A double-blind crossover comparison of clomipramine and desipramine in the treatment of panic disorder

Sasson, Yehuda; Iancu, Iulian; Fux, Mendel; Taub, Migdala; Dannon, Pinhas N.; Zohar, Joseph

doi:10.1016/s0924-977x(98)00024-8

Cited by 34 publications

(14 citation statements)

References 23 publications

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“…Nevertheless, electrical stimulation of human locus coeruleus (LC) which caused a 4 to 9 fold increase in NE plasma metabolites produced only alertness (Libet & Gleason, 1994). Although the latter data makes unlikely the LC contribution to aversiveness, NE may play roles either modulatory or permissive in panic attacks as suggested by several reports of successful treatments of PD with selective or preferential inhibitors of NE reuptake (Bertani et al, 2004;Dannon, Iancu, & Grunhaus, 2002;Kalus et al, 1991;Lydiard, 1987, Lydiard et al, 1993Nardi et al, 2003;Sasson et al, 1999;Seedat et al, 2003;Versiani et al, 2002;). More important, whereas the α 2 -adrenergic antagonist yohimbine is an established panicogen (Bremner, Krystal, Southwick, & Charney, 1996;Charney, Woods, Goodman, & Heninger, 1987;Charney, Woods, Krystal, Nagy, & Heninger, 1992), appropriate doses of the α 2 -adrenergic agonist clonidine promote a rapid but transient improvement of PD patients (Liebowitz, Fyer, McGrath, & Klein, 1981).…”

Section: Challenging the Modelmentioning

confidence: 99%

Towards a translational model of panic attack.

Schenberg

2010

Psychology & Neuroscience

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About 20 years ago, Deakin and Graeff proposed that whereas generalized anxiety disorder is produced by the overactivity of 5-HT excitatory projections from dorsal raphe nucleus to the areas of prefrontal cortex and amygdala which process distal threat, panic attacks are a dysfunction of 5-HT inhibitory projections from dorsal raphe nucleus to the dorsal periaqueductal gray matter, thereby releasing the responses to proximal threat, innate fear or anoxia. Besides, they suggested that the decrease in 5-HT1A neurotransmission in the hippocampus results in learned helplessness and depression. Accordingly, the Deakin Graeff hypothesis provided a unified frame to the widespread use of 5-HT selective reuptake inhibitors in generalized anxiety, panic disorder and depression. Competitor hypotheses implicate panic attacks with the abnormal functioning of locus coeruleus, basolateral amygdala, dorsomedial hypothalamus or an as-yet-unknown suffocation alarm system. Conversely, cognitive psychologists suggest that panic attacks result from the catastrophic (cortical) interpretation of bodily symptoms. In any event, translational models of panic attack are expected to reproduce the main features of clinical panic, namely, the patient's higher sensitivity to both lactate and CO2, the drug specific sensitivity, the lack of stress hormone responses during panic attacks, the higher vulnerability of women and the high comorbidity with agoraphobia, major depression and childhood separation anxiety. Therefore, here we review the main steps in the experimental approach to anxiety disorders which are paving the route towards a translational model of panic attack.

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Section: Challenging the Modelmentioning

confidence: 99%

Towards a translational model of panic attack.

Schenberg

2010

Psychology & Neuroscience

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“…According to this pharmacological profile, each antidepressant differs in its clinical efficacy. For the treatment of anxiety disorders, such as obsessive-compulsive disorder, panic disorder and premenstrual dysphoria, reuptake inhibitors with a serotonergic profile are clearly superior to antidepressants with a noradrenergic profile (Thoren et al 1980;Modigh et al 1992;Eriksson et al 1995;Sasson et al 1999;Eriksson 2000). In contrast, reuptake inhibitors with a noradrenergic profile are effective for the treatment of attention deficit hyperactivity disorder (Biederman and Spencer 1999;Bymaster et al 2002).…”

Section: Introductionmentioning

confidence: 94%

Contrasting Fos expression induced by acute reboxetine and fluoxetine in the rat forebrain: neuroanatomical substrates for the antidepressant effect

et al. 2004

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“…The results of studies examining the efficacy of noradrenergic antidepressants including reboxetine (Dannon et al 2002;Seedat et al 2003;Perna et al 2004;Versiani et al 2002), desipramine (Lydiard 1987) and bupropion (Simon et al 2003) for panic disorder are suggestive of potential efficacy although mixed with, for example, a negative study with bupropion ) and comparative studies of reboxetine and paroxetine ) and desipramine and clomipramine (Sasson et al 1999) demonstrating efficacy of the noradrenergic agent, but less that that of the serotonergic agent.…”

Section: Introductionmentioning

confidence: 95%