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.     

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.     

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.     

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.     

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.     

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.