Search PubMed⌕ Search

Biomedical subjects

D F Klein

Publications and source records attributed to D F Klein.

At least 91 records · Page 5Linked to original sources

Sodium lactate response and familial risk for panic disorder.

OBJECTIVE: The authors used the family study method to test the hypothesis that sodium lactate response defines two subtypes of panic disorder. METHOD: Rates of panic disorder in 142 first-degree relatives of patients who responded to sodium lactate, 88 first-degree relatives of patients who did not respond to sodium lactate, and 231 first-degree relatives of never mentally ill subjects were compared. RESULTS: No difference in familial transmission of panic disorder was found between the two patient groups. CONCLUSIONS: The findings do not support the notion that panic disorder subtypes are associated with lactate sensitivity.

Biomarkers↗

Testing the suffocation false alarm theory of panic disorder.

The need for hypotheses concerning the nature of those functions that have been impaired in stereotyped psychiatric syndromes is emphasized. With regard to panic disorder, the key role of the spontaneous panic attack became apparent from several viewpoints. However, panics seem to be a type of misreleased fear, which guided the thinking concerning the nature of possible psychological or physiological malfunctions. We indicate that spontaneous panic cannot be fear, but must represent some other malfunction and suggest that the spontaneous panic is a suffocation false alarm. The development of this idea is outlined, and attempts to develop tests of this hypothesis are indicated. In particular, studies of children with congenital central hypoventilation syndrome, patients with Chronic Obstructive Pulmonary Disease, dyspnea, field measures of panic, pregnancy, childbirth and the postpartum period, as well as the premenstrual syndrome afford pointed opportunities, new information and potential tests of the theory. A recent challenge to the theory from acetazolamide infusion is discussed. Developing a possible antecedent for the pathologically depressed threshold for the suffocation alarm, in the form of a phasic endorphinergic deficiency, is presented.

Adult↗

Consistencies between recalled panic and lactate-induced panic.

This study investigated the frequency and severity of symptoms during naturally occurring panic attacks recollected as "usual" and during sodium lactate-induced attacks. Seventy-six male and 126 female patients with panic disorder or agoraphobics with panic attack (DSM-III criteria) underwent lactate infusion studies and were serially administered the Acute Panic Inventory (API). Fifty-nine percent of the subjects were rated by an attending psychiatrist to have experienced lactate-induced panic attacks. Patients were also asked to API symptom rate their "usual" panic attacks. For panic recollected as usual, the most frequently reported symptoms (> or = 75%) at the moderate to severe levels included: afraid in general, difficulty concentrating, difficulty performing a job, desire to flee, afraid of losing control, palpitations, feeling hot or cold or both, dyspnea, dizzy-lightheaded. During lactate infusion, 25 of 29 API symptoms increased significantly from prelactate to point of panic; however, particularly robust effect sizes were exhibited for the desire to flee, dyspnea, tingling, twitching/trembling and difficulty doing a job. Comparison of panic recollected as usual and lactate-induced panic showed that more than half of the symptoms did not differ after Bonferroni correction; however, the most notable were fear in general, dyspnea, chest pain/discomfort, difficulty swallowing, feeling weak, desire to flee, and feeling hot/cold or both. These data point to a very distinctive role during both recollected and lactate-induced panic attacks for fearfulness the desire to flee (by definition), and for dyspnea, difficulty performing a job and fear of losing control. During lactate-induced panic, dyspnea exhibited the most robust effect size of all physical symptoms.

Adolescent↗

Anxiogenic effects of CO2 and hyperventilation in patients with panic disorder.

