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Biochemical Basis of Anxiety

Recent work suggests that some patients may be biochemically more sensitive to the development of anxiety symptoms in the presence of particular diseases. Mathew et al have reported that patients with generalized anxiety disorders have higher plasma catecholamine levels than normal controls. These patients may down regulate catechol receptors as a result of these higher plasma concentrations and thus experience reduced receptor sensitivity in their adrenergic nervous system. Other investigators, however, have failed to confirm these findings. Abelson et al have noted that patients with generalized anxiety have a blunted growth hormone response to clonidine (an alpha2-partial agonist) stimulation , suggesting a decreased sensitivity of alpha2 adrenergic receptors. It may be that higher levels of catecholamines lead to down regulation of selective patients' post-synaptic alpha2-adrenoceptors.

Brawman-Mintzer and Lydiard in reviewing research data in this area suggest that patients at risk for generalized anxiety disorder may have deficits in the regulatory mechanisms of the hypothalamic-pituitary-axis associated with an abnormal response to stress. They hypothesize that such patients are more sensitive than controls in terms of the number and intensity of symptoms that they develop following a panic challenge paradigm, and that they are therefore biologically distinct from patients with a primary panic disorder. The generalized anxiety patients appear to have alterations in the sensitivity of their central benzodiazepine receptors, abnormalities of serotonergic function and alteration of their 5-HT1 and 5-HT2 receptors. These researchers also cite data to suggest abnormalities in the cholecystokinin system in patients who develop severe anxiety, as well as significant changes in brain activity in this population.

Wu et al noted higher relative metabolic rates in the brains of patients with generalized anxiety disorder, particularly in the occipital temporal (right posterior temporal lobe) and frontal lobes (left interior frontal gyrus), as well as in the cerebellum. They also noted decreased absolute metabolic activity in the area of the basal ganglion, the cingulate gyrus, the temporal lobes, the amygdala, and the hippocampus of these patients. Patients with general anxiety disorder had significant increases in activity in their basal ganglion and right parietal lobes and a decrease in metabolism in their right temporal and occipital lobes during vigilant tasks. When benzodiazepines were administered to these patients, cerebral glucose metabolism over the cortical surface, particularly the occipital cortex and in the limbic system and basal ganglion, diminished markedly.

Brawmin-Mintzer and Lydiard summarized the currently existing data and suggest that there are several cellular structural abnormalities and changes in regulatory mechanisms that may be important biological components in the production of anxiety. Maladaptive responses to stressful stimuli occur in the locus ceruleus-norepinephrine-sympathetic nervous system, the hypothalamic-pituitary-axis, and the cholecystekinen system. Other abnormalities have been noted in the 5-HT and GABA-modulating systems.

Gray proposes a behavioral inhibition system as a model for anxiety disorder. In this system he defines the neuroanatomic circuits that modulate response to stress. When overstimulated, these systems produce persistent anxiety states in humans. The septohippocampal system processes threat-relevant stimuli. Discharge of this system increases arousal. Noradrenergic and serotonergic stimulation to the septohippocampal area activates the system, which in turn generates impulses to the limbic structures and the prefrontal cortex.

Medical conditions that alter the hypothalamic-pituitary-axis or which alter transmitter or receptor function may impact this system and produce anxiety-like states. Neuroimaging data provides support for this concept. It is hoped that further research into this area will help define the biological correlates of medically induced and primary anxiety disorders.

Diagnosis and Coding DSM-IV establishes specific criteria for determining that a mental disorder is due to a general medical condition. "There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition. When a mental disorder is due to a general medical condition, one does not diagnose the primary psychiatric disorder with the same symptom, but rather codes the symptom secondary to the general medical condition. Thus, with anxiety one would not code 300.02, generalized anxiety disorder, but rather 293.89, anxiety disorder due to a general medical condition. The 293.89 code may be used for those specific presentations of anxiety states which include generalized anxiety symptoms, panic attacks, obsessions and/or compulsions. When the 293.89 code is used, it is important that the anxiety symptoms be well defined and prominent and that there is evidence from history, physical examination and laboratory findings that these symptoms are a physiological consequence of the patient's general medical condition. Clinicians should also be sure that the disturbance is not better accounted for by some other mental disorder such as an adjustment disorder with secondary anxiety brought on by the diagnosis of a disease. This diagnosis should not be used if anxiety symptoms occur only during the course of a delirium. Finally, the anxiety symptoms associated with the medical disorder must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

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