August 2012  << Back  

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 LETTERS TO THE EDITOR

Agomelatine for the treatment of posttraumatic stress disorder: A case report

Domenico De Berardis, MD, PhD

National Health Service, Department of Mental Health, Psychiatric Service of Diagnosis and Treatment, Hospital G. Mazzini, Teramo, Italy, Department of Neurosciences and Imaging, Chair of Psychiatry, Università G. d’Annunzio, Chieti, Italy

Nicola Serroni, MD

National Health Service, Department of Mental Health, Psychiatric Service of Diagnosis and Treatment, Hospital G. Mazzini, Teramo, Italy

Stefano Marini, MD

National Health Service, Department of Mental Health, Psychiatric Service of Diagnosis and Treatment, Hospital G. MazziniTeramo, Italy, Department of Neurosciences and Imaging, Chair of Psychiatry, Università G. d’Annunzio, Chieti, Italy

Francesco Saverio Moschetta, MD

National Health Service, Department of Mental Health, Psychiatric Service of Diagnosis and Treatment, Hospital G. Mazzini, Teramo, Italy

Giovanni Martinotti, MD, PhD

Department of Neurosciences and Imaging, Chair of Psychiatry, Università G. d’Annunzio, Chieti, Italy

Massimo Di Giannantonio, MD

Department of Neurosciences and Imaging, Chair of Psychiatry, Università G. d’Annunzio, Chieti, Italy

KEYWORDS: posttraumatic stress disorder, agomelatine, treatment

ANNALS OF CLINICAL PSYCHIATRY 2012;24(3):241-242

TO THE EDITOR:

Posttraumatic stress disorder (PTSD) is a severe psychiatric disorder that develops in the aftermath of a severe emotionally traumatic event.1 Agomelatine is a melatonergic agonist (MT1 and MT2 receptors) and a 5-HT2C antagonist.2 We report on a patient with PTSD who remitted after agomelatine monotherapy.

A 44-year-old female housewife with no history of psychiatric disorders voluntarily came to our outpatient facility in July 2011, 5 months after a traffic accident. Her symptoms included intrusive memories and flashbacks, nightmares, hyperarousal, emotional numbing, irritability, central insomnia, symptoms triggers by certain cues (eg, the sound of passing cars), and severe avoidance behavior. The Structured Clinical Interview for DSM-IV confirmed the PTSD diagnosis. Impact of Event Scale (IES) score was 68, indicating severe impact. On the basis of our patient’s request and her refusal to take medications because she feared weight gain and sexual side effects, we prescribe agomelatine, 25 mg/d. We also considered that insomnia and nightmares were her most disturbing symptoms. Our patient categorically rejected any psychological intervention because of financial hardships. After 2 weeks of agomelatine, 25 mg/d, we observed an improvement in PTSD symptoms (IES score of 50) and sleep quality and her medication was titrated to 50 mg/d. At the end of the fourth week, further improvement was observed (IES score of 31). After another 5 weeks of continuous improvement, our patient reported full remission with an IES score of 10. At her last observation in February 2012, our patient was taking agomelatine, 50 mg/d, and had an IES score of 6. No adverse effects related to agomelatine were observed.

To our knowledge, this is the first report that documented a positive effect of agomelatine on PTSD. Evidence suggests that agomelatine may alleviate anxiety symptoms.2 Furthermore, the tolerability profile of agomelatine, including a low propensity to cause sexual dysfunction and weight gain, together with positive effect on sleep may have contributed to our patient’s improvement.3

The neurobiologic hypothesis of agomelatine’s effect on PTSD is that the drug may enhance the levels of dopamine and norepinephrine in the frontal cortex because of blockade of the inhibitory input of 5-HT2C receptors to cortical dopaminergic and adrenergic pathways.4 On the other hand, it also is possible to hypothesize that restoring circadian rhythms (increasing sleep efficiency and decreasing intra-sleep awakening) via MT1 and MT2 agonism may contribute to improved symptomatology because disruption of circadian rhythms has been reported in PTSD patients.5,6 However, because this is a case report, we cannot exclude a placebo or “tincture of time” effect and prospective double-blind, placebo-controlled studies are needed.

DISCLOSURES: The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products. This manuscript was entirely funded by the authors, and no pharmaceutical companies were informed of or were involved in the paper. All authors have contributed to this case report with equal efforts.

    REFERENCES

  1. Farina B, Venturi P, Onofri A, et al. Usefulness of a DSM criteria-based inventory for screening for post-traumatic stress disorder.  Prehosp Disaster Med.  2007;22:454–456.
  2. De Berardis D, Di Iorio G, Acciavatti T, et al. The emerging role of melatonin agonists in the treatment of major depression: focus on agomelatine.  CNS Neurol Disord Drug Targets.  2011;10:119–132.
  3. Stein DJ, Ahokas AA, de Bodinat C. Efficacy of agomelatine in generalized anxiety disorder: a randomized, double-blind, placebo-controlled study.  J Clin Psychopharmacol.  2008;28:561–566.
  4. Fornaro M, Prestia D, Colicchio S, et al. A systematic, updated review on the antidepressant agomelatine focusing on its melatonergic modulation.  Curr Neuropharmacol.  2010;8:287–304.
  5. Di Giannantonio M, Di Iorio G, Guglielmo R, et al. Major depressive disorder, anhedonia and agomelatine: an open-label study.  J Biol Regul Homeost Agents.  2011;25:109–114.
  6. Tempesta D, Mazza M, Iaria G, et al. A specific deficit in spatial memory acquisition in post-traumatic stress disorder and the role of sleep in its consolidation.  Hippocampus.  2012;22:1154–163.

CORRESPONDENCE: Domenico De Berardis, MD, PhD, National Health Service, Department of Mental Health, Psychiatric Service of Diagnosis and Treatment, Hospital G. Mazzini, Piazza Italia 1, 64100 Teramo, Italy, E-MAIL: dodebera@aliceposta.it