Pathophysiology Of Panic Disorder Research Articles

Plasma gamma-amino-butyric acid (GABA) levels in cholecystokinine-tetrapeptide (CCK-4) induced anxiety.

Dysregulation of the GABA system is supposed to play an important role in the pathophysiology of panic disorder. Moreover, prior investigations revealed an association between GABA plasma levels and experimental induced panic with lactate. To evaluate a possible relationship between plasma GABA and CCK-4 induced panic plasma GABA levels in healthy volunteers were investigated. 12 healthy subjects were challenged with 50 micro g CCK-4. Blood samples for determination of plasma GABA were drawn at baseline, 5 and 10 minutes after CCK-4 injection. Plasma GABA levels did not change significantly during the CCK-4 challenge as revealed by ANOVA for repeated measurements. There was no correlation between baseline GABA levels and anxiogenic response to CCK-4. In contrast to previous findings with lactate our study does not suggest a possible relationship between plasma GABA levels and experimental induced panic with CCK-4.

L -5-Hydroxytryptophan induced increase in salivary cortisol in panic disorder patients and healthy volunteers

Hypersensitivity of brain serotonin receptors has been proposed as a causal mechanism in the pathophysiology of panic disorder. This theory can be tested, using serotonergic stimulation of the HPA axis. Up to now, plasma cortisol has generally been used as the outcome measure in such studies. Assessment of salivary cortisol is a non-invasive alternative to measure HPA axis activity. Salivary cortisol levels were measured in 24 panic disorder patients and 24 healthy volunteers, following ingestion of 200 mg L-5-hydroxytryptophan or placebo. A significant rise in cortisol was observed in both patients and controls following ingestion of L-5-hydroxytryptophan. No such effects were seen in the placebo condition. The results show that L-5-hydroxytryptophan stimulated salivary cortisol is a useful probe of serotonin function in healthy volunteers as well as panic disorder patients, and provide some evidence against a serotonin receptor hypersensitivity in panic disorder.

Panic disorder patients have reduced cyclic AMP in platelets

Little is known about the intracellular mechanisms involved in the pathophysiology of panic disorder (PD). Abnormalities in the cyclic AMP system have been described in several psychiatric disorders but there are no studies in panic patients. We evaluated not only the levels of platelet cyclic AMP, but also cyclic GMP and nitric oxide synthase (NOS) activity in patients with PD at baseline and after treatment with clomipramine and in healthy volunteers. Platelet cyclic AMP was determined by enzymeimmunoassay, cyclic GMP by radioimmunoassay and NOS activity by the conversion of 3H-arginine to 3H-citruline in 17 PD patients before treatment with clomipramine, after remission of panic attacks and in 22 healthy volunteers. Average baseline cyclic AMP of PD patients was lower than after remission of panic attacks ( P<0.005) and lower than in healthy volunteers ( P<0.005). Average cyclic AMP after remission of panic attacks was not significantly different than in healthy volunteers. There were no significant differences in cyclic GMP and NOS analysis. Our results suggest that PD patients without treatment have lower platelets cyclic AMP levels than healthy volunteers and that this decrease may be corrected by clomipramine.

Persistent respiratory irregularity in patients with panic disorder

Background: Dysregulated respiratory control may play a role in the pathophysiology of panic disorder. This could be due to abnormalities in brain stem respiratory nuclei or to dysregulation at higher brain levels. Results from previous studies using the doxapram model of panic have yielded an unclear picture. A brief cognitive manipulation reduced doxapram-induced hyperventilation in patients, suggesting that higher level inputs can substantially alter their respiratory patterns. However, respiratory abnormalities persisted, including a striking irregularity in breathing patterns. Methods: To directly study respiratory irregularity, breath-by-breath records of tidal volume (V t) and frequency ( f) from previously studied subjects were obtained. Irregularity was quantified using von Neumann’s statistic and calculation of “sigh” frequency in 16 patients and 16 matched control subjects. Half of each group received a standard introduction to the study and half received a cognitive intervention designed to reduce anxiety/distress responses to the doxapram injection. Results: Patients had significantly greater V t irregularity relative to control subjects. Neither the cognitive intervention nor doxapram-induced hyperventilation produced significant changes in V t irregularity. The V t irregularity was attributable to a sighing pattern of breathing that was characteristic of panic patients but not control subjects. Patients also had somewhat elevated f irregularity relative to control subjects. Conclusions: The irregular breathing patterns in panic patients appear to be intrinsic and stable, uninfluenced by induced hyperventilation or cognitive manipulation. Further study of V t irregularity and sighs are warranted in efforts to localize dysregulated neural circuits in panic to brain stem or midbrain levels.

