Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using aperiodic analysis, we examined the impact on the electroencephalogram (EEG) of muscle activity from opiate-induced rigidity with alfentanil. We compared two groups of patients, one receiving alfentanil with neuromuscular blocking agents and the other group receiving no relaxants. The alfentanil-induced muscle rigidity exerted a noticeable effect on the EEG, with a moderate effect on total power at 1 Hz; a marked effect on the total number of waves, cumulative percent power at 3 Hz, and average power at 17 to 19 Hz; and a striking effect on F90, the frequency below which 90% of the power resides. The presence of electromyographic (EMG) noise in the EEG consistently altered the variables derived from the EEG, so that anesthetic depth appeared less than it actually was. This was true in spite of the fact that we gave slightly more alfentanil in the group not receiving a relaxant. Although the observed muscle activity was greater than that usually seen clinically, and may have differed qualitatively, the results do serve as a warning that muscle noise can interfere with the EEG. Currently, there is no computerized technique that will reject or account for this noise, and we must depend on observation to recognize the EMG patterns within the EEG, either with the raw recording or with a detailed analysis (such as aperiodic analysis), and to compensate for this noise if possible. Techniques that average the EEG or that present a single number have difficulty providing this information. These results do not detract from the usefulness of the EMG contained in EEG recordings as a supplementary or complementary indicator of anesthetic lightness.
J Clin Monit 1986 Jan
PMID:The effect of muscle movement on the electroencephalogram during anesthesia with alfentanil. 287 79

MDMA (3,4-methylenedioxymethamphetamine, ecstasy) is a widely misused psychostimulant drug abused among large segments of the young population. Pharmacologically it displays effects related to amphetamine-type drugs and a set of distinctive effects (closeness to others, facilitation to interpersonal relationship, and empathy) that have been named by some authors "entactogen" properties. MDMA is a potent releaser and/or reuptake inhibitor of presynaptic serotonin (5-HT), dopamine (DA), and norepinephrine (NE). These actions result from the interaction of MDMA with the membrane transporters involved in neurotransmitter reuptake and vesicular storage systems. The most frequent effects after MDMA/ecstasy administration are euphoria, well-being, happiness, stimulation, increased energy, extroversion, feeling close to others, increased empathy, increased sociability, enhanced mood, mild perceptual disturbances, changed perception of colors and sounds, somatic symptoms related to its cardiovascular and autonomic effects (blood pressure and heart rate increase, mydriasis), and moderate derealization but not hallucinations. Acute toxic effects are related to its pharmacologic actions. The serotonin syndrome (increased muscle rigidity, hyperreflexia, and hyperthermia), among others, is characteristic of acute toxicity episodes. MDMA metabolism is rather complex and includes 2 main metabolic pathways: (1) O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation; and (2) N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine. The fact that the polymorphic enzyme CYP2D6 partially regulates the O-demethylenation pathway prompted some expectations that subjects displaying the poor metabolizer phenotype may be at higher risk of acute toxicity episodes. In this metabolic pathway a mechanism-based inhibition of the enzyme operates because the formation of an enzyme-metabolite complex that renders all subjects, independently of genotype, phenotypically poor metabolizers after the administration of 2 consecutive doses. Therefore, the impact of CYP2D6 pharmacogenetics on acute toxicity is limited. One of the interesting features of MDMA metabolism is its potential involvement in the development of mid- to long-term neurotoxic effects as a result of progressive neurodegeneration of the serotonergic neurotransmission system.
Ther Drug Monit 2004 Apr
PMID:Human pharmacology of MDMA: pharmacokinetics, metabolism, and disposition. 1522 54