Kerskens, C.

The mechanical origin of cerebrospinal fluid (CSF) and interstitial fluid (ISF) transport remains unresolved. High-frequency arterial pulsations ([~]1 Hz) have long been proposed as a driver of CSF flow, yet multiple biomechanical analyses suggest that their ability to support deep bulk interstitial transport is severely limited by the poroelastic resistance of neural tissue. At the same time, slow-wave sleep is associated with large, synchronous CSF oscillations and enhanced clearance-related dynamics near[~]0.05 Hz. What selects this low-frequency regime remains unclear. Here we propose a theoretical framework in which this frequency selection is not incidental, but mechanically necessary. When neural populations update their state, local thermodynamic demand induces microvascular dilation. Under intracranial volume constraints, this blood-volume expansion must, to leading order, be compensated by displacement of other intracranial volume components, including CSF. We model the poroelastic response of the interstitial matrix and obtain an effective low-pass filter for this displacement, with a nominal cut-off frequency in the slow-wave range (rc {approx}0.05 Hz). This mechanical filter implies two distinct forcing regimes. During wakefulness, rapid commitment and sensorimotor resetting are hypothesized to generate spectrally sharp, high-frequency transients in vascular volume. Because this spectral content lies largely above the poroelastic passband, waking dynamics are predicted to be inefficient at driving deep bulk transport. Slow-wave sleep, by contrast, reduces rapid commitment-like transitions and permits smoother, more globally synchronized vascular-volume oscillations that fall within the passband and support larger-scale CSF motion. The framework yields several falsifiable predictions, including load-dependent modulation of sleep-associated CSF pulsation amplitudes, a BOLD-first/CSF-second temporal ordering during slow-wave events, and a mechanical discrepancy between deep interstitial transport and the rapid dispersion of superficial exogenous tracers. More generally, the theory advances a strong claim: the sleeping brain is mechanically privileged for large-scale CSF dynamics not because sleep introduces a new driver, but because sleep permits forcing in a frequency range that brain tissue can actually transmit.