Increased response to a putative panicogenic nocebo administration in female patients with panic disorder

Experimental challenge studies may generate and test hypotheses regarding the pathophysiology of panic disorder and may serve to identify pathophysiologically relevant subtypes. It has been suggested that gender-related differences may be relevant in the development and maintenance of panic disorder. In a randomized double blind design the effects of placebo and sodium lactate administration in 14 female and 16 male patients with panic disorder and 23 healthy control subjects were compared using the Acute Panic Inventory (API) score and derived formal criteria for a panic attack. Panic attack frequency following sodium lactate was 76.6% in the patient group. Although control subjects had a lacate-induced increase in the API score as well, this effect was much weaker. No panic attacks occurred in patients with panic disorder or healthy control subjects receiving a placebo. However, a gender effect was observed in the putative panicogenic placebo condition: female patients with panic disorder had more subthreshold panic anxiety as measured with the API score. The data give evidence for an increased nocebo response in female patients with panic disorder.

Panic provocation procedures in the treatment of panic disorder: Early perspectives and case studies

Although panic provocation procedures have been utilized for many decades to generate and test hypotheses about the pathophysiology of panic disorder, very little is known about the value of these procedures for treatment. In this article, we discuss the theoretical and practical issues related to panic provocation procedures in the treatment of panic disorder. We conclude that hyperventilation, physical exercise, and other activities that induce paniclike symptoms are among the most suitable provocation procedures for use in treatment. Two cases illustrate the use of such procedures in cognitive-behavioral intervention.

Panic patients in the non-panic state: physiological and cognitive dysfunction

Panic attacks and the antipanic effect of antidepressants are claimed to distinguish panic disorder (PD) from generalised anxiety disorder. However, most studies showing neurochemical disturbances in PD overlook the non-panic state. We compared panic patients in the non-panic state with controls on biochemical, psychological and physiological measures. There were no differences on the neuroendocrine tests. Self-ratings of bodily and psychological symptoms of anxiety were significantly higher in patients and they scored worse on word recall. Patients had significantly more skin conductance fluctuations and slow wave activity in the electroencephalogram, a sign of hyperventilation which may have implications for brain activity. Discrepancies between patients' self-ratings and objective measures of pulse rate and psychomotor performance indicated that panic patients have distorted perceptions of both physical and mental functioning. Hyperventilation and cognitive distortions in the non-panic state may facilitate panic attacks and are part of the pathophysiology of PD.

Respiratory psychophysiology of panic disorder: three respiratory challenges in 98 subjects.

Respiratory abnormalities may play a central role in the pathophysiology of panic disorder. The current study was undertaken to examine the respiratory response in the largest series of subjects to date during three respiratory challenges that used improved methodology. Fifty-nine patients with DSM-III-R panic disorder and 39 normal volunteers were challenged with 5% and 7% CO2 inhalation and room air hyperventilation separated by room air breathing with continuous spirometry. Patients with panic disorder were more sensitive to the anxiogenic effects of CO2 than were normal subjects, and CO2 was a more potent stimulus to panic than hyperventilation. Patients increased their respiratory rate more quickly during CO2 inhalation than did comparison subjects, and this increase preceded the panic attacks. Patients who panicked in response to 5% CO2 demonstrated continued rise in end-tidal CO2, while the end-tidal CO2 of the comparison groups stabilized. Low end-tidal CO2 and high variance in minute ventilation at baseline predicted panic attacks during CO2 inhalation. Following CO2 or hyperventilation challenges, respiratory rate dropped sharply, while tidal volume remained elevated longer in patients than in comparison subjects. The findings confirm the greater behavioral and physiological sensitivity of patients with panic disorder to CO2 inhalation and identify a series of respiratory abnormalities. Panic attacks in panic disorder may be explained by inefficient compensatory mechanisms, primarily of respiratory rate.

