PubMed Health⌕ Search

Biomedical subjects

J De Veaugh-Geiss

Publications and source records attributed to J De Veaugh-Geiss.

4 recordsLinked to original sources

The Brief Social Phobia Scale: a psychometric evaluation.

The Brief Social Phobia Scale (BSPS) is an observer-rated scale designed to assess the characteristic symptoms of social phobia, using three subscales-fear, avoidance, and physiological arousal-which may be combined into a total score. Each of 18 BSPS items is anchored to a 5-point rating scale. Psychometric evaluation of the BSPS in a sample of 275 social-phobia patients yielded a high level of reliability and validity. Test-retest reliability was excellent, as was internal consistency. The fear and avoidance subscales demonstrated highly significant correlations with remaining item totals; however, the physiological subscale did not. The BSPS also demonstrated significant relationships with other established scales that assess anxiety and disability, and it proved sensitive to treatment effects in a trial of a 5-HT3 antagonist and placebo. Factor analysis yielded six meaningful factors. We conclude that the BSPS provides a reliable, valid, and sensitive measure for the evaluation of social phobia.

Analysis of Variance↗

Chronic benztropine and haloperidol administration induce behaviorally equivalent pharmacological hypersensitivities separately but not in combination.

This study reports the pharmacologic induction of behavioral pharmacologic hypersensitivity in an animal model of tardive dyskinesia. Four groups of rats received IP injections twice daily of 2.5 mg/kg haloperidol (H), 10 mg/kg benztropine (B), 2.5 mg/kg H plus 10 mg/kg benztropine (H + B), or saline for 4 weeks. Drug-induced catalepsy and spontaneous oral activity were measured daily during treatment. At 1 and 2 weeks after withdrawal of treatment, all groups were tested with apomorphine (AP) for the induction of stereotyped behavior. At 6 weeks after withdrawal of treatment, all animals were tested for catalepsy after receiving 2.5 mg/kg H. During the chronic treatment phase, H inhibited and B enhanced spontaneous oral activity. Also, H induced profound catalepsy during week 1, with partial tolerance to this effect observed during weeks 2-4. At 2 weeks after withdrawal, equivalent enhancement of AP stereotypy was seen in the H and B groups, but H + B (and saline) did not cause enhancement. At 6 weeks after withdrawal, enhancement of catalepsy was observed in the H and B groups, while H + B and control groups did not differ. Both H and B administered chronically can produce hypersensitivity when given alone, but this effect is attenuated when H and B are given in combination. While preservation of the dopamine-(DA)-acetylcholine balance during treatment appears to protect against hypersensitivity, the blockade of DA reuptake by benztropine, rather than its anticholinergic properties, may explain both the failure of combined treatment to induce hypersensitivity and the ability of B alone to induce hypersensitivity.

Animals↗

Differential liabilities of haloperidol and thioridazine for inducing apomorphine hypersensitivity.

In an animal model of tardive dyskinesia, sensitivity to apomorphine-induced stereotyped behavior reflects increased dopamine receptor activity induced by chronic neuroleptic treatment. Four groups of Sprague-Dawley rats received haloperidol (H) 0.5 mg/kg, haloperidol 0.5 mg/kg + benztropine 2.0 mg/kg (H + B), thioridazine (T) 25 mg/kg, or saline (S) ip daily for 18 days, were withdrawn for 21 days, and then received another 10 days of drug. Drug-induced catalepsy was measured daily during the second phase of drug treatment. Sensitivity to apomorphine 0.125 mg/kg and 0.250 mg/kg was assessed during the first and second weeks of withdrawal from each phase of drug treatment. Catalepsy scores for H, H + B, and T groups showed an unexpected progressive increase over treatment days. Following withdrawal from the first drug phase, only H and H + B rats showed enhanced apomorphine stereotypy. H rats were hypersensitive for both weeks of testing while H + B rats were only hypersensitive for the first week. All rats showed changes in apomorphine sensitivity after withdrawal from the second drug phase. H and H + B rats showed significant enhancement of stereotypy at both apomorphine dose levels and at both weeks of testing. T rats showed a significant enhancement but only at the higher apomorphine dose level and only during the first withdrawal week. S rats had a significant enhancement of apomorphine-induced stereotypy during the second withdrawal week. We conclude that H, H + B, and T have differential liability for inducing dopamine receptor hypersensitivity, with haloperidol being most effective and thioridazine being least effective.

Animals↗