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)

Occupational exposure to manganese can cause early neurobehavioral effects in low- or a-symptomatic workers. A battery of neuropsychological tests was administered to a group of 61 ferroalloy male workers and 87 controls. The average (geometric mean) manganese concentrations in total dust at the plant have changed from 1981 to 1997 respectively from 1597.03 micrograms/m3 to 239 micrograms/m3 at the furnace area; from 151.53 to 255.76 micrograms/m3 at the casting area; from 167 to 54.7 micrograms/m3 at the maintenance (welding operations), yielding a current overall value of 54.25 micrograms/m3. A cumulative exposure index was calculated for each alloy worker and the average value (geometric mean) resulted to be 1204.87 micrograms/m3 x years, which divided by the average length of exposure (15.17 years), showed the concentration of 70.83 micrograms/m3 of manganese in total dust. Blood and urinary manganese geometric means resulted significantly higher in the exposed workers (9.18 micrograms/l and 1.53 micrograms/g creatinine, respectively) than in controls (5.74 micrograms/l and 0.40 microgram/g creatinine, respectively). A positive correlation was observed between the airborne manganese concentrations in total dust and blood manganese (n = 55; R = 0.36; R2 = 0.13; p = 0.0068), whereas no association resulted between cumulative exposure index and both blood manganese and urinary manganese. Higher prevalence of symptoms reporting was observed in the alloy workers concerning irritability, loss of equilibrium and rigidity. Tremor parameters including the central frequency and its dispersion, resulted to be statistically different in the exposed workers compared to the controls. Motor functions exploring the coordination of rapid and alternating movements and memory functions resulted to be impaired in the manganese workers. Dose-effect relationships were observed between the cumulative exposure index and some of the test results, whereas no relationship was found with the airborne manganese concentrations and the biological indicators of exposure. These findings are consistent with the existing knowledge of a cumulative mechanism of action of manganese, which must be carefully considered when setting safe exposure levels. In order to be protective for the entire working life, the average annual exposure level should be lower than 100 micrograms/m3.
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PMID:Long-term exposure to "low levels" of manganese oxides and neurofunctional changes in ferroalloy workers. 1038 91

1. Administration of MK-801 a selective antagonist of the NMDA receptors (50, 100 and 150 micrograms/kg, s.c.) elicited in adult cats ataxia and loss of equilibrium. A dose-response effect was observed. 2. Administration of DNQX, a selective antagonist of the non-NMDA receptors, even with doses 20 times higher than those employed with MK-801, did not produce any behavioural disturbances. 3. Previous injection of SCH 23390, a selective parenteral antagonist of dopamine D1 receptor, reduced significantly the intense ataxic effects of MK-801, while sulpiride only increased the latency of the symptoms. 4. The results are discussed considering the reported interactions between the dopaminergic and glutamatergic systems.
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PMID:Behavioural motor effects of MK-801 and DNQX parenteral administration in adult cats: dose-response analysis. Modulatory role of dopaminergic D1 and D2 antagonists on MK-801 induced motor behaviours. 1078 56

Early mortality syndrome (EMS) is a non-infectious disease affecting lake trout and other salmonids in the Great Lakes and in inland lakes. It is characterised by loss of equilibrium, hyperexcitability, anorexia, and eventually death. EMS is associated with low thiamine and treatment of eggs or fry with thiamine-HCl eliminates symptoms and mortality. To verify the role of the active form of the vitamin as the prophylactic agent, we used thiamine pyrophosphate (TPP) to reverse EMS symptoms. We also investigated the ability of specific thiamine antagonists that either block TPP production or interfere with its function to induce EMS. When graded doses of TPP were administered to EMS-susceptible sac-fry, there was a dose-dependent reduction in EMS. The egg concentration of TPP that was associated with reduced EMS was similar to the threshold thiamine concentration found in feral lake trout stocks where EMS occurs. A thiamine deficient stock from Lake Ontario was very sensitive to the thiamine antagonist oxythiamine (OXY) with total mortality associated with developmental arrest occurring at an antagonist to thiamine molar ratio (ATR) above 7:1. The threshold ATR with OXY for development of EMS-like neurological signs in this stock was 1.6:1. In addition to EMS-like neurological signs, OXY caused dose-dependent increases in hydrocephalus, developmental arrest, and vitelline congestion in the Lake Ontario stock. These signs are consistent with those observed in feral fish exhibiting EMS. Much higher doses of antagonists were required (both pyrithiamine (PT) and OXY) to induce EMS-like clinical signs in the thiamine replete Lake Manitou stock. PT was a more potent inducer in this stock as the ATR associated with development of clinical signs was 111:1 for PT compared with 892:1 for OXY. These data provide experimental evidence supporting the hypothesis that a thiamine deficiency in the natural environment is the cause of EMS.
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PMID:The use of thiamine and thiamine antagonists to investigate the etiology of early mortality syndrome in lake trout (Salvelinus namaycush). 1123 84

