This article examines the ability of the “Panic Attack–PTSD Model” to predict how panic attacks are generated and how panic attacks worsen posttraumatic stress disorder (PTSD). The article does so by determining the validity of the Panic Attack–PTSD Model in respect to one type of panic attacks among traumatized Cambodian refugees: orthostatic panic (OP) attacks, that is, panic attacks generated by moving from lying or sitting to standing. Among Cambodian refugees attending a psychiatric clinic, we conducted two studies to explore the validity of the Panic Attack–PTSD Model as applied to OP patients, meaning patients with at least one episode of OP in the previous month. In Study 1, the “Panic Attack–PTSD Model” accurately indicated how OP is seemingly generated: among OP patients (N = 58), orthostasis-associated flashbacks and catastrophic cognitions predicted OP severity beyond a measure of anxious–depressive distress (SCL subscales), and OP severity significantly mediated the effect of anxious–depressive distress on CAPS severity. In Study 2, as predicted by the Panic Attack–PTSD Model, OP had a mediational role in respect to the effect of treatment on PTSD severity: among Cambodian refugees with PTSD and comorbid OP who participated in a CBT study (N = 56), improvement in PTSD severity was partially mediated by improvement in OP severity.
stress disorder; posttraumatic; panic disorder; panic attack; flashbacks; catastrophic cognitions; Cambodian refugees; orthostatic intolerance
This study surveys Khmer refugees attending two psychiatric clinics to determine both the prevalence of panic disorder as well as panic attack subtypes in those suffering panic disorder. A culturally valid adaptation of the SCID-panic module, the Cambodian Panic Disorder Survey (CPDS), was administered to 89 consecutive Cambodian refugees attending these psychiatric clinics. Utilizing culturally sensitive panic probes, the CPDS provides information regarding both the presence of panic disorder and panic-attack subtypes during the month prior to interview. Of 89 patients surveyed at two psychiatric clinics, 53 (60%) currently suffered panic disorder. Among the 53 patients suffering panic disorder, the most common panic attack subtypes during the previous month were the following: “sore neck” [51% of the 53 panic disorder patients (PDPs)], orthostatic dizziness (49% of PDPs), gastro-intestinal distress (26% of PDPs), effort induced (21% of PDPs), olfactory induced (21% of PDPs), and “while-sitting dizziness” (16% of PDPs).
Because a large proportion of patients with panic attacks receiving approved pharmacotherapy do not respond or respond poorly to medication, it is important to identify additional therapeutic strategies for the management of panic symptoms. This article describes a randomized, rater-blind study comparing low-dose risperidone to standard-of-care paroxetine for the treatment of panic attacks.
Fifty six subjects with a history of panic attacks were randomized to receive either risperidone or paroxetine. The subjects were then followed for eight weeks. Outcome measures included the Panic Disorder Severity Scale (PDSS), the Hamilton Anxiety Scale (Ham-A), the Hamilton Depression Rating Scale (Ham-D), the Sheehan Panic Anxiety Scale-Patient (SPAS-P), and the Clinical Global Impression scale (CGI).
All subjects demonstrated a reduction in both the frequency and severity of panic attacks regardless of treatment received. Statistically significant improvements in rating scale scores for both groups were identified for the PDSS, the Ham-A, the Ham-D, and the CGI. There was no difference between treatment groups in the improvement in scores on the measures PDSS, Ham-A, Ham-D, and CGI. Post hoc tests suggest that subjects receiving risperidone may have a quicker clinical response than subjects receiving paroxetine.
We can identify no difference in the efficacy of paroxetine and low-dose risperidone in the treatment of panic attacks. Low-dose risperidone appears to be tolerated equally well as paroxetine. Low-dose risperidone may be an effective treatment for anxiety disorders in which panic attacks are a significant component.
ClinicalTrials.gov Identifier: NCT100457106
Panic attacks are common, and while they are not life-threatening events, they can lead to the development of panic disorder and agoraphobia. Appropriate help at the time that a panic attack occurs may decrease the fear associated with the attack and reduce the risk of developing an anxiety disorder. However, few people have the knowledge and skills required to assist. Simple first aid guidelines may help members of the public to offer help to people who experience panic attacks.
