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Mood disorders are the leading cause of health‐related disability, with ‘anxiety disorders’ being commonest in New Zealand. But diagnosis is still based on clinical symptom checklists not biological causes. We have developed a detailed theory of the brain systems controlling threat‐avoidance and threat‐approach—in which activity generates specific behaviours, and hyper‐reactivity (hypersensitivity to input) generates specific clinical syndromes. A key foundation of the theory is a measure of rhythmic brain activity that, in rats, perfectly predicts anti‐anxiety drug action. This led us to a specific non‐invasive measure of activation of the threat‐approach system in the brain of humans: conflict‐specific rhythmicity. We are currently testing whether our new biological marker divides untreated ‘anxiety’ patients with superficially similar clusters of symptoms into distinct high‐scoring and low‐scoring groups with different treatment‐responses, which would validate the first human biological marker for a theoretically‐defined ‘anxiety’ syndrome. This marker should predict treatment efficacy better than current symptom‐based diagnoses; greatly improving treatment outcomes and cost‐effectiveness. Abbreviations: BIS: Behavioural Inhibition System; DSM‐5: Diagnostic and Statistical Manual of the American Psychiatric Association, 5th edition; FFFS: Fight, Flight, Freeze System; GAD: Generalised Anxiety Disorder; ICD‐10: International Classification of Diseases, 10th edition; OCD: Obsessive Compulsive Disorder; RDoC: Research Domain Criteria Professor Neil McNaughton
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Neil McNaughton (2017) studied this question.
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