β-Adrenoreceptor coupling to gs protein in alcohol dependence, panic disorder, and patients with both conditions

Ethanol may downregulate G-protein-coupled beta-adrenoreceptors (beta AR). beta AR may also be dysregulated in panic disorder (PD). In clinical samples, many patients have comorbid alcohol dependence (AD) and PD. Therefore, we investigated beta AR coupling in patients with these disorders. We harvested polymorphonuclear leukocytes from 24 healthy volunteers (Vs), and from 22 abstinent AD patients, 7 PD patients, and 9 patients with comorbid AD/PD. beta AR were assayed using saturation and agonist-displacement experiments. Group differences were tested using one-way analysis of variance (ANOVA). All beta AR binding parameters were similar in AD patients and Vs. The ratio of the agonists' dissociation constant from the receptor in the low affinity state (KL) to that in the high affinity state (KH) was significantly higher in PD patients than in AD patients and Vs (930.97 +/- 440.80 vs. 226.2 +/- 94.47 vs. 197.05 +/- 61.03, respectively, p < .01). This finding suggests that beta AR are supercoupled to GS in patients with PD. There was a trend for higher total receptor density (RT) in AD/PD and PD patients (Vs = 39.06 +/- 42.57 vs. AD = 27.93 +/- 23.07 vs. AD/PD = 66.85 +/- 79.02 vs. PD = 68.36 +/- 49.20, p < .08). There were no differences between AD/PD and PD patients, who combined had a significantly higher RT than Vs and AD patients (Vs = 38.95 +/- 8.81 vs. AD = 29.63 +/- 5.07 vs. AD/PD = 67.51 +/- 17.00, fmol/mg protein, p < .04). Finally, AD/PD patients had a significantly higher receptor density in the low-affinity conformational state than Vs and AD patients, but not PD patients (25.96 +/- 11.59 vs. 10.69 +/- 1.53 vs. 7.62 +/- 1.08 vs. 17.07 +/- 5.26 fmol/mg protein, respectively, p < .005). beta AR function in polymorphonuclear leukocytes is normal in abstinent alcoholics. The previously reported abnormal beta AR regulation in alcoholism may be state dependent. The higher RT and KL/KH ratio in AD/PD and PD, but not in AD patients, suggest that increased beta AR function may be important in the pathophysiology of PD.

Behavioral, neuroendocrine and biochemical effects of different doses of 5-HTP in panic disorder

To investigate the role of serotonin (5-HT) in the pathophysiology of panic disorder (PD) a challenge test with l-5-hydroxy-tryptophan (5-HTP) was conducted. Seven patients suffering from PD and seven healthy controls received an i.v. challenge with 10 mg, 20 mg and 40 mg 5-HTP and placebo in random order on four different occasions. Before, during and until 2 h after 5-HTP administration anxious and depressive symptomatology was assessed. In addition, plasma levels of 5-HTP, cortisol, and 5-HIAA were measured at several timepoints. During and after infusion of placebo or any of the different dosages of 5-HTP, none of the patients or controls experienced a panic attack or showed an increase in anxiety or depressive symptoms. There was a dose-related increase in side effects, like nausea, dizziness and fatigue. Only infusion with 40 mg 5-HTP led to an increase in plasma cortisol in both patients and controls. The observed increase in plasma cortisol level was higher for patients compared to controls only at 30 min after infusion. In conclusion, stimulation of the serotonergic neuronal system by three different dosages of 5-HTP did not induce panic or anxiety in PD patients and healthy controls. The 5-HT hypersensitivity hypothesis of PD could not be confirmed in the present study.

