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At least 919 records · Page 51Linked to original sources
PubMed1998

Is the efficacy of topical corticosteroid therapy for psoriasis vulgaris enhanced by concurrent moclobemide therapy? A double-blind, placebo-controlled study.

BACKGROUND: Psychosocial factors have been implicated in the onset and exacerbation of psoriasis. OBJECTIVE: We conducted a randomized, placebo-controlled, double-blind study to investigate the effect of an antidepressant agent, moclobemide, on the course of psoriasis vulgaris. METHODS: Sixty subjects were enrolled in the study. Patients were randomly assigned to treatment groups. Patients received moclobemide 450 mg/day or placebo and a topical corticosteroid ointment (diflucortolone valerate) for 6 weeks. Patients were examined at the beginning of the study and at 2-week intervals. At each visit, the severity of psoriasis and psychologic status were evaluated with the Psoriasis Area Severity Index (PASI), Beck Depression Inventory (BDI), Hamilton Rating Scale for Anxiety (HAM-A), Hamilton Rating Scale for Depression (HRS-D-17) and State-Trait Anxiety Inventory including state (STAI-1) and trait anxiety (STAI-2). RESULTS: Treatment efficacy was able to be evaluated in 22 patients in the moclobemide-treated group and in 20 in the placebo-treated group. The improvement rates in PASI, BDI, STAI-1, and HAM-A scores were significantly higher in the moclobemide treatment group. The level of state anxiety was diminished in the moclobemide group. Correlation was positive between improvement rates of the psoriatic lesions and state anxiety in all patients. CONCLUSION: Our results suggest that an antidepressant drug is useful in the treatment of psoriasis.

Administration, Topical↗
PubMed2006

Effects of tianeptine on onset time of pentylenetetrazole-induced seizures in mice: possible role of adenosine A1 receptors.

Depression is a common psychiatric problem in epileptic patients. Thus, it is important that an antidepressant agent has anticonvulsant activity. This study was organized to investigate the effects of tianeptine, an atypical antidepressant, on pentylenetetrazole (PTZ)-induced seizure in mice. A possible contribution of adenosine receptors was also evaluated. Adult male Swiss-Webster mice (25-35 g) were subjects. PTZ (80 mg/kg, i.p.) was injected to mice 30 min after tianeptine (2.5-80 mg/kg, i.p.) or saline administration. The onset times of 'first myoclonic jerk' (FMJ) and 'generalized clonic seizures' (GCS) were recorded. Duration of 600 s was taken as a cutoff time in calculation of the onset time of the seizures. To evaluate the contribution of adenosine receptors in the effect of tianeptine, a nonspecific adenosine receptor antagonist caffeine, a specific A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a specific A2A receptor antagonist 8-(3-chlorostyryl) caffeine (CSC) or their vehicles were administered to the mice 15 min before tianeptine (80 mg/kg) or saline treatments. Tianeptine (40 and 80 mg/kg) pretreatment significantly delayed the onset time of FMJ and GCS. Caffeine (10-60 mg/kg, i.p.) dose-dependently blocked the retarding effect of tianeptine (80 mg/kg) on the onset times of FMJ and GCS. DPCPX (20 mg/kg) but not CSC (1-8 mg/kg) blocked the effect of tianeptine (80 mg/kg) on FMJ. Our results suggest that tianeptine delayed the onset time of PTZ-induced seizures via adenosine A1 receptors in mice. Thus, this drug may be a useful choice for epileptic patients with depression.

Adenosine A1 Receptor Agonists↗
PubMed2000

Depression and ischemic heart disease.

Major depression is a common comorbidity associated with ischemic heart disease (IHD). There is growing evidence that psychological stress in general and depression in particular predispose to cardiovascular disease. Persons who have mental stress during daily life are at twice the risk of myocardial ischemia, and patients with post-myocardial infarction depression have higher mortality rates than nondepressed controls. These data suggest a psychophysiologic mechanism underlying the vulnerability of depressed patients to IHD. Clinical studies have demonstrated that depression is associated with a much higher risk of both cardiovascular morbidity and mortality, which could be caused by platelet activation. Physicians should maintain a heightened level of clinical suspicion for depression and depressive disorders in persons with IHD, particularly those individuals who are recovering from an acute ischemic event, such as myocardial infarction. Furthermore, depression may complicate the recovery of IHD, but in most cases depression can be effectively treated with antidepressant agents.

