In addition to HINTS, or how to improve the differential diagnosis of acute vestibular syndrome in the emergency department | Ukrainian Medical Journal

Acute vestibular syndrome (AVS) most commonly presents as acute unilateral vestibulopathy (AUVP)/vestibular neuritis (VN); however, it may be caused by posterior circulation ischemic stroke, hemorrhage, or other lesions of the posterior cranial fossa (e.g., multiple sclerosis). The HINTS examination is not invariably a reliable marker for confirming central AVS. Recent data suggest that a «negative» HINTS result may be falsely negative in 20–30% of cases, and early brain magnetic resonance imaging (MRI) (48–72 h) may miss 12–50% of posterior circulation strokes. This underscores the need to identify additional bedside markers to improve the differential diagnosis of AVS in the emergency department (ED). We present sensitivity and specificity data for the Babinski asynergy test to increase clinical suspicion of cerebellar involvement, as well as for the penlight-cover test (penlight with monocular occlusion) to improve detection of spontaneous nystagmus (SN) in ED patients with AVS, as adjuncts to the HINTS protocol. The aim of the research: to improve the differential diagnosis of central versus peripheral AVS by incorporating the Babinski asynergy test and the penlight-cover test as adjuncts to the HINTS protocol. Materials and methods. A total of 120 patients with symptoms of AVS were examined in the ED. Initial assessment included symptom review, medical history, and otoneurological examination; when SN was not visualized clinically, the penlight-cover test was performed (smartphone flashlight with monocular occlusion). Ten patients with benign paroxysmal positional vertigo, vestibular migraine, or Ménière’s disease were identified and excluded from further analysis. The remaining 110 patients were stratified according to HINTS findings. The Babinski asynergy test was considered positive if the patient raised the legs when attempting to sit up from the supine position with arms crossed over the chest. Test sensitivity and specificity were assessed against videonystagmography (VisualEyes™ 505) and brain MRI performed no earlier than 72 h after symptom onset. Otoscopy and audiometry were performed in all patients, with audiologist consultation as needed. Results. Among 110 patients, the HINTS examination suggested AUVP in 85 (77.3%) and central nervous system (CNS) involvement in 25 (22.7%). Of the 85 patients classified as peripheral by HINTS, a positive Babinski asynergia test was recorded in 5 (5.9%); brain MRI demonstrated CNS pathology in all five. Among 25 patients with a central-type HINTS pattern, the asynergy test was positive in 20 (80%). Brain MRI performed at 72 h verified CNS pathology in 6 of 85 patients initially classified as peripheral by HINTS. In 1 (4%) patient within the central-type HINTS group, the clinically assessed horizontal head impulse test (h-HIT) was normal (suggesting CNS involvement); however, MRI showed no pathological findings and AUVP was ultimately diagnosed. In this study, the sensitivity of the HINTS protocol was 80.0% (95% CI 65.7–94.3%) and specificity was 98.8% (95% CI 96.3–100%). The sensitivity of the Babinski asynergia test was 83.3% (95% CI 65.5–94.5%) and specificity was 100% (95% CI 96.3–100%). In 21 (19.1%) of 110 patients, nystagmus was not visualized on routine clinical examination; the penlight-cover test detected unidirectional SN in 19 (90.5%) of these patients. Videonystagmography revealed unidirectional SN in all 21 patients. The sensitivity of the penlight-cover test for detecting unidirectional SN relative to videonystagmography (VisualEyes™ 505) was 90.5% (95% CI 71–99%). Conclusion. The Babinski asynergia test may be recommended as an adjunct to the HINTS protocol to improve bedside screening for central AVS; the method demonstrated 100% specificity. The penlight-cover test substantially increases detection of spontaneous nystagmus in the ED when instrumental recording methods are unavailable. Nevertheless, the search for additional specific clinical markers for differentiating central AVS remains warranted.

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