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Clonazepam probably improves TDD and ginkgo biloba probably improves TDS (both Level B); both should be considered as treatment. Risperidone may improve TDS but cannot be recommended as treatment because neuroleptics may cause TDS despite masking symptoms. Amantadine and tetrabenazine might be considered as TDS treatment (Level C). Diltiazem should not be considered as TDD treatment (Level B); galantamine and eicosapentaenoic acid may not be considered as treatment (Level C). Data are insufficient to support or refute use of acetazolamide, bromocriptine, thiamine, baclofen, vitamin E, vitamin B6, selegiline, clozapine, olanzapine, melatonin, nifedipine, fluperlapine, sulpiride, flupenthixol, thiopropazate, haloperidol, levetiracetam, quetiapine, ziprasidone, sertindole, aripiprazole, buspirone, yi-gan san, biperiden discontinuation, botulinum toxin type A, electroconvulsive therapy, α-methyldopa, reserpine, and pallidal deep brain stimulation as TDS treatments (Level U). Data are insufficient to support or refute TDS treatment by withdrawing causative agents or switching from typical to atypical DRBA (Level U).
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Preference for immediate reward, taken as an index of impulsiveness, has been suggested to be under the preferential control of central serotonin (5-HT) function. The present study examined the effects of the acute administration of drugs which directly or indirectly alter 5-HT transmission on tolerance to delay of reward in rats subjected to a procedure of discrete-trial choice in an operant chamber. Different groups of rats were trained to choose between two levers giving access to reinforcers differing in both magnitude and delay: one food pellet, delayed by 0 or 5 s, vs. five pellets delivered after a prereinforcer interval fixed at either 15, 30, 45, or 60 s, depending on the experiments. The learning curves indicated that rats were able to adjust their choice strategy precisely according to various factors: the respective duration of the delays before the small and large rewards, the immediacy of the small reward delivery, and the lengthening of the trials by a postreinforcer delay (or intertrial interval). Whatever the experimental parameters and stage of the learning, an acute administration of drugs able to reduce 5-HT neuronal activity (benzodiazepines; 5-HT1A receptor partial agonists: buspirone and MDL 73005EF) or enhance 5-HT transmission (5-HT reuptake inhibitors: indalpine and zimelidine; 5-HT1A receptor full agonist: 8-OH-DPAT) failed significantly to alter choice strategy (decreased or increased preference for the large but delayed reward, respectively), as they did in other situations such as a T-maze procedure. Only d-amphetamine (0.5 mg/kg), on one occasion, significantly reduced preference for the larger reward. The choice strategy was also insensitive to acute changes in experimental parameters such as a reduction in delay or increase in the magnitude of the large reinforcement. These results indicate that the present operant paradigm is not sensitive to acute modifications in the internal state of the animals and in the reward contingencies, and therefore is not useful to evaluate tolerance to delay and variations in impulsiveness in rats.
Buspirone HCl has very low oral bioavailability (4%) due to deactivation by extensive first pass effect. It also has very limited transdermal permeation due to its high hydrophilicity.
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Children 2-6 years of age with ASD (N = 166) were randomized to receive placebo or 2.5 or 5.0 mg of buspirone twice daily. The primary objective was to evaluate the effects of 24 weeks of buspirone on the Autism Diagnostic Observation Schedule (ADOS) Composite Total Score. Secondary objectives included evaluating the effects of buspirone on social competence, repetitive behaviors, language, sensory dysfunction, and anxiety and to assess side effects. Positron emission tomography measures of tryptophan metabolism and blood serotonin concentrations were assessed as predictors of buspirone efficacy.
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There is poor evidence in management of HD today. The analysis of the twenty level-I studies fails to result in any treatment recommendation of clinical relevance. High-quality RCT are highly warranted to advance HD treatment in clinical practice.
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A within-subject design was used to characterize the effects of dose manipulations on discriminative and self-reported effects of oral diazepam and buspirone. Subjects were trained to discriminate diazepam (10 mg) versus placebo (n = 10), or buspirone (10 or 15 mg) versus placebo (n = 9). The compounds were identified to subjects by letter code before discrimination training began. In later sessions, correct identifications at 2 hr after the oral administration of drug earned money. All subjects showed accurate discrimination performance during the test-of-acquisition phase. In a low-dose generalization phase, diazepam and buspirone produced dose-related increases in drug identifications across a four-fold range of doses. In a subsequent low-dose training phase, in which subjects were trained to discriminate progressively lower drug doses, the median lowest discriminable dose of diazepam and buspirone was 2.5 and 7.5 mg, respectively. Dose-response functions for drug identifications were shifted leftward in the low-dose training phase relative to the low-dose generalization phase, suggesting that reinforcement of progressively lower doses enhances drug discriminability. The self-reported effects of diazepam and buspirone were similar (e.g., both drugs increased ratings of drug strength and clumsy/uncoordinated) and different (e.g., diazepam but not buspirone increased ratings of drowsy/sleepy; buspirone but not diazepam increased ratings of tense/nervous). This study demonstrates discriminative and self-reported effects of diazepam and buspirone at doses lower than previously shown to be behaviorally active, and suggests that at commonly used clinical doses, diazepam is relatively more discriminable than buspirone.
