Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278126 (loss of equilibrium)
 140 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A bovine cerebellar disorder of recurrent seizures characterized by loss of equilibrium, extension of the head and thoracic limbs, opisthotonus, nystagmus and falling to the side or backwards is described from 16 farms in the Brazilian state of Rio Grande do Sul. The main pathologic features were vacuolation, degeneration and loss of Purkinje cells with axonal spheroids in the cerebellar granular layer and white matter. Electron microscopic study of Purkinje cells showed cytoplasmic membranous bodies, similar to those observed in human and animal gangliosidoses. Feeding trials in calves demonstrated that the disease is an intoxication caused by ingestion of Solanum fastigiatum var. fastigiatum. A hypothesis is proposed that the intoxication is an induced lysosomal storage disease, probably a gangliosidosis.
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PMID:Intoxication by Solanum fastigiatum var. fastigiatum as a cause of cerebellar degeneration in cattle. 641 29

This study concerned the suitability of rainbow trout as an experimental host for plerocercoids of Triaenophorus crassus. Twenty-five trout were exposed to Cyclops bicuspidatus thomasi infected with procercoids of T. crassus. Plerocercoids were recovered from 11 of these fish. Hemorrhaging in the muscle was the first evidence of infection in live fish between Days 22-58 postinfection (PI). Migration of worms created extensive lesions in the muscle by Day 30 PI followed by formation of granulomas between Days 45-75 PI. One to three plerocercoids were wound throughout the muscle after Day 30 PI, and penetration into the body cavity and through the integument was common. Mortality of infected trout was first observed at Day 44 PI, and by Day 56 PI, 45% of the trout died. The swimming behavior of infected trout was marked by decreased activity and loss of equilibrium.
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PMID:Experimental infections of rainbow trout, Salmo gairdneri Richardson, with plerocercoids of Triaenophorus crassus Forel. 671 58

Experiments of chronic intoxication with three concentrations (10, 20, and 40 ppm) of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) were conducted in the freshwater mollusc Lymnaea stagnalis. Snail survival was concentration dependent. In all cases the growth can be described by the von Bertalanffy pattern (ht = h (1 - e-k(t-to)) and the variations of the k values showed that growth was significantly altered in all the groups treated. The overall fecundity (F) was always reduced; the decrease was due both to a lower number of eggs per egg mass (-7.8 to -12%) and to an earlier death of the intoxicated snails. Fecundity studied in terms of size, according to the law F = ahz, points out the loss of equilibrium between growth and fecundity: in all groups treated the values of the exponent z were increased. The importance of these perturbations can be quantified by the calculation of a "Snail Yield" which is reduced by 72.6% in the 40 ppm group. Egg fertility was also reduced. It can be concluded that 2,4,5-T disturbs the physiological equilibrium of Lymnaea stagnalis leading even to earlier death of the snails.
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PMID:Chronic intoxication by an herbicide, 2,4,5-trichlorophenoxyacetic acid, in the pond snail, Lymnaea stagnalis L. 688 2

An experiment was carried out with 100 broiler birds of the Leghorn breed, aged 20 days. The birds were divided into groups and were given various amounts of methionine--0,5, 2, and 3 per cent with the basic standard mixture. The clinical signs of methionine intoxication were followed up--drowsiness, weakness in the legs, opisthotonus, and twisting of the neck (torticollis) alons with the loss of equilibrium. It was found that with birds receiving 0.5 per cent methionine with the diet the amount of vitamins A, E, and B1 in the blood serum and the liver rose considerably, while with birds given 2 and 3 per cent methionine with the feed the amount of these vitamins dropped essentially. Therepeutic treatment with 3 mg of vitamin E and vitamin B1 each in the course of 4 to 6 days yielded a good effect. An improvement of the general condition and disappearance of the most typical symptoms of methionine intoxication were recorded.
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PMID:[Effect of vitamin B1 and vitamin E on methionine poisoning in broiler chickens]. 734 83

A prospective investigation of 98 patients with acute loss of inner ear function showed that such patients display changes in the pulsatility of the basilar artery; however, the differences can be appreciated only by comparison with control sonograms during the course of the disease. Patients with sudden deafness or sudden loss of equilibrium generally showed unremarkable findings on duplex sonography of the cervical portions of vessels supplying the brain.
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PMID:[Color-coded duplex ultrasound findings and transcranial color duplex ultrasound findings in patients with acute inner ear disorders--a preliminary observation]. 767 32