Bullfrog (Rana catesbeiana) tadpoles were exposed to malathion in water in a 28-d static renewal test. The effects of malathion on survival, growth, development, and loss of equilibrium posture were determined. Survival was significantly decreased at malathion concentrations of 2,500 micrograms/L and higher. Development of tadpoles was delayed significantly by malathion exposure as indicated by a dose-related decrease in developmental stage over time. Development of tadpoles in the 1,000-microgram/L and higher treatment groups was significantly delayed from that observed in the control. The effects of malathion on developmental stage suggest that malathion may decrease thyroid function in tadpoles, as it does in other species. Maintenance of equilibrium posture following agitation of the test containers was significantly impaired in tadpoles in all the malathion treatment groups (500 to 3,000 micrograms/L) relative to the control. Maintenance of equilibrium posture was thus the most sensitive end point measured in this study. Loss of equilibrium posture could increase predation losses and decrease feeding in populations of bullfrog tadpoles in the field. However, concentrations of malathion that produced adverse effects in our study are higher than published, measured concentrations found in wetlands or streams.
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PMID:Effects of malathion on survival, growth, development, and equilibrium posture of bullfrog tadpoles (Rana catesbeiana). 1135 6

Juvenile rainbow trout (Oncorhynchus mykiss) were exposed to high dietary concentrations of six polychlorinated n-alkane (PCAs) (C(10)H(15.5)C(6.5), C(10)H(15.3)Cl(6.7),C(11)H(18.4)Cl(5.6),C(12)H(19.5)Cl(6.5),C(14)H(24.9)Cl(5.1) and C(14)H(23.3)Cl(6.7)) for 21 to assess their effects on behavior and liver and thyroid histology and for 85 days to assess histology for a longer term exposure. This is the first histological work using PCAs of known carbon chain length and chlorine content and the first effort to examine the histopathology of fish exposed to PCAs. PCAs, also known as chlorinated paraffins, are complex industrial products for which there is a lack of toxicological data on individual congeners. With the exception of trout exposed to C(14)H(24.9)Cl(5.1), which had much lower exposure concentrations, many of the trout exposed to the PCAs (whole fish concentrations 0.22-5.5 microg g(-1)) showed a diminished or no startle response, loss of equilibrium, and developed a dark coloration. These responses are indicative of a narcotic toxicological mode-of-action. Histopathological lesions were observed in the livers of trout from each exposure group. However, the most severe histopathologies were observed in the livers of fish exposed to C(10)H(15.3)Cl(6.7) and C(11)H(18.4)Cl(5.6) (whole fish concentrations 0.92 and 5.5 microg g(-1), respectively), in which extensive fibrous lesions were present that were not observed in any other exposure group. Other alterations observed in all treatment groups included hepatocyte necrosis, sites of inflammation, and glycogen/lipid depletion. The relative sizes of hepatocytes of PCA exposed trout were smaller than control trout, although only a few of the observed differences were statistically significant. No lesions were present in the thyroid, although trout exposed to C(10)H(15.5)Cl(6.5) (whole fish concentration 0.84 microg g(-1)) had slightly more active thyroids, as indicated by an increased mean thyroid epithelium cell height relative to controls. It would appear that PCA toxicity is inversely related to carbon chain length, as has been observed in similar studies using mammals. The concentrations in the fish from this experiment were at levels that have been reported in invertebrates and fish from contaminated sites in the Great Lakes. However, the exposure concentrations were likely much greater in these experiments compared with the environment and require further study.
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PMID:Examination of the behavior and liver and thyroid histology of juvenile rainbow trout (Oncorhynchus mykiss) exposed to high dietary concentrations of C(10)-, C(11)-, C(12)- and C(14)-polychlorinated n-alkanes. 1145 28

