Tuesday 21 June 2016 5:00pm
What do we mean by ‘anxiety’? This was the fundamental question of Professor Neil McNaughton’s public lecture on June 8th. We are often taught that fear and anxiety are two points on a continuum. But, depending on who you ask, on the language you speak, or on the culture you come from, anxiety and fear will mean something different. For some, fear is strong and anxiety is weak. But for others, fear is normal and anxiety abnormal. The words can become muddled together and the real underlying concepts become impossible to separate out. How can we study anxiety if we don’t know what it means? One trick is to look at drugs used in the clinic.
Ask any two psychiatrists what anxiety is and you can get three different answers. But ask them which drugs are ’anxiolytic’, that is types of drug which target clinical anxiety and they can agree. Professor McNaughton’s focus fell on examples of three chemically different classes of anxiolytic: triazolam (a benzodiazepine), buspirone, and pregablin. The only effect these three classes share is their capacity to reduce the symptoms of generalised anxiety disorder. So he tried to identify what these three very different drugs were doing that was the same in the brain and find out how that controls anxiety.
The cells of your brain fire in many different rhythmic patterns. These rhythms reflect different processes, changing as your brain’s needs change. We can record some of these rhythms as electrical currents from the scalp using an electroencephalograph, or EEG. But what do these rhythms have to do with anxiety? Over the course of his decades long research Professor McNaughton discovered that, in a part of the brain called the hippocampus, all anxiolytics reduce a slow rhythm (5-12 Hz, which means that it has between five and twelve peaks per second). Professor McNaughton believes that this rhythm is important for the generation of clinical anxiety.
With the help of his team Professor McNaughton developed a test which would reliably generate a functionally similar 5-12Hz rhythm in human EEG. His team are now able to determine whether or not a group have been given anxiolytics. This is an important step for drug testing, as it may now give us a biologically based test for showing whether or not a newly developed anxiolytic actually works to reduce anxiety. More importantly, this EEG response may provide a ‘biomarker’ that allows us to tell whether someone has a particular cause of anxiety disorder – his group is testing this at the moment. If you, or someone you know, experiences anxiety and is not on medication contact email@example.com to be a part of further testing for this anxiety biomarker.
The subjectivity of mental illness and diagnosis with symptom checklists often makes treatment difficult. With an objective tool, like the test Professor McNaughton has developed, we can make the process easier. Being able to quickly and accurately determine whether or not a drug will help people with anxiety is an incredible step forward and we hope that, after further testing, this method will be accepted into anxiolytic testing standards.
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