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 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

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

On the morning after taking alcohol in large amounts together with intranasal heroin, a 25-year-old man experienced pain, swelling and blistering in both arms together with right brachial plexus paresis. Creatine kinase (1930 U/l), acute phase proteins and IgE (238 IU/ml) were elevated. The pain was largely relieved by guanethidine block (given once only), and the swelling and blisters responded to methylprednisolone (80 mg daily for 7 days, then gradually reduced). Function returned in the lower division of the brachial plexus within ten days, but the upper division was still paretic 2.5 months later. After injecting heroin intravenously, a 27-year-old man woke up next morning with fever (39 degrees C) and proximal flaccid paralysis of the right arm. In addition to leucocytosis (25,600/microliters), creatine kinase was raised to 28,890 U/l and pANCA to a titre of 1:50 (antineutrophil cytoplasm antibody, perinuclear fluorescence pattern). The cerebrospinal fluid showed increases in cell count (15/microliters) and protein (73 mg/dl). Acute renal failure supervened after two days but was successfully treated. The paresis was still present at four months, though improved. A 21-year-old woman developed an upper brachial plexus lesion after attempting suicide with intravenous heroin accompanied by flunitrazepam (20 mg by mouth) and a bottle of whisky. She had raised levels of C-reactive protein (12 mg/dl) and IgM (4.0 milligrams). The paresis cleared up within six weeks without specific therapy. In view of the immunological abnormalities it seems possible that the immune system was involved in the pathogenesis of the plexus lesions and the rhabdomyolysis.
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PMID:[Brachial plexus lesions and rhabdomyolysis following heroin abuse. Indications for an immunological cause]. 782 62

Acute compartmental syndrome (CS) is a surgical emergency. Different conditions in which high non-physiological pressure appears within a closed fascial space reduce the necessary blood perfusion. CS is caused by trauma, burns, bleeding in patients with coagulopathies arterial injuries, nephrotic syndrome or unusual physical exercise with secondary compartmental swelling. When decompression occurs too late, permanent loss of function and limb contracture may result. In the following paper we report on a case of four-compartmental syndrome in the lower legs of a patient with drug intoxication. After cannabis consumption, the patient fell asleep sitting cross-legged. During our first examination several hours later, the signs of compartmental syndrome with spontaneous pain, turgid swelling and paresis were present. Bilateral skin incision technique was used to gain entrance into the four compartments in both lower legs. Immediately after the operation, the patient showed crush syndrome with high serum creatine kinase activity 140.501 U/l and acute renal failure caused by rhabdomyolysis. Within 2 weeks of haemofiltration and dialysis, a full recovery to a normal serum creatinine level of 0.7 mg/dl was achieved. After emergency treatment and rehabilitation, the patient showed neither vascular nor neural defects.
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PMID:[Bilateral tibial compartment syndrome with crush symptoms after cannabis abuse]. 937 97

The 39-year-old male in this report was a victim of C4 spinal cord injury for 7 years. He was regularly followed up at our pain clinic and psychiatric out-patient department (OPD) for treatment of his chronic pain with morphine, anticonvulsant and sedatives. At the night of December 15, 1997, he took approximately 0.1 gm of morphine and a certain number of flurazepam pills. On the next day, he experienced numbness and paresis in both legs in association with painful swelling of both thighs. Then he sought medical advice at our hospital and was admitted for investigation on December 20, 1997. Laboratory examination revealed elevated creatine kinase activity, increased urine myoglobin concentration and raised plasma creatinine, signifying the development of acute muscle damage. The excreted urine morphine concentration was as high as 6,384 ng/mL. Increased PYP uptake in the proximal portion of both thighs was noted on muscle scan. These abnormalities were resolved gradually over two weeks under conservative treatment. Morphine-induced rhabdomyolysis complicated by acute renal failure was highly suspected.
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PMID:Rhabdomyolysis-induced acute renal failure after morphine overdose--a case report. 1060 51


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