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Heating efficacy and core rewarming rates were similar with full-body forced-air and full-body resistive polymer heating in healthy volunteers.
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Ninety-four subjects were recruited by mass media announcements and were seen in a university-based outpatient psychiatric clinic. Assessments were 1) questionnaires for all 94 subjects, 2) diagnostic interview of 50 subjects, and 3) laboratory performance of 34 subjects. Treatment conditions were 1) 6 weeks of buspirone, 2) 6 weeks of placebo, 3) a five-session, group cognitive-behavior therapy program with buspirone, or 4) the cognitive-behavior therapy program with placebo. Treatment outcome measures included subjective anxiety ratings and heart rate measures during a laboratory performance, a questionnaire measure of performance confidence, and a blind rating of musical performance quality.
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Neuro-inflammation in Parkinson's disease (PD) is associated with glial cell activation and production of different inflammatory cytokines. In this study we investigated the effect of chronic administration of buspirone and fluoxetine on cerebrospinal fluid (CSF) levels of inflammatory cytokines, TNF-α, IL-1β and IL-6 in 6-hydroxydopamine (6-OHDA)-lesioned rats.6-OHDA (8 μg/2 μl/rat) was injected unilaterally into the central region of the substantia nigra pars copmacta (SNc) and after 21 days lesioned rats were treated with buspirone and fluoxetine intraperitonealy (i.p.) for 10 days. CSF samples were collected at tenth day of drugs administration and were analysed by ELISA method to measure TNF-α, IL-1β and IL-6 levels.The results showed that the CSF levels of TNF-α was increased 3 weeks after 6-OHDA injection while there was a significant decrease in TNF-α levels of parkinsonian animals treated with buspirone (1 mg/kg) and fluoxetine (1 mg/kg). IL-1β and IL-6 both were decreased in parkinsonian rats, while their level was increased in buspirone (1 mg/kg) and fluoxetine (1 mg/kg) treated parkinsonian rats.Our study indicates that chronic administration of buspirone and fluoxetine in 6-OHDA-lesioned rats restores central concentration of inflammatory cytokines to the basal levels. We suggest that serotonergic agents can be used as adjuvant therapy along with commonly used anti-parkinsonian drugs by modulation of cerebral inflammatory cytokines. We suggest that the further clinical investigations may be carried out to prove this hypothesis.
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Eight patients with mild to severe tardive dyskinesia (TD) were treated for 12 weeks with buspirone in dosages of up to 180 mg/day in an open-label study. Changes in TD severity were assessed by the Abnormal Involuntary Movement Scale. The rater was blind to buspirone dosage. Buspirone was well tolerated by most subjects. A within-subjects comparison of pretreatment and post-treatment Abnormal Involuntary Movement Scale scores revealed a mean improvement of 4.4 (p < 0.01). Improvement was also observed in neuroleptic-induced extrapyramidal side effects such as parkinsonism and akathisia. Scores on the Hamilton Rating Scale for Anxiety and the Brief Psychiatric Rating Scale did not change during the 12-week study. The results of this open-label pilot study suggest that relatively high doses of buspirone may be efficacious in the treatment of TD.
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Baboons were trained to discriminate either pentylenetetrazole (PTZ) or beta-carboline-3-carboxylic acid ethyl ester (beta-CCE) from the no-drug condition. Both drugs specifically bind sites in the gamma-aminobutyric acid A (GABA(A)) receptor complex and decrease GABAergic transmission. beta-CCE occasioned drug-lever responding in baboons trained to discriminate PTZ and vice versa. Flumazenil, the benzodiazephine receptor antagonist, blocked beta-CCE, consistent with beta-CCE's receptor binding activity. The azaspirodecanedione anxiolytics buspirone and ipsapirone produced full generalization in all baboons; gepirone and tandospirone yielded full generalization in some baboons and partial in others. These anxiolytics are inactive in the GABA(A) complex and potently bind 5-HT(1A) sites. A specific 5-HT(1A) ligand, 8-hydroxy-2-(di-n-propylamino)tetralin, produced generalization similar to gepirone and tandospirone, which show the most specific 5-HT(1A) binding. The major azaspirodecanedione metabolite, 1-(2-pyrimidinyl)piperazine (an alpha(2)-adrenergic antagonist), occasioned the least drug-appropriate responding. Full generalization to buspirone and ipsapirone may have resulted from dopaminergic or alpha(1)-adrenergic activity combined with 5-HT(1A) activity. The molecular mechanism of the generalization profile for PTZ and beta-CCE shown by the present results is unclear. The data may reflect altered relationships between GABAergic and serotonergic transmission, and altered stimulus effects of the training drugs, in the context of chronically decreased GABAergic transmission.