Alprazolam in Panic Disorder and Agoraphobia: Results From a Multicenter Trial

Ballenger, James C.; Burrows, Graham D.; DuPont, Robert L.; Lesser, Ira M.; Noyes, Russell; Pecknold, John C.; Rifkin, Arthur; Swinson, Richard P.

doi:10.1001/archpsyc.1988.01800290027004

Cited by 527 publications

(145 citation statements)

References 40 publications

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“…Á Alprazolam was superior to placebo and as effective as comparator drugs in a number of studies (Andersch et al 1991;Ballenger et al 1988;CNCPS 1992;Lydiard et al 1992;Noyes et al 1996;Uhlenhuth et al 1989). In a relapse prevention study (8 weeks acute study, followed by up to 35 weeks relapse prevention), it was superior to placebo and as effective as imipramine (Curtis et al 1993).…”

Section: Tricyclic Antidepressants (Tcas) Treatment Withmentioning

confidence: 99%

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Pharmacological Treatment of Anxiety, Obsessive-Compulsive and Post-Traumatic Stress Disorders – First Revision

Bandelow

Zohar

Hollander

et al. 2008

The World Journal of Biological Psychiatry

711

410

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In this report, which is an update of a guideline published in 2002 (Bandelow et al. 2002, recommendations for the pharmacological treatment of anxiety disorder, obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD) are presented. Since the publication of the first version of this guideline, a substantial number of new randomized controlled studies of anxiolytics have been published. In particular, more relapse prevention studies are now available that show sustained efficacy of anxiolytic drugs. The recommendations, developed by the World Federation of Societies of Biological Psychiatry (WFSBP) Task Force for the Pharmacological Treatment of Anxiety, Obsessive-Compulsive and Post-Traumatic Stress Disorders, a consensus panel of 30 international experts, are now based on 510 published randomized, placebo-or comparator-controlled clinical studies (RCTs) and 130 open studies and case reports. First-line treatments for these disorders are selective serotonin reuptake inhibitors (SSRIs), serotonin-noradrenaline reuptake inhibitors (SNRIs) and the calcium channel modulator pregabalin. Tricyclic antidepressants (TCAs) are equally effective for some disorders, but many are less well tolerated than the SSRIs/ SNRIs. In treatment-resistant cases, benzodiazepines may be used when the patient does not have a history of substance abuse disorders. Potential treatment options for patients unresponsive to standard treatments are described in this overview. Although these guidelines focus on medications, non-pharmacological were also considered. Cognitive behavioural therapy (CBT) and other variants of behaviour therapy have been sufficiently investigated in controlled studies in patients with anxiety disorders, OCD, and PTSD to support them being recommended either alone or in combination with the above medicines.

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Section: Tricyclic Antidepressants (Tcas) Treatment Withmentioning

confidence: 99%

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Pharmacological Treatment of Anxiety, Obsessive-Compulsive and Post-Traumatic Stress Disorders – First Revision

Bandelow

Zohar

Hollander

et al. 2008

The World Journal of Biological Psychiatry

711

410

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“…Alterations have also been found in concentrations of neuroactive steroids, which are known to act as allosteric modulators at the GABA A receptor (Strohle et al, 2002). Finally, the well-known rapid and strong anxiolytic effects of benzodiazepines are mediated by the benzodiazepine-binding site at the GABA Areceptor (Ballenger et al, 1988;Zwanzger and Rupprecht, 2005;Domschke and Zwanzger, 2008).…”

Section: Introductionmentioning

confidence: 99%

Acute Shift in Glutamate Concentrations Following Experimentally Induced Panic with Cholecystokinin Tetrapeptide—A 3T-MRS Study in Healthy Subjects

