Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperbaric chamber dives at 31 ATA with helium-oxygen were performed at the Japan Marine Science and Technology Center in 1987. During simulated underwater experiments, auditory brain stem responses were recorded in 4 professional divers for assessment of brain stem function. All divers had no clinical symptoms at 150 m below sea level, and their ABRs also showed no significant changes. During the 150-250 m depth saturation dives, all divers complained of various symptoms such as euphoria, ataxia, joint pain, tremor and dyspnea, while, I-III and I-V interpeak latencies on their ABRs increased with a tendency of recovery. Furthermore, the changes of both interpeak latency were independent of each other. These results indicate that transient dysfunction clinically or subclinically occurred at the processes between 150-300 m below sea level. Moreover, independent changes of I-III and I-V interpeak latencies in this study may mean that the pathways reached to the generation sites of wave III and V were different.
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PMID:Effects of a hyperbaric environment on human brain stem function with specific reference to auditory brain stem responses. 317 89

Heliox compression deeper than 16 ATA can lead to EEG changes associated with confusion and somnolence. In man the symptoms termed the high pressure neurologic syndrome (HPNS) can also include increased tremor, memory problems, dizziness, nausea, and vomiting. In a series of 3 dives at NUTEC, a compression profile developed for operational use down to 360 msw was evaluated. In each dive 6 different divers were compressed to 360 msw on heliox. Neuropsychologic and neurophysiologic testing were performed repeatedly. The HPNS testing revealed only mild effects of the compression. Only 3 divers had impairments of more than 2 SD in peripheral motor function compared to their predive average. Memory was impaired periodically in 2 divers. The same was found for perceptual speed and reasoning. Fifty percent of the divers had an increase of more than 2 SD in postural tremor, but that had minimal effect on their motor performance. Six of the 18 divers had an EEG power spectrum with both alpha band inhibition and theta increase. While the performance impairment was most marked around 240 msw, the EEG changes occurred mainly deeper than 300 msw. In only 1 of the 18 divers marked EEG changes, marked tremor increase, and marked cognitive performance impairment were observed at the same time. Although mild HPNS was observed, the divers were little impaired during the compression to 360 msw. The results confirm that using a compression profile with rates decreasing progressively with increasing depth, and with several intermediate stops, provides fit divers at depth. By using standard batteries of HPNS testing we were able to obtain evidence for the acceptability of this compression profile.
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PMID:HPNS effects among 18 divers during compression to 360 msw on heliox. 321 42

Exposure to high pressure produces neurologic changes in humans which manifest as tremor, EEG changes, and convulsions. Since previous studies have implicated the involvement of the serotoninergic system in these symptoms, it was of interest to study serotonin release at high pressure. Synaptosomes isolated from guinea pig striatum were used to follow serotonin efflux at 68 ATA. The major observation was a decrease in [3H]serotonin release from depolarized striatal synaptosomes at 68 ATA. In view of the role of serotonin as an inhibitory neurotransmitter in this area, the observed decrease in synaptic release leads us to conclude that decreased serotoninergic activity in striatal neurons probably is contributing to the hyperexcitability associated with HPNS.
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PMID:Pressure suppresses serotonin release by guinea pig striatal synaptosomes. 336 53

Adverse neurological manifestations of exposure to high hydrostatic pressure include tremor and convulsions, suggesting an alteration in synaptic transmission, particularly with inhibitory pathways. Because striatal transmission has been implicated in the high pressure neurologic syndrome (HPNS), we investigated the effect of pressure exposure on the release of a major inhibitory neurotransmitter in this region. Synaptosomes isolated from the guinea pig striatum were used to study the effect of compression to 67.7 ATA on [3H]dopamine release. Pressure was found to have a suppressive effect on the initial release of [3H]dopamine by synaptosomes isolated from the striatum of guinea pigs. This finding suggests that decreased inhibitory regulation at the level of the striatum contributes to the hyperexcitability associated with compression to high pressure.
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PMID:Release of dopamine from striatal synaptosomes: high pressure effects. 336 91

Excitatory amino acid neurotransmission may be involved in the tremor component of the high pressure neurological syndrome (HPNS). 2-Amino-7-phosphonoheptanoic acid (2-APH) is a novel antagonist of excitatory amino acids with preferential activity at the N-methyl-D-aspartate receptor. Rats were injected either i.p. or intracerebroventricularly with 2-APH and subsequently exposed to pressure. The EEG changes that occur after treatment with 2-APH at 1 ATA, namely, a marked increase in delta waves (1-4 Hz) in the centro-occipital region, continue at pressure. However, the apparent duration of action of 2-APH is shorter: the power spectra of delta waves reached its maximum value after a mean time of 37 min (SD 12) compared with 60 min (SD 5) in unpressurized rats. Behavioral results include an increase in the onset pressure for tremor--82.6 ATA (SEM 4.7) in treated rats compared with 49.4 ATA (SEM 3.4) in saline controls (P less than 0.005). It is probable that the antitremor effect and the EEG changes resulting from 2-APH are due to decreased postsynaptic activity of an excitatory neurotransmitter, and these data support the hypothesis that tremor may be central rather than peripheral in origin.
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PMID:Effect of 2-aminophosphonoheptanoic acid on the EEG of rats exposed to high pressure. 372 81

