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PubMed1997

Measurement of panic disorder by a modified panic diary.

The psychometric characteristics of panic diary measures were investigated in a sample of 37 patients suffering from panic disorder with agoraphobia. Following recommendations made in the recent consensus development conference on the assessment of panic disorder, daily ratings included not only the occurrence of panic attacks but also fear of panic, expectancy of panic, and expected aversiveness of panic. These new measures were reliable and, on the whole, demonstrated good divergent and convergent validity. Further, adding such measures increased the incremental validity of panic disorder assessment.

Adult↗
PubMed1989

'Fear of panic': an investigation of its role in panic occurrence, phobic avoidance, and treatment outcome.

The concept of 'fear of fear' has recently received empirical attention regarding its role in panic occurrence and phobic avoidance. Overall, the results of such studies have indicated that anticipation of panic is positively correlated (albeit weakly) with self-reports of avoidance. The present study examined the relationship of panic anticipation--panic occurrence, phobic avoidance and treatment outcome, using a more direct measure of this fear than has been used in previous studies. Results indicated that anticipation of panic was slightly correlated with breadth and severity of avoidance, and moderately correlated with overall clinical severity. In addition, anticipation of panic was found to decrease significantly throughout treatment, but appeared to be independent of actual panic experience. These results may suggest the operation of an intervening variable which accounts for the reduction of both anticipated and actual panic events. Implications for assessment and treatment are discussed.

Adolescent↗
PubMed1992

Noradrenergic function in panic disorder. Effects of intravenous clonidine pretreatment on lactate induced panic.

To assess the role of noradrenergic stimulation during lactate-induced panic, ten patients with panic disorder who panicked during a standard sodium-lactate infusion underwent a repeat infusion following intravenous clonidine pretreatment. Although clonidine significantly lowered prelactate systolic blood pressure, the drug did not significantly lower prelactate anxiety levels, as reflected by the Acute Panic Inventory (API). Clonidine blocked lactate-induced panic in four of ten subjects, a significant effect. Clonidine treatment also significantly attenuated lactate-panic symptoms, as reflected by time to panic and API comparison between trials. Nevertheless, over half the subjects still panicked in response to lactate despite clonidine. This preliminary study suggests that reduction of central noradrenergic activity by clonidine, at least at the dosage levels employed in the current study, only partially attenuates panic response to lactate. Noradrenergic theories of panic may not therefore fully account for lactate panicogenesis.

Adult↗
PubMedDate not supplied

Specificity of lactate response in panic disorder, panic with concurrent depression and major depression.

Lactate infusions with 0.5 molar sodium lactate in a dose of 10 ml/kg within 20 min were given to patients with panic disorder (n = 6), panic attacks with concurrent major depression (n = 7) and major depression without panic (n = 5). Lactate-induced anxiety and symptom attacks without panic were seen more often in the groups with panic attacks, but a full-blown panic attack was provoked in only four subjects, all belonging to the groups with a history of panic attacks. The low incidence of lactate-induced panic attacks can be explained by differences in the procedure that aimed at reducing expectancy biases and baseline anxiety.

Adolescent↗
PubMedDate not supplied

Follow-up study of patients with panic disorder and agoraphobia with panic attacks treated with tricyclic antidepressants.

One hundred and seven patients with panic disorder or agoraphobia with panic attacks were studied 1-4 years after treatment with a tricyclic antidepressant. At follow-up more than 80% of the patients remained symptomatic but fewer than half were experiencing panic attacks and only 40% were avoiding phobic situations. Although patients with agoraphobia were more severely ill and had been ill longer than those with panic disorder, their response to tricyclics and eventual outcome was similar to that for patients with panic disorder. Panic and agoraphobic patients who had the most severe symptoms initially showed the least improvement. The results suggest that panic disorder and agoraphobia with panic attacks are variants of a single illness and that, despite its chronicity, this illness has a favorable outcome.

Adult↗
PubMed2005

Panic attack symptom dimensions and their relationship to illness characteristics in panic disorder.

