Disease relevance of Anxiety Disorders

• Buspirone for anxiety disorders in patients with severe lung disease [1].
• This study examined the interrater reliability of generalized anxiety disorder (GAD) and major depressive disorder (MDD) diagnoses derived from the Structured Clinical Interview for DSM-III (SCID) [2].
• This review covers the roles of GABAergic neurotransmission in epilepsy, anxiety disorders, schizophrenia, stiff-person syndrome, and premenstrual dysphoric disorder [3].
• BACKGROUND: It is still unknown whether anxiety disorders observed in Graves' disease are a consequence of increased thyroid hormone levels or precede the onset of Graves' disease [4].
• OBJECTIVE: To examine the association between chronic headaches and DSM-III-R-defined psychiatric disorders, including depression, anxiety disorders, conduct disorder, oppositional defiant disorder and attention-deficit hyperactivity disorder, in a population-based sample of children and adolescents [5].

Psychiatry related information on Anxiety Disorders

• Impaired 5-HT and BDNF signaling is central to depression and anxiety disorders, but could also play important roles in the pathogenesis of several age-related disorders, including insulin resistance syndrome, Alzheimer's disease and Huntington's disease [6].
• To examine the role of the noradrenergic system in anxiety disorders, 23 patients (nine with generalized anxiety disorders and 14 with panic disorders) were studied for four weeks with clonidine hydrochloride, a predominantly presynaptic noradrenergic agonist, and with placebo [7].
• To determine whether nicotine dependence, classified by level of severity, was associated with other substance dependence, major depression, and anxiety disorders, we studied a random sample of 1007 young adults in the Detroit (Mich) area using the National Institute of Mental Health Diagnostic Interview Schedule, revised according to DSM-III-R [8].
• Relatives of children in the nonaffective psychiatric control (PC) group had low rates of alcoholism, high rates of other (anxiety) disorder diagnoses, and intermediate rates of MDD (accounted for by those children with separation anxiety) [9].
• 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 [10].

High impact information on Anxiety Disorders

• Fluvoxamine for the treatment of anxiety disorders in children and adolescents [11].
• Benzodiazepine tranquilizers are used in the treatment of anxiety disorders [12].
• As reviewed in this chapter, the existing preclinical and clinical literature is suggestive of, but not conclusive, concerning a role of substance P and NK(1) receptors in the pathophysiology of depression and/or anxiety disorders [13].
• CONTEXT: Evidence suggests that early adverse experiences play a preeminent role in development of mood and anxiety disorders and that corticotropin-releasing factor (CRF) systems may mediate this association [14].
• Efficacy of venlafaxine extended-release capsules in nondepressed outpatients with generalized anxiety disorder: A 6-month randomized controlled trial [15].

Chemical compound and disease context of Anxiety Disorders

• Efficacy of paroxetine for relapse prevention in social anxiety disorder: a 24-week study [16].
• Antidepressants for the treatment of generalized anxiety disorder. A placebo-controlled comparison of imipramine, trazodone, and diazepam [17].
• OBJECTIVE: To assess the anxiolytic efficacy of pregabalin in patients with generalized anxiety disorder [18].
• CONCLUSIONS: In humans with mood and anxiety disorders, small hippocampal volumes have been taken as evidence that excessive stress levels of cortisol induce hippocampal volume loss [19].
• Heart rate and plasma norepinephrine responsivity to orthostatic challenge in anxiety disorders. Comparison of patients with panic disorder and social phobia and normal control subjects [20].

Biological context of Anxiety Disorders

• The current study evaluates the association between salivary cortisol concentrations and response to carbon-dioxide inhalation in children and adolescents with anxiety disorders, mood disorders, or no psychiatric illness [21].
• BACKGROUND: Although citalopram has gained wide acceptance in the treatment of depression and anxiety disorders, its use during pregnancy and lactation has been poorly characterized [22].
• This article highlights multiple neurobiological interactions that play a role in anxiety and reviews selected studies of plasma neurosteroid levels, plasma GABA levels, and benzodiazepine binding site sensitivity and density in patients with anxiety disorders [23].
• Benzodiazepine-induced chemotaxis is impaired in monocytes from patients with generalized anxiety disorder [24].
• The DRD2 NcoI C allele frequency is significantly higher (Chi-square = 17.13; p < 0.00002) in individuals with MWA, anxiety disorders, and/or major depression (C allele frequency = 0.80) than in individuals who have none of these disorders (C allele frequency = 0.67) [25].

Anatomical context of Anxiety Disorders

• 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 [10].
• RESULTS: Generalized anxiety disorder patients had a 16.5% higher N-acetylaspartate/creatine ratio in the right dorsolateral prefrontal cortex compared with healthy participants; 13 of 15 matched patient-comparison subject pairs displayed a difference in this direction [26].
• METHOD: N-Acetylaspartate/creatine resonance ratios were measured in the left and right dorsolateral prefrontal cortex and hippocampus of 15 medication-free generalized anxiety disorder patients and 15 age- and sex-matched healthy volunteers [26].
• CONCLUSIONS: With use of pure depression and anxiety groups and careful control of other factors known to affect GH, these results demonstrate central nervous system noradrenergic dysfunction in anxiety disorders [27].
• Moreover, CRF has also been implicated in the pathogenesis of a variety of anxiety disorders, mainly through CRF neurocircuits connecting the amygdala and the locus ceruleus [28].

Gene context of Anxiety Disorders

• Cholecystokinin (CCK) may mediate human anxiety and animal data suggest that cholecystokinin antagonists could provide an important advance in the treatment of anxiety disorders [29].
• RATIONALE: Hypersecretion of corticotropin releasing factor (CRF) has been implicated in both severe anxiety disorders and major depression [30].
• The zinc metalloenzyme glyoxalase I (GLO1) is thought to play a role in anxiety disorders because a reduced brain expression of GLO1 has been associated with increased anxiety-behaviours in mice [31].
• Our data support the hypothesis that the hyperactivity of the noradrenergic system in response to stress is associated with anxiety disorders in adolescents and might influence the responses of GH and Te [32].
• Polymorphisms in the regulatory region of the serotonin transporter (5-HTT), in intron 7 of the tryptophan hydroxylase (TPH) gene and in the MAOA gene were previously reported to be associated with mood and anxiety disorders, impulsivity and aggression [33].

Analytical, diagnostic and therapeutic context of Anxiety Disorders

• Accordingly, though benzodiazepines (which reinforce transmission at GABA(A) receptors), serotonin (5-HT)(1A) receptor agonists and 5-HT reuptake inhibitors are currently the principle drugs employed in the management of anxiety disorders, there is considerable scope for the development of alternative therapies [34].
• In 984 patients with generalized anxiety disorder who received buspirone in double-blind studies, the incidence of drowsiness (9 percent) did not differ significantly from that (10 percent) reported in 334 patients who received placebo [35].
• Positron emission tomography (PET) measurements of cerebral glucose use were made in 18 patients with generalized anxiety disorder (GAD) during a passive viewing task off medication, and an active vigilance viewing task before and after medication or placebo treatment [36].
• Topographic EEG changes with benzodiazepine administration in generalized anxiety disorder [37].
• BACKGROUND: Selective serotonin reuptake inhibitors are effective in the treatment of social anxiety disorder and are currently regarded as the pharmacotherapy of choice [38].

References