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Biomedical subjects

D F Klein

Publications and source records attributed to D F Klein.

At least 199 records · Page 11Linked to original sources
PubMed1987

Pituitary adrenocortical unresponsiveness in lactate-induced panic.

The hypothalamic-pituitary adrenal (HPA) axis responds to a variety of physical and emotional stimuli with increased output of adrenocorticotropic hormone (ACTH) and cortisol, yet there is little known about the activity of this system during episodes of severe anxiety in patients with DSM-III-defined anxiety disorders. To explore further whether alterations of the HPA axis occur during various anxiety states, we measured ACTH and cortisol during lactate infusion in patients with panic disorder and agoraphobia. In eight patients who panicked during lactate infusion, there were no elevations in either ACTH or cortisol. Further, the patterns of hormone secretion did not differ among patients who panicked, nonpanicking patients, or controls. This negative result suggests that the neurobiological mechanisms that mediate panic differ from those responsible for other fear responses.

Adolescent↗
PubMed1987

An objective marker of lactate-induced panic.

There are a number of agents claimed effective in provoking panic attacks in the laboratory. For each case, however, the determination of whether an attack has occurred is largely subjective. An objective index of panic would be of great benefit in standardizing laboratory provocation studies. Using heart rate (HR) recordings during sodium lactate infusion, we developed a formula--the heart rate index (HRI)--which appears to correlate well with the subjective experience of panic. Of note is the fact that the HRI was most powerful in identifying attacks that occurred in the first 15 min of the 20-min infusions. In an accompanying study, we examined HR variability during the infusions using the successive difference mean square statistic. HR variability did not change during lactate-induced panic attacks. Therefore, tachycardia during lactate-induced panic probably does not result from decreased vagal tone to the heart.

Adult↗
PubMed1987

A model of panic and agoraphobic development.

A model for the development of agoraphobia with panic attacks is proposed. The initiating clinical manifestation is the sudden appearance of spontaneous panic. The inter-panic chronic anxiety may have several components: i.e. conditioning, increasing autonomic distress, and sensitization to the panic leading to avoidance. The illness course is quite variable but usually chronic. The spontaneous panic is blocked by imipramine with primary pharmacological anti-panic effects. However, no direct effect of imipramine upon either anticipatory anxiety or avoidance behaviour is hypothesized. Among the psychotherapies, direct in vivo exposure mobilizes the patient more rapidly than office based therapy. Our data are consonant with the theory that the avoidances of agoraphobia are secondary to spontaneous panic attacks, and that the primary benefits of imipramine and exposure therapy are in their respective effects on panic and avoidance. Moreover, laboratory challenge studies, brain imaging studies, and genetic studies all point to a biological diathesis for panic disorder.

Agoraphobia↗
PubMed1987

Idiopathic cardiomyopathy and panic disorder: clinical association in cardiac transplant candidates.

Patients under evaluation for cardiac transplant surgery were seen for routine psychiatric diagnosis and treatment. Of 35 patients with idiopathic cardiomyopathy, 83% (N = 29) had definite or probable panic disorder. Of 25 patients with postinfarction cardiac failure, rheumatic heart disease, or congenital heart disease, only 16% (N = 4) had definite or probable panic disorder. The authors suggest that autonomic mechanisms may underlie the association of cardiomyopathy and panic disorder and that increased cardiac sympathetic tone or circulating catecholamines may cause myocarditis and cardiomyopathy.

Adult↗
PubMed1987

Discontinuation of alprazolam treatment in panic patients.

Alprazolam treatment was tapered in 17 panic patients at a rate of 10% of the starting dose every 3 days. Only four subjects completed withdrawal on schedule (4-5 weeks); four additional subjects discontinued treatment in 7-13 weeks. During withdrawal 15 patients had recurrent or increased panic attacks and nine had significant new withdrawal symptoms. Most common among the latter were malaise, weakness, insomnia, tachycardia, lightheadedness, and dizziness. None had seizures, psychosis, or significant neurological or EEG abnormalities. Results indicate that relapse and withdrawal are important considerations in the choice of alprazolam treatment for panic attacks.

Acute Disease↗
PubMed1987

CO2 challenge of patients with panic disorder.

In an open trial, five of eight panic disorder patients and none of five control subjects panicked after inhalation of two breaths of 35% CO2 and 65% O2; none panicked after placebo. Using 35% CO2 to induce panic is safe, simple, and well tolerated and may provide a valuable laboratory model of panic.

Administration, Inhalation↗
PubMed1987

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.

Adult↗
PubMed1986

Blood gas changes and hypophosphatemia in lactate-induced panic.