Effects of tryptophan depletion in panic disorder

Tryptophan (TRP) depletion is a useful paradigm for evaluating serotonin (5-HT) function in psychiatric disease. Primate studies have shown that plasma TRP depletion can be induced by the ingestion of an amino acid (AA) mixture lacking TRIP (Young et al ! 989). In this report the AA mixture without TRP reduced cerebrospinal fluid (CSF) TRP by 61% relative to a control AA mixture, which effect was associated with a 34% reduction in 5-hydroxyindole, acetic acid. Oral administration of this AA mixture following a Iow-TRP diet is known to reduce plasma TRP levels in healthy humans by over 80% of baseline levels (Zimmerman et a l i 993). In other clinical studies we have found that TRP depletion by this method produces a transient exacerbation of depressive symptoms in antidepressant-remitted depressed (Delgado et al 1990) and obsessive-compulsive patients (Barr et al 1994); however, to date there have been no studies utilizing TRP depletion in panic disorder (PD) patients. The norepinephrine (NE) and 5-HT systems have been implicated in the pathophysiology of PD (Kahn et al ! 988a, Charney et al 1992). Furthermore, the 5-HT system may provide inhibitory inputs to the principal NE nucleus, the locus coeruleus (AstonJones et ai ! 99 I). If TRP depletion sufficiently reduced presynaptic 5-HT inhibition of NE function in PD patients, this could lead to a transient increase in NE function with accompanying increases in anxiety, blood pressure, and the NE metabolite 3-methoxy-4hydroxyphenylglycol (MHPG).

Somatic Symptoms, Fear, and Panic

Back to table of contents Previous article Next article ArticleNo AccessSomatic Symptoms, Fear, and PanicDAVID A. KATERNDAHLDAVID A. KATERNDAHLSearch for more papers by this authorPublished Online:1 Apr 2006https://doi.org/10.1176/ajp.150.9.1434-aAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail "Somatic Symptoms, Fear, and Panic." American Journal of Psychiatry, 150(9), pp. 1434-a–1434 Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - American Journal of Psychiatry $35.00 Add to cart PPV Articles - American Journal of Psychiatry Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byPrevalence of Obsessive-Compulsive Disorder in Patients With Schizophrenia and Outcome on Positive and Negative Symptoms, Cognition, and Quality of LifeJournal of Nervous & Mental Disease, Vol. 207, No. 4Genome-wide association analysis of pain severity in dysmenorrhea identifies association at chromosome 1p13.2, near the nerve growth factor locus19 July 2016 | Pain, Vol. 157, No. 11The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies20 November 2012 | Biology of Mood & Anxiety Disorders, Vol. 2, No. 1A Cross-Ethnic Comparison of Lifetime Prevalence Rates of Anxiety DisordersJournal of Nervous & Mental Disease, Vol. 198, No. 8Journal of Addictive Diseases, Vol. 29, No. 1Depression and Anxiety, Vol. 26, No. 10Psychotherapy and Psychosomatics, Vol. 77, No. 3Ethnicity & Health, Vol. 12, No. 3Current Psychiatry Reports, Vol. 8, No. 4Relationship between perfectionism, personality disorders and agoraphobia in patients with panic disorder28 August 2002 | Acta Psychiatrica Scandinavica, Vol. 106, No. 3Obsessive-Compulsive and Panic Symptoms in Patients With First-Admission PsychosisThomas Craig, M.D., M.P.H., Michael Y. Hwang, M.D., and Evelyn J. Bromet, Ph.D.1 April 2002 | American Journal of Psychiatry, Vol. 159, No. 4Panic attacks in psychosis26 February 2002 | Acta Psychiatrica Scandinavica, Vol. 105, No. 1The Journal of Nervous and Mental Disease, Vol. 190, No. 8Depression and Anxiety, Vol. 13, No. 4Depression and Anxiety, Vol. 9, No. 3Depression and Anxiety, Vol. 9, No. 3The Journal of Nervous & Mental Disease, Vol. 187, No. 9Journal of Psychosomatic Research, Vol. 44, No. 1Use of health care services by persons with panic symptoms1 April 2006 | Psychiatric Services, Vol. 48, No. 8Human Psychopharmacology: Clinical and Experimental, Vol. 12, No. S1Human Psychopharmacology: Clinical and Experimental, Vol. 12, No. S1Plastic &amp Reconstructive Surgery, Vol. 100, No. 2American Journal of Medical Genetics, Vol. 60, No. 2Panic and panic disorder in the United States1 April 2006 | American Journal of Psychiatry, Vol. 151, No. 3 Volume 150Issue 9 September 1993Pages 1434-a-1434 Metrics PDF download History Published online 1 April 2006 Published in print 1 September 1993

