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Biomedical subjects

M H Pollack

Publications and source records attributed to M H Pollack.

At least 37 records · Page 2Linked to original sources
PubMed1996

Panic anxiety, dyspnea, and respiratory disease. Theoretical and clinical considerations.

There is intriguing evidence suggesting pathophysiologic relationships among dyspnea, hyperventilation, and panic anxiety. The symptoms of panic attacks and pulmonary disease overlap, so that panic anxiety can reflect underlying cardiopulmonary disease and dyspnea can reflect an underlying anxiety disorder. The pathogenesis of panic may be related to respiratory physiology by several mechanisms: the anxiogenic effects of hyperventilation, the catastrophic misinterpretation of respiratory symptoms, and/or a neurobiologic sensitivity to CO2, lactate, or other signals of suffocation. In a subset of patients with PD, incipient pulmonary dysfunction may also contribute to their anxiety symptoms. Patients with pulmonary disease, particularly those with obstructive lung disease, have a high rate of panic symptoms and PD. There is reason to believe that pulmonary disease constitutes a risk factor for the development of panic related to repeated experiences with dyspnea and life-threatening exacerbations of pulmonary dysfunction, repeated episodes of hypercapnia or hyperventilation, the use of anxiogenic medications, and the stress of coping with chronic disease. Panic in pulmonary patients may carry significant morbidity, including phobic avoidance of activity, overly aggressive treatment with anxiogenic medications, and more prolonged and frequent hospitalization. Successful treatment of panic in these patients can improve functional status and quality of life by relieving anxiety and dyspnea. Nonpharmacologic treatment of panic, including cognitive-behavioral approaches, can be useful in patients with concomitant respiratory disease. Sedating medications such as benzodiazepines should be used with caution in patients with pulmonary disease to avoid respiratory depression. Serotonergic antidepressants (SSRIs) and anxiolytics (buspirone) may be effective treatments for panic or generalized anxiety in pulmonary patients and have relatively little potential for significant adverse effects.

Anxiety↗
PubMed1996

Prevalence of panic in patients referred for pulmonary function testing at a major medical center.

OBJECTIVE: The authors examined the prevalence and correlates of panic disorder in a group of patients who were referred for pulmonary function testing. METHOD: Patients (N = 115) were screened for the presence of panic attacks and panic disorder with a self-report questionnaire; a subgroup (N = 25) received structured diagnostic assessment. RESULTS: Of the 115 patients, 41% (N = 47) reported panic attacks and 17% (N = 20) met screening criteria for panic disorder. From the confirmed rate of panic disorder among the subgroup who received structured diagnostic assessment, the overall prevalence rate of panic disorder was estimated to be 11% and included six of the nine patients (67%) who had a diagnosis of chronic obstructive pulmonary disease. There were no significant differences between patients with and without panic in the severity of pulmonary function abnormalities or in the response to bronchodilators. However, patients with panic attacks were significantly more likely to report dyspnea at rest and irritable bowel symptoms and tended to report difficulty swallowing. CONCLUSIONS: This study suggests that panic disorder and subsyndromal panic are relatively common and may be unrecognized and inadequately treated in patients who present with respiratory symptoms.

Airway Obstruction↗
PubMed1996

Relationship of childhood anxiety to adult panic disorder: correlates and influence on course.

