Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the course of multiple episodes of thiamine deficiency in the rhesus monkey, the triad of anorexia, apathy, and hind limb weakness is the earliest clinical manifestation. In later episodes, nystagmus, abducens paresis, midline ataxia, dysmetria, and congestive heart failure are also seen. With the exception of dysmetria, the neurologic signs promptly respond to thiamine administration. Pair-fed controls showed no clinical signs. Neither peripheral neuropathy nor edema was observed. Thiamine-deficiency in the experimental animals was confirmed by blood transketolase assays.
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PMID:Clinical manifestations of chronic thiamine deficiency in rhesus monkey. 40 80

Cattle consuming only Kochia scoparia in a pasture southeastern Colorado became ill. Clinical signs were lacrimation, depression, anorexia, nystagmus, head pressing, and recumbency. Some cattle died acutely, with the only clinical signs being recumbency, nystagmus, and occasionally opisthotonos. Pathologic findings were pulmonary edema and congestion, hepatic necrosis and fibrosis, necrosis of proximal convoluted tubular epithelium in the kidneys, epidermal necrosis of lightly pigmented areas, and laminar cerebrocortical necrosis. When the cattle were removed from the pasture, the problem ceased.
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PMID:Polioencephalomalacia and photosensitization associated with Kochia scoparia consumption in range cattle. 50 Apr 79

Clinical signs of toxicosis, neurologic lesions, and increased tissue residues of methylmercury (MM)were produced in 9 cats by oral administration of 1.29 and 0.86 mg of Hg/kg of body weight/day as methylmercuric hydroxide. Clinical signs, which began after 15 days of exposure, included anorexia, ataxia, hypermetria, proprioceptive impairment, blindness, vertical nystagmus, and grand mal convulsions. Significant lesions occurred in cerebrum, brainstem, and cerebellum and correlated well with clinical signs. Microscopic central nervous system lesions consisted of neuronal degeneration, necrosis and loss of neurons, swollen axons, demyelination, loss of nerve cell processes, vacuolation of neuropil, gliosis, neuronophagia, perivascular cuffs, endothelial hypertrophy and hyperplasia, leptomeningitis, and infrequent vascular necrosis. Overall distribution of central nervous system lesions was unrelated to daily dose, but more advanced lesions were produced by the smaller daily dose. Mean tissue residues of MM were generally directly related to daily dose, and the average distribution among tissues was constant, with highest concentrations in liver, followed by kidney, spleen, muscle, and brain. In utero exposure of kittens to MM, revealed transplacental accumulation.
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PMID:Pathology of subacute methylmercurialism in cats. 83 68

A case of acute lymphoblastic leukemia (ALL) which showed extensive demyelinated lesion of the brain stem during complete remission is presented. A 13 year-old girl who was diagnosed as ALL in February, 1987 was treated according to the TCCSG L84-11 protocol, which induced complete remission in June, 1987. Her condition had been stable until April, 1988 when she abruptly complained of gait disturbance, vertigo and anorexia. She was subsequently admitted to our hospital. At the time of admission, she had ataxic gait, horizontal nystagmus towards right at dextroversion, bilateral exaggerated patellar tendon reflex, emotional incontinence, urinary incontinence and left 6th and 7th nerve palsy. In the middle of May, right spastic hemipalesia and hypesthesia became apparent. Left caudal pontine-basal lesion was suspected and was confirmed by MRI. Her synptoms progressed. Five months after admission, suffered repeated central apnea and died. Autopsy disclosed extensive cervical spinal cord. Cerebrum and cerebellum were intact. No evident findings suggesting the etiology were obtained. Whole skull radiation, intrathecal methotrexate, cytosine arabinoside and hydrocortisone might have contributed to the development of the demyelinated lesion.
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PMID:[Acute lymphoblastic leukemia with extensive demyelinated lesion of the brain stem during complete remission]. 140 57

Metronidazole, administered to 5 dogs for periods ranging from 3 to 14 days, was associated with acute development of CNS dysfunction. Metronidazole dosage ranged from 67.3 to 129.0 mg/kg of body weight/d. Clinical signs of toxicosis began with anorexia and intermittent vomiting and progressed rapidly to include pronounced, generalized ataxia and vertical, positional nystagmus. These signs were consistent with lesions of the vestibular nuclei and/or cerebellum. High CSF protein content was detected in 2 of 3 dogs from which CSF was collected. Two dogs were euthanatized because of severe neurologic dysfunction. Three dogs improved slowly and recovered completely over several months. These findings suggest that currently recommended dosages of metronidazole may be too high for some dogs.
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PMID:Central nervous system toxicosis associated with metronidazole treatment of dogs: five cases (1984-1987). 276 64

Infection with rickettsiae of the spotted fever group was clinically and serologically diagnosed in four dogs from two households on Long Island. In two dogs, clinical signs included high fever (to 40.5 C), abdominal pain, lethargy, depression, anorexia, and nystagmus. One of these dogs had conjunctivitis and petechial hemorrhages in the oral mucous membranes. The third dog initially had high fever, evidence of abdominal pain, anorexia, and depression. The fourth dog appeared clinically normal. Clinical signs disappeared following treatment with tetracycline given orally.
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PMID:Rocky Mountain spotted fever in dogs. 738 Jul 21

