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Purpose: We examined the relationship between economic, physical, and social characteristics of neighborhoods, where men who have sex with men (MSM) lived and socialized, and symptom scores of depression and generalized anxiety disorder (GAD)., Methods: Participants came from a cross-sectional study of a population-based sample of New York City MSM recruited in 2010-2012 (n = 1126). Archival and survey-based data were obtained on neighborhoods, where the men lived and where they socialized most often., Results: MSM who socialized in neighborhoods with more economic deprivation and greater general neighborhood attachment experienced higher GAD symptoms. The relationship between general attachment to neighborhoods where MSM socialized and mental health depended on the level of gay community attachment: in neighborhoods characterized by greater gay community attachment, general neighborhood attachment was negatively associated with GAD symptoms, while in low gay community attachment neighborhoods, general neighborhood attachment had a positive association with GAD symptoms., Conclusions: This study illustrates the downsides of having deep ties to social neighborhoods when they occur in the absence of broader access to ties with the community of one's sexual identity. Interventions that help MSM cross the spatial boundaries of their social neighborhoods and promote integration of MSM into the broader gay community may contribute to the reduction of elevated rates of depression and anxiety in this population.

Clinical characteristics predicting response and remission to psychopharmacological treatment of bipolar disorder (BD) and co-occurring anxiety disorders have been understudied. We hypothesized that non-response to risperidone or placebo in individuals with co-occurring BD and anxiety symptoms would be associated with a more severe clinical course of BD, and certain demographic variables. This study was a secondary analysis of a randomized, double-blind, parallel, 8-week study comparing risperidone monotherapy and placebo in individuals with BD plus current panic disorder, current generalized anxiety disorder (GAD), or lifetime panic disorder (n=111) [31]. We compared clinical characteristics of responders (50% improvement on the Hamilton Anxiety Scale [HAM-A]) and non-responders as well as remitters (HAM-A<7) and non-remitters in risperidone treatment (n=54) and placebo (n=57) groups. For non-responders in the risperidone group, co-occurring lifetime panic disorder was significantly more common than for non-responders in the placebo group. Apart from this, no significant differences in course of illness or demographics were found either between or across groups for patients with BD and co-occurring anxiety symptoms receiving risperidone or placebo in this acute phase study., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

Objective: This study assessed the efficacy of two fixed doses of paroxetine in the treatment of generalized anxiety disorder., Method: Outpatients (N=566) with generalized anxiety disorder and no other axis I disorder were eligible if they scored >/=20 on the Hamilton Rating Scale for Anxiety (with a score of 2 or higher on the anxious mood and tension items). Following a 1-week placebo run-in phase, patients were randomly assigned to 8 weeks of treatment with paroxetine, 20 or 40 mg/day, or placebo. The primary outcome measure was the change from baseline in total score on the Hamilton anxiety scale. Response was defined as a rating of "very much improved" or "much improved" on the Clinical Global Impression global improvement measure; remission was defined as a Hamilton anxiety scale score

Generalized anxiety disorder (GAD) is a severe and chronic anxiety disorder characterized by uncontrollable worrying and somatic anxiety (tension, insomnia and hypervigilance). It is a common condition, with lifetime prevalence rates for DSM-IV GAD in the general population of approx. 5-6% being reported. In addition, like other anxiety disorders, GAD also shows comorbidity with depression and most of the other anxiety disorders. This article reviews data on the prevalence of GAD, its comorbidity with depression, and its social and economic impact. Proposed neurobiological mechanisms for GAD are discussed, since an understanding of these may help in the development of future therapies. Finally, current pharmacological and non-pharmacological treatment options for GAD are reviewed, with particular attention being paid to published clinical-trial data.

Generalized anxiety disorder (GAD) is a chronic mental disorder that is characterized by excessive anxiety or worry. Traditionally, the treatment goal for GAD has been the attainment of a treatment response, clinically defined as a 40% to 50% symptomatic improvement relative to baseline. However, there is growing consensus among clinical psychiatrists that the treatment goal should be remission, a virtually asymptomatic state that corresponds to a score of < or = 7 on the Hamilton Rating Scale for Anxiety (HAM-A) or a > or = 70% symptomatic improvement from baseline. Venlafaxine extended release (XR), a serotonin-norepinephrine reuptake inhibitor, is the first pharmacotherapeutic agent to be indicated for both depression and GAD. This article reviews the efficacy data from several short- and long-term placebo-controlled studies of venlafaxine conducted to evaluate the potential of this agent to facilitate remission. Total scores on the HAM-A and the Clinical Global Impressions scale were used as the primary variables; scores for the HAM-A psychic and somatic anxiety factors and for the Hospital Anxiety and Depression scale were used as secondary variables. Venlafaxine XR showed a substantial effect size in the individual HAM-A items of worry, anxiety, and behavior at interview. The pooled analysis of 2 long-term studies indicated that the scores of venlafaxine remitters separated from those of responders by the second month, resulting in an overall increase in remitters. The results of these studies demonstrate the strong potential of venlafaxine XR in facilitating remission in GAD.