The Delphi method was used to reach consensus in a panel of experts. Experts included 50 professionals and 6 people who had experience of panic attacks and were active in mental health advocacy. Statements about how to assist someone who is having a panic attack were sourced through a systematic search of both professional and lay literature. These statements were rated for importance as first aid guidelines by the expert and consumer panels and guidelines were written using the items most consistently endorsed.
Of 144 statements presented to the panels, 27 were accepted. These statements were used to develop the guidelines appended to this paper.
There are a number of actions which are considered to be useful for members of the public to do if they encounter someone who is having a panic attack. These guidelines will be useful in revision of curricula of mental health first aid programs. They can also be used by members of the public who want immediate information about how to assist someone who is experiencing panic attacks.
Panic disorder is a severe anxiety disorder with recurrent, debilitating panic attacks. In subjects with panic disorder there is evidence of decreased central GABAergic activity as well as marked increases in autonomic and respiratory responses following intravenous infusions of 0.5M sodium lactate1–3. In an animal model of panic disorder, chronic inhibition of GABA synthesis in the dorsomedial/perifornical hypothalamus of rats produces anxiety-like states and a similar vulnerability to sodium lactate-induced cardioexcitatory responses4–9. The dorsomedial/perifornical hypothalamus is enriched in orexin (ORX, also known as hypocretin)-containing neurons10 that play a critical role in arousal10,11, vigilance10 and central autonomic mobilization12, all of which are key components of panic. Here, we demonstrate that activation of the ORX neurons is necessary for developing a panic-prone state in the animal model, and either silencing the hypothalamic ORX gene (Hcrt) product with RNA interference or systemic ORX1 antagonists blocks the panic responses. Moreover, we show that subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety. Taken together our results suggest that the ORX system may be involved in the pathophysiology of panic anxiety, and that ORX antagonists constitute a potential novel treatment strategy for panic disorder.
Panic disorder has an elevated prevalence in Parkinson’s disease (PD). To explore the basis for this co-occurrence, the familial aggregation of panic disorder was examined in patients with PD. Probands and relatives of patients with PD and panic disorder (PD-PANIC; N=20, N=115) and control probands with PD and no active psychiatric illness (PD-NA; N=17, N=108) were interviewed by phone, using a structured interview to determine panic status. Lifetime prevalence of panic and “panic-like” disorders was higher in PD-PANIC than in PD-NA relatives. Panic and “panic-like” disorders are familial disorders in PD.
Panic disorder is a severe anxiety disorder characterized by susceptibility to induction of panic attacks by subthreshold interoceptive stimuli such as 0.5 M sodium lactate infusions. Although studied for four decades, the mechanism of lactate sensitivity in panic disorder has not been understood. The dorsomedial hypothalamus/perifornical region (DMH/PeF) coordinates rapid mobilization of behavioral, autonomic, respiratory and endocrine responses to stress, and rats with disrupted GABA inhibition in the DMH/PeF exhibit panic-like responses to lactate, similar to panic disorder patients. Utilizing a variety of anatomical and pharmacological methods, we provide evidence that lactate, via osmosensitive periventricular pathways, activates neurons in the compromised DMH/PeF, which relays this signal to forebrain limbic structures such as the bed nucleus of the stria terminalis to mediate anxiety responses, and specific brainstem sympathetic and parasympathetic pathways to mediate the respiratory and cardiovascular components of the panic-like response. Acutely restoring local GABAergic tone in the DMH/PeF blocked lactate induced panic-like responses. Autonomic panic-like responses appear to be a result of DMH/PeF-mediated mobilization of sympathetic responses (verified with atenolol) and resetting of the parasympathetically-mediated baroreflex. Based on our findings, DMH/PeF efferent targets such as the C1 adrenergic neurons, paraventricular hypothalamus and the central amygdala are implicated in sympathetic mobilization; the nucleus of the solitary tract is implicated in baroreflex resetting; and the parabrachial nucleus is implicated in respiratory responses. These results elucidate neural circuits underlying lactate induced panic-like responses and the involvement of both sympathetic and parasympathetic systems.
panic; c-Fos; hypothalamus; GABA; anxiety; lactate; l-allylglycine
Classical conditioning features prominently in many etiological accounts of panic disorder. According to such accounts, neutral conditioned stimuli present during panic attacks acquire panicogenic properties. Conditioned stimuli triggering panic symptoms are not limited to the original conditioned stimuli but are thought to generalize to stimuli resembling those co-occurring with panic, resulting in the proliferation of panic cues. The authors conducted a laboratory-based assessment of this potential correlate of panic disorder by testing the degree to which panic patients and healthy subjects manifest generalization of conditioned fear.
