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)

Mutants of Drosophila melanogaster that lack Cu/Zn superoxide dismutase or urate are hypersensitive to reactive oxygen species (ROS) generated in vivo by the redox-cycling agent paraquat. We have subsequently employed paraquat as a selective agent to identify adult viable mutants potentially defective in other, perhaps unknown, components of ROS metabolism. Paraquat screening of ethyl methanesulfonate-induced second- and third-chromosome mutations yielded 24 paraquat hypersensitive mutants. Two mutants were identified as being new alleles of the previously identified doublesex (dsx) and pink (p) genes. The remainder of the mutations identified previously undescribed genes, including one second chromosome paraquat hypersensitive mutant that was found to exhibit shaking legs, abdomen pulsations, and body shuddering under ether anaesthesia. This recessive mutation was mapped to the polytene chromosome region of 48A5-48B2 and defines a new gene we named quiver (qvr). This mutation is similar in phenotype to the Shaker (Sh), ether-a-gogo (eag), and Hyperkinetic (Hk) mutations, all of which affect potassium channel function in D. melanogaster.
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PMID:Genetic analysis of oxygen defense mechanisms in Drosophila melanogaster and identification of a novel behavioural mutant with a Shaker phenotype. 877 66

Recent neuropathological findings define that 10-20% of the Parkinson patients belong to the atypical Parkinson's syndrome due to multi-system disease marked by typical Parkinsonian symptoms such as rigor, tremor and akinesia and early onset of severe autonomic, cerebellar or pyramidal disorders. Symptoms like postural hypotension, dysphagia, hypersalivation, urinary bladder dysfunction, thermodysregulation, abnormalities in eye movement, early falls or dementia etc. are frequently seen in these patients. In these patients dopamin depletion in the nigrostriatal pathway is combined with degeneration of other cerebral structures like olivopontocerebellar and intermediolateral columns. Patients need high dosages of L-dopa and other antiparkinsonian drugs with poor prognosis in general. First, we report on an atypical Parkinson patient who developed acute dyspnoea and muscle rigidity after general anaesthesia; second, on another patient who took a long time to recover from general anaesthesia. Both responded to antiparkinsonian drugs, the first to orally applied L-dopa, the second to intravenous amantadine. Most probably the interruption of the treatment with high dosages of L-dopa (in these patients given in 2-4 hours intervals) had caused these complications. The special nature of the anaesthesiological management of atypical Parkinson patients is reviewed.
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PMID:[Perioperative management of the patient with atypical Parkinson disease]. 886 35

With estimates as high as 1 million patients in the United States, Parkinson's disease is a relatively common neurological disorder. It has long been thought that the primary biochemical disturbance in Parkinson's disease is dopamine related. Accordingly, many drugs have been developed that increase the supply of dopamine, affect the biochemical balance of dopamine, or act as a dopamine substitute. These drugs may have significant interactions with anesthetic agents. In addition, there are several disease and drug-induced physiological aberrancies that can have profound anesthetic implications in the patient with Parkinson's disease (e.g., aspiration pneumonitis, myocardial irritability, hypotension, hypertension, and respiratory impairment). Although surgical therapy for Parkinson's disease has a long history, with the advent of advanced neuroimaging techniques there has been a resurgence of these procedures (e.g., pallidotomy and thalamotomy) for advanced stages of Parkinson's disease. It is likely that these surgical procedures will become more commonplace, possibly prolonging the lifespan of patients with Parkinson's disease. Even though these cases are typically performed with local anesthesia, there are several important caveats to consider in the management of these patients (e.g., airway access with CNS changes, hypertension, and tremor). It's incumbent on anesthesiologists to become familiar with the special needs of patients with Parkinson's disease and alter the "days in hell" attitude among these patients toward surgery and anesthesia.
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PMID:Surgical intervention and anesthetic management of the patient with Parkinson's disease. 895 68