A postural control system in the lamprey is driven by vestibular input and maintains the dorsal-side-up orientation of the animal during swimming. After a unilateral labyrinthectomy (UL), the lamprey continuously rolls toward the damaged side. Normally, a recovery of postural equilibrium ("vestibular compensation") takes about 1 mo. However, illumination of the eye contralateral to UL results in an immediate and reversible restoration of equilibrium. Here we used eye illumination as a tool to examine a functional recovery of the postural network. Important elements of this network are the reticulospinal (RS) neurons, which are driven by vestibular input and transmit commands for postural corrections to the spinal cord. In this study, we characterized modifications of the vestibular responses in individual RS neurons caused by UL and the effect exerted on these responses by eye illumination. The activity of RS neurons was recorded from their axons in the spinal cord by chronically implanted electrodes, and spikes in individual axons were extracted from the population activity signals. The same neurons were recorded both before and after UL. Vestibular stimulation (rotation in the roll plane through 360 degrees ) and eye illumination were performed in quiescent animals. It was found that the vestibular responses on the UL-side changed only slightly, whereas the responses on the opposite side disappeared almost completely. This asymmetry in the bilateral activity of RS neurons is the most likely cause for the loss of equilibrium in UL animals. Illumination of the eye contralateral to UL resulted, first, in a restoration of vestibular responses in the neurons inactivated by UL and in an appearance of vestibular responses in some other neurons that did not respond to vestibular input before UL. These responses had directional sensitivity and zones of spatial sensitivity similar to those observed before UL. However, their magnitude was smaller than before UL. Second, the eye illumination caused a reduction of the magnitude of vestibular responses on the UL side. These two factors tend to restore symmetry in bilateral activity of RS neurons, which is the most likely cause for the recovery of equilibrium in the swimming UL lamprey. Results of this study are discussed in relation to the model of the roll control system proposed in our previous studies as well as in relation to the vestibular compensation.
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PMID:Modifications of vestibular responses of individual reticulospinal neurons in lamprey caused by unilateral labyrinthectomy. 1178 25

There is considerable evidence from studies on cats and monkeys that several cortical areas such as area 2v at the tip of the intraparietal sulcus, area 3av in the sulcus centralis, the parietoinsular vestibular cortex adjacent to the posterior insula (PIVC) and area 7 in the inferior parietal lobule are involved in the processing of vestibular information. Microelectrode recordings from these areas have shown that: (1) most of these cortical neurons are connected trisynaptically to the labyrinthine endorgans and (2) they receive converging vestibular, visual and somatosensory inputs. These data suggest that a multimodal cortical system is involved in postural and gaze control. In humans, recent positron emission tomography (PET) scans and functional magnetic resonance imaging (fMRI) studies have largely confirmed these data. However, because of the limited temporal resolution of these two methods, the minimum time of arrival of labyrinthine inputs from the vestibular hair cells to these cortical areas has not yet been determined. In this study, we used the evoked potential method to attempt to answer this question. Due to its excellent temporal resolution, this method is ideal for the investigation of the tri- or polysynaptic nature of the vestibulocortical pathways. Eleven volunteer patients, who underwent a vestibular neurectomy due to intractable Meniere's disease (MD) or acoustic neurinoma resection, were included in this experiment. Patients were anesthetized and the vestibular nerve was electrically stimulated. The evoked potentials were recorded by 30 subcutaneous active electrodes located on the scalp. The brain electrical source imaging (BESA) program (version 2.0, 1995) was used to calculate dipole sources. The latency period for the activation of five distinct cortical zones, including the prefrontal and/or the frontal lobe, the ipsilateral temporoparietal cortex, the anterior portion of the supplementary motor area (SMA) and the contralateral parietal cortex, was 6 ms. The short latency period recorded for each of these areas indicates that several trisynaptic pathways, passing through the vestibular nuclei and the thalamic neurons, link the primary vestibular afferents to the cortex. We suggest that all these areas, including the prefrontal area, process egomotion information and may be involved in planning motor synergies to counteract loss of equilibrium.
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PMID:Vestibular projections in the human cortex. 1181 Jan 47

