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Our results suggest that bipolar patients prone to mood conversion constitute one third of the inpatient population with this illness. The switch from depression to mania occurred significantly more frequently during treatment with TCA than with non-TCA drugs. It is hypothesized that anticholinergic activity may contribute to the higher frequency of TCA-induced mood conversions.
Paroxetine (PAR) is a potent and selective inhibitor of serotonin uptake, and it has been demonstrated that 3H-PAR is a favorable candidate for labeling of the serotonin transport system. In this report, the binding of 3H-PAR to rat brain membranes was further investigated to obtain a better understanding of its role in the neuronal serotonin-uptake mechanism. Consistent with previous reports, it is indicated that 3H-PAR binds with high affinity to a site closely related to the serotonin-uptake mechanism. This binding is highly sodium dependent. The finding that depletion of brain serotonin content with p-chlorophenylalanine did not induce any alteration in the number and the affinity of the 3H-PAR-binding sites suggests the lack of serotonergic modulation on these sites. Repeated administration of desipramine, clomipramine, mianserin or deprenyl also failed to change 3H-PAR-binding sites in cerebral cortex and hippocampus. Such findings are compared to previous studies on the serotonin-uptake mechanism and the site labeled by 3H-imipramine, and discussed in respect to the biochemistry of affective disorders.
Studies investigating a possible relationship between the plasma concentration of tricyclic antidepressants and clinical response have measured only the tertiary and secondary amine forms of these drugs. The present study shows that the hydroxy metabolites of tricyclic antidepressants might also be active. Hydroxylated imipramine, desipramine, chlorimipramine, and nortriptyline inhibit the uptake of norepinephrine and serotonin into synaptosomes to the same extent as do their parent compounds. Hydroxylated nortriptyline and imipramine reverse or prevent reserpine-induced motor retardation and ptosis. Following chronic imipramine, significant steady-state concentrations of unconjugated hydroxylated metabolites are present in rat tissues including the cerebrospinal fluid. Accounting for steady-state concentrations of hydroxylated metabolites of tricyclic antidepressants in man may help to clarify whether there is a relationship between active drug concentration and clinical effect.
Subchronic (14 days) administration of chlorimipramine and zimelidine, and a new morpholine derivative produces different effects on 3H-imipramine binding with synaptic membranes of the mouse brain. Chlorimipramine increases the concentration of the binding sites (Bmax), zimelidine raises both the Bmax and the dissociation constant, while the new morpholine derivative does not significantly change these characteristics. It has been demonstrated that the changes in the Bmax that occur during prolonged administration of chlorimipramine depend on the method for the obtaining of membrane brain preparations.
The patient's aquagenic pruritus resolved after discontinuing the clomipramine but reemerged when treatment was restarted.
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To compare, via a pilot study, the effectiveness of behavior therapy and of drug treatment in children and adolescents with obsessive-compulsive disorder.
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As shown in 3 short term placebo-controlled trials in patients with panic disorder with or without agoraphobia, oral paroxetine 10 to 60 mg/day is significantly more effective than placebo for most variables measuring reduction in panic attack frequency. The drug also produced significantly greater improvements in various anxiety and depression scales than placebo. An extension phase of one of the placebo-controlled studies showed that the efficacy of paroxetine in reducing panic attack frequency is maintained during up to 6 months' treatment and that the drug reduces the risk of relapse. Oral paroxetine 10 to 60 mg/day was at least as effective as clomipramine 10 to 150 mg/day in a comparative study. During weeks 7 to 9 of treatment, 51% of paroxetine recipients had no full panic attacks, compared with 37% of clomipramine recipients. The onset of action appeared to be more rapid for paroxetine than for clomipramine. The 2 drugs were equally effective in improving generalised anxiety, phobic avoidance and social, family and work interactions. In patients who elected to continue treatment for a further 36 weeks in an extension phase of the above study, response rates increased further in all groups, including the placebo group. During weeks 34 to 36 of extended treatment, 85% of paroxetine recipients, 72% of clomipramine recipients and 59% of placebo recipients had no panic attacks. The difference between paroxetine and placebo was statistically significant at this time point; however, there was no significant difference between groups at the primary efficacy endpoint (weeks 22 to 24).
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This short-term but intensive study supported theories of OCD as an illness with fluctuating severity. Previous findings, that OCD seems to be chronic in approximately half of the cases, were supported by this study.
