Effect of the selective serotonin reuptake inhibitor fluvoxamine on CCK-4 induced panic attacks

vanMegen, Hjgm; Westenberg, H. G. M.; DenBoer, JA; Slaap, B.R.; Scheepmakers, A

doi:10.1007/s002130050201

Cited by 64 publications

(35 citation statements)

References 35 publications

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“…The CCK-4-induced panic rate dropped significantly from 76% to 29% within eight weeks of treatment in the fluvoxamine group, whereas there was only a nonsignificant decrease from 67% to 56% in the placebo group. In contrast to treatment with imipramine or fluvoxamine (Bradwejn and Koszycki 1994b;van Megen et al 1997), we found no statistically significant effect of vigabatrin on the physiological response to CCK-4 such as heart rate.…”

Section: Discussioncontrasting

confidence: 93%

“…Although it has to be considered that our study was not placebo-controlled and a certain placebo effect cannot be ruled out, the pronounced anxiolytic effects of vigabatrin are unlikely to be merely caused by a placebo effect. Previous studies investigating the effects of fluvoxamine on CCK-4-induced panic in a placebo-controlled study revealed a marked effect of fluvoxamine on CCK-4-induced panic in view of a slight and non-significant effect in the placebo group (van Megen et al 1997). The CCK-4-induced panic rate dropped significantly from 76% to 29% within eight weeks of treatment in the fluvoxamine group, whereas there was only a nonsignificant decrease from 67% to 56% in the placebo group.…”

Section: Discussionmentioning

confidence: 77%

“…Besides the GABAergic system, also the serotonergic system is involved in the neurobiology of CCK-4-induced anxiety (Harro et al 1993). Treatment with serotonin reuptake inhibitors (SSRIs) commonly used for antipanic treatment reduces or even blocks CCK-4-induced panic in patients with panic disorder (van Megen et al 1997;Bradwejn and Koszycki 1994b;Shlik et al 1997).…”

Section: Discussionmentioning

confidence: 99%

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Vigabatrin Decreases Cholecystokinin-Tetrapeptide (CCK-4) Induced Panic in Healthy Volunteers

Zwanzger

Baghai

Schuele

et al. 2001

Neuropsychopharmacology

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Vigabatrin increases gamma aminobutyric acid (GABA) levels by irreversible inhibition of the GABA-catabolizing enzyme GABA-transaminase (GABA-T). Preclinical studies suggest anxiolytic effects in vigabatrin treated rats. Anxiolytic effects in patients with panic disorder (PD) could therefore be expected. To evaluate putative anxiolytic properties of vigabatrin in humans, CCK-4-induced panic symptoms were studied in healthy volunteers before and after vigabatrin treatment. After placebo-controlled administration of 50 g CCK-4, ten healthy volunteers received vigabatrin for seven days with a daily dosage of 2 g. The treatment period was followed by a second CCK-4 challenge. Panic and anxiety were assessed using the Acute Panic Inventory (API) score and a DSM-IV derived panicsymptom-scale (PSS). ACTH and cortisol plasma levels were determined during the CCK-4 challenge. All subjects reported a marked reduction of CCK-4-induced panic symptoms and anxiety after seven days of vigabatrin treatment both in the API-and PSS-scores. MoreoverThe new antiepileptic drug vigabatrin is a selective irreversible inhibitor of GABA-transaminase (GABA-T), the main degradative enzyme of GABA (Harden 1994). Vigabatrin increases CSF GABA levels by 2 to 3-fold when administered in anticonvulsant doses (Ben-Menachem 1989). Preclinical studies suggest that vigabatrin has anxiolytic properties in addition to its anticonvulsant effects. Sayin et al. (1992) compared the anxiolytic effects of diazepam and vigabatrin in rats and found a significant decrease of anxiety with both substances using the elevated plus maze test. Sherif and colleagues investigated the effects of GABA-transaminase inhibition on exploratory behaviour in socially isolated rats using both the elevated plus maze and the open field NO . 5 test (Sherif et al. 1994;Sherif and Oreland 1995). Despite these promising results in animal models it is still unclear whether vigabatrin exerts anxiolytic properties also in humans.CCK-4 has potent anxiogenic properties both in patients with panic disorder and in healthy volunteers (Bradwejn et al. 1990;Bradwejn et al. 1991a;Bradwejn et al. 1991b). Recent data suggest that CCK-4-induced panic is attenuated by antipanic treatment. A decrease of the anxiogenic effects of CCK-4 has been shown after treatment with benzodiazepines in healthy volunteers (de Montigny 1989). Moreover, antidepressants that are commonly used as antipanic treatment, e.g. imipramine (Bradwejn and Koszycki 1994a), fluvoxamine (van Megen etal. 1997) and citalopram (Shlik et al. 1997) reduced CCK-4-induced panic in patients with panic disorder.CCK-4-induced panic appears to be a suitable model to assess anxiolytic properties of psychopharmacological drugs in humans. To evaluate the putative anxiolytic properties of the selective GABA transaminase inhibitor vigabatrin, we therefore studied the effects of treatment with vigabatrin for seven days on CCK-4-induced panic symptoms in healthy male volunteers. METHODSTen male healthy volunteers (mean age ϭ 30.7 years, S...

