Abstract
There is consensus among scientists in considering Panic Attack (PA) as an exaggerated fear response triggered by intense activation of the amygdala and related Fear brain network. Current guidelines for treatment (e.g. National Institute for Clinical Excellence, NICE, 2011), that are based on this view, do not achieve satisfactory results: one-third of all treated patients report persistent PAs and other Panic Disorder (PD) symptoms, and several meta-analyses report the high likelihood of relapse. Here we review findings from Affective Neuroscience and clinical insights from a phenomenological-Gestalt perspective, putting into question the link between PD and activation of the Fear brain network. We propose an alternative hypothesis about PD etiology: PD is mainly connected to the Panic system, that is activated in situations of separation from affective support and overexposure to the environment. In our view, PA can be understood as an acute attack of solitude which is not adequately recognized by the patient due to the intervention of a dissociative component that makes it impossible to integrate all neuro-physiological responses activated by the Panic/Separation brain system within a coherent emotional feeling. This perspective can explain many evidences that otherwise remain isolated elements without a comprehensive frame: i.e., the association with agoraphobia, the onset of PD during adolescence and young adult life, the need to be accompanied, the connection with air hunger and other respiratory anomalies, the efficacy of antidepressants and the lack of activation of the Hypothalamic-Pituitary-Adrenal (HPA) axe. We discuss future steps to test this hypothesis and the consequences for psychotherapeutic treatment.