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)

A 3-year-old female ferret died five days after admission to a veterinary clinic for treatment of acute dyspnea and posterior paresis. Blood chemistry showed no hypergammaglobulinemia. Histopathological examination revealed mild to severe inflammatory infiltrates, composed mostly of plasma cells, in multiple organs. Lesions were especially severe in the kidneys, where focal segmental membranous glomerulopathy was also present. In the liver, in addition to lymphocytic and plasmacytic infiltration in periportal areas, dilatation and proliferation of the bile ducts were seen. On analysis of PCR products, using primers directed against the gene encoding Aleutian disease (AD) viral capsid and formalin-fixed kidney samples, we detected a single band of about 400 bp, specific to the AD virus.
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PMID:Spontaneous Aleutian disease in a ferret. 1085 10

This report describes a case of a 17-year-old girl with Charcot-Marie-Tooth disease (CMT) representing rigid spine and respiratory failure. At age 11, she tended to walk on her toes and had difficulty in getting up from the floor without support. She became aware of flexion limitation of the neck at the age of 12. At 15 years of age, She began to have dyspnea on effort. When she was 17 years old, neurological examination revealed mild weakness of the upper extremities and severe weakness of the distal lower extremities, generalized wasting and areflexia. Superficial sensation was mildly impaired distally, and vibration sensation was severely impaired in the lower extremities. Motor and sensory nerve conduction velocities were mildly reduced, and compound muscle action potential of the tibial and peroneal nerves and sensory nerve action potential on ulnar and sural nerves were absent. Electromyography showed neurogenic changes with denervation potentials. Sural nerve biopsy revealed severe loss of myelinated fibers without any onion-bulb formation. As for family history, her elder sister showed moderate loss of vibration sensation in the lower extremities. On the basis of these findings, she was diagnosed as having CMT type 2, though a mode of inheritance was uncertain. She also had peculiar findings of flexion limitation of the spine (rigid spine), contracture of the hip joint, and fatty degeneration of paraspinal muscles on CT. Percent vital capacity (VC) was 22.5%, and arterial blood gas analysis showed PaO2 of 60.5 mmHg and PaCO2 65.0 mmHg. To our knowledge, this is the first case of CMT accompanied by rigid spine and respiratory failure. Motor and sensory neuropathy combined with rigid spine also have not been reported previously. The relationship between rigid spine syndrome with neurogenic muscular atrophy and CMT type 2C with the clinical characteristics of diaphragm and vocal cord paresis is discussed.
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PMID:[A patient of Charcot-Marie-tooth disease with rigid spine and respiratory failure]. 1100 24

A 22-week-old 21-kg female Bernese Mountain Dog ingested a topical antipsoriatic preparation containing the synthetic vitamin D analog tacalcitol. The dog died after a history of lethargy, recumbency, paresis of the hindlimbs, increased rectal temperature, dyspnea, and hematemesis. Histologic examination revealed metastatic calcification in the kidneys, lungs, myocardium, brain, stomach, and tear glands. The appearance of soft tissue mineralization in multiple organs is consistent with hypercalcemia derived from excessive vitamin D uptake. Oral toxicity studies for tacalcitol in the dog are not available, but the present report emphasizes the extraordinary toxic risk of drugs containing this vitamin D analog to dogs.
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PMID:Metastatic calcification in a dog attributable to ingestion of a tacalcitol ointment. 1105 79

The lower cranial nerves (CN. IX-XII) are responsible for the nerve supply of the pharyngolaryngeal region. Loss of innervation is manifested by dysphagia, aspiration, altered speech production, dyspnea and/or stridor, and visible loss of movement. In general electrophysiological testing should be applied in every kind of paresis. Beside standard equipment for electromyography limited special equipment is necessary. Examination under local anaesthesia is possible and can serve as a basis for therapeutic consequences. In this article general aspects as seen from an oto-rhino-laryngological standpoint are presented.
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PMID:[Electrophysiological diagnosis of the caudal cranial nerves]. 1119 66

Fourteen patients with severe neuroparalytic snake envenomation, resulting in acute type II respiratory failure, admitted to respiratory critical care unit for mechanical ventilation during one year period, were studied. Ventilatory requirements, amount of anti snake venom (ASV) infused, period of neurological recovery and hospital survival were evaluated. All patients had severe manifestations such as ptosis, extraocular muscle paresis and limb weakness along with dyspnoea. Seven patients (50%) had additional complaints of dysphagia and dysphonia. ASV was administered to all, with a median requirement of 900 ml. Mechanical ventilation was required for a median duration of 17 hours and all except one patient, who had suffered irreversible hypoxic cerebral injury prior to resuscitation, survived with complete neurological recovery. We conclude, that the timely institution of ventilatory support and anti-venom therapy in such patients, is associated with an excellent outcome.
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PMID:Management of respiratory failure in severe neuroparalytic snake envenomation. 1130 37

