Objective Alcohol use disorder (AUD) is a chronic, relapsing brain disorder characterized by compulsive alcohol drinking and impaired control over alcohol use. Its pathogenesis involves functional abnormalities in neural circuits underlying reward, cognitive control, and emotion regulation. Current clinical assessments primarily rely on psychometric scales, which rely on subjective experience, are susceptible to recall bias and concealment, and provide limited insight into the aberrant neural responses underlying AUD. Addiction involves state-dependent, non-stationary neural dynamics, necessitating analytical approaches capable of capturing the time-varying features of brain states. Microstate analysis characterizes the spatiotemporal dynamics of brain activity by identifying brief, recurrent, quasi-stable spatial patterns in electroencephalography (EEG), and thus provides a useful tool for investigating neural mechanisms in resting-state and task states. Previous studies have shown that microstate parameters can reflect addiction-related pathological craving and functional impairment. However, the alcohol cue-induced temporal reorganization of microstates in patients with AUD remains to be investigated. In this study, we applied microstate analysis to investigate aberrant microstate patterns in patients with AUD in response to alcohol cue exposure.Methods Twenty-one patients with AUD admitted to Shandong Daizhuang Hospital from October 2023 to January 2024 were enrolled. All participants met the ICD-11 diagnostic criteria. A visual cue exposure paradigm containing alcohol cues was used. EEG data were recorded sequentially during eyes-open resting state, neutral cue exposure, and alcohol cue exposure, with eyes-closed resting-state data collected after each condition for microstate analysis. Subjective craving intensity was assessed using a visual analogue scale (VAS) before and after cue exposure.Results The microstate topographies across conditions were largely consistent with the four topographies of microstate classes A–D. Compared with the resting state, after exposure to alcohol cues, AUD patients showed a significant increase in the mean duration (t=4.341, P<0.001), coverage (t=12.645, P<0.001), and occurrence (t=2.740, P=0.030) of microstate B, while the mean duration (t=–5.196, P<0.001) and coverage (t=–7.623, P<0.001) of microstate A significantly decreased. Under neutral cues, the occurrence (t=5.806, P<0.001), mean duration (t=6.541, P<0.001), and coverage (t=9.496, P<0.001) of microstate C significantly increased. In addition, under alcohol cues, the transition probabilities between microstates A and B and between microstates C and D were significantly increased (A→B: t=12.401, P<0.001; B→A: t=2.637, P=0.024; C→D: t=3.390, P=0.007; D→C: t=3.690, P=0.004), whereas the bidirectional transition probabilities between microstates A and C were significantly decreased (A→C: t=–7.861, P<0.001; C→A: t=–3.253, P=0.008).Conclusion Alcohol cues can induce the retrieval of past drinking experiences and pathological craving in patients with AUD. These cue-elicited responses are reflected in EEG microstate parameters, which could serve as potential electrophysiological markers of cue reactivity in AUD and provide a basis for understanding the neural mechanisms underlying alcohol addiction.