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Anxiety: Anxiety

The biological theories on anxiety developed from preclinical studies with animal models of anxiety, the study of patients in whom biological factors were highlighted, from the increasing knowledge of basic neuroscience and the actions of psychoactive drugs. One school of thought argues that biological variation in patients with measurable distur bo anxiety reflect the result of psychological conflicts. One side asserts that current biological events prior psychological conflicts. The two situations may coexist in certain subjects and a whole range of feelings with a biological basis may exist among individuals with symptoms of anxiety disorder.


autonomic nervous system.

Stimulation of the autonomic nervous system causes certain symptoms - cardiovascular (eg, tachycardia), muscle (eg, headache), gastrointestinal ones (eg, diarrhea) and respiratory (eg, tachypnea). These peripheral manifestations of anxiety are neither unique nor necessarily of anxiety disorders related to the subjective experience of anxiety.

Currently it is generally believed that anxiety precedes the central nervous system manifestations of anxiety devices, except when there is a specific Because device, such as when the subject has a pheochromocytoma. Some individuals with anxiety disorders, particularly panic disorder , have an autonomic nervous system shows an increase of sympathetic tone, it adapts slowly to repeated stimuli and responds to stimuli too moderate.


Neurotransmitters

The three main neurotransmitters associated with anxiety on the basis of animal studies and drug response are adrenaline, serotonin and gamma-amino butyric acid (GABA). Much of the information of the basic sciences neuro anxiety derived from animal experiments involving behavioral paradigms and psychoactive substances. One of these animal models of anxiety is the test of the conflict, in which the animal is simultaneously shown that stimuli are positive (eg, food) and negative (eg, electric shock). The anti-anxiety drugs (eg, zodiazepine well) tend to facilitate the adjustment of the soul in this situation, while other drugs (eg, amfeta mine) that do not worsen the behavioral response of the animal.

Noradrenaline

The general theory on the role of noradrenaline in anxiety disorders is that the patient may have hit a noradrenergic system is poorly regulated that has occasional bursts of activity. The cell bodies of the noradrenergic system are located mainly in the rostral locus coeruleus in the pons and project their axons to the cerebral cortex, the system lim bique, the trunk and spinal cord.

Human studies have found that in patients with disorder pa nico adrenergic agonists (eg, isoproterenol) and adrenergic antagonists (eg, yohimbine) can cause you frequent and severe attacks panic.

On the contrary, clonidine, an adrenergic agonist, reduces symptoms of anxiety in some experimental and therapeutic situations. Less frequently, patients with the disorder anxiety, particularly panic disorder have high levels of urinary or CSF noradrenergic metabolite 3-methoxy-4-hydroxy-sifenilglicole (MHPG).

SEROTONIN

The identification of many types of receptors if rotonina has stimulated the search for a role in the pathogenesis of anxiety disorders. The interest in this report was originally motivated by the observation that serotonergic antidepressants have some therapeutic effects in anxiety disorders - for example, clomipramine in obsessive-compulsive disorder. The efficacy of buspirone, an agonist of the serotonin receptor na lA receptor (5-HT1A) in the treatment of anxiety disorders also suggests the possibility of an association between anxiety and serotonin.