Nineteen patients with a DSM-IV-TR diagnosis of panic disorder and 19 healthy comparison subjects were recruited for the study. The fear-generalization paradigm consisted of 10 rings of graded size presented on a computer monitor; one extreme size was a conditioned danger cue, the other extreme a conditioned safety cue, and the eight rings of intermediary size created a continuum of similarity from one extreme to the other. Generalization was assessed by conditioned fear potentiating of the startle blink reflex as measured with electromyography (EMG).
Panic patients displayed stronger conditioned generalization than comparison subjects, as reflected by startle EMG. Conditioned fear in panic patients generalized to rings with up to three units of dissimilarity to the conditioned danger cue, whereas generalization in comparison subjects was restricted to rings with only one unit of dissimilarity.
The findings demonstrate a marked proclivity toward fear overgeneralization in panic disorder and provide a methodology for laboratory-based investigations of this central, yet understudied, conditioning correlate of panic. Given the putative molecular basis of fear conditioning, these results may have implications for novel treatments and prevention in panic disorder.
Individuals with anxiety often report greater smoking and drinking behaviors relative to those without a history of anxiety. In particular, smoking and alcohol use have been directly implicated among individuals experiencing panic attacks, diagnosed with panic disorder, or high on panic-relevant risk factors such as anxiety sensitivity. Less is known, however, about specific features of panic that may differentiate among those who do or do not use cigarettes or alcohol. The purpose of the current study was to replicate previous research findings of an association between panic symptomatology, cigarette smoking, and alcohol consumption, as well as extend findings by examining whether specific symptoms of panic attacks differentiated among those who do or do not use cigarettes or alcohol. Participants (n = 489) completed the Panic Attack Questionnaire-IV, a highly detailed assessment of panic attacks and symptoms, as well as self-report measures of smoking history and alcohol use. Consistent with previous research, participants who reported a history of panic attacks (n = 107) were significantly more likely to report current daily or lifetime daily cigarette smoking, and significantly greater hazardous or harmful alcohol use than participants with no panic history (n = 382). Although smoking and hazardous alcohol use were highly associated regardless of panic status, participants with panic attacks showed elevated hazardous alcohol use after controlling for daily or lifetime smoking. Surprisingly, although participants who reported having had at least one panic attack were more likely to smoke, panic attack symptoms, intensity, or frequency did not differentiate panickers who did or did not smoke. Furthermore, panic-related variables were not shown to differentially relate to problematic drinking among panickers. Implications for understanding the complex relationship between panic attacks and smoking and drinking behaviors are discussed.
smoking; alcohol; panic attacks; comorbidity
Comprehensive cognitive behavior therapies have been proved to be more effective than behavioral interventions. However, the efficacy of CBT is not studied in the Indian context and also, the amount of change brought about by CBT is not known. Aims: This study aims to examine the efficacy of cognitive behavioral intervention (CBI) in the treatment of panic disorder. Our specific objectives were to assess the effectiveness of CBI in reducing symptom severity as well as cognitions related to panic and panic-related behaviors. Design: The study adopted a two-group comparison with pre- and postassessments design.
Materials and Methods:
The sample consisted of 30 patients sequentially allotted to the CBI (n = 15) and behavioral intervention (BI, n = 15) groups. Assessment was done using a semistructured interview schedule, panic disorder severity scale, Texas panic attack record form, Anxiety Sensitivity Index, Agoraphobic cognitions questionnaire, Behavioral avoidance checklist, and Panic appraisal inventory. The CBI group was provided with comprehensive cognitive behavior therapy and the BI group with psycho-education and applied relaxation.
CBI was found to be superior to BI in the reduction of panic symptoms, behavioral avoidance, safety behaviors, and cognitions. A large percentage of the CBI group patients met the criteria for clinically significant change with a large magnitude of change.
