Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta-Adrenoceptor blocking drugs have been used for the treatment of acute stress reactions, adjustment disorders, generalised anxiety, panic disorder and agoraphobia. In general they are effective in these disorders if somatic or autonomic symptoms are prominent but not extreme in degree. Thus, they are of more value for the relatively mild tremor of the anxious violinist in public performance than in the severe shaking noticed during a panic attack. It is most likely that beta-blockers act primarily by blocking peripheral adrenergic beta-receptors; symptoms that are mediated through beta-stimulation, such as tremor and palpitations, are helped most. Improvement is noted within 1 to 2 hours and with relatively low doses (e.g. propranolol 40 mg/day). Some recent studies, however, have suggested that when longer treatment using higher doses (e.g. propranolol 160 mg/day) is given, improvement in other forms of anxiety is noted after several weeks of treatment. beta-blocking drugs are useful adjuncts to existing treatments for anxiety and are likely to enjoy wider use now that benzodiazepines are being avoided due to their dependence risks.
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PMID:Current status of beta-blocking drugs in the treatment of anxiety disorders. 290 81

Stress induces an imbalance of neuroimmunomodulation, a phenomenon involving the immune, central nervous and endocrine systems. Receptors to substances involved in stress reactions and anxiety, like adrenaline, acetylcholine, histamine, endomorphines, ACTH and several neuropeptides, are present on lymphocytes and lymphocytes can secrete various hormones and neuropeptides. Peripheral and central, cortical and subcortical nervous structures influence immune response. Steroids play a dose dependent inhibitory role perhaps via GIF (Glucocorticoid Increasing Factor) and cytokines (IL 1). In rats, stress induces an increase of corticosterone levels and a lymphopenia depending on the presence of adrenals and pituitary, whereas functional responses to mitogens appear decreased in animals even after surgical removal of adrenals and/or pituitary. Immune response vary according to the degree of control over stressors, to the type of stressor and the animal species. Chronic or repeated stress tends to stimulate immune reaction, contrary to acute stress. In man grief reactions, terminal illness of a spouse, divorce, examinations, caregiving to Alzheimer patients have been used as models of stress, with immune consequences. Pathological anxiety has been less studied, with only few anomalies reported in DSM III-R panic disorder. The immune system participation in the adaptive response to stress is reviewed.
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PMID:[Stress and panic. Immunologic aspects]. 828 94

This study applied the corticotropin-releasing hormone (CRH) stimulation test to patients with panic disorder, before and during treatment with alprazolam, and to control subjects. In contrast to some, but not all prior studies, untreated, nondepressed panic disorder patients failed to show blunted adrenocorticotropic hormone or cortisol responses to CRH. In fact, the responses were subtly enhanced in that they were more rapid than those of controls. After 12 weeks of alprazolam treatment, repeat testing gave results that were indistinguishable from those of controls. Inconsistency among reports of CRH testing in panic disorder may be related to interactions among illness mechanisms, concurrent subthreshold depressive symptoms, the chronic stress of the illness, and hyperresponsiveness of panic patients to the acute stress of experimental manipulations. Pretreatment abnormalities in hypothalamic-pituitary-adrenal axis function appear to resolve with alprazolam treatment. Preliminary observations suggest that pretreatment dysregulation of the hypothalamic-pituitary-adrenal system may predict a more difficult or less satisfactory treatment.
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PMID:Adrenocorticotropic hormone and cortisol responses to corticotropin-releasing hormone: changes in panic disorder and effects of alprazolam treatment. 898 98

