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

Ten clinically intact weaned piglets were experimentally intoxicated by intravenous injection of lipoproteide-free lipopolysaccharide endotoxin according to Westphal of E. coli O 127:B8. Severe endotoxin shock with all clinical manifestations of experimental coli-enterotoxaemia was induced in all animals and included circulatory disorder with tachycardia, intermittent pallor and/or cyanosis, symptoms of severe systemic intoxication, neurological symptoms, such as lack of coordination, hindleg staggering, spasm, paresis, paralysis, changes in respiration, such as rise in respiratory frequency and deepened breathing premortal deceleration of respiration and gasping for breath, temperature, variation, including hyperthermia and aggravating hypothermia, gastro-intestinal symptoms, such as temporary vomiting and persistent diarrhoea, leucopenia, eosinopenia, variation of haematocrit, edematisation, increased transudation, congestion, and gastro-intestinal shock lesions. Eight animals died. These experiments quite obviously have confirmed that endotoxin shock is the common pathogenetic principle behind all forms of coli-entertoxaemia (i.e, the forms of edematisation, cardiovascular failure, and gastro-intestinal processes.) Lipopolysaccharide endotoxin alone may be responsible for the development of both edemas and neurotoxic symptoms (edema disease) and diarrhoea (gastro-intestinal form of coli-enterotoxaemia). The pathogenetic relevance of additional toxins (neurotoxin and enterotoxin) is discussed under this aspect.
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PMID:[Experimental studies on the pathogenesis of Coli-enterotoxemia in swine. 4. Effect of lipopolysaccharide endotoxin on weaned piglets following parenteral administration]. 33 9

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

Medical personnel should be able to recognize vascular injuries. Knowing the key signs of ischemia, namely pallor, pulselessness, pain, paresis, and paresthesia and the soft signs of vascular injury will help to prevent limb loss.
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PMID:Recognition of vascular injury in the trauma patient. 211 86

The feeding of monensin as a coccidiostat in three separate flocks of turkeys was associated with increased mortality, posterior paresis, and a skeletal muscle myopathy. Mortality attributed to the disease was 1.65%, 1.86%, and 4.80% in the three flocks. Samples of monensin-supplemented feed fed to the flocks when showing clinical signs contained 88, 85, and 106 g/ton of complete feed, respectively. Clinically, the turkeys showed posterior paresis, inability to rise, incoordination, reluctance to move, and leg trembling and weakness. Necropsy findings included consistent lesions of pallor within the type I muscles of the legs, wings, and backs. Microscopic lesions included myofiber degeneration and necrosis with massive cellular proliferation interpreted as sarcolemmal nuclei proliferation. Occasional axonal degeneration with loss of axons was present in peripheral nerves embedded in the damaged musculature. In the youngest flock, multifocal areas of acute coagulation necrosis of the myocardium were also present. These outbreaks occurred following intake of monensin in the complete feed at levels considered therapeutic; however, no associated predisposing clinical condition, drug/toxin interaction, or excessive monensin levels in the feed could be demonstrated.
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PMID:Skeletal muscle lesions in turkeys associated with the feeding of monensin. 319 76

Acute arterial occlusions of the extremities present with the classical five P's: pain, pallor, pulselessness, paresthesia, paresis. Loss of sensitivity and motility are symptoms of the most severe grade of ischemia. The occlusions are due to embolism in about 70% of subjects and to local thrombosis in 30%. These patients have to be treated immediately with heparin. In the mildest forms, deobliteration is desirable, but in the more severe cases rapid restoration of flow not only saves limbs but also life. Deobliteration may be performed surgically or by means of catheters (local thrombolysis or thrombus aspiration) if available. Deep vein thrombosis, the other kind of emergency situation, requires immediate anticoagulation as soon as pulmonary embolism is suspected. It should be initiated by heparin and followed by oral anticoagulation. In patients presenting without pulmonary embolism but a swollen leg, ruptured Baker cysts or muscle hematomas should be ruled out before anticoagulation is started. Systemic thrombolysis or surgical thrombectomy is reserved for young patients with acute isolated thromboses. Thrombectomy must also be kept in reserve for the most severe form of deep venous thromboses, the phlegmasia cerulea dolens. In thrombophlebitis, no anticoagulation is indicated except in bedridden patients. The others must remain mobile and may be treated by systemic and local antiinflammatory drugs, incision of thrombosed varices, and bandages.
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PMID:[Emergencies in angiology]. 849 73

Turkey knockdown was diagnosed in three of five flocks of hen turkeys on a single farm within a 12-mo period. The age of birds in the flocks affected ranged from 6 wk 2 days to 7 wk 4 days. The attack rate ranged from 0.02% to 0.30% with a case fatality rate in affected birds ranging from 0 to 74%. The diagnosis was made on the basis of clinical signs and histopathologic lesions associated with knockdown. The feed in all flocks contained bacitracin methylene disalicylate and monensin (Coban). Affected birds were recumbent, demonstrated paresis, and were unable to vocalize. Postmortem examination revealed few significant lesions although pallor of the adductor muscles and petechiation in adductor and gastrocnemius muscles were noted. Birds that had been recumbent for extended periods were severely dehydrated. Consistent microscopic lesions included degeneration, necrosis, and regeneration of adductor, gastrocnemius, and abdominal muscles. No lesion in cardiac tissue was noted. Results of our investigation indicated that changes in water consumption, vitamin E status, and brooder to finisher movement correlated with the occurrence of knockdown. Turkey knockdown was defined in 1993 as any condition identified in a turkey flock that has affected the neuromuscular system to a degree that a turkey is unable to walk or stand. This definition was later modified to...neuromuscular or skeletal systems to a degree that a turkey is unable to walk or stand properly. Knockdown may be associated with numerous feed, management, or disease factors alone or in combination. Dosage of monensin, feed restriction/gorging, water restriction, heat stress, copper, mycotoxins, sodium chloride in feed, and sulfa drugs have all been suggested as contributing factors; however, laboratory studies to duplicate this have not been successful. This report presents observations from a single farm at which three of five hen flocks in a single year experienced knockdown. When a flock was reported as affected, a detailed investigation was initiated within 3 hr. The fifth flock was followed on a twice weekly basis from 0 to 8 wk of age to determine if initiating events were evident, but knockdown did not occur.
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PMID:Turkey knockdown in successive flocks. 1100 29