Multicomponent CBI is superior to BI in terms of the amount of change it brings about with respect to panic symptoms, avoidance, safety behaviors, and cognitions.
Clinically significant change; magnitude of change; multicomponent cognitive behavioral intervention
This study surveys Vietnamese refugees attending two psychiatric clinics to determine both the prevalence of panic disorder (PD) as well as panic attack subtypes in those suffering PD. A culturally valid adaptation of the SCID-panic module (the Vietnamese Panic Disorder Survey or VPDS) was administered to 100 Vietnamese refugees attending two psychiatric clinics. Utilizing culturally sensitive panic probes, the VPDS provides information regarding both the presence of PD and panic attack subtypes during the month prior to interview. Of 100 patients surveyed, 50 (50%) currently suffered PD. Among the 50 patients suffering PD, the most common panic attack subtypes during the previous month were the following: “orthostatic dizziness” (74% of the 50 panic disorder patients [PDPs]), headache (50% of PDPs), wind-induced/temperature-shift-induced (24% of PDPs), effort-induced (18% of PDPs), gastro-intestinal (16% of PDPs), micturition-induced (8% of PDPs), out-of-the-blue palpitations (24% of PDPs), and out-of-the-blue shortness of breath (16% of PDPs). Five mechanisms are adduced to account for this high PD prevalence as well as the specific profile of subtypes: 1) a trauma-caused panic attack diathesis; 2) trauma-event cues; 3) ethnic differences in physiology; 4) catastrophic cognitions generated by cultural syndromes; and 5) a modification of Clark’s spiral of panic.
Vietnamese refugees; Panic disorder; Panic disorder subtypes; Trauma; Catastrophic cognitions
Although there is increasing evidence that panic attacks are common in posttraumatic stress disorder (PTSD), little is known if posttraumatic panic is comparable to panic attacks observed in panic disorder (PD).
This study examined the cognitive responses to panic attacks in participants with PD and PTSD.
Participants with PD (n=22) and PTSD (n=18) were assessed on the Anxiety Disorder Interview Schedule for DSM-IV and subsequently administered the Agoraphobic Cognitions Questionnaire and a measure of fears related to trauma memories.
Although participants did not differ in terms of catastrophic appraisals about somatic sensations, PTSD participants were more likely to experience fears about trauma memories and being harmed by trauma again during their panic attacks than PD participants.
These findings suggest that although PTSD participants fear somatic outcomes during panic attacks, their panic attacks are distinguished by a marked fear of trauma memories.
Panic attack; posttraumatic stress disorder; panic disorder; trauma memories
In cognitive theory it is hypothesized that panic attacks are provoked by catastrophic misinterpretations of bodily sensations. The aim of the present study was to investigate the ability of associated word pairs referring to catastrophic thinking (e.g. palpitations-heart attack) in producing panic attacks. Patients with PD (n = 20), patients with mixed anxiety disorders (n = 20), and a healthy control group (n = 30) participated in the present study. To enhance ecological validity we first conducted a stimulus validation experiment. Subsequently, nine suitable panic and neutral word pairs were presented in block to the participants. Anxiety levels were assessed before and after the presentation. PD patients were more anxious when reading these word pairs, compared to neutral word pairs. However, none of the participants experienced a panic attack upon reading the word pairs. From the present results it seems that catastrophic thinking is rather related to the anticipatory anxiety for panic attacks, but not necessarily with the occurrence of the panic attacks themselves.
Panic is characterized as a disorder of interoceptive physiological hyperarousal, secondary to persistent anticipation of panic attacks. The novel aim of the present research was to investigate whether severity of agoraphobia within panic disorder covaries with the intensity of physiological reactions to imagery of panic attacks and other aversive scenarios.
A community sample of principal panic disorder (n=112; 41 without agoraphobia, 71 with agoraphobia) and control (n=76) participants imagined threatening and neutral events while acoustic startle probes were presented and the eye-blink response (orbicularis oculi) recorded. Changes in heart rate, skin conductance level, and facial expressivity were also measured.