Subtyping panic disorder by predominant symptom constellations, such as cognitive or respiratory, has been done for some time, but criteria have varied considerably between studies. We sought to identify statistically symptom dimensions from intensity ratings of 13 DSM-IV panic symptoms in 343 panic patients interviewed with the Anxiety Disorders Interview Schedule for DSM-IV Lifetime Version. We then explored the relation of symptom dimensions to selected illness characteristics. Ratings were submitted to exploratory maximum likelihood factor analysis with a Promax rotation. A three-factor solution was found to account best for the variance. Symptoms loading highest on the first factor were palpitations, shortness of breath, choking, chest pain, and numbness, which define a cardio-respiratory type (with fear of dying). Symptoms loading highest on the second factor were sweating, trembling, nausea, chills/hot flashes, and dizziness, which defines a mixed somatic subtype. Symptoms loading highest on the third factor were feeling of unreality, fear of going crazy, and fear of losing control, which defines a cognitive subtype. Subscales based on these factors showed moderate intercorrelations. In a series of hierarchical multiple regression analyses, the cardio-respiratory subscale was a strong predictor of panic severity, frequency of panic attacks, and agoraphobic avoidance, while the cognitive subscale mostly predicted worry due to panic. In addition, patients with comorbid asthma had higher scores on the cardio-respiratory subscale. We conclude that partly independent panic symptom dimensions can be identified that have different implications for severity and control of panic disorder.

Adult↗
PubMed2002

Pentagastrin-induced sleep panic attacks: panic in the absence of elevated baseline arousal.

BACKGROUND: It has been suggested that pharmacological challenges that induce panic attacks are confounded by effects of environmental stress, elevated baseline arousal, and expectancy bias. METHODS: To control for effects of arousal and cognition on the panicogenic effects of pentagastrin, pharmacological challenges were conducted during sleep in seven patients with panic disorder or social phobia. All patients had previously experienced pentagastrin-induced panic while awake. Infusions of normal saline and pentagastrin (0.6 microg/kg) were administered in fixed order and timed so that pentagastrin infusions took place during the transition from Stage 2 to Stage 3 sleep. Long intravenous lines were placed for remote blood sampling and subsequent analysis of plasma adrenocorticotropic hormone and cortisol. Measures of anxiety and panic were obtained at baseline and upon awakening after pharmacological challenge. RESULTS: All seven subjects awoke within seconds following pentagastrin infusion. Four patients reported symptoms that met criteria for panic. Neither baseline anxiety nor neuroendocrine measures were predictive of panic. CONCLUSIONS: These data demonstrate the ability to induce panic during a period of diminishing arousal and indicate that panic attacks can occur in the absence of elevated arousal and environmental stress.

Arousal↗
PubMed2000

LY354740, a potent group II metabotropic glutamate receptor agonist prevents lactate-induced panic-like response in panic-prone rats.

LY354740 is a potent and selective agonist at the group II metabotropic glutamate receptors and is shown to be an effective inhibitor of glutamate release with significant anxiolytic and drug withdrawal alleviating properties in certain animal models. Rats with chronic inhibition of GABA synthesis in the dorsomedial hypothalamus (DMH) are highly anxious and exhibit panic-like responses to peripheral lactate infusions similar to patients with panic disorder. Using these panic-prone rats, we tested the efficacy of LY354740 in preventing the lactate-induced panic-like response, comparing it to alprazolam, a clinically effective anti-panic drug. Rats were fitted with femoral arterial and venous catheters and implanted with Alzet pumps infusing the GABA synthesis inhibitor L-allylglycine into the DMH. After four days of recovery, they were confirmed to be panic-prone to lactate infusions as indicated by increases in heart rate, blood pressure, respiratory rate and "anxiety" measured in the social interaction test. Next, they were pretreated with either vehicle, LY354740 (0.3 and 0.6 mg/kg) or alprazolam (0.5 and 1.0 mg/kg) and re-challenged with lactate infusions. LY354740 treatment was equally efficacious as alprazolam in preventing lactate-induced panic attacks in this model. These data suggest that LY354740 could be a novel anti-panic drug, as effective as alprazolam in acute treatment.

