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Race morning until the LA Marathon!!

02 · My Journey

Surgeries, VNS & DBS

2017 — right after surgery (blurred for comfort — tap to reveal)
2017 — after the resection (blurred for comfort — tap to reveal)

2017

Left anterior temporal lobectomy

In 2017, I went all in. Surgeons performed a left anterior temporal lobectomy — they cut out part of my brain in a desperate, calculated fight to stop the seizures. For a moment, it felt like the war might finally be over.

That decision was not casual. The left temporal lobe is where a lot of what makes you you lives — language, naming, verbal memory, the ability to pull a word when you need it. On the dominant side, a resection like mine carries real risk: lasting speech problems, memory loss, trouble finding words, changes in mood or personality, infection, bleeding, stroke, even deficits that don’t fully reverse. You don’t sign those papers lightly. You sit with the fear that the cure could cost pieces of who you are.

I knew the stakes. My family knew the stakes. The surgeons were clear: this was major brain surgery, and there were no guarantees — not that the seizures would stop, and not that I’d walk out exactly the same person who walked in. Still, the seizures were already stealing my life. So I chose the risk. I chose the operating room. I chose to fight.

Then, a few months later, lightning struck again: a breakthrough seizure. Hope cracked. The operating room hadn’t been enough. Back to the drawing board.

2017 — the next day (blurred for comfort — tap to reveal)
A little medical history Where the anterior temporal lobectomy came from

Cutting into the brain to stop seizures isn't new. British surgeon Victor Horsley performed the first deliberate epilepsy operation in 1886, removing scar tissue he'd traced to a patient's seizures using the still-new idea that different parts of the cortex controlled different functions. The temporal lobe version came decades later, out of the Montreal Neurological Institute, where Wilder Penfield and Herbert Jasper operated on patients who stayed awake under local anesthetic through the 1930s–50s. Electrically stimulating the exposed cortex let them map speech and memory in real time and mark the boundary of what could safely come out — the same awake-mapping idea that still guides surgery near language areas today.

The operation itself was standardized in the 1950s by Murray Falconer at the Maudsley Hospital in London, who removed the anterior temporal lobe en bloc — as one connected piece, hippocampus included — rather than piecemeal. Falconer's version is, in its essentials, the same anterior temporal lobectomy still performed now, built around a simple finding: a huge share of drug-resistant temporal lobe epilepsy traces back to hippocampal sclerosis, scarring in that one structure, and taking it out along with the surrounding lobe stops the seizures far more often than medication alone ever does.

That last part took a long time to become official. Surgery sat on the shelf as a "last resort" for decades, used only after years of failed drugs, until a 2001 randomized controlled trial by Wiebe et al. in the New England Journal of Medicine finally put it head-to-head against continued medication — and found most surgical patients became seizure-free, versus almost none on drugs alone. Determining which side was safe to cut had its own breakthrough: the Wada test, developed by Juhn Wada in 1949, sedates one hemisphere at a time through the carotid artery so surgeons can confirm which side actually handles language before committing to a dominant-side resection like mine.

2019

Vagus nerve stimulator

In 2019 I chose to have a vagus nerve stimulator put in. I wasn’t finished fighting. It helped a little — but breakthrough seizures still came. That didn’t stop me. Resection and VNS were already in. The big guns were out to play — and I was still standing.

By then I’d already walked a long road to get there. Cerebral hemiatrophy as a kid. A massive seizure and hospital days. Years of focal aware seizures I didn’t even recognize. Then the big tonic-clonic seizures in community college, breakthroughs that kept coming, UCLA and telemetry to map the storm, and in 2017 a left anterior temporal lobectomy that still couldn’t finish the war. The VNS was the next move after all of that — resection plus stimulator, everything we had short of going deeper. And when the breakthroughs still showed up, the path ahead pointed somewhere harder: DBS.

How it works How a vagus nerve stimulator actually calms a seizure network

A VNS doesn’t touch the brain at all. The device — a pulse generator about the size of a matchbook — sits under the skin in the upper chest, with a thin lead wrapped around the left vagus nerve in the neck. Left, not right: the right vagus carries more of the fibers that regulate heart rate, so stimulating it risks slowing the heart down. The left side avoids most of that.

Those pulses travel up afferent vagal fibers into the brainstem, into a relay station called the nucleus tractus solitarius. From there, signals fan out to the locus coeruleus and the raphe nuclei — the brain’s main noradrenaline and serotonin sources — which project diffusely across the whole cortex. The net effect is a broad rise in inhibitory tone: more GABAergic activity, a higher threshold the next hypersynchronous discharge has to clear. It isn’t aimed at one spot. It raises the floor everywhere at once.

