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

Report on 5 cases of adenoidcystic carcinoma of the larynx and review of the literature, containing about 60 further reports. About 80% of these tumors arise in the subglottice laryngo-tracheal transition region, 20% in the ventricular cord and the epiglottis. The vocal cords containing no mucus glands are never the origin of adenoid cystic carcinomas. These tumors grow under an intact mucosa and reach very often an enormous extension until dyspnoea, dysphagia and recurrent never paresis lead to diagnosis. The clinical course of these tumors ist not preditable--even not by their histological structure. In some cases the outcome is rapidely fatal by local growth and metastases, in others a many year long survival can be reached, but there exists no reliable report on a "cured" adenoid cystic carcinoma of the larynx. By radical surgery only better results can be expected. Irradiation produces long lasting remissions in some cases.
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PMID:[Adenoid-cystic carcinoma of the larynx (author's transl)]. 65 64

Twenty-four 4-week-old poults, free from Mycoplasma meleagridis and M. gallisepticum, were inoculated with a velogenic viscerotropic strain of Newcastle disease virus. Clinical signs (gasping, coughing, and dyspnea) developed 4-5 days postinoculation, continued until nervous derangement appeared, and then (usually 3 days after initial clinical signs appeared) declined in severity. Prominent nervous signs were paresis and paralysis of the extremities, with pronounced head-shaking. The most constant gross lesions detected involved the airsacs. The abdominal sacs of a few poults contained a large accumulation of yellowish, cheesy exudate and there was cloudiness of the thoracic airsacs of all inoculated poults. A few turkeys had tracheitis with some catarrhal exudates and casts in the lower part of the tracheal lumen. Congestion of lepto-meningeal vessels usually correlated with the severity of the nervous signs. The histologic lesions were characterized by both degenerative and proliferative changes with predominantly mononuclear cell and heterophil infiltrations throughout the body. The obvious lesion seen in the recovery stage of the disease was proliferation of lymphofollicular nodules in the parenchymatous organs.
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PMID:Pathology of velogenic Newcastle Disease virus infection in turkeys. 116 10

Interscalene block may cause phrenic nerve block and decreased diaphragmatic motion. We evaluated the effect of continuous interscalene block on ventilatory function and diaphragmatic motion. We studied ten patients scheduled for surgery or manipulation of the shoulder. Preoperatively, the patients underwent spirometry and double-exposure chest radiography. They received an interscalene block with 0.75% bupivacaine. Thereafter, 0.25% bupivacaine was infused into the interscalene space for 24 h. Spirometry was repeated three times and double-exposure radiography twice. The maximal inspiratory and expiratory pressures were measured repeatedly. Haemoglobin oxygen saturation (SPO2) was monitored with pulse oximetry. The block provided adequate anaesthesia for surgery or manipulation. All patients had a marked ipsilateral paresis of the diaphragm in the radiographs 3 h after the initial block. Twenty-one hours later five patients had diaphragmatic motility comparable to the situation before the block. In the other five patients, the amplitude of diaphragmatic motility on the side of the block was only 4-37% of the values before the block. All patients had a clear reduction in forced vital capacity (FVC), forced expiratory volume in 1s (FEV1) and peak expiratory flow (PEF) 3 and 8 h after the block without signs of dyspnoea. In conclusion, in all our patients interscalene block caused an ipsilateral hemidiaphragm paresis, which in five of ten patients persisted until the end of the continuous block.
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PMID:Effect of continuous interscalene brachial plexus block on diaphragm motion and on ventilatory function. 153 80

The report describes seven SMA-cases in descendents of crossbreeds of American Brown Swiss x Deutsches Braunvieh. Symptoms and course: After initially normal development of the calves for one to six weeks the disease set in suddenly followed by a rapid lethal course of one to one and a half weeks duration due to asphyxia and/or secondary diseases. Only one case was reported having been sick since birth (?). Characteristic signs were rapidly progressing muscular atrophy, paresis and paralysis of the limbs, the trunk and the diaphragm, usually accompanied by progressive dyspnoea. Signs of congenital neuromyodysplasia (arthrogryposis) of different degree were present in four of the seven calves. Six calves had contracted a secondary pneumonia. Blood gas analysis (6/7) revealed a compensated (1x) or decompensated (4x) respiratory acidosis. Neurohistological findings: Degeneration and loss of motor neurons in the ventral horns of the spinal cord and neurogenic muscular atrophy. Immunohistochemistry revealed a pronounced accumulation of type 200 kD-neurofilaments in perikarya and dendrites of ventral horn motoneurons indicating disturbed mechanisms of the axonal transport. The disease seems to be inherited as a recessive trait.
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PMID:[Spinal muscle atrophy in Brown Swiss x Braunvieh cross calves]. 163 59