Overall panic disorder patients exceeded controls in startle reflex and heart rate during imagery of standard panic attack scenarios, concordant with more extreme ratings of aversion and emotional arousal. Accounting for the presence of agoraphobia revealed that both panic disorder with and without situational apprehension showed the pronounced heart rate increases during standard panic attack imagery observed for the sample as a whole. In contrast, startle potentiation to aversive imagery was more robust in those without versus with agoraphobia. Reflex diminution was most dramatic in those with the most pervasive agoraphobia, coincident with the most extreme levels of comorbid broad negative affectivity, disorder chronicity, and functional impairment.
Principal panic disorder may represent initial, heightened interoceptive fearfulness and concomitant defensive hyperactivity, which through progressive generalization of anticipatory anxiety, ultimately transitions to a disorder of pervasive agoraphobic apprehension and avoidance, broad dysphoria and compromised mobilization for defensive action.
imagery; anxiety; panic; agoraphobia; comorbidity; depression; anhedonia; anxiety sensitivity; chronicity; emotional reactivity; narrative imagery; diagnostic subtypes; psychophysiology; startle; heart rate; facial expressivity; skin conductance; corrugator; EMG; SCL
Panic disorder is one of the chronic and disabling anxiety disorders. There has been evidence for either genetic heterogeneity or complex inheritance, with environmental factor interactions and multiple single genes, in panic disorder's etiology. Linkage studies have implicated several chromosomal regions, but no research has replicated evidence for major genes involved in panic disorder. Researchers have suggested several neurotransmitter systems are related to panic disorder. However, to date no candidate gene association studies have established specific loci. Recently, researchers have emphasized genome-wide association studies. Results of two genome-wide association studies on panic disorder failed to show significant associations. Evidence exists for differences regarding gender and ethnicity in panic disorder. Increasing evidence suggests genes underlying panic disorder overlap, transcending current diagnostic boundaries. In addition, an anxious temperament and anxiety-related personality traits may represent intermediate phenotypes that predispose to panic disorder. Future research should focus on broad phenotypes, defined by comorbidity or intermediate phenotypes. Genome-wide association studies in large samples, studies of gene-gene and gene-environment interactions, and pharmacogenetic studies are needed.
Panic Disorder; Genetics; Genome-Wide Association Study; Polymorphism
Spontaneous or unexpected panic attacks, per definition, occur out-of-the blue, in absence of cues or triggers. Accordingly, physiological arousal or instability should occur at the onset of or during the attack, but not preceding it. To test this hypothesisweexaminedif points of significant autonomic changes preceded the onset of spontaneous panic attacks.
Forty-three panic disorder patients underwent repeated 24-hour ambulatory monitoring. Thirteen naturally panic attacks were recorded during 1,960 hours of monitoring. Minute-by-minute epochs beginning 60 minutes before, and continuing to 10 minutes after, the onset of individual attacks were examined for respiration, heart rate, and skin conductance level. Measures were controlled for physical activity and vocalization, and compared to time matched control periods within the same person.
Significant patterns of instability across a numberof autonomic and respiratory variables were detected as early as 47 minutes before panic onset. The final minutes prior to onset were dominated by respiratory changes, with significant decreases in tidal volume followed by abrupt PCO2 increases. Panic attack onset was characterized by heart rate and tidal volume increases and a drop in PCO2. Symptom report was consistent with these changes. Skin conductance levels were generally elevated in the hour before and duringthe attacks. Changes in the matched control periods were largely absent.
Significant autonomic irregularities preceded the onset of attacks that were reported as abrupt and unexpected. The findings invite reconsideration of the current diagnostic distinction betweenuncuedand cued panic attacks.
panic attacks; physiology; respiration; ambulatory; autonomic; diagnostic
Two studies examined the contributing factors for panic symptoms following trauma. In Study 1, survivors of sexual and nonsexual assaults (N = 105) were assessed at 2 weeks postcrime. Prior trauma, psychiatric history, crime characteristics, and peritraumatic dissociation were assessed. Posttraumatic panic was modestly predicted by childhood sexual abuse (CSA) experiences, a history of Anxiety and Depression, and peritraumatic dissociation. Childhood physical abuse (CPA), Adult Victimization, crime variables, and a prior history of Substance Use disorders and posttraumatic stress disorder (PTSD) were not implicated. In Study 2, the role of peritraumatic panic in predicting later arousal was also examined in a similar sample who were assessed within 6 weeks of their trauma (N = 93). Presence of significant arousal during trauma predicted frequency of posttrauma panic attacks, but not its severity. In contrast to Study 1, prior history of PTSD, perception of life threat, and the index trauma being a sexual assault all predicted posttrauma panic, whereas prior trauma exposure and depression did not. These findings are discussed in terms of cognitive and arousal factors that may influence posttrauma panic.