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Section: Discussioncontrasting

confidence: 93%

Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

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Vigabatrin Decreases Cholecystokinin-Tetrapeptide (CCK-4) Induced Panic in Healthy Volunteers

Zwanzger

Baghai

Schuele

et al. 2001

Neuropsychopharmacology

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“…Studies so far have shown that treatment with SSRIs significantly decreased the sensitivity of patients with PD to the panicogenic effects of CCK-4, flumazenil, and CO 2 (Bell et al, 2002;Bertani et al, 1997;Perna et al, 1997;Shlik et al, 1997;van Megen et al, 1997). These results support the view that 5-HT-ergic enhancement by SSRIs leads to antipanic effects.…”

Section: Effects Of Treatment On Panic Challengementioning

confidence: 60%

Serotonin Function in Panic Disorder: Important, But Why?

Maron

Shlik

2005

Neuropsychopharmacol

106

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The essential role of serotonin (5-hydroxytryptamine (5-HT)) system in the neurobiology and pharmacotherapy of panic disorder (PD) continues to be a topic of intensive interdisciplinary research. Interest in the involvement of 5-HT in PD has been fuelled by clinical studies demonstrating that medications increasing the synaptic availability of 5-HT, such as selective 5-HT re-uptake inhibitors, are effective in the treatment of PD. Rival theories of 5-HT deficiency vs excess have attempted to explain the impact of 5-HT function in PD. In the past decade, knowledge of the role of 5-HT in the neurobiology of PD has expanded dramatically due to much new research including experimental, treatment, brain-imaging, and genetic studies. The current review attempts to summarize the new data and their implications. The challenge and treatment studies generally confirm the specific inhibitory influence of 5-HT on panicogenesis. The brainimaging studies in PD patients demonstrate functional and clinically relevant alterations in various elements of 5-HT system affecting the neurocircuitry of panic. The findings of genetic association studies suggest that certain 5-HT-related genes may contribute to the susceptibility to PD; however, these data are rather limited and inconsistent. It appears that, even if not the primary etiological factor in PD, the 5-HT function conveys important vulnerability, as well as adaptive factors. A better understanding of these processes may be critical in achieving progress in the treatment of patients suffering from PD.

