Seizure · 2026
Distinguishing isolated epileptic vertigo/dizziness from vestibular paroxysmia: Clinical clues from a retrospective comparative study.
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Lu Xi, Peng Yufen, Fang Bo, Xu Min, Tu Qi, Li Xiaobing, Xie Xufang
Аннотация
PURPOSE: Recurrent brief vestibular attacks are often evaluated as peripheral disorders, but some reflect epileptic vestibular seizures requiring electroencephalographic (EEG) assessment. We sought to identify clinical clues distinguishing isolated epileptic vertigo/dizziness (iEVD) from vestibular paroxysmia (VP).
METHODS: We retrospectively compared 50 patients with iEVD and 50 with VP at a tertiary centre. Vestibular symptom descriptions were summarised according to the predominant motion percept documented in the initial clinical account. Clinical features, associated symptoms, EEG findings, and short-term treatment outcomes were reviewed. Independent discriminators were assessed using Firth's penalised logistic regression.
RESULTS: Attack frequency independently distinguished iEVD from VP (odds ratio 0.024, 95% confidence interval 0.005-0.120, p < 0.001); daily attacks were uncommon in iEVD but typical in VP (10.0% vs. 88.0%). Heave-like vertical linear motion (floating, rising, sinking, or falling) occurred in 13/50 patients with iEVD (26.0%) and in no patient with VP (specificity 100.0%, 95% CI 92.9-100.0; sensitivity 26.0%). Cortical sensory auras (auditory or visual hallucinations, paraesthesia) affected 20.0% of iEVD patients; auditory hallucinations occurred only in iEVD and unilateral tinnitus only in VP. EEG abnormalities most often involved the temporal region (56.0%).
CONCLUSION: Lower attack frequency and heave-like vertical linear motion help distinguish iEVD from VP. Heave-like motion is specific but insensitive, so its absence does not argue against iEVD. Targeted history-taking on motion quality and associated symptoms may help physicians identify patients warranting epilepsy or EEG evaluation before epileptic vestibular events are misclassified as VP.
METHODS: We retrospectively compared 50 patients with iEVD and 50 with VP at a tertiary centre. Vestibular symptom descriptions were summarised according to the predominant motion percept documented in the initial clinical account. Clinical features, associated symptoms, EEG findings, and short-term treatment outcomes were reviewed. Independent discriminators were assessed using Firth's penalised logistic regression.
RESULTS: Attack frequency independently distinguished iEVD from VP (odds ratio 0.024, 95% confidence interval 0.005-0.120, p < 0.001); daily attacks were uncommon in iEVD but typical in VP (10.0% vs. 88.0%). Heave-like vertical linear motion (floating, rising, sinking, or falling) occurred in 13/50 patients with iEVD (26.0%) and in no patient with VP (specificity 100.0%, 95% CI 92.9-100.0; sensitivity 26.0%). Cortical sensory auras (auditory or visual hallucinations, paraesthesia) affected 20.0% of iEVD patients; auditory hallucinations occurred only in iEVD and unilateral tinnitus only in VP. EEG abnormalities most often involved the temporal region (56.0%).
CONCLUSION: Lower attack frequency and heave-like vertical linear motion help distinguish iEVD from VP. Heave-like motion is specific but insensitive, so its absence does not argue against iEVD. Targeted history-taking on motion quality and associated symptoms may help physicians identify patients warranting epilepsy or EEG evaluation before epileptic vestibular events are misclassified as VP.