Experimental evidence indicates that intracellular chloride concentration regulates the excitation–inhibition (EI) balance, yet the mechanisms by which activity-dependent chloride dynamics drive seizure evolution and stage transitions remain unclear. We present a conductance-based neuronal network in which EI balance emerges from chloride homeostasis via channel-mediated influx and transporter-mediated extrusion. We show that the fraction of inhibitory synaptic conductance contributing to channel-mediated influx acts as a control parameter that organizes seizure dynamics into distinct stages–preictal, ictal-tonic, and ictal-clonic–distinguished by characteristic amplitude and frequency signatures. Decreasing this fraction shortens ictal activity and suppresses seizure initiation, whereas high fraction promotes the emergence of ictal-tonic and ictal-clonic stages and spiral-wave dynamics, rendering seizure dynamics largely insensitive to inhibition. At intermediate values, seizures bypass the ictal–tonic stage and emerge directly as the ictal–clonic stage. Moreover, joint variation of fractions with synaptic strengths reveals that recurrent excitation expands the tonic–clonic seizure, while recurrent inhibition prolongs preictal states and suppresses ictal-clonic activity.

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• Network phase transitions
• Neuronal dynamics
• Neuronal network activity