OBJECTIVE: Previous studies have indicated that patients with panic disorder are more likely than normal subjects to have acute panic attacks during inhalation of CO2, but methodological objections have been raised. In this study the authors attempted to address three of these methodological problems by ensuring that raters who assessed whether panic attacks occurred were blind to subjects' diagnoses, by randomizing the order of administration of 5% CO2 and hyperventilation, and by challenging a greater number of subjects with 7% CO2. METHOD: Patients with panic disorder and normal subjects underwent 20-minute inhalations of 5% CO2 and 7% CO2 and 15 minutes of room-air hyperventilation. Ratings of panic/no panic during each condition were made separately by an assessor blind to diagnosis and by the subject. Scores on four panic rating scales were also recorded before and after each intervention. RESULTS: Room-air hyperventilation caused panic attacks in a small number of patients; the difference in panic rate between patients and comparison subjects was statistically significant by the subjects' but not by the raters' assessment. Panic rates during 5% CO2 and 7% CO2 were significantly greater among the patients by both assessments; the panic rate was greatest during 7% CO2. Order of administration did not significantly affect panic rates for hyperventilation and 5% CO2. CONCLUSIONS: Panic patients were clearly more sensitive to the anxiogenic effects of CO2 than comparison subjects, and CO2 was a more potent anxiogenic stimulus than room-air hyperventilation. Seven percent CO2 discriminated best between patients and comparison subjects and should be the focus of further research.

Administration, Inhalation↗

Effects of informant mental disorder on psychiatric family history data.

OBJECTIVE: In family history interviews, mentally ill individuals ascribe their own disorders to relatives more frequently than informants who are not ill. Whether this reflects increased or decreased reporting accuracy remains unknown. This study addressed this issue by examining the sensitivity and specificity of diagnoses based on information from different types of informants classified by their own illness status. METHOD: Both members of 2,193 pairs of individuals participating in a psychiatric family study were directly interviewed. One individual in each pair (the informant) also provided family history data about the other (the subject). Informant-subject pairs were grouped according to the illness status of the informant based on the direct interview. Patterns of ascription of mental illness to subjects by groups of ill and not-ill informants were then compared with the subjects' psychiatric status based on direct interview. RESULTS: For depression, alcoholism, panic disorder, and "any diagnosis," ill informants demonstrated significantly increased sensitivity in family history reports when compared to never-mentally-ill informants; specificity, by contrast, was always significantly reduced. For each disorder, the aggregate disorder rate derived from family history reports was closer to the rate derived from direct interviews if information from ill informants as a group was used. CONCLUSIONS: The sensitivity and specificity of family history information appears to vary systematically with informant mental illness status. This may introduce a serious bias into psychiatric family study data, leading to overestimation of the strength of the tendency for mental disorders to "run in families." Family studies that rely on the informant method in their diagnostic evaluations should be aware of this problem.

Adult↗

Anxiety and congenital central hypoventilation syndrome.

OBJECTIVE: It has been hypothesized that individuals who cannot perceive elevations of CO2 will be less anxious than individuals with intact CO2 perception. To test this hypothesis, children with congenital central hypoventilation syndrome, who have a potentially lethal chronic illness associated with lack of CO2 perception and thus provide a natural experimental group, were studied. METHOD: Rates of anxiety symptoms and disorders in children with congenital central hypoventilation syndrome (N = 13) were compared with rates in an age-matched, nonreferred group of community subjects (N = 292) that included subgroups of children with asthma (N = 15) and other chronic medical illnesses (N = 66). Anxiety symptoms were assessed with information obtained from structured interviews of the parents, which provided both total symptom scores and DSM-III-R diagnoses. RESULTS: The children with congenital central hypoventilation syndrome exhibited significantly fewer anxiety symptoms than all other comparison subjects. Two of these children (15%) met criteria for anxiety disorders, a rate lower than that of the whole community group (24%) and of the chronically ill comparison subgroups (32%-47%). The largest difference in the prevalence of disorder emerged between the children with congenital central hypoventilation syndrome (15%) and those with asthma (47%). In the comparison of children with congenital central hypoventilation syndrome and children with other chronic illnesses, a priori analysis showed that the former had significantly lower rates of disorders that have been linked to panic in the literature. CONCLUSIONS: This study supports theories of anxiety that implicate CO2 perception in the pathophysiology of panic and related anxiety states.

Adolescent↗

Childhood separation anxiety disorder in patients with adult anxiety disorders.

