Liaison psychiatry and HIV infection (II): Application of relaxation in HIV positive patients

Abstract We examined the efficacy of relaxation techniques in a sample of HIV patients without AIDS in the early stages after infection, by comparing the three groups: relaxation group (progressive muscle relaxation and modified autogenic training); ordinary supportive psychotherapy group, and finally no psychiatric treatment group. Scores for anxiety, fatigue, depression and confusion , as measured by the profile of mood states (POMS), were significantly lower after relaxation than before. There were no significant differences in the POMS scores (except for anger ) among the three groups. These two results suggest that a combination of progressive muscle relaxation and modified autogenic training is a useful method, which can be easily employed in HIV patients without AIDS.     

Respiratory control as a treatment for panic attacks

Eighteen patients who experienced frequent panic attacks were given a treatment derived from the literature on hyperventilation and anxiety. The treatment consisted of (i) brief, voluntary hyperventilation. This was intended to induce a mild panic attack; (ii) explanation of the effects of overbreathing and reattribution of the cause of a patient's attacks to hyperventilation; (iii) training in a respiratory control technique. Substantial reductions in panic attack frequency and in self-reported fear during a behaviour test were obtained after 2 weeks' treatment and these reductions occurred in the absence of exposure to feared situations. Further reductions in panic attack frequency were evident at 6-month and 2-year follow-up though interpretation of these results is complicated by the addition of exposure and other psychological treatments.     

Hyperventilation-induced panic attacks in panic disorder with agoraphobia

Eight minutes of hyperventilation to an end-tidal PCO2 of less than 20 mmHg led to a panic attack in 7 of 12 patients with panic disorder with agoraphobia and only 1 of 12 normal controls. Patients experienced greater increases in panic symptoms than controls during hyperventilation. Patients who reported more distress from somatic symptoms of hyperventilation during the preceding week were more likely to panic during hyperventilation. Patients who panicked during hyperventilation exhibited a delayed recovery of normocapnia following hyperventilation. Hyperventilation by this protocol is an effective means of inducing panic attacks in the laboratory. A hyperventilation challenge may identify a subgroup of patients for whom hyperventilation symptoms are frequently associated with panic.     

Panic attacks during relaxation and relaxation-induced anxiety: a hyperventilation interpretation

This paper explains how a hyperventilation theory of panic disorder accounts for panic attacks during relaxation and relaxation-induced anxiety. The explanation is based on the observation that chronic hyperventilators maintain a steady state of low pCO2 (arterial carbon dioxide tension) and are, therefore, sensitive to relatively small increases in ventilation when metabolism is low and to relatively sudden reductions in metabolism when ventilation is relatively constant. Thus, if minute volume of air breathed remains constant while the metabolic production of CO2 decreases, as in the case of one who sits down or lies down to relax, respiratory hypocapnea may increase in intensity until it produces the familiar sensations which mark the panic attack. Data from relevant studies of panic attacks during relaxation support the hyperventilation interpretation.     

Lactate provocation of panic attacks. II. Biochemical and physiological findings

Thirty-one of 43 patients with panic disorder or agoraphobia with panic attacks and none of 20 normal controls panicked in response to infusions of sodium lactate. Before receiving lactate, patients showed higher heart rates than controls and also signs of hyperventilation. During lactate infusion, patients who did not panic, nevertheless, developed higher lactate and pyruvate levels and greater ionized calcium and pH changes than controls. Lactate-induced panic attacks were regularly accompanied by biological changes consistent with hyperventilation and central noradrenergic activation and irregularly by elevation of plasma norepinephrine and cortisol levels. Panic attacks were not associated with changes in epinephrine or calcium levels or pH. Baseline arousal increased the likelihood of panic during lactate infusion. It is hypothesized that lactate-induced panic primarily involves central noradrenergic discharge with inconsistent peripheral manifestations.     

Experimental pathophysiology of panic

In this article, we review how the knowledge of the pathophysiology of panic disorder has expanded, with special emphasis on laboratory models using lactate and carbon dioxide challenges. Experiments in the late 1960s revealed that lactate infusion can induce panic attacks. A prominent feature of these attacks is hyperventilation. Because lactate infusion induces a metabolic alkalosis, one would rather expect a compensatory hypoventilation. For years hyperventilation was thought to be causally linked to panic, but it has since been proven to be a symptom rather than a cause of panic attacks. Similarly, it is not hypocapnia but hypercapnia that has proven to be capable of provoking panic attacks. Carbon dioxide challenges are comparable to lactate infusion in the degree to which they meet the criteria for an ideal model of panic disorder. Experiments with carbon dioxide in first-degree relatives of panic disorder patients and in monozygotic twins support the idea of a constitutional predisposition to panic disorder. Of the various other agents that have been used to trigger panic attacks, cholecystokinin seems particularly promising as a valid laboratory model of panic disorder and may provide valuable data regarding the mechanism of panic attacks. The false suffocation alarm theory, proposed by Klein, is an integrative hypothesis that may account for a large number of the laboratory as well as clinical observations.     