Alkalosis is prominent among the many physiologic and biochemical effects of sodium lactate infusion. Though this is partially due to the conversion of lactate to bicarbonate, the metabolic component, it may also be secondary to hyperventilation before and during the infusion, the respiratory component. We analyzed pH, carbon dioxide pressure, bicarbonate, and inorganic phosphate from patients with panic disorder and agoraphobia with panic attacks and from normal controls both before and during lactate infusion. Our findings extend earlier work demonstrating that many such patients are chronic hyperventilators. Both metabolic and respiratory alkalosis develop in all subjects during lactate infusion, but only hyperventilation-induced hypocapnia differentiates patients at the point of lactate-induced panic from nonpanicking patients and normal controls. Finally, low inorganic phosphate levels at baseline appear associated with patients who will panic during the subsequent lactate infusion. This last unexpected finding may reflect hyperventilation or an abnormality in intracellular glycolysis.

Adult↗
PubMed1986

Schedule for Affective Disorders and Schizophrenia--Lifetime Version modified for the study of anxiety disorders (SADS-LA): rationale and conceptual development.

The SADS-LA, a modification of the Lifetime Version of the Schedule for Affective Disorders and Schizophrenia, was designed specifically for studies requiring detailed lifetime information on anxiety disorders, symptoms and traits. This article focuses on current difficulties in assessing and conceptualizing anxiety disorders, as addressed in the SADS-LA. The following topics are discussed: conceptual differentiation of certain anxiety disorders; sub-threshold symptoms and syndromes; the relationship between affective and anxiety syndromes; the residual category, Generalized Anxiety Disorder. We emphasize a lifetime sequential approach to diagnostic assessment for a comprehensive understanding of the interrelationships between mental disorders.

Agoraphobia↗
PubMed1986

How blind is blind? Assessment of patient and doctor medication guesses in a placebo-controlled trial of imipramine and phenelzine.

The purpose of the double blind is to protect the internal validity of a clinical trial by preventing knowledge of treatment conditions from influencing outcome or its assessment. We studied medication guesses of 137 depressed patients and/or their doctors at the end of a 6-week randomized trial of placebo, imipramine, and phenelzine. Overall, 78% of the patients and 87% of the doctors correctly distinguished between placebo and active medication. Clinical outcome, treatment condition, and their interaction each contributed to guessing accuracy, while medication experience and side effects assessed only in week 6 did not. Accuracy was high, however, even when cases were stratified for clinical outcome, indicating that other cues were available to the patients and doctors. These may include patterns and timing of side effects and clinical response not detectable in this end-point analysis.

Adolescent↗
PubMed1986

Possible mechanisms for lactate's induction of panic.

Forty-three patients with panic disorder or agoraphobia with panic attacks and 20 control subjects received 0.5 M racemic sodium lactate intravenous infusions, single-blind as to duration and sequence. During the procedure, pulse; blood pressure; blood L-lactate and pyruvate; plasma ionized calcium, phosphate, prolactin, epinephrine, norepinephrine, and cortisol levels; and venous PCO2, pH, and bicarbonate were measured in an attempt to clarify the mechanism of lactate-induced panic attacks. During the infusion, 72% of the patients but none of the control subjects had panic attacks. The laboratory findings suggest that peripheral catecholamine surge is not the mechanism by which lactate causes panic, although elevated epinephrine may be a predisposing factor. Heightened central noradrenergic activity was present in many but not all of the attacks. Contrary to previous hypotheses, neither depression of ionized calcium nor induction of metabolic alkalosis appears sufficient to cause panic during lactate infusion.

Agoraphobia↗
PubMed1986

Agitated depression, alprazolam, and panic anxiety.

Three patients with agitated depression showed rapid and persistent response to alprazolam. At least two of the patients had prior panic disorder. Several lines of evidence suggest that agitated depression may sometimes be caused by unremitting panic anxiety.

Adult↗
PubMed1986

Alprazolam in the treatment of panic disorders.

An open clinical trial of alprazolam therapy of patients with panic disorder or agoraphobia with panic attacks was undertaken to clarify certain issues not resolved by previous studies. These included the proportion of patients who significantly improve with alprazolam; the relative time courses for improvement in panic attacks, anticipatory anxiety, and phobic avoidance; whether successful alprazolam treatment alters vulnerability to panic with sodium lactate infusion; and what factors predict response to alprazolam in panic patients. Thirty patients meeting DSM-III criteria for panic disorder or agoraphobia with panic attacks completed a 12-week open clinical trial, and 22 were considered responders. In responders, panic attacks showed rapid improvement, whereas improvement of anticipatory anxiety and phobic avoidance was more variable. Successful alprazolam therapy appeared to block lactate vulnerability. High pretreatment Hamilton Anxiety Scale scores were associated with poor treatment response. The data suggest that alprazolam is an effective treatment for panic disorder and agoraphobia with panic attacks, and acts by directly blocking panic attacks.

Adult↗