The authors examined the relation between retrospectively reported childhood separation anxiety disorder and adult DSM-III-R anxiety disorders in 252 outpatients at an anxiety disorders research clinic. The prevalence of childhood separation anxiety disorder was significantly greater among patients with two or more lifetime adult anxiety disorder diagnoses than it was among patients with only one anxiety disorder, suggesting that childhood separation anxiety disorder may be a risk factor for multiple anxiety syndromes in adulthood.

Adolescent↗

Cognitive therapy.

Explore the source record for details and available documents.

Cognitive Behavioral Therapy↗

Timing of neuroendocrine responses and effect of m-CPP and fenfluramine plasma levels in OCD.

The present study assesses the timing of and relationship between neuroendocrine response and metabolite blood levels following the partial serotonin (5-HT) agonist m-CPP and the 5-HT releaser/reuptake blocker fenfluramine. Cortisol levels peaked significantly earlier than did prolactin, m-CPP, fenfluramine, or norfenfluramine blood levels by time-to-peak analysis. This earlier cortisol response to both 5-HT agents raises the possibility that peripheral mechanisms may play a role in cortisol release. Since peak m-CPP level correlated even more closely to peak prolactin rise than did peak fenfluramine, this suggests that prolactin response to oral m-CPP challenge is useful in assessing 5-HT function.

Adult↗

Panic attacks during placebo procedures in the laboratory. Physiology and symptomatology.

Heart rate, respiratory measurements, and Acute Panic Inventory symptoms of 17 patients with panic disorder who experienced panic attacks during a placebo infusion (situationally provoked panic) were analyzed and compared with similar data from a group of 19 patients with panic disorder who panicked during lactate infusion. Previously, it was shown that the group with lactate-induced panic attacks exhibited increased minute ventilation compared with normal control subjects and nonpanicking patients with panic disorder during lactate infusion. The group with situationally provoked panic attacks exhibited significant increases in both heart rate and minute ventilation immediately preceding the onset of the panic attack. The increase in minute ventilation appeared to be caused more by increase in tidal volume than in respiratory frequency. The increase in heart rate in the group with situationally provoked panic attacks was very similar to that seen in the group with lactate-induced panic attacks, but the group with situationally provoked panic attacks appeared to have somewhat greater increase in minute ventilation than the group with lactate-induced panic attacks. This suggests that the metabolic alkalosis produced by lactate infusion might actually blunt the full expression of panic-associated respiratory stimulation. These data validate the belief that significant cardiorespiratory stimulation occurring during panic attacks in the laboratory is not simply secondary to the intrinsic physiologic effects of panic-inducing substances such as lactate, yohimbine, and carbon dioxide.

Adult↗

A direct interview family study of social phobia.

Risks for DSM-III-R anxiety and affective disorders and "subdisorder" (nonimpairing) irrational social fears, among directly interviewed first-degree relatives (n = 83) of probands who met criteria for social phobia but for no other lifetime anxiety disorder diagnosis, were contrasted to risks for disorder among similarly evaluated relatives (n = 231) of never mentally ill controls. Relatives of social phobia probands had a significantly increased risk for social phobia (16% vs 5%, relative risk = 3.12) but not for other anxiety disorders. These results suggest a familial contribution to the development of some cases of social phobia. The specificity of the pattern of intergenerational transmission is consistent with the current nosologic distinction between social phobia and other anxiety disorders.

Adult↗

False suffocation alarms, spontaneous panics, and related conditions. An integrative hypothesis.

A carbon dioxide hypersensitivity theory of panic has been posited. We hypothesize more broadly that a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system. This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic, and the urge to flee. Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor. If other indicators of potential suffocation provoke panic this theoretical extension is supported. We broadly pursue this theory by examining Ondine's curse as the physiologic and pharmacologic converse of panic disorder, splitting panic in terms of symptomatology and challenge studies, reevaluating the role of hyperventilation, and reinterpreting the contagiousness of sighing and yawning, as well as mass hysteria. Further, the phenomena of panic during relaxation and sleep, late luteal phase dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety, and treatment are used to test and illuminate the suffocation false alarm theory.

Asphyxia↗