Reactivity to interoceptive cues in nocturnal panic

In this study, patients with panic disorder (PD) who suffered nocturnal panic (NP) attacks were compared with PD patients who never experienced NP attacks and healthy controls. Three tasks were chosen to evaluate attention to cardiac cues, reactivity to induction of respiratory cues, and reactivity to relaxation cues. Relative to healthy controls, PD groups reported more fear of all three tasks and showed more physiological arousal in response to the hyperventilation task. The only task on which the two PD groups differed was the relaxation task, where nocturnal panickers were significantly more distressed. These findings are consistent with the notion that nocturnal panickers are fearful of states involving a diminution of conscious awareness or vigilance.     

Panic disorder and hyperventilation

Respiratory abnormalities are associated with anxiety, particularly with panic attacks. Symptoms such as shortness of breath, "empty-head" feeling, dizziness, paresthesias and tachypnea have been described in the psychiatric and respiratory physiology related to panic disorder. Panic disorder patients exhibit both behaviorally and physiologically abnormal responses to respiratory challenges tests. OBJECTIVE: We aim to observe the induction of panic attacks by hyperventilation in a group of panic disorder patients (DSM-IV). METHOD: 13 panic disorder patients and 11 normal volunteers were randomly selected. They were drug free for a week. They were induced to hyperventilate (30 breaths/min) for 3 minutes. Anxiety scales were taken before and after the test. RESULTS: 9 (69.2%) panic disorder patients and one (9.1%) of control subjects had a panic attack after hyperventilating (p < 0.05). CONCLUSION: The panic disorder group was more sensitive to hyperventilation than normal volunteers. The induction of panic attacks by voluntary hyperventilation may be a useful and simple test for validating the diagnosis in some specific panic disorder patients.     

Exogenous factors in panic disorder: clinical and research implications

Because panic disorder has an underlying biologic and probably genetic basis, the role of factors outside the organism in initiating and sustaining panic is often overlooked. The authors review certain exogenous factors that seem capable of triggering attacks and/or increasing their frequency and intensity: self-administered pharmacologic agents (caffeine, alcohol, nicotine, over-the-counter cold preparations, cannabis, cocaine); habits (sleep deprivation, diet, exercise, relaxation, hyperventilation); and aspects of the environment (fluorescent lighting, life stressors). There may be a specificity to the action of some of these factors, because certain factors previously thought to trigger panic attacks (e.g., pain, hypoglycemia) have been proved not to have this effect. Although the clinical significance of many of the exogenous factors discussed still awaits empirical confirmation, attention to such factors during the initial evaluation of a patient with panic disorder may be helpful in formulating a successful treatment plan.     

Hyperventilation and panic attacks

The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviews the role of hyperventilation and abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paCO2 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a need to integrate cognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiological factors, the applicability of hyperventilation in the aetiology and treatment of panic attacks remains in question.     

Emotional responding to hyperventilation as a predictor of agoraphobia status among individuals suffering from panic disorder

Some data suggest that panic patients with extensive agoraphobia (PDA) display more intense respiratory distress during their panic attacks than Panic disorder (PD) patients. However, no studies have determined if PDA patients also show heightened sensitivity to a respiratory challenge compared to PD patients. The current study examined the differential emotional responding to hyperventilation among PDA patients, PD patients, and a non-clinical group with a history of panic attacks. Response to hyperventilation challenge did not distinguish non-clinical panickers from panic patients; however, behavioral tolerance to hyperventilation challenge significantly predicted agoraphobia status among panic disorder patients, even after controlling for demographic and clinical status variables.     

Panic attacks during sleep: a hyperventilation-probability model

Panic attacks during sleep are analysed in terms of a hyperventilation theory of panic disorder. The theory assumes that panic attacks during sleep are a manifestation of severe chronic hyperventilation, a dysfunctional state in which renal compensation has led to a relatively steady state of diminished bicarbonate. Reductions in respiration during deep non-REM sleep lead to respiratory acidosis which triggers hyperventilatory hypocapnea and subsequent panic. A probability model designed to predict when during sleep panic attacks are likely to occur is supported by relevant data from studies of sleep and panic attacks. Implications for treatment are discussed.     

