The Neuroscience of Sleep Paralysis: What 2024–2025 Imaging Studies Reveal
2024–2025 neuroimaging review of sleep paralysis: EEG, MRI, DWI and molecular studies clarifying REM–wake dissociation, hallucinations, and clinical implications.
Introduction — sleep paralysis at the REM–wake boundary
Sleep paralysis (SP) is a transient inability to move while falling asleep or upon awakening, often accompanied by vivid hypnagogic or hypnopompic hallucinations such as a sensed presence, pressure on the chest, and intense fear. SP is widespread: population and clinical studies estimate that roughly one in three people will report at least one episode in their lives, with higher rates among students and psychiatric populations.
Neuroscientists conceptualize SP as an example of sleep–wake dissociation in which REM-sleep motor atonia persists or intrudes into wakefulness while elements of REM dreaming (visual and auditory imagery) co-occur with regained meta‑awareness. This mixed REM/wake state explains both the paralysis and the dreamlike hallucinations and frames the question: what do modern imaging and electrophysiology tell us about the neural mechanisms of SP?
What 2024–2025 EEG and polysomnography studies show
Recent case reports and small-sample polysomnographic (PSG) studies have reinforced the electrophysiological signature of SP as a mixed REM/wake state. For example, a 2024 PSG case report documented co‑occurrence of REM features alongside alpha intrusions—an electrophysiological marker of partial cortical arousal—supporting the view that SP episodes reflect simultaneous activation of REM circuitry and waking cortical networks. These PSG/EEG data help explain why patients are conscious and aware yet unable to move.
However, many EEG findings remain descriptive and frequently derive from single cases or small cohorts; spectral analyses and advanced EEG metrics (time irreversibility, connectivity) are being applied only recently and need larger samples for replication. Emerging computational approaches to EEG sleep staging and arousal detection promise better identification of SP‑relevant transitions in future cohort studies.
Structural and molecular imaging insights (MRI, DWI, molecular reviews)
Diffusion and structural MRI studies in related REM‑predominant disorders (notably narcolepsy) have identified white‑matter microstructural differences that may form a structural backdrop for abnormalities in REM regulation and associated phenomena such as SP and dream‑related hallucinations. A 2024 diffusion‑weighted imaging (DWI) synthesis highlights widespread white‑matter changes in narcolepsy that could contribute to altered network dynamics between brainstem REM generators and cortical regions responsible for perception and threat detection. While direct MRI studies of isolated SP remain limited, these findings demonstrate plausible structural pathways that imaging researchers should test in dedicated SP cohorts.
At the molecular level, reviews published through 2025 have begun to explore intracellular signaling mechanisms that may influence hallucination‑proneness during REM intrusions. A 2025 molecular review proposed candidate pathways (including β‑arrestin‑2 and related modulatory systems) that could mediate sensory gating, affective amplification, or abnormal cortical‑subcortical communication during SP—pointing to potential pharmacological targets for future translational research. These molecular proposals remain preliminary but are an important complement to electrophysiology and structural imaging.
Clinical, cultural and research implications — where imaging takes us next
Clinically, converging imaging and electrophysiology reinforce that SP is rooted in a physiological REM–wake boundary phenomenon rather than primary psychosis. This distinction is important because hypnagogic/hypnopompic hallucinations and sensed presences are common in SP and cross cultural narratives, and they can be misinterpreted as psychiatric or supernatural phenomena without appropriate education and evaluation. Imaging reinforces the neurobiological basis of these experiences, which may reduce stigma and guide targeted care.
Research priorities emergent from 2024–2025 work include: standardizing PSG/EEG markers for SP, recruiting larger and better‑characterized cohorts (including isolated SP vs narcolepsy‑associated SP), applying multimodal imaging (simultaneous EEG‑fMRI, DWI, PET where feasible), and integrating molecular data. Limitations of the current literature are clear: many published imaging observations are case reports or small samples, and causal mechanisms remain unproven. Nonetheless, the combined electrophysiological, structural, and molecular findings of 2024–2025 set a roadmap for mechanistic studies and for trials that might target neurotransmitter or signaling pathways implicated in REM intrusions.
Takeaway: Modern imaging across 2024–2025 strengthens the model of sleep paralysis as a REM‑wake dissociation with identifiable electrophysiological and structural correlates. Translational progress will depend on larger multimodal studies, clearer phenotyping, and integration of molecular findings into clinical hypotheses.