High hydrostatic pressure has been shown to produce neurological changes in humans which manifest, in part, as tremor, myoclonic jerks, electroencephalographic changes, and convulsions. This clinical pattern has been termed high-pressure nervous syndrome (HPNS). These symptoms may represent an alteration in synaptic transmission in the central nervous system with the inhibitory neural pathways being affected in particular. Since gamma-aminobutyric acid (GABA) transmission has been implicated in other seizure disorders, it was of interest to study GABAergic function at high pressure. Isolated synaptosomes were used to follow GABA release at 67.7 ATA of pressure. The major observation was a 33% depression in total [3H]GABA efflux from depolarized cerebrocortical synaptosomes at 67.7 ATA. The Ca2+-dependent component of release was found to be completely blocked during the 1st min of [3H]GABA efflux with a slow rise over the subsequent 3 min. These findings lead us to conclude that high pressure interferes with the intraterminal cascade for Ca2+-dependent release of GABA.
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PMID:Effect of pressure on [3H]GABA release by synaptosomes isolated from cerebral cortex. 380 14

The possibility that hyperbaric helium can modify membrane function in nonneural cells was investigated by measuring the effect of pressure (29.6 atm He + 1.0 atm O2) on transport of the organic anion p-aminohippurate (PAH) and the organic cation tetraethylammonium (TEA) by renal cortex slices. Control slices were exposed to 100% O2 at 1 ATA. A unique incubating and shaking apparatus was built to allow remote control of the incubation conditions in a sealed chamber containing hyperbaric O2. In rat or rabbit renal tissue incubated for 90 min, pressure did not affect the uptake of either substance and was without effect on the total water content and inulin space of rat renal cortex. The kinetic characteristics of the transport systems were investigated by incubating tissue for 15, 30, 45, 60, 75, or 90 min. These experiments were analyzed by fitting a mathematical model to the data and calculating values for parameters representing the active and passive components of the transport processes. Pressure did not affect either of the parameters for PAH or for TEA transport. Thus, if helium elicits its known neural effects through an action on cell membranes, that action is not large enough to be detected by this assay system.
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PMID:In vitro renal transport of organic ions during exposure to hyperbaric helium. 663 42

The hypothesis that non-anaesthetic compounds, structurally related to specific anaesthetics, can protect against the high pressure neurological syndrome was tested. Infusion of two structural analogues of alphaxalone (3 alpha-hydroxy-5 alpha pregnane-11,20 dione) during pressurisation of rats with helium and oxygen gas mixtures (total pressure 80-100 ATA; inspired oxygen partial pressure 0.5 ATA) ameliorated the severe tremors associated with the high pressure neurological syndrome without any shift in tremor frequency (11-14 Hz). The steroid analogues which were selected (delta 16 and 3 beta-hydroxy-alphaxalone) have no known general anaesthetic effects and present an unexpected structural approach to the pharmacology of the syndrome. It may now be possible to investigate, treat or prevent the syndrome by the use of selective drugs without more generalised anaesthetic effects.
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PMID:Non-anesthetic steroids ameliorate the high pressure neurological syndrome in rats. 684 78

The neurophysiological effects of the novel anticonvulsant lamotrigine on the high pressure neurological syndrome, HPNS, were investigated in the rat and nonhuman primate Papio anubis. Rats were exposed to pressure at a rate of 3 ATA per min in a helium/oxygen environment. They were pretreated with either lamotrigine isethionate 15, 30, or 60 mg/kg IP or control vehicle. After 15 and 30 mg/kg there were no changes in onset pressures for any of the grades of tremor or myoclonus. After 60 mg/kg, tremor was much slower, at 7-9 Hz, than the 15-20 Hz seen in controls. Four baboons were exposed to pressure at 0.33 ATA per min in the same environment and treated with lamotrigine isethionate at 7.5 mg/kg/h i.v. Each animal underwent a control and a drug-treated exposure. No changes in the onset or severity of HPNS behavioural signs were observed. However, an increase in alpha wave amplitude of the EEG was almost prevented. In both species sustained myoclonic jerking occurred at pressures similar to those at which seizure activity was observed in control exposures. It is concluded that although lamotrigine is protective in several models of neuronal excitation, it is ineffective in protecting against behavioural signs associated with high atmospheric pressure.
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PMID:Lack of effect of lamotrigine against HPNS in rodent and primate models. 791 27

The neurophysiological effects of 2 novel AMPA/kainate receptor antagonists, GYKI 52466 and LY 293558, on the high pressure neurological syndrome have been investigated in the rat and baboon (GYKI 52466) and rat (LY 293558). Rats were exposed to increasing ambient pressures of helium and oxygen at 3 ATA/min, on one occasion each. GYKI 52466 at 20 mumol/kg i.v. immediately before, followed by 70 mumol/kg/hr i.v. during compression delayed tremor by 85% and myoclonus by 30%, compared with control vehicle, and no side effects were observed. Seizure activity was not affected by any of the doses used. LY 293558 at 36 mumol/kg i.p. delayed tremor and myoclonus (44% and 12%), LY 293558 72 mumol/kg additionally delayed seizure activity (21%). Side effects, principally tranquilization at the higher dose, were also noted. Six baboons were exposed to a maximum pressure of 91 ATA at 0.3 ATA/min, in the same environment, on two occasions. One exposure was treated with an i.v. infusion of GYKI 52466 15.2 mumol/kg/hr, the other with the same volume of control vehicle. Limb and face tremor and myoclonus were delayed and the severity of signs reduced. No seizures were observed in the drug treated group before 91 ATA. EEG changes associated with exposure to pressure were not affected. It is concluded that antagonism at the AMPA/kainate receptor by GYKI 52466 and LY 293558 beneficially alters HPNS signs but in a manner which is dependent on both the drug and species being studied.
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PMID:Protection from high pressure induced hyperexcitability by the AMPA/kainate receptor antagonists GYKI 52466 and LY 293558. 793 94


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