The bispectral (BIS) index and 95% spectral edge frequency (SEF) of the electroencephalograph (EEG) have been used to study the anesthetic and sedative effects of intravenously (i.v.) administered drugs. This prospective study was designed to evaluate the effectiveness of the BIS index and 95% SEF for assessing the level of propofol-induced sedation and amnesia during regional anesthesia. Ten consenting adult patients undergoing surgery with regional anesthesia were administered propofol in increments of 10-20 mg i.v., every 5-10 min until they became unresponsive to tactile stimulation (i.e., mild prodding or shaking). The BIS index and 95% SEF were continuously recorded from a bifrontal montage (Fp1-Cz and Fp2-Cz) using the Aspect B500 monitor. The depth of sedation was assessed clinically at 5- to 10-min intervals using the observer's assessment of alertness/sedation (OAA/S) scale, with 1 = no response to tactile stimulation to 5 = wide awake. Each patient was shown a picture of an animal (cat) prior to administration of an initial dose of propofol, 40 mg i.v.. Subsequently, patients were administered intermittent bolus doses of propofol, 10-20 mg i.v., and shown different pictures upon achieving OAA/S scores of 4, 3, and 2 during the onset of and recovery from propofol-induced sedation. Picture recall was tested upon arrival of the patient in the postanesthesia care unit (PACU). Of the two EEG variables studied, the BIS index exhibited a better correlation with the OAA/S scores during both the onset (Spearman's rho = 0.744) and recovery (Spearman's rho = 0.705) phases of propofol-induced sedation. With the increasing depth of sedation, there was a progressive decrease in the BIS index (OAA/S score of 5, BIS = 94.5 +/- 2.9; 4, 93.3 +/- 3.3; 3, 89 +/- 6.1; 2, 80.1 +/- 8.7; 1, 75.6 +/- 7.5; mean +/- SD). Conversely, there was a progressive increase in the BIS value during recovery from propofol sedation (OAA/S score of 1, BIS = 75.6 +/- 7.5; 2, 82.4 +/- 10.5; 3, 84.9 +/- 5.9; 4, 93.8 +/- 0.8). Although the changes in the 95% SEF values were less consistent during the onset phase, this EEG variable increased from 16.4 +/- 5.0 to 19.3 +/- 5.6 as the OAA/S score increased from 1 to 4 during the recovery phase. Patient recall of the intraoperative pictures decreased with increasing depth of sedation and decreasing BIS values (OAA/S:% BIS:% recall = 5:94.5 +/- 2.9:100%; 4:93.4 +/- 3:63%; 3:87.3 +/- 6.1:40%; 2:80.8 +/- 8.3:0%; 1:75.6 +/- 7.5:0%). The BIS index appears to be a useful variable for assessing the depth of propofol-induced sedation. Increasing depth of sedation was associated with a significant decrease in intraoperative picture recall.
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PMID:Electroencephalographic bispectral index correlates with intraoperative recall and depth of propofol-induced sedation. 898 22

Tremors are common in mammals emerging from anesthesia. To determine whether appropriate thermal manipulations immediately before emergence from anesthesia are sufficient to eliminate these tremors, electroencephalographic (EEG) and electromyographic (EMG) activities, hypothalamic temperature (Thy), and O2 consumption were monitored in 12 rats recovering from halothane anesthesia under three thermal regimes. EEG and EMG activities were recorded throughout anesthesia and served as feedback signals for controlling anesthetic depth. During anesthesia, Thy was either 1) allowed to fall to 32-34 degrees C, 2) maintained at 37-39 degrees C, or 3) allowed to fall to 32-34 degrees C and then raised to 37-39 degrees C. When hypothermic on emergence from anesthesia, all of the animals exhibited postanesthetic tremors that persisted until Thy values returned to normothermia. None of the animals expressed postanesthetic tremors when normothermic on emergence from anesthesia. In addition, the time between emergence from anesthesia (as determined by EEG/EMG parameters) and the initiation of coordinated motor activities was significantly decreased in the normothermic animals.
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PMID:Appropriate thermal manipulations eliminate tremors in rats recovering from halothane anesthesia. 901 5

To test the hypothesis that altered neuronal activity may influence the extent and severity of the glio-vascular lesions produced by 1,3-dinitrobenzene (DNB), rats were either given the tremorgenic pyrethroid, Bifenthrin, or anaesthetised during various dosing schedules of DNB. When compared with controls dosed only with DNB, Bifenthrin tremor made both the ataxia and other functional effects caused by DNB more pronounced. Lesions in the brain stem were made significantly more severe and widespread across three dose levels of DNB. Centres such as facial nuclei, motor nuclei of fifth nerve, subthalamic nuclei and mamillary bodies, not damaged by DNB alone, were also affected in some animals. In contrast, general anaesthesia by either isoflurane ur urethane decreased the severity of the lesions, this being more pronounced with urethane. The character of the tissue changes, however, was not altered by these additional procedures. These findings support the suggestion that neuronal activity is one important determinant of the selective vulnerability of sensitive brain stem nuclei to glio-vascular damage from DNB intoxication.
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PMID:Increasing or decreasing nervous activity modulates the severity of the glio-vascular lesions of 1,3-dinitrobenzene in the rat: effects of the tremorgenic pyrethroid, Bifenthrin, and of anaesthesia. 903 63

