Acute vertigo in a 67-year-old woman: Peripheral or central?

INITIAL EVALUATION

On arrival, her temperature was 98.1°F (36.7°C), heart rate 82 beats per minute, respiratory rate 18 breaths per minute, and oxygen saturation 97% on room air. Her blood pressure was elevated at 230/107 mm Hg. Body mass index was 31.42 kg/m2. She was alert and oriented to person, place, and time.

A cardiac evaluation was performed to assess for arrhythmia or myocardial ischemia as potential causes of her symptoms, particularly given her advanced age, severe hypertension, and significant cardiovascular risk profile. In addition, myocardial ischemia was considered because women, especially those with diabetes or multiple cardiometabolic risk factors, may present with atypical or nonspecific symptoms, including epigastric discomfort, nausea, and dizziness. Cardiovascular examination did not reveal murmurs, pulse deficits, or other findings suggestive of aortic dissection, and there were no clinical signs of acute heart failure. Electrocardiogram showed normal sinus rhythm without evidence of arrhythmia or acute ischemia, and serum troponin levels were within normal limits. A previously obtained transthoracic echocardiogram showed normal cardiac structure and function, with no intracardiac thrombus or other potential cardioembolic source.

Initial laboratory studies were obtained to evaluate alternative causes of dizziness and to assess for evidence of hypertensive emergency, given the patient’s markedly elevated blood pressure. A basic metabolic panel was performed to assess for electrolyte disturbances, renal function, and dehydration related to vomiting, and a complete blood cell count was obtained to evaluate for anemia and hematologic abnormalities. Both studies were within normal limits, with no abnormalities to explain her symptoms and no laboratory evidence of nonneurologic end-organ injury.

Dizziness is a common but diagnostically challenging symptom. Initial descriptions are often nonspecific, and patients may use terms such as “dizziness,” “lightheadedness,” or “spinning” interchangeably.^1–5 Because symptom quality alone is unreliable, we explained the different types of dizziness to the patient in simple terms—vertigo (a sensation of spinning or motion), presyncope (a feeling of impending faint), and disequilibrium (a sense of imbalance)—and asked her which best matched her experience. With this guided approach, she identified her symptoms as most consistent with vertigo.

DIFFERENTIAL DIAGNOSIS

The patient’s vertigo was spontaneous, continuous for more than 24 hours, and worsened with head movement. Once vertigo is established, a useful diagnostic framework is the TiTrATE approach, which relies on timing, triggers, and targeted examination findings to classify dizziness into vestibular syndromes that guide the differential diagnosis.^2,6

1. Which vestibular syndrome best describes this patient’s presentation?

• Benign paroxysmal positional vertigo

• Spontaneous episodic vestibular syndrome

• Acute vestibular syndrome

The answer depends on whether her symptoms are episodic or continuous, and whether they are triggered or spontaneous.

Benign paroxysmal positional vertigo was considered because her symptoms worsened with head movement. However, benign paroxysmal positional vertigo is characterized by brief, triggered episodes of vertigo lasting seconds, with patients typically asymptomatic between episodes. This patient had continuous symptoms, making benign paroxysmal positional vertigo unlikely.

Spontaneous episodic vestibular syndrome is characterized by recurrent spontaneous episodes of vertigo lasting minutes to hours, with symptom-free intervals between episodes. Common causes include vestibular migraine and Ménière disease. This patient’s symptoms were continuous with no symptom-free intervals, making a spontaneous episodic syndrome unlikely. Vestibular migraine was considered within this category. It typically presents with recurrent episodes of vertigo, often associated with migraine features such as photophobia, phonophobia, or headache. The patient had no history of migraine and no recurrent episodes, arguing against this diagnosis.

Ménière disease was also considered; it is characterized by episodic vertigo associated with auditory symptoms, including fluctuating hearing loss, tinnitus, and aural fullness. The absence of auditory symptoms in this patient makes this diagnosis unlikely.

Acute vestibular syndrome, defined by continuous symptoms lasting days to weeks, best fits with this patient’s sudden onset of continuous vertigo lasting more than 24 hours and the associated nausea, vomiting, and head-motion intolerance.^3,4 Once acute vestibular syndrome is identified, the diagnostic focus shifts from syndrome classification to determining the underlying cause. The key task then is to distinguish peripheral from central causes.^1,7,8

CASE CONTINUED: FURTHER ASSESSMENT

Distinguishing central from peripheral causes of acute vestibular syndrome relies heavily on history and physical examination. The most common peripheral causes include vestibular neuritis and labyrinthitis, while the central cause of greatest concern is posterior circulation stroke.

