Hello, thank you for the opportunity to share information on ECT Injury.
Hopefully increasing understanding can improve quality of life after ECT, by identifying appropriate rehabilitation interventions based on the kind of injury involved.
The information presented here is not medical advice.
It may be triggering for some, if accurate and complete risks, were not explained honestly, during the legal informed consenting process.
This brief presentation covers:
- Why every patient has a uniquely different ECT experience
- What device manufacturers mean when they warn that ECT can cause brain damage
- Discuss how ECT qualifies as a repetitive, mild or moderate, traumatic brain injury
- Discuss the importance of looking at ECT as repeated electrical injury
- Understanding how the damage impacts life after treatment
Unregulated variables in electrical dosing
When talking about ECT, we must remember, not all ECT is the same, because of the number of variables involved in generating the electrical field strength, or what we can think of as the electrical dose, and the circumstances under which it is generated.
Let’s take a look at how many unregulated variables are involved in creating an electrical dose.
Keep in mind, psychiatrists have specialty training in human biology, not the physics of bioengineering.
Variables include the current strength. It is fixed at either 800 or 900 milliamps, depending on the device.
Yes, you heard correctly, every device in every country has different electrical dosing capacity, even when made by the same manufacturer.
Fixed amperage is an arbitrary number without clinical or scientific rationale.
Pulse width and pulse type.
Frequency is an important variable, the hertz setting determines how long the current is pulsed through the brain, depending on hertz settings, it could be pulsed for up to eight, seconds.
Modern ECT machines produce different voltages.
MECTA is 250 volts. Thymatron generates 450 volts.
To continue with variables:
- Percent of Power?
- Where are electrodes put on the head?
- In bilateral electrode placement, the charge’s focus, is the “anterior of the frontal lobes and brain stem.”
Additional variables include:
- How much electricity was given to a patient compared to the dose needed to cause a seizure?
- How long the brain was exposed to the pulsed charge?
- How long each seizure lasted?
- How long did the brain activity turn off before it restarted? Which medicines are in the blood during ECT?
- Medicine and anything else in the blood is delivered at a cellular level, amplifying their effects.
Other variables include:
- Length of time between treatments.
- The number of ECT treatments a person endures.
ECT’s 7 variables of risk
Here is a screenshot of the 2018 Regulatory Update for the Thymatron, ECT machine.
It was published within days of the confidential settlement in an American Federal court case against the device manufacturer.
Notice how they cite the American Psychiatric Association as recognizing seven independent risks associated with ECT’s permanent memory loss and permanent brain damage.
It’s important to know that each of these risks are independent which means patients can be exposed to any number of risks during each and every treatment.
I had 5 of the 7 risks.
Understanding ECT induced brain damage
So, how can we better understand ECT’s damage?
I’d like to introduce you to Dr Bennet Omalu.
He’s a forensic neuropathologist.
The coroner, who first identified chronic traumatic encephalopathy in American Football players.
Will Smith played him in the movie, Concussion.
Doctor Omalu explained ECT injury during a Brain Injury Advisory board meeting for the State of California’s Department of Rehabilitation.
He confirmed that repetitive head trauma causes functional injuries that aren’t readily seen on standard brain scans, but that the neuropathology of electrical injury and people with a history of ECT is easily recognized under a microscope.
He said it causes extensive functional changes which must be considered in the context of both an electrical injury and repetitive head trauma.
He explained, the natural laws governing electricity do not change based on a doctor’s intent.
ECT as a Repititive traumatic brain injury
Let’s talk Repetitive, mild to moderate, traumatic, brain injury.
ECT is rarely a single event.
The more a person has, the worse the outcome.
Acute or Index courses are typically three times a week in America, twice a week In England.
Can you imagine sending an athlete with a brain injury back in to play before they healed?
We now understand how dangerous that is.
ECT injury is referred to as mild to moderate because, like a concussion, micro structural cell damage cannot be seen on standard brain scans.
In ECT, Brain activity silence, referred to as postictical suppression, happens after the seizure.
Doctors cannot control how long the brain turns off.
Without brain activity, the lungs are not pumping oxygen through the brain, and the brainstem’s ability to regulate heart rate, is compromised.
Yes, the person has an oxygen mask on, but there’s no brain activity to breathe it in, and respiratory muscles are paralyzed without mechanical support to inflate the lungs properly until the paralytic wears off completely.
This creates anoxia and hypoxia.
Doctors are not required to document how long brain activity silence and coma lasted.
It varies in every patient and every treatment based on the variables mentioned previously.
Without oxygen circulation and erratic profusion, cell death begins at four minutes.