We studied the effects of propofol on electrophysiologic monitoring for functional neurosurgery. In six patients with intractable epilepsy, electrocorticograms (ECoGs) were monitored for epilepsy surgery, and in two of them, somatosensory evoked potentials (SEPs) were monitored because of the focus adjacent to the central sulcus. In four patients with hemifacial spasm, brain stem auditory evoked potentials (BAEPs) and abnormal muscle responses (AMRs) were monitored during microvascular decompression (MVD). In two patients with Parkinson's disease and in one patient with post-traumatic tremor, neural noise levels were recorded from microelectrodes during posteroventral pallidotomy and Vim thalamotomy. In each case of epilepsy surgery, during intravenous anesthesia with propofol, spike activity was recordable enough to identify the resective area and the residual spikes. SEP phase reversal was obtained in two patients and an exact determination of the central sulcus was possible. BAEPs and AMRs were obtained in all MVDs. To record neural noise levels, the infusion of propofol was decreased in two cases of posteroventral pallidotomy, and it was stopped in one case of Vim thalamotomy. In these patients, neural noise levels were recorded and were useful for identifying the target. Propofol is a potentially useful anesthetic agent for electrophysiologic monitoring during functional neurosurgery.
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PMID:[Intraoperative monitoring for functional neurosurgery during intravenous anesthesia with propofol]. 905 30

The use of ondansetron, a selective serotonin 5-HT3 receptor antagonist, is well established in patients with nausea and vomiting associated with cancer chemotherapy, radiotherapy or anaesthesia and surgery. The wide distribution of 5-HT3 receptors in the body and the role of these receptors in disease have provided the rationale for investigation of ondansetron in novel applications. Preliminary data have shown ondansetron to have clinical benefit in patients with nausea and vomiting associated with drug overdosage or poisoning, anti-infective or antidepressant therapies, uraemia or neurological trauma, and in patients with pruritus. Patients with gastrointestinal motility disorders (e.g. carcinoid syndrome, irritable bowel syndrome, diarrhoea associated with cryptosporidiosis or diabetes, and chronic refractory diarrhoea) have also shown some improvement when treated with ondansetron, as have patients with certain pain or CNS-related disorders [e.g. alcohol (ethanol) dependence, opiate withdrawal, vertigo, cerebellar tremor and Parkinson's disease treatment-related psychosis]. In contrast to conventional antiemetics, ondansetron is generally well tolerated with a lower incidence of sedation and only isolated case reports of extrapyramidal reactions. Furthermore, unlike dopamine receptor-blocking neuroleptics, ondansetron does not appear to worsen the symptoms of Parkinson's disease. Thus, in addition to its established indications, preliminary results suggest that ondansetron may be beneficial in a number of novel applications. This drug may represent a treatment alternative in patients with refractory disease, or an effective treatment of conditions for which current therapies are either poorly tolerated or not available. Further investigation of ondansetron in a range of potential new applications appears to be warranted.
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PMID:Ondansetron. A review of its pharmacology and preliminary clinical findings in novel applications. 911 22

Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardized questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychologic origin of chemical sensitivity. Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research. Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals). Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitization (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation.
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PMID:Profile of patients with chemical injury and sensitivity. 916 75

The output from the central nervous system to muscles may be rhythmic in nature. Previous recordings investigating peripheral manifestations of such rhythmic activity are conflicting. This study attempts to resolve these conflicts by employing a novel arrangement to measure and correlate rhythms in tremor, electromyographic (EMG) activity and muscle vibration sounds during steady index finger abduction. An elastic attachment of the index finger to a strain gauge allowed a strong but relatively unfixed abducting contraction of the first dorsal interosseous (1DI). An accelerometer attached to the end of the finger recorded tremor, surface electrodes over 1DI recorded EMG signals and a heart-sounds monitor placed over 1DI recorded vibration. This arrangement enabled maintenance of a constant overall muscle contraction strength while still allowing measurement of the occurrence of tremulous movements of the finger. Ten normal subjects were studied with the index finger first extended at rest and then contracting 1DI to abduct the index finger against three different steady forces up to 50% of maximal voluntary contraction (MVC). Power spectral analysis of tremor, EMG activity and muscle vibration signals each revealed three frequency peaks occurring together at around 10 Hz, 20 Hz and 40 Hz. Coherence analysis showed that the same three peaks were present in the three signals. Phase analysis indicated a fixed time lag of tremor behind EMG of around 6.5 ms. This is compared with previous measurements of electromechanical delay. Other experiments indicated that the three peaks were of central nervous origin. Introducing mechanical perturbations or extra loading to the finger and making recordings under partial anaesthesia of the hand and forearm demonstrated preservation of all the peaks, suggesting that they did not originate from mechanical resonances or peripheral feedback loop resonances. It is concluded that, at least for a small hand muscle, there exist not one but a number of separate peak frequencies of oscillation during active contraction, and that these oscillations reflect synchronization of motor units at frequencies determined within the central nervous system. It is proposed that the multiple oscillations may be a means of frequency coding of motor commands.
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PMID:Frequency peaks of tremor, muscle vibration and electromyographic activity at 10 Hz, 20 Hz and 40 Hz during human finger muscle contraction may reflect rhythmicities of central neural firing. 918 89


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