Objective: This study evaluated the efficacy and safety of fixed doses of once-daily extended-release (XR) venlafaxine in outpatients with generalized anxiety disorder without concomitant major depressive disorder., Method: Adult outpatients with generalized anxiety disorder but not major depressive disorder with total scores of 18 or higher on the Hamilton Rating Scale for Anxiety and scores of 2 or higher on its anxious mood and tension factors were eligible. Patients were randomly assigned to receive placebo or venlafaxine XR (75, 150, or 225 mg/day) for 8 weeks. Primary efficacy variables were final total and psychic anxiety factor scores on the Hamilton anxiety scale and final severity and global improvement item scores on the Clinical Global Impression (CGI) scale., Results: Of the 377 patients entering the study, 370 were included in a safety analysis and 349 in an efficacy analysis. Adjusted mean scores at 8 weeks (last-observation-carried-forward analysis) were significantly lower for one or more of the venlafaxine XR groups in four of four primary and three of four secondary outcome measures than for the placebo group. These included a change of 1.7 (versus 1.3) from baseline on CGI severity item scores and a final score of 2.2 (versus 2.6) on the CGI global improvement item. All doses of venlafaxine XR were well tolerated., Conclusions: Venlafaxine XR is an effective and well-tolerated option for the short-term treatment of generalized anxiety disorder in outpatients without major depressive disorder.

This article reviews results of reports suggesting that venlafaxine extended release (XR) may play an important role in the treatment of anxiety disorders, particularly generalized anxiety disorder (GAD). Statistically significant improvements in GAD for venlafaxine XR compared with placebo on the basis of the Hamilton Rating Scale for Anxiety were seen in the acute treatment studies up to 8 weeks and were maintained for 6 months. One comparative study found venlafaxine XR to be as effective as, or on some measures more effective than, buspirone at relieving GAD. Venlafaxine XR was safe and well tolerated in the GAD studies, with discontinuation rates due to adverse effects similar to the rates seen with placebo or buspirone.

The literature and clinical experience suggest a higher-than-normal incidence of mitral valve prolapse in patients with panic disorder, although the relationship between these two conditions is currently a matter of speculation. Patients with panic disorder are likely to first consult their family practitioner or internist, who may then refer them to a psychiatrist. Hence psychiatrists should be familiar with the signs, symptoms, and management of mitral valve prolapse. The authors describe mitral valve prolapse, panic disorder, and their association, then suggest a strategy for evaluation and treatment of these conditions.

Buspirone was compared with imipramine and placebo in the treatment of panic disorder in an 8-week, double-blind controlled study of 52 randomly assigned patients. The side effect profile of buspirone was less disruptive than that of imipramine. Buspirone was not significantly superior to placebo in its antipanic or anxiolytic effects in panic disorder patients.

This article reviews the evidence on the efficacy of monoamine oxidase inhibitors (MAOIs) and of alprazolam in the treatment of panic disorder and agoraphobia. It also presents guidelines to the clinician on how to implement these treatments in practice.

Previously unrecognized similarities among metabolic responses to various maneuvers used to evoke anxiety in patients with panic disorder are described. On the basis of these observations, a new biological model is proposed for panic disorder, in which the primary defect--which is neuroendocrine rather than psychiatric--is operationally placed within the redox-regulating apparatus of the brain stem. This model is consistent with many clinical features of panic disorder and also provides a theoretical framework for further studies of the pathophysiology of this and related conditions (e.g., hyperventilation syndrome).

Of 51 patients with panic attacks, 11.8% (7.8% with a correction factor) had a positive dexamethasone suppression test. This is significantly lower than the rate for melancholia. This difference suggests that panic attacks and major depression may be associated with different biological mechanisms.

