Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective double blind randomized trial comparing two different dose schedules of continuous steroid coverage during prophylactic cranial radiotherapy (CRT) in leukemic children was conducted to find out the optimum dose to be prescribed to reduce the incidence of Somnolence Syndrome (SS). Between April 1994 and February 1996, 32 patients with acute lymphoblastic leukemia received CRT of 18 Gy in 10 fractions. Patients were randomized to receive oral dexamethasone of 2 or 4 mg/m2 during radiotherapy. The diagnosis of SS was made clinically based on symptoms of somnolence. All patients were followed for a minimum of 8 months. The overall incidence of SS was 40%. The development of SS was steroid dose dependent. In low dose steroid arm the incidence of SS was 64.3% (9/14), compared to 17.6% (3/17) in high dose arm with statistically significant difference (P = 0.008). The median time to development of SS was 4 weeks. The most common symptom of SS was drowsiness followed by anorexia, headache, nausea, vomiting, decreased activity, irritability, fever and ataxia, respectively. The duration of symptoms ranged from 2 to 14 days. The development of SS was not related to the presence of acute reactions, age at the time of CRT and sex. In all cases the symptoms subsided completely and spontaneously. Our results suggest that steroid coverage at a dose of 4 mg/m2 during CRT reduces the incidence of SS. However, a multicentric prospective randomized trial is needed to determine the role and the optimal dose of steroid.
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PMID:Reduced incidence of the somnolence syndrome after prophylactic cranial irradiation in children with acute lymphoblastic leukemia. 975 69

Since 1984, a significant number of privately owned and feral horses on Easter Island have died of a syndrome consisting of progressive anorexia, weight loss, obtundation, and other central nervous system abnormalities. A single horse experiencing clinical signs of the reported syndrome was identified, examined and necropsied. Clinical signs included inappetence, emaciation, ataxia and icterus. Gross necropsy findings included hepatic enlargement and mottling, ascites and gastric impaction. Histopathological lesions included hepatic hemorrhage and necrosis, periportal megalocytosis, portal fibrosis, bile duct hyperplasia and multinucleate hepatocytes. Crotalaria grahamiana and C pallida, were identified in the pasture of the presenting horse, and found to be widespread on the island. Alkaloid fingerprinting identified grahamine, monocrotalin, and a grahamine analog in C grahamiana. A retrorsine analog and a senecionine analog were identified in C pallida. The highly characteristic lesions and the identification of pyrrolizidine alkaloids in the 2 plants strongly suggest that ingestion of 1 or both of the Crotalaria species led to chronic liver damage and hepatic encephalopathy in the presenting horse. Widespread distribution of C grahamiana on the island and reported temporal and seasonal trends in incidence among horses and cattle suggest that C grahamiana may be responsible for extensive morbidity and mortality among horses and cattle on Easter Island.
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PMID:Hepatotoxicity associated with pyrrolizidine alkaloid (Crotalaria spp) ingestion in a horse on Easter Island. 1019 40

Here we report a case of acute cerebellitis, in which the patient developed right peripheral facial palsy during the recovery phase of cerebellar ataxia. A 67-year-old man developed truncal and limb ataxia following a fever, general fatigue and anorexia. He was diagnosed to have acute cerebellitis. While the ataxia symptoms were improving without any treatment, right peripheral facial nerve palsy developed and an MRI revealed an enhancement of the right facial nerve proximal to the geniculate ganglion. After treatment with acyclovir and corticosteroids, his facial nerve palsy and ataxia both gradually improved. There has been no previous report of an adult case who developed peripheral facial nerve palsy during the recovery phase of acute cerebellitis. This case indicates that a wide spectrum of neurological complications may develop in association with a varicella-zoster virus infection.
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PMID:[An adult case of peripheral facial nerve palsy following acute cerebellitis associated with high antibody titers against varicella-zoster virus]. 1034 52

