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Biomedical subjects

J D Coplan

Publications and source records attributed to J D Coplan.

At least 55 records · Page 3Linked to original sources
PubMed1997

Psychiatric symptoms in adolescence as predictors of obesity in early adulthood: a longitudinal study.

OBJECTIVES: This study examined the longitudinal relationship between psychopathology and obesity in young adulthood. METHODS: More than 700 youth in a population-based sample were psychiatrically assessed in 1983 (mean age = 14 years) and 1992 (mean age = 22 years). Self-reported body mass index (BMI) in 1992 was regressed on measures of depression and conduct disorder as well as a set of covariates including indices of physical health, social class, intelligence, and cigarette and alcohol use. Associations were examined with BMI treated as a continuous variable and with a binary index of obesity derived from the BMI distribution in each gender. RESULTS: BMI in young adults was positively related to a number of covariates. With all covariates controlled, BMI was inversely related to adult depressive symptoms in males but not females. BMI was positively related to adolescent symptoms of conduct disorder in both sexes. Similar associations were found between psychiatric symptoms and obesity. CONCLUSIONS: Conduct disorder symptoms in adolescence predicted BMI and obesity in early adulthood. These associations remained after controlling for factors that can affect the association between psychopathology and obesity.

Adolescent↗
PubMed1997

Clomipramine treatment of panic disorder: pros and cons.

BACKGROUND: Controlled trials suggest that clomipramine may be a highly effective antipanic drug. Lowering the starting dose may alleviate troublesome initial side effects and increase acceptability and compliance. METHOD: Fifty-eight patients with DSM-III-R panic disorder with or without agoraphobia underwent 13 weeks of clomipramine treatment. Starting at 10 mg/day, the dose was gradually increased to a mean dose of 97 mg/day. RESULTS: While completers showed highly significant improvement, the benefits were severely limited by a high dropout rate due to adverse reactions occurring mostly during the first 2 weeks of treatment. CONCLUSION: Given the alternatives, clomipramine should not be used as a first-line antipanic medication.

Adult↗
PubMed1996

Ventilatory effects of tryptophan depletion in panic disorder: a preliminary report.

On the basis of preclinical studies, we hypothesized that deficient serotonin neurotransmission may be associated with the respiratory hyperactivity and carbon dioxide sensitivity seen in panic disorder. We used the tryptophan depletion method to investigate the effects of transient reductions in serotonin on respiration in five patients with panic disorder and seven normal control subjects. During room air breathing, the patients showed significantly increased ventilation when tryptophan-depleted, while the normal subjects showed no significant changes in respiration. These preliminary data suggest that serotonergic manipulation may affect ventilatory indices, with panic disorder patients being particularly sensitive to the effect of tryptophan depletion.

Adult↗
PubMed1996

Persistent elevations of cerebrospinal fluid concentrations of corticotropin-releasing factor in adult nonhuman primates exposed to early-life stressors: implications for the pathophysiology of mood and anxiety disorders.

There is increasing evidence for an important role of adverse early experience on the development of major psychiatric disorders in adulthood. Corticotropin-releasing factor (CRF), an endogenous neuropeptide, is the primary physiological regulator of the mammalian stress response. Grown nonhuman primates who were exposed as infants to adverse early rearing conditions were studied to determine if long-term alterations of CRF neuronal systems had occurred following the early stressor. In comparison to monkeys reared by mothers foraging under predictable conditions, infant monkeys raised by mothers foraging under unpredictable conditions exhibited persistently elevated cerebrospinal fluid (CSF) concentrations of CRF. Because hyperactivity of CRF-releasing neurons has been implicated in the pathophysiology of certain human affective and anxiety disorders, the present finding provides a potential neurobiological mechanism by which early-life stressors may contribute to adult psychopathology.

Animals↗
PubMed1996

Comorbidity of depression and panic disorder.

The high comorbidity of panic disorder and depression might be anticipated on epidemiologic grounds alone. Both are common disorders with a characteristically chronic course, increasing the probability that a given patient with one disorder will develop the other. Symptoms of anxiety are highly prevalent among depressed patients; however, not all such symptoms represent an actual comorbid anxiety disorder. Conversely, about 50% of patients with panic disorder ultimately experience an episode of major depression. The comorbidity of panic disorder and depression has significant and potentially ominous prognostic implications; the high rate of suicide attempts observed in panic disorder are further exacerbated by the presence of a comorbid depression. Panic disorder and depression share well-defined disturbances in hypothalamic-pituitary-adrenal axis function, serotonergic neurotransmission, and growth hormone response to pharmacologic challenge. In addition, most of the available medications used to treat depression are also first-line therapy for panic disorder. Although initial studies suggested that patients with comorbid panic disorder and depression have a poorer treatment outcome, recent data show similar outcomes for patients with both disorders and those with panic disorder uncomplicated by depression.

