Psychomotor impairment

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... 

First-generation antihistamines are effective, but associated sedation and psychomotor impairment limit chronic use. Efficacy and safety of second-generation antihistamines in children have been demonstrated in clinical trials.33 Cetirizine is indicated for children 6 months of age and older, loratadine for children 2 years of age and older, and fexofenadine for children 6 years of age and older.15... 

Volkow, N.D., Chang, L., Wang, G.J. et al. Association of dopamine transporter reduction with psychomotor impairment in methamphetamine abusers. Am. J. Psychiatry. 158 377, 2001. 

The most common side effect of BZs is CNS depression. Tolerance usually develops to this effect. Other side effects are disorientation, psychomotor impairment, confusion, aggression, excitement, and anterograde amnesia. 

Fluoxetine Alprazolam Increased plasma concentrations and half-life of alprazolam increased psychomotor impairment... 

Zaleplon also binds to the GABAa receptor. It has a rapid onset, a half-life of about 1 hour, and no active metabolites. It does not reduce nighttime awakenings or increase the total sleep time. It may be best used for middle-of-the-night awakenings. It does not appear to cause significant rebound insomnia or next-day psychomotor impairment. The most common side effects are dizziness, headache, and somnolence. The recommended dose is 10 mg (5 mg in the elderly). 

Tolerance to the daytime CNS effects (e.g., drowsiness, psychomotor impairment, decreased concentration) may develop in some individuals. 

Psychomotor Impairments were measured by such test batteries as the numerical facility, speed of closure, Purdue pegboard, and Strom-berg manual dexterity tests. Anecdotal reports, both by subjects and by staff, of changes In behavior and mood generally paralleled the other symptoms. The spectrum of the effects and their Intensity is similar to that commonly reported in the recent literature on cannabis studies in other volunteer populations. However, DMHP acetate seemed to elicit more orthostatic hypotension, and cannabis, a greater degree of mental effects. 

Ability to Communicate. The mental status exam is critical to the determination of a patient s capacity to consent, and the ability to communicate is an absolute prerequisite (see the section Diagnostic Assessment in Chapter 1). Psychomotor impairments such as mutism or catatonia (withdrawn type) would severely affect an individual s fundamental ability to communicate any appreciation of the issues involved and their ramifications. Although an individual may actually be well oriented and may intellectually appreciate and even later remember events that occurred and the issues involved, that person is not capable of consenting if unable to demonstrate these faculties. 

Buspirone causes less psychomotor impairment than benzodiazepines and does not affect driving skills. The drug does not potentiate effects of conventional sedative-hypnotic drugs, ethanol, or tricyclic antidepressants, and elderly patients do not appear to be more sensitive to its actions. Nonspecific chest pain, tachycardia, palpitations, dizziness, nervousness, tinnitus, gastrointestinal distress, and paresthesias and a dose-dependent pupillary constriction may occur. Blood pressure may be significantly elevated in patients receiving MAO inhibitors. 

Buspirone Mechanism uncertain Partial agonist at 5-HT receptors but affinity for D2 receptors also possible Slow onset (1-2 weeks) of anxiolytic effects t minimal psychomotor impairment—no additive CNS depression with sedative-hypnotic drugs Generalized anxiety states Oral activity forms active metabolite short half-life Toxicity Tachycardia paresthesias t gastrointestinal distress Interactions CYP3A4 inducers and inhibitors... 

Raymon, L.P., Steele, B.W., and Walls, H.C., Benzodiazepines in Miami-Dade County, Florida driving under the influence (DUI) cases (1995-1998) with an emphasis on Rohypnol GC-MS confirmation, patterns of use, psychomotor impairment, and results of Florida legislation, J. Anal. Toxicol., 23, 490, 1999. 

More importantly, buspirone has a much better side-effect profile than traditional antianxiety drugs. Buspirone seems to produce less sedation and psychomotor impairment than benzodiazepine agents.2... 

Volkow, N., L. Chang, G. Wang, et al. Association of Dopamine Transporter Reduction with Psychomotor Impairment in Methamphetamine Abusers. The American Journal of Psychiatry 3 (March 2001) 377-382. 

The earliest signs of CS poisoning appear to be psychologic/behavioral. Symptoms are headache, fatigue, insomnia, rapid mood changes, intellectual and slight psychomotor impairment. 

Mustafa, S.J., and D. M.S. 1999. Adenosine A1 receptor antisense oligonucleotide treatment of alcohol and marijuana-induced psychomotor impairments. In US Patent 5932557. 

King, D. J. 1994, Psychomotor impairment and cognitive disturbances induced by neuroleptics, Acta Psychiatr.Scand.Suppl., vol. 380, pp. 53-58. 

Any prescription for benzodiazepines must be preceded by a careful risk-benefit analysis considering the issues of an individual s particular life situation, personality style and psychiatric diagnosis. Risks of both abuse and cognitive/ psychomotor impairments have to be balanced against therapeutic benefits. 

The important advantages of the benzodiazepines over their predecessors are that they cause relatively less psychomotor impairment, drowsiness, and respiratory inhibition, and are consequently relatively safe in overdose. However, it must be emphasized that these advantages are relative, and that the low toxicity potential does not apply when they are combined with other agents, particularly alcohol (18) and opioids (19). 

Macrolides cause increases in the serum concentrations, AUCs, and half-lives and reductions in the clearance of triazolam and midazolam (138-140). These changes can result in clinical effects, such as prolonged psychomotor impairment, amnesia, or loss of consciousness (141). Erythromycin can increase concentrations of midazolam and triazolam by inhibition of CYP3A4, and dosage reductions of 50% have been proposed if concomitant therapy is unavoidable (142). 

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