The Dizzy Patient: A Framework Beyond "Vertigo vs. Presyncope"

A systematic neurological approach to a notoriously difficult complaint

Dr Neeraj Manikath , claude.ai

Abstract

Dizziness represents one of the most challenging complaints in internal medicine, affecting approximately 15-20% of adults annually and accounting for over 4 million emergency department visits in the United States each year. The traditional binary classification of "vertigo versus presyncope" oversimplifies a complex symptom with diverse etiologies ranging from benign peripheral vestibular disorders to life-threatening posterior circulation strokes. This review provides internists with a structured, evidence-based approach to the dizzy patient, emphasizing bedside examination techniques that can differentiate benign from dangerous causes, particularly in the acute setting. We focus on practical clinical tools including the HINTS examination for acute vestibular syndrome, recognition of benign paroxysmal positional vertigo (BPPV) with appropriate treatment maneuvers, understanding persistent postural-perceptual dizziness (PPPD) as a common cause of chronic symptoms, and identifying red flags requiring urgent neuroimaging.

Introduction: Moving Beyond Outdated Paradigms

The conventional approach to dizziness—asking patients whether their symptom represents "spinning" (vertigo) versus "lightheadedness" (presyncope)—has significant limitations. Research demonstrates that patients use descriptive terms inconsistently, with poor correlation between symptom descriptors and underlying diagnoses. Newman-Toker and colleagues found that timing and triggers provide more diagnostic value than quality of dizziness alone.

A more clinically useful framework categorizes dizziness by temporal pattern:

Acute vestibular syndrome (AVS): Continuous dizziness lasting days, associated with nausea, vomiting, gait instability, and nystagmus
Episodic vestibular syndrome: Recurrent attacks lasting seconds to hours
Chronic vestibular syndrome: Persistent symptoms lasting weeks to months

This temporal approach, combined with careful examination, substantially improves diagnostic accuracy.

The HINTS Exam for the Internist: Using Nystagmus to Differentiate Vestibular Neuritis from Cerebellar Stroke in the Acute Setting

The Clinical Challenge

Acute vestibular syndrome presents a critical diagnostic dilemma. Approximately 25% of patients presenting with acute continuous dizziness, nausea, vomiting, and gait instability have a posterior circulation stroke, most commonly involving the cerebellum. However, the majority have benign vestibular neuritis. Critically, early CT imaging misses up to 50% of posterior circulation strokes in the first 48 hours, making clinical examination paramount.

The HINTS Examination: More Powerful Than MRI

The HINTS examination (Head Impulse, Nystagmus, Test of Skew) represents one of the most valuable bedside tools in internal medicine. When applied correctly to patients with acute vestibular syndrome, HINTS demonstrates higher sensitivity for stroke than early MRI with diffusion-weighted imaging (DWI).

Head Impulse Test (HIT)

The head impulse test assesses vestibulo-ocular reflex function. With the patient fixating on the examiner's nose, the examiner rapidly rotates the patient's head approximately 10-20 degrees to one side. A normal response shows smooth eye movement maintaining fixation. An abnormal (positive) test shows a corrective saccade—the eyes move with the head, then rapidly jump back to maintain fixation.

Pearl: A positive head impulse test (corrective saccade) indicates peripheral vestibular dysfunction, suggesting vestibular neuritis rather than stroke. A bilaterally normal head impulse test in acute vestibular syndrome is concerning for central pathology.

Nystagmus Assessment

Direction-changing nystagmus with gaze is the most specific finding for central pathology. In peripheral vestibular disorders, nystagmus is unidirectional—it beats in the same direction regardless of gaze direction, typically with the fast phase away from the affected ear. Central lesions may produce direction-changing nystagmus, purely vertical nystagmus, or purely torsional nystagmus.

Oyster: Many clinicians misinterpret end-point nystagmus (a few beats of nystagmus at extreme gaze, seen in normal individuals) as pathologic. Pathologic direction-changing nystagmus must be present at least 30 degrees from midline and sustained.