The case of dyspnoea, exaggerated when in the supine position and during exertion, as a result of severe weakness of the diaphragm is reported. The aim of the study was to present a rare case of idiopathic bilateral diaphragmatic paresis (BDP) and to describe all the diagnostic procedures necessary to perform differential diagnostics. In order to establish the final diagnosis, chest radiography, haemodynamic evaluation of the circulatory system, ultrasonography, ultrasonocardiography, measurement of transdiaphragmatic pressures, scintiscanning of the lungs, spirometry, analysis of arterial blood gases, computed tomography of the thorax and external stimulation of the phrenic nerve were performed. The measurement of transdiaphragmatic pressure was crucial to establish and confirm the diagnosis of BDP, as only a small difference in gastric and oesophageal pressures during tidal breathing and inspiratory efforts was recorded. As no cause of diaphragmatic paresis was found, the case was classified as idiopathic. The final diagnosis of non-trauma related bilateral diaphragmatic weakness was generally delayed. In the case of the described patient, dyspnoea, the main symptom he was suffering from, was supposed to result from his congenital heart defect. We recommend that the suspicion of idiopathic diaphragmatic paresis should always be raised in patients suffering from respiratory failure of unknown origin. It is, however, necessary to perform extensive diagnostics to exclude the other causes of phrenic-diaphragmatic impairment. It's also necessary to consider all infections, injuries and surgical procedures within the thorax as possible causes of diaphragmatic paresis.
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PMID:Dyspnoea exaggerated in the supine position and during exertion--diagnostic challenge. 1140 3

The acute toxicity of dried Nerium oleander leaves to Najdi sheep is described in 12 sheep assigned as untreated controls, N. oleander-treated once at 1 and 0.25 g/kg body weight and N. oleander-treated daily at 0.06 g/kg body weight by drench. Single oral doses of 1 or 0.25 g of dried N. oleander leaves/kg body weight caused restlessness, chewing movements of the jaws, dyspnea, ruminal bloat, incoordination of movements, limb paresis, recumbency and death 4-24 hr after dosing. Lesions were widespread congestion or hemorrhage, pulmonary cyanosis and emphysema, hepatorenal fatty change and catarrhal abomasitis and enteritis. The daily oral doses of 0.06 g dried N. oleander leaves/kg body weight caused less severe signs and death occurred between days 3 and 14. In these animals, the main lesions were hepatonephropathy and gelatinization of the renal pelvis and mesentry and were accompanied by significant increases in serum AST and LDH activities, in bilirubin, cholesterol and urea concentrations and significant decreases in total protein and albumin levels, anemia and leucopenia.
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PMID:Acute toxicity of various oral doses of dried Nerium oleander leaves in sheep. 1178 96

Myotonic dystrophy type 1 (DM1) is the most common inherited muscle disorder and may present in numerous ways due to characteristic multisystem involvement. We report a 47-year-old man who presented with an 8-year history of slowly progressive dyspnea and episodic stridor. The laryngeal paresis was documented with videostroboscopy and laryngeal electromyography, and treated with tracheostomy and antimyotonia agents.
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PMID:Myotonic dystrophy type 1 (DM1) presenting with laryngeal stridor and vocal fold paresis. 1193 83

A 76-yr-old woman was scheduled for left upper extremity orthopedic procedure. Preoperative examinations were within normal limits except forced vital capacity. Interscalene brachial plexus block with 0.25% bupivacaine 15 ml, was performed under general anesthesia. Her intraoperative course was uneventful. She, however, complained of the dyspnea after removal of a tracheal tube, and Spo2 dropped to 89%. A chest X-ray demonstrated the elevation of hemidiaphragm. She was diagnosed as ipsilateral hemidiaphragmatic paresis, treated with oxygen inhalation under deep breathing for approximately one hour, and then transferred to the common ward. We conclude that respiratory movement should be carefully observed following interscalene brachial plexus block especially in geriatric patients.
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PMID:[A case report of hemidiaphragmatic paresis caused by interscalene brachial plexus block]. 1222 42

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are distinct but related aspects of the same dynamic disease process known as venous thromboembolism (VTE). An estimated 200,000 new cases occur in the United States every year, including 94,000 with PE, resulting in an incidence of 23 per 100,000 patients per year-cases. Without treatment, pulmonary embolism is associated with a mortality rate of approximately 30%, causing nearly 50,000 deaths per year. Moreover, based on post-mortem studies, two-thirds of the patients with pulmonary emboli remain undiagnosed. Clinically, PE may present as (1) isolated dyspnea, (2) pleuritic pain and/or hemoptysis, and (3) circulatory collapse. However, clinical history and examination can be notoriously misleading in reaching a diagnosis. A number of acquired etiologic risk factors (predispositions) are associated with a tendency to develop VTE. These include increasing age, immobilization, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, as well as certain types of oral contraception and hormone replacement therapy. In addition, a variety of genetic risk factors, such as factor V Leiden, protein S or C deficiency have also been identified. However, in at least half of the instances, no predisposing factors can be identified (idiopathic PE). In the majority of cases thromboemboli originate in the deep veins of the calf or pelvis. The pathogenic conditions for VTE comprise a triad of factors and include (1) venous stasis, (2) hypercoagulable states, and (3) vascular endothelium injury. Occlusion of pulmonary arteries has variable and transient clinical and pathophysiologic consequences, involving both mechanical and reflex effects of vascular occlusion with a consecutive perfusion defect as well as the release of vasoactive and other inflammatory mediators. The objectives of this article are to present an overview of the etiologic and pathogenic factors promoting VTE as well as the pathophysiologic and inflammatory processes following PE.
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PMID:Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis. 1258 87


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