Global cerebral blood flow after CO2 inhalation in normal subjects and patients with panic disorder determined with []water and PET

Ponto, Laura L. Boles; Kathol, Roger G.; Kettelkamp, Richard; Watkins, G. Leonard; Richmond, John C.; Clark, Jo; Hichwa, Richard D.

doi:10.1016/s0887-6185(02)00094-4

Cited by 21 publications

(4 citation statements)

References 18 publications

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“…Panic patients exhibited a decrease in global CBF (gCBF) and stable pCO 2 -adjusted gCBF values in comparison with air and CO 2 inhalations, whereas normals exhibited stable gCBF and increasing pCO 2 -adjusted gCBF values [Ponto et al, 2002]. Recent SPECT and PET studies found abnormalities in temporal cortical and hippocampal areas of panic disorder patients [Bisaga et al, 1998;Bremner et al, 2000;Meyer et al, 2000].…”

Section: Discussionmentioning

confidence: 99%

Frontal Brain Hypoactivity as a Biological Substrate of Anxiety in Patients with Panic Disorders

Akiyoshi

Hieda²,

Aoki³

et al. 2003

Neuropsychobiology

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Frontal brain asymmetry is associated with differences in the basic dimensions of emotion. It seems to reflect the activation of specialized systems for avoidance-withdrawal behavior. Since patients with panic disorder are characterized by having both negative emotions and avoidance-withdrawal behavior, we expected them to show greater asymmetry in the frontal hemisphere change activation. Near-infrared reflection spectroscopy was recorded from the left and right frontal regions of 23 patients with panic disorder without depression and from 31 healthy control participants in the following conditions: confrontation at rest with neutral (mushroom), anxiety-relevant (spider and snake) or anxiety-irrelevant but emotionally relevant stimuli (erotic picture). Emotional states and traits were assessed by the State-Trait Anxiety Inventory. The left frontal oxyhemoglobin in patients was significantly lower than in control subjects when confronted with anxiety-relevant or anxiety-irrelevant but emotionally relevant stimuli. There was no frontal brain asymmetry when patients or control subjects observed any stimuli. These data suggest that patients with panic disorder are characterized by having a greater decrease in the activation of a left frontal avoidance-withdrawal system in situations with a negative valence. The findings are interpreted as biological evidence for a disturbed cortical processing in patients with panic disorder.

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Section: Discussionmentioning

confidence: 99%

Frontal Brain Hypoactivity as a Biological Substrate of Anxiety in Patients with Panic Disorders

Akiyoshi

Hieda²,

Aoki³

et al. 2003

Neuropsychobiology

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“…Both pharmacological and psychological methods have been used to examine anxiety in humans. These include pharmacological methods such as cholecystokinin tetrapeptide (CCK-4), lactate, carbon dioxide and pentagastrin induced anxiety (Benkelfat et al, 1995;Bellodi et al, 1998;Ponto et al, 2002;Bradwejn et al, 1995;Javanmard et al, 1999;Boshuisen et al, 2002;Zedkova et al, 2003;Zwanzger et al, 2003aZwanzger et al, , 2003b, and psychological (experimental) methods such as extemporaneous public speaking, aversive conditioning, fear-potentiated startle response, Stroop colour word task performance and anticipation of electric shock (Baas et al, 2002;Chua et al, 1999;Graeff, 2002Graeff, , 2003Grillon and Ameli, 2001;Grillon et al, 1991Grillon et al, , 1993aPalma et al, 1994;Reiman et al, 1989;Riba et al, 2001;Silva et al, 2001;Simpson et al, 2001;Tillfors et al, 2002). Recently, it has been shown that some of these models of experimental anxiety, particularly the fear-potentiated startle response are also sensitive to benzodiazepine anxiolytic agents (Zuardi et al, 1993;Patrick et al, 1996;Hellewell et al, 1999;Leite et al, 1999;Bitsios et al, 1999;Riba et al, 2001;Graeff, 2003).…”

Section: Introductionmentioning

confidence: 99%

The acute effects of L‐theanine in comparison with alprazolam on anticipatory anxiety in humans

Gray

Oliver³

et al. 2004

Human Psychopharmacology

126

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L-Theanine (delta-glutamylethylamide) is one of the predominant amino acids ordinarily found in green tea, and historically has been used as a relaxing agent. The current study examined the acute effects of L-theanine in comparison with a standard benzodiazepine anxiolytic, alprazolam and placebo on behavioural measures of anxiety in healthy human subjects using the model of anticipatory anxiety (AA). Sixteen healthy volunteers received alprazolam (1 mg), L-theanine (200 mg) or placebo in a double-blind placebo-controlled repeated measures design. The acute effects of alprazolam and L-theanine were assessed under a relaxed and experimentally induced anxiety condition. Subjective self-reports of anxiety including BAI, VAMS, STAI state anxiety, were obtained during both task conditions at pre- and post-drug administrations. The results showed some evidence for relaxing effects of L-theanine during the baseline condition on the tranquil-troubled subscale of the VAMS. Alprazolam did not exert any anxiolytic effects in comparison with the placebo on any of the measures during the relaxed state. Neither L-theanine nor alprazalam had any significant anxiolytic effects during the experimentally induced anxiety state. The findings suggest that while L-theanine may have some relaxing effects under resting conditions, neither L-theanine not alprazolam demonstrate any acute anxiolytic effects under conditions of increased anxiety in the AA model.

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“…Healthy nonclinical samples have also played an important role in such research. They are used for comparative purposes when studying clinical populations to elucidate the nature and phenomenology of panic, including clarifying subtypes of panic attacks (Forsyth, Eifert, & Canna, 2000;Schmidt, Forsyth, Santiago, & Trakowski, 2002), biological and psychological vulnerabilities that may affect panic (Forsyth, Palav, & Duff, 1999;Gorman, Kent, Sullivan, & Coplan, 2004;Karekla, Forsyth, & Kelly, 2004;McNally & Eke, 1996;Ponto et al, 2002;, the effects of induced anxiety on cognitive processes (e.g., Hopko et al, 2003), and to study the role of fear conditioning in the etiology of anxiety disorders (Bouton, Mineka, & Barlow, 2001;Forsyth, Eifert, & Thompson, 1996;, to name a few.…”

mentioning

confidence: 99%

Repeated exposure to 20% CO2 challenge and risk for developing panic attacks: A controlled 6- and 12-month follow-up in a nonclinical sample

Prenoveau

Forsyth

Kelly

et al. 2006

Journal of Anxiety Disorders

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Global cerebral blood flow after CO2 inhalation in normal subjects and patients with panic disorder determined with []water and PET

Cited by 21 publications

References 18 publications

Frontal Brain Hypoactivity as a Biological Substrate of Anxiety in Patients with Panic Disorders

Frontal Brain Hypoactivity as a Biological Substrate of Anxiety in Patients with Panic Disorders

The acute effects of L‐theanine in comparison with alprazolam on anticipatory anxiety in humans

Repeated exposure to 20% CO2 challenge and risk for developing panic attacks: A controlled 6- and 12-month follow-up in a nonclinical sample

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