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Psychomotor

The pharmacological profile of buspirone in both animals and humans differs substantially from that of the ben2odia2epine anxiolytics. Buspirone lacks anticonvulsant, myorelaxant, and hypnotic effects. It also produces less sedation resulting in less psychomotor impairment in conjunction with... [Pg.226]

Desipramine [50-47-5] (35) and nortriptyline [72-69-5] (36) are demethylated derivatives and principal metaboHtes of (32) and (33), respectively. Both compounds possess less sedative and stronger psychomotor effects than the tertiary amine counterparts, probably because tricycHcs containing secondary amine groups generally show greater selectivity for inhibiting the reuptake of norepinephrine compared with the reuptake of serotonin. Protriptyline [438-60-8] (37), a stmctural isomer of nortriptyline, is another important secondary amine that displays a similar clinical profile. [Pg.467]

It is estimated that concentrations of 3000 ppm cause unconsciousness in less than 10 minutes (39). Anesthetic effects have been reported at concentrations of 400 ppm after 20-min exposure. Decrease in psychomotor performance at a trichloroethylene concentration of 110 ppm has been reported in one study (33), whereas other studies find no neurotoxic effects at concentrations of 200 ppm (40—43). [Pg.25]

The anticonvulsant primidone (1035) resembles phenobarbital but lacks the 2-oxo substituent. It was introduced in 1952 and has remained a valuable drug for controlling grand mal and psychomotor epilepsy. As might be expected, primidone is metabolized to yield phenobarbital (1034 X = 0) and C-ethyl-C-phenylmalondiamide (1036), both of which have marked anticonvulsant properties however, primidone does have intrinsic activity and an appropriate mixture of its metabolites has only a fraction of its activity (73MI21303). Primidone may be made in several ways, of which desulfurization by Raney nickel of the 2-thiobarbiturate (1034 X = S) or treatment of the diamide (1036) with formic acid (at 190 °C) seem to be the most satisfactory (54JCS3263). [Pg.153]

FAS is normally characterized by growth retardation, anomalies of the head and face, and psychomotor dysfunctions. Excessive consumption of ethyl alcohol may lead to malformations of the heart, extremities, and kidneys. Since consumption of ethyl alcohol is socially acceptable and prevalent even in pregnant women, the risks associated with the use of ethyl alcohol are remarkable. However, it should be kept in mind that there are several chemical compounds in tlie occupational environment that may also cause malformations even at low doses. The oc-cupationally-important known human teratogens include methyl mercury, ethyl alcohol, PCB compounds, tobacco smoke, lead, TCDD, 2,4,5- F, carbon monoxide, nitrogen dioxide, gasoline, and fluoride. [Pg.316]

Stimulants Stimulant drugs Psychomotor stimulant drugs... [Pg.1038]

The characteristic behavioral effects of acute and chronic psychomotor stimulant diugs are locomotor activation, stereotypy, and conditioned reward and stimulus-reward learning. The most important brain regions involved in these effects are summarized in Table 3. [Pg.1041]

Psychedelic Hallucinogen Psycho Energizers Psychomotor Stimulant Diugs Psychostimulants Psychotogenic Psychotomimetic Drugs PT... [Pg.1500]

Learning occurs in three domains cognitive, affective, and psychomotor. When developing a teaching plan for the patient, the nurse must consider each domain. [Pg.52]

The psychomotor domain involves learning physical skills (such as injection of insulin) or tasks (such as performing a dressing change). The nurse teaches a task or skill using a step-by-step method. The patient is allowed hands-on practice under die supervision of the nurse. The nurse assesses die patient mastery of the skill by having the patient or caregiver perform a return demonstration under the watchful eye of the nurse ... [Pg.53]

Psychomotor seizures occur most often in children 3 years of age through adolescence. The individual may experience an aura with perceptual alterations, such as hallucinations or a strong sense of fear. Repeated coordinated but inappropriate movements,... [Pg.253]

When severe anxiety is present, it is important to obtain the history from a family member or friend. During the time the history is taken, the nurse observes the patient for behavioral symptoms indicating anxiety (eg, psychomotor agitation [extreme restlessness], facial grimaces, tense posture). Physiologic manifestations of anxiety include increased blood... [Pg.277]

Short-chain acyl-CoA dehydrogenase (SCAD) deficiency has been recorded in only a few patients and these show wide variation in clinical presentation. The defect has been seen in infants with a syndrome of psychomotor retardation and failure to thrive. These infants showed abnormal organic aciduria, and drastically decreased SCAD activity was demonstrable in cultured fibroblasts. Muscle symptoms were only part of a wider syndrome in all infants and children so far reported to have SCAD deficiency, but were the sole presenting feature in two adult patients, in whom lipid storage was demonstrable in skeletal muscle. The gene encoding for human SCAD has been mapped to chromosome 12. [Pg.306]

