In the UK, thousands of people with depression continue to undergo electroconvulsive “shock” therapy (ECT) each year, usually if their symptoms have not improved following talking therapy or anti-depressants, and especially if they are considered to be at high risk of suicide, and the numbers may be rising. The technique, which involves using an electric shock to induce a seizure, carries risks, such as memory problems, but the majority of patients experience symptom improvements, and patient surveys show they generally view it positively. However, some experts remain opposed to its use and question its evidence base.
Despite the continued use of ECT, and its apparent benefits, exactly how it works remains largely unexplained. However, new clues come from a Chinese study, published in Social Cognitive and Affective Neuroscience, in which patients showed increased grey matter volume in the amygdala, a brain structure involved in emotional processing.
Jiaojian Wang at the University of Electronic Science and Technology of China, and her colleagues, recruited 23 patients (average age 39; 12 women) with major depression who had not responded to other treatments and/or were acutely suicidal, and who were due to receive a course of ECT.
The researchers scanned the patients’ brains using fMRI 12-24 hours before their first ECT session and then again 24-72 hours after their last session (the patients averaged seven sessions over a 2-3 week period). The scan was used to assess basic brain structure and to look for connectivity patterns between brain areas while the patients rested. For comparison, the researchers also scanned the brains of 25 healthy controls of similar age and educational background.
After treatment, the patients with depression showed not only improved symptoms but also increased grey matter volume in the left amygdala, specifically in a subregion known as the superficial nuclei. The amygdala is involved in emotional processing; the superficial nuclei is involved specifically in interpreting facial expressions.
Post-treatment, the patients also showed increased connectivity between the fusiform face area (FFA) in the temporal lobe, so-called because of its role in processing faces, and the amygdala. Statistical analysis suggested this was because of an increased effect of the FFA on the amygdala, but this remains somewhat speculative.
At pre-treatment, the patients had reduced grey matter in the amygdala and reduced amygdala–FFA connectivity as compared with the healthy controls, and the more extreme these structural and connectivity features, the more severe the patients’ depression symptoms. This suggests the ECT had acted on aspects of brain structure and function relevant to depression.
Wang and her colleagues speculated that the brain changes they observed in the depressed patients may indicate that ECT “alleviates the symptoms of depression by improving … social abilities to enhance the gaze fixation of face stimuli”. More generally the findings are consistent with previous suggestions that ECT helps promote neuronal growth.
This was a small study and the patients were taking different anti-depressants throughout, so larger, more tightly controlled research is needed to confirm and build on the results.