Early recognition of limb ischemia may allow prompt, effective therapy for peripheral arterial injuries. A review of cases of peripheral arterial trauma at the Toronto General Hospital since 1953 revealed that 50% of the injuries were not immediately recognized. An expanding hematoma, pulsatile hemorrhage or the onset of a bruit and thrill signifies arterial damage in penetrating wounds. Ischemia may be difficult to recognize in patients with soft tissue or skeletal trauma, but the presence of distal pallor, coolness, paresis, cyanosis, anesthesia, poor capillary refill and disproportionate pain indicates significant arterial damage and necessitates surgical exploration. The diagnosis of arterial "spasm" in such instances is untenable and can only be made after direct inspection, or on the return of pulses after reduction of a fracture or release of a tight cast. Restoration of arterial continuity by end-to-end anastomosis is the recommended technique for all arterial injuries, since after ligation of even minor vessels, ischemia may ensue, and amputation may occasionally be necessary.
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PMID:THE RECOGNITION AND MANAGEMENT OF PERIPHERAL ARTERIAL INJURIES. 1428 3

Spontaneous and experimental poisoning with the swainsonine-containing and calystegine-containing plant Ipomoea carnea subsp fistulosa is described. Three of 8 goats presenting with emaciation, weakness, symmetrical ataxia, posterior paresis, proprioceptive deficits, abnormal posture, abnormal postural reaction, and muscle hypertonia were necropsied. I fistulosa was suspected to be the cause of the neurologic disease in all cases. An experiment was conducted to confirm the diagnosis using 12 goats and diets containing 3 different concentrations of the plant. All goats fed I fistulosa developed neurological signs that were similar to those observed in the spontaneous intoxication. Muscle atrophy and pallor were the only macroscopic changes observed in spontaneous and in experimental intoxication. Histological lesions of spontaneous and experimental animals were similar. The most prominent lesion was cytoplasmic vacuolation in neurons of the central and the autonomous nervous system, pancreatic acinar cells, hepatocytes, Kupffer cells, follicular epithelial cells of the thyroid gland, and macrophages of the lymphatic tissues. Neuronal necrosis, axonal spheroids formation, and astrogliosis were additionally observed in the brain. Ultrastructurally, the cytoplasmic vacuoles consisted of distended lysosomes surrounded by a single-layered membrane. Nonreduced end-rests or sequence of alpha-Man, alpha-Glc, beta(1-4)-GlcNAc, and NeuNAc on lysosomal membrane were revealed by lectin histochemistry. Samples of plants used in the experimental trial contained swainsonine and calystegine and their intermediary derivate. We conclude that I fistulosa induces a glycoprotein storage disease primarily based on the inhibition of the lysosomal alpha-mannosidase by the alkaloid swainsonine.
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PMID:Spontaneous and experimental glycoprotein storage disease of goats induced by Ipomoea carnea subsp fistulosa (Convolvulaceae). 1731 94

During February-April 2004, an estimated 400-500 free-ranging elk (Cervus elaphus) developed paresis, became recumbent, and died or were euthanized in the Red Rim Wildlife Habitat Management Area (RRWHMA), Wyoming, USA. Elk were found in sternal recumbency, alert and responsive, but unable to rise. Their condition progressed to lateral recumbency followed by dehydration, obtundation, and death. Gross lesions were limited to degenerative myopathy, with pallor and streaking in skeletal muscles. Microscopically, affected muscles had degenerative lesions of varying duration, severity, and distribution, some with early mineralization and attempts at regeneration. Diagnostic testing ruled out common infectious, inflammatory, toxic, and traumatic causes. Tumbleweed shield lichen (Xanthoparmelia chlorochroa) was found in the area and in the rumen of several elk. This lichen was collected and fed to three captive elk. Two of these elk exhibited signs of ataxia, which rapidly progressed to weakness and recumbency after 7 and 10 days on this diet, respectively, and a degenerative myopathy, consistent with lesions observed in the elk affected at RRWHMA, was observed. All remaining elk migrated from the RRWHMA during the spring and no subsequent losses have been documented.
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PMID:Paresis and death in elk (Cervus elaphus) due to lichen intoxication in Wyoming. 1769 88

Juvenile myelomonocytic leukemia (JMML) is a distinct myeloproliferative malignancy of early childhood with a varied clinical presentation that may include failure to thrive, malaise, fever, bleeding, pallor, lymphadenopathy, and hepatosplenomegaly. Skin, pulmonary, and gastrointestinal involvement have also been reported. There are no reports of central nervous system (CNS) involvement at diagnosis of this disease. This is a report of a 21-month old boy who had a right facial paresis at presentation. A brain mass was demonstrated on magnetic resonance imaging and cerebrospinal fluid analysis confirmed CNS leukemic infiltration. We report the presence of CNS infiltration as a part of the natural course of JMML and provide a review of the literature.
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PMID:Juvenile myelomonocytic leukemia presenting with facial nerve paresis: a unique presentation. 1798 96


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