Allylglycine↗
PubMed1994

Definitions of panic attacks and panic disorder in the DSM-IV: implications for research.

The authors review various definitions of panic and recent conceptual and empirical evidence that led to the revised definitions of panic in the Diagnostic and Statistical Manual of Mental Disorders. Fourth Edition (DSM-IV; American Psychiatric Association, 1994). The DSM-IV definitions of panic are more precise and more empirically based than those contained in the DSM-III-R, but are designed primarily for clinicians rather than researchers. Thus, it is possible that definitions of panic used in research under the DSM-IV system will encompass a heterogeneous mix of emotional phenomena. Recommendations on essential components of a conservative definition of panic are proposed for research purposes. Implications of this definition for limited symptom attacks and "non-fearful" panic are elaborated and related to final definitions of panic attacks and panic disorder in the DSM-IV.

Electromyography↗
PubMed1985

The epidemiology of panic attacks and panic disorder. Results of three community surveys.

The authors report findings pertaining to panic disorder from the first three sites of the National Institute of Mental Health Epidemiologic Catchment Area Program. Probability samples of about 3,000 persons aged 18 years or older were interviewed in the New Haven, Connecticut area, eastern Baltimore City, Maryland, and the greater St. Louis, Missouri area in 1980-1982. Information on panic attacks and panic disorder was obtained using the Diagnostic Interview Schedule. The prevalence rate of panic attacks in the prior six months was found to be about 3% at each of the sites, while the prevalence of panic disorder varied from 0.6 to 1.0%. Age at onset was found to peak at 15-19 years. Simple panic attacks, severe and recurrent panic attacks, and panic disorder were found to be characterized by similar symptom profiles and age at onset distributions, and to have similar distributions by demographic factors.

Adolescent↗
PubMed2002

Does nocturnal panic represent a more severe form of panic disorder?

Nocturnal panic (NP), or waking from sleep in a state of panic, occurs in 18% to 45% of panic disorder patients. This relatively common phenomenon, however, is not well understood. In this study, the authors tested the hypotheses that NP represents a more severe form of panic disorder or is a manifestation of heightened vulnerability to sleep disturbance. Patients with NP ( = 51) were compared with patients with panic disorder without a history of NP ( = 41) on measures of panic disorder severity, comorbidity, interpersonal functioning, and sleep disturbance. There was no evidence for more severe psychopathology and only weak evidence for more sleep disturbance. Instead, patients with NP showed less agoraphobic avoidance, perhaps suggesting that they are less likely to associate panic with situational factors. The authors conclude that NP may be a specific version of panic disorder characterized by fearful associations with sleep and sleeplike states.

Adult↗
PubMed2005

Panic disorder with and without agoraphobia: comorbidity within a half-year of the onset of panic disorder.

The present study was performed to compare the clinical features of patients with panic disorder with and without agoraphobia. The subjects were 233 outpatients with panic disorder (99 males and 134 females) diagnosed according to DSM-IV criteria. Sixty-three patients met the criteria for panic disorder without agoraphobia, and 170 met the criteria for panic disorder with agoraphobia. Patients with agoraphobia showed a significantly longer duration of panic disorder and higher prevalence of generalized anxiety disorder. However, there were no significant differences in prevalence of major depressive episodes, in current severity of panic attacks, or in gender ratio between the two groups. The second aim of the present study was to investigate the effects of onset age and sex differences on the development of agoraphobia within a half-year. The subjects were divided into two groups according to their self-report: patients who did or did not develop agoraphobia within 24 weeks of onset of panic disorder. A total of 40.6% of the patients developed agoraphobia within 24 weeks of the onset of panic disorder, and onset age and sex differences had no robust effect on the development of agoraphobia within 24 weeks.

Adult↗
PubMed1997

Long-term evaluation of paroxetine, clomipramine and placebo in panic disorder. Collaborative Paroxetine Panic Study Investigators.

