Meeting #2: Agenda and Summary

Articles he's been sending me through the week were unbelievably validating to the SOVM theory. I'm super glad I've been recording the meetings, chat's done a great job summarizing.

NUMBERS 2, AND 6-9 complete our understanding of exactly what's happening at the brink of sleep state shifting

We are not religious but had what some people would call a "come to jesus" moment during our meeting after exploring the oscillatory and gap junction pieces. It became obvious that the enigma has unraveled and the mystery is no more. Then he turned to me and said "So, time for you to re-write your paper, integrating this in there". Thus my sense of overwhelm on two fronts!

Summary: Advancing the SOVM Framework

With Dr. Jay Lombard | July 2025

I'm excited to share key highlights from my second strategy meeting with Dr. Jay Lombard, as we continue refining our understanding of Sleep-Onset Oscillatory Vasomotor Myoclonus (SOVM)—the name we’ve now officially adopted for the condition many of us have been struggling to name, explain, and get treated seriously.

Summary of transcription:

✅New Official Name:

Sleep-Onset Oscillatory Vasomotor Myoclonus (SOVM)This name reflects the condition’s core features:• Sleep-onset timing• Oscillatory instability across neural, vascular, and autonomic systems• Vasomotor dysfunction (problems with blood flow and tone)• Myoclonic jerking

🧠 Oscillation is the Key: Our jerking likely results from instability in how the brain shifts between states—especially at the boundary between wakefulness and light sleep (N1/N2). In some cases, features of REM sleep (like dream imagery or muscle movement) intrude too early, without the protective paralysis REM should bring. This "REM without REM" overlap helps explain the dream-like, startling experiences many of us report.

✅ Case Criteria for Inclusion: We’re now identifying participants for the first published case series. Dr. Lombard recommended focusing on those with several overlapping features:

• Ion channel mutations

• Vivid dreaming or physical dream enactment

• Evidence of inflammation

• Hypnic headaches or "exploding head" symptoms

• CSF flow issues or signs of intracranial hypertension

• Tinnitus (optional)

If you’ve submitted to the registry and checked off several of these, you will be contacted!

💡 Treatments on the Horizon

We’re beginning to explore how these patterns may point to targeted treatment paths, including:

• Medications that stabilize ion channels

• Therapies that regulate CSF flow

• Anti-inflammatory strategies

• New ideas like Gap Junction inhibitors, which may reduce hypersynchrony in the brain

🧠 Structural Pathway = Separate Paper

Some participants (like Tracy) show strong evidence of structural compression or CSF flow blockage, often confirmed by upright MRIs or MRVs. Dr. Lombard encouraged developing this as a separate paper focused on structural contributors to SOVM—likely submitted to Medical Hypotheses.

💬 Reflections from Dr. Lombard

Dr. Lombard shared his deep appreciation for what we’ve built together:

“I’m very impressed by the work that’s been done here… this paper is already so well written. To see that you've taken the lead on something like this is — I love working to help figure this out. We’re going to put this on the map.”

Breakdown of the "come to Jesus":

New research on REM motor control and brain synchronization strongly supports the SOVM model.

In normal REM sleep, the brainstem’s sublaterodorsal nucleus (SLD) activates a motor suppression system (via the ventromedial medulla, or VMM), which silences muscles through glutamate and GABA-mediated inhibition. When this fails—as in REM Behavior Disorder—dreams are physically acted out. But in Sleep-Onset Oscillatory Vasomotor Myoclonus (SOVM), similar motor discharges appear too early, at the N1–N2 sleep transition. This suggests REM-like motor circuits may activate prematurely, before inhibitory pathways are in place—pointing to a failure of state segregation between wake, NREM, and REM.

In parallel, research on gap junctions—the electrical “wiring” between neurons and glial cells—offers further insight. These intercellular channels can amplify abnormal oscillations and contribute to hypersynchrony across motor networks. Gap junction blockers, like carbenoxolone, reduce seizure-like discharges by disrupting this synchronization. These same gap junctions regulate astrocytic buffering of potassium, calcium, and pH—aligning with the SOVM model’s vascular and fluid tone vulnerabilities (e.g., Diamox responsiveness).

Together, these findings suggest that SOVM reflects a hybrid dysfunction involving:

• REM-related motor disinhibition at sleep onset

• Electrophysiological hypersynchrony via gap junctions

• Astroglial and vascular-autonomic instability

  
  

🔍 Lay Person Summary

We’re learning that SOVM (Sleep-Onset Oscillatory Vasomotor Myoclonus) is not just a sleep problem—it’s a breakdown of how different brain systems are supposed to work together during the transition into sleep.

We now see SOVM through three main lenses:

1. 🧠 The cellular view: How brain cells communicate—some of us have nerves that are too electrically sensitive or mistimed, possibly due to gap junctions over-activating circuits.

2. 💓 The blood flow view: Sleep requires blood vessels to relax at the right time. In SOVM, that may happen too soon or too strongly—causing instability in how fluid and pressure move in the brain.

3. 🎶 The rhythm view (oscillatory): Sleep stages are supposed to “flow” smoothly—like a rhythm. But in SOVM, the brain may accidentally mix features of REM sleep (like dream activity or movement) into earlier stages, leading to jerking and wake-ups.

This is why SOVM is so disruptive—and so misunderstood. It’s not just neurological or just vascular. It’s a fragile coordination problem that throws the body offbeat at the exact moment it tries to rest.