The historical roots of the current avoidance of MAOIs are reviewed. A practical approach to the careful prescription of MAOIs is outlined. Medical contraindications, side effects and their management and drug and food interactions with MAOIs are discussed. With careful patient selection, adequate caution by the physican, and appropriate preparation of the patient, MAOIs are often uniquely effective (as in endogenous anxiety) and have an acceptably low potential for serious toxicity.

The unpredictability of spontaneous unexpected panic attacks has inhibited the controlled study of this phenomenon. Previous studies demonstrated that an increase in blood lactic acid occurred concomitant with symptoms of anxiety in anxiety-prone patients who underwent standard physical exercise. The question of whether these patients had an excessive sensitivity to lactate led to the development of the lactate infusion model, in which anxiety is induced in a controlled environment. The history and current application of the lactate infusion model in the study of neurochemical correlates of panic are described, and a methodology for lactate infusion procedures is outlined.

Panic disorder with or without agoraphobia is dominated by the occurrence of panic attacks. However, panic attacks are also reported to occur as part of the clinical picture in several medical conditions, notably thyroid disease, hypoglycemia, and pheochromocytoma. The authors examine these conditions, review the relevant literature, and offer an evaluation strategy. Routine screening is not recommended. Panic disorder is also associated with mitral-valve prolapse and temporal lobe seizures. The authors explore the possible consequences of this association and outline an evaluation strategy. Again, routine screening is not recommended.

The focus of this paper is the treatment of panic disorder with alprazolam. Drug treatments alone are sometimes not sufficient by themselves, to adequately control all of the symptoms or components of this disorder. In the typical case we can identify four targets of treatment: The first target is the biological core of the condition, that is characterized by the unexpected, unprovoked attacks of anxiety. This responds best to medication. The second target is the phobic avoidance behaviour. It appears to be a conditioned or learned complication of the biological core, and appears to follow the laws of learning theory. Unlearning treatments, like behaviour therapy (notably in vivo exposure) are usually necessary to make a full impact against the phobic avoidance behaviour. Thirdly, there is no drug that reverses the psycho-social problems these patients have. Not all of them have such problems, but those that do may need psychotherapy to deal with their conflicts and stresses. Finally, the evidence in several chronic studies, suggest that this is a chronic relapsing disorder in the majority of cases. It is not enough to treat these patients acutely. They must be followed chronically and monitored carefully over many years, if they are to be protected against relapse.

Studies of the treatment of panic anxiety and various other states with monoamine oxidase (MAO) inhibitors are critically reviewed. It is concluded that MAOIs have differential effects on several dimensions of pathologic anxiety. The association between depression and anxiety states is also reviewed; it is observed that MAOIs effectively treat severe anxiety and phobic disorders without operating strictly via their antidepressant mechanism. In addition, it is proposed that biologic depression and biologic anxiety should be considered to have some independence from one another. Guidelines for the clinical delineation of anxiety disorders are provided, and the clinical and research implications of the proposal for revision of DSM-III anxiety and phobic disorders section, are outlined in detail. It is suggested that anxiety and phobic disorders be classified into endogenous (disease) and exogenous (nondisease) types.

The authors describe two HLA identical sibling pairs with panic disorder. To their knowledge, this is the first report of histocompatibility testing in patients with anxiety disorders.

Infusions of sodium lactate evoke panic symptoms in patients with panic disorder but not in normal subjects. Although plasma vasopressin (AVP) is known to rise in response to other forms of stress, its response during this maneuver has not previously been reported. We measured plasma AVP in double-blind infusions of sodium lactate in 5 normal subjects, 6 patients with panic disorder, and, again in 4 patients after chronic alprazolam. In all groups administered lactate, AVP rose significantly above baseline values (p less than 0.05) though no change was seen in a control group of patients during D5NS infusion. No difference in AVP response to lactate was apparent between untreated patients (who experienced panic) and normals or chronically treated patients (who had minimal symptoms). Thus, the presence of panic symptoms induced by lactate is insufficient to provoke an abnormal pattern of AVP release.

Of 131 patients with panic disorder or agoraphobia, 44 (34%) had definite mitral valve prolapse on the basis of clinical findings of an apical mid- or late systolic click and a murmur and/or a two-dimensional echocardiogram showing prolapse of one leaflet in two views or of two leaflets in a single view. Seven other patients (5%) had a probable diagnosis of mitral prolapse on the basis of a typical murmur alone or an intermittent apical mid- or late systolic click and a prolapsing leaflet in a single echocardiographic view. This finding confirms previous reports of the association between panic disorder and mitral valve prolapse.

