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)

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

We reported a 49-year-old mother and her 28-year-old son with autosomal dominantly inherited bulbar spinal muscular atrophy (AD-BSMA). They showed progressive bulbar paresis, muscle wasting and weakness dominant in the proximal groups of limb muscles, and finger tremor. Onset of illness was in adult life. In laboratory examinations, elevated creatine kinase in serum and neurogenic changes either in EMG or muscle biopsy were noted. The son had neither gynecomastia nor abnormal sexual hormone levels which were observed in the sex-linked recessive bulbar spinal muscular atrophy (SR-BSMA). Elongation due to the CAG repeats at the androgen receptor gene of the X chromosome in SR-BSMA was not detected. In conclusion, it is clear that AD-BSMA is different from SR-BSMA on the basis of clinical and genetical aspects.
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PMID:[A mother and her son with autosomal dominant bulbar spinal muscular atrophy]. 130 Feb 63

An 11-year-old girl presented to the emergency department with hypoventilation and shock after being bitten by a Mojave rattlesnake. Intubation was required, and she improved rapidly after fluid resuscitation and antivenom administration. She was extubated four hours after envenomation and did well. The patient subsequently developed increased weakness and cranial nerve paresis and required reintubation for respiratory failure at 30 hours after envenomation despite administration of 30 vials of antivenom. She improved after administration of additional antivenom and was extubated ten hours later. Twenty-four hours after envenomation, signs of rhabdomyolysis were noted with myoglobinuria and a creatine phosphokinase level of 96,400 units/L. Myoglobinuric renal failure was treated with mannitol, hydration, and alkalinization of the urine. The patient's renal and neurological functions improved steadily during the following three to four days. Neurotoxic and myotoxic effects of Mojave venom are known to occur but are not well documented in human beings. Recognition of potential complications from envenomation such as respiratory paralysis and rhabdomyolysis with myoglobinuric renal failure is critical.
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PMID:Mojave rattlesnake envenomation: prolonged neurotoxicity and rhabdomyolysis. 153 96

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

A patient with serologically confirmed infection by Borrelia burgdorferi presenting with painful paresis and atrophy of the proximal muscles of both upper extremities and bilateral facial paresis is described. Electromyography showed a neurogenic and myopathic pattern, and creatine kinase was raised. Muscle biopsy revealed the typical signs of focal myositis. Treatment with i.v. penicillin led to dramatic clinical and serological improvement. Muscle biopsy was repeated 2 months later; neurogenic changes were still present, but no inflammatory signs could be seen anymore. Thus, the presented case may be the first reported of meningopolyneuritis accompanied by focal nodular myositis, in the second stage of Lyme borreliosis.
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PMID:Meningopolyneuritis Bannwarth with focal nodular myositis. A new aspect in Lyme borreliosis. 380 66

In 18 patients with myotonic dystrophy, spontaneous aggregation and platelet aggregation induced by thrombin, adenosine diphosphate and epinephrine were compared with normal aggregation patterns. In 17 of the 18 patients the results were not significantly different from normal. In 1 patient spontaneous aggregation and hypersensitive platelets were found. These results are in disagreement with earlier reports on a specific hypersensitivity to epinephrine in myotonic dystrophy. Neither the clinical data (myotonia, paresis) nor the laboratory data (creatine kinase, myoglobin, immunoglobulin G) were correlated with the platelet aggregations.
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PMID:Normal platelet aggregation in myotonic dystrophy. 629 58

Paresis of the limbs of two 4-month-old ostriches fed a diet predominantly of crushed maize was investigated. Raised levels of serum aspartate transaminase and creatine kinase were demonstrated in both birds. The less severely affected ostrich recovered after a single intramuscular injection of a vitamin E-selenium preparation but the other died despite therapy. An autopsy of the latter revealed focal pale areas in the thigh muscle. Microscopically affected muscle fibres showed degeneration, necrosis and regenerative changes. Fibrinoid degeneration and necrosis of some arterioles was observed as well as varying degrees of interstitial fibrosis. The above findings suggest a diagnosis of vitamin E-selenium deficiency.
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PMID:Suspected vitamin E-selenium deficiency in two ostriches. 663 92

