Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Motor phenomena - mostly in the form of myoclonus in the widest sense - are not rare in aeromedical studies conducted at flight altitudes and involving severe and acute hypoxia. At the same time medium to severe general changes can be observed in the EEG. When oxygen is supplied the motor phenomena stop after a few seconds, and the EEG results become normal again. These reversible changes are contrasted with clinical findings after anoxic coma conditions and hypoxic accidents which occurred during flights and where the myoclonus survives the coma, which is an extremely grave prognostic indication.
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PMID:[Prognostic significance of myoclonias in aerospace altitude studies and others with acute hypoxia-accompanied status]. 12 75

The neurophysiological interactions between the high pressure neurological syndrome (HPNS) and a new beta carboline, abecarnil, were studied in the non-human primate Papio anubis. Abecarnil is a partial agonist at the benzodiazepine site on the GABA/benzodiazepine receptor. Six animals were exposed on two occasions to pressures of 91 ATA in an environment of helium and oxygen. One exposure was pretreated with a total dose of abecarnil 1.0 mg/kg, the other with an equivalent volume of vehicle. Treatment with abecarnil prevented the severe signs of HPNS occurring between 51 and 91 ATA. Onset pressures of the various signs were unaffected. Some signs, e.g. myoclonus, became more frequent when abecarnil was used. A residual protective effect of abecarnil was present 4 weeks after the dose was given, active at pressures less than 71 ATA. Changes with pressure in the EEG were recorded primarily from the frontal cortex, but were also present in the parietal and occipital areas of the left cortex. Amplitude and frequency spectra were calculated and changes with pressure in the four conventional wavebands, plus two others, analysed. The most striking change was the prevention by abecarnil of the pressure-induced 100% increase in alpha wave amplitude in the frontal region. It is concluded that modulation of GABA transmission is important in controlling the expression of HPNS.
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PMID:Interactions of the beta carboline abecarnil with the high pressure neurological syndrome in a primate model. 136 51

When human divers and experimental animals are exposed to high pressure of helium-oxygen mixture, they develop the high pressure neurological syndrome, characterized by nausea, vertigo, tremor, myoclonus, EEG modifications and convulsions. Free-moving rats were stereotaxically implanted in the anterior caudate nucleus with a microdialysis probe to measure dopamine, dihydroxyphenylacetic acid and homovanillic acid levels during different phases of a simulated dive up to 5.1 MPa. Compression was found to cause an increase in extracellular dopamine and dihydroxyphenylacetic acid concentrations, but not in homovanillic acid. This represents a specific effect of high pressure on the dopaminergic pathway. Recent findings on D2 autoreceptors, showing a decrease in receptor affinity under pressure, allow us to conclude that pressure increases dopamine synthesis through a direct action on D2 autoreceptors.
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PMID:Effects of high pressure on striatal dopamine release in freely moving rats: a microdialysis study. 149 92

Neurophysiological interactions between the competitive N-methyl-D-aspartate (NMDA) preferring receptor antagonist, CPP (3-((+-)-2-carboxypiperazine-4-yl)-propyl-1-phosphonate) and the high pressure neurological syndrome (HPNS) have been investigated in the non-human primate Papio anubis. Eight animals were exposed on two occasions to environmental pressures of 81 atmospheres absolute (ATA) in a hyperbaric chamber, using helium and oxygen. One exposure followed pretreatment with CPP (either 5 or 10 mg/kg i.v. plus 5 mg/kg/hr infusion), the other a saline control. Pretreatment with CPP delayed moderate signs of face tremor and myoclonus and abolished severe signs of whole body tremor and seizure activity. By 81 ATA, scores representing severity of HPNS were significantly reduced by CPP to a mean score, reflecting a level of just mild to moderate limb tremoring (P less than 0.001). Changes in the EEG were observed in channels associated with the frontal, parietal and occipital regions of the left cortex. Amplitude and frequency spectra were calculated and changes with pressure in the 4 conventional wavebands were analysed. The most striking change was the complete prevention by CPP of the 100% increase in the amplitude of alpha waves at 81 ATA in the frontal region (P less than 0.001). It is concluded that NMDA transmission has a major role in the expression of HPNS.
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PMID:The effects of the competitive NMDA receptor antagonist CPP on the high pressure neurological syndrome in a primate model. 183 61

