OBJECTIVES: Clinical and electrophysiological studies suggest that panic disorder (PD) patients show disturbed response inhibition to sensory stimuli. Thus, habituation of neuronal activation after repeated sine tone stimulation was assessed by functional magnetic resonance imaging (fMRI) in patients with PD. METHODS: Twenty patients with PD and 20 age- and gender-matched healthy controls were assessed by 3T fMRI for auditory habituation. During three stimulation cycles of digitally generated pulsed (ν=5 Hz) 800-Hz sine tones alternating with silent periods, activation of the auditory cortex and other anxiety- or sensory integration-related regions was assessed. Brain activation was further analyzed dependent on functional serotonin transporter (5-HTT) gene variation (5-HTTLPR). RESULTS: PD patients demonstrated an extended brain activity in the first stimulation block, which normalized during the second stimulation cycle. A positive correlation with anxiety measures (HAMA) and an increased activity of distinct anxiety- or sensory integration-related areas (e.g., BA 22, BA 10) were seen during the third block of auditory stimulation. There was a significant interaction of left amygdala activation and the 5-HTTLPR S allele. CONCLUSIONS: Our results support the hypothesis of an aberrant processing of sensory information in PD patients. This phenomenon may underlie an enhanced responsiveness to anxiety-relevant or irrelevant stimuli possibly increasing PD vulnerability.
OBJECTIVES: Clinical and electrophysiological studies suggest that panic disorder (PD) patients show disturbed response inhibition to sensory stimuli. Thus, habituation of neuronal activation after repeated sine tone stimulation was assessed by functional magnetic resonance imaging (fMRI) in patients with PD. METHODS: Twenty patients with PD and 20 age- and gender-matched healthy controls were assessed by 3T fMRI for auditory habituation. During three stimulation cycles of digitally generated pulsed (ν=5 Hz) 800-Hz sine tones alternating with silent periods, activation of the auditory cortex and other anxiety- or sensory integration-related regions was assessed. Brain activation was further analyzed dependent on functional serotonin transporter (5-HTT) gene variation (5-HTTLPR). RESULTS:PDpatients demonstrated an extended brain activity in the first stimulation block, which normalized during the second stimulation cycle. A positive correlation with anxiety measures (HAMA) and an increased activity of distinct anxiety- or sensory integration-related areas (e.g., BA 22, BA 10) were seen during the third block of auditory stimulation. There was a significant interaction of left amygdala activation and the 5-HTTLPR S allele. CONCLUSIONS: Our results support the hypothesis of an aberrant processing of sensory information in PDpatients. This phenomenon may underlie an enhanced responsiveness to anxiety-relevant or irrelevant stimuli possibly increasing PD vulnerability.
Authors: Thomas Dresler; Anne Guhn; Sara V Tupak; Ann-Christine Ehlis; Martin J Herrmann; Andreas J Fallgatter; Jürgen Deckert; Katharina Domschke Journal: J Neural Transm (Vienna) Date: 2012-06-13 Impact factor: 3.575
Authors: K R Engel; K Obst; B Bandelow; P Dechent; O Gruber; I Zerr; K Ulrich; D Wedekind Journal: Eur Arch Psychiatry Clin Neurosci Date: 2015-11-19 Impact factor: 5.270
Authors: Nina C Donner; Philip L Johnson; Stephanie D Fitz; Karen E Kellen; Anantha Shekhar; Christopher A Lowry Journal: Depress Anxiety Date: 2012-04 Impact factor: 6.505
Authors: Peter Zwanzger; M Zavorotnyy; J Diemer; T Ruland; K Domschke; M Christ; N Michael; B Pfleiderer Journal: J Neural Transm (Vienna) Date: 2012-08-25 Impact factor: 3.575