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A simple and selective high-performance liquid chromatographic method for the determination of amitriptyline in human plasma has been developed. For plasma samples, the protein was removed with 1 M NaOH and 0.7 M ZnSO4. aqueous solutions. The chromatographic separation was performed on an analytical mbondapak C18 column (250 3.9 mm, i.d) with an isocratic mobile phase consisting of phosphate buffer-acetonitrile-triethylamine (65:35:0.1 v/v/v) adjusted to pH 5.1. Clomipramine was used as an internal standard. Using ultraviolet detection at 239 nm, the detection limit for amitriptyline in plasma was 5 ng/ml. No interferences were found with tricyclic antidepressant drugs, which allows this method to be used in clinical studies. The calibration curve was linear over the concentration range 5-200 ng/ml. The recovery was complete for plasma. The inter-day and intra-day assay coefficients of variation were found to be less than 10%.
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Behaviour therapy consisting of specific exposure in vivo is reviewed in terms of its clinical usefulness for the treatment of agoraphobia, obsessive compulsive neurosis and related conditions. A combined behavioural and psychological formulation of individual target problems is advocated. These can be rated in terms of discomfort, disability, and physiological indices of anxiety. Although discomfort and disability have been found to correlate, their relationship with anxiety measures is questioned. Variables affecting the outcome of exposure are reviewed, including: duration--best results with prolonged, frequent sessions over a short period; arousal--experience of high anxiety not essential; adjunctive cognitive therapy--considered to add nothing to effectiveness during exposure treatment. The author goes on to argue that simple response prevention is effective in reducing ritualising activities in obsessive compulsive neurosis, without effecting concomitant anxiety. Whereas anxiety responds independently to exposure therapy, and hence that the anxiety reduction model of obsessive compulsive neurosis is inadequate. The putative anti-obsessional properties of clomipramine are questioned, and the utility of imipramine in agoraphobia is disputed.
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Sertraline was first developed and approved for the treatment of depression. However, considerable research has been conducted on its use in anxiety disorders. This paper reviews the data emerging from controlled and open trials of the use of sertraline in anxiety disorders. Sertraline has been tested extensively in the treatment of panic and obsessive-compulsive disorders. Less extensive testing has been completed on social phobia and post-traumatic stress disorder. The reviewed studies show that sertraline is an effective and well-tolerated treatment of all of these disorders. A comparison of sertraline with other pharmacotherapeutic options shows it to be at least equivalent to other medications for anxiety disorders.
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To date, no universally applicable recommendations are available for the treatment of patients with postherpetic neuralgia. A mixture of clinical anecdotes, experimental findings and observations from clinical trials form the basis of the medical arsenal for this condition. Tricyclic antidepressants are commonly used, and clinical experience and several investigations have documented their effectiveness. Today, single entity antidepressants, which can be combined with neuroleptics to increase analgesia, are generally recommended for the treatment of postherpetic neuralgia. Some authors also recommend the additional administration of an opioid if analgesia is inadequate. Just over a decade ago, opioids were considered ineffective for the treatment of neuropathic pain; however, more recent investigations relating to the use of opioids, primarily in the treatment of nontumour-related chronic pain, have led to a revision of their use in neuropathic pain. Nevertheless, the use of opioid therapy for neurogenic pain remains controversial. Tramadol is a synthetic, centrally acting analgesic with both opioid and nonopioid analgesic activity. The nonopioid component is related to the inhibition of noradrenaline (norepinephrine) reuptake and stimulation of serotonin (5-hydroxytryptamine; 5-HT) release at the spinal level. In this regard, there are parallels with antidepressants, which are believed to potentiate the effect of biogenic amines in endogenous pain-relieving systems. There is evidence that, in tramadol, both mechanisms act synergistically with respect to analgesia. The aim of this pilot study was to investigate, for the first time, the analgesic efficacy and tolerability of tramadol, compared with the antidepressant clomipramine, in the treatment of postherpetic neuralgia. If necessary, clomipramine was used in combination with the neuroleptic levomepromazine. The study allowed individualised dosages at predetermined intervals up to a maximum daily dose of tramadol 600mg and clomipramine 100mg, or clomipramine 