Clomipramine and initial worsening in panic disorder: beyond the 'jitteriness syndrome'

The time course and the phenomenology of the initial response to clomipramine (10-20 mg/day) was investigated in 70 patients with panic disorder with or without agoraphobia. Nineteen (27.1%) patients reported worsening of their clinical state which, on average, began 28 h after the first dose and lasted for 5 days. Increase in the frequency and severity of panic attacks was the most frequent finding (14 patients), followed by psycho- stimulant (jitteriness; n=9), depressive (n=8) and tonic anxiety symptoms (n=7). This pattern of initial worsening is different from the 'jitteriness syndrome' described for other antidepressants. Its implications for the understanding of the pathophysiology of panic disorder are discussed.

Brain perfusion abnormalities in drug-naive, lactate-sensitive panic patients: A SPECT study

Using single photon emission computed tomography (SPECT) and 99mTc-hexamethylpropyleneamine oxime (HM-PAO), we assessed brain perfusion in seven patients with panic disorder (PD) and in five age-matched normal subjects at rest. No patient had ever received drug treatment for panic. All patients were sensitive to lactate-induced panic. Computer tomography (CT) scans did not reveal any morphological abnormalities of the brain in any of the PD patients. Two indices of cerebral perfusion were calculated; these demonstrated alterations of brain perfusion in the PD group. Significant right—left asymmetry was found in the inferior frontal cortex of the PD patients. We also observed a significant blood flow increase in the left occipital cortex and a significant decrease in the hippocampal regions bilaterally. Although the changes seen in the inferior frontal cortex and occipital cortex may be related to anxiety experienced by the patients during the study, the pattern of hippocampal hypoperfusion appears to be characteristic of panic disorder. This suggests that the hippocampal structures may play an important role in the pathophysiology of panic disorder.

Serotonin, Panic Disorder and Agoraphobia

A serotonin-anxiety connection has been widely recognized. In panic disorder (PD), however, most researchers have emphasized noradrenergic mechanisms. Serotonin related findings in PD, e.g. the documented antipanic potential of selective serotonin reuptake inhibitors (SSRIs), are reviewed, lending support for a serotonergic deficit contributing to the pathophysiology of PD. Since citalopram is the most selective SSRI described, it was chosen as a tool for testing whether the serotonin reuptake inhibition per se is responsible for this antipanic effect. Twenty patients with PD with or without agoraphobia (DSM-III-R criteria) were treated openly with citalopram and assessed with CAS, MADRS, SCL-90 the Agoraphobia Scale, other self-ratings, and a panic diary. Thirteen of the 17 patients completing 8 weeks of treatment were judged as responders. The response seemed similar to or better than that seen with other antidepressants. The response covered broad aspects of morbidity, e.g. anticipatory anxiety, agoraphobia and somatization. In the first week, a transient increase of panic-related symptoms was observed. Sixteen of the patients were enrolled in a 15 months' study of long-term maintenance treatment; 11 patients completed this phase. The gains were maintained during this follow-up, and further improvement was observed. Side-effects were similar to those of other SSRIs and mostly mild. For instance, weight-gain was not associated with citalopram treatment. The results support the hypothesis that serotonin reuptake inhibition is essential for the antipanic effect of antidepressants as well as for the initial paradoxical increase of anxiety often seen with these drugs. Thus, an initial deterioration, possibly due to transient decrease of serotonin transmission, turns to improvement when serotonergic potentiation has occurred.

A cerebrospinal fluid study of the pathophysiology of panic disorder associated with alcoholism

In order to investigate the neurochemistry of panic disorder in alcoholics, we measured various cerebrospinal fluid (CSF) parameters in subjects with both conditions and compared them with an age- and sex-matched population of alcoholics and normal controls. When height, age and weight were covaried, subjects with panic disorder had higher levels of B-endorphin in CSF. There were no differences in other CSF measures between the groups. Alcoholics with panic disorder had higher plasma MHPG concentrations compared with alcoholics without panic disorder but these were not statistically different from controls.