Trauma; Panic; PTSD; Assault; Physiological arousal
Panic disorder is a severe anxiety disorder characterized by recurrent panic attacks that can be consistently provoked with intravenous (i.v.) infusions of hypertonic (0.5M) sodium lactate (NaLac), yet the mechanism/CNS site by which this stimulus triggers panic attacks is unclear. Chronic inhibition of GABAergic synthesis in the dorsomedial hypothalamus/perifornical region (DMH/PeF) of rats induces a vulnerability to panic-like responses following i.v. infusion of 0.5 M NaLac providing an animal model of panic disorder. Using this panic model, we previously demonstrated that inhibiting the anterior 3rd ventricle region [A3Vr; containing the organum vasculosum lamina terminalis (OVLT), the median preoptic nucleus (MnPO), and anteroventral periventricular nucleus (AVP)] attenuates cardiorespiratory and behavioral responses elicited by i.v. infusions of NaLac. Here we demonstrate that i.v. infusions of 0.5M NaLac or sodium chloride, but not iso-osmolar D-mannitol, increased “anxiety” (decreased social interaction) behaviors; heart rate; and blood pressure responses. Utilizing whole-cell patch clamp preparations, we also show that bath applications of NaLac (positive control), but not lactic acid (lactate stimulus) or D-mannitol (osmolar stimulus) increases firing rates of neurons in the A3Vr, that are retrogradely labeled from the DMH/PeF; which are most likely glutamatergic based on a separate study using retrograde tracing from the DMH/PeF in combination with in situ hybridization for vesicular glutamate transporter 2. These data demonstrate that hypertonic sodium, but not hyper-osmolarity or changes in lactate, is the key stimulus that provokes panic attacks in panic disorder, and is consistent with human studies (Gorman et al, 1989; Peskind et al, 1998).
sodium lactate; panic; DMH; OVLT; MnPO; osmotic; hypothalamus; anxiety
Panic disorder is a severe anxiety disorder characterized by recurrent panic attacks that can be consistently provoked with intravenous (i.v.) infusions of hypertonic (0.5 M) sodium lactate (NaLac), yet the mechanism/CNS site by which this stimulus triggers panic attacks is unclear. Chronic inhibition of GABAergic synthesis in the dorsomedial hypothalamus/perifornical region (DMH/PeF) of rats induces a vulnerability to panic-like responses after i.v. infusion of 0.5 M NaLac, providing an animal model of panic disorder. Using this panic model, we previously showed that inhibiting the anterior third ventricle region (A3Vr; containing the organum vasculosum lamina terminalis, the median preoptic nucleus, and anteroventral periventricular nucleus) attenuates cardiorespiratory and behavioral responses elicited by i.v. infusions of NaLac. In this study, we show that i.v. infusions of 0.5 M NaLac or sodium chloride, but not iso-osmolar -mannitol, increased ‘anxiety' (decreased social interaction) behaviors, heart rate, and blood pressure responses. Using whole-cell patch-clamp preparations, we also show that bath applications of NaLac (positive control), but not lactic acid (lactate stimulus) or -mannitol (osmolar stimulus), increases the firing rates of neurons in the A3Vr, which are retrogradely labeled from the DMH/PeF and which are most likely glutamatergic based on a separate study using retrograde tracing from the DMH/PeF in combination with in situ hybridization for vesicular glutamate transporter 2. These data show that hypertonic sodium, but not hyper-osmolarity or changes in lactate, is the key stimulus that provokes panic attacks in panic disorder, and is consistent with human studies.