OBJECTIVE: This study investigated the correlates of a childhood history of anxiety disorders in adult patients participating in a longitudinal study of panic disorder. The authors hypothesized that a history of anxiety during childhood would be associated with higher rates of comorbid anxiety and depressive disorders, greater likelihood of anxiety disorders in family members, and greater chronicity, as reflected by decreased time spent in remission. METHOD: The presence of a childhood history of anxiety disorders was assessed by structured interview, and its association with comorbid anxiety and depressive disorders, family history, and select anxiety severity variables was examined in a replication sample of 94 patients. The influence of childhood anxiety on the prospectively ascertained course of disorder was assessed in a full group of 194 patients. RESULTS: Over half (54%) of the patients experienced anxiety disorders during childhood. These patients experienced higher rates of comorbid anxiety and depression, family history of anxiety, and increased levels of agoraphobia, panic frequency, and global severity of illness at baseline evaluation. Childhood anxiety disorders were not independently associated with the number of months in remission or the severity of illness over time, although a modest effect for this variable was evident when degree of avoidance and anxiety sensitivity at baseline were statistically controlled. CONCLUSIONS: Adult panic patients with a history of anxiety disorders in childhood have elevated rates of comorbid anxiety and depressive disorders and a tendency toward increased avoidance, but there was not strong evidence that these patients respond differently to treatment over time.

Adult↗
PubMed1996

The pharmacotherapy of panic disorder.

The biological model for panic disorder posits a specific, genetically inherent neurochemical dysfunction; pharmacological treatment attempts to reregulate the dysregulated physiological system, thereby achieving remission (or, ideally, recovery) or amelioration of the symptoms sufficient for nonpharmacological therapies to be viable. This article will review the evidence of the efficacy of single classes of pharmacological agents (antidepressants, including TCAs, MAOIs, and SSRIs; benzodiazepines; and other agents) and integrated treatments, involving coadministration of medications within or across classes or a combination of pharmacological and nonpharmacological therapies, such as cognitive-behavioral therapy. Research pertaining to the relative efficacy of administering combination treatments concurrently or sequentially is examined. Individualized treatment plans for patients maximize the benefits of integrated treatments.

Antidepressive Agents, Tricyclic↗
PubMed1996

Clinical issues in the long-term treatment of panic disorder.

Longitudinal studies in naturalistic settings have shed new light on the course and value of therapeutic interventions in panic disorder and agoraphobia. Patients, their families, and clinicians need additional information about the natural course of the disorders and the factors that predispose patients to sustained illness, recovery, and relapse during treatment and upon treatment discontinuation. Clinical experience and controlled studies confirm the efficacy of pharmacologic and cognitive-behavioral therapy (CBT). Newer antidepressants, especially the serotonin selective reuptake inhibitors, represent a significant advance in effective pharmacologic intervention. However, despite the availability of effective treatment options, panic disorder often remains a chronic condition characterized by intermittent remissions and relapses over many years. Depression and comorbid anxiety disorders are associated with increased disease severity, treatment refractoriness, and relapse. The role of CBT as both a primary intervention and as an aid in the discontinuation of pharmacotherapy is reviewed.

Age Factors↗
PubMed1996

Venlafaxine for panic disorder: results from a double-blind, placebo-controlled study.

Venlafaxine has demonstrated efficacy for depression, and recent reports and clinical experience suggest that it may be effective for the treatment of anxiety disorders as well. We present what we believe are the first data from a controlled study designed to test the efficacy of venlafaxine for the treatment of panic disorder. There were 25 patients enrolled at one site of a five-center study; 13 received venlafaxine and 12 received placebo. There were more dropouts for placebo than for venlafaxine (8/12 vs. 2/13) in this 8-week acute trial. Patients treated with venlafaxine experienced significantly greater global improvement than those on placebo and exhibited trends toward greater improvement on anxiety and depression symptoms as assessed by the Hamilton rating scales. These data encourage further evaluation of venlafaxine for the treatment of panic disorder.

Adult↗
PubMed1995

Pattern of placebo response in panic disorder.