Paroxetine has been shown to be effective in panic disorder in three 10- to 12-week studies. This trial studied the longer term effects of paroxetine in patients with DSM-III-R defined panic disorder. Patients who satisfactorily completed a 12-week, double-blind, placebo-controlled study of paroxetine and clomipramine could choose to continue receiving their randomized treatment for a further 36 weeks. Efficacy assessments included the daily panic attack diary, the Clinical Global Impression Scale, the Hamilton Anxiety Rating Scale, the Marks Sheehan Phobia Scale and the Sheehan Disability Scale. In total, 176 patients were included in the intention-to-treat population. The number of full panic attacks decreased in all three groups during the 12-week study, and improvements continued with long-term therapy. Paroxetine was statistically significantly more effective than placebo throughout the long-term study with respect to reduction from baseline of full panic attacks, and at the end of treatment with respect to the proportion of patients who eventually experienced no panic attacks. There were no significant differences between paroxetine and clomipramine. The proportion of patients who withdrew from the study due to adverse effects was greater in the clomipramine group (19%) than in either the paroxetine group (7%) or the placebo group (9%). Paroxetine was significantly more effective than placebo and as effective as (but better tolerated than) clomipramine in the long-term treatment of panic disorder. Not only was efficacy maintained, but continued improvement was also seen, indicating the importance of long-term treatment in patients with panic disorder.

Adolescent↗
PubMed2004

Psychopathological description of hyperventilation-induced panic attacks: a comparison with spontaneous panic attacks.

Our aim was to describe the clinical features of hyperventilation-induced panic attacks (HPA) in panic disorder patients - DSM-IV - and to compare them with their spontaneous panic attacks and with spontaneous panic attacks in panic disorder (PD) patients not sensible to the hyperventilation challenge test. We reexamined 88 previously studied PD patients when they were submitted to a hyperventilation challenge test. They were induced to hyperventilate (30 breaths/min) for 4 min and anxiety scales were applied before and after the test. A total of 51.1% (n = 45) PD patients had a panic attack after hyperventilating - HPA (chi(2) = 13.11, d.f. = 1, p = 0.017). The clinical symptoms of the most severe panic attack were recorded by the HPA patient and by the PD patients not sensible to this test (non-HPA; n = 43, 48.9%) in a diary during a 1-week period and then compared. The HPA group had more respiratory symptoms (chi(2) = 15.26, d.f. = 1, p < 0.001), fulfilling the criteria for the respiratory PD subtype (75.6%), the disorder started later (Mann-Whitney, p < 0.001), had a higher familial prevalence of PD (chi(2) = 19.45, d.f. = 1, p = 0.036), and had more previous depressive episodes (chi(2) = 18.74, d.f. = 1, p < 0.001). The HPA group had similar symptomatology in spontaneous attacks and HPA. The HPA group may be regarded as a subgroup of the respiratory panic disorder subtype with diagnostic and therapeutic implications.

Adult↗
PubMed1992

Evidence for hypothalamo-growth hormone dysfunction in panic disorder: profile of growth hormone (GH) responses to clonidine, yohimbine, caffeine, glucose, GRF and TRH in panic disorder patients versus healthy volunteers.

Given the abrupt and time-limited nature of daytime-awake and nocturnal-sleep panic attacks, several chemical and neuroendocrine challenge tests have been employed to investigate the neurobiology of "spontaneous" panic attacks. Previously we demonstrated that panic disorder patients have blunted growth hormone (GH) responses to clonidine, an alpha 2-adrenergic agonist. However, the mechanism of this blunted response and the role of hypothalamic-GH dysfunction, if any, remains unclear. To further delineate the status of hypothalamic-GH function in panic disorder, we review the literature and present original data on the GH responses to a number of different chemical and neuroendocrine challenge paradigms. Although stress-mediated increases in GH are thought to be a common correlate of stress in humans, our findings indicate that panic disorder patients have significantly blunted GH responses to clonidine, yohimbine, growth-hormone releasing factor, and caffeine compared to normal control subjects. A similar trend was noted in the delayed rise in GH after glucose challenge. There was no difference in the rate of abnormal GH responses to thyrotropin-releasing hormone in panic disorder compared to normal control subjects. No drug or neuroendocrine challenge, even if associated with marked increases in anxiety, produced a significantly enhanced GH response compared to normal control subjects. These findings provide support for a hyporesponsive hypothalamic-GH system in panic disorder. These observations, combined with preliminary observations from our clinic of short stature in several cases of prepubescent children with anxiety disorders, also underscore the need for assessing early growth patterns in individuals with panic disorder. Strategies for investigating the site(s) of possible neurotransmitter or hypothalamic-GH-somatomedin dysfunction are discussed.