Antidepressive Agents↗
PubMed1988

Depression in vascular dementia.

Vascular dementia results from ischemic injury to the brain. Depression is a frequent complication of cerebrovascular dementia (CVD) occurring in 25 to 80% of patients during the course of their illness. Depression is unrelated to the severity of intellectual compromise or to the co-existence of delusions. The symptom profile of depression in CVD is indistinguishable from that of late-onset idiopathic major depressive episodes. The frequency of depression differs with the subtype of CVD and is most common in disorders with lesions of the frontal lobes, either cortical or subcortical. In addition to lesion site, other contributors to depression in CVD include vascular disease of other organs, drug therapy of co-existing medical conditions, and psychological reactions to disability. The depression of CVD responds to treatment with antidepressant agents.

Aged↗
PubMed1989

[Drug treatment of obesity].

Anorectic agents constitute the most widely used supportive drug treatment in obesity as well as that most often prescribed. A large number of substances have been proposed for this purpose, and some have been found to be reasonably effective, while others exhibiting side effects which forbid their use, as thyroid hormones and diuretic agents. There are other substances with properties that might justify their use, such as ballast preparations, some antidepressive agents, and a few compounds acting principally on the gastrointestinal tract. Of current interest are substances furthering thermogenesis, but for the time being these remain in the realm of pure research. The anorectic agents usually available bring about a weight loss of about 0.5 lb (0.230 kg) per week more than prescription of a placebo, though only over a limited period of time. Once the drug is discontinued, weight regain is the rule and it appears even that association of an anorectic agent to behavioural therapy might have an unfavourable effect on maintenance of the weight loss. Their use is therefore difficult to justify except in the rare cases where a short-term reduction in weight is desired or in patients suffering from an illness linked to their overweight. Differences in eating habits observed with amphetamines compared with fenfluramine and its dextrorotatory isomer dexfenfluramine suggest that these compounds could play a supportive role in the management of obese patients along with the dietetic training and changes in eating habits which are still fundamental to the medical treatment of obesity.

Antidepressive Agents↗
PubMed2005

[Remarkably low blood pressure induced by combination of SSRI and a small dose of TCA].

Recently, selective serotonin reuptake inhibitors (SSRI) have been frequently used as the first choice of antidepressants because of their safety in comparison with tricyclic antidepressive agents (TCA). On the other hand, when SSRIs are not effective, they are frequently replaced with another antidepressant. In that case, a small dose of a TCA is often added without cross tapering. We report two elderly patients with depression who exhibited markedly low blood pressure when a small dose of a TCA was added to a SSRI. The combination of a SSRI and a TCA can be hazardous because it can cause unexpected adverse effects especially in elderly patients.

Aged↗
PubMed1996

Functional classification of antidepressants based on antagonism of swim stress-induced fos-like immunoreactivity.

Autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake and immunocytochemical assessment of Fos-like immunoreactivity (Fos-LI) were used to assess swim stress-induced changes in metabolic activity in brain and to define the effect of chronic treatment with antidepressants from different pharmacological classes. Saline-treated rats processed in the forced swim test exhibited marked increases in Fos-LI in limbic cortical regions, lateral septum, medial amygdala and paraventricular nucleus of the hypothalamus (PVN). Uptake of 2-DG was increased by swim stress in some of the same brain regions where Fos-LI was induced, with the notable exception of a lack of a change in the PVN. Rats received injections for 3 wk with imipramine, desipramine, fluoxetine, nisoxetine, tranylcypromine or mianserin before being processed in the forced swim test. Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis. After tranylcypromine treatment, Fos-LI was induced in many brain regions including limbic cortex, amygdala and paraventricular nucleus of the hypothalamus. None of the other antidepressants induced Fos-LI in any brain region examined. Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices. Chronic treatment with fluoxetine, tranylcypromine and mianserin did not alter swim stress-induced Fos-LI in any brain region. Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI. In contrast to the action of chronic imipramine on Fos-LI induced by swim, chronic administration of imipramine did not antagonize the stress-induced changes in 2-DG uptake in limbic cortical regions. Acute administration of propranolol, which blocks beta-adrenergic receptors, reduced the number of cells staining for Fos-LI in limbic cortical regions, resembling the effects produced by chronic imipramine, desipramine and nisoxetine. In the PVN, neither propranolol nor prazosin (an alpha 1 antagonist) blocked the swim-induced Fos-LI, suggesting that swim-induced Fos-LI in the PVN is not under control of beta- or alpha 1-adrenergic receptors. These latter results imply that adaptation of noradrenergic receptors by chronic imipramine may not be related to the antagonism of stress-induced Fos-LI. The clear functional differences of the various antidepressant agents on swim stress-induced Fos-LI after chronic administration provide a functional classification of antidepressant drug action not previously identified.

