Central stroke presenting as acute vestibular syndrome: case report and scoping literature review

Posterior inferior cerebellar artery (PICA) strokes often present with acute vestibular symptoms that may mimic peripheral disorders, posing significant diagnostic challenges. Prompt recognition and targeted management are essential to prevent misdiagnosis and improve outcomes. A 55-year-old woman with acute isolated vertigo showed only a horizontal spontaneous nystagmus, and a diagnosis of stroke on MRI was obtained. Multiple databases (MEDLINE, EMBASE, Web of Science, Scopus, PubMed, and Cochrane) were searched, using a cutoff date of May 2025, to identify English-language studies on pseudo-vestibular neuritis, which mimic a peripheral disease. We reviewed 112 full-text articles and found 33 reporting data that met the inclusion criteria. We found 79 patients that presented at diagnosis with a spontaneous nystagmus of central origin. Every patient was submitted to MRI and a stroke or infarction was found. The most frequent localization of the lesions was the cerebellum. Instrumental oculomotor assessment, in conjunction with advanced neuroimaging techniques, enables early and accurate localization of posterior circulation infarcts.

In brainstem strokes, vertigo and dizziness are often accompanied by other neurological signs as in Wallenberg's syndrome. Isolated vestibular syndromes may result from small, localized lesions involving the vestibular nuclei or the root entry zone of the eighth cranial nerve at the pontomedullary junction, dorsolateral medulla, pontine or midbrain tegmentum, or the cerebellar peduncles (Kuybu et al., 2025; Nickel et al., 2018; Salerno et al., 2022; Choi et al., 2013; Kim et al., 2014). Despite advances in diffusion-weighted imaging (DWI), which has significantly improved the detection of posterior circulation strokes, expert bedside neuro-otologic evaluation remains more sensitive than acute MRI (including DWI) during the first 48 h in detecting small infarcts (Kim et al., 2022; Kilburg et al., 2017).

We introduce the case of a 55-year-old woman, a non-smoker, who presented to the emergency department with acute isolated vertigo associated with nausea. She had no comorbidities and no cardiovascular risk factors. She had an III-grade right-beating horizontal spontaneous nystagmus with truncal ataxia. The head shake test (HST) showed an enhancement of the spontaneous nystagmus, and the clinical head impulse test (cHIT) was negative. Skew deviation (SD) was also negative. The instrumental vestibular examination with videonystagmography and video head impulse test (vHIT) confirmed a normal vestibular ocular reflex (VOR) bilaterally. A head CT and an angio-CT scan were performed, both of which were negative for acute lesions. She was hospitalized in the neurology department, and an MRI was obtained, which found an area of water molecular diffusivity restriction in the left paramedian medulla, hyperintense on T2 and FLAIR, consistent with recent ischemic focus (Figure 1). A 75 mg acetylsalicylic acid therapy was indicated. A week later the patient reported improved vertiginous symptoms and absence of ataxia; the videonystagmography showed a persistent horizontal right-beating spontaneous nystagmus, with a reduced slow phase velocity, and VOR hypergain in the right lateral semicircular canal. She did not develop neurological symptoms or signs later.

Literature search

Multiple databases (MEDLINE, EMBASE, Web of Science, Scopus, PubMed, and Cochrane) were searched using a cutoff date of May 2025, to identify English-language studies on central stroke presenting as acute vestibular syndrome. The string used was ((“Vertigo”[Mesh]) AND “Stroke”[Mesh]) AND “Nystagmus, Pathologic”[Mesh]. Titles and abstracts of identified articles were screened independently by two reviewers (FB and AGT). Articles were excluded if they lacked full-text and were not in English. The inclusion criteria were: patients with spontaneous nystagmus of central origin mimicking acute unilateral vestibulopathy, without auditory symptoms and neurological symptoms (except for ataxia). The exclusion criteria were: patients with auditory symptoms, or any neurological sign (except for ataxia), either at the beginning of evaluation or subsequently; patients with a nystagmus of central origin (i.e., vertical, changing direction nystagmus, gaze-evoked nystagmus); patients under 18 years old; positional nystagmus. Full-text versions of eligible articles were reviewed independently by the same two reviewers.

