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)

Unprecedented mortality occurred in bald eagles (Haliaeetus leucocephalus) at DeGray Lake, Arkansas, during the winters of 1994-1995 and 1996-1997. The first eagles were found dead during November, soon after arrival from fall migration, and deaths continued into January during both episodes. In total, 29 eagles died at or near DeGray Lake in the winter of 1994-1995 and 26 died in the winter of 1996-1997; no eagle mortality was noted during the same months of the intervening winter or in the earlier history of the lake. During the mortality events, sick eagles were observed overflying perches or colliding with rock walls. Signs of incoordination and limb paresis were also observed in American coots (Fulica americana) during the episodes of eagle mortality, but mortality in coots was minimal. No consistent abnormalities were seen on gross necropsy of either species. No microscopic findings in organs other than the central nervous system (CNS) could explain the cause of death. By light microscopy, all 26 eagles examined and 62/77 (81%) coots had striking, diffuse, spongy degeneration of the white matter of the CNS. Vacuolation occurred in all myelinated CNS tissue, including the cerebellar folia and medulla oblongata, but was most prominent in the optic tectum. In the spinal cord, vacuoles were concentrated near the gray matter, and occasional swollen axons were seen. Vacuoles were uniformly present in optic nerves but were not evident in the retina or peripheral or autonomic nerves. Cellular inflammatory response to the lesion was distinctly lacking. Vacuoles were 8-50 microns in diameter and occurred individually, in clusters, or in rows. In sections stained by luxol fast blue/periodic acid-Schiff stain, the vacuoles were delimited and transected by myelin strands. Transmission electron microscopy revealed intramyelinic vacuoles formed in the myelin sheaths by splitting of one or more myelin lamellae at the intraperiodic line. This lesion is characteristic of toxicity from hexachlorophene, triethyltin, bromethalin, isonicotinic acid hydrazide, and certain exotic plant toxins; however, despite exhaustive testing, no etiology was determined for the DeGray Lake mortality events. This is the first report of vacuolar myelinopathy associated with spontaneous mortality in wild birds.
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PMID:Epizootic vacuolar myelinopathy of the central nervous system of bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana). 982 89

The comparative effects of diazinon and malathion on Najdi sheep were described in sheep allotted as untreated controls, diazinon-treated at 25 mg/kg/d or 50 mg/kg/d, and malathion-treated at 25 mg/kg/d or 50 mg/kg/d. Although serum cholinesterase (ChE) activity was reduced, neither significant clinical signs nor severe pathological changes were produced in sheep dosed orally with 25 or 50 mg diazinon/kg/d for 21 d. Both oral dose levels of malathion were lethal to sheep between 1 and 6 d and caused, prior to death, hyperexcitability, tremors, clonic convulsions, salivation, nasal discharge, incoordination of movement, paresis of the limbs and recumbency. Lesions were widespread congestion and hemorrhage, patchy pulmonary cyanosis, gastroenteritis and hepatonephropathy. These changes were accompanied by increases in the activities of serum SDH and AST, in the concentrations of urea, triglyceride and cholesterol, and decreases in ChE activity and in RBC, PCV and Hb values.
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PMID:Comparative effects of diazinon and malathion in Najdi sheep. 1050 28

Three-mo-old male Wistar rats were sprayed with 250, 500, 1000 and 2000 ppm amitraz 2 w apart or given single doses of 50, 100, or 250 mg/kg p.o, i.m. or i.p. No effects were observed in the amitraz-sprayed rats. Single doses of amitraz p.o, i.m. or i.p. was non-toxic at 50 mg/kg, toxic at 100 mg/kg and lethal at 250 mg/kg within 24 h of dosing. Survivors were killed 48 h post-dosing. Features of toxicity were depression, incoordination of movement, paresis of the limbs, hepatonephrotoxicity, muscular hemorrhage at site of injection and peritonitis following i.p. injection. These changes, accompanied by leucopenia, were correlated with alterations in serum AST and concentrations of serum constituents. Amitraz did not inhibit serum ChE activity.
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PMID:Effects of amitraz given by different routes on rats. 1059 39

Experimental spinal cord injury (SCI) via contusion of moderate severity results in residual locomotor deficits, including a lack of coordination and trunk stability. Given that muscle contractile properties and fiber composition adapt to reduced neural input and/or weight bearing, contusion-induced locomotor deficits may reflect changes in hindlimb skeletal muscle. Therefore, we examined muscle adaptations during early (1 week), intermediate (3 week), and late (10 week) stages of motor recovery after moderate SCI. Forty-two Sprague Dawley rats underwent SCI via 1.1mm cord displacement with the OSU impact device or served as age and weight-matched or laminectomy controls. Subsets of rats had soleus (SOL) in vitro physiological testing or SOL and extensor digitorum longus (EDL) myosin heavy chain (MHC) fiber type analysis. At 1 week post-SCI during paralysis/paresis, a significant decrease in wet weight occurred in the plantaris, medial/lateral gastrocnemius (MG/LG), tibialis anterior, and SOL. Changes in contractile properties of the SOL did not accompany muscle wet weight changes. By 3 weeks, the loss of weight-bearing activity early after SCI induced significant decreases in SOL peak twitch and peak tetanic tension as well as significantly greater IIx MHC expression in the EDL. By 10 weeks post-SCI, after several weeks of weight supported stepping, muscle wet weight, contractile properties and MHC composition returned to baseline levels except for MG/LG atrophy. Thus, muscle plasticity appears to be extremely sensitive to locomotor deficits and their resolution after moderate spinal cord contusion.
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PMID:Skeletal muscle adaptations following spinal cord contusion injury in rat and the relationship to locomotor function: a time course study. 1168 94