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“…Criterium seven, i.e., drugs which are clinically ineffective in panic disorder are unable to block CCK-4 induced attacks, has been studied only in healthy volunteers (de Montigny 1989;. Like sodium lactate-and CO 2 -induced panic, CCK-4-induced attacks are blocked by antipanic treatment with antidepressants van Megen et al 1997;Shlik et al 1997) or benzodiazepines (de Montigny 1989. Although CCK antagonists have so far failed to be effective in the treatment of panic disorder (Kramer et al 1995) or benzodiazepine withdrawal induced anxiety (Abelson et al 1995), CCK-4 induced attacks are a promising strategy to elucidate the neurobiological correlates of panic disorder.…”

Section: Discussionmentioning

confidence: 99%

Increased ACTH Concentrations Associated with Cholecystokinin Tetrapeptide-Induced Panic Attacks in Patients with Panic Disorder

Ströhle

Holsboer

Rupprecht

2000

Neuropsychopharmacology

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Preclinical findings on the role of corticotropin releasing hormone (CRH) in stress and anxiety, on the interaction of CRH and cholecystokinin (CCK) in modulating anxiety, as well as the blunted corticotropin (ACTH) response to CRH in panic disorder suggest that CRH may play a role in panic disorder. To further characterize the role of the hypothalamic-pituitary-adrenocortical (HPA) system in panic disorder, we compared patients with and without CCK tetrapeptide (CCK-4) induced panic attacks. Twenty-four patients with panic disorder were given injections of CCK-4 (25 g). Panic attacks, psychopathological changes, as well as ACTH and cortisol secretion were recorded. Fifteen of the 24 patients experienced a panic attack after CCK-4. ACTH secretion was significantly higher in the patients with CCK-4-induced panic attacks than in those without such attacks. The patients without CCK-4-induced attacks had a brief but less pronounced increase in ACTH concentrations. Cortisol concentrations were not significantly increased after CCK-4 administration. The increased ACTH concentrations suggest that the activation of the HPA system in CCK-Cholecystokinin tetrapeptide (CCK-4) has been reported to have an enhanced panicogenic effect in panic disorder . Like sodium lactateand CO 2 -induced panic, CCK-4-induced attacks are accompanied by hyperventilation and resemble the pattern of panic symptoms induced by CO 2 administration . In contrast to the "respiratory" panicogens sodium lactate and CO 2 (Coplan and Klein 1996), CCK has been further reported to activate the hypothalamic-pituitary-adrenocortical (HPA) system (de Montigny 1989;Koszycki et al. 1996;Kellner et al. 1997). It has been suggested that this effect is primarily pharmacological and unrelated to the experimentally-induced panic (Abelson et al. 1994). However, in healthy control subjects, enhanced corticotropin (ACTH) and cortisol secretion has been linked recently to panic-like symptoms (Koszycki et al. 1998).To further characterize the role of the HPA system in experimentally-induced panic attacks in patients with panic disorder we compared ACTH and cortisol concentrations in patients with and without CCK-4-induced panic attacks. METHODSTwenty-four patients (nine women and fifteen men; mean age ϭ 38.1 years, SD ϭ 10.8) with a diagnosis of panic disorder but without a comorbid axis I disorder, as assessed with the Structured Clinical Interview for DSM-IV (Wittchen et al. 1997) were studied. These subjects had been medication-free for at least 10 days and had undergone thorough medical examination to rule out other illnesses, drug intake, and lifestyles that could interfere with the study. The protocol was approved by the local ethics committee for human experiments. After complete description of the study to the subjects, written informed consent was obtained.All subjects were studied from 9:00 a.m. to 1:00 p.m. in a supine position in a soundproof room with a single bed (Kellner et al. 1995(Kellner et al. , 1997Ströhle et al. 1998bStröhle et al. , 1999. Each su...

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Effect of the selective serotonin reuptake inhibitor fluvoxamine on CCK-4 induced panic attacks

Cited by 64 publications

References 35 publications

Vigabatrin Decreases Cholecystokinin-Tetrapeptide (CCK-4) Induced Panic in Healthy Volunteers

Vigabatrin Decreases Cholecystokinin-Tetrapeptide (CCK-4) Induced Panic in Healthy Volunteers

Serotonin Function in Panic Disorder: Important, But Why?

Increased ACTH Concentrations Associated with Cholecystokinin Tetrapeptide-Induced Panic Attacks in Patients with Panic Disorder

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