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Anxiety disorders


Anxiety disorders can be triggered by a number of factors, including life experiences and psychological traits. In particular, increased stress and inadequate coping mechanisms may contribute to anxiety. Family history and genetics have also been implicated in the aetiology of anxiety disorders.

Studies show that there is a link between anxiety disorders and specific areas of the brain, and that an imbalance in certain neurotransmitters in the brain that regulate anxiety, such as noradrenaline, serotonin and Gamma-aminobutyric acid (GABA), may contribute to the symptoms of the disease.

The forebrain is the area most affected in people with anxiety disorders. The limbic system, which is involved in storing memories and creating emotions, is also thought to play a central role in processing all anxiety-related information. Both the locus coeruleus and the dorsal raphe project to the septohippocampal circuit, which in turn projects to other areas of the limbic system that mediate anxiety. The hippocampus and amygdala are of particular importance, as they are interconnected and also project to both subcortical and cortical nuclei. Interestingly, in some people with post-traumatic stress disorder (PTSD), the hippocampus appears to be smaller. This may be because of degeneration of dendrites in this part of the brain, which is thought to be caused by a stress-induced increase in the concentrations of glucocoticoids.

Other brain structures involved in controlling emotion, such as the hypothalamus, may also be involved in the pathogenesis of anxiety disorders. People with obsessive-compulsive disorder (OCD) often show increased activity in the basal nuclei, in particular the striatum and other frontal lobe areas of the forebrain.

Serotonin Hypothesis

The serotoninergic systems are involved in controlling anxiety and are almost certainly involved in the pathogenesis of anxiety disorders. Although there has been much research into the role of serotonin in the brain, in particular its function and influence in the synaptic cleft, a full understanding of its function, particularly in disease, is yet to be found (Fuller and Wong, 1997). However, the discovery that selective serotonin reuptake inhibitors (SSRIs), which enhance serotonin-mediated neurotransmission in the brain, are useful in treating mood and anxiety disorders led to the hypothesis that serotonin dysfunction is important in the aetiology of these disorders.

The fact that at least some antidepressant agents, such as the SSRIs, appear to relieve anxiety symptoms suggests that both anxiety disorders and depression share some common aetiopathological mechanisms (Boulenger et al, 1997). This is further illustrated by twin studies showing a common genetic susceptibility between anxiety and depression (Kendler et al, 1987, 1992). The discovery of a common biological basis for anxiety disorders and depression would simplify and improve the treatment of these related disorders (Stahl, 1997).

There are various theories linking the function of serotonin and its receptors to the actions of both anxiolytic and antidepressant drugs. Pharmacological manipulation to enhance serotonin concentration in the brain increases anxiety, and a reduction in serotonin concentrations is associated with reduced anxiety. This suggests that anxiety is caused by abnormally increased serotonin concentrations and depression due to abnormally decreased serotonin concentrations. However, this is an oversimplification of the issue and it has been hypothesised that serotonin receptors actually adapt to the increased concentrations of serotonin and there is a down-regulation of inhibitory 5-HT1A receptors leading to excessive neuronal impulse flow (Stahl, 1997).

Animal models of anxiety have been used to clarify the precise involvement of serotonergic mechanisms in anxiety disorders (Sánchez, 1993). The 5-HT2A/2C receptor antagonist, ritanserin, the partial 5-HT1A receptor agonists, buspirone and ipsapirone, and the 5-HT3 receptor antagonists, zacopride and ondansetron, have all shown anxiolytic effects in a variety of animal test models (Sánchez, 1993). In addition, creating an overall increase in serotonergic activity, using the SSRI citalopram and the serotonin-releasing agent, fenfluramine, relieved symptoms of anxiety in mice. Furthermore, the panic- and anxiety-inducing effects of m-CPP, a serotonin receptor agonist, are well documented (Eriksson et al, 1991).


Last updated: 20.12.2011





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