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

The ceroid-lipofuscinoses comprise a group of inherited storage diseases of human beings and animals that are characterised by progressive neurodegenerative disease and the accumulation within cells of a fluorescent lipopigment. A distinct syndrome occurs in Cocker spaniel dogs in which there is a generalised accumulation of a lipofuscin-like pigment, with such a heavy accumulation in smooth muscle that the intestine and other organs have a brown discolouration. Such discolouration is not observed in other forms of ceroid-lipofuscinosis. Dogs are clinically affected in adulthood and show progressive hind limb paresis, incoordination, and deficient postural reactions and proprioception. Spinal reflexes may be exaggerated. Behavioural or temperament changes, seizures or blindness may occur.
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PMID:Generalised ceroid-lipofuscinosis and brown bowel syndrome in Cocker spaniel dogs. 1603 90

There have been anecdotal reports since 1962 of 'staggers' in sheep grazing Romulea rosea infested pastures, but this is the first detailed account. In September 2005, a locomotor disorder developed in 12 of 120 Merino wethers that had grazed R. rosea infested pasture at Albury, New South Wales, over several months. Affected sheep displayed signs that included limb paresis, knuckling over in the fetlocks, fine head tremor, incoordination, and an equilibrium disturbance characterised by frequent falling. The microscopic examination of brain and spinal cord tissues from two affected sheep revealed mild vacuolation, occasional lymphocytic cuffing around blood vessels, mild Wallerian degeneration, and occasional glial cells that contained honey-brown cytoplasmic pigments. The most significant changes were found in the cerebellum, where there were decreased numbers of Purkinje cells, increased numbers of glial cells, scattered vacuoles and occasional swollen axons. Previous reports of cerebellar toxicoses in ruminants have involved goats and cattle and have been associated with the ingestion of six Solanum spp. The Purkinje cell loss in this type of disorder is ultimately extensive and consequently affected animals may survive, but will remain permanently disabled.
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PMID:Cerebellar ataxia in sheep grazing pastures infested with Romulea rosea (onion grass or Guildford grass). 1878 18

A 3-year-old Thoroughbred gelding presented with a history of neurological signs, including incoordination in his hindlimbs, of about 7 months' duration. On initial examination, the horse exhibited ataxia and paresis in all limbs with more severe deficits in the hindlimbs. Cervical radiographs displayed severe osteoarthritis of the articular processes between C5 and C6. On subsequent cervical myelography the dorsal contrast column was reduced by 90% at the level of the intervertebral space between C5 and C6. Cervical vertebral canal endoscopy, including epidural (epiduroscopy) and subarachnoid endoscopy (myeloscopy), was performed under general anaesthesia. A substantial narrowing of the subarachnoid space at the level between C6 and C7 was seen during myeloscopy, while no compression was apparent between C5 and C6. Epiduroscopy showed no abnormalities. After completion of the procedure, the horse was subjected to euthanasia and the cervical spinal cord submitted for histopathological examination. Severe myelin and axon degeneration of the white matter was diagnosed at the level of the intervertebral space between C6 and C7, with Wallerian degeneration cranially and caudally, indicating chronic spinal cord compression at this site. Myeloscopy was successfully used to identify the site of spinal cord compression in a horse with cervical vertebral stenotic myelopathy, while myelography results were misleading.
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PMID:Cervical vertebral canal endoscopy in a horse with cervical vertebral stenotic myelopathy. 2169 35

Lacunar syndrome is a neurodeficit secondary to a deep cerebral lesion, usually because of microatheroma of small arteries. Ataxic hemiparesis (AH) is a lacunar syndrome with unilateral pyramidal weakness and ipsilateral ataxia. Thalamic tuberculoma, as a cause of AH, has not been previously described in the literature. We describe an elderly man who presented with left hemiparesis and ipsilateral ataxia. Clinical examination revealed upper motor neuron left facial paresis and left-sided hemiparesis. The patient had incoordination in left upper and lower limbs. Mantoux test was positive and erythrocyte sedimentation rate was elevated. MRI of brain showed a conglomerated hypointense lesion in the right thalamus with a peripheral hyperintensity on T1-weighted imaging and a hyperintense lesion in T2-weighted imaging with significant perilesional oedema, suggesting a tuberculoma. The patient was treated with antitubercular therapy and was symptomatically better at the 9 months follow-up.
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PMID:Isolated thalamic tuberculoma presenting as ataxic hemiparesis. 2358 Jun 86

In the last five years in western Mongolia, a neurological disorder and resultant economic loss have developed in goats, sheep, cattle and horses: association of the disease with ingestion of Oxytropis glabra, a toxic plant, was suggested. Affected goats showed neurological signs, including ataxia, incoordination, hind limb paresis, fine head tremor and nystagmus. Three goats, one with moderate clinical signs and the other two with severe clinical signs, were necropsied and examined to describe and characterize the histologic, immunohistochemical and ultrastructural lesions. Although no gross pathological changes were observed in a variety of organs including the central nervous system of these goats, microscopic examination of the cerebellum demonstrated degenerative changes in all these goats, such as vacuolar changes and loss of Purkinje cells, torpedo formation in the granular layer, increased number of spheroids in the cerebellar medulla, and loss of axons and myelin sheaths of Purkinje cells. The chemical analysis of the dried plant detected 0.02-0.05% (dry weight basis) of swainsonine. This is the first report describing the clinical and pathological findings in Mongolian goats suspected to be affected by O. glabra poisoning.
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PMID:Cerebellar ataxia suspected to be caused by Oxytropis glabra poisoning in western Mongolian goats. 2457 29


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