Panic Disorder Medication

  • Author: Mohammed A Memon, MD; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych (UK)   more...
 
Updated: Mar 29, 2011
 

Intermediate-Acting Benzodiazepines

Class Summary

By binding to specific receptor sites, intermediate-acting benzodiazepines appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. These agents are effective on standing-dose and prn schedules.

Lorazepam (Ativan)

 

Lorazepam is a sedative hypnotic with a short onset of effects and a relatively intermediate half-life. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the CNS, including the limbic and reticular formations.

Clonazepam (Klonopin)

 

Clonazepam facilitates inhibitory GABA neurotransmission and other inhibitory transmitters. It has a relatively longer half-life (approx 36 h).

Alprazolam (Xanax, Xanax XR)

 

Alprazolam is for the management of anxiety attacks. It binds to receptors at several sites within the CNS, including the limbic system and the reticular formations. Its effects may be mediated through the GABA receptor system. Alprazolam has been reviewed in the literature, although its use is currently discouraged because of its higher potential to elicit dependency.

Diazepam (Valium, Diastat, Diazepam Intensol)

 

Diazepam depresses all levels of the CNS (eg, the limbic and reticular formations), possibly by increasing the activity of GABA.

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Serotonin Reuptake Inhibitor/Antagonist

Class Summary

The mechanism of antidepressant action of this class of drugs is not fully understood in humans. These agents are not MAOIs and, unlike amphetamine-type drugs, do not stimulate the CNS.

Trazodone

 

Trazodone is useful in the treatment of panic disorder and agoraphobia with panic attacks. It is an antagonist at the 5-HT2 receptor and inhibits the reuptake of 5-HT. It also has a negligible affinity for cholinergic and histaminergic receptors.

In animals, this drug selectively inhibits serotonin uptake by brain synaptosomes and potentiates the behavioral changes induced by the serotonin precursor, 5-hydroxytryptophan.

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Selective Serotonin Reuptake Inhibitors

Class Summary

SSRIs are first-line agents for long-term management of anxiety disorders. Control is gradually achieved over a 2- to 4-wk course, depending on required dosage increases.

All commonly used SSRIs appear to have a role in the treatment of panic disorder. Fluoxetine is covered herein, because it has a very long half-life. This makes it well suited for patients who have difficulty remembering to take all of their medications each day. The longer half-life also minimizes the risk and severity of SSRI withdrawal that can occur when patients exhaust or abruptly discontinue their SSRI.

Fluoxetine (Prozac)

 

Fluoxetine selectively inhibits presynaptic serotonin reuptake, with minimal or no effect on reuptake of norepinephrine or dopamine.

Paroxetine (Paxil, Paxil CR)

 

This is an alternative sedating SSRI. Paroxetine is a potent selective inhibitor of neuronal serotonin reuptake. It also has weak effect on norepinephrine and dopamine neuronal reuptake.

Sertraline (Zoloft)

 

This agent selectively inhibits presynaptic serotonin reuptake. It also has a weak inhibitory effect on norepinephrine and dopamine neuronal reuptake.

Fluvoxamine (Luvox, Luvox CR)

 

Fluvoxamine is a potent selective inhibitor of neuronal serotonin reuptake. It does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors and therefore has fewer adverse effects than do tricyclic antidepressants.

Citalopram (Celexa)

 

Citalopram enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane. SSRIs are the antidepressants of choice due to minimal anticholinergic effects.

Escitalopram (Lexapro)

 

Escitalopram is a selective serotonin reuptake inhibitor and S-enantiomer of citalopram. Its mechanism of action is thought to be potentiation of serotonergic activity in the CNS resulting from the inhibition of CNS neuronal reuptake of serotonin.

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Tricyclic Antidepressants

Class Summary

TCAs have the advantages of once-daily dosing, low risk of dependence, and no dietary restrictions. However, they are discontinued in 35% of cases because of adverse effects, such as blurred vision, dry mouth, dizziness, weight gain, gastrointestinal disturbance, agitation, insomnia, headache, and decreased libido or ability to orgasm. TCAs must be started in low doses to avoid amphetamine like stimulation and can require up to 8-12 weeks for treatment response.