We report a 50-year-old male having metamorphopsia associated with retinal edema. He was well until one month prior to the present admission when he developed occipital headache and backache. Three weeks later, he noted a sudden onset of twisting of visual images. On admission, he was in no acute distress with well preserved general conditions. Only neurological abnormalities were bilateral papilledema, retinal edema and horizontal nystagmus with a rotatory component. Routine blood chemistries were unremarkable. The CSF contained 28 cells/cmm with 60% consisting of large atypical cells. Cranial CT scans revealed no mass, however, the magnified orbital CT showed bilateral swelling of the optic nerve. He was treated with ventriculoperitoneal shunt and Ommaya tube placement through which methotrexate, cytarabine and prednisolone were administered. He was also treated with systemic cisplatin, mitomycin-C and 5-fluorouracil. With these therapy, his headache, metamorphopsia and papilledema improved. He was discharged for out-patient follow-up, however, he had to admitted again because of progressive difficulty of gait and loss of appetite. On admission, he complained of severe backache, and his gait disturbance appeared to be in part due to his backache. A slight weakness was noted in all four limbs with loss of deep reflexes. Mentally he was alert and cranial nerves appeared intact without papilledema. But nuchal rigidity was noted. Cranial CT scan revealed attenuation of all the cortical sulci and marked diffuse low density changes in the cerebral white matter, and his chest film revealed a ring-shape shadow in his left lung field. He deteriorated progressively with terminal gastrointestinal hemorrhage. He expired three weeks after his second admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 50-year-old man with metamorphopsia and optic nerve swelling]. 819 34

Male rhesus monkeys (Macaca mulatta) were administered daily doses of the antimalarial drug arteether. The 14-day treated group received either 24 mg/kg/day, 16 mg/kg/day, or 8 mg/kg/day. The seven-day treatment group received either 24 mg/kg/day or 8 mg/kg/day. All control cases in each group received the sesame oil vehicle alone. Neurologic signs were absent for animals in the seven and 14-day treatment groups except for one monkey which showed diffuse piloerection on day 14, and another monkey receiving 24 mg/kg/day for seven days showed mild lethargy after the fourth day. Mild, sporadic anorexia was noted in all animals by day 14, and a single animal showed diffuse piloerection on day 14. Surgical anesthesia preceded killing by exsanguination and was accompanied by perfusion fixation of the central nervous system. Brain sections were cut and then stained for study by light microscopy. Evidence of neuronal pathology, both descriptive and numerical, was collected. The neuroanatomic and neuropathologic findings demonstrated that arteether produced extensive brainstem injury when administered for 14 days. The magnitude of brainstem neurotoxicity was dose-dependent, where injury was greatest at the 24 mg/kg/day dose level, less at the 16 mg/kg/day dose level, and least at the 8 mg/kg/day dose level. Arteether induced multiple systems injury to brainstem nuclei of 1) the reticular formation (cranial and caudal pontine nuclei, and medullary gigantocellular and paragigantocellular nuclei); 2) the vestibular system (medial, descending, superior, and lateral nuclei); and 3) the auditory system (superior olivary nuclear complex and trapezoid nuclear complex). The vestibular nuclei and the reticular formation were most severely injured, with the auditory system affected less. The cranial nerve nuclei (somatic and splanchnic) appeared to escape damage, with the exception of the abducens nerve nucleus. The same brainstem nuclear groups of seven-day treated monkeys appeared normal. The statistical data are concordant with the descriptive data in demonstrating neurotoxic effects. In summary, no neurologic deficits were detected in any of the vehicle control monkeys (14-day and seven-day cases). Monkeys in the 14-day treatment group were free of clinical neurologic signs throughout the first week. At day 14, fine horizontal nystagmus was seen in one monkey, and another monkey exhibited diffuse piloerection. Monkeys in the seven-day treatment group were free of clinical neurologic signs except for one case. This monkey was treated with 24/mg/kg/day of arteether and exhibited lethargy after the fourth day. These indications of dysfunction arose too late to be practical indicators of neurotoxicity.
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PMID:Arteether: risks of two-week administration in Macaca mulatta. 915 46

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

A 19-yr-old female lynx (Lynx canadensis) presented for an acute onset of anorexia and reluctance to move. Physical examination, radiography, hematology, and serum biochemistry revealed evidence of renal failure, presumptive uremic gastritis, chronic intervertebral disk disease at T13-L1, and markedly low serum levels of total thyroxine (1.54 nmol/L) and total triixodothyronine (0.55 nmol/L). Twenty-five hours after its original presentation, the lynx exhibited horizontal nystagmus, which has been suggested as a clinical sign associated with hypothyroidism in domestic dogs. The lynx was euthanatized because of poor prognosis, and medical management concerns related to its chronic renal failure. Necropsy examination substantiated that the lynx had true hypothyroidism with 60-90% of the thyroid gland replaced with adipose tissue. Although feline adult-onset hypothyroidism may have low incidence, it should still be considered as a cause of nonspecific signs of disease in cats, as well as signs suggestive of hypothyroidism. Routine monitoring of baseline exotic felid thyroid levels throughout life would help to identify normal values and diagnose a potential disease that has obscure clinical signs.
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PMID:Adult-onset hypothyroidism in a lynx (Lynx canadensis). 1458 93


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