Hyperventilation in panic disorder and social phobia

The aim of our study was to observe the induction of panic attacks by hyperventilation in a group of panic disorder and social phobia patients (DSM-IV). We randomly selected 26 panic disorder patients, 22 social phobics and 25 normal volunteers. They were drug-free for 1 week. Hyperventilation (30 breaths/min) was induced for 3 min. Anxiety scales were taken before and after the test. 61.5% (n = 16) of panic disorder patients, 22.7% (n = 5) of social phobics and 4.0% (n = 1) of control subjects had a panic attack after hyperventilating (p < 0.01, panic disorder vs. control; p < 0.05, panic disorder vs. social phobia; p = n.s., social phobia vs. control). Both anxiety disorder groups were more sensitive to hyperventilation than normal volunteers. The induction of panic attacks by voluntary hyperventilation may be an easy and useful test for validating the diagnosis in some specific panic disorder patients.     

Hyperventilation challenge test in panic disorder and depression with panic attacks.

Our aim was to determine whether panic disorder (PD) patients, major depressive patients without panic attacks (MD) and major depressive patients with panic attacks (MDP) respond similarly to hyperventilation challenge tests. We randomly selected 35 PD patients, 33 MDP patients, 27 MD patients and 30 normal volunteers with no family history of anxiety or mood disorder. The patients had not been treated with psychotropic drugs for at least 1 week. They were induced to hyperventilate (30 breaths/min) for 4 min, and anxiety was assessed before and after the test. A total of 16 (45.7%) PD patients, 12 (36.4%) MDP patients, four (11.1%) MD patients, and two (6.7%) normal volunteers had a panic attack after hyperventilating. The PD and MDP patients were significantly more responsive to hyperventilation than the MD patients and the normal volunteers. The MD patients had a significantly lower heart-rate response to the test than all the other groups. There is growing evidence that PD patients are more sensitive to the vasoconstrictive effects on basilar arterial blood flow caused by hyperventilation-induced hypocapnia than are comparison subjects. Our data suggest that there is an association between panic attacks and hyperreactivity to an acute hyperventilation challenge test.     

Panic disorder and agoraphobia: Fear of fear or fear of the symptoms produced by hyperventilation?

Two versions of the fear-of-fear hypothesis of panic disorder are discussed. The fear-of-fear-somatic-effects-of-fear version, which is distinguished from the classical conditioning version, is compared with the hyperventilation theory of panic disorder and agoraphobia. The fear-of-the-somatic-effects-of-fear hypothesis is criticized on the basis of its inability to explain adequately (a) the initiation of panic attacks, (b) the growth in intensity of panic attacks, and (c) the termination of panic attacks. The tenability of the hyperventilation theory is supported by evidence from programs of treatment derived from the basic assumptions of the theory.     

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.     

Frequency of panic as an outcome measure in agoraphobia research: Latent effects of exposure on panic

The frequency of panic attacks during treatment of patients with panic disorder and agoraphobia was studied with an event sampling method. Treatment comprised panic management techniques followed by exposure in vivo. Results revealed that the frequency of panic attacks varied considerably across patients. There was a group of patients that responded to treatment with a decrease in both panic attacks and avoidance. Another group of patients, however, experienced little panic in the initial phase of treatment, but during the exposure phase they evidenced an increase in the frequency of panic attacks along with a decrease in avoidance. Consequently, merely focusing on panic frequency could lead to considering some patients as treatment failures, while in fact they did respond to the treatment. Recommendations for the use of panic attack frequency as an outcome measure in the evaluation of treatment for panic disorder with agoraphobia are discussed.     

Normalization of venous pH, pCO2, and bicarbonate levels after blockade of panic attacks

Recent evidence suggests that hyperventilation may be associated with spontaneous panic attacks in patients with panic disorder. This is reflected in abnormal patterns of blood gas and blood pH levels in these patients. In this study, absolute levels and variances of pH, pCO2, and bicarbonate were compared between controlled patients before and after successful pharmacological treatment. The results indicate that successful treatment of panic disorder results in a normalization of pH, pCO2, and bicarbonate levels.     

Atypical panic attacks and lack of resolution of mourning

A number of psychologic and biologic contributors to panic disorder have been identified. Three cases of young adult women who experienced atypical panic attacks are described. The attacks are atypical because they had ideational or situational precipitants and because they were inevitably accompanied by intrusive visual images of a deceased loved one. In each case, there was also the persistence of irrational beliefs and/or unintegrated feelings about the deceased, corroborating that the intrusive images and panic attacks occurred in the context of unresolved mourning. Although the association between panic attacks and intrusive images apparently has not been reported previously, both phenomena have been associated with lack of resolution of mourning. The discussion considers similarities in these cases and in reports of Vietnam veterans suffering from posttraumatic stress disorder and panic attacks. Together, these similarities suggest that unresolved traumas of various kinds may at times contribute to the development of atypical panic attacks accompanied by intrusive visual images.