A study on modern, modified ECT documented that brain activity suppression can last more than six minutes in some patients who later awakes from coma activity.
ECT’s anesthesia wears off fast, the person is actually awaking from coma after the fast-acting anesthesia wore off.
Traumatic brain injuries are typically measured by how long the person was unconscious.
For ECT recipients, this refers to how long there was no brain activity, plus how long coma activity lasted, at each treatment.
Mild means loss of consciousness was less than 30 minutes.
Moderate means the person was unconscious for more than 30 minutes, but less than 24 hours.
This picture is from an actual ECT neuro pathology study, using an electric field more than four times weaker than modern ECT.
There is hypertrophy and hyperplasia of astrocytes around irregularly dilated blood vessels.
I’m genuinely curious what my brain will look like at autopsy under a microscope.
People are familiar with acute electrical injury, but only electrical injury specialists are familiar with delayed low voltage electrical injury.
Please remember all the variables involved in ECT, to understand every ECT recipient has a unique outcome.
No two people get ECT the same way.
electrical injury and seizure risks
Electrical injury and violent seizure activity can potentially cause
- Pathological neurogenesis
- Reactive gliosis
- Perivascular hemorrhage
- chronic micro bleeding
- Cerebral anoxic injury
- Vascular problems
- Changes in brain metabolism
- Acquired channelopathies
- Reversible or Irreversible
- Leaky Blood-Brain Barrier
- Leaky blood-cerebro spinal fluid barrier
potential long term conseqences of Electrical injury
Delayed low-voltage electrical injury typically begins emerging with unexplained neuromuscular episodes long after shock.
It can happen anywhere from several months, to more than a decade after low voltage shock.
Repeated exposure to pulsed, high energy fields, changes how the body uses sodium, potassium, calcium and other electrolytes.
The body transfers electronic messages across cell membranes by exchanging electrolytes through voltage gated ion channels.
Electrical injury changes ion channel function, causing Acquired channelopathies.
Gradually, the body loses ability to regulate electrolytes.
Channelopathies cause episodes depending on which electrolyte the body is struggling to process.
Symptoms can include a broad spectrum of sudden onset events including:
- Paralysis on one side of the body
- Tetany seizures
- Full body weakness
- Writhing movements
- Muscle spasms
- Muscle twitching
- Involuntary muscle movements
- Cardiac arrhythmia
Symptoms can resolve as quickly as they hit, sometimes they last for several minutes, other times several days, depending upon how long it takes the body to regain homeostasis.
Over time, there is a progressive loss of ion channel function in electrical injury patients.
Episodes happen more frequently and people begin losing the ability to fully recover after an episode.
We don’t know if that’s because ion channels continue to deteriorate, or if it’s because with the loss of regulation, surrounding cells slowly lose capacity to regulate ion channels.
It may be a combination of both.
Electroporation after ECT
Electroporation is what happens when cell membranes are exposed to Rapidly Pulsed, medium or high electric fields.
It creates tiny holes in the cell membrane.
This allows anything outside the cell, to get into the cell.
During ECT, this allows medicine and anything else in the blood stream to be delivered at a cellular level, amplifying effects.
Where the electrical fields are strongest, pores are too large to heal.
These holes cause the cells to leak like a sinking ship.
The cells take on water, and lose their contents.
Though they try to keep up, eventually they cannot, and cells die.
This is referred to as irreversible Electroporation.
Initial damage is isolated to the path that receives the highest electrical fields.
As time progresses, surrounding cells, previously dependent on damaged cells, no longer receive nutrition, pulses, or oxygen.
Slowly cells starve and begin to die off, causing additional degeneration.
Though typically used for tumor ablation, one article on brain cancer treatment explained they chose to use the low end of electric field parameters outlined in the American Psychiatric Association’s Electroconvulsive therapy handbook.
When I read that, I stared, in disbelief, thinking about my own brain stem getting 900 milliamps pulsed through it, more than 100 times, rupturing chronic micro bleeding in the central pontine area.
ECT device safety and efficacy remain unproven
The cumulative effects of cellular micro structure damage is likely why, after more than 80 years of ECT use, now the US FDA requires device manufacturers to put warnings in their user manuals and hospitals to display warnings that ECT’s long term safety and efficacy is not proven.
And long term follow up may be needed.
Psychiatrists are not routinely taught the neuropathology or histopathology of ECT, neither are neurologists.
This makes it nearly impossible for ECT recipients to find appropriate long-term follow up recommended by the FDA.
Doctors who deny damage caused by ECT, highlight gaps in their medical education which cause major problems for people navigating life after ECT.