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

There are several protozoan infections that cause relatively benign illness in normal individuals but result in severe disease manifestations in patients with AIDS. These diseases include Pneumocystis carinii pneumonia, CNS toxoplasmosis, cryptosporidiosis, and isosporiasis. Pneumocystis carinii pneumonia (PCP) caused by Pneumocystis carinii, is the most common opportunistic infection in AIDS. It is seen in more than 80% of individuals with this syndrome. Although historically classified as a protozoan, this organism shares many biochemical characteristics with fungi. The onset of PCP may be insidious, and cough and dyspnea are the most common presenting symptoms. Auscultation of the lungs is often unremarkable, but diffuse infiltrates are commonly seen on chest radiographs. The diagnosis of PCP can be confirmed by identifying the organism on specimens obtained by sputum induction or bronchoalveolar lavage. Trimethaprim-sulfamethoxazole is the treatment of choice but is unfortunately associated with leukopenia and rash in many individuals. Both trimethaprim-sulfamethoxazole and aerosolized pentamidine are used prophylactically in patients at high risk for initial or relapsing infection. The appropriate use of these agents has resulted in improved survival for AIDS patients with PCP. Toxoplasmosis, due to Toxoplasma gondii, affects the central nervous system in patients with AIDS. Headache is a common presenting symptom, and both seizures and paresis can occur. A diagnosis of toxoplasmosis is strongly suspected in symptomatic individuals with ringed mass lesions noted on head CT. Patients with this condition are treated with a combination of sulfadiazine, pyrimethamine, and folinic acid. Cryptosporidiosis and isosporiasis are coccidian protozoan diseases that can result in severe, acute, and chronic diarrhea in immunocompromised individuals. Cryptosporidiosis is the more common of the two and is caused by an unknown species of the genus crytosporidium. Isosporiasis is due to infection with Isospora belli. Dehydration and weight loss are a common result of infection with either agent. A definitive diagnosis can be made by examining an acid fast stain of a diarrheal stool specimen and demonstrating oocysts that are specific for each of these organisms. Fluid replacement and general supportive care are essential in the treatment of both of these diseases. Spiramycin is an unproven treatment modality that is often used in patients with cryptosporidiosis. Isosporiasis responds to initial therapy with trimethaprim-sulfamethoxazole, followed by prophylaxis with pyrimethamine. The adoption of safe sexual practices that minimize fecal-oral contamination should decrease the future prevalence of these diseases and other enteric parasitic infections.
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PMID:Parasitic diseases. Diseases associated with acquired immunodeficiency syndrome. 201 33

A 13-year-old boy, with no past medical history, was admitted after a car accident on October 29, 1989. On admission, he was alert. Physical examination revealed a bruise on the left frontal region, a fracture of right clavicula and right hemopneumothorax. He was treated with respirator due to dyspnea. On November 1, 1989, he was removed from respirator and expressed diplopia. Neurological examination showed bilateral ptosis, mild anisocoria, normal light reflex and horizontal gaze nystagmus in lateral gaze. Both eyes were deviated outward slightly in the primary position and showed inability to converge. The external ocular movements of both eyes were mildly limited in elevation and adduction. Ataxia was observed in bilateral upper extremities. Deep reflexes were normal and no pathological reflexes were observed. Brain CT scans showed no abnormality. On November 6, 1989, his ptosis and diplopia improved. On November 8, he was completely recovered. A magnetic resonance imaging on November 10 revealed no abnormality. We suggested that transient dysfunction of midbrain associated with head injury might cause transient bilateral primary oculomotor nerve paresis, nystagmus and ataxia.
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PMID:[A case of transient bilateral primary oculomotor nerve paresis associated with head injury]. 224 37

The toxicity of sodium selenite was studied in 28 Nubian goats, 20 of which died or were killed in extremis 2 h to 21 d after dosing. Single or repeated daily oral doses of 160, 80, 40, 20 and 5 mg sodium selenite/kg were toxic to goats while daily doses of selenite ranging from 0.25 to 1 mg/kg/d for 225 d were not toxic to this species of animals. The main signs of poisoning were uneasiness, inappetence, dyspnea, salivation, diarhea, paresis of the hind limbs, arching of the back, and recumbency. The main lesions were hemorrhages in the rumen, reticulum, osmasum and abomasum, hemorrhagic or catarrhal abomasitis and enteritis, fatty change and necrosis of the centrilobular hepatocytes and of the cells of the renal convoluted tubules, splenic hemosiderosis, pulmonary congestion, haemorrhage, edema and emphysema, accumulation of lymphocytes in the vital organs, and straw-colored fluid in the serous cavities.
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PMID:Experimental selenium poisoning in Nubian goats. 235 37

Clinical signs in dogs with pseudorabies (Aujeszky's disease) were tabulated from 25 confirmed cases. The duration of disease was short, ranging from 6 to 96 hours. Eight dogs were euthanatized. Of those not euthanatized, 12 (71%) died within 24 hours of onset, 16 (94%) died within 48 hours, and only 1 (6%) lived longer than 48 hours (96 hours) after the onset of clinical signs. All of the dogs had ptyalism, 84% were restless, 84% were anorectic, 76% were atactic, and 64% wandered aimlessly. Sixty-four percent of the dogs had tachypnea, 60% had dyspnea, 56% vocalized, 52% were pruritic, 48% held their necks rigidly, 36% vomited, 36% had muscle spasms, 36% were aggressive, 28% had trismus, and 24% had dysphagia. Five of 25 dogs (20%) had abnormal pupillary light responses. Two of the 25 dogs circled and 2 walked backwards. Each of the following were detected once: blindness, ptosis, facial paresis, excessive lacrimation, head-tilt, head-pressing, signs of abdominal pain, and photophobia. All dogs had been exposed to swine, although in some instances the farmer was unaware pseudorabies existed in the herd or believed it was not in the herd on the basis of negative results on serologic testing.
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PMID:Clinical signs associated with pseudorabies in dogs. 277 5


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