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)

Hyperkalaemic periodic paralysis(HYPP) is characterized by intermittent episodes of muscular tremor, weakness, and collapse, and is probably caused by abnormal electrolyte transport in the muscle cell membrane. During an episode of HYPP, most animals are severely hyperkalaemic. HYPP is a hereditary disease and occurs only in American Quarter horses or crossbreds. Because these horses are now being imported into the Netherlands, HYPP should be included in the differential diagnosis of horses showing signs of muscle tremor, paresis, or paralysis. The present article reviews the literature on HYPP and describes a case showing typical signs of the disease.
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PMID:[HYPP: hyperkalemic periodic paralysis in the horse]. 1018 80

A 2-year-old Thoroughbred filly was admitted to the hospital for evaluation of exercise intolerance. Resting videoendoscopic evaluation (i.e., while the horse was standing) of the nasopharynx and trachea revealed right arytenoid paresis and a tracheal defect that was 100 cm distal to the external nares. Surgery, consisting of a right prosthetic laryngoplasty, was performed. However, postoperative videoendoscopic evaluation revealed minimal abduction of the affected arytenoid cartilage. Dynamic videoendoscopic evaluation (i.e., while the horse was exercising) revealed the right arytenoid to be fixed in a submaximal position with no evidence of collapse into the airway. When the endoscope was positioned in the midcervical tracheal region, marked tracheal collapse was identified during exercise. Tracheal collapse can critically limit athletic function. Treatment of tracheal collapse depends on causative factors, the length of the trachea involved, and accessibility of the affected tracheal segment. The use of dynamic tracheal videoendoscopy should be considered in athletic horses with exercise intolerance in which the cause cannot be determined from resting or dynamic videoendoscopic evaluations of the nasopharynx.
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PMID:Dynamic tracheal collapse as a cause of exercise intolerance in a thoroughbred. 1070 89

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

Blastomycosis was diagnosed in six nondomestic felids from eastern Tennessee, including two Asian lions (Panthera leo persicus), one African lion (Panthera leo), one Siberian tiger (Panthera tigris), one cheetah (Acinonyx jubatus), and one snow leopard (Panthera uncia). Clinical signs included lethargy, anorexia, weight loss, dyspnea, sneezing. ataxia, and paresis. Variable nonspecific changes included leukocytosis, monocytosis, moderate left shift of neutrophils, moderate hypercalcemia, hyperproteinemia, and hyperglobulinemia. Thoracic radiographs revealed interstitial and alveolar changes, consolidation or collapse of a lung lobe, bullae formation, and a pulmonary mass. Agar gel immunodiffusion (AGID) serology for Blastomyces dermatitidis was performed in five felids and was positive in three. The tiger had cerebral blastomycosis and was positive for AGID serologic tests of both cerebrospinal fluid and serum. One percutaneous lung aspirate in the snow leopard and one bronchial aspirate in an Asian lion demonstrated B. dermatitidis organisms. whereas tracheal wash samples and a nasal discharge were nondiagnostic in others. Treatment with itraconazole was attempted in four cats. The tiger improved before euthanasia, whereas the others did not survive beyond initial treatments. In four felids, B. dermatitidis was found in the lungs and tracheobronchial lymph nodes associated with a florid pyogranulomatous reaction; the tiger had a pyogranulomatous encephalomyelitis, and the cheetah had a single pulmonary granuloma. Thoracic radiography, cytologic examination of lung lesion aspirates, and B. dermatitidis AGID serology should be performed on clinically ill zoo felids in endemic areas to rule out blastomycosis.
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PMID:Blastomycosis in nondomestic felids. 1458 83

A 4-year old, female spayed terrier was referred for hind end paresis that rapidly progressed to paralysis. Spinal radiographs revealed vertebral collapse and bony lysis. Myelography confirmed spinal cord compression and surgical exploration found an extradural soft tissue mass. Metastatic anal sac adenocarcinoma was diagnosed at postmortem examination.
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PMID:Metastatic anal sac adenocarcinoma in a dog presenting for acute paralysis. 1536 42

Ten dogs with neuroendocrine carcinoma of the liver were selected for inclusion in the study. Clinical signs were anorexia (7), vomiting (5), polydipsia/polyuria (3), icterus (2), lethargy (2), weight loss (2), paresis (1), ataxia (1), weakness (1), collapse (1), and urinary tract infection (1). Hematologic and biochemical abnormalities included anemia (2/8), leukocytosis (4/8), high liver enzyme activity (serum alkaline phosphatase, 7/9; alanine transaminase, 7/9; aspartate transaminase, 8/9), and high total bilirubin (6/9). Grossly, the tumors were diffuse, involving all liver lobes in six dogs, and two dogs had various-sized nodules in addition to diffuse involvement. Histologically, there were eight tumors with solid or trabecular pattern (group A), one tumor with cords or rows of neoplastic cells (group B), and one tumor with multiple rosette-like structures (group C). Immunohistochemical studies revealed that all 10 neoplasms were positive for at least one of the endocrine markers used: neuron-specific enolase (NSE; 8/10), synaptophysin (5/10), and chromogranin-A (3/10). A panel of NSE, chromagranin-A, and synaptophysin detected 100% of the tumors in our series. Electron microscopy confirmed the diagnosis by the presence of intracytoplasmic neurosecretory granules in the two examined cases. Our results show that neuroendocrine markers commonly used in humans can be used for the diagnosis of hepatic neuroendocrine carcinoma in dogs, preferably a panel of synaptophysin, chromagranin-A, and NSE because chromogranin-A alone is not as useful in dogs as in humans.
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PMID:Canine hepatic neuroendocrine carcinoma: an immunohistochemical and electron microscopic study. 1575 67

Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation.
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PMID:Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau. 1690 61

This paper describes two different cases of acute suicidal arsenic trioxide intoxication. Case no 1. A 38-year-old man, alcohol abuser, who ingested 4-5 g dental paste, which corresponds to 2.2-2.7 g of pure arsenic trioxide, developed gastritis with vomiting and abdominal pain, but without diarrhea. No cardiovascular collapse or renal failure were observed. The patient developed also symptoms of central nervous system injury (minor left paresis) and transient hepatic impairment. A head CT revealed no pathological changes in the brain. Hepatic disturbance recovered in a few days and the patient could be discharged on the 12 day. Case no 2. A 57-year-old man, who ingested few grams of pure arsenic developed vomiting, abdominal pain and severe diarrhea. Cardiovascular collapse as a result of intravascular volume depletion, vasodilatation and myocardial dysfunction was observed. The patient died on the first day of hospitalization. In both cases treatment included gastric lavage, BAL therapy, haemodialysis and supportive measures.
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PMID:[Two different clinical cases of acute arsenic trioxide intoxication]. 1772 5

Femoral nerve palsy, mostly of iatrogen cause, leads to paresis of quadriceps muscle with complete loss of knee extension. Therapeutical options include neurolysis, nerve reconstruction or functional muscle transplantations. Another concept is the transfer of hamstring muscles as described in post polio surgery. We describe our experience of biceps femoris and semitendinosus muscle transfer for reconstruction of knee extension. From 2003 to 2007 seven patients (mean age 43) with complete loss of knee extension after femoral nerve lesion were treated. Nerve palsy was caused by direct lesion, traction, hematoma after collapse, lesion of lumbosacral plexus and an unclear muscle dystrophy. Indication for muscle transfer was due to long standing muscle paresis. All patients received a transfer of biceps femoris and semitendinosus muscle/tendon into the quadriceps tendon. Patients were immobilised in a cast for 6 weeks in extended knee position. Weight bearing started after 8 weeks. Operations went uneventfully. All patients were able to extend the knee postoperatively against gravity and were able to climb stairs without help. 4 Patients had complete knee extension, 2 had a lack of 20 degrees , one of 30 degrees. Daily routine was possible in all cases. No instability of knee joints occurred postoperatively. In a nerve lesion close to the muscle a nerve reconstruction should be aimed. If not performed or with unsuccessful outcome, muscle transfer is a good option to restore function. All recent studies describe good to excellent results with stable knees, allowing the patient to manage daily routine without assistance and to climb stairs up and down. Long term complications such as dislocation of patella or genu recurvatum were not observed in our patients. The latter results as typical complication in polio from weakening knee flexion through biceps femoris transfer, if the gastrocnemius muscle is not forceful enough. However in an isolated femoral nerve lesion this will rarely occur.
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PMID:[Reconstruction of quadriceps femoris muscle function with muscle transfer]. 2023 8

The surgical treatment of ventral spinal canal compression has traditionally required either an anterior or combined anterior-posterior decompression and stabilization. These types of approaches carry a significant morbidity and may not be appropriate for all patients. We report our experience with multi-level corpectomies and reconstruction performed via a single, posterolateral approach. A retrospective review was performed of six consecutive patients at a single institution who were treated for ventral multi-level spinal cord compression via a single posterolateral approach. All six patients underwent reconstruction and stabilization with an expandable cage and posterior fixation. Five patients had metastatic cancer with spinal cord compression and one patient had osteomyelitis with a ventral epidural abscess and vertebral body collapse. All patients underwent 2-level corpectomies. Pre-operative and post-operative neurologic function and stabilization construct integrity were analyzed. All patients had successful decompression and stabilization and there were no hardware complications. Three peri-operative complications were encountered: post-operative pleural effusion needing thoracostomy drainage, transient leg paresis that resolved at 2months and a post-operative wound infection needing operative debridement. At last follow-up all patients had improvement or stabilization of their neurological function. Long-term follow-up was limited by the progression of metastatic disease and death in all the patients with cancer. This study demonstrates that symptomatic improvement can be achieved in select patients requiring multi-level corpectomies when using a single posterolateral approach with expandable cage reconstruction and posterior stabilization.
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PMID:Multi-level corpectomies and reconstruction via a single posterolateral approach. 2069 72


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