Pub Date : 2007-12-01DOI: 10.1097/01.IDT.0000299133.95994.b1
V. Pirec
Learning Objectives fter reading this article, the practitioner should be able to:Discuss the assessment of depression in pregnant women and treatment approaches.Describe potential risks of using selective serotonin reuptake inhibitors in pregnant patients.Summarize basic concepts regarding treatment decisions in pregnant patients with depression.
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Pub Date : 2007-11-01DOI: 10.1097/01.IDT.0000296678.53190.e6
P. L. Dago
of monoamine oxidase inhibitors (MAOIs) in the treatment of depression. This dopaminergic, noradrenergic, and serotonergic antidepressant class may be of particular value in the treatment of atypical depression, where it has demonstrated superior efficacy to tricyclics. Three MAOIs (isocarboxazid, phenelzine, and tranylcypromine) have long been approved in the United States for the treatment of depression. They irreversibly inhibit both forms of the monoamine oxidase enzyme: MAO-A and MAO-B. Their widespread use, however, has been limited by the need for strict dietary restrictions. In February 2006, the FDA approved the selegiline transdermal system (STS) (Emsam, Bristol-Myers Squibb) for the treatment of major depressive disorder (MDD). The agent, the first antidepressant patch, delivers selegiline transdermally and at the starting and potentially therapeutic dose of 6 mg/24 h can be used without dietary restrictions. This article will: • Describe the rationale for the development of STS;
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Pub Date : 2007-10-01DOI: 10.1097/01.IDT.0000290219.07082.4c
J. Jefferson
it was not until 1930 that Lucy Wills started it on the path to discovery when she found that a yeast extract (Marmite, the bane of monoamine oxidase inhibitor users) prevented macrocytic anemia of pregnancy. Folic acid was named in 1941 after its isolation from four tons of spinach (folium = leaf in Latin). It was synthesized in pure crystalline form in the early 1940s and received the formal name of pteroylglutamic acid because of its structure. If one cares to split hairs, folic acid refers to the chemical compound not found naturally in foods while folate encompasses both natural folates (pteroylglutamates) and synthetic folic acid. Other names that have popped up over the years include vitamin M, vitamin B 9 , and folacin. Dietary sources of this water-soluble B vitamin include dark leafy greens, lentils, and enriched grain products such as cereals, breads, pasta, and rice. In January 1998, the FDA required folic acid fortification of grain products to reduce the risk of neural tube defects. Mandatory fortification has not been implemented universally throughout the world for a variety of reasons, including concern about masking symptoms of vitamin B12 deficiency. 2
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Pub Date : 2007-09-01DOI: 10.1097/01.IDT.0000288127.14560.b9
J. Pilitsis, R. Bakay
Additional Reference As a psychiatrist and psychotherapist I read this article with great interest. However, my intention is not actually to comment substantially on the many questions raised by deep brain stimulation (DBS) but to provide a literature reference and give my reasons for doing so. In his book “Tief im Hirn [Deep in the brain],” Helmut Dubiel, who had undergone DBS, published an impressive description of his treatment (1). Although in his case it was Parkinson’s disease that led to his having DBS, not a psychiatric disorder in the narrower sense, this book seems to me to be of great value for the article by Kuhn and colleagues. The doctor in charge of advice and treatment and the reader are given an exact description of the situation of a patient who is treated with DBS. The book is, of course, totally subjective, but also entirely credible and authentic. However: is this science? An idea of the importance of patients’ (or “service users’”, as they are often referred to in English speaking countries) experiences came through in the 2009 schizophrenia guidelines from Britain’s National Institute for Health and Clinical Excellence. Tilmann Steinert comments that in spite of their formal evidence base, these official guidelines influencing English health policy contain substantial qualitative and subjective passages, for example, several detailed case histories giving patients’ own perspectives. Dubiel’s book is such an example of a narrative contribution from a patient. In my opinion, the discussion around DBS would also be of benefit in psychiatric settings. In any case, we should be discussing the option. Dubiel`s book is a fine example of a narrative contribution from a patient. In my opinion, the discussion around DBS would benefit from this in psychiatric illness, too. In any case, we should be discussing the option DOI: 10.3238/arztebl.2010.0644a
作为一名精神病学家和心理治疗师，我怀着极大的兴趣阅读了这篇文章。然而，我的意图实际上并不是对深部脑刺激(DBS)引发的许多问题进行实质性的评论，而是提供文献参考并给出我这样做的理由。接受过DBS的Helmut Dubiel在他的书《大脑深处》(Tief im Hirn [Deep In brain])中对他的治疗进行了令人印象深刻的描述(1)。虽然在他的案例中，是帕金森病导致了他的DBS，而不是狭义的精神疾病，但在我看来，这本书对库恩及其同事的文章有很大的价值。负责建议和治疗的医生和读者都得到了一个准确的描述病人的情况，谁接受DBS治疗。当然，这本书是完全主观的，但也完全可信和真实。然而，这是科学吗?2009年，英国国家健康与临床卓越研究所(National Institute for Health and Clinical Excellence)发布了精神分裂症指南，其中体现了患者(或“服务使用者”，在英语国家经常这样称呼他们)经历的重要性。Tilmann Steinert评论说，尽管他们有正式的证据基础，这些影响英国卫生政策的官方指导方针包含大量定性和主观的段落，例如，几个详细的病例史给出了患者自己的观点。Dubiel的书就是这样一个病人叙述贡献的例子。在我看来，关于DBS的讨论对精神病学也有好处。无论如何，我们应该讨论一下这个选择。Dubiel的书是病人叙述贡献的一个很好的例子。在我看来，围绕DBS的讨论也会从精神疾病中受益。在任何情况下，我们都应该讨论DOI: 10.3238/arztebl.2010.0644a选项
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Pub Date : 2007-08-01DOI: 10.1097/01.IDT.0000282901.77256.88
Jeffrey Rado
and a leading cause of disability worldwide. While many effective antidepressant treatments are available, the neurobiology of depression, as well as the mechanism of action (MOA) of antidepressants, remains unclear. Recent investigations of brain-derived neurotrophic factor (BDNF) support its putative role in both the pathophysiology of depression and antidepressants’ MOA. Preclinical studies of depression indicate that BDNF has effects comparable to those of antidepressants. Brain levels of BDNF in animals decrease in response to stress while increases occur in response to antidepressants, electroconvulsive shock (ECS), vagus nerve stimulation (VNS), and transcranial magnetic stimulation (TMS). In addition, a growing number of clinical studies support its role as a marker of antidepressant activity.
