Thalamocortical correlates of sleep spindle and slow oscillation dysfunction in Lewy body disorders
Thalamocortical correlates of sleep spindle and slow oscillation dysfunction in Lewy body disorders
Publication status: preprint
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Original abstract
Abstract Sleep disturbances are pervasive in Lewy body disorders (LBD), but their neurophysiological basis remains unclear. Non-rapid eye movement (NREM) sleep offers an objective window into thalamocortical circuit function, minimally confounded by the motor and cognitive fluctuations of wake. Sleep spindles, slow oscillations (SOs) and their coupling reflect complementary aspects of this system, and may be differentially affected in LBD. We characterised NREM microarchitecture in 109 participants (55 controls, 32 Parkinson's disease [PD], 22 dementia with Lewy bodies [DLB]), quantifying spindle density and morphology, SOs, spindle–SO coupling and spectral power, and related these to thalamic volumes and cortical thickness in the 77 participants with MRI, adjusting for age and sex. Macroarchitecture was broadly similar between groups. Slow and fast spindle densities were reduced in LBD and lowest in DLB (all p FDR <0.05), with PD reductions more prominent for fast spindles. Additionally, DLB showed reduced central and occipital SO density (p FDR ≤0.018), altered slow spindle–SO coupling, and increased frontal beta power (p FDR =0.004). Within LBD, reduced thalamic volume was associated with lower spindle density and weaker slow spindle–SO coupling. These dissociable abnormalities of spindle generation and thalamocortical coordination support sleep EEG as an accessible physiological readout of circuit dysfunction in LBD.