Neurobiological Hypotheses in Panic Disorder

Česká verze

Authors: P. Šilhán ¹; MUDr. Martin Hýža ¹; D. Kamarádová ²; K. Látalová ²; J. Praško ²
Authors place of work: Oddělení psychiatrické, FN Ostrava ¹; Klinika psychiatrie LF UP a FN Olomouc ²
Published in the journal: Cesk Slov Neurol N 2014; 77/110(3): 314-319
Category: Přehledný referát

Summary

Panic disorder is a mental disorder characterized by recurrent panic attacks accompanied by significant somatic and psychological symptoms. Ethiopathogenesis of panic disorder remains unclear although clinical manifestation and proven algorithms of treatment are known. Due to paroxysmal nature of the disorder and its symptoms, functional imaging techniques provide ambiguous results. Leading neurotransmitter theories are based on the proven efficacy of antidepressants treatment. This includes the role of the neurotransmitters involved in modulation of fear circuit (serotonin, norepinephrine, gamma-aminobutyric acid, glutamate, cortikoliberin etc.). From neuroanatomical point of view, the nucleus of amygdala, with a large number of pathways involved in the panic reaction, plays the key role in triggering panic attacks. In contrast, prolonged anxiety is associated with activation of bed nucleus striae terminalis. The entire process is complex and involves interaction of the brainstem and cortical centres, the role of which consists of affective modulation of the limbic system and its regulation by volitional processes.

Key words:
panic disorder – magnetic resonance imaging – positron emission tomography –serotonin – norepinephrine – amygdala –locus coeruleus – prefrontal lobes

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.

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