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Horizontal nystagmus is still commonly interpreted at the bedside through a pragmatic peripheral-versus-central dichotomy. Although this heuristic is often clinically useful, it may be misleading because distributed brainstem–cerebellar disorders can generate peripheral-appearing phenotypes. This paper presents a narrative clinical–conceptual review proposing that a substantial subset of horizontal nystagmus patterns may be understood more coherently as expressions of dysfunction within a coupled vestibulo-ocular integrative network rather than as direct signatures of a single lesion site. Within this framework, two core dynamical domains are separated conceptually: a vestibular nuclei (VN)-centered velocity-storage process and an NPH-centered gaze-holding integrator. These processes are proposed to operate under cerebellar regulatory influence, with the nodulus–uvula (NU) acting as a plausible regulator of storage gain, temporal persistence, adaptation stability, and oscillatory behavior. Clinically, the velocity-storage domain is expressed through low-frequency vestibulo-ocular reflex behavior and optokinetic after-nystagmus-related dynamics, whereas the gaze-holding domain is expressed through eccentric gaze stability, gaze-evoked nystagmus, and post-saccadic drift. This framework carries a clinically relevant implication: horizontal nystagmus phenotypes may be interpreted more effectively by asking which functional process is predominantly abnormal—gaze holding, storage-related vestibular persistence, or cerebellar regulatory stability—rather than by relying solely on a binary peripheral–central label. On this basis, we outline a clinician-facing workflow linking gaze dependence, periodicity, direction reversals, head-shaking behavior, and Alexander-law mismatch to operational bedside criteria and candidate quantitative readouts. The proposed model is intended as a clinical–conceptual framework rather than a deterministic localization tool. Its main value lies in organizing discordant vestibular findings, strengthening the mechanistic interpretation of bedside and instrumented observations, and identifying testable directions for future validation studies in acute dizziness and ocular motor disorders.
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Leonardo Manzari (2026) studied this question.
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