Imipramine (Tofranil, Tofranil-PM)

 

Imipramine inhibits the reuptake of norepinephrine and serotonin (5-hydroxytryptamine, 5-HT) at presynaptic neurons.

Desipramine (Norpramin)

 

Desipramine may increase the synaptic concentration of norepinephrine in the CNS by inhibiting the reuptake by the presynaptic neuronal membrane. It may have effects in the desensitization of adenyl cyclase, down-regulation of beta-adrenergic receptors, and down-regulation of serotonin receptors.

Clomipramine (Anafranil)

 

This agent affects serotonin uptake while it affects norepinephrine uptake when converted into its metabolite, desmethylclomipramine.

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Monoamine Oxidase Inhibitors

Class Summary

These are effective in patients with social phobia. Advantages of MAOIs are low risk of dependence and less anticholinergic effect than TCAs. Disadvantages are the higher number of adverse effects, including sexual difficulty, hypotension, weight gain, dry mouth, tachycardia, insomnia, drowsiness, headache, weakness, and constipation.

Phenelzine (Nardil)

 

Nardil is the MAOI that is most commonly used for panic disorder. It has demonstrated clear superiority over placebo in double-blind trials for treating specific symptoms of panic disorder. The drug is usually reserved for patients who do not tolerate or respond to traditional cyclic or second-generation antidepressants.

Tranylcypromine (Parnate)

 

This drug is also effective against panic disorder. It binds irreversibly to MAO, thereby reducing monoamine breakdown and enhancing synaptic availability.

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Serotonin Norepinephrine Reuptake Inhibitors

Class Summary

The dual serotonin-norepinephrine reuptake inhibitor antidepressant (SNRI), venlafaxine (Effexor, Effexor XR), is indicated for panic disorders.

Venlafaxine (Effexor, Effexor XR)

 

Venlafaxine is a serotonin/norepinephrine reuptake inhibitor. It may treat depression by inhibiting neuronal serotonin and norepinephrine reuptake. In addition, it causes beta-receptor down-regulation.

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Alpha-2 Antagonists

Class Summary

The alpha-2 adrenergic antagonists increase synaptic norepinephrine and serotonin, while also blocking some postsynaptic serotonergic receptors that conceptually mediate excessive anxiety when stimulated with serotonin.

Mirtazapine (Remeron, Remeron SolTab)

 

Mirtazapine has a much more sedating effect, generally reducing its potential to aggravate initial anxiety. Remeron may cause residual morning sedation that often improves with continued therapy and may cause an increase in appetite or weight gain.

Sedating antidepressants, such as Remeron are usually prescribed for use only at night before bed to help improve sleep, but they should include a warning for the patient not to operate a motor vehicle or machinery if he or she is feeling sedated or directly after the dose.

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Contributor Information and Disclosures
Author

Mohammed A Memon, MD  Chairman and Attending Geriatric Psychiatrist, Department of Psychiatry, Spartanburg Regional Medical Center

Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

Coauthor(s)

Colin Y Daniels, MD  Consulting Staff, Department of Psychiatry, Madigan Army Medical Center

Colin Y Daniels, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Robert Harwood, MD, MPH, FACEP, FAAEM  Senior Physcian, Department of Emergency Medicine, Advocate Christ Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine

Robert Harwood, MD, MPH, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Samuel M Keim, MD  Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine

Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michael C Plewa, MD  Research Coordinator, Consulting Staff, Department of Emergency Medicine, Lucas County Emergency Physicians, Inc, and Mercy Saint Vincent Medical Center

Michael C Plewa, MD, is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Physicians for Social Responsibility, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Iqbal Ahmed, MBBS, FRCPsych (UK)  Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Iqbal Ahmed, MBBS, FRCPsych (UK) is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, American Psychiatric Association, American Society of Clinical Psychopharmacology, and Royal College of Psychiatrists

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Sandra Yerkes to the development and writing of this article.

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