Ears are special sense organs whose principal functions are hearing and maintaining equilibrium. Aminoglycoside antibiotics, erythromycin, polymyxin B, and cisplatin can affect either or both of these functions by binding with, injuring, and/or destroying special receptor cells associated with these functions. Severe hearing loss manifests itself as deafness, whereas loss of equilibrium will present as abnormal righting reflexes, nausea, and vomiting. Damage is proportional to levels of these ototoxins in the endolymphatic fluids. Evidence suggests that toxicity may be influenced by endolymphatic calcium concentrations, and levels of cAMP and cGMP are altered in specialized cochlear cells during ototoxicity, suggesting an additional mechanism for ototoxicity. The administration of salicylates and loop diuretics may potentiate the action of ototoxins, especially aminoglycoside antibiotics, probably by increasing the levels of these toxins in the endolymphatic fluid. Although many of these assessments have been made in laboratory animals, applicability may also be expected in small domestic animals, and extreme care should be taken in prescribing potentially ototoxic drugs to small animals. Cochlear damage from ototoxic compounds occurs initially in the cells detecting high-frequency sounds located at the lower basal region. In aging dogs and humans, this sensitivity of receptors in the lower basal region is enhanced. Early auditory damage is detectable by BAER and cochlear microphonic potentials. Vestibular responses can also be detected early as vestibular ocular reflexes and visual-vestibulo-ocular reflexes. Early detection is especially important because early changes can sometimes be reversible. Cavinton (apovincaminic acid) and fosfomycin represent examples of experimental agents being evaluated in laboratory animals for application as potential treatments to limit the ototoxicity associated with various drugs.
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PMID:Ototoxicity in dogs and cats. 845 3

Vestibular compensation, i.e. recovery after unilateral labyrinthectomy (UL) in the lamprey (a lower vertebrate, Cyclostome), as well as different means of promoting the compensation, is described. UL results in a loss of equilibrium and rotation during swimming which is compensated in about 60 days. The deficit can, however, be immediately abolished by applying asymmetrical tonic visual or vestibular input (electrical stimulation of the optic or vestibular nerve, illumination of one eye, removal of one eye). In addition, asymmetrical visual input promotes plastic changes underlying the vestibular compensation. The compensation is discussed in relation to the neuronal network responsible for postural control in the lamprey and identified in our previous studies.
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PMID:Vestibular compensation in the lamprey. 874 71

Removal of a vestibular organ (unilateral labyrinthectomy, UL) in the lamprey (Lampetra fluviatilis) results in a loss of equilibrium, so that the animal rolls (rotates around its longitudinal axis) almost continuously when swimming. This paper describes (i) UL-evoked disturbances of the pattern of locomotory movements responsible for rolling, (ii) recovery of equilibrium control after UL (vestibular compensation), and (iii) the role of vision in the recovery of equilibrium control. It was found that rolling is caused by an asymmetry in the undulatory locomotory movements, with larger deviations of the head towards the side with an intact labyrinth. The rolling appeared to be synchronized with the undulatory locomotory rhythm: during one complete roll turn (360 °), two cycles of locomotion were performed. A characteristic feature of the UL-induced motor deficit in the lamprey is the alternation of episodes of impaired swimming (with a distortion of the body shape and of the locomotor pattern and with a loss of equilibrium) with episodes of normal swimming (without any marked distortion of the locomotor pattern or loss of equilibrium). In the course of recovery after UL, the duration and frequency of the appearance of episodes of normal swimming increased, whereas episodes of impaired swimming became less frequent and shorter. The recovery of equilibrium control and the role of vision in recovery were investigated in lampreys with different combinations of lesions to the vestibular and visual sensory organs. In group 1 (UL only) animals, the time required for 80 % recovery was, on average, 33 days. In group 2 (UL and removal of both eyes) and in group 3 (UL and removal of the contralateral eye) animals, vestibular compensation was considerably retarded, and normal functioning of the roll control system was not regained even 3 months after UL. In contrast, in group 4 (UL and removal of the ipsilateral eye) animals, no impairment of the equilibrium control was observed, and the animals swam without rolling immediately after surgery. These findings indicate (i) that the visual system is important for the process of vestibular compensation, and (ii) that the deficiency in equilibrium control caused by UL can be abolished by means of unilateral (contralateral to UL) visual input. The hypothesis is advanced that the main UL-evoked motor deficit in the lamprey (loss of equilibrium) is primarily caused not by a persistent static distortion of the body shape, but by a loss of function of the roll control system responsible for stabilization of the dorsal-side-up orientation during swimming. A conceptual model of the roll control system of the lamprey, formulated in our previous studies, is used here to present arguments in favour of this hypothesis.
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PMID:Vestibular compensation in lampreys: impairment and recovery of equilibrium control during locomotion 931 61