Animals↗
PubMed2003

S-adenosyl-methionine in depression: a comprehensive review of the literature.

As many as 29% to 46% of patients with major depressive disorder (MDD) show only partial or no response to an adequate course of an antidepressant. The current practice is to increase the dose, switch to another antidepressant, or to combine the initial antidepressant with an antidepressant of a different class or a non-antidepressant agent. A growing number of studies have also been directed toward exploring the potential use of augmenting traditional antidepressants with nonpharmaceutic supplements, or even using such supplements as monotherapy for depression. S-adenosyl-methionine (SAMe) is one such compound. Compared with many other nonpharmaceutic supplements, SAMe has been extensively studied, and impressive literature extending back three decades suggests the antidepressant efficacy of SAMe. In the present work, the authors summarize the literature, focusing on the potential role of SAMe and its precursors in the pathophysiology of MDD, followed by a review of studies examining the use of SAMe for the treatment of MDD. Finally, the authors propose a model that would explain the actions of SAMe in the central nervous system.

Antidepressive Agents↗
PubMedDate not supplied

Serial electrocardiographic changes as a predictor of cardiovascular toxicity in acute tricyclic antidepressant overdose.

Tricyclic antidepressant agents continue to be a leading cause of significant morbidity and mortality in reported poisonings involving pharmaceutical agents. Although the history and physical examination play an important role in the assessment of patients with tricyclic antidepressant overdose, the presence of anticholinergic features on examination cannot predict the severity of the overdose. Several clinical variables, in particular electrocardiographic (ECG) changes, have been proposed as a guide to determine the severity of the tricyclic antidepressant poisoning. The authors describe a patient with tricyclic antidepressant overdose who presented with altered mental status and whose serial ECG changes played a significant role in diagnosing and predicting the impending cardiovascular toxicity. The role of ECG changes in making the diagnosis and assessing the severity of the tricyclic antidepressant overdose is reviewed.

Amitriptyline↗
PubMed2006

Metabotropic glutamate 5 receptor antagonism is associated with antidepressant-like effects in mice.

Antidepressant-like effects of metabotropic glutamate (mGlu)5 receptor antagonists have been reported previously. We now provide definitive identification of mGlu5 receptors as a target for these effects through the combined use of selective antagonists and mice with targeted deletion of the mGlu5 protein. In these experiments, the mGlu5 receptor antagonists 2-methyl-6-(phenylethynyl)-pyridine (MPEP) and the more selective and metabolically stable analog 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]-pyridine (MTEP) decreased immobility in the mouse forced swim test, a test predictive of antidepressant efficacy in humans. mGlu5 receptor knockout mice had a phenotype in the forced swim test that was congruent with the effects of receptor blockade; mGlu5 receptor knockout mice were significantly less immobile than their wild-type counterparts. Consistent with mGlu5 receptor mediation of the antidepressant-like effects of MPEP, the effects of MPEP were not observed in mGlu5 receptor knockout mice, whereas comparable effects of the tricyclic antidepressant imiprimine remained active in the mutant mice. MPEP and imiprimine resulted in a synergistic antidepressant-like effect in the forced swim test. The drug interaction was not likely because of increased levels of drugs in the brain, suggesting a pharmacodynamic interaction of mGlu5 and monoaminergic systems in this effect. Thus, the present findings substantiate the hypothesis that mGlu5 receptor antagonism is associated with antidepressant-like effects. This mechanism may not only provide a novel approach to the therapeutic management of depressive disorders but also may be useful in the augmentation of effects of traditional antidepressant agents.

Animals↗
PubMed1980

Treatment of depression in the medically ill elderly with methylphenidate.

Three depressed geriatric patients had a marked therapeutic response to the psychostimulant drug methylphenidate. These patients either had been unable to tolerate tricyclic antidepressants or had a medical illness that contraindicated tricyclic therapy. The lack of adverse effects in our elderly patients and methylphenidate's effectiveness as an antidepressant were consistent with the findings of other investigators. These results suggest that psychostimulants deserve further evaluation as antidepressant agents in the geriatric population.