Literature review

As seen in the flowchart (Figure 2), our systematic search identified 1,487 citations. We eliminated 764 duplicates, and 381 were excluded for not being in English and for lacking a full-text article. Of the remaining 342 abstracts, we excluded 230 articles for being background articles or for there being a mismatch between the study group and the required target population. We finally reviewed 112 full-text articles and found 33 reporting data that met the inclusion criteria (Ataç et al., 2020; Choi et al., 2014; León Cejas et al., 2019; Braun et al., 2011; Casani et al., 2013; Chen et al., 2011; Choi et al., 2015, 2018; Huang and Yu, 1985; Kikuchi and Yamasoba, 2007; Kim et al., 2001, 2013; Kim and Kim, 2019; Kim and Lee, 2010; Lee and Sohn, 2002; Lee et al., 2003; Lee and Cho, 2004; Lee et al., 2015; Ling et al., 2019; Mazagri et al., 1992; Moon et al., 2009; Ogawa et al., 2013, 2018; Park et al., 2014; Pavlin-Premrl et al., 2015; Schwartz et al., 2007; Su and Young, 2011; Tseng and Chiu, 2014; Usui et al., 2019; Seo et al., 2004; Volgger and Gürkov, 2017; von Brevern et al., 2014; Witsch et al., 2018). Every patient report can be found in the Supplementary Table S1.

Patient characteristics

We found 79 patients who presented at diagnosis with a spontaneous nystagmus of central origin mimicking a peripheral one. Patients had a mean age of 61.89 years (±14.07), range 22–86, the M/F ratio was 1.4, and 38 patients had at least one cardiovascular risk factor (48.1%). Every patient had spontaneous nystagmus (horizontal or torso-horizontal), and 43 (54.4%) also had ataxia at presentation. Supplementary Table S2 describes the patient characteristics.

Patient evaluation

Initially, most patients did not have a complete evaluation: the cHIT, HST, and cover test for SD were unknown in 40 (50.7%), 63 (79.7%), and 56 patients (73.4%), respectively. Every patient was referred for an MRI, and a stroke or infarction was found. The most frequent localization of the lesions was the cerebellum (36 patients, 45.6%), followed by the nodulus, the cerebellar peduncle, the medulla, and the vermis cerebelli (10, 7, 7, and 6 patients, respectively); other sites were less involved.

The HIT was the most used test, with results from 39 patients being available. It was positive in 12 patients (30.8%) and negative in 27 (69.2%). The HST and SD cover tests were less commonly undertaken. When described, HST was positive (enhancement of the spontaneous nystagmus) in 9 patients and negative (spontaneous nystagmus not enhanced) in 7 patients. The SD cover test was positive in 3 patients and negative in 20 patients. In some cases where HIT was positive for peripheral disease, the HST and SD cover tests were useful to lead the diagnosis to a central lesion.

The literature showed that HIT, when performed, is a valid tool to address a peripheral or a central lesion, and when it is associated with other tests, it increases its specificity. As well-described in emergency department protocols evaluating vertigo and dizziness, the HINTS and STANDING protocol are gold standard in clinical practice (Gerlier et al., 2021). However, instrumental quantitative vestibular function tests have a critical role in confirming a suspicion of peripheral or central lesions (Jaganathan et al., 2024; Mantokoudis et al., 2015), as MRI in the first 48 h does not have great sensitivity (Kattah et al., 2009). Furthermore, in follow-ups the results are more comparable to see progresses and modifications from the symptoms' onset.

In our case report, the patient did not present any cardiovascular or stroke risk factor. Only the cHIT and the confirmation with vHIT lead us to suspect a central stroke. The support provided by the instrumental tests enabled us to refer the patient to the neurology department to perform an MRI although the angioTC did not detect any acute lesion or vessel obstruction.

Evaluation in acute vestibular syndromes should always find its basics in HINTS and STANDING protocols, using instrumental tests to confirm and strengthen the clinical bedside examination, in order to correctly assess the patient (Figure 2).

Distinguishing isolated central vascular vertigo/dizziness from peripheral causes—such as acute unilateral vestibulopathy or vestibular neuritis, which affect the labyrinth or vestibular nerve—is essential, as these conditions differ significantly in both treatment strategies and prognosis (Strupp et al., 2022). Misdiagnosing a stroke may result in missed opportunities for effective treatment, potentially increasing morbidity and mortality, whereas overdiagnosis of vascular causes can lead to unnecessary and costly investigations and treatments (Saber Tehrani et al., 2013; Dong et al., 2020).

In a prospective, cross-sectional study at an academic hospital conducted in the emergency department, consecutive patients with acute vestibular syndrome with 1 or more stroke risk factor were considered. One hundred one high-risk patients were included, 25 peripheral and 76 central lesions (69 ischemic strokes, 4 hemorrhages, 3 other). Initial MRI diffusion-weighted imaging was falsely negative in 12% (all <48 h after symptom onset; Kattah et al., 2009). Therefore, the matter carries a special weight in terms of health and healthcare costs.