Changes in Cerebral Cortex and Limbic Brain Functions after Short-Term Paroxetine Treatment in Panic Disorder: An [18F]FDG-PET Pilot Study

Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Psychiatry investigation (Impact Factor: 1.28). 09/2010; 7(3):215-9. DOI: 10.4306/pi.2010.7.3.215
Source: PubMed


Panic disorder (PD) is a common and often chronic psychiatric illness, and serotonin-specific reuptake inhibitors (SSRIs) are the drugs of choice for the treatment of PD. Previous studies suggested the cerebral cortex and limbic brain structures played a major role in the development of PD, but the therapeutic effect of SSRIs on specific brain structures remains unclear in PD. We examined the changes in PD patients' glucose metabolism using the [(18)F] Fluorodeoxy-glucose-positron emission tomography (FDG-PET) before and after 12 weeks of paroxetine treatment.
We assessed the brain glucose metabolism of 5 PD patients, using the [(18)F]FDG-PET, and treated them with paroxetine (12.5-37.5 mg/day) for 12 weeks. Then, we compared before and after treatment PET images of the patients, using voxel-based statistical analysis and a post hoc regions of interest analysis. Furthermore, we measured the patients' clinical variables, including information from the Panic Disorder Severity Scale (PDSS), Clinical Global Impression for Severity (CGI-S), and Hamilton Anxiety Rating Scale (HAMA).
After 12 weeks of paroxetine treatment, the patients showed significant clinical improvement in terms of PDSS, CGI-S and HAMA scores (12.8±1.8 vs. 3.8±2.3, 4.6±0.5 vs. 2.0±1.4, and 15.2±4.0 vs. 5.0±1.2, respectively; all p values<0.05). After treatment, patients' glucose metabolism increased significantly in global brain areas: the right precentral gyrus, right middle frontal gyrus, right amygdala, right caudate body, right putamen, left middle frontal gyrus, left precentral gyrus, left insula, left parahippocampal gyrus, and left inferior frontal gyrus (All areas were significant at uncorrected p<0.001 and cluster level corrected p<0.05).
In these PD patients, cerebral cortex and limbic brain functions changed after short-term treatment with paroxetine. The therapeutic action of paroxetine may be related to altered glucose metabolism at both the cerebral cortex and limbic brain areas.

1 Follower
22 Reads
  • Source
    • "And third, patients who were on medications differed from those who were not in some olfactory measures, specifically, in the olfactory reactivity and the odor awareness. Since medications may have an effect on the neuroanatomical circuits involved in the olfactory function (Outhred et al., 2013; Sim et al., 2010), the influence of drug intake in these outcomes cannot be ruled out. However, it should be noted that medicated patients showed a greater clinical severity that at the same time was positively correlated with olfactory questionnaires Therefore, it is plausible that the clinical severity would also explain the olfactory results. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The olfactory function in panic disorder (PD) has been scarcely approached in the literature. The purpose of this paper is to study this question by focusing on the olfactory sensitivity (i.e. detection threshold), the reactivity to odors, and the odor awareness in patients suffering from PD. 41 patients with PD and 41 healthy controls performed Sniffin׳ Sticks Test (threshold subtest) and completed the Affective Impact of Odors scale (AIO), the Relational Scale of Olfaction (EROL) and the Odor Awareness Scale (OAS). Clinical symptoms rating scales were concurrently obtained. PD patients showed lower olfactory detection thresholds (i.e. higher sensitivity) along with an enhanced reactivity to odors as well as a greater olfactory awareness compared to the healthy controls. The severity of PD was significantly associated with the olfactory questionnaires ratings, but not with the detection ability. Olfactory measures were intercorrelated in most cases. i) The results of the olfactory sensitivity are limited to one odorant (phenyl ethyl alcohol) and thus may not be generalizable to other odorants. ii) As comorbid Axis II disorders were not screened, it is not possible to exclude the influence of personality traits in our results. iii) The involvement of the medications in some olfactory outcomes cannot be ruled out. The current findings highlight the importance of the olfactory function in PD as patients appeared to be highly sensitive, reactive and aware of odors. These results are discussed in the light of the common neural substrates involved in the olfactory processing and in the pathophysiology of PD, and also related to the clinical features of this disorder. Copyright © 2015. Published by Elsevier B.V.
    Journal of Affective Disorders 01/2015; 175C:292-298. DOI:10.1016/j.jad.2015.01.049 · 3.38 Impact Factor
  • Source
    • "When untreated patients and treated patients were compared with healthy comparison subjects, patients treated with antidepressants showed no difference in amygdalar serotonin binding potential, while untreated patients showed significantly lower serotonin binding potential [100]. Treatment with paroxetine for 12 weeks in psychotropic medication-naive PD patients altered amygdalar glucose metabolism [101]. In the report of Prasko and colleagues, treatment with antidepressants did not change the amygdalar glucose metabolism [102]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Although the neurobiological mechanisms underlying panic disorder (PD) are not yet clearly understood, increasing amount of evidence from animal and human studies suggests that the amygdala, which plays a pivotal role in neural network of fear and anxiety, has an important role in the pathogenesis of PD. This article aims to (1) review the findings of structural, chemical, and functional neuroimaging studies on PD, (2) relate the amygdala to panic attacks and PD development, (3) discuss the possible causes of amygdalar abnormalities in PD, (4) and suggest directions for future research.
    Biology of Mood and Anxiety Disorders 11/2012; 2(1):20. DOI:10.1186/2045-5380-2-20
  • [Show abstract] [Hide abstract]
    ABSTRACT: In 2000, Gorman et al. published a widely acknowledged revised version of their 1989 neuroanatomical hypothesis of panic disorder (PD). Herein, a 'fear network' was suggested to mediate fear- and anxiety-related responses: panic attacks result from a dysfunctional coordination of 'upstream' (cortical) and 'downstream' (brainstem) sensory information leading to heightened amygdala activity with subsequent behavioral, autonomic and neuroendocrine activation. Given the emergence of novel imaging methods such as fMRI and the publication of numerous neuroimaging studies regarding PD since 2000, a comprehensive literature search was performed regarding structural (CT, MRI), metabolic (PET, SPECT, MRS) and functional (fMRI, NIRS, EEG) studies on PD, which will be reviewed and critically discussed in relation to the neuroanatomical hypothesis of PD. Recent findings support structural and functional alterations in limbic and cortical structures in PD. Novel insights regarding structural volume increase or reduction, hyper- or hypoactivity, laterality and task-specificity of neural activation patterns emerged. The assumption of a generally hyperactive amygdala in PD seems to apply more to state than trait characteristics of PD, and involvement of further areas in the fear circuit, such as anterior cingulate and insula, is suggested. Furthermore, genetic risk variants have been proposed to partly drive fear network activity. Thus, the present state of knowledge generally supports limbic and cortical prefrontal involvement as originally proposed in the neuroanatomical hypothesis. Some modifications might be suggested regarding a potential extension of the fear circuit, genetic factors shaping neural network activity and neuroanatomically informed clinical subtypes of PD potentially guiding future treatment decisions.
    Journal of Neural Transmission 06/2012; 120(1). DOI:10.1007/s00702-012-0811-1 · 2.40 Impact Factor
Show more

Similar Publications

Preview (3 Sources)

22 Reads
Available from