anxiety; hypothalamus; panic; sodium lactate; DMH; OVLT; Mood/Anxiety/Stress Disorders; Psychiatry & Behavioral Sciences; Animal models; Neuroanatomy; panic; hypothalamus; sodium lactate; osmotic; MnPO
BACKGROUND. Increased general practice attendance rates have been associated with the diagnosis of mental illness but panic disorder has not been specifically investigated in this respect. In addition, studies have failed adequately to assess type and frequency of secondary care referral and patterns of psychotropic prescription in patients with panic disorder in relation to matched controls. AIM. This study set out to compare subjects with panic disorder with age and sex matched controls on measures of general practice consultation rate; psychotropic and non-psychotropic drug use; referral to secondary care, laboratory and radiological tests and hospital admissions; history of illness and complaints; and psychiatric comorbidity. METHOD. The study was carried out in nine practices in the Forth Valley area. One hundred patients with panic disorder, previously diagnosed using DSM III-R criteria, were identified and matched by age and sex with controls. Data were collected by review of general practice case notes. RESULTS. Subjects with panic disorder had significantly higher rates of general practice consultation over the 10 year period prior to DSM III-R diagnosis of panic disorder than controls. Subjects with panic disorder had also been prescribed a significantly greater number of psychotropic and non-psychotropic medications over this period, had had more secondary care investigations and had higher rates of mainly minor illness and related complaints than controls. High comorbidity of panic disorder with depression which had been diagnosed over the 10 year period prior to DSM III-R diagnosis of panic disorder was found. CONCLUSION. The results of this study describe a population of subjects with panic disorder who are long-term heavy users of primary care services. The results also suggest an association between panic disorder and both minor illness and psychiatric comorbidity over the 10 year period prior to DSM III-R diagnosis of panic disorder.
OBJECTIVE: To examine the medical services and treatment for anxiety disorders reported by patients who had either panic disorder with agoraphobia or else social phobia. DESIGN: Archival research of consecutive records of psychiatric interviews conducted between January 1990 and December 1991. The records were examined by a trained research assistant who had had no contact with the patients. PATIENTS: One hundred patients who had panic disorder with agoraphobia and twenty-eight patients who had social phobia. SETTING: An anxiety disorders clinic in a university-affiliated psychiatric institute. OUTCOME MEASURES: Variables related to the use of medical services included history of hospitalization, emergency department visits and referrals to specialists. Variables related to treatment included types of medication received, whether behaviour therapy was received and types of health care professionals seen. RESULTS: Almost 30% of the patients with panic disorder and more than 20% of those with social phobia had a history of a major depressive episode at some time in their lives; 30% and 25% respectively had a current nonpsychiatric medical diagnosis. In the past year nearly one-third of both patient groups had seen three or more different health care professionals and almost one-fifth of those with panic disorder had gone to a general hospital emergency department. Of the patients with panic disorder 9% had previously been assessed by a cardiologist and 17% by a neurologist. At least two-thirds of each group had received benzodiazepines, often for use as needed. Although most of the patients in both groups had been seen by mental health professionals such as psychiatrists, few had received optimal treatment. Of those with panic disorder, only 15% had received the tricyclic antidepressant imipramine, 13% alprazolam and 11% cognitive-behavioural therapy. Only 4% of the patients with social phobia had received cognitive-behavioural therapy. CONCLUSIONS: Both groups of patients, and particularly those with panic disorder, are frequent users of medical services. Although most have had contact with mental health professionals, few have received appropriate treatment. Benzodiazepines appear to be overprescribed, whereas forms of treatment that have been shown to reduce the use of medical services, such as cognitive-behavioural therapy, are infrequently given.
Both insufficient sleep and oversleeping have been reported as precipitating and aggravating factors of tension-type headache (TTH). However, previous studies relied on recalled self-reports, and the relationship has not been confirmed prospectively and objectively in a daily life situation. Recently, ecological momentary assessment (EMA) using electronic diaries, i.e., computerized EMA, is used to record subjective symptoms with the advantages of avoiding recall bias and faked compliance in daily settings. In addition, actigraphy has become an established method to assess sleep outside laboratories. Therefore, the aim of this study was to investigate the within-individual effect of sleep on the following momentary headache intensity in TTH patients during their daily lives utilizing EMA and actigraphy.
