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C.01.01 From strength to strength – Escitalopram the cornerstone of treatment in depression
S441
Satellite symposia
C.01. Outstanding needs in depression and how multimodal antidepressants may solve them C.01.01 From strength to strength − Escitalopram the cornerstone of treatment in depression Y. Barak1 ° 1 Abarbanel Mental Health Center, Tel-Aviv University, Bat-Yam, Israel The introduction of selective serotonin reuptake inhibitors (SSRIs) was a major revolution in antidepressant pharmacotherapy [1]. In the 20 years and more since their introduction, SSRIs have captured the antidepressant market and become a household name. However, the results of ‘real world’ studies emphasise that remission is still hard to achieve for patients suffering from depression [1]. We have come to realise that SSRIs and their derivative compounds, the serotonin-norepinephrine reuptake inhibitors and norepinephrine reuptake inhibitors, represent only a limited advance over older antidepressants. The therapeutic efficacy of these mechanistically simple monoamine-based antidepressants is limited by slow onset, modest remission rates and lower effectiveness for certain depressive symptoms [1]. Multiple pharmacological approaches exist to augment the effects of SSRIs, including atypical antipsychotics and mirtazapine. Furthermore, promising novel compounds may also fulfil the goal of enhanced control of depressive symptoms. Among these is a new class, not previously much discussed: multimodal antidepressants. These compounds combine inhibition of the 5-HT transporter with blockade and/or (partial) agonism of 5-HT receptors [2]; early examples are trazodone and nefazodone. Newer multimodal antidepressants are currently under investigation, including vilazodone (a 5-HT reuptake inhibitor with 5-HT1A agonist properties) and Lu AA21004 (a 5-HT reuptake inhibitor with 5-HT3 antagonist, 5-HT7 antagonist, 5-HT1B partial agonist and 5-HT1A agonist properties). New multimodal compounds combining 5-HT ‘augmenting moieties’ with 5-HT reuptake inhibition may provide a more effective and well-tolerated antidepressant in a single molecule. References [1] Chang, T., Fava, M., 2010 The future of psychopharmacology of depression. J Clin Psychiatry 71, 971–975. [2] Nutt, D.J., 2009 Beyond psychoanaleptics − can we improve antidepressant drug nomenclature? J Psychopharmacol 23, 343–345.
C.01.02 The symptom of depression that nobody understands E. Lenze1 ° 1 Washington University, School of Medicine, Washington, USA Major depressive disorder (MDD) is characterised by a variety of symptoms, including low mood or loss of interest. Cognitive dysfunction, encompassing a diminished ability to think, concentrate or make decisions, is a core symptom of MDD; it is highly
prevalent at presentation and often persists during remission [1]. Cognitive dysfunction negatively impacts functional recovery, including work/life functioning, and is a significant burden to the patient, their family and wider society [2]. Furthermore, residual symptoms, including persistent cognitive dysfunction, increase the likelihood of relapse in patients with MDD [3]. Despite being identified within diagnostic criteria for depression and its role in achieving functional recovery, cognitive dysfunction is often overlooked by mental health professionals [3], patients and the general community. Cognitive dysfunction can be easily identified (patients have impaired ability to concentrate [attention], remember [memory], plan [executive function] and may be slow to respond [psychomotor speed] [2,3]) and can be assessed by self-report, clinician rating by interview or behavioural observation, and via a variety of objective neuropsychological tests. Increased awareness and improvements in the ease of assessment are needed [3]. Treatment directed specifically toward this neglected symptom of MDD is warranted. To further this goal, a battery of neuropsychological tests should be incorporated as outcome measures in clinical trials of antidepressants. Cognitive dysfunction is an under-appreciated but common symptom of MDD. It is hoped that improvements in cognitive function will reduce disability and help patients with MDD maintain/return to normal functioning. References [1] Conradi, H.J., Ormel, J., de Jonge, P., 2011 Presence of individual (residual) symptoms during depressive episodes and periods of remission: a 3-year prospective study. Psychol Med 41, 1165–1174. [2] Jaeger, J., Berns, S., Uzelac, S., Davis-Conway, S., 2006 Neurocognitive deficits and disability in major depressive disorder. Psychiatry Res 145, 39−48. [3] Greer, T.L., Kurian, B.T., Trivedi, M.H., 2010 Defining and measuring functional recovery from depression. CNS Drugs 24, 267–284.
