peaked at 48 hours, and returned to base-line values 120 hours after injection. An injection of 350 microgram of 1alpha(OH)CC was given to 23 parturient-paresis-prone Israeli-Friesian cows from 7 days to 6 hours prepartum; 13 cows were injected once, 6 were injected twice, and 4 were injected 3 times, all at 48-hour intervals. Parturient-paresis-prone cows (n = 23) of the same breed were used as controls. Within 0 to 36 hours postpartum, plasma calcium concentrations were found to be higher in cows injected with 1alpha(OH)CC than in the control cows. The increase was highly significant (P less than 0.01) in cows injected at least twice. None of the cows injected with 1alpha(OH)CC, within 72 to 24 hours prior to calving developed parturient paresis; but 9 of 23 control cows developed parturient paresis. Prior to calving, none of the injected cows developed hypercalcemia and there was no local or systemic clinically detectable signs of toxiosis. When given at the right time prepartum, 1alpha(OH)CC is considered to be an improvement over previous methods of preventing bovine parturient paresis.
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PMID:Use of 1alpha-hydroxycholecalciferol in the prevention of bovine parturient paresis. 24 72

One hundred and thirty four cases of hypocalcaemia (parturient paresis) between April and Jul 1976 from 72 herds in the UK and Eire were used to compare the response to intravenous treatments with one of three solutions containing calcium salts. Two solutions contained 8 g calcium, one with added magnesium (1.03 g), a third solution contained 6.2 g calcium. The biochemical response obtained 24 hours after successful treatment from all solutions was similar. The clinical response with both 8 g calcium solutions was similar and significantly superior to that obtained with 6.2 g calcium (P less than 0.02 greater than 0.01). More cases (44 per cent) relapsed after treatment with 6.2 g calcium. There was no evidence that the added magnesium to the calcium solution improved the clinical response of parturient paresis cases in this spring claving season, as had been suggested previously. The herds providing these 134 cases had recorded an incidence of 8.04 per cent for parturient paresis in 1975.
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PMID:Milk fever: a case against polypharmacy solutions. 24 19

The endocrine factors associated with parturient paresis have not been defined totally. Estrogens stimulate uptake of calcium by bone. Since secretion of estrogen increases dramatically as parturition approaches, estrogen may be involved in homeostatic mechanisms regulating calcium metabolism. Plasma was collected for 30 days (-30) prepartum to 5 days (+5) postpartum from six Holstein and nine Jersey cows approaching three or more lactations. Of all cows, six Jerseys contracted parturient paresis. Estradiol and estrone were analyzed by radioimmunoassay, total calcium and total magnesium by atomic absorption spectrophotometry, and total phosphorus by colorimetry. Data were grouped into periods respresenting days -30 to -21, -20 to -11, -10 to -6, -5 to -4, -3 to -2, -1, 0 (parturition), +1, +2 to +3, and +4 to +5. Calcium in plasma was lower in parturient paresis cows on days +1 and +2 to +3, and magnesium was higher during the same periods but lower on days -4 to -5. Total phosphorus, estrone, and estradiol of normal cows and those with parturient paresis were not different. During the entire sampling period, phosphorus and estradiol were similar in both groups while magnesium was higher and calcium lower in cows with parturient paresis. Estrone was lower in cows with parturient paresis. Lower estrone in cows with parturient paresis may be predisposing for parturient paresis.
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PMID:Estrogen in plasma of parturient paretic and normal cows. 45 85

Twelve cows, at least third parity, were assigned randomly to either a control or treatment group. Treated cows received .4 mg of the vitamin D metabolite, 1,25-dihydroxycholecalciferol intramusculary in 5 ml corn oil. Intramuscular injections were started 5 days before predicted calving with reinjections every 5 days until calving. Incidence of parturient paresis was 0 and 33% (2 of 6) in the treated and control groups. Response to treatment was rapid with elevated calcium in serum approximately 12 h postinjection. Treatment maintained or elevated calcium and phosphorus concentrations in serum during the critical period, 24 h pre- to 48 h postpartum, when milk fever is most likely to occur. There was, however, no significant difference between treatments at 72 h postpartum. Based on these observations 1,25-dihydroxycholecalciferol holds promise as a preventative of parturient paresis; however, further studies are needed on application and safety.
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PMID:Potential use of 1,25-dihydroxycholecalciferol for prevention of parturient paresis. 50 Aug 93

Four trials involved intravenous or intramuscular injections of 1alpha-hydroxyvitavin D3 to test efficacy in preventing parturient paresis. Use of .1 mg intravenously afforded total protection compared with an incidence of 33% (2/6) in controls. Intramuscular injections of .1 mg in 2 ml propylene glycol and .3, .5, and 1.0 mg in 5 ml corn oil resulted in 0, 15.7, 20, and 0% incidence of parturient paresis compared with 33, 16.7, 37.5, and 37.5% incidence of parturient paresis in the controls. There was a rapid increase in serum calcium (12 to 24 h) in response to intravenous treatment, whereas the response to intramuscular injections was gradual but was maintained longer. To evaluate the safety of 1alpha-hydroxyvitamin D3, eight cows, two per treatment, were given intramuscular doses of .5, 1.0, 1.5, or 3.0 mg (three 1.0 mg injections) in 5 ml corn oil. No clinical or pathological evidence of hypervitaminosis C or soft tissue calcification was found. Tissue taken from the injection site 15 days after last injection contained 3 to 38 IU vitamin D activity per 100 g wet tissue compared with control of 8 to 15 IU per 100 g. Total vitamin D activity of milk taken the 11th milking postpartum from cows receiving .5 or 1.0 mg had a mean of 13.4 and 22.6 IU vitamin D activity per liter compared to 19 IU per liter for control milk. Milk from the 5th milking postpartum in the cows receiving .5 mg had a mean activity of 14.5 IU per liter. Milk from animals slaughtered for retention studies had a mean activity of 22 IU per liter.
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PMID:Efficacy and safety of 1alpha-hydroxyvitamin D3 for prevention of parturient paresis. 59 4

1. The effect of 1-alpha-hydroxycholecalciferol (1 alpha-OH-D3) on calcium and phosphorus metabolism has been studied in ewes at peak lactation by a combination of a mineral balance and a radioisotope technique. 2. The rate of Ca absorption was substantially higher in the treated ewes than in controls. The rates of endogenous loss of Ca into urine, faces and milk, however, were only slightly higher. 3. In consequence, the net retention of Ca was increased and the loss of skeletal reserves of Ca normally associated with peak lactation, prevented. 4. Although the rate of bone accretion increased slightly, the increase in skeletal retention of Ca resulted mainly from a decrease in the rate of bone resorption. 5. This finding conflicts with the generally held belief that bone resorption is increased by cholecalciferol treatment. 6. The rates of apparent absorption and retention of P were increased by the treatment probably as a result of a direct effect of the 1 alpha-OH-D3 on P absorption. 7. These results provide a possible explanationof the beneficial effect of 1 alpha-OH-D3 in preventing parturient paresis (milk fever) in the dairy cow.
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PMID:The effect of 1-alpha-hydroxycholecalciferol on calcium and phosphorus metabolism in the lactating ewe. 69 76


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