Test of Skew Deviation

Skew deviation represents vertical misalignment of the eyes caused by brainstem or cerebellar dysfunction. Perform the alternate cover test: have the patient fixate on your nose while you alternately cover each eye. Observe for vertical refixation movements when uncovering each eye.

HINTS Interpretation

A "HINTS-negative" examination (reassuring for peripheral cause) includes:

Positive (abnormal) head impulse test
Unidirectional, horizontal nystagmus
Absent skew deviation

A "HINTS-positive" examination (concerning for stroke) includes ANY of:

Normal (negative) head impulse test bilaterally
Direction-changing nystagmus
Present skew deviation

Kattah and colleagues demonstrated 100% sensitivity and 96% specificity for stroke when HINTS was applied by trained examiners in patients with acute vestibular syndrome. This exceeds the sensitivity of MRI-DWI performed within 48 hours of symptom onset.

Hack: Remember "INFARCT" for concerning features:

Impulse normal (negative head impulse)
Nystagmus direction-changing
Fast phase alternating
Articulation abnormal (dysarthria)
Refixation on cover test (skew)
Contralateral hearing loss (suggests AICA stroke)
Truncal ataxia severe and out of proportion

The Triad of PPPD (Persistent Postural-Perceptual Dizziness): A Common Cause of Chronic Dizziness

An Underrecognized Entity

Persistent postural-perceptual dizziness represents one of the most common causes of chronic dizziness yet remains underdiagnosed in internal medicine practice. Formally defined by the Bárány Society in 2017, PPPD affects approximately 15-20% of patients presenting to subspecialty dizziness clinics.

Diagnostic Criteria

PPPD diagnosis requires all five of the following:

Dizziness, unsteadiness, or non-spinning vertigo present on most days for ≥3 months
Persistent symptoms without regard to position, though standing and upright posture may worsen symptoms
Symptoms triggered or exacerbated by:
- Active or passive motion without regard to direction or position
- Visual stimuli (complex patterns, scrolling screens, moving objects)
- Environments with complex visual motion (grocery stores, crowds)
Precipitated by conditions causing vestibular symptoms, acute medical illnesses, or psychological distress
Symptoms cause significant functional impairment

Pathophysiology

PPPD represents a maladaptive response to an initial vestibular insult or other precipitant. Following events like vestibular neuritis, BPPV, concussion, or even panic attacks, some patients develop persistent high postural tone and increased visual dependence for balance. Rather than normal sensory reweighting and adaptation, these patients maintain maladaptive strategies.

Neuroimaging studies demonstrate altered processing in multisensory vestibular cortical regions and limbic structures. The condition involves both sensorimotor and psychological components, though it is not primarily psychiatric.

Clinical Recognition

Pearl: Patients with PPPD often describe "feeling off-balance" or "like walking on a boat" rather than discrete vertigo episodes. They frequently report symptom exacerbation in visually complex environments—supermarkets are a classic trigger. Unlike anxiety disorders, the primary complaint is dizziness, not anxiety, though secondary anxiety about symptoms is common.

Oyster: PPPD commonly follows BPPV that was successfully treated. Patients report the positional vertigo resolved, but they "never felt quite right afterward." This presentation should prompt consideration of PPPD rather than persistent BPPV.

Management

Treatment requires a multimodal approach:

Vestibular rehabilitation therapy (VRT): First-line treatment, focusing on habituation, adaptation, and substitution exercises
Cognitive behavioral therapy: Addresses maladaptive behavioral responses and anxiety
Pharmacotherapy: Selective serotonin reuptake inhibitors (SSRIs), particularly sertraline and escitalopram, show efficacy in randomized trials
Patient education: Explaining the condition's mechanism helps reduce anxiety and improve compliance

Hack: When prescribing SSRIs for PPPD, warn patients that symptoms may initially worsen for 1-2 weeks before improvement. Starting with half the usual starting dose and slow titration improves tolerability.

BPPV: Diagnosis with the Dix-Hallpike and Treatment with the Epley Maneuver

The Most Common Vestibular Disorder

Benign paroxysmal positional vertigo affects approximately 2.4% of the population at some point in their lives, with increasing prevalence in older adults. Despite its frequency, BPPV is often mismanaged, with patients undergoing unnecessary testing or receiving inappropriate medications.

