Reduced benzodiazepine receptor binding in panic disorders measured by iomazenil SPECT

Kaschka, Wolfgang P.; Feistel, H.; Ebert, Dieter

doi:10.1016/0022-3956(95)00019-2

Cited by 106 publications

(52 citation statements)

References 10 publications

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“…Brain SPECT has shown hypoperfusion in the frontal lobes of patients with panic disorder with yohimbine challenge; however, the same drug did not cause any changes in healthy volunteers [Devous., 1992]. With 123 I-iomazenil, a significant decrease in activity occurred 2 h after injection in the lateral inferior temporal lobes, left medial inferior temporal lobe, and inferior frontal lobes [Kaschka et al, 1995].…”

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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“…18 Evidence supports a decreased benzodiazepinesensitive receptor function in anxious patients, 19,20 but studies investigating benzodiazepine binding in PD patients concentrated on cortical areas and did not examine the receptor density in the brainstem, probably due to issues of resolution. [21][22][23][24] Compared to healthy volunteers, pre-or post-treatment plasma or cerebrospinal fluid GABA concentrations are not significantly altered in PD patients, [25][26][27] although Rímon et al 25 found that low pretreatment levels of cerebrospinal fluid GABA correlated significantly with poor therapeutic outcome.…”

Section: Introductionmentioning

confidence: 99%

Common effects of chronically administered antipanic drugs on brainstem GABAA receptor subunit gene expression

et al. 2001

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Panic disorder is an anxiety disorder that can be treated by long-term administration of tricyclic antidepressants such as imipramine, monoamine oxidase inhibitors such as phenelzine, or the selective serotonin reuptake inhibitor (SSRI) antidepressants. Clinical data also indicate that some benzodiazepines, such as alprazolam, are effective antipanic agents, and that their therapeutic onset is faster than that of antidepressants. Benzodiazepines are well known for their action at GABA A receptors, and preclinical data indicate that imipramine and phenelzine also interfere with the GABAergic system. In addition some clinical data lend support to decreased benzodiazepine-sensitive receptor function in panic disorder patients. Using imipramine, phenelzine and alprazolam, we investigated, in rats, the possibility that the therapeutic efficacy of antipanic agents stems from the remodeling of GABAergic transmission in the pons-medulla region. Of the 12 GABA A receptor subunit (␣1-6, ␤1-3, ␥1-3) steady-state mRNA levels investigated, we observed an increase in the levels of the ␣3-, ␤1-and ␥2-subunit transcripts with all three antipanic agents tested. The effects of imipramine and phenelzine on these subunits occurred after 21 days of treatment, while alprazolam effects were observed after 3 days of administration. Histochemical data suggest that the ␣3␤1␥2 subunits comprise a receptor subtype in the pons-medulla region. Therefore, we conclude that these molecular events parallel the therapeutic profile of the drugs examined. We further propose that these events may correspond to a remodeling of the GABA A receptor population, and may be useful markers for investigation of the antipanic properties of drugs. Molecular Psychiatry (2001) 6, 404-412.

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“…In another study of depressed patients with or without panic disorder (N = 18), radiolabeled iomazenil SPECT scans demonstrated that those patients with panic disorder had a significant decrease (P , 0.05) in the regional activity index in the lateral inferior temporal lobes (right and left), medial inferior temporal lobes (left), and inferior frontal lobes (right and left) after 2 hours (Kaschka et al, 1995). The findings may be due to either regional blood flow differences or BZDR effects, but the former hypothesis is confirmed to some extent by similar findings in the scans acquired after 10 minutes.…”

Section: Single Photon Emission Computed Tomographymentioning

confidence: 95%

Targeting the Modulation of Neural Circuitry for the Treatment of Anxiety Disorders

Farb

Ratner

2014

Pharmacol Rev

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Reduced benzodiazepine receptor binding in panic disorders measured by iomazenil SPECT

Cited by 106 publications

References 10 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

Common effects of chronically administered antipanic drugs on brainstem GABAA receptor subunit gene expression

Targeting the Modulation of Neural Circuitry for the Treatment of Anxiety Disorders

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