1. To distinguish GAD from panic disorder is not difficult if a patient has frequent, spontaneous panic attacks and agoraphobic symptoms, but many patients with GAD have occasional anxiety attacks or panic attacks. Such patients should be considered as having GAD. An even closer overlap probably exists between GAD and social phobia. Patients with clear-cut phobic avoidant behavior may be distinguished easily from patients with GAD, but patients with social anxiety without clear-cut phobic avoidant behavior may overlap with patients with GAD and possibly should be diagnosed as having GAD and not social phobia. The cardinal symptoms of GAD commonly overlap with those of social phobia, particularly if the social phobia is more general and not focused on a phobic situation. For example, free-floating anxiety may cause the hands to perspire and may cause a person to be shy in dealing with people in public, and thus many patients with subthreshold social phobic symptoms have, in the authors' opinion, GAD and not generalized social phobia. The distinction between GAD and obsessive-compulsive disorder, acute stress disorder, and posttraumatic stress disorder should not be difficult by definition. At times, however, it may be difficult to distinguish between adjustment disorder with anxious mood from GAD or anxiety not otherwise specified, particularly if the adjustment disorder occurs in a patient with a high level of neuroticism or trait anxiety or type C personality disorder. Table 2 presents features distinguishing GAD from other psychiatric disorders. 2. Lifetime comorbid diagnoses of other anxiety or depression disorders, not active for 1 year or more and not necessitating treatment during that time period, should not effect a diagnosis of current GAD. On the other hand, if concomitant depressive symptoms are present and if these are subthreshold, a diagnosis of GAD should be made, and if these are full threshold, a diagnosis of MDD should be made. 3. If GAD is primary and if no such current comorbid diagnosis, such as other anxiety disorders or MDD, is present, except for minor depression and dysthymia, or if only subthreshold symptoms of other anxiety disorders are present, GAD should be considered primary and treated as GAD; however, patients with concurrent threshold anxiety or mood disorders should be diagnosed according to the definitions of these disorders in the DSM-IV and ICD-10 and treated as such. 4. Somatization disorders are now classified separately from anxiety disorders. Some of these, particularly undifferentiated somatization disorder, may overlap with GAD and be diagnostically difficult to distinguish. The authors believe that, as long as psychic symptoms of anxiety are present and predominant, patients should be given a primary diagnosis of GAD. 5. Two major shifts in the DSM diagnostic criteria for GAD have markedly redefined the definition of this disorder. One shift involves the duration criterion from 1 to 6 months, and the other, the increased emphasis on worry and secondary psychic [table: see text] symptoms accompanied by the elimination of most somatic symptoms. This decision has had the consequence of orphaning a large population of patients suffering from GAD that is more transient and somatic in its focus and who typically present not to psychiatrists but to primary care physicians. Therefore, clinicians should consider using the ICD-10 qualification of illness duration of "several months" to replace the more rigid DSM-IV criterion of 6 months and to move away from the DSM-IV focus on excessive worry as the cardinal symptom of anxiety and demote it to only another important anxiety symptom, similar to free-floating anxiety. One also might consider supplementing this ICD-10 criterion with an increased symptom severity criterion as, for example, a Hamilton Anxiety Scale of 18. Finally, the adjective excessive, not used in the definition of other primary diagnostic criteria, such as depressed mood for MDD, should be omitted (Table 3). 6. One may want to consider the distinction of trait (chronic) from state (acute) anxiety, but whether the presence of some personality characteristics, particularly anxious personality or Cluster C personality and increased neuroticism, as an indicator of trait [table: see text] anxiety is a prerequisite for anxiety disorders; occurs independently of anxiety disorders; or is a vulnerability factor that, in some patients, leads to anxiety symptoms and, in others, does not, is unknown. 7. Symptoms that some clinicians consider cardinal for a diagnosis of GAD, such as extreme worry, obsessive rumination, and somatization, also are present in other disorders, such as MDD. (ABSTRACT TRUNCATED)
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PMID:Overview and clinical presentation of generalized anxiety disorder. 1122 2

Thought Field Therapy (TFT) is a self-administered treatment developed by psychologist Roger Callahan. TFT uses energy meridian treatment points and bilateral optical-cortical stimulation while focusing on the targeted symptoms or problem being addressed. The clinical applications of TFT summarized included anxiety, adjustment disorder with anxiety and depression, anxiety due to medical condition, anger, acute stress, bereavement, chronic pain, cravings, depression, fatigue, nausea, neurodermatitis, obsessive traits, panic disorder without agoraphobia, parent-child stress, phobia, posttraumatic stress disorder, relationship stress, trichotillomania, tremor, and work stress. This uncontrolled study reports on changes in self-reported Subjective Units of Distress (SUD; Wolpe, 1969) in 1,594 applications of TFT, treating 714 patients. Paired t-tests of pre- and posttreatment SUD were statistically significant in 31 categories reviewed. These within-session decreases of SUD are preliminary data that call for controlled studies to examine validity, reliability, and maintenance of effects over time. Illustrative case and heart rate variability data are presented.
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PMID:Thought Field Therapy clinical applications: utilization in an HMO in behavioral medicine and behavioral health services. 1152 9