Urinary output of homovanillic acid and 4-hydroxy-3-methoxymandelic acid was decreased both in patients with panic attacks and in normal controls during lactate infusion, whereas that of tribulin (an endogenous monoamine oxidase inhibitor and benzodiazepine receptor binding inhibitor) was increased. There was no change in urinary excretion of any of these compounds during saline infusion. These findings provide further evidence of a link between tribulin output and stress and anxiety in man and point to its possible in vivo action as a monoamine oxidase inhibitor.

The authors review the role of the serotonergic system in panic disorder and the potential for use of the new serotonin (5-HT) reuptake inhibitors in treating panic disorder. Data currently available are only preliminary but suggest a future potential for this class of drug in the treatment of panic/anxiety disorders. The authors present a succinct and comprehensive overview of the data available, which aims to assist in the planning of future research in this area.

Anxiety, phobic and related neurotic disorders lend themselves to diagnostic confusion because of the large and variable array of symptoms associated with them. This has complicated attempts at coherent classification. This paper examines the problems in diagnosis and classification and the diversity of causal models of these disorders. It offers an alternative integrated perspective that may have heurestic merit in guiding clinicians to a practical choice of treatment and in delineating a useful starting point for the biological investigation of these disorders.

In the historical review and empirical delineation of the classification of anxiety and hysterical states (Part I), it was concluded that the existing classifications are unsatisfactory and require some reconceptualization if they are to be useful clinically and empirically. In keeping with more recent developments in the genetic, behavioral, pharmacological, biochemical, and psychophysiological investigation of these disorders, a new classification is proposed. The two major categories of anxiety and hysterical disorders have a different clinical presentation and course, a different mean age of onset, distribution of age of onset, sex distribution, response to treatment modalities, and habituation response on galvanic skin response. Empirical evidence supporting this proposal is cited. This classification has heuristic merit in guiding research efforts and discussions and in directing clinicians to a simple and practical solution to their patients' anxiety disorders.

A more detailed measurement instrument for dental anxiety has been developed. To investigate the dimensionability of the response, two instruments were administered to 452 persons. The first set of items (33) concerned stimuli which might prove fearsome to patients. Some of these were dental specific, others were not. A second instrument (20 items) elicited the anxiety symptoms experienced. By comparing separate Kaiser-Caffrey Alpha Factor Analyses two factors were identified within each instrument. These were labelled "generalized" phobias and "dental specific" phobias; and "endogenous" and "exogenous" (anticipatory) anxiety symptoms. Four scales were constructed using simple summations of highly loaded variables. The scales are quite reliable. Although correlations among the scales proved to be significant they are all quite low, indicating that the four scales give more or less non-redundant information about the patient. The scale had discriminating validity in differentiating between patients who acknowledge experiencing spontaneous panic/anxiety attacks and those who did not. The data confirm that dental fears are relatively independent of other generalized anticipatory fears. The results cast doubt on previously held assumptions regarding the unidimensionality of anxiety. They are consistent with a new classification of anxiety and phobic disorders presented elsewhere. The implications for research and patient management are discussed.

Lactate infusions are anxiogenic in patients with panic disorder or agoraphobia with panic attacks, but few neuroendocrine profiles of this effect have appeared. The authors measured the number and intensity of panic symptoms and blood hormone levels during double-blind lactate infusions in 25 patients and 10 normal subjects and during placebo infusions in another five patients. Each patient was rechallenged with an identical infusate after chronic double-blind outpatient treatment with alprazolam or placebo. The results confirm the effectiveness of lactate infusions in evoking anxiety, extend previous hormone profiles of this maneuver, and indicate that chronic alprazolam treatment minimizes the neuroendocrine response to lactate challenges in patients with panic disorder or agoraphobia with panic attacks.

Eighty-two patients suffering from panic attacks with or without phobias were examined for evidence of thyroid disease. None of the patients had abnormal total T4 or T3 resin uptake measurements, regardless of whether they were nonmedicated or treated with one of three antipanic drugs: alprazolam, phenelzine, or imipramine. A higher than expected incidence of undetectable TSH levels (22% overall) appeared in all groups. The clinical relevance of this finding is currently uncertain.

The authors studied in vitro immune function as measured by lymphocytic proliferative response to mitogen stimulation in 36 patients with agoraphobia and panic attacks who were participating in a double-blind placebo-controlled psychopharmacological study of anxiety disorder. No significant difference in immune status was observed between panic patients and healthy controls.