Impairment Of Psychomotor Skills Research Articles

The psychopharmacology of clobazam

The psychopharmacology of clobazam, specifically its effects on CNS arousal, cognitive and memory functions and psychomotor performance, is reviewed. Compared with the 1,4-benzodiazepine tranquillizers, clobazam is characterized by a lack of sedative and amnestic effects and no impairment of psychomotor skills including car driving, both in volunteer and clinically anxious patient populations. Clobazam also compares favourably with buspirone, a nonbenzodiazepine anxiolytic agent. Differentiation of the psychopharmacological profile of clobazam from the 1,4-benzodiazepines suggests important pharmacodynamic differences between the two groups. These in turn represent significant advantages for the clinical use of clobazam in the management of ambulant patients with anxiety.

Psychomotor Effects of Diazepam in Anxious Patients and Healthy Volunteers

Psychomotor effects of diazepam, 5 and 10 mg, were compared to placebo in 30 highly anxious, nonpsychotic outpatients and age and sex-matched healthy volunteers. Diazepam did not reduce anxiety according to psychiatrists' ratings, but 10 mg of diazepam three times a day reduced the scores of the self-rated visual analogue scale for anxiety compared to placebo. Diazepam, 5 mg, was devoid of adverse psychomotor effects, but diazepam, 10 mg, impaired tracking and divided attention task performance in patients and volunteers alike. Plasma, erythrocyte, and saliva diazepam and N-desmethyldiazepam concentrations did not correlate with the impairment of psychomotor skills over time.

Counteraction by doxapram of the alcohol-induced impairment of psychomotor skills in man.

Counteraction by doxapram of the alcohol-induced impairment of psychomotor skills in man.

Unchanged Protein Binding and the Increase of Serum Diazepam Levels after Food Intake

Seven subjects received diazepam 0.3 mg/kg intravenously twice with a 2-week interval between the doses. The subjects ingested a fatty or carbohydrate meal in a cross-over fashion 4 hours after the injection on both experimental days. Venous blood samples were drawn 2, 3, 4, 5 and 6 hours after the injection of diazepam for measurement of the serum levels of total and free (unbound) diazepam, N-desmethyldiazepam, and free fatty acids. Serum levels of diazepam decreased progressively with time until the food intake, after which a significant (P less than 0.01) postprandial increase (average 23%) occurred with both diets as compared to the preprandial levels at 4 hours (average 240 ng/ml). Serum levels of free fatty acids decreased significantly both after a fatty (P less than 0.01) and a carbohydrate (P less than 0.05) meal. Diazepam was extensively (96 to 98%) bound to proteins and no changes in its protein binding was found. It is concluded that the late impairment of psychomotor skills that occurs with an increase in the diazepam serum level after its intravenous administration is due rather to its re-mobilization from a storage site than to variations in its protein binding.