C.01.03 Outstanding needs in depression and how multimodal antidepressants may solve them P. Blier1 ° 1 University of Ottawa, Institute of Mental Health Research, Room 6411, Ottawa, Canada Major depression is a heterogeneous disorder. For instance, it is possible to have two patients meeting diagnostic criteria and yet not have a single sign or symptom in common. This indicates that pathophysiology may differ widely. From a therapeutic point of view, such clinical observations may also begin to explain why only about half of patients respond (i.e. 50% improvement) and a third achieve remission with any first therapeutic attempt. Despite this rather inefficient performance of antidepressants, it is nevertheless possible to determine if any given medication will not work within a standard therapeutic trial. Many studies have shown that if an antidepressant has not produced a minimal improvement (<20%) after two weeks, there is about 10% chance that this regimen will induce remission [1]. Consequently, doses may be increased for an extra two weeks, or if drug titration
Satellite symposia
C.01. Outstanding needs in depression and how multimodal antidepressants may solve them C.01.01 From strength to strength − Escitalopram the cornerstone of treatment in depression Y. Barak1 ° 1 Abarbanel Mental Health Center, Tel-Aviv University, Bat-Yam, Israel The introduction of selective serotonin reuptake inhibitors (SSRIs) was a major revolution in antidepressant pharmacotherapy [1]. In the 20 years and more since their introduction, SSRIs have captured the antidepressant market and become a household name. However, the results of ‘real world’ studies emphasise that remission is still hard to achieve for patients suffering from depression [1]. We have come to realise that SSRIs and their derivative compounds, the serotonin-norepinephrine reuptake inhibitors and norepinephrine reuptake inhibitors, represent only a limited advance over older antidepressants. The therapeutic efficacy of these mechanistically simple monoamine-based antidepressants is limited by slow onset, modest remission rates and lower effectiveness for certain depressive symptoms [1]. Multiple pharmacological approaches exist to augment the effects of SSRIs, including atypical antipsychotics and mirtazapine. Furthermore, promising novel compounds may also fulfil the goal of enhanced control of depressive symptoms. Among these is a new class, not previously much discussed: multimodal antidepressants. These compounds combine inhibition of the 5-HT transporter with blockade and/or (partial) agonism of 5-HT receptors [2]; early examples are trazodone and nefazodone. Newer multimodal antidepressants are currently under investigation, including vilazodone (a 5-HT reuptake inhibitor with 5-HT1A agonist properties) and Lu AA21004 (a 5-HT reuptake inhibitor with 5-HT3 antagonist, 5-HT7 antagonist, 5-HT1B partial agonist and 5-HT1A agonist properties). New multimodal compounds combining 5-HT ‘augmenting moieties’ with 5-HT reuptake inhibition may provide a more effective and well-tolerated antidepressant in a single molecule. References [1] Chang, T., Fava, M., 2010 The future of psychopharmacology of depression. J Clin Psychiatry 71, 971–975. [2] Nutt, D.J., 2009 Beyond psychoanaleptics − can we improve antidepressant drug nomenclature? J Psychopharmacol 23, 343–345.
C.01.02 The symptom of depression that nobody understands E. Lenze1 ° 1 Washington University, School of Medicine, Washington, USA Major depressive disorder (MDD) is characterised by a variety of symptoms, including low mood or loss of interest. Cognitive dysfunction, encompassing a diminished ability to think, concentrate or make decisions, is a core symptom of MDD; it is highly
prevalent at presentation and often persists during remission [1]. Cognitive dysfunction negatively impacts functional recovery, including work/life functioning, and is a significant burden to the patient, their family and wider society [2]. Furthermore, residual symptoms, including persistent cognitive dysfunction, increase the likelihood of relapse in patients with MDD [3]. Despite being identified within diagnostic criteria for depression and its role in achieving functional recovery, cognitive dysfunction is often overlooked by mental health professionals [3], patients and the general community. Cognitive dysfunction can be easily identified (patients have impaired ability to concentrate [attention], remember [memory], plan [executive function] and may be slow to respond [psychomotor speed] [2,3]) and can be assessed by self-report, clinician rating by interview or behavioural observation, and via a variety of objective neuropsychological tests. Increased awareness and improvements in the ease of assessment are needed [3]. Treatment directed specifically toward this neglected symptom of MDD is warranted. To further this goal, a battery of neuropsychological tests should be incorporated as outcome measures in clinical trials of antidepressants. Cognitive dysfunction is an under-appreciated but common symptom of MDD. It is hoped that improvements in cognitive function will reduce disability and help patients with MDD maintain/return to normal functioning. References [1] Conradi, H.J., Ormel, J., de Jonge, P., 2011 Presence of individual (residual) symptoms during depressive episodes and periods of remission: a 3-year prospective study. Psychol Med 41, 1165–1174. [2] Jaeger, J., Berns, S., Uzelac, S., Davis-Conway, S., 2006 Neurocognitive deficits and disability in major depressive disorder. Psychiatry Res 145, 39−48. [3] Greer, T.L., Kurian, B.T., Trivedi, M.H., 2010 Defining and measuring functional recovery from depression. CNS Drugs 24, 267–284.
C.01.03 Outstanding needs in depression and how multimodal antidepressants may solve them P. Blier1 ° 1 University of Ottawa, Institute of Mental Health Research, Room 6411, Ottawa, Canada Major depression is a heterogeneous disorder. For instance, it is possible to have two patients meeting diagnostic criteria and yet not have a single sign or symptom in common. This indicates that pathophysiology may differ widely. From a therapeutic point of view, such clinical observations may also begin to explain why only about half of patients respond (i.e. 50% improvement) and a third achieve remission with any first therapeutic attempt. Despite this rather inefficient performance of antidepressants, it is nevertheless possible to determine if any given medication will not work within a standard therapeutic trial. Many studies have shown that if an antidepressant has not produced a minimal improvement (<20%) after two weeks, there is about 10% chance that this regimen will induce remission [1]. Consequently, doses may be increased for an extra two weeks, or if drug titration