Pathophysiology

BPPV results from calcium carbonate crystals (otoconia) that dislodge from the utricle and migrate into the semicircular canals, most commonly the posterior canal (90% of cases). Head position changes cause the crystals to move, deflecting the cupula and producing inappropriate signals interpreted as motion.

The Dix-Hallpike Maneuver

This provocative test confirms posterior canal BPPV. Technique:

Seat the patient on the examination table with head turned 45 degrees to one side
Warn the patient about expected symptoms
Rapidly lay the patient back with the head extended 20 degrees below horizontal, maintaining the 45-degree rotation
Observe for nystagmus and vertigo for up to 1 minute

Positive test characteristics:

Latency: 5-20 seconds before symptoms begin
Upbeating and torsional nystagmus (top pole of eye beating toward the affected ear)
Duration: typically <60 seconds
Fatiguability: symptoms decrease with repeated testing

Pearl: The side producing symptoms when turned downward (e.g., right Dix-Hallpike positive) indicates the affected ear. The nystagmus beats toward the affected ear in posterior canal BPPV.

The Epley Maneuver (Canalith Repositioning)

The Epley maneuver successfully treats posterior canal BPPV in approximately 80% of patients with a single treatment, with higher success after repeated treatments. Proper technique requires:

Start with positive Dix-Hallpike position (head extended and turned toward affected ear)
Wait for nystagmus to cease
Rotate head 90 degrees to the opposite side (now looking 45 degrees away from affected ear)
Wait 30 seconds
Roll patient onto side, continuing to turn head so nose points downward
Wait 30 seconds
Sit patient upright, head tilted forward 30 degrees

Hack: Video the Epley maneuver on the patient's phone so they can repeat it at home if symptoms recur. Many patients successfully self-treat recurrences using video guidance.

Oyster: Not all positional vertigo is BPPV. Horizontal canal BPPV (10% of cases) requires the supine roll test for diagnosis and different treatment (Lempert/BBQ roll maneuver). Central positional vertigo from cerebellar lesions may produce atypical nystagmus—pure downbeating, immediate onset without latency, or duration >1 minute.

Post-Treatment Recommendations

Traditional post-Epley restrictions (sleeping upright, avoiding head positions) lack strong evidence but remain common practice. Recent studies suggest restrictions may not improve outcomes. However, many practitioners recommend:

Sleeping with head elevated 45 degrees for one night
Avoiding the affected ear-down position for 48 hours

When to Order an MRI: Red Flags in the History and Exam That Warrant Urgent Imaging

The Imaging Dilemma

Neuroimaging for dizziness has low yield but high utilization. Studies indicate that only 3-5% of patients presenting with isolated dizziness have clinically significant findings on MRI, yet imaging rates exceed 50% in many emergency departments. This results in substantial healthcare costs, incidental findings requiring follow-up, and false reassurance when early MRI appears normal despite posterior circulation stroke.

Historical Red Flags

Certain historical features substantially increase stroke probability and warrant urgent MRI with attention to posterior fossa:

Vascular risk factors: Multiple stroke risk factors (particularly combination of age >60, hypertension, diabetes, atrial fibrillation) increase pre-test probability

Abrupt onset: Stroke typically begins suddenly at a definable moment, whereas vestibular neuritis often develops over hours

Severe headache: Particularly occipital headache, may indicate vertebral artery dissection or cerebellar hemorrhage

Neck trauma or manipulation: Recent chiropractic manipulation or trauma raises concern for vertebral artery dissection

Neurological symptoms: Any focal weakness, numbness, diplopia, dysarthria, or dysphagia

Severe imbalance: Inability to walk independently suggests central pathology

Hearing loss: Sudden unilateral hearing loss with vertigo may indicate anterior inferior cerebellar artery (AICA) stroke

Examination Red Flags

HINTS-positive examination: As discussed, any concerning features on HINTS (normal head impulse, direction-changing nystagmus, or skew deviation) in acute vestibular syndrome

Severe truncal ataxia: Inability to sit unsupported suggests midline cerebellar involvement

