کاهش اتصال ناقل سروتونین مغزی در بیماران مبتلا به اختلال پانیک
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|31611||2004||9 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research: Neuroimaging, Volume 132, Issue 2, 15 December 2004, Pages 173–1819
There is strong evidence for the importance of the serotonin (5-HT) system in the neurobiology of panic disorder (PD); however, the exact role of this system remains unclear. The 5-HT transporter (5-HTT) is a key element in 5-HT neurotransmission. The current study aimed to investigate the binding of 5-HTT in the brain of patients with PD. We used single-photon emission computed tomography with a radioligand that specifically labels the 5-HTT, [123I]nor-β-CIT. Subjects comprised eight patients with current PD, eight patients with PD in remission, and eight healthy control subjects. The patients with current PD showed a significant decrease in 5-HTT binding in the midbrain, in the temporal lobes and in the thalamus in comparison to the controls. The binding of 5-HTT in patients with PD in remission was similar to findings in the control group in the midbrain and in the temporal lobes, but lower in the thalamus. Regional 5-HTT binding significantly and negatively correlated with the severity of panic symptoms. These findings point to a dysregulation of the 5-HT system in PD patients. Altered function of 5-HTT appears to be related to the clinical status of patients. Clinical improvement in the patients in remission is associated with normalization of 5-HTT binding.
Panic disorder (PD) is a prevalent and potentially disabling condition characterized by recurrent panic attacks, anticipatory fear and avoidance. There is strong evidence for the involvement of the brain serotonin [5-hydroxytryptamine (5-HT)] system in the pathophysiology of PD. The impact of this system in PD is substantiated by the established clinical efficacy of the selective 5-HT reuptake inhibitors (SSRI) in the treatment of PD (Kent et al., 1998). The mechanism of action of the SSRIs supports the involvement of the 5-HT transporter (5-HTT) in PD, but the exact role of the 5-HTT is unclear. Genetic studies have failed to demonstrate an association between a functional polymorphism in the 5-HTT gene promoter region and PD (Deckert et al., 1997, Hamilton et al., 1999 and Ishiguro et al., 1997). There is some evidence for decreased 5-HTT binding in platelets of patients with PD (Faludi et al., 1994 and Marazziti et al., 1999), an abnormality that is normalized after successful treatment with antidepressants (Marazziti et al., 1999). However, other studies have not found differences in platelet 5-HTT binding between patients with PD and normal controls (Maguire et al., 1995 and Stein et al., 1995). Moreover, a study of Malison et al. (1998), which demonstrated a lack of correlation between the binding of 5-HTT in platelets and in the brain in patients with depression, raises doubts on the validity of the platelet binding model. To our knowledge, so far there have been no brain-imaging studies of the function of 5-HTT in PD. Therefore, we investigated brain 5-HTT binding potential in patients with PD in comparison to healthy subjects. The aims of this study were to detect whether there are quantitative alterations in 5-HT re-uptake sites in brain regions that are involved in the neurobiology of PD, and whether the 5-HTT binding characteristics are related to the symptomatic status of the patients.