Adjustment Disorders↗
PubMed1980

[Functional headache].

Not all functional types of headache are of psychogenic orgin. Many are due to minor irritative lesions or to refractory anomalies. Only a very small number of headache types can be regarded as psychogenic without further examination. In most cases functional and organic causes are involved. A detailed analysis of the evolution and localization of headache, together with thorough internal and neurological examinations are necessary to enable one to categorize a headache with any confidence. If depression and tension prevail, it is important to reduce the patient's consumption of painkillers by means of antidepressive agents, autogenic training or betablockers.

Adrenergic beta-Antagonists↗
PubMed1984

Second-generation antidepressants.

The host of newly developed antidepressant drugs offer important clinical advantages to some patients, although their promises of improved therapeutic efficacy and reduced adverse effects compared with conventional treatments are not fully realized. Increased biochemical specificity and unique mechanistic or clinical profiles render these compounds valuable in research into the pathophysiology of affective disorders and mode of action of antidepressant agents.

Alprazolam↗
PubMed2005

Review article: drugs interfering with visceral sensitivity for the treatment of functional gastrointestinal disorders--the clinical evidence.

At present, the concept of visceral hypersensitivity provides the leading hypothesis regarding the generation of symptoms in functional gastrointestinal disorders. This paper discusses the current clinical evidence for drugs that have been proposed to interfere with visceral sensitivity in functional gastrointestinal disorders. Several possible pharmacological targets have been identified to reduce visceral pain and to reverse the processes underlying the persistence of visceral hypersensitivity. However, most of the available evidence comes from experimental animal models and cannot simply be extrapolated to patients with functional gastrointestinal disorders. In this review, we selected five drug classes that have been shown to exhibit visceral analgesic properties in experimental studies, and of which data were available regarding their clinical efficacy. These included opioid substances, serotonergic agents, antidepressants, somatostatin analogues and alpha(2)-adrenergic agonists. Although clinical trials show a limited benefit, in particular for serotonergic agents, the evidence illustrating that these effects result from normalization of visceral sensation is currently lacking. Therefore, we conclude that the concept of targeting visceral hypersensitivity as a treatment for functional gastrointestinal disorders is still controversial. Future evaluations require patient selection based on the presence of visceral hypersensitivity and application of compounds that exhibit 'true' viscerosensory effects.

Abdominal Pain↗
PubMed2004

Treatment of insomnia associated with clinical depression.

Sleep disturbances are almost always present in patients with depression. Though sleep disturbances generally abate with the resolution of depression, some patients continue to report poor sleep. Since a number of studies have demonstrated that insomnia increases the risk of new-onset depression and recurrence of depression, optimal management of insomnia associated with depression becomes an important clinical goal. Antidepressant agents have variable effects on sleep and in fact, some antidepressants seem to worsen sleep in patients with depression. This article reviews various treatment options in the management of patients presenting with insomnia and depression, including single agents, combination strategies and behavioral interventions.

Antidepressive Agents, Tricyclic↗
PubMed1995

[Effects of chronic administration of antidepressants on microtubule assembly in rat cerebral cortex].

We examined the effects of chronic treatment with several types of antidepressants on microtubule assembly and phosphorylation of microtubule-associated proteins (MAPs) in the rat cerebral cortex. The microtubule assembly was monitored in turbidity at 350 nm using a spectrophotometer. Chronic but not acute treatment with desipramine (DMI), maprotiline (MPR) or citalopram (CTR) inhibited microtubule assembly, assayed in the presence of protein phosphatase inhibitors (PPI). In contrast, this inhibitory effect was completely nullified in the absence of PPI. The three compounds had no direct effect on microtubule assembly. The phosphorylation of MAPs (MAP2 and tau) was investigated by immunoblotting with monoclonal antibodies (phosphoserine, phosphothreonine and phosphotyrosine) after immunoprecipitation of MAPs. The serine but not threonine or tyrosine phosphorylation of MAP2 was significantly increased after chronic treatment with DMI, MPR or CTR. The phosphorylation of tau was not altered following chronic administration of antidepressants. These results suggest that the inhibition of microtubule assembly observed after chronic antidepressant treatment is attributable to an increase in the phosphorylated MAP2 and this effect may represent a novel and common action of typical and atypical antidepressant agents. Our results show that besides second messengers system, protein phosphorylation might be involved in the therapeutic effects of antidepressants.

Animals↗