This study characterizes the pattern of placebo response in depressed panic disorder patients who participated in a randomized clinical trial. We compared placebo-treated subjects whose panic attacks remitted, with those whose attacks did not remit, and with remitting and nonremitting subjects treated with active medication. Seventy-one subjects who met criteria for panic disorder and for a concurrent depressive diagnosis (major depression, dysthymia, or depressive disorder not otherwise specified [NOS]) were treated with either imipramine (n = 36) or alprazolam (n = 35), and 28 patients were treated with placebo. Sixteen placebo-treated and 40 medication-treated patients were panic free at Week 8. Placebo panic remitters were significantly more ill than active-medication remitters on all measures. In contrast, subjects who achieved panic remission on placebo showed no difference on other clinical measures from active medication nonremitters, and little difference from placebo nonremitters. Results support the need for assessment of all core panic disorder symptoms in determining treatment efficacy and in considerations of response and remission.

Alprazolam↗
PubMed1995

EEG abnormalities in patients with atypical panic attacks.

BACKGROUND: Panic attacks and certain partial seizures have phenomenologic similarities which suggest that they may somehow be related. No evidence of such a relationship, however, was found when the routine EEGs of patients with panic attacks were examined. METHOD: Fifteen subjects with atypical panic attacks who met DSM-III-R criteria for panic disorder agreed to have routine followed by prolonged ambulatory EEG monitoring with sphenoidal electrodes. Fourteen subjects actually underwent monitoring; 1 had a panic attack during premonitoring routine EEG. RESULTS: Focal paroxysmal EEG changes consistent with partial seizure activity occurred during panic attacks in 33% (N = 5) of the 15 subjects; 2 (40%) of the 5 subjects with panic-related EEG changes had normal routine EEGs. Multiple attacks were recorded before panic-related EEG changes were demonstrated in several subjects. CONCLUSION: It may be necessary to monitor the EEG during multiple panic attacks to reveal an association between atypical panic attacks and epileptiform EEG changes.

Adult↗
PubMed1995

Integrated treatment of panic disorder.

Epidemiological studies suggest that about 3.5% of the adult United States population meet criteria for panic disorder, and that an additional 2-5% suffer from agoraphobia with or without panic. Both biological and behavioral models have been proposed to elucidate the nature of this disorder. The authors review research findings regarding these models, as well as pharmacological and cognitive-behavioral treatment approaches. The complexity of factors contributing to the disorder suggests the need for an integrated treatment approach involving considerations of combination drug therapy and psychosocial interventions.

Adaptation, Psychological↗
PubMed1995

The longitudinal course and outcome of panic disorder.

Converging lines of evidence from a variety of methods of inquiry support a developmental model for panic disorder that includes a constitutional predisposition for anxiety influenced by genetic, familial, cognitive-behavioral and psychosocial factors, early expression during childhood, and variable manifestations during the life-cycle. Studies of patients followed up after acute pharmacotherapy trials and those treated naturalistically are consistent with this model and portray panic disorder as a generally chronic condition with a longitudinal course marked by relatively brief intervals of remission and high rates of recurrence and relapse. Longitudinal and follow-up studies suggest that panic attack frequency responds more readily and rapidly to pharmacotherapy than do other aspects of panic disorder such as agoraphobia and generalized anxiety. In general, the presence of agoraphobia is associated with more severe symptoms, greater chronicity, and more limited response to treatment. Other variables associated with chronicity and treatment resistance include patient-related factors (psychiatric and medical comorbidity, anxiety sensitivity) and pharmacologic factors (adequacy of dose, duration, and compliance). Although it is currently difficult to predict the duration of treatment needed for an individual patient, available evidence suggests that a substantial proportion of patients may require chronic treatment for panic disorder.

Adult↗
PubMed1994

Sleep panic attacks: an association with childhood anxiety and adult psychopathology.

The authors examine whether the presence of sleep panic attacks identifies a subgroup of panic disorder patients. Subjects (n = 95) were consecutive patients with panic disorder participating in the MGH longitudinal study of panic disorder. Patients were evaluated with structured interviews to establish adult anxiety and affective disorders, and the presence of childhood anxiety disorders. Patients were queried whether they had ever experienced at least one panic attack during sleep. Patients with a history of sleep panic had significantly higher rates of comorbid generalized anxiety disorder (p < 0.01), social phobia (p < 0.03), and major depression (p < 0.005). The trend was toward longer length of illness (p < 0.09) and were more likely to have a history of an anxiety disorder during childhood (p < 0.005). The presence of sleep panic attacks may delineate a subgroup of panic disorder patients with early difficulties with anxiety, and comorbid mood and anxiety disorders as adults.