Occult Thyroid Dysfunction in Refractory Depression

Back to table of contents Previous article Next article ArticleNo AccessOccult Thyroid Dysfunction in Refractory DepressionMURRAY B. STEIN, and THOMAS W. UHDEMURRAY B. STEINSearch for more papers by this author, and THOMAS W. UHDESearch for more papers by this authorPublished Online:1 Apr 2006https://doi.org/10.1176/ajp.146.2.281AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail "Occult Thyroid Dysfunction in Refractory Depression." American Journal of Psychiatry, 146(2), p. 281 Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - American Journal of Psychiatry $35.00 Add to cart PPV Articles - American Journal of Psychiatry Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited ByInternational Journal of Psychiatry in Clinical Practice, Vol. 18, No. 1Serotonin and Female Psychopathology1 January 2013 | Women's Health, Vol. 9, No. 1The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies20 November 2012 | Biology of Mood & Anxiety Disorders, Vol. 2, No. 1Archives of Women's Mental Health, Vol. 15, No. 6The World Journal of Biological Psychiatry, Vol. 7, No. 3BMC Psychiatry, Vol. 4, No. 1Patterns of Psychopathology and Dysfunction in High-Risk Children of Parents With Panic Disorder and Major DepressionJoseph Biederman, M.D., Stephen V. Faraone, Ph.D., Dina R. Hirshfeld-Becker, Ph.D., Deborah Friedman, B.A., Joanna A. Robin, B.A., and Jerrold F. Rosenbaum, M.D.1 January 2001 | American Journal of Psychiatry, Vol. 158, No. 1Depression and Anxiety, Vol. 11, No. 3Journal of Endocrinological Investigation, Vol. 21, No. 11International Journal of Psychiatry in Clinical Practice, Vol. 2, No. 1Cognitive Therapy and Research, Vol. 19, No. 4Acta Psychiatrica Scandinavica, Vol. 92, No. 5Setting diagnostic thresholds for social phobia: considerations from a community survey of social anxiety1 April 2006 | American Journal of Psychiatry, Vol. 151, No. 3Acta Psychiatrica Scandinavica, Vol. 90, No. 2Acta Psychiatrica Scandinavica, Vol. 89, No. s376Baylor University Medical Center Proceedings, Vol. 6, No. 3Postgraduate Medicine, Vol. 91, No. 7Psychiatry and Clinical Neurosciences, Vol. 45, No. 2Acta Psychiatrica Scandinavica, Vol. 83, No. S365International Review of Psychiatry, Vol. 3, No. 2Major depression in patients with social phobia1 April 2006 | American Journal of Psychiatry, Vol. 147, No. 5Social Psychiatry and Psychiatric Epidemiology, Vol. 25, No. 6Journal of Psychosomatic Obstetrics & Gynecology, Vol. 11, No. 3Postgraduate Medicine, Vol. 86, No. 6International Review of Psychiatry, Vol. 1, No. 3 Volume 146Issue 2 February 1989Pages 281-281 Metrics PDF download History Published online 1 April 2006 Published in print 1 February 1989

An Open Trial of Fluoxetine in the Treatment of Panic Attacks

Fluoxetine is a new antidepressant with pharmacologic effects apparently limited to blockade of neuronal serotonin reuptake. We entered 20 patients who met DSM-III criteria for either panic disorder or agoraphobia with panic attacks into an open, uncontrolled pilot study of fluoxetine. Four responded to placebo in the week before fluoxetine administration and were dropped from the study. Of the remaining 16 patients, nine were nonresponders and seven were responders, with complete cessation of their panic attacks. Eight of the nine nonresponders were unable to tolerate the side effects of fluoxetine. In contrast, all of the responders (and one nonresponder) experienced minimal side effects. Fluoxetine may be effective in the treatment of panic attacks, perhaps implicating the serotonergic system in the pathophysiology of panic disorder. Future studies should use very low doses of fluoxetine to initiate treatment.