This study examined the prevalence of peritraumatic and persistent panic symptoms following trauma. Survivors of civilian trauma (n=30) with either acute stress disorder (ASD) or no acute stress disorder (non-ASD) were administered the Panic Module of the Structured Clinical Interview for DSM-IV (SCID). Participants also completed the Impact of Event Scale, Acute Stress Disorder Scale, Beck Depression Inventory, Beck Anxiety Inventory, and the Anxiety Sensitivity Index. Panic attacks were experienced by 77% of participants during their trauma, and 47% reported recurrent panic attacks post-trauma. ASD participants demonstrated more panic symptoms during and after their trauma than non-ASD participants. Posttraumatic panic was most strongly associated with anxiety sensitivity. These findings are discussed in terms of cognitive factors that may mediate posttrauma panic and treatment implications for managing posttraumatic anxiety. There is increasing evidence that panic attacks play a role in psychopathological response to trauma. A significant proportion of people with panic disorder report a history of trauma (). Moreover, two-thirds of trauma survivors report panic attacks within the previous 2 weeks (). There is also evidence that people with posttraumatic stress disorder (PTSD) display elevated levels of anxiety sensitivity (). Recent attention has focused on acute panic reactions because of proposals that panic during trauma may condition trauma-related cues to subsequent panic (). There is evidence that panic attacks occur in 53-90% of trauma survivors during the traumatic experience (). Further, people with acute stress disorder (ASD) are more likely to report peritraumatic panic attacks than non-ASD individuals. ASD is a useful framework in which to investigate the role of panic in posttraumatic stress because ASD describes acute responses to trauma that are strongly predictive of chronic PTSD (). This study investigated the relationship between peritraumatic panic and ongoing panic attacks following trauma. Specifically, we indexed panic attacks during trauma and subsequent to trauma in trauma survivors with and without ASD. We also indexed the extent to which distorted interpretations about somatic sensations may be associated with panic attacks following trauma. We considered that the strong evidence that maladaptive appraisals of somatic sensations mediate panic () is directly relevant to posttraumatic panic. We hypothesized that ASD participants would report more peritraumatic and persistent panic than non-ASD participants, and that this panic would be associated with dysfunctional interpretations about somatic stimuli.
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PMID:Peritraumatic and persistent panic attacks in acute stress disorder. 1297 43

Stress increases plasma and brain concentrations of corticosteroids and neuroactive steroids. Cortisol is the most important stress hormone in the hypothalamic pituitary adrenocortical system. However, significant amounts of the mineralocorticoid deoxycorticosterone are also released during stress. Deoxycorticosterone undergoes biotransformation to allotetrahydrodeoxycorticosterone, a neuroactive steroid with anxiolytic and anticonvulsant properties. Our studies indicate that the anticonvulsant activity of deoxycorticosterone is mediated by its conversion to allotetrahydrodeoxycorticosterone, which is a potent positive allosteric modulator of GABA(A) receptors. Although the role of allotetrahydrodeoxycorticosterone within the brain is undefined, recent studies indicate that stress induces increases in allotetrahydrodeoxycorticosterone to levels that can activate GABA(A) receptors. These results might have significant implications for human stress-sensitive conditions such as epilepsy, panic disorder, post-traumatic stress disorder, and major depression. In epilepsy, a role for adrenal allotetrahydrodeoxycorticosterone in seizure susceptibility has been suggested. Recent preclinical studies indicate a role of neuroactive steroids in ethanol actions. Although these studies provide a better understanding of the role of allotetrahydrodeoxycorticosterone and related neuroactive steroids in acute stress, further studies are clearly warranted to ascertain the specific role of neuroactive steroids in the pathophysiology of chronic stress and related brain conditions.
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PMID:Physiological role of adrenal deoxycorticosterone-derived neuroactive steroids in stress-sensitive conditions. 1632 48

Serotonin-promoting drugs show cardioprotective properties in patients with anxiety or depression, but it is not known if this is a direct effect of increasing serotonin. We aimed to characterize the effect of serotonin manipulation through acute tryptophan depletion on cardiovascular and psychological responses to stress challenge in recovered patients with anxiety disorders. In 27 recovered patients with anxiety disorders (panic disorder treated by selective serotonin reuptake inhibitors (SSRIs) or cognitive behavioral therapy, social anxiety disorder treated by SSRIs), we performed a double-blind randomized crossover study. On 2 separate days, the subjects ingested an acute tryptophan-depleting (aTD) or nondepleting (nD) drink in random order and underwent a stress challenge at time of maximum depletion. Systolic blood pressure (P = 0.007; diff = 9.0 mm Hg; 95% confidence interval (CI), 2.6-15.3 mm Hg) and diastolic blood pressure (P = 0.032; diff = 5.7 mm Hg; 95% CI, 0.6-10.9 mm Hg) responses to stress were significantly greater under aTD than nD, as were the psychological responses to stress (for Spielberger state anxiety, difference in stress response between aTD and nD = 7.11; P = 0.025). Blood pressure responses to stress showed no correlation with psychological responses. The significant increases in acute stress sensitivity in both cardiovascular and psychological domains on serotonin depletion suggest that serotonin is involved in the control of both cardiovascular and psychological aspects of the acute stress response. The lack of correlation in the difference between aTD and nD conditions in cardiovascular and psychological responses suggests that serotonin may have distinct effects on these 2 domains, rather than the cardiovascular responses being merely a secondary consequence of psychological changes.
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PMID:Depleting serotonin enhances both cardiovascular and psychological stress reactivity in recovered patients with anxiety disorders. 1685 62