The mean plasma concentration of cortisol at the time of the first treatment for hypocalcaemia at calving was significantly higher in 17 cows which did not recover, than in 53 cows which recovered. Healthy periparturient cows had significantly lower cortisol levels than cows with hypocalcaemia. There was a negative correlation between plasma cortisol and plasma calcium at the time of the first treatment. After adjustment for differences in plasma calcium there was no significant difference between cortisol concentrations in healthy cows and paretic cows which recovered. Plasma cortisol was positively correlated with both packed cell volume (PCV) and serum creatine kinase (CK). At first treatment cows which did not recover had higher levels of PCV and serum CK than cows which recovered, and the difference between the mean plasma cortisol concentrations of these two groups was related to differences in plasma calcium, PCV and serum CK. Plasma cortisol concentrations remained high in cases of protracted paresis.
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PMID:Plasma concentrations of cortisol in cows with hypocalcaemia in relation to their responses to treatment with calcium. 671 15

Experimental downer cows were produced by maintaining healthy cows in sternal recumbency for 6, 9, or 12 hours with the right pelvic limb positioned under the body. Halothane anesthesia was used to create this artificial parturient paresis-like position. In 8 of 16 experiments, cows were able to stand within 3 hours after anesthesia, but the others remained recumbent until death or euthanasia. There was no correlation between duration of the treatment and ability to stand after enforced recumbency. The appearance of the right pelvic limb of downer cows resembled the injured limbs of human patients with compartmental/crush syndrome, as well as the limbs of clinical downer cows. The affected limbs were swollen and held in rigid extension. Some animals which were able to stand also had swollen right pelvic limbs. Systemic signs of crush syndrome included dark yellow or brown urine suggestive of myoglobinuria, and marked elevation of serum creatine kinase enzyme levels. Highest creatine kinase levels were observed at 24 hours in the ambulatory group and at 48 hours in the downer group. Necropsy of downer animals revealed ischemic necrosis of the caudal thigh muscles and inflammation of the sciatic nerve caudal to the proximal end of the femur. Evidence of peroneal nerve damage was observed in at least 9 animals.
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PMID:The role of pressure damage in pathogenesis of the downer cow syndrome. 692 Feb 48

We report two cases of compartment syndrome of the lower leg that occurred in male patients aged 62 and 57 years, respectively, after 10 and 12-h urological surgery in the lithotomy position. During sedation and mechanical ventilation creatine kinase (CK) activity of more than 8,000 U/l was found in both patients. After extubation, clinical symptoms of the compartment syndrome were found. On the 1st day after surgery patient 2 underwent fasciotomy of both lower legs (Fig. 2). No lasting neurologic defects were observed. Patient 1 was treated by fasciotomy on the 4th postoperative day after paresis of the peroneal nerve had developed in the left lower leg. This paresis had shown no tendency to regression when the patient left hospital. On phlebography, both patients showed blockage of the deep lower leg veins up to the knee. DISCUSSION. The compartment syndrome is a rare but serious complication resulting from prolonged surgery in the lithotomy position. Symptoms are neuromuscular lesions of the affected limb. Severe complications of the compartment syndrome are acute renal failure resulting from myoglobin residues in the tubules, electrolyte disturbances, and disorders of acid-base balance. A decrease in perfusion due to the elevated position of the legs, on the one hand, and the impeded venous back-flow due to the positioning on the other are discussed. While positioning the legs, it is important to ensure that the lower legs are lifted only slightly above left atrial level. When rehabdomyolysis occurs, serum CK activity increases. CK values of over 2,000 U/l after surgery may be considered a warning sign in ventilated and sedated patients, in whom early clinical symptoms of the compartment syndrome such as pain and paresthesias cannot be ascertained. Frequent and regular checks of these parameters starting shortly after surgery are recommended. A thorough examination of the lower legs and, if necessary, measurement of the tissue pressure in the compartment should follow. The deep veins of the legs should be checked by phlebography. In cases of verified compartment syndrome, early fasciotomy is the best choice of therapy, because neuromuscular defects are known to be irreversible after 12 to 24 h. Enforced diuresis is recommended in order to avoid renal complications.
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PMID:[Postoperative bilateral compartment syndrome resulting from prolonged urological surgery in lithotomy position. Serum creatine kinase activity (CK) as a warning signal in sedated, artificially respirated patients]. 769 79


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