Adult↗
PubMed1994

Anxiety psychopathology predictive of outcome in patients with panic disorder and depression treated with imipramine, alprazolam and placebo.

This study examines clinical predictors of outcome for patients with panic disorder and depression in a 16 week, placebo-controlled trial of alprazolam and imipramine (n = 126). Baseline global severity of illness and phobic avoidance were differentially predictive of acute response to treatment. Patients in the mild to moderate range of global distress experienced smaller degrees of improvement on alprazolam than on imipramine at week 4. At endpoint, the relative effectiveness of the active medication versus placebo was diminished in patients with higher levels of phobic avoidance. This relationship was not evident for completers, suggesting that the adverse effects of avoidance on outcome after sustained treatment was reduced.

Adult↗
PubMed1994

Predicting prospective episodes of depression in patients with panic disorder: a longitudinal study.

This study used a naturalistic, longitudinal study to examine predictors of the emergence of major depression among 90 nondepressed patients with panic disorder who were followed for a 2-year period. Twenty-four percent of the sample experienced a major depressive episode during the study period. Adequacy and type of medication treatment were not associated with decreased risk. Past history of major depression was associated with a greater risk for a prospective episode. The degree of assertiveness, presence of comorbid generalized anxiety disorder, and severity of agoraphobia were each significant predictors of the occurrence of depression when considered alone and when the influence of past history of depression was statistically controlled. The implications of these findings for the clinical management of patients with panic disorder are discussed.

Adolescent↗
PubMed1994

Treatment of fluoxetine-induced sexual dysfunction with bupropion: a case report.

Antidepressant-induced sexual dysfunction is a common and significant cause of patient distress and noncompliance with treatment. A number of adjunctive pharmacologic strategies, including yohimbine, cyproheptadine, bethanechol, and amantadine, have been employed previously. We report a case of using bupropion to treat fluoxetine-induced sexual dysfunction in a 50-year-old man with a history of recurrent major depression. This is the first case of such treatment we know. Sexual dysfunction induced by fluoxetine is thought secondary to effects on the serotonin system. Bupropion is an antidepressant with minimal sexual side effects. The mechanism by which bupropion resolved this sexual dysfunction is unknown, but it may be related to its mild dopamine uptake blockade.

Bupropion↗
PubMed1994

The relationship of alprazolam and clonazepam dose to steady-state concentration in plasma.

This report addresses the correlation between dose and concentration of both alprazolam and clonazepam in plasma. Patients were 43 participants in a double-blind, placebo-controlled study of alprazolam and clonazepam for the treatment of panic disorder. The concentration of clonazepam in plasma was linearly related with dose, measured as milligrams per day (R = 0.724; F = 24.2; p = 0.0001) or milligrams per kilogram per day (R = 0.863; F = 58.3; p = 0.0001). The correlation between drug concentration and daily dose of alprazolam was also significant (R = 0.60; F = 9.5; p = 0.007), although the correlation between dose measured as milligrams per kilogram per day and drug level was not significant (R = 0.361; F = 2.4; p = 0.14). This replicates previous findings that, for each additional milligram per day dose of alprazolam, there is a corresponding increase of approximately 10 ng/ml in the plasma and presents preliminary data that, for each added 1 mg/day dose of clonazepam, there is approximately an increase of 12 ng/ml in the plasma. For both drugs, however, there may be considerable variation in level in plasma for a given dose. Weight-adjusted clonazepam concentration may be more predictable than weight-adjusted alprazolam concentration.

Adolescent↗