Corticobasal degeneration presents with an asymmetric akinetic-rigid syndrome, apraxia and combinations of supranuclear gaze palsy, myoclonus, and an alien limb. Six patients aged 59-77 yrs, diagnosed on clinical criteria as having corticobasal degeneration, have been studied with positron emission tomography using tracers of dopamine storage capacity and oxygen metabolism. Striatal 18F-6-fluorodopa uptake was reduced in an asymmetric pattern, caudate and putamen being involved in all cases. Uptake into medial frontal cortex was also impaired. Regional cortical oxygen metabolism was most significantly depressed in the superior and posterior temporal, inferior parietal, and occipital associated cortices. Within the frontal lobe, the hypometabolism was chiefly posterior. This unique combination of regional hypometabolism and disruption of the nigrostriatal system is discussed in relation to the clinical features of the disease and is compared with reported findings in other disorders of cognition and movement.
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PMID:Corticobasal degeneration. A unique pattern of regional cortical oxygen hypometabolism and striatal fluorodopa uptake demonstrated by positron emission tomography. 190 Jul 28

Four right-handed patients (69, 58 and 68 year-old men; 85 year-old woman) complained of motor difficulties with their left hand (3 cases), or both hands predominant on the left side (1 case). Continuous (1 case) or intermittent (2 cases) myoclonus was noted in the left arm. These disorders gradually progressed for 3 to 10 years. Clinical examination disclosed absence of motor, sensory (except in 1 case), or visual deficit. There were no cerebellar signs, no parkinsonian features (except for mild rigidity in 1 case), and no oculomotor abnormality. On the other hand, neuropsychological examination showed evidence of visuo-constructive apraxia in all cases, dressing apraxia in 3/4 cases and writing impairment in 3/4 cases. There was no amnesia, no aphasia and no intellectual impairment. MRI showed atrophy of the parietal areas, predominant on the right side. A positron emission tomography study was performed in all cases, and twice in 1 case. Cortical energy metabolism was measured using either 18 F-fluorodeoxyglucose or 15 O-Oxygen, to calculate the cerebral metabolic rate of glucose (CMRglu) or oxygen (CMRO2) respectively. Cortical metabolism was significantly decreased in the whole cortex of the right hemisphere in 3 cases, and was also reduced in the cortex of the left hemisphere, significantly in 1/3 studied planes. Moreover, regional metabolic indices (CMRO2 or CMRglu/cortex) showed a significant decrease in both the right and left posterior associative areas (temporo-parieto-occipital cortex), predominantly marked on the right side in 3 cases, indicating bilateral cortical dysfunction. At follow-up, one patient became progressively demented, another had visuo-spatial disorders indicating a lesion of both parietal areas. The relationships of our cases with the slowly progressive apraxia syndrome and with corticobasal degeneration are discussed.
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PMID:[Slowly progressive apraxia: a MRI and positron tomography in 4 cases]. 206 64

Anesthetic doses of fentanyl (46 +/- 1.3 micrograms/kg) and oxygen (group I) were compared to a moderate dose of fentanyl (3 to 4.7 micrograms/kg; mean = 3.54 +/- 0.1 micrograms/kg) + etomidate (0.4 mg/kg) intravenously (IV) (group II) during the anesthetic induction-endotracheal intubation sequence to evaluate hemodynamic changes and the incidence of side effects in 23 New York Heart Association class III and IV patients. Chest wall rigidity only occurred in group I (27%), and pain on injection (8%) and myoclonus (25%) only in group II. Patients in group I experienced transient, small increases in central venous pressure (immediately after induction) and mean pulmonary artery pressure (after tracheal intubation). Patients in group II had small, transient decreases in heart rate, mean arterial blood pressure and cardiac index after induction which returned to baseline levels immediately after tracheal intubation. The data indicate that a modest dose of fentanyl with etomidate is similar to a large (anesthetic) dose of fentanyl in terms of avoiding cardiovascular depression and preventing hemodynamic stimulation during and following the induction-tracheal intubation sequence. Our findings also demonstrate that these doses of fentanyl before etomidate decrease but do not eliminate side effects of etomidate. The results suggest that a modest dose of fentanyl followed by etomidate may be an attractive alternative to high doses of fentanyl in patients with limited cardiovascular reserve, especially when prolonged postoperative respiratory depression secondary to high doses of an opioid is undesirable.
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PMID:Induction of anesthesia with fentanyl or fentanyl plus etomidate in high-risk patients. 297 66