We further reviewed the patient’s history to refine the differential diagnosis. She had no hearing loss, tinnitus, or aural fullness, making labyrinthitis less likely. She reported no recent upper respiratory infection, which is commonly associated with vestibular neuritis. While these findings reduce the likelihood of peripheral causes, they do not exclude them.^7,8 A comprehensive neurologic examination, including assessment of mental status, cranial nerves, pupils, motor and sensory function, and reflexes, revealed no focal neurologic deficits. However, the absence of focal deficits also does not reliably exclude posterior circulation stroke, as these strokes may present with isolated vestibular symptoms.^7,8

2. On examination, which finding would most strongly suggest a central cause of vertigo in this patient?

• Direction-changing gaze-evoked nystagmus

• Unidirectional horizontal nystagmus

• Positive head impulse test

• Vertigo worsened by head movement

The HINTS (head-impulse, nystagmus, test of skew) examination is a bedside tool used to differentiate peripheral from central causes of acute vestibular syndrome.^8–12 It should be applied only in the appropriate clinical context; that is, in patients with continuous symptoms and spontaneous nystagmus. Nystagmus consists of involuntary repetitive eye movements that have a slow phase in which the eyes drift away from the target followed by a fast corrective phase that brings the line of sight back to the target.

The HINTS examination is not intended for use in brief, triggered episodic vertigo, such as typical benign paroxysmal positional vertigo. The HINTS examination is highly technique-dependent; clinicians unfamiliar with its performance and interpretation may find instructional video demonstrations helpful.¹³ It has 3 components:

• Head impulse test. This evaluates the vestibuloocular reflex. The patient is asked to fix their gaze on a target while the examiner rapidly turns the head horizontally to one side. A positive test, defined by the presence of additional eye movements to maintain gaze (ie, corrective refixation saccades) after the head turn, indicates impaired vestibulo-ocular reflex function on the side to which the head was turned and typically suggests a peripheral vestibular lesion. In contrast, a normal (negative) head impulse test in a patient with continuous vertigo is concerning for a central cause.^8,9

• Nystagmus assessment. Peripheral causes typically produce unidirectional horizontal nystagmus (ie, eye movement to the side and then back to center) that does not change direction with gaze and usually follows Alexander’s law (ie, nystagmus intensity increases when gazing in the direction of the fast corrective phase and diminishes with gaze in the slow-phase direction).¹⁴ In contrast, direction-changing gaze-evoked nystagmus—for example, right-beating nystagmus in right gaze and left-beating nystagmus in left gaze—suggests a central lesion. Vertical (upbeat or downbeat) or pure torsional (rotary eye movements) nystagmus is highly suggestive of a central cause.^8,9

• Test of skew. Vertical misalignment of the eyes (skew deviation) detected with alternate eye covering indicates a central cause, often involving the brainstem.^8,9

Notably, individual components of the HINTS examination have limitations. Posterior circulation strokes can occasionally produce findings suggestive of a peripheral cause of acute vestibular syndrome, including unidirectional nystagmus and an abnormal head impulse test.^12,15 Although a normal head impulse test strongly suggests a central lesion, abnormal results may occasionally occur in stroke, particularly in infarctions involving vestibular pathways.^9,16 This principle has been summarized succinctly by Kerber and Baloh¹⁷: “… with only rare exception, central lesions can mimic a ‘peripheral’ pattern of nystagmus, but peripheral lesions cannot cause ‘central’ patterns of nystagmus.”

This teaching point underscores the importance of recognizing central patterns of nystagmus when present, while also appreciating that apparently peripheral findings do not entirely rule out a central lesion. Further, the clinical manifestations of cerebellar infarction vary according to lesion size and location, and smaller cerebellar strokes may not produce the classic ocular motor findings typically associated with central vertigo.

CASE CONTINUED: HINTS EXAMINATION

Our patient’s horizontal head-impulse test was positive, with corrective saccades, favoring a peripheral vestibular process. She demonstrated spontaneous unidirectional horizontal nystagmus, which is typically associated with peripheral causes. The test of skew was negative, arguing against a central lesion. Taken together, the HINTS examination suggested a peripheral vestibular etiology. Two physicians confirmed the findings independently.

Gait and truncal stability are important components of the neurologic examination, as severe truncal ataxia or inability to sit or stand unsupported is concerning for central pathology. In this case, gait assessment was deferred because the patient’s severe dizziness and active vomiting limited safe evaluation at the time of examination. This incomplete component of the examination became clinically relevant, as it reduced confidence in excluding a central cause and contributed to the decision to pursue further evaluation.

DIAGNOSTIC REASONING

3. In this patient with acute vestibular syndrome and an examination suggesting a peripheral cause, which clinical factors would most strongly justify further evaluation for stroke?

• Advanced age and vascular risk factors

• Persistent symptoms despite supportive therapy

• Normal neurologic examination

• Absence of auditory symptoms

Despite a HINTS examination suggesting a peripheral cause of acute vestibular syndrome, the patient’s vascular risk profile significantly increased the pretest probability of stroke. She had long-standing hypertension with medication nonadherence, a greater than 30-year smoking history, and obesity (body mass index 31.42 kg/m2).

