KEY ARTICLES FOR SOVM

Article Integration Summary – SOVM Sleep-Onset Oscillatory Vasomotor Myoclonus

1. RAAS in PTSD: ACE and ARBs Reduce Symptoms (J Clin Psychiatry, 2012)

ACE inhibition linked to reduced PTSD symptoms; implicates central RAAS in stress resilience and neurovascular modulation. In the case of SOVM, provides outside validation that RAAS signaling impacts CNS function, supporting SOVM's theory that low ACE/A2 worsens sleep-state regulation. https://www.psychiatrist.com/jcp/renin-angiotensin-pathway-posttraumatic-stress-disorder/

2. Cyclic-Periodic Phenomena During NREM and REM Sleep (Ferri et al., J Sleep Res, 2024)

Reviews oscillatory phenomena in sleep, especially autonomic, EEG, vascular, and motor coupling. In the case of SOVM, directly supports the idea that vascular-autonomic rhythms shape sleep transitions. Parallels drawn with SOVM instability at the N1-N2 transition. https://pmc.ncbi.nlm.nih.gov/articles/PMC11911051/

3. Coupled Electrophysiological, Hemodynamic, and CSF Oscillations (Fultz et al., Science, 2019)

Demonstrates that CSF pulsations are driven by slow waves and vascular tone. Glymphatic activity is sleep-phase dependent. Likely the cornerstone for SOVM’s core mechanism: that failure to synchronize vascular and CSF oscillations leads to sleep-state disruption. https://pubmed.ncbi.nlm.nih.gov/31672896/

4. REM Sleep Switch in REM Behavior Disorder (Vetrivelan et al., Sleep Med, 2013)

SLD and VMM circuits regulate REM atonia. RBD arises from their dysfunction. Suggests dream enactment when motor inhibition fails. Suggests that SOVM may reflect premature or mistimed activation of REM motor programs at sleep onset, without proper atonia. Supports hybrid state theory. https://pubmed.ncbi.nlm.nih.gov/23768838/

5. Gap Junction Blockers and Induced Seizures (Curr Neuropharmacol, 2016)

Gap junction blockers reduce seizure-like hypersynchrony. Highlights roles in thalamocortical and brainstem oscillations. Gap junctions may amplify oscillatory instability in SOVM. Blocking them could reduce synchronous discharge at state transitions. https://pubmed.ncbi.nlm.nih.gov/27262601/

6. Na(V)1.1 Channels in Circadian Rhythms (Proc Natl Acad Sci, 2012)

SCN-specific loss of Nav1.1 impairs interneuronal coupling and circadian rhythm entrainment. Demonstrates how ion channelopathy can disrupt system-level timing and neuronal synchrony—key features of SOVM oscillatory mistiming at sleep onset. https://pubmed.ncbi.nlm.nih.gov/22223655/

7. Voltage-Gated Ion Channels and Sleep (J Membrane Biol, 2024)

Review of Ca²⁺, Na⁺, and K⁺ channel roles in sleep regulation across species; links dysfunction to sleep disorders and potential therapies. Evidence shows Nav, K⁺, and especially Cav3.x channels regulate sleep-onset oscillations via thalamocortical circuits; disruption fragments NREM and alters transitions, supporting SOVM’s channelopathy-driven oscillation–vasomotor mismatch model. Serves as the primary citation for why voltage-gated ion channels are central to sleep onset stability. Supports the genetics link between your cohort’s variants and altered oscillatory gating. Provides a mechanistic bridge to the vasomotor dysregulation component —integrated from the other neurovascular literature. https://doi.org/10.1007/s00232-024-00325-0