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Antidepressants/antidepressant therapy

Patients receiving monoamine oxidase inhibitors (MAOI) as antidepressant therapy have been especially subject to the hypertensive effects of vasoactive amines (52). These dietary amines have also been impHcated as causative agents ia migraine. Other aaturaHy occurring alkaloids (qv) have been recognized for centuries as possessing neurological stimulant and depressant properties. [Pg.478]

Antidepressant therapy is usually associated with a delay of up to about two to three weeks before the onset of a cleat beneficial effect. Therefore, it... [Pg.228]

Promoting Patient Responsibility for Antidepressant Drug Therapy... [Pg.292]

Croghan TW, Lair TJ, Engelharr LE, er al (1997). Effect of antidepressant therapy on health care utilization and costs in primary care. Psychiatr Serv 48) 1420-6. [Pg.53]

McCombs JS, Nichol MB, Stimmel GL, et al (1990). The cost of antidepressant drug therapy failure a study of antidepressant use patterns in a Medicaid population. J Clin Psychiatry (6, suppL), 60—9. [Pg.54]

Monitor antidepressant therapy for relief of lower abdominal pain. [Pg.320]

It is widely accepted that it takes approximately 2 to 4 weeks of treatment before improvement is seen in emotional symptoms of depression, such as sadness and anhedonia. Furthermore, it may take as long as 6 to 8 weeks of treatment to see the full effects of antidepressant therapy. [Pg.569]

Since the typical major depressive episode lasts 6 months or longer, if antidepressant therapy is interrupted for any reason following the acute phase, the patient may relapse into the depressive episode. When treating the first depressive episode, antidepressants must be given for an additional 4 to 9 months in the continuation phase for the purpose of preventing relapse. [Pg.569]

Lack of patient understanding concerning optimal antidepressant drug therapy frequently leads to partial compliance or non-compliance with therapy, thus, the primary purpose of antidepressant counseling is to enhance compliance and improve outcomes. [Pg.569]

Unfortunately, antidepressants do not produce a clinical response immediately. Improvement in physical symptoms, such as sleep, appetite, and energy, can occur within the first week or so of treatment. Although a recent meta-analysis suggests earlier effects of antidepressant treatment,36 it is widely accepted that it takes approximately 2 to 4 weeks of treatment before improvement is seen in emotional symptoms of depression, such as sadness and anhedonia. Furthermore, it may take as long as 6 to 8 weeks of treatment to see the full effects of antidepressant therapy.7 22 23... [Pg.578]

Approximately one-third of patients with MDD do not respond satisfactorily to their first antidepressant medication.37 In such cases, the clinician must evaluate the adequacy of antidepressant therapy, including dosage, duration, and patient compliance.17 Treatment reappraisal also should include verification of the patient s diagnosis and reconsideration of clinical factors that could be impeding successful therapy, such as concurrent medical conditions (e.g., thyroid disorder), comorbid psychiatric conditions (e.g., alcohol abuse), and psychosocial issues (e.g., marital stress).16... [Pg.578]

Duration of antidepressant therapy is also an unsettled question. It may be possible in some patients to prevent depressive relapse with a mood-stabilizing drug without maintenance antidepressant therapy following acute treatment with an antidepressant. If so, the risk of a mood switch with continued antidepressant therapy would be reduced. [Pg.601]

Benzodiazepines are recommended for acute treatment of generalized anxiety disorder when short-term relief is needed, as an adjunct during initiation of antidepressant therapy, or to improve sleep. [Pg.605]

Steimer, W., et al., "Pharmacogenetics A New Diagnostic Tool in the Management of Antidepressive Drug Therapy," Clin. Chim. Acta, 308, 33-41 (2001). [Pg.187]

Gupta, R. and Molnar, G. 1980. Plasma levels and tricyclic antidepressant therapy Part I. A review of assay method. Biopharmacol Drug Dispos. 1 259. [Pg.316]

In contrast to MDD, the bipolar disorders consist of episodes of depression and episodes of hypomania or mania. This poses a problem for treating the depressed phase of this illness, becanse, as noted earlier, antidepressants can trigger hypomania, mania, or mixed dysphoric mania and can increase the freqnency of manic episodes. Therefore, the hallmark of treating BPAD is the nse of mood stabilizers, with and withont snpplemental antidepressant therapy. Please refer to Table 3.16 for a comparison of the traditional mood stabilizers. [Pg.78]

We do not use benzodiazepines as readily when treating GAD as we do when treating panic disorder. In comparison to those with panic disorder, most patients with GAD can more easily tolerate the delay in treatment response and even any transient exacerbation of anxiety associated with antidepressant therapy. Benzodiazepines are reserved for those who present with especially severe anxiety that necessitates more rapid relief than an antidepressant can afford and for those who do not achieve a satisfactory response to antidepressant or buspirone therapy. Due to the persistent nature of the anxiety experienced by patients with GAD, shortacting benzodiazepines such as alprazolam are not especially helpful unless dosed 3-4 times per day. Instead, we prefer long-acting agents such as clonazepam. When used to treat GAD, clonazepam should be started at a low dose (0.25-0.5 mg/day) and titrated to higher doses (1-4 mg/day) if clinically necessary. [Pg.152]

A recent open label retrospective report indicates that tiagabine, which acts by blocking GABA reuptake, might be an effective augmentation strategy for patients who are only partially responsive to antidepressant therapy. [Pg.165]

The long-acting benzodiazepine clonazepam can be used as a first-line agent for those patients with particularly severe symptoms who are unable or unwilling to wait for the delayed therapeutic benefit of an antidepressant. Clonazepam can be initiated as a monotherapy for those without comorbid depression or in conjunction with an antidepressant for those who are also depressed. In the latter case, clonazepam can be used transiently with a plan to taper and discontinue it once sufficient time has elapsed to experience benefit from antidepressant therapy. [Pg.166]

Generalized Sociai Anxiety Disorder, Treatment Resistance. A significant minority of patients will not experience a satisfactory treatment response to antidepressant therapy, even after a trial of adequate duration at full strength doses. For those with comorbid depression who are experiencing no benefit from SSRI treatment for either the anxiety or depression, then switching treatment is advisable. The options include switching to another SSRI, a SNRI (venlafaxine or perhaps dulox-etine), or, when other alternatives fail, phenelzine. [Pg.166]


See other pages where Antidepressants/antidepressant therapy is mentioned: [Pg.291]    [Pg.570]    [Pg.571]    [Pg.578]    [Pg.578]    [Pg.580]    [Pg.580]    [Pg.581]    [Pg.1337]    [Pg.178]    [Pg.3]    [Pg.470]    [Pg.152]    [Pg.809]    [Pg.13]    [Pg.151]    [Pg.197]   
See also in sourсe #XX -- [ Pg.570 , Pg.571 ]

See also in sourсe #XX -- [ Pg.570 , Pg.571 ]




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