100mg with or without levomepromazine 100mg. 21 (60%) of 35 randomised patients (> or = 65 years) received the study medication over the 6-week period [tramadol n = 10; clomipramine with or without levomepromazine) n = 11]. After 3 weeks' treatment the dosage in both groups remained almost constant for the rest of the 6-week treatment phase (mean daily dose: tramadol 250 to 290mg; clomipramine 59.1 to 63.6mg). Only 3 patients required the combination of clomipramine and levomepromazine. At the outset, both groups recorded an average pain level of 'moderate' to 'very severe'. In correlation with increasing the study medication, this had decreased to 'slight' by the end of the treatment, when 9 of 10 patients in the tramadol group and of 6 of 11 patients in the clomipramine group retrospectively rated their analgesia as excellent, good or satisfactory. The psychological/physical condition of the patients did not change significantly during tramadol treatment. Sensitivity and depression parameters decreased in the clomipramine group. The incidence of adverse events for all patients was similar in both groups (tramadol 76.5%; clomipramine with or without levomepromazine 83.3%). In conclusion, tramadol would appear to be an interesting therapeutic alternative for pain relief in postherpetic neuralgia, particularly in patients who are not depressed. In clinical practice, tramadol and clomipramine can best be used differentially. For example, tramadol could be the drug of first choice in patients with obvious cardiovascular disease (not an uncommon problem in the > or = 65 year age group) in whom antidepressants are contraindicated, and similarly in patients in whom an antidepressant effect is not required. (ABSTRACT TRUNCATED)
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To investigate to what extent the primary depression subtype atypical depression can predict differential outcome of the mono-amino-oxidase inhibitor (MAO-I) moclobemide and the tricyclic antidepressant clomipramine in the Danish University Antidepressant Group Study (DUAG).
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Magnetic resonance images were used to measure the volume of the head of the caudate nucleus in 20 patients with obsessive-compulsive disorder and 16 normal control subjects. The obsessive-compulsive patients showed a significant increase in the volume of the right side of the head of the caudate nucleus compared with that of control subjects. This finding was not correlated with demographic, psychopathological, or clinical characteristics.
1. It has been shown that thyrotropin releasing hormone (TRH) can potentiate the effects of the antidepressant, imipramine, as measured by the mouse forced-swimming test. This potentiation is not associated with an increase of effective levels of noradrenaline in the synaptic clefts, but depends upon the integrity of opioid systems. The present study was designed to investigate: (a) the potentiation by TRH of the effects of other antidepressants, using the same test; (b) the possible involvement of other neuronal systems, such as the 5-hydroxytryptaminergic and dopaminergic systems; (c) the contribution of the opioid and dopaminergic systems to the potentiation of the actions of other antidepressants by TRH. 2. The effects of nortriptyline, amineptine, maprotiline, nomifensine and mianserin, but not that of clomipramine, were potentiated by TRH (2 mg kg-1, i.p.). The inhibitor of 5-hydroxytryptamine synthesis, p-chlorophenylalanine (PCPA), did not prevent the effect induced by imipramine plus TRH. Blockade of dopaminergic systems by gamma-butyrolactone (GBL) (37.5 mg kg-1, i.p.), alpha-methyl-p-tyrosine (AMPT) (125 mg kg-1, i.p.) and apomorphine (0.025 mg kg-1, i.p.) antagonized the effects induced by various antidepressants alone (at high, effective doses) or at lower ineffective doses in association with TRH. The effect induced by imipramine plus TRH was also blocked by sulpiride (16 mg kg-1, i.p.). Pretreatment with the opioid antagonist, naloxone, inhibited the effects induced by nomifensine plus TRH or mianserin plus TRH but not those induced by nortriptyline plus TRH, maprotiline plus TRH or amineptine plus TRH. When high active doses of the antidepressants were used alone, only the clomipramine effect was blocked by naloxone. 3. These data indicate that TRH is able to potentiate the effect not only of imipramine but of other antidepressants in the mouse forced-swimming test, although these other antidepressants act in various ways on cerebral amines. The antagonism of the effects induced by the antidepressants alone or in association with TRH after blockade of dopaminergic systems may indicate a reversal of the effect of the antidepressants by blockade of dopaminergic systems. Hence, the same mechanisms would be involved in the effects induced by antidepressants alone or in association with TRH, with respect to dopaminergic systems. However, different mechanisms of action seem to be responsible for the potentiation of TRH of the effect of the various antidepressants, since the involvement of the opioid systems varies according to the antidepressant tested.