Unusual clinical and pathological observations in the field in goats and sheep suffering from Strongyloides papillosus infection prompted experimental work on this parasite. Goats were infected percutaneously with either single or multiple, low or high levels of S. papillosus. Young goats up to 12 months of age were found to be the most susceptible. Some animals, however, showed substantial resistance to infective doses. Clinical signs included transient diarrhoea, misshapen, elongated faecal pellets terminally, dehydration, anorexia, cachexia, gnashing of teeth, foaming at the mouth, anaemia and nervous signs such as ataxia, a wide-based stance, stupor and nystagmus. A 'pushing syndrome' was seen in 22% of the animals. The pathological changes are described and included enteritis, status spongiosus in the brain, hepatosis leading to rupture of the liver, nephrosis, pulmonary oedema, interstitial pneumonia and pneumonia. About 6% of the goats died acutely from fatal hepatic rupture. The development of an acquired immunity was determined. The immunity elicited an allergic skin reaction at the application site of larvae or injection sites of larval metabolites. This immunity, however, could be breached by large doses of larvae. The most profound clinicopathological changes induced by the parasites were an anaemia (most pronounced in the young goats) and hypophosphataemia. Trace element analyses provided evidence of Cu, Mn and possibly Se deficiencies in some goats.
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PMID:Experimental studies with Stronglyloides papillosus in goats. 1063 9

Equine granulocytic and monocytic ehrlichiosis caused by Ehrlichia equi and E. risticii, respectively, are seasonal diseases in horses that occur throughout the United States E. equi is transmitted by lxodes ticks and causes high fever, depression, anorexia, limb edema, petechiation, icterus, ataxia, and stiffness in gait. E. risticii, also known as the agent of Potomac horse fever, causes a febrile illness with a colitis of variable severity. Its occurrence is associated with aquatic habitats. The natural route of transmission is oral, through the ingestion of E. risticii infected trematode stages either free in water or in an intermediate host, such as aquatic animals.
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PMID:Ehrlichial diseases. 1121 45

Susceptibility of sheep to oral administration of Citrullus colocynthis fruits, Nerium oleander leaves or their mixture is described in 12 sheep assigned as untreated controls, C. colocynthis-treated at 0.25g/kg/day, N. oleander-treated at 0.25g/kg and plant mixture-treated at 0.25g of C. colocynthis/kg plus 0.25g of N. oleander/kg. The daily use of 0.25g of C. colocynthis/kg for 42 days was not fatal to sheep and caused slight diarrhoea, catarrhal enteritis, centrilobular hepatocellular fatty change and degeneration of the renal tubular cells. Single oral doses of 0.25g of N. oleander/kg were lethal to sheep within 18-24h and caused uneasiness, grinding of the teeth, dyspnoea, anorexia, frequent urination, ruminal bloat, ataxia and recumbency before death. The main lesions were widespread congestion and haemorrhage, pulmonary cyanosis and emphysema and severe hepatonephropathy. Rapid death was also observed in sheep receiving single doses of the mixture of the two plants. Effects were correlated with changes in the activities of serum lactic dehydrogenase (LDH) and aspartate transaminase (AST) and concentrations of cholesterol, bilirubin, total protein, albumin, globulin and urea and haematological parameters.
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PMID:Response of Najdi sheep to oral administration of Citrullus colocynthis fruits, Nerium oleander leaves or their mixture. 1132 8

