Pituitary volume in patients with panic disorder Sukru Kartalci a, ⁎, Metin Dogan b , Suheyla Unal a , A. Cemal Ozcan c , Serdal Ozdemir a , Murad Atmaca d a Inonu University, Medical School, Department of Psychiatry, Malatya, Turkey b Inonu University, Medical School, Department of Radiology, Malatya, Turkey c Inonu University, Medical School, Department of Neurology, Malatya, Turkey d Fırat University, Medical School, Department of Psychiatry, Elazig, Turkey abstract article info Article history: Received 1 September 2010 Received in revised form 3 November 2010 Accepted 3 November 2010 Available online 12 November 2010 Keywords: Agoraphobia HPA axis Magnetic resonance imaging Panic disorder Pituitary gland volume Panic patients have many functional deficiencies in the hypothalamic–pituitary–adrenal (HPA) axis. Previous studies have shown changed pituitary gland volume in some psychiatric disorders that have functional deficiencies in the HPA axis. However, to date no study has evaluated the pituitary gland volume in patients with panic disorder (PD). We investigated the pituitary gland volume in patients with PD (n = 27) and age- and sex-matched healthy controls (n = 27), using 1.5-T magnetic resonance imaging in this study. Analysis showed that patients with PD had significantly smaller pituitary volume compared to healthy subjects. Patients with agoraphobia especially had a significantly smaller pituitary volume than patients without agoraphobia. There was a significant relationship between the pituitary volume and both the severity of symptoms and the illness duration in the patient group. The results show that patients with PD have reduced pituitary volume, which may reflect the functional abnormalities seen in this disorder. These findings may help us better understand the pathology of PD. © 2010 Elsevier Inc. All rights reserved. 1. Introduction Panic disorder (PD) is an incapacitating and overwhelming condition characterized by the occurrence of unexpected and repeated panic attacks. Such panic attacks include intense, sudden and unexpected surge of extreme fear accompanied by major neurovegetative and psychological changes such as dyspnea, palpitations, tachycardia, sweating, tremor, nausea, depersonalization and fear of losing control which lasts for about 20 min. As a consequence of these attacks, a persistent concern about additional attacks and avoidance of places where an attack would be embarrassing may gradually develop. This extreme avoidance is known as agoraphobia, in which case the patient is afraid of leaving home unaccompanied, becoming incapacitated for most social functions (American Psychiatry Association, 1994). Around 2/3 of patients with PD also demonstrate agoraphobia (Del-Ben and Graeff, 2009). Several brain structures that organize defensive reactions and represent the neural substrate of fear and anxiety have been implicated in the functional neuroanatomy of PD. Some authors have reported that some structural alterations in the periaqueductal gray matter and locus coeruleus, hippocampus and parahippocampal gyrus, anterior cingulate cortex, amygdala, hypothalamic paraven- tricular and lateral nucleus, brain stem structures, and the temporal and right frontal lobes are more frequently observed in panic patients than in controls (Al-Haddad et al., 2001; Engel et al., 2009; Gorman et al., 2000; Massana et al., 2003; Sobanski et al., 2010; Uchida et al., 2008). The amygdala and paraventricular nucleus especially play an important role in the pathophysiology of PD. According to Gorman et al. (2000), the hypothalamic paraventricular nucleus that activates the hypothalamic–pituitary–adrenal (HPA) axis is controlled by the amygdala, indicating that the HPA axis is a component of the panic pathway that starts from the amygdala. The abnormalities of HPA that are specifically implicated in the pathophysiology of depression (Nemeroff et al., 1992; Sheline, 2000; Swaab et al., 2005) have also been reported in other psychiatric disorders (Bailly et al., 1994; Carroll et al., 1981; Krishnan et al., 1985; Lammers et al., 1995; Volsan and Berzewski, 1985; Walker et al., 2008), including anxiety disorders (Risbrough and Stein, 2006; Young et al., 2003). There is some evidence for abnormalities in the HPA system regulation in PD. For example, increased basal cortisol production, abnormal dexamethasone suppression test(DST) and blunted adrenocorticotropic hormone (ACTH) and cortisol responses to corticotropin-releasing hormone (CRH) infusion are reported in patients with PD, along with differences in the feedback sensitivity of the axis (Abelson et al., 2007). Furthermore, some studies have demonstrated that patients with PD also have numerous Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 203–207 Abbreviations: ACTH, adreno-corticotropic hormone; ANCOVA, analysis of covari- ance; ANOVA, analysis of variance; CRH, corticotropin-releasing hormone; DST, dexamethasone suppression test; HPA, hypothalamic-pituitary-adrenal; HPT, hypo- thalamus-pituitary-thyroid; ICV, intracranial volume; OCD, obsessive-compulsive disorder; PAS, panic and agoraphobia scale; PD, panic disorder; RPV, relative pituitary volume; SCID- IV, structured clinical interview for the DSM-IV; STAI, state-trait anxiety inventory; TRH, thyrotropin releasing hormone; TSH, thyrotropin stimulating hormone. ⁎ Corresponding author. Inonu University, Medical School, Department of Psychiatry, 44280 Malatya, Turkey. Tel.: + 90 422 3410660/5410; fax: + 90 422 3410787. E-mail address: skartalci@inonu.edu.tr (S. Kartalci). 0278-5846/$ – see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.pnpbp.2010.11.005 Contents lists available at ScienceDirect Progress in Neuro-Psychopharmacology & Biological Psychiatry journal homepage: www.elsevier.com/locate/pnp