The main motor disorder evoked by unilateral labyrinthectomy (UL) in the lamprey (Lampetra fluviatilis) is a complete loss of equilibrium and rolling (rotation about the longitudinal axis) during swimming. A previous study has shown that the recovery of equilibrium control in the lamprey takes, on average, 33 days. However, lampreys were able to maintain equilibrium if UL was combined with removal of the ipsilateral eye ('surgical compensation' of the vestibular deficit). It was suggested that tonic excitatory inflow, rather than specific information about the orientation of the animal in space delivered by the remaining eye, is important for the recovery of equilibrium control. In the present study, a number of experiments were designed to test this hypothesis. It was found that illumination of the eye contralateral to the UL or continuous electrical stimulation (10 Hz) of the corresponding optic nerve resulted in immediate restoration of equilibrium control. The same result was obtained when the vestibular nerve on the UL side was stimulated. Thus, the roll control system in the lamprey, driven by only one labyrinth, is able to maintain equilibrium provided that the lack of tonic inflow from the missing labyrinth is compensated for by tonic vestibular or visual input. The present study has also shown that the importance of visual input for maintaining equilibrium after UL decreases with time. In animals that achieved a high degree of compensation, removal of the eyes on day 23 after UL evoked decompensation, whereas removal on day 70 did not. A reduction of the significance of visual input was also observed in surgically compensated UL lampreys. In these animals, removal of the remaining eye on days 1-3 after the first surgery resulted in a complete loss of equilibrium, removal on day 7 resulted in a partial loss, whereas removal on days 48-55 did not affect the postural stability. Three lines of evidence suggest that asymmetrical visual input evokes plastic changes in the roll control system. (i) In one group of animals, initially one eye was removed, and then 50 days later the labyrinth ipsilateral to the missing eye and remaining eye were removed. These animals exhibited a mild impairment of equilibrium control, in contrast to the animals in which both surgeries were performed simultaneously. (ii) In another group of animals, initially one eye was removed, and then 50 days later the remaining eye and both labyrinths were removed. These animals exhibited rolling towards the eye that remained intact for longer. (iii) A short-term electrical stimulation (5-10 min daily for 3 days) of the optic nerve (contralateral to UL) in blinded animals considerably improved the equilibrium control compared with that of non-stimulated animals; the improvement was observed for 60 days after stimulation.
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PMID:Vestibular compensation in lampreys: role of vision at different stages of recovery of equilibrium control. 935 82

Gliomas represent the majority of primary central nervous system tumors in adults. The moderate overall impact of conventional therapeutic regimens on these inherently aggressive neoplasms raises the need for a direct intervention in the biology of neoplastic change. In the last decade important achievements in the molecular genetic basis of deregulated cell-cycle have been brought about, the neuro-oncologic implications of which are reviewed here. Loss of equilibrium between promoting factors and negative control of mitosis emergeus as a general principle, with gene amplification-overexpression operating in the former group, while deletions, loss of function-type mutations and post-transcriptional events prevail at the opposite pole. Damage to regulatory mechanisms will result, as a major consequence, in transgression of one or more of the so-called restriction points of the cell-cycle. Lesions of the genome are further ramified by supracellular processes involving autocrine and paracrine growth-stimulating loops. Malignant progression of gliomas, therefore, can be envisaged as a cumulative sequence of genetic alterations and interactions of tumor cells with their microenvironment.
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PMID:[Molecular genetics of gliomas]. 965 63


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