This is the therapeutic approach that dr puledda suggests in her recent eeg imaging study based on results.

Low-frequency parietal activity may constitute a pivotal neurophysiological signature underlying the pathophysiology of VSS. This finding suggests potential therapeutic targets aimed at restoring cortical excitability balance and improving sensory–attentional regulation. First, alpha-regulating neurofeedback could be employed to enhance parieto-occipital alpha oscillatory control, thereby reinforcing inhibitory gating mechanisms and suppressing the intrusion of irrelevant visual percepts [48, 49]. Second, parietal transcranial magnetic stimulation (TMS) protocols designed to downregulate pathological theta activity may modulate top-down attentional control and recalibrate thalamocortical rhythmicity, potentially normalizing dysrhythmic network activity [54, 55]. Third, GABAergic modulation, either through pharmacological enhancement of inhibitory neurotransmission or noninvasive interventions that increase cortical inhibition, may help rebalance the excitatory–inhibitory dynamics [56, 57] and attenuate visual hyperexcitability. Collectively, these approaches offer a rational framework for developing frequency-specific neuromodulation strategies that directly target the cortical and thalamocortical dysrhythmia underlying VSS, warranting systematic investigation in future clinical trials.