Olanzapine in the Treatment of Apathy in Previously Depressed Participants Maintained With Selective Serotonin Reuptake Inhibitors

Marangell, Lauren B.; Johnson, Christopher R.; Kertz, Barbara; Zboyan, Holly A.; Martinez, J. Michael

doi:10.4088/jcp.v63n0503

Cited by 54 publications

(23 citation statements)

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“…Although pharmacologic studies in animal models of apathy have also lent insight into mechanisms contributing to the regulation of motivated behaviors, the lack of full model validation constrains use of the results. Drugs claimed to benefit apathy in humans include serotonergic antidepressants (Siddique et al 2009), antipsychotics (Marangell et al 2002), catecholaminergic psychostimulants (Padala et al 2010), antidementia cholinomimetics, and antiglutamatergics (Swanberg 2007;Rodda et al 2009), and antiparkinsonian dopaminergics ). All presumably act through effects on neurotransmitters mediating frontal-subcortical circuit function.…”

Section: Pathophysiologymentioning

confidence: 99%

“…The successful use of methylphenidate to treat stroke-induced apathy has been reported (Spiegel et al 2009). Atypical antipsychotics given to patients with schizophrenia (clozapine alone or with mirtazapine, respiradone, olanzapine) as well as certain antidepressants (buproprion) and psychostimulants (amphetamine, methylphenidate, and modafinil) used in the treatment of various brain disorders are also said to have benefited apathy (Marangell et al 2002;Corcoran et al 2004;Daiello 2007;Padala et al 2007Padala et al , 2010. Thus, although recent therapeutic studies have identified approaches worthy of further evaluation, as yet there is insufficient evidence to indicate that any pharmacological treatment actually ameliorates apathy (Drijgers et al 2009).…”

Section: Current Therapeutic Approachesmentioning

confidence: 99%

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Apathy in Neuropsychiatric Disease: Diagnosis, Pathophysiology, and Treatment

Chase¹

2010

Neurotox Res

117

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Apathy is an increasingly recognized concomitant of a broad range of central nervous system disorders. Nevertheless, its nosology, pathogenesis and therapy remain shrouded in confusion and controversy. As yet, there is little consensus regarding methods for detecting apathy, or distinguishing it from depression, or for assessing its severity. Many now regard the apathy syndrome as primarily reflecting a lack of motivation that compromises emotional, cognitive, and overt behavioral function. Even though under-recognized and under-diagnosed, apathy hardly appears uncommon: current epidemiologic studies suggest over 10 million Americans may be affected. Its reported frequency in various neurologic and psychiatric conditions varies widely, from less than 10 to over 80%, reflecting differences in population characteristics and assessment procedures. Often apathy has been associated with such neurodegenerative disorders as Alzheimer's disease, Parkinson's disease, and fronto-temporal dementia. But it also occurs in those with psychiatric disorders such as schizophrenia and major depression. Clinical, neuropathologic, and neuroimaging observations increasingly suggest that apathy reflects dysfunction of frontal-subcortical circuits, especially those linking the ventromedial prefrontal cortex to related regions in the basal ganglia. Therapeutically, numerous small studies suggest that psychostimulants, dopaminergics, and cholinesterase inhibitors may benefit those manifesting this syndrome. However, no adequately powered, randomized controlled trials have reported success and no medication have ever been approved for this disorder. The accelerating pace of current research nevertheless promises to improve our understanding of apathy and to better address the unmet medical needs of those suffering its consequences.