Conversely, a normal neurologic examination does not exclude posterior circulation stroke, and the absence of auditory symptoms does not reliably distinguish central from peripheral causes of acute vestibular syndrome.

Given these risk factors and her limited engagement with routine medical care, a lipid panel and hemoglobin A1c were obtained to assess for additional, previously unrecognized cardiometabolic risk factors. Laboratory evaluation revealed marked dyslipidemia:

• Total cholesterol 311 mg/dL (reference range < 200)

• Low-density lipoprotein cholesterol 232 mg/dL (< 100)

• Non–high-density lipoprotein cholesterol 252 mg/dL (< 130).

Hemoglobin A1c was elevated at 7.2% (< 5.7%), consistent with previously undiagnosed diabetes. Further, her blood pressure on presentation was severely elevated at 230/107 mm Hg.

Taken together, these findings represent a high burden of atherosclerotic cardiovascular risk.¹⁸ The patient’s estimated PREVENT score, incorporating factors such as age, blood pressure, lipid profile, glycemic status, and smoking history, was about 31% (derived from the American Heart Association Predicting Risk of Cardiovascular Disease Events calculator), reflecting a high predicted 10-year risk of cardiovascular events.¹⁹ This elevated risk further increased concern for an underlying cerebrovascular process.

Also, her symptoms persisted despite initial supportive management, including antiemetics and vestibular suppressants. These findings lowered the threshold for evaluating a central cause. Although benign vestibular disorders are common, posterior circulation stroke must be strongly considered in patients presenting with acute vestibular syndrome in the presence of vascular risk factors.^{10,11,20–23}

BRAIN IMAGING AND DIAGNOSIS

Brain magnetic resonance imaging subsequently revealed patchy restricted diffusion in the right cerebellar hemisphere, consistent with acute ischemic cerebellar infarction (Figure 1).

• Download figure
• Open in new tab
• Download PowerPoint

Figure 1

Diffusion-weighted brain magnetic resonance imaging showed patchy areas of restricted diffusion in the right cerebellar hemisphere (arrows), consistent with acute ischemic infarction.

CASE DISCUSSION AND TREATMENT CONSIDERATIONS

Dizziness accounts for about 4% to 5% of emergency department visits, and stroke represents an important cause of these presentations.^20,22 Observational studies have shown that posterior circulation stroke may present with isolated vestibular symptoms, including vertigo, nausea, vomiting, and imbalance, in the absence of focal neurologic deficits, making early diagnosis challenging.^7,10,15 Small cerebellar infarctions, in particular, may closely mimic peripheral vestibular disorders such as vestibular neuritis.^16,21

Importantly, this patient’s experience does not provide support for routine neuroimaging in all patients with vertigo. Most cases of vertigo are due to benign peripheral vestibular disorders, and indiscriminate imaging may lead to unnecessary testing and increased healthcare costs. However, neuroimaging should be pursued when clinical features raise concern for central pathology, including significant vascular risk factors, discordant or incongruent examination findings, or persistent diagnostic uncertainty.^1,5 In this patient, the discordance between the clinical history, a bedside examination suggesting a peripheral cause, and a high-risk vascular profile, along with incomplete gait assessment and persistent symptoms, justified further evaluation for stroke.

Management of posterior circulation stroke presenting with isolated vestibular symptoms can be challenging. These patients often have low National Institutes of Health Stroke Scale scores, which may underestimate the functional impact of severe vertigo and gait instability.^24,25 Evidence guiding the use of intravenous thrombolysis in this population remains limited, and treatment decisions must often be individualized based on clinical suspicion, symptom severity, and imaging findings.^24,25 In this case, the patient was treated with dual antiplatelet therapy and high-intensity statin therapy, with gradual improvement in symptoms, and was referred for vestibular rehabilitation.

TAKE-HOME POINTS

• Evaluation of vertigo must be approached on a case-by-case basis, integrating findings from the history, physical examination, and overall risk profile.

• Although most cases of vertigo are benign, clinicians must remain vigilant for posterior circulation stroke, particularly when clinical features and risk factors raise concern.

• Acute vestibular syndrome is characterized by continuous vertigo, nausea or vomiting, spontaneous nystagmus, and gait instability lasting days to weeks.

• The key diagnostic task in acute vestibular syndrome is distinguishing peripheral vestibular disorders from posterior circulation stroke.

• Posterior circulation stroke can present with isolated vertigo, even in the absence of focal neurologic deficits.

• Even when bedside findings appear peripheral, clinicians must interpret them in the context of the patient’s vascular risk profile and overall clinical picture.

• Neuroimaging should not be performed routinely in all patients with vertigo but should be considered when clinical features raise suspicion for central pathology.

DISCLOSURES

The authors report no relevant financial relationships which, in the context of their contributions, could be perceived as a potential conflict of interest.