Hemodynamic changes and side effects of anesthesia induction with etomidate or thiopental were evaluated in 83 ASA class I or II patients. Patients were randomly assigned to one of 12 groups according to pretreatment drug (fentanyl, 100 micrograms, or normal saline intravenously), induction agent (etomidate, 0.4 mg/kg, or thiopental, 4 mg/kg), and maintenance anesthetic technique (isoflurane-oxygen, isoflurane-nitrous oxide-oxygen, or fentanyl-nitrous oxide-oxygen). The purpose of this experiment, of factorial design, was to evaluate the combined effects of two or more experimental variables used simultaneously and to observe interaction effects. There were significant increases in heart rate in all groups, especially after tracheal intubation. These increases were attenuated but not eliminated by fentanyl pretreatment. Systolic arterial blood pressure increased significantly after intubation and was not affected either by fentanyl pretreatment or by the induction agent. Patients in whom anesthesia was induced with etomidate had a greater incidence of pain on injection and myoclonus and a lesser incidence of apnea than patients in whom anesthesia was induced with thiopental. Fentanyl pretreatment significantly decreased the incidence of pain on injection and myoclonus, but it increased the incidence of apnea when anesthesia was induced with etomidate. The incidence of postoperative nausea and vomiting was similar after thiopental and etomidate and was unaffected by fentanyl pretreatment. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etomidate versus thiopental for induction of anesthesia. 402 53

We studied a patient with somatic growth failure with easy fatigability, myopathy with mitochondrial abnormality, increased lactate and pyruvate in blood and CSF, mental retardation, seizure, myoclonus, deafness, cerebellar ataxia, and blindness with macular degeneration and optic atrophy. Pathologic findings included multiple brain infarctions and massive calcification in the basal ganglia. Biochemical studies of isolated mitochondria revealed decreased oxygen consumption in skeletal muscle, diaphragm, and brain, suggesting an abnormality in the respiratory chain.
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PMID:Mitochondrial encephalomyopathy with lactate-pyruvate elevation and brain infarctions. 653 55

A 39 years old man with severe action myoclonus and epileptic seizure was reported. He had been in good health and worked as an occupational diver until August 16, 1966, when he had to dive into the sea bottom about 35 m deep without diving equipment. After finishing his work, he fell into unconsciousness and drowned. Sometime later, he was rescued and treated as decompression sickness. When he became alert, severe action myoclonus and epileptic seizure appeared. 8 years later, he was admitted to our hospital for rehabilitation. The danger of diving without equipment was indicated, because in sea bottom alveolar oxygen pressure (Pao2) is about 450 mmHg and alveolar air pressure 4.5 atmospheric pressure. In this condition patient could hold his breath longer time than in sea surface. When he finished his work and floated with muscle relaxing, however, his blood supply to the brain decreased. It was thought, therefore, that he fell into unconsciousness and drowned. In somatosensory evoked potentials (SEP) by median nerve stimulation, giat patterns were recognized but there were differences between SEP of myoclonus epilepsy and that of this patient. P50 and N70-80 were giant in him, suggesting that he had a brain stem disturbance. Since the inhibition system of fast conducted fiber did not work well in this state, the component of slow conducted fiber was magnified. Action myoclonus may be due to the disturbance of inhibition system in the brain stem.
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PMID:[A Lance-Adams syndrome of a diver (author's transl)]. 679 51


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