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)

Sixteen ASA class II or III male patients (aged, 52 to 66 years) undergoing elective cardioversion were randomly assigned to receive either thiopental or etomidate according to an observer-blinded, parallel study design. The appropriate drug was administered in 2-mL aliquots every 15 seconds until the patient no longer responded to verbal commands, at which time cardioversion was attempted. The total dose for induction was 0.22 +/- 0.2 mg/kg and 3.2 +/- 0.4 mg/kg for etomidate and thiopental, respectively. The cardiorespiratory data after induction were evaluated for maximal percent change from baseline. The baseline heart rate was 106 +/- 6 beats/min and 98 +/- 8 beats/min for the etomidate and thiopental groups, respectively (mean +/- SEM). The heart rate decreased 5% after induction with etomidate and increased 7% with thiopental (P less than 0.05). The baseline mean arterial pressure (MAP) was 96 +/- 3 mm Hg and 105 +/- 11 mm Hg for the etomidate and thiopental groups, respectively (mean +/- SEM). The MAP decreased 4% with etomidate and 3% with thiopental. Respiratory rate was significantly increased by 22% after etomidate compared with a 22% decrease in respiratory rate with thiopental (P less than 0.05). Seven of eight patients in the thiopental group required only one countershock, whereas four of eight patients in the etomidate group required only one shock. One patient in each group could not be successfully cardioverted. Recovery time and clinical side effects were similar between groups except for mild myoclonus in the etomidate group. Titration to effect of either etomidate or thiopental provided satisfactory anesthesia for elective cardioversion in hemodynamically stable patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of etomidate and thiopental anesthesia for cardioversion. 176 19

The minimal alveolar concentrations for halothane, enflurane, and isoflurane in the domestic cat were found to be 1.19 +/- 0.05 (SEM)%, 2.37 +/- 0.06%, and 1.61 +/- 0.04%, respectively. During the potency studies, it was observed that enflurane and isoflurane resulted in shorter wake-up times, compared with halothane. However, enflurane and isoflurane produced electroencephalographic (EEG) and clinical signs of CNS irritability (EEG spiking, myoclonus) in normocapnic or mildly hypocapnic cats. In addition, enflurane and isoflurane caused greater airway irritability (coughing, salivation) than did halothane.
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PMID:Minimal alveolar concentrations for halothane, enflurane, and isoflurane in the cat. 686 22

Patients with cortical myoclonus may have purely focal or multifocal jerks, or they may have additional bilateral or generalized jerks, suggesting the spread of excitatory myoclonic activity between the cerebral hemispheres and across the sensorimotor cortex. The factors contributing to this spread of activity were investigated in 10 patients with multifocal cortical myoclonus and eight patients with multifocal and bilateral or generalized cortical myoclonus. The two groups were termed 'non- spreaders' and 'spreaders' respectively. Eight of the patients were also epileptic. Motor thresholds to single transcranial magnetic shocks at rest were higher in 'non- spreaders' (median 88%, range 45-100% of stimulator output) than either 'spreaders' (50%, range 26-90%, P=0.023) or health controls (38%, range 28-53%, P<0.001). This pathological elevation in motor threshold was not simply an effect of treatment with antiepileptic drugs. Paired transcranial magnetic stimuli were used to investigate ipsilateral cortico-cortical and transcallosal inhibition, There was less (MANOVA, P<0.05) ipsilateral inhibition at interstimulus intervals (ISIs) of 1-6 ms in 'spreaders' (mean 107+/-SEM 23% of control) compared with 'non- spreaders' (75+/-15%) or healthy subjects (59+/-10%). There was also less (P<0.05) transcallosal inhibition across inhibitory timings (10, 12 and 14 ms) in the 'spreaders' (98+/-6% of control) compared with the 'non-spreaders' (64+/-8%) or healthy subjects (59+/-6%). There was no relationship between ipsilateral cortico-cortical and transcallosal inhibition and the presence or absence of epilepsy, although non-epileptic patients did have higher motor thresholds (median 85%, range 32-100% of stimulator output) than either epileptic patients (50%, range 26-90%, P<0.001) or healthy controls (38%, range 28-53%, P=0.002). Abnormalities in ipsilateral and transcallosal inhibition appear to facilitate the spread of the cortical myoclonic activity responsible for bilateral and generalized jerks. However, these abnormalities in inhibition do not play a major role in the development of generalized seizures in patients with cortical myoclonus.
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PMID:Abnormalities of the balance between inhibition and excitation in the motor cortex of patients with cortical myoclonus. 862 91

We describe a pedigree in which eight individuals presented with a non-progressive disorder with onset between the ages of 12 and 50 years. It was characterized by predominantly distal, semi-continuous rhythmic myoclonus (all patients), generalized tonic-clonic seizures (all patients) and complex partial seizures (three patients). Most individuals had rarely suffered seizures and had a normal cognitive level, but three individuals with intractable seizures had mild mental retardation. The pattern of inheritance was autosomal dominant with high penetrance. We defined this disorder as autosomal dominant cortical myoclonus and epilepsy (ADCME). All patients had frontotemporal as well as generalized interictal EEG abnormalities. A neurophysiological study of the myoclonus suggested a cortical origin. Back-averaging of the data generated a series of waves with a frequency that mirrored the frequency of EMG bursts. Frequency analysis identified significant peaks with coherence between EMG and EEG, which were recorded over the contralateral rolandic area in five patients. The frequency of coherence was 8-25 Hz and phase spectra confirmed that EEG activity preceded EMG activity by 8-15 ms. In two individuals there was also significant coherence between the ipsilateral EEG and EMG, consistent with the transcallosal spread of myoclonic activity. The C-reflex at rest was enhanced and somatosensory and visual evoked potentials were of high amplitude. The resting motor threshold intensity to transcranial magnetic stimulation was significantly reduced (38%; SD +/- 7; P = 0.01) and the post-motor evoked potential silent period (101 ms; SEM +/- 10) was significantly shortened compared with the controls (137 ms; SEM +/- 18). These clinical and neuro- physiological characteristics suggest diffuse cortical hyperexcitability and high propensity for intra-hemispheric and inter-hemispheric cortical spread, as well as rhythmic myoclonic activity. Genome-wide linkage analysis identified a critical region spanning 12.4 cM between markers D2S2161 and D2S1897 in 2p11.1-q12.2, with a maximum two-point LOD score of 3.46 at Theta 0.0 for marker D2S2175. Multipoint LOD score values, reaching 3.74 around D2S2175, localize the ADCME gene to the centromeric region of chromosome 2. The exclusion of the locus for familial adult myoclonic epilepsy on chromosome 8q23.3-q24 from linkage to our family and the new localization of the responsible gene to chromosome 2cen, together with the different phenotype, define a new epilepsy syndrome. We hypothesize that the responsible gene causes cortical hyperexcitability that is widespread but particularly involves the frontotemporal circuits.
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PMID:Autosomal dominant cortical myoclonus and epilepsy (ADCME) with complex partial and generalized seizures: A newly recognized epilepsy syndrome with linkage to chromosome 2p11.1-q12.2. 1170