Long-Term Effects of Alprazolam and Imipramine on Cerebrospinal Fluid Monoamine Metabolites and Neuropeptides in Panic Disorder

Lepola, Ulla; Jolkkonen, Jukka; Rimón, Ranan; Riekkinen, P.

doi:10.1159/000118574

Cited by 12 publications

(1 citation statement)

References 25 publications

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“…In the latter instance for panic, plasma and cerebrospinal homovanillic acid (HVA) concentrations, a DA metabolite, fail to discriminate panic and control subjects [29,99,100]. The lack of a neurochemical panic index is not without precedent since NE alterations, for example, have likewise failed to discriminate panic from non-panic subjects [101,102]. Some laboratories have identified DA perturbations among panic patients with increased anxiety as measured on the Spielberger State Anxiety scale, augmented panic frequency in the 12 months preceding clinical interview and reduced symptom free periods relative to other panic patients [30,31,68].…”

Section: Central Dopamine Turnover: Prelude To Anxiety and Emergence mentioning

confidence: 99%

The Myth of Panic Spontaneity: Consideration of Behavioral and Neurochemical Sensitization

Hebb

Anger

Mendella

et al. 2007

TOPJ

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Panic disorder is characterized by a progression of panic symptom severity with repeated attacks. Repeated panic episodes evoke heightened anticipatory anxiety, phobic avoidance and are typically associated with comorbid symptoms of depression. Due to the heterogeneity of the disorder, reliable neurochemical correlates attending panic have not been identified. However, variable neuropeptide interfacing with major and minor transmitter systems may modulate individual vulnerability to panic and account for variable panic profiles. The extensive colocalization of cholecystokinin (CCK) with other neurotransmitters, including dopamine (DA), enkephalin (ENK) and GABA, in specific central sites may influence various aspects of anxiety and panic. The behavioral correlates attending panic likely follow from variable neurochemical release and conditioning/sensitization. Clinicians maintain that recurrent panic attacks are spontaneous (unexpected, uncued) and fail to acknowledge the wealth of information implicating a prominent role for stressful life events in panic. Conditioning and sensitization of both behavior (e.g., fear-motivated) and neurochemical events (e.g., DA and CCK) in response to uncontrollable stressors parallel the diverse heterogeneity of panic amongst clinical samples. Cholecystokinin-4, pentagastrin, lactate acid, and CO 2 induce panic attacks that are dependent on subjective history, expectancy measures and panic profiles. Panic disorder is associated with chronic illness and familial sick-role modeling exacerbates the course of the illness. The current review outlines the evidence in support of a conditioning/sensitization model for panic, a model that may explain the variable efficacies of pharmacological interventions.

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Section: Central Dopamine Turnover: Prelude To Anxiety and Emergence mentioning

confidence: 99%

The Myth of Panic Spontaneity: Consideration of Behavioral and Neurochemical Sensitization

Hebb

Anger

Mendella

et al. 2007

TOPJ

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Antidepressants and benzodiazepines for panic disorder in adults

Bighelli

Trespidi

Castellazzi

et al. 2016

Cochrane Database of Systematic Reviews

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The identified studies are not sufficient to comprehensively address the objectives of the present review. The majority of studies enrolled a small number of participants and did not provide data for all the outcomes specified in the protocol. For these reasons most of the analyses were underpowered and this limits the overall completeness of evidence. In general, based on the results of the current review, the possible role of antidepressants and benzodiazepines should be assessed by the clinician on an individual basis. The choice of which antidepressant and/or benzodiazepine is prescribed can not be made on the basis of this review only, and should be based on evidence of antidepressants and benzodiazepines efficacy and tolerability, including data from placebo-controlled studies, as a whole. Data on long-term tolerability issues associated with antidepressants and benzodiazepines exposure should also be carefully considered.The present review highlights the need for further higher-quality studies comparing antidepressants with benzodiazepines, which should be conducted with high-methodological standards and including pragmatic outcome measures to provide clinicians with useful and practical data. Data from the present review will be included in a network meta-analysis of psychopharmacological treatment in panic disorder, which will hopefully provide further useful information on this issue.

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