Twenty-seven patients with TTH wore watch-type computers as electronic diaries for seven consecutive days and recorded their momentary headache intensity using a visual analog scale of 0-100 approximately every six hours, on waking up, when going to bed, and at the time of headache exacerbations. They also recorded their self-report of sleep quality, hours of sleep and number of awakenings with the computers when they woke up. Physical activity was continuously recorded by an actigraph inside the watch-type computers. Activity data were analyzed by Cole's algorithm to obtain total sleep time, sleep efficiency, sleep latency, wake time after sleep onset and number of awakenings for each night. Multilevel modeling was used to test the effect of each subjective and objective sleep-related variable on momentary headache intensity on the following day.
Objectively measured total sleep time was significantly positively associated with momentary headache intensity on the following day, while self-reported sleep quality was significantly negatively associated with momentary headache intensity on the following day.
Using computerized EMA and actigraphy, longer sleep and worse sleep quality were shown to be related to more intense headache intensity on within-individual basis and they may be precipitating or aggravating factors of TTH.
We examined mediational models of panic-fear, panic disorder (PD), and asthma outcomes among adult asthma patients. PD was assessed by the Anxiety Disorders Interview Schedule. Twenty-one asthma-PD patients and 27 asthma-only patients completed spirometry and questionnaires. Asthma-PD patients reported greater illness-specific and generalized panic-fear than asthma-only patients, despite no differences in asthma severity or physical symptoms during asthma attacks. Illness-specific panic-fear mediated the relationship between PD and poorer health-related quality of life, including emotional disturbance due to asthma. Illness-specific panic-fear was associated with more primary care office visits for asthma. Asthma-PD patients reported greater irritability during asthma attacks than asthma-only patients. Generalized panic-fear was directly associated with restriction of activities due to asthma and use of rescue medication for asthma. Neither measure of panic-fear was associated with asthma severity. Panic-fear experienced during asthma attacks may be an important area to target for improving health-related quality of life among asthma-PD patients.
asthma; generalized panic-fear; illness-specific panic-fear; panic disorder; quality of life
Recent evidence suggests that the GABA transporter 1 (GAT-1; SLC6A1) plays a role in the pathophysiology and treatment of anxiety disorders. In order to understand the impact of genetic variation within SLC6A1 on pathological anxiety, we performed a case–control association study with anxiety disorder patients with and without syndromal panic attacks. Using the method of sequential addition of cases, we found that polymorphisms in the 5′ flanking region of SLC6A1 are highly associated with anxiety disorders when considering the severity of syndromal panic attacks as phenotype covariate. Analysing the effect size of the association, we observed a constant increase in the odds ratio for disease susceptibility with an increase in panic severity (OR ~ 2.5 in severely affected patients). Nominally significant association effects were observed considering the entire patient sample. These data indicate a high load of genetic variance within SLC6A1 on pathological anxiety and highlight GAT-1 as a promising target for treatment of anxiety disorders with panic symptoms.
Electronic supplementary material
The online version of this article (doi:10.1007/s00702-008-0075-y) contains supplementary material, which is available to authorized users.
GAT-1; Single nucleotide polymorphisms; Anxiety disorders and panic; Sequential addition of cases; GABA system genetics
The present study is the first to attempt to determine rates of panic attacks, especially ‘somatically focused’ panic attacks, panic disorder, symptoms of post-traumatic stress disorder (PTSD), and depression levels in a population of Rwandans traumatized by the 1994 genocide. The following measures were utilized: the Rwandan Panic-Disorder Survey (RPDS); the Beck Depression Inventory (BDI); the Harvard Trauma Questionnaire (HTQ); and the PTSD Checklist (PCL). Forty of 100 Rwandan widows suffered somatically focused panic attacks during the previous 4 weeks. Thirty-five (87%) of those having panic attacks suffered panic disorder, making the rate of panic disorder for the entire sample 35%. Rwandan widows with panic attacks had greater psychopathology on all measures. Somatically focused panic-attack subtypes seem to constitute a key response to trauma in the Rwandan population. Future studies of traumatized non-Western populations should carefully assess not only somatoform disorder but also somatically focused panic attacks.
Panic disorder; Stress disorders; post-traumatic; Depression; Rwanda; Holocaust