Most VNS devices run open-loop: a fixed schedule — stimulate for 30 seconds, rest for 5 minutes, repeat, all day — regardless of what the brain is actually doing. Newer models add a closed-loop layer: an onboard algorithm that watches heart rate, because many seizures cause a sudden spike (ictal tachycardia), and fires an extra burst of stimulation automatically the moment it detects one. Patients also carry a magnet they can swipe over the device by hand, to trigger stimulation on demand the second they feel an aura coming on.

A little medical history Where DBS came from — and how it reached epilepsy

Deep brain stimulation traces back to 1947, when Spiegel and Wycis built the first human stereotactic frame for precisely targeting deep brain structures. In 1963, researchers found that high-frequency electrical pulses to the thalamus could calm tremor instead of destroying tissue — and in 1987, Dr. Alim-Louis Benabid pioneered chronic, implanted stimulation for tremor, kicking off the modern DBS era. The FDA approved DBS for essential tremor in 1997, Parkinson’s disease in 2002, and dystonia in 2003.

DBS for epilepsy came later. Researchers targeted the anterior nucleus of the thalamus (ANT) — a hub in the brain’s seizure-spreading circuitry — and Medtronic ran the pivotal SANTE trial from 2003–2008 across 17 U.S. centers. The results held up: a 40% median seizure reduction at three months, improving further over years of follow-up. On April 27, 2018, the FDA approved DBS as a treatment for drug-resistant epilepsy — just four years before my own leads went in.

2022

Deep brain stimulation

I was done waiting for epilepsy to decide my life. DBS was next — and I chose it on purpose. In consultation with my surgeon, I committed to putting two deep leads in my brain. In 2022, I walked into that operating room ready. This was the line I would not retreat from.

DBS is not a small step. You’re asking a surgical team to place hardware deep in the brain — leads, wires, a stimulator under the skin — and live with it. The risks are real: bleeding, infection, hardware problems, stroke, pain at the implant site, unwanted stimulation side effects, mood changes, and the chance it simply doesn’t help enough. You can need revisions. Batteries don’t last forever. You’re signing up for appointments, programming sessions, and a device that becomes part of your body.

The reward, if it works, is the reason people still choose it: a chance to turn the volume down on seizures, to get days back, to feel like yourself again. For me the upside was worth the gamble — not because the risk disappeared, but because living without trying was already costing too much.

Then came the long fight after the fight: nearly four years with my doctors and the team at Medtronic, refusing to quit until we found a golden setting. On March 18, 2026, they started testing low pulse stimulation 24/7. It’s been about seven months since they added that setting — and it was the right choice. The DBS has changed my life. My depression has evaporated. I stayed the course. And it held.

2022 — the incisions, close up (blurred for comfort — tap to reveal)
2022 — right after surgery (blurred for comfort — tap to reveal)
2022 — after DBS (blurred for comfort — tap to reveal)
How it works What's actually inside a DBS system — and why "finding a setting" takes years

The hardware is deceptively simple: two thin leads, each with multiple metal contacts, placed deep in the brain through small burr holes using a stereotactic frame and MRI guidance precise enough to land within a millimeter of the target. The leads run under the scalp and skin to an implantable pulse generator (IPG) — the actual battery and electronics — tucked under the skin, usually below the collarbone or in the abdomen.

Unlike a VNS’s one-size-fits-all schedule, a DBS system has a huge number of adjustable variables: which contacts on each lead are active, in what polarity (monopolar vs. bipolar), the pulse frequency (Hz), pulse width (microseconds), amplitude (mA or volts), and whether stimulation runs continuously or in a duty cycle (minutes on, minutes off). That’s thousands of possible combinations per side — which is exactly why “programming” is its own ongoing process, not a one-time setup. Each visit, the amplitude or contact gets nudged, the effect gets tracked over weeks, and the search continues.

Mechanistically, high-frequency stimulation at the anterior thalamus doesn’t destroy anything — it jams the signal. It disrupts the thalamus’s ability to relay and synchronize rhythms across the cortex, through a mix of depolarization blockade, synaptic depression, and masking of the pathological oscillations a seizure focus needs to recruit the rest of the network. Instead of silencing the spark, it makes it much harder for the spark to catch.

That’s the backdrop for the “golden setting” from March 2026: nearly four years of incremental adjustments — this contact, that amplitude, this duty cycle — until one specific combination, low pulse stimulation running continuously, finally held. A search.

Freedom from my depression. I’m still having seizures — but the sting is no longer there.

The science

Curious exactly what's happening in the brain during a seizure — and what the VNS and DBS above are each actually interrupting? I pulled the full explanation and two live, interactive simulations (a small cortical network you can push into a spreading seizure, and a real Hodgkin-Huxley neuron you can fire yourself) out onto their own page, so this chapter doesn't turn into a neuroscience textbook.

Try the seizure & neuron simulations →

Curious about the medical side? Switch to dark mode to see the surgery photos from this story — blurred by default, tap any photo to reveal it.

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