This complex consists of four subunits, all of which are encoded on nuclear DNA, synthesized on cytosolic ribosomes, and transported into mitochondria. The succinate dehydrogenase (SDH) component of the complex oxidizes succinate to fumarate with transfer of electrons via its prosthetic group, FAD, to ubiquinone. It is unique in that it participates both in the respiratory chain and in the tricarboxylic acid (TC A) cycle. Defects of complex II are rare and only about 10 cases have been reported to date. Clinical syndromes include myopathy, but the major presenting features are often encephalopathy, with seizures and psychomotor retardation. Succinate oxidation is severely impaired (Figure 11). [Pg.309]

Matrila MJ, Aranko K, Seppala T Acute effects of huspirone and alcohol on psychomotor skills. J Clin Psychiatry 43 56-60, 1982 McMahon T, Andersen R, Merten P, et al Protein kinase C epsilon mediates upregu-lation ofN-type calcium channels by ethanol. Mol Pharmacol 37 33-58, 2000 Merry], Reynolds CM, Bailey], et al Prophylactic treatment of alcoholism by lithium carbonate. Lancet 2 481 82, 1976... [Pg.50]

Pharmacodynamic tolerance to the psychomotor effects of benzodiazepines has been demonstrated after single or multiple doses (File 1985 Greenblatt and Shader 1978 Rosenberg and Chiu 1985). Pharmacodynamic tolerance to the anxiolytic effect (over a 6-month period) has not been demonstrated (Rickels et al. 1983), and clinical experience supports the view that many patients with anxiety disorders require long-term therapy with benzodiazepines or alternative antianxiety agents. An important clinical consequence of tolerance to sedative effects is observed in benzodiazepine overdoses, when patients may initially be... [Pg.123]

Schuster CR The behavioral pharmacology of psychomotor stimulant drugs, in Psychotropic Agents, Part II. Edited by Hoffineister F, Stille G. New York, Springer-Verlag, 1981, pp 587-605... [Pg.207]

Cami J, FarreM, Mas M, etal. Human pharmacology of 3,4-methylenedioxymetham-phetamine ( ecstasy ) psychomotor performance and subjective effects. J Clin Psychopharmacol 20 455 66, 2000... [Pg.261]

Dohrn CS, Lichtor JL, Finn RS, et al Subjective and psychomotor effects of nitrous oxide in healthy volunteers. Behav Pharmacol 3 19-30, 1992 Dohrn CS, Lichtor JL, Coalson DW, et al Reinforcing effects of extended inhalation of nitrous oxide in humans. Drug Alcohol Depend 31 263-280, 1993 Evans AC, Raistrick D Phenomenology of intoxication with toluene-based adhesives and butane gas. Br J Psychiatry 130 769-773, 1987 Evans EB, Balster RL CNS depressant effects of volatile organic solvents. Neurosci Biobehav Rev 13 233—241, 1991... [Pg.306]

Whitwam JG, Morgan M, Hall GM, et al Pain during continuous nitrous oxide administration. Br J Anaesth 48 423 29, 1976 WileyJL, Bale AS, Balster RL Evaluation of toluene dependence and cross-sensitization to diazepam. Life Sci 72 3023—3033, 2003 Wise RA, Bozarth MA A psychomotor stimulant theory of addiction. Psychol Rev 94 469-492, 1987... [Pg.313]

Laboratory activities have the distinct advantage of engaging both the stndents psychomotor and the cognitive domains of learning. They begin with the... [Pg.111]


See other pages where Psychomotor is mentioned: [Pg.384]    [Pg.461]    [Pg.467]    [Pg.215]    [Pg.315]    [Pg.764]    [Pg.1038]    [Pg.1043]    [Pg.53]    [Pg.58]    [Pg.253]    [Pg.255]    [Pg.255]    [Pg.255]    [Pg.255]    [Pg.257]    [Pg.282]    [Pg.306]    [Pg.37]    [Pg.124]    [Pg.168]    [Pg.189]    [Pg.192]    [Pg.209]    [Pg.287]    [Pg.291]    [Pg.305]   
See also in sourсe #XX -- [ Pg.398 ]

See also in sourсe #XX -- [ Pg.475 ]




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Agitation psychomotor

Bayley Psychomotor Development

Cocaine psychomotor stimulants

Depressive disorders psychomotor disturbances

Iodine deficiency psychomotor development

Marijuana psychomotor performance

Psychomotor Stimulant Diugs

Psychomotor Vigilance Performance Neurocognitive Assay Sensitive to Sleep Loss

Psychomotor Vigilance Task

Psychomotor Vigilance Task (PVT) as a Neurocognitive Assay for Sleep Loss

Psychomotor ability

Psychomotor behavior

Psychomotor development

Psychomotor dysfunction

Psychomotor effects

Psychomotor functioning

Psychomotor impairment

Psychomotor impairment Motor activity

Psychomotor performance

Psychomotor performance benzodiazepines

Psychomotor retardation

Psychomotor skill

Psychomotor stimulants

Psychomotor test

Psychomotor vigilance performance

Psychomotor vigilance testing

Psychomotoric system

Sympathomimetic Agents (Psychomotor Stimulants)

Syndrome type psychomotor retardation

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