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Anorexia is defined as diminished appetite or aversion to food. Clinical manifestations of anorexia have multiple etiologies, which include systemic illness, pain, fever, stress, metabolic disorders, and decreased palatability and learned aversion to food. Disorders of appetite are common in companion and laboratory animal medicine. Anecdotal evidence and personal experience suggest that propofol (2, 6-diisopropylphenol), when given intravenously at subhypnotic doses, causes acute appetite stimulation in dogs. The establishment of a dose-response effect could have important clinical applications; therefore, this study attempts to qualify and quantify the effect of propofol on appetite stimulation in healthy young adult dogs. Six purpose-bred male dogs (age, 6 months) were obtained from a Class A vendor. Dogs were housed individually and provided water ad libitum throughout the study period. All dogs were fed ad libitum to ensure that test conditions and degree of satiety were identical. Each dog was assigned randomly to either an experimental group or control each day of the study. The experimental groups received single bolus intravenous injections of propofol at different dosage levels (0.5, 1.0, 1.5, 2.0, or 3.0 mg/kg of body weight), and the control group received saline. The administrator was blinded to the animals identification and dose. Dosages greater than 3.0 mg/kg resulted in profound sedation and ataxia, which physically inhibited the dogs from obtaining the food; therefore 3.0 mg/kg was the highest dose tested. Dogs were weighed daily to ensure accurate dosing. Dosing was performed at the same time each day to minimize variability. Food intake amounts were recorded at 15, 30, 60, 120, and 1440 min after injection. Food intake was expressed as [food intake (g)/ body weight (kg)/ unit time (min)]. After a 1-w rest period, the study was repeated. Data were analyzed with a type RBF-65 randomized-block factoral design (ANOVA). Each dog served as its own control. The two experiments were analyzed separately, and a P-value of less than 0.05 was used to declare statistical significance. A significant (P, 0.05) increase in food consumption was observed solely during the 0-to-15-min time interval; no significant increase in food consumption was observed at any other time point. This data supports propofols appetite stimulating effect in the initial 15 min after injection. Additional studies are required to explore the mechanism for this effect and to determine whether it occurs in other species.
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PMID:The effect of propofol administered intravenously on appetite stimulation in dogs. 1148 52

A 12-year-old crossbred female cat was presented for necropsy with a history of anorexia, ataxia, convulsions, and blindness. Grossly, a whitish, firm, and well-circumscribed nodule with an irregular surface of approximately 1.5 cm in diameter was observed in the right dorsal, parietal, and occipital lobes of the brain. Histologically, the tumor was composed of neoplastic astrocytes forming irregular interweaving sheets and bundles. These cells were elongated, spindle-shaped, and bipolar, and some had clear cytoplasm and a dense nuclear chromatin pattern. Extensive areas of cartilaginous and osseous metaplasia were observed. By immunohistochemistry, the neoplastic cells were found to be markedly positive for S-100 protein and glial fibrillary acidic protein. On the basis of morphologic and immunohistochemical features, the diagnosis of pilocytic astrocytoma was made.
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PMID:Pilocytic astrocytoma in a cat. 1245 Feb 12

For the first time Ovine Herpesvirus 2 (OvHV-2) was identified in Swiss pigs as the causative agent of Porcine Malignant Catarrhal Fever (MCF). Diseased animals from two farms were observed to show weakness, anorexia, fever up to 41 degrees C, and neurological symptoms, i.e. ataxia, convulsions and hyperesthesia, erosion on the snout and in the oral and nasal mucosa, as well as multiple skin lesions. Histopathological findings included severe non-purulent inflammation with mononuclear cell infiltration in several organs. Most dominant were meningo-encephalitis, disseminated nephritis as well as purulent catarrhalic bronchopneumonia. The findings were quite reminiscent of the lesions due to MCF in cattle and give therefore substantial proof to use Porcine Malignant Catarrhal Fever as the term for the disease. Identification of the causative agent was done with a quantitative PCR specific for OvHV-2. Different tissues from diseased animals were positive. Furthermore, one animal which had been ill for more than five days tested positive for antibodies against an epitope conserved among MCF viruses. Serum samples from diseased animals reacted negative towards Classical Swine Fever- and Pseudorabies virus antigen. A weakly positive reaction against porcine enterovirus type I argued against the involvement of enteroviruses in the observed disease. Moreover, by means of different conventional PCRs, we detected the newly discovered porcine lymphotropic herpesviruses for the first time in Switzerland and could at the same time exclude their involvement in Porcine Malignant Catarrhal Fever.
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PMID:[Porcine malignant catarrhal fever: diagnostic findings and first detection of the pathogenic agent in diseased swine in Switzerland]. 1264 51


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