Adult↗
PubMed1996

Ambulatory monitoring of respiration in anxiety.

An ambulatory monitor, body suit, and calibration procedure were developed to compare the respiration of seven patients with panic disorder and twelve normal volunteers. Subjects wore a body suit with Respitrace bands, connected to a portable respiratory monitor for a period of 24 hours. Breath by breath values for respiratory rate and tidal volume were computed every two minutes. There was a significant difference between patients and controls in their patterns of minute ventilation during sleep. Tidal volume, rather that respiratory rate increases characterized the periods of anxiety and limited symptom attacks.

Adult↗
PubMed1995

Effects of intravenous diazepam pretreatment on lactate-induced panic.

The psychological and physiological effects of acute low-potency benzodiazepine administration on lactate-induced panic were examined in 10 patients with panic disorder (PD). The patients, who had panicked during a standard sodium-lactate infusion, underwent a repeat infusion modified by pretreatment with intravenous diazepam (5 mg). Acute Panic Inventory (API) scores preceding the second lactate infusion, which were associated with diazepam pretreatment, were significantly reduced in compared with those measured before the first lactate infusion. However, the second visit "fear of doom" item of the API was significantly reduced relative to the same time point of the first visit 35 min before lactate infusion, when diazepam had not yet been administered. Thus, the reduction of prelactate anxiety preceding the second infusion appeared to reflect both pharmacological and nonpharmacological contributions. The diazepam pretreatment condition was associated with a significantly increased infusion duration and a significant attenuation of rate of API symptom increase in response to lactate. Despite significant attenuation of lactate infusion effects associated with the diazepam pretreatment condition, 7 of 10 patients experienced a second panic attack. This pilot study suggests that diazepam pretreatment is associated with a marked reduction of symptomatic response during a second lactate infusion, although the magnitude of attenuation observed was insufficient to block lactate-induced panic in a majority of lactate-vulnerable PD patients.

Adult↗
PubMed1995

Rebreathing tests in panic disorder.

In order to compare the ventilatory response of panic patients and normal controls, 21 panic disorder patients with agoraphobia and 21 normal controls underwent the Read rebreathing test. Panic patients panicked significantly more during the test, responded with more respiratory rate and less tidal volume, but showed no hypersensitivity to inhaled carbon dioxide compared to normal controls.

Adult↗
PubMed1995

Uncoupling of the noradrenergic-hypothalamic-pituitary-adrenal axis in panic disorder patients.

In this paper the authors examine the interrelationship of both the noradrenergic (NA) system and the hypothalamic-pituitary-adrenal (HPA) axis and its implications for panic disorder (PD). Seventeen PD patients and 16 healthy volunteers were challenged orally 12 weeks apart with the alpha 2-agonist clonidine (13 healthy volunteers and 12 patients repeated the challenge). Between challenges, PD patients were treated with fluoxetine, with 10 of 12 improving at least moderately. Both during the acute phase of the illness and during the phase of pharmacological improvement, patients demonstrated a greater percentage of reductions of plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) and plasma cortisol during clonidine challenge. We used correlational matrices to examine the relationship between the NA system, as reflected by plasma MHPG, and the HPA axis, as reflected by plasma cortisol measures. Healthy volunteers exhibited multiple significant "couplings" between either baseline or maximal decrease (delta max) of plasma MHPG, with either baseline or delta max plasma cortisol measures both within the first and second challenges and between the first and second challenges. In contrast, PD patients demonstrated "uncoupling" of the NA system and the HPA axis, with no significant correlations observed between either baseline and/or maximal decrease (delta max) measures of MHPG with the same cortisol measures for either the first or second challenge. The same uncoupling was observed for NA/HPA correlations between the first and second challenges. These data suggest that the hyperresponsivity to clonidine in PD patients persists during fluoxetine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1995

Persistence of blunted human growth hormone response to clonidine in fluoxetine-treated patients with panic disorder.