Stressful life events increase the susceptibility for subsequent onset of psychiatric disorders in humans. Previous research has implicated neurotrophins in the onset of some stress-related diseases, such as major depression disorder, post-traumatic stress disorder or panic disorder. We have tested the hypothesis that the neurotrophin-3 (NT-3)/TrkC system is a genetic interface mediating the deleterious effects of stress on the initiation of panic disorder and other pathologies. To this aim, we have analyzed the functionality of HPA axis and the behavioral consequences of different types of stressful conditions in a mouse model of panic disorder, which overexpresses TrkC, the high affinity-receptor for NT-3 (TgNTRK3). Our results reveal that TgNTRK3 mice exhibit an altered circadian corticosterone rhythm that is reversed by clonidine treatment, but normal expression of genes involved in the control of the hypothalamus-pituitary-adrenal (HPA) axis (CRH, GR) and normal corticosterone response to acute and chronic stressors. In contrast, they exhibit an altered pattern of activation of stress-related brain areas and showed enhanced anxiety-related behavior and more passive strategies than wild types under some chronic stress conditions. We conclude that TgNTRK3 mice present differences in their response to stress characterized by subtle changes in the HPA axis, marked changes in acute stress-induced brain activation and altered coping strategies, suggesting a key role of TrkC receptor in the stress neural circuitry and in the behavioral consequences of chronic stress.
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PMID:Susceptibility to stress in transgenic mice overexpressing TrkC, a model of panic disorder. 1969 58

In Japan, the impact of DSM-5 has been greater than we had imagined. The Japanese Society of Psychiatry and Neurology organized a group for translation and the members spent many hours in this volunteer effort over a 2-year period. This highlights the significance of and expectations for DSM-5 in clinical practice in Japan. Regarding anxiety disorders, the highlights of changes from DSM-IV-TR to DSM-5 are as follows. Firstly, the DSM-5 chapter on anxiety disorder no longer includes obsessive-compulsive disorder (which is included with obsessive-compulsive and related disorders) or posttraumatic stress disorder and acute stress disorder(which are included with trauma- and stressor-related disorders). However, the sequential order of these chapters in DSM-5 reflects the close relationships among them. Secondly, in DSM-IV, selective mutism and separation anxiety disorder were classified in the section "Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence." They are now classified as an anxiety disorder. Through these two changes, at the beginning of the chapter, it can be clearly noted that anxiety disorders include disorders that share features of excessive fear and anxiety and related behavioral disturbances. Thirdly, panic disorder and agoraphobia are not associated in DSM-5. Thus, the former DSM-IV diagnoses of panic disorder with agoraphobia, panic disorder without agoraphobia, and agoraphobia without a history of panic disorder are now replaced by two diagnoses, panic disorder and agoraphobia, each with separate criteria. The co-occurrence of panic disorder and agoraphobia is now coded with two diagnoses. This change recognizes that a marked number of individuals with agoraphobia do not experience panic symptoms. For the present, this change ends the. controversy over the hierarchy between panic disorder and agoraphobia. The diagnostic criteria for agoraphobia are derived from the DSM-IV descriptors for agoraphobia, although the clarification of fears from two or more agoraphobia-related situations is now required, because this is a robust means for distinguishing agoraphobia from specific phobias. Also, the criteria for agoraphobia are now extended to be consistent with criteria sets for other anxiety disorders (e.g., a clinician's judgment of the fears as being out of proportion to the actual danger in the situation, with a typical duration of 6 months or more). From the above, these changes from DSM-IV-TR to DSM-5 in anxiety disorders make our judgments faster and more efficient in clinical practice, and DSM-5 is more useful to elucidate the pathology. In this manuscript, we discuss the application and problems based on clinical and research viewpoints regarding anxiety disorders in DSM-5.
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PMID:[Impact of DSM-5: Application and Problems Based on Clinical and Research Viewpoints on Anxiety Disorders]. 2682 11


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