Thank you! Great question – it seems that global infraslow dynamics continue during transitional states for sleep and anesthesia (i.e., where you see these spatial maps persisting). Some interesting perspectives on this: doi.org/10.1016/j.co... doi.org/10.1016/j.ne... doi.org/10.1016/j.ce...

Takeaway: We have been missing a huge brain event during ECT. Further research can help us learn more to optimize stimulation and outcomes for this life-saving treatment. If CSD proves central to the mechanism of ECT, we could develop novel brain stimulation therapies that don’t require seizure!

ECT can cause side effects, most often temporary memory issues. As with any treatment, we discuss this risk with patients and weigh against potential benefits, so that patients can make informed decisions. We are now testing if memory effects might also be modulated by spreading depolarization.

ECT is stigmatized and misrepresented in popular media and by anti-psychiatry activists. The reality is ECT is not painful, violent, or a form of punishment. Patients are asleep and immobilized with general anesthesia during the seizure. There is no evidence that ECT causes ‘brain damage’.

We are now testing if CSD mediates the clinical effects of ECT. This hypothesis could explain:
- why seizure intensity predicts therapeutic effects
- why stimulation parameters modulate outcomes
- why ECT is inhibitory and raises seizure thresholds (CSD is an intrinsic anti-seizure mechanism)

We then showed that CSD waves also occur in routine ECT treatments in human patients. This required a novel tool – bedside, non-invasive optical monitoring of brain hemodynamics – developed by our colleagues in the Penn Physics dept!

Clinically, ECT stimulation parameters are known to modulate outcomes. Here, we found that electrode placement shapes where seizure is most intense and where CSD is triggered. Increasing pulse current and frequency increase seizure amplitude, which in turn predicts the likelihood of triggering CSD.

Why has this gone undetected for nearly 86 years? CSD wavefronts travel very slowly (millimeters per minute), such that when they are subjected to routine low frequency EEG filtering (our mainstay tool for brain monitoring during ECT), they’re rendered virtually invisible (right video panel).

In a mouse model, we observed that seizure is followed by a slow-traveling wave of maximal neural and hemodynamic activation followed by suppression, consistent with cortical spreading depolarization (CSD). Only high amplitude seizures cross the threshold of triggering this all-or-none event.

ECT remains the most effective treatment for severe, medication-resistant depression, achieving rapid remission in 60-80% of patients. It also works for psychosis, mania, catatonia, and more, when other treatments have failed. Why electrically-induced seizure is therapeutic has remained a mystery.

Takeaway: We have been overlooking a huge brain event during ECT due to understudy. Research can help us optimize stimulation and outcomes for this life-saving treatment. If CSD proves central to the mechanism of ECT, we could develop novel brain stimulation therapies that don’t require seizure!

ECT can cause side effects, most often temporary memory issues. As with any treatment, we discuss this risk with patients and weigh against potential benefits, so that patients can make informed decisions. We are now testing if memory effects might also be modulated by spreading depolarization.

ECT is stigmatized and misrepresented in popular media and by anti-psychiatry activists. The reality is ECT is not painful, violent, or a form of punishment. Patients are asleep and immobilized with general anesthesia during the seizure. There is no evidence that ECT causes ‘brain damage’.

We are now testing if CSD mediates the clinical effects of ECT. This hypothesis could explain:
- why seizure intensity predicts therapeutic effects
- why stimulation parameters modulate outcomes
- why ECT is inhibitory and raises seizure thresholds (CSD is an intrinsic anti-seizure mechanism)

We then showed that CSD waves also occur in routine ECT treatments in human patients. This required a novel tool – bedside, non-invasive optical monitoring of brain hemodynamics – developed by our colleagues in the Penn Physics dept!