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Section: Pathophysiologymentioning

confidence: 99%

Section: Current Therapeutic Approachesmentioning

confidence: 99%

Apathy in Neuropsychiatric Disease: Diagnosis, Pathophysiology, and Treatment

Chase¹

2010

Neurotox Res

117

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“…There are studies showing that 5-HT 2A/2C antagonism has a significant role in the mechanism underlying the antidepressant-like effect of conventional antidepressants in the FST. The down regulation of 5-HT 2A receptors is proposed to mediate the longterm actions of antidepressants 24,25 C In recent years, a number of open-label and placebo controlled studies have suggested that atypical antipsychotic drugs and some antidepressants (e.g., mirtazapine and mianserin) augment the clinical response to SSRIs in treatment-resistant patients [26][27][28][29] . One common feature of these agents is their ability to occupy 5-HT 2 In order to investigate the possible involvement of the serotonergic system in the antidepressant and antiepileptic activity of CDE, the effect of the CDE on lithium induced head-twitches, a serotonin mediated behavior was investigated.…”

Section: Discussionmentioning

confidence: 99%

Dual Protective Effect of Cynodon dactylon in Epilepsy as Well as Depression

Ingale¹,

Gupta²

2015

Pharmacologia

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Background and Objective: Depression and epilepsy are considered as the strongest predictor of poor quality of life. A complex relation has been established between the two conditions which suggest that the high co morbidity of depression and epilepsy is related to the existence of common neurobiologic and pathogenic mechanisms involved in them. Plants and their extracts are better choice to treat such type of diseases (in which treatment of one worsens the other), because of presence of antagonistic substances in them, due to which they show lesser or no side effects. Hence, the present study was designed to investigate the effect of ethanolic extract of Cynodon dactylon on epilepsy and depression in mice. Methodology: Antidepressant activity was investigated using forced swim test and reserpine induced hypothermia model and antiepileptic activity was explored using MES test and PTZ induced seizure test. Results:The results of the present study showed that ethanolic extract of C. dactylon possess promising antidepressant as well as antiepileptic activity. From the mechanistic study performed using baclofen induced catatonia and lithium induced head twitch model, it was demonstrated that the antiepileptic effect of C. dactylon may be mediated through its GABA-mimetic action and antidepressant activity may be mediated through 5 HT 2 antagonistic action (like atypical antidepressants). Conclusion: Thus, it may be concluded that dual protective effect of C. dactylon in epilepsy and depression is associated with diverse mechanism, namely GABA-mimetic and 5-HT 2 antagonistic action.

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“…There is also a small case study of risperidone augmentation of milnacipran (Tani et al, 2004). Open trials also support a potential role for augmentation of SSRIs with olanzapine in the treatment of apathy in SSRI-remitters (Marangell et al, 2002). In addition, the acute antidepressant effects of olanzapine also appear to be sustained during the continuation and maintenance phases of treatment (Corya et al, 2003) while the addition of olanzapine to fluoxetine in depression also appears to reduce outpatient, and inpatient utilization and medical costs (Corey-Lisle et al, 2003).…”

Section: Older Antipsychotic Agents: Amisulpride (Solian) and Molindomentioning

confidence: 96%

Monoaminergic‐based Pharmacotherapy for Depression

Papakostas¹,

Fava²

2005

Biology of Depression

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Although recent advances in neuropharmacology, neuroendocrinology, molecular biology, and pharmacogenetics have been instrumental in bringing about potential treatments for depression which are fundamentally unrelated to their predecessors, including substance P antagonists, glutaminergic agents, and corticotropinreleasing factor (CRF) antagonists, nevertheless it was agents that influenced the function of monoamine receptors and transporters that were discovered initially by serendipity and then developed as treatments for depression. The development of such compounds also served as a framework for the understanding of depression as a medical illness affecting brain functioning. As a result of these efforts, our field has gained further understanding of the role of monoamines in depression. In previous chapters, the relevance of monoamines in the underlying pathophysiology of depression was reviewed. In the following chapter we will focus on describing the contemporary role of monoaminergic agents in the treatment of depression. 6.

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Olanzapine in the Treatment of Apathy in Previously Depressed Participants Maintained With Selective Serotonin Reuptake Inhibitors

Cited by 54 publications

References 0 publications

Apathy in Neuropsychiatric Disease: Diagnosis, Pathophysiology, and Treatment

Apathy in Neuropsychiatric Disease: Diagnosis, Pathophysiology, and Treatment

Dual Protective Effect of Cynodon dactylon in Epilepsy as Well as Depression

Monoaminergic‐based Pharmacotherapy for Depression

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