Caffeine↗
PubMed1989

Avoidance behaviour and major depression in panic disorder: a report from the Cross-National Collaborative Panic Study.

Avoidance behaviour and secondary major depression are both frequent in clinical samples of patients with panic disorder. Their status is unclear: indicators of severity of panic disorder or indicators of separate psychiatric disorders. Among the data of the Cross-National Collaborative Panic Study (n = 1,168) we found that especially avoidance behaviour defines more severe states of panic disorder (earlier age at onset, higher frequency of panic attacks and higher level of psychopathology); co-occurrence of major depression is less clearly associated with more severe panic disorder. The results are compatible with the DSM-III-R concepts of comorbidity of panic disorder and major depression and of subtyping panic disorder by avoidance behaviour.

Adult↗
PubMed2006

35% Carbon dioxide and breath-holding challenge tests in panic disorder: a comparison with spontaneous panic attacks.

Respiration and its control mechanisms may represent an important system involved in abnormal anxiety. Our aim was to compare the demographic and clinical features of patients with panic disorder (PD) with agoraphobia (DSM-IV) who had a panic attack after both the 35% carbon dioxide (CO(2)) test and the breath-holding test (CPA group), and compare them with PD patients who did not have a panic attack after both tests (NPA group). We examined 76 patients with PD who were administered a 35% CO(2)test and a breath-holding test within a 1-week interval. Anxiety scales were applied before and after each test. A panic attack was induced in 50 (65.8%) patients during the CO(2)test (chi(2) = 28.44, df = 1, P<.001) and in 40 (52.6%) patients during the breath-holding test (chi(2) = 15.35, df = 1, P = .036). All patients who had a panic attack during the breath-holding test also had a panic attack during the CO(2)test (n = 40; CPA group). Twenty-six (34.2%) patients with PD did not have a panic attack after both respiratory tests (NPA group). The CPA group had more (chi(2) = 21.67, df = 1, P = .011) respiratory PD subtype. In the CPA group, the disorder started earlier (Mann-Whitney, P<.001), had a higher familial prevalence of PD (chi(2) = 18.34, df = 1, P = .028), and had more previous depressive episodes (chi(2) = 23.59, df = 1, P<.001). Our data suggest that there is an association between respiratory PD subtype and the response to respiratory challenge tests: CO(2)and breath-holding. The CPA may be confirmed as a subgroup of respiratory PD subtype.

Adolescent↗
PubMed1996

The panic-inducing properties of the cholecystokinin tetrapeptide CCK4 in patients with panic disorder.

We studied the effect of the cholecystokinin tetrapeptide (CCK4), a potent CCKB antagonist, in patients with panic disorder. Two different dosages (25 and 50 micrograms) of CCK4 and saline were tested in 12 patients who were randomly allocated to 2 of the 3 possible treatment groups. Patients were tested on 2 separate occasions, 1 week apart, using an unbalanced single-blind incomplete block design. A total of 24 intravenous injections were carried out. The panic rate with 25 micrograms CCK was 44% (4/9) and 71% (5/7) with 50 micrograms. None of the patients panicked with saline (0/8). Patients' symptom responses were very similar to their spontaneous panic attacks. Taking the Panic Symptom Scale (PSS) as outcome variable, we found that CCK4 provoked symptoms of panic in a dose-dependent fashion. The behavioral response to CCK4 was not accompanied by activation of the hypothalamic-pituitary-adrenal (HPA) axis as measured by the prolactin and cortisol responses. Moreover, CCK4-induced panic symptoms were not correlated with plasma increases in the principal noradrenergic metabolite, 3-methoxy-4-hydroxy-phenylglycol (MHPG), suggesting that activation of the locus coeruleus may not be critical for CCK4-induced panic.

Adult↗