Zwanzger

Zavorotnyy

Gencheva

et al. 2013

Neuropsychopharmacol

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According to preclinical studies, glutamate has been implicated in the pathogenesis of anxiety. In order to elucidate the role of glutamate in anxiety and panic in humans, brain glutamate þ glutamine (Glx) levels were measured during cholecystokinin-tetrapeptide (CCK-4)-induced panic using magnetic resonance spectroscopy (MRS). Eighteen healthy subjects underwent a CCK-4 challenge. MR spectra were obtained from the anterior cingulate cortex (ACC) using a single voxel point-resolved spectroscopy method and analyzed using LCModel. A combined fitting of Glx was performed. Panic was assessed using the Acute Panic Inventory (API) and Panic Symptom Scale (PSS) scores. Moreover, hypothalamic-pituitary-adrenal axis stimulation was monitored throughout the challenge. There was a significant panic response following CCK-4 as revealed by a marked increase in both the panic scores (API: F(1,17) ¼ 149.41; po0.0001; PSS: F(1,17) ¼ 88.03; po0.0001) and heart rate (HR: F(1,17) ¼ 72.79; po0.0001). MRS measures showed a significant increase of brain Glx/creatine (Glx/Cr) levels peaking at 2-10 min after challenge (F(1,17) ¼ 15.94; p ¼ 0.001). There was also a significant increase in CCK-4-related cortisol release (F(6,11) ¼ 8.68; p ¼ 0.002). Finally, significant positive correlations were found between baseline Glx/Cr and both API max (r ¼ 0.598; p ¼ 0.009) and maximum heart rate (HR max ) during challenge (r ¼ 0.519; p ¼ 0.027). Our results suggest that CCK-4-induced panic is accompanied by a significant glutamate increase in the bilateral ACC. The results add to the hypothesis of a disturbance of the inhibitory-excitatory equilibrium and suggest that apart from static alterations rapid and dynamic neurochemical changes might also be relevant for the neural control of panic attacks.

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“…In view of the well-established use of benzodiazepines for the treatment of panic and anxiety (Ballenger et al, 1988) it is surprising that apart from the preliminary report of de Montigny (1989) in four subjects no controlled study on the effects of benzodiazepines on CCK-4-induced panic is available so far. Therefore, we conducted a double-blind, placebo-controlled parallel-group study and investigated CCK-4-induced panic symptoms after treatment with alprazolam, which has been shown to be highly effective and well tolerated in the treatment of panic and anxiety in PD patients (Ballenger et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, we conducted a double-blind, placebo-controlled parallel-group study and investigated CCK-4-induced panic symptoms after treatment with alprazolam, which has been shown to be highly effective and well tolerated in the treatment of panic and anxiety in PD patients (Ballenger et al, 1988). According to clinical use, we administered a single dose of 1 mg alprazolam prior to a challenge with CCK-4, which is a suitable dose both for acute anxiolytic effects and for medium-term treatment of patients with PD (Ballenger et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Effects of Alprazolam on Cholecystokinin-Tetrapeptide-Induced Panic and Hypothalamic–Pituitary–Adrenal-Axis Activity: A Placebo-Controlled Study

Zwanzger

Eser

Aicher

et al. 2002

Neuropsychopharmacol

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Cholecystokinin-tetrapeptide (CCK-4) induces panic attacks both in patients with panic disorder (PD) and healthy volunteers. It has been shown that panic elicited by CCK-4 is improved after treatment with antidepressants. Moreover, a reduction of CCK-4-induced panic has also been demonstrated after treatment with lorazepam in single subjects and after selective GABAergic treatment with vigabatrin. Although benzodiazepines are widely used as anxiolytics, no controlled study on the effects of benzodiazepines on CCK-4-induced panic symptoms is available so far. Therefore, we investigated the effects of alprazolam and placebo on CCK-4-induced panic symptoms in a double-blind, placebo-controlled study. A total of 30 healthy subjects were challenged with 50 mg CCK-4. Out of these 30 subjects, 26 showed a marked panic response to CCK-4. Subjects were rechallenged after a 7-day interval and treated with 1 mg alprazolam or placebo 1 h prior to the second CCK-4 challenge. Panic was assessed using the acute panic inventory (API) and a DSM-IV-derived panic symptom scale (PSS). Moreover, the number of reported symptoms and self-rated anxiety and arousal were recorded. We found a significant reduction of the API and PSS scores and of the number of reported symptoms compared to placebo. Moreover, compared to placebo the CCK-4-induced ACTH and cortisol release were significantly attenuated during the CCK-4 challenge after alprazolam treatment. However, also placebo treatment reduced CCK-4-induced anxiety and HPA-axis activation to a certain extent. In conclusion, our data show that alprazolam reduces CCK-4-induced panic, which supports the hypothesis of a possible interaction between the GABA and the CCK system.

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Alprazolam in Panic Disorder and Agoraphobia: Results From a Multicenter Trial

Cited by 527 publications

References 40 publications

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Pharmacological Treatment of Anxiety, Obsessive-Compulsive and Post-Traumatic Stress Disorders – First Revision

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Pharmacological Treatment of Anxiety, Obsessive-Compulsive and Post-Traumatic Stress Disorders – First Revision

Acute Shift in Glutamate Concentrations Following Experimentally Induced Panic with Cholecystokinin Tetrapeptide—A 3T-MRS Study in Healthy Subjects

Effects of Alprazolam on Cholecystokinin-Tetrapeptide-Induced Panic and Hypothalamic–Pituitary–Adrenal-Axis Activity: A Placebo-Controlled Study

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