OBJECTIVE: The authors determined the effects of antipanic treatment with fluoxetine on human growth hormone (GH) response to the alpha 2 agonist clonidine. METHOD: Seventeen patients with panic disorder and 15 healthy volunteers were challenged with clonidine. Thirteen of the patients and 12 of the volunteers were given a second challenge with clonidine 12 weeks later. The patients received open fluoxetine and the healthy subjects received no treatment between challenges. Subjects with high baseline human GH levels (greater than 2 ng/ml) at the first and second challenges were excluded from further analysis. RESULTS: The patients with panic disorder (N = 13 for the first challenge and N = 9 for the second) had significantly lower human GH responses to clonidine than the healthy subjects (N = 14 during the first challenge and N = 9 for the second) during both challenges, despite clinical improvement in eight of the nine patients at the time of the second challenge. CONCLUSIONS: Blunted secretion of human GH in response to clonidine in patients with panic disorder persists despite clinical recovery.

Clonidine↗
PubMed1995

Primate models of anxiety. Longitudinal perspectives.

In summary, VFD subjects appear to have sustained long-term behavioral and biologic sequelae following disruption of normative maternal-infant attachment patterns. The sequelae are primarily manifest as stable anxiety or affective traits and, from a biologic perspective, are most analogous to recent data that have emerged from studies of patients with PTSD. Multiple abnormalities are observed of systems directly involved in affect regulation. Further studies are required to clarify the pathologic ontogeny of the VFD condition and its potential relevance to human psychopathology.

Adolescent↗
PubMed1994

Adverse early experiences affect noradrenergic and serotonergic functioning in adult primates.

It has been proposed that certain adverse early experiences may play a role in determining subsequent susceptibility to adult anxiety and affective disorders and this relationship may be the result of altered neurodevelopment of the noradrenergic and/or serotonergic systems. In this study of nonhuman primates, the predictability of foraging requirements for mothers during an early period of their infants' lives was manipulated. When the offspring were young adults, these early manipulations were related to differences in behavioral response to acute administration of two putative anxiety-provoking agents: the noradrenergic probe, yohimbine, and the serotonergic probe, mCPP. These long-term effects of the developmental environment on subsequent pharmacological responsivity suggest that both neuronal systems may be permanently altered by early experiential factors.

Animals↗
PubMed1994

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↗
PubMed1994

Augmentation strategies with tricyclic or fluoxetine treatment in seven partially responsive panic disorder patients.

BACKGROUND: Although panic disorder is generally responsive to single antidepressant pharmacotherapy, a substantial percentage of patients fail either to respond adequately or to maintain a therapeutic response. METHOD: The authors report on seven consecutive openly treated patients with panic disorder who showed inadequate antipanic responses to treatment regimens including either a tricyclic (TCA) or fluoxetine. Those patients taking a TCA had fluoxetine added and those patients taking fluoxetine had a TCA added. RESULTS: All seven patients showed an improvement in antipanic response to the combination treatment. CONCLUSION: The current case series is the first, to our knowledge, to suggest that the combination of a TCA and fluoxetine may provide a viable pharmacotherapeutic option for panic disorder patients who have failed to respond to an adequate trial of either a TCA or fluoxetine. Appropriate controlled studies are recommended.

Adult↗
PubMed1993

Therapeutic strategies for the patient with treatment-resistant anxiety.

Outcome of anxiety disorder treatment with psychotherapy and medication is generally as good as or better than that of other psychiatric illnesses. Nevertheless, refractory cases occur. The first step in approaching the treatment-resistant patient with an anxiety disorder is to be certain that the treatment has been adequate. Failure to provide an adequate dose of medication for adequate periods of time may be the most common cause of "treatment resistance." The second step is to reconsider the diagnosis and/or determine if new diagnoses have emerged since the original consultation. Depression and substance abuse are especially likely to complicate anxiety disorders. Several studies have shown that concomitant personality disorders (axis II) increase the occurrence of resistance to standard treatment and must be addressed through psychotherapy. Last, a variety of possible underlying medical conditions, including thyroid disorder, arrhythmia, and complex partial seizure, should be considered. Then, the clinician should consider a variety of pharmacologic approaches that are specific to each anxiety disorder. Panic disorder patients who are refractory to imipramine frequently respond to high-potency benzodiazepines, monoamine oxidase (MAO) inhibitors, serotonin reuptake inhibitors, or various combinations. Generalized anxiety disorder, if unresponsive to benzodiazepines, may respond to buspirone or a tricyclic antidepressant. Patients with obsessive compulsive disorder who have failed to respond to clomipramine or fluoxetine and other serotonin reuptake blockers may benefit from augmentation strategies using combination therapies including buspirone, fenfluramine, and neuroleptics. Social phobia refractory to beta-blockers and MAO inhibitors may benefit from buspirone, fenfluramine, and neuroleptics. Social phobia refractory to beta-blockers and MAO inhibitors may benefit from buspirone, fluoxetine, or alprazolam.

Anxiety Disorders↗