Benign paroxysmal positional vertigo (BPPV) is a disorder in which patients suffer from acute rotatory vertigo due to the presence of free otoconial debris migrating into one or more semicircular canals during head movements and resulting in abnormal stimulation of the ampullary crest. A prolonged loss of equilibrium of unclear origin is also present. Static posturography is a useful tool for the study of postural control systems and their role in these abnormalities. The aim of the present study was to evaluate the frequency of body sway and long-term instability of BPPV patients by posturography frequency analysis. Twenty patients with canalithiasis of the posterior semicircular canal and 20 normal controls were subjected to static posturography. Informed consent was obtained from all subjects. Patients were tested 1 h after diagnosis, and 3 days and 12 weeks after the characteristic Epley repositioning maneuver. Patients with BPPV showed significantly increased body sway both on lateral (X) and anteroposterior (Y) planes compared to normal subjects. Corporal oscillation with a broad-frequency spectrum was observed in both closed and open eye tests. The repositioning maneuver decreased the X plane body sway, while the anteroposterior sway was unchanged. Twelve weeks after treatment, a normalization of the anteroposterior sway was observed. Results of this study suggest that the long-term postural disturbance associated with BPPV differs from the acute disequilibrium that subsides after canalith repositioning: the former is a sagittal plane/broad spectrum body sway, while the latter is primarily a frontal plane/low frequency sway. The Epley maneuver was shown to reduce frontal sway, a postural abnormality that might therefore be linked to posterior semicircular canal function. Conversely, the observed sagittal body sway was only partially relieved by the restoration of canal function, and therefore, may be more related to the chronic dizziness observed in these patients.
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PMID:Long-term postural abnormalities in benign paroxysmal positional vertigo. 1223 67

A series of experiments were conducted to determine the physiological impact of acute sublethal molybdenum exposure to juvenile kokanee salmon (Oncorhynchus nerka Kennerlyi). Molybdenum was found to be relatively non-toxic to kokanee as the 96 h LC(50) was greater than 2,000 mg Mo l(-1). Exposure to either 25 or 250 mg Mo x l(-1) for 7 days was found to stimulate a significant 1.6- to 1.7-fold increase in ventilation which was later characterized to be dose-dependent between 5 and 250 mg Mo l(-1). Acute sublethal molybdenum exposure was found to have little or no impact on kokanee oxygen consumption at rest or immediately following a bout of forced activity or on physiological indicators of stress such as plasma lactate, sodium and cortisol. Despite these findings, prior exposure to 25 or 250 mg Mo l(-1) resulted in post-exercise loss of equilibrium and exercise-induced delayed mortality that were not observed in controls. Molybdenum accumulation in gill and liver of kokanee was also characterized. The findings of this study suggest that despite the non-toxic nature of molybdenum, acute sublethal exposure to this metal has physiological consequences to those fish exposed even for only a brief period. Further studies are needed to more fully elucidate the metabolism and mode of action of this metal in fish.
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PMID:Physiological impact of acute molybdenum exposure in juvenile kokanee salmon (Oncorhynchus nerka). 1237 20

We report a Japanese family with acetazolamide-responsive episodic ataxia. The proband was a 41-year-old woman with interictal nystagmus. She experienced recurrent attacks of loss of equilibrium and loss of coordination of the extremities accompanied by dysarthria and nausea beginning at about 10 years old. These episodes usually lasted for several hours two or three times a week. Direct sequence of CACNA1A demonstrated a novel insertion mutation in the patient and her father. This mutation is estimated to cause early stop of the gene transcription, producing a truncated protein. This is the first report of episodic ataxia type 2 of which the mutation was identified in a Japanese family.
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PMID:A novel insertion mutation of acetazolamide-responsive episodic ataxia in a Japanese family. 1273 95


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