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Pub Date : 2007-07-01DOI: 10.1097/01.IDT.0000280816.38955.e1
J. Zacher, Sarah E Grady
T he second-generation antipsychotics (SGAs) have become the first-line treatment for schizophrenia. They hold the distinct advantage of fewer unwanted extrapyramidal effects, especially tardive dyskinesia, compared with first-generation antipsychotics (FGAs). They also may produce less worsening of negative symptoms, greater improvement in cognitive impairment, and better relapse prevention. Recently, the Clinical Antipsychotic Trials of Intervention Effectiveness found that while firstand second-generation agents are effective in treating the positive and negative symptoms of schizophrenia, there is a high discontinuation rate. The most common reasons for discontinuation in Phase 1 of this trial were lack of efficacy, intolerability, and patient decision. This emphasizes the need for effective new agents that are more tolerable and will facilitate medication adherence. Paliperidone extended-release tablet (paliperidone ER, Invega, Janssen L.P., Titusville, NJ) is the newest SGA on the U.S. market. INDICATIONS Paliperidone ER is indicated for the acute and maintenance treatment of schizophrenia. The efficacy of paliperidone ER was established in three placebo-controlled trials, each 6 weeks in duration.
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Pub Date : 2007-06-01DOI: 10.1097/01.IDT.0000271143.75925.33
M. Demitrack
M ajor depression is among the most common and disabling of human diseases. The Global Burden of Disease Study notes that by the year 2020, the societal impact of unipolar major depression alone will be exceeded by only that of ischemic heart disease as estimated by a measure of disease morbidity, disability-adjusted life years. While modern pharmaceutical options have a clear record of success in randomized, controlled clinical trials, real-world experience in their use leaves room for improvement. The percentage of all patients who seek treatment for whom current options do not provide an acceptable solution ranges to 30%. The results of the Sequenced Treatment Alternatives to Relieve Depression (or STAR*D) trial have recently been reported. This study used a semi-naturalistic treatment algorithm designed to model as closely as possible the sequence of treatment options most commonly used in clinical practice. Among the observations are that for patients who may generally be expected to respond to treatment, the likelihood of achieving remission of symptoms (defined by a Hamilton Depression Rating Scale score of < 8) after either one (Level 1) or two (Level 2) sequential treatment trials ranges over 50%. However, once prospective evidence of failure to achieve benefit has been demonstrated, the likelihood of good clinical outcome drops precipitously, and hovers at exceedingly low levels after three prospective treatment failures. For example, the reported incidence of categorical remission in patients treated with tranylcypromine was 6.9%, which was observed after patients had failed to receive benefit from any of the three preceding adequately administered antidepressants. Equally informative is a review of the information in the STAR*D study regarding overall tolerability of treatments. For instance, as patients proceeded through the sequential treatment levels, the discontinuation rate due to treatment intolerance or adverse events rose steadily (8.6% at Level 1; 20.5% [range: 12.5%–27.2%] at Level 2; 35.2% [range: 34.2%–36.2%] at Level 3; and 32.1% [range 21.6%–41.4%] at Level 4). In other words, as the expectations of efficacy diminished with increasing resistance to prior treatment, the non-adherence to, and likely intolerability of, treatment options increased quite dramatically. Overall, these data paint a picture of measurable but limited benefit with the most commonly used pharmaceutical treatments. Does this picture improve over the longer term for individuals who achieve acceptable acute benefit? Unfortunately, it appears that, similar to the acute outcomes, as the degree of prior treatment non-response increases, the likelihood that any efficacy will be lost After reading this article, the practitioner should be able to:
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