Limb ataxia: Finger-nose-finger or heel-shin ataxia on one side suggests cerebellar hemisphere involvement

Vertical or purely torsional nystagmus: Unlike horizontal nystagmus seen in peripheral disorders

Gaze-evoked nystagmus: Nystagmus present only with sustained eccentric gaze suggests central pathology

Abnormal saccades: Slow or inaccurate saccades indicate brainstem or cerebellar dysfunction

Dysmetric saccades: Saccades that overshoot or undershoot target (hypermetric or hypometric)

Cranial nerve abnormalities: Any cranial nerve finding beyond expected CN VIII involvement

Horner syndrome: Ptosis, miosis, and anhidrosis suggest lateral medullary (Wallenberg) syndrome

The ABCD² Score Limitation

The ABCD² score, developed for transient ischemic attack risk stratification, has been adapted for posterior circulation TIA but performs poorly for isolated dizziness. Isolated vertigo without other neurological symptoms typically receives low ABCD² scores despite significant stroke risk. Therefore, ABCD² should not guide imaging decisions in isolated dizziness.

Imaging Recommendations

Urgent MRI with DWI (preferably within 24 hours) indicated for:

Acute vestibular syndrome with any HINTS-positive feature
Acute dizziness with any additional neurological symptom or sign
Acute dizziness with multiple vascular risk factors and any atypical feature
New severe headache accompanying acute dizziness
Recent neck trauma or manipulation

Routine outpatient MRI may be considered for:

Progressive chronic dizziness
Chronic dizziness with unexplained progressive hearing loss (acoustic neuroma)
Atypical positional vertigo not responding to treatment
Associated tinnitus and progressive hearing loss (cerebellopontine angle lesion)

Imaging generally not indicated for:

Classic BPPV with typical Dix-Hallpike findings
Vestibular neuritis with reassuring HINTS examination
PPPD meeting diagnostic criteria without red flags

Pearl: When ordering MRI for acute dizziness, specifically request attention to the posterior fossa and request DWI sequences. Standard stroke protocols may focus on anterior circulation.

Practical Approach: Putting It All Together

Initial Assessment

Characterize temporal pattern: Acute continuous (AVS), episodic, or chronic
Identify triggers: Positional, visual, orthostatic
Screen for red flags: Review historical and examination red flags systematically
Focused examination: Include HINTS components (even in non-acute presentations to assess for any chronic central signs), Dix-Hallpike if episodic positional symptoms, orthostatic vitals, cardiovascular and neurological examination

Decision Pathway

For acute vestibular syndrome:

Perform complete HINTS examination
If HINTS-positive or any red flag → urgent MRI
If HINTS-negative → diagnose vestibular neuritis, provide symptomatic treatment (meclizine, ondansetron for acute phase only), early vestibular rehabilitation

For episodic positional vertigo:

Perform Dix-Hallpike maneuver
If positive → Epley maneuver, patient education, consider video instructions
If negative or atypical features → consider horizontal canal BPPV (supine roll test), vestibular migraine, or TIA (if vascular risk factors present)

For chronic dizziness:

Assess for PPPD diagnostic criteria
Evaluate for persistent vestibular deficit (head thrust, balance testing)
If meets PPPD criteria → vestibular rehabilitation, consider SSRI, CBT referral
If progressive or atypical → outpatient MRI, consider subspecialty referral

Conclusion

Dizziness evaluation requires moving beyond simplistic classification schemes to embrace a structured approach based on temporal patterns and focused examination. The HINTS examination provides stroke detection superior to early MRI in acute vestibular syndrome and should be mastered by all internists. Recognition of BPPV allows immediate treatment with the Epley maneuver, providing dramatic symptom relief. Understanding PPPD enables appropriate management of chronic symptoms that might otherwise lead to extensive unnecessary testing. Finally, systematic attention to red flags ensures that dangerous causes are not missed while avoiding excessive imaging in benign conditions.

The dizzy patient need not be diagnostically dizzying. With these tools, internists can confidently evaluate and manage most dizzy patients, reserving neuroimaging and subspecialty referral for appropriate cases.

References

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