Two important areas of the brain send a specific type of signal between them when people are on the road to becoming depressed or anxious. We don't yet know if disrupting this signal could improve people’s mental health, but at minimum, there is exciting potential to use it as an early diagnosis tool facilitating other interventions.
Electrical signals within the brain are essential for communication between different regions, but can also trigger severe effects when they misbehave. Neuroscientists at the University of California, San Francisco used intracranial electroencephalography (iEEG) machines to study the brain activity of 21 epilepsy patients preparing for brain surgery. The patients were also asked to describe their mood over the period of time in which the measurements were taken.
The 13 participants who suffered bouts of depression or anxiety had signals passing between the amygdala and hippocampus at frequencies between 13 and 30 Hertz, which were not seen in the other participants. These brainwaves, called β-AH ICNs, coincided with periods when anxiety was increasing.
Both regions are known to have important, but poorly understood, roles in processing emotion and mood. The authors also looked for signals between the amygdala and several other brain regions, but found nothing corresponding to mood.
Finding a reliable way to diagnose depression and anxiety, particularly their severity, would mark a major step forward in the treatment of these conditions. Several biomarkers are under investigation for this purpose. However, the finding that β-AH ICNs are associated with a change in mood could make it more valuable still.
“We were surprised to find such a clear and consistent signal,” Dr Vikaas Sohal, a senior author of a paper in Cell reporting the findings, said in a statement.
Searches for a measurable indicator of changing mood have used PET and functional MRI imaging, but, besides being very expensive, these don't last long enough to track changes that take hours, let alone days.
A crucial unanswered question is whether β-AH ICNs cause, or perhaps reinforce, mood changes, or if they are a symptom. In the former case, it may be possible to deliver controlled frequencies to the relevant parts of the brain to disrupt them, as is already done for some patients with Parkinson’s disease.
Although some of the patients were prone to anxiety, for others it was a relatively new experience, presumably triggered by the approaching neurosurgery. As is so often the case, larger sample sizes are needed to confirm the findings. Unfortunately, iEEG requires drilling through the skull to place electrodes directly onto the brain, unlike conventional EEG. This may make finding participants without epilepsy to test the general applicability of the findings challenging, unless fewer interventionist methods are found. Similar limitations may obstruct clinical applications.
