Vertigo: What Could Be Causing It

Peripheral vs. Central Vertigo: Why the Distinction Matters

The single most important question when evaluating vertigo is whether the cause is peripheral (inner ear or vestibular nerve) or central (brainstem or cerebellum). Peripheral causes account for approximately 80% of cases seen in primary care and carry a generally favorable prognosis. Central vertigo, while less common, can signal life-threatening pathology like posterior circulation stroke.

The HINTS exam (Head Impulse, Nystagmus, Test of Skew) is a bedside tool that helps clinicians separate these two categories. A 2009 study published in Stroke (N=101) found that HINTS had a sensitivity of 100% and specificity of 96% for identifying stroke in patients with acute vestibular syndrome, outperforming early MRI. The presence of a normal horizontal head impulse test, direction-changing nystagmus, or skew deviation raises suspicion for a central lesion [1].

Peripheral vertigo typically produces unidirectional horizontal-torsional nystagmus that worsens when gaze is directed away from the affected ear. Central vertigo often presents with vertical or purely torsional nystagmus, and patients may report associated neurological deficits. A thorough cranial nerve examination, gait assessment, and Romberg test should be part of every vertigo evaluation. The distinction between these categories guides both the urgency of neuroimaging and the treatment pathway.

BPPV: The Most Common Culprit

Benign paroxysmal positional vertigo causes brief episodes of spinning triggered by specific head movements, such as rolling over in bed, looking up, or bending forward. Episodes typically last less than 60 seconds and resolve spontaneously once the provoking position is maintained [2]. BPPV results from displaced calcium carbonate crystals (otoconia) migrating into the semicircular canals.

The posterior canal is affected in roughly 85% to 90% of BPPV cases. The Dix-Hallpike maneuver confirms this variant with an estimated sensitivity of 82% and specificity of 71%, according to a systematic review in the Journal of the American Academy of Audiology [3]. Horizontal canal BPPV, diagnosed via the supine roll test, accounts for 5% to 15% of cases.

Treatment is mechanical, not pharmaceutical. The Epley canalith repositioning maneuver resolves posterior canal BPPV in approximately 80% of patients within one to two sessions [4]. The 2017 American Academy of Otolaryngology Clinical Practice Guideline strongly recommends repositioning maneuvers as first-line therapy and advises against routine use of vestibular suppressants for BPPV [2]. Recurrence rates range from 15% in the first year to nearly 50% over five years. Patients with vitamin D deficiency may face higher recurrence risk, and supplementation has shown benefit in a 2020 randomized trial published in Neurology (N=957) that demonstrated a 24% reduction in annual BPPV recurrence with vitamin D and calcium supplementation [5].

Vestibular Neuritis and Labyrinthitis

Vestibular neuritis presents as sudden, severe, continuous vertigo lasting days to weeks, typically accompanied by nausea and postural instability but without hearing loss. When hearing loss accompanies the vertigo, the diagnosis shifts to labyrinthitis. Both conditions are believed to result from viral inflammation of the vestibular nerve, with herpes simplex virus type 1 implicated in postmortem studies [6].

Vestibular neuritis is the second most common cause of peripheral vertigo. The acute phase produces spontaneous unidirectional nystagmus with a positive head impulse test toward the affected side. Caloric testing shows reduced or absent response in the affected ear in over 90% of cases.

A short course of corticosteroids during the first 72 hours may improve vestibular recovery. The Strupp et al. trial (N=141, published in the New England Journal of Medicine) found that methylprednisolone significantly improved caloric response at 12 months compared to placebo, while valacyclovir showed no benefit [7]. Vestibular rehabilitation therapy is the most important long-term intervention. A Cochrane review of 39 trials (N=2,441) confirmed that vestibular rehabilitation produces moderate to strong evidence of benefit for unilateral vestibular hypofunction, reducing symptoms and improving balance function [8]. Most patients achieve substantial compensation within three to six months, though older adults and those with comorbid anxiety may recover more slowly.

Meniere Disease: Episodic Vertigo with Hearing Loss

Meniere disease is defined by recurrent episodes of spontaneous vertigo lasting 20 minutes to 12 hours, accompanied by fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness. The 2015 diagnostic criteria from the Barany Society and the American Academy of Otolaryngology require at least two definite vertigo episodes lasting 20 minutes to 12 hours, documented low-to-mid frequency hearing loss on at least one audiogram, and fluctuating aural symptoms in the affected ear [9].

Prevalence estimates vary widely, from 34 to 190 per 100,000. The pathological hallmark is endolymphatic hydrops, an excess accumulation of endolymph in the inner ear. Gadolinium-enhanced inner ear MRI can now visualize hydrops in vivo, though this imaging is not yet required for diagnosis.

First-line management includes dietary sodium restriction (targeting <1,500 mg daily) and betahistine, which is widely used outside the United States. A 2016 Cochrane review found insufficient high-quality evidence to confirm betahistine's efficacy, though clinical experience supports its use in many patients [10]. Intratympanic dexamethasone injections offer a less invasive option for refractory cases. Intratympanic gentamicin, which selectively ablates vestibular hair cells, reduces vertigo attacks in roughly 80% to 90% of patients but carries a risk of hearing loss in 20% to 30% of cases [11]. The condition is bilateral in 25% to 40% of patients over a 20-year follow-up period, which has significant implications for treatment planning.

Vestibular Migraine: An Underdiagnosed Entity

Vestibular migraine is the most common cause of episodic vertigo in patients with a history of migraine headaches, and it may be the single most underdiagnosed vestibular disorder. The ICHD-3 diagnostic criteria require at least five episodes of vestibular symptoms lasting 5 minutes to 72 hours, a current or past history of migraine, and migrainous features during at least half of the vestibular episodes. Population-based studies estimate the prevalence at roughly 1% of the general population and up to 11% of patients seen in dizziness clinics [12].

A defining characteristic is that headache does not need to accompany the vertigo. Some patients experience vertigo as their primary or sole migraine manifestation. Photophobia, phonophobia, or visual aura during episodes helps confirm the diagnosis. There is no confirmatory test; it remains clinical.

"Vestibular migraine should be considered in any patient with episodic vertigo and a personal or family history of migraine, even when headache is absent during attacks," per the Barany Society consensus document published in the Journal of Vestibular Research [12].

Prophylactic treatment follows migraine prevention principles. Beta-blockers, tricyclic antidepressants (nortriptyline or amitriptyline at 10 to 75 mg nightly), venlafaxine, and topiramate are all used. A retrospective study of 100 patients at Johns Hopkins found that lifestyle modifications combined with pharmacologic prophylaxis reduced vertigo episode frequency by over 75% in the majority of treated patients [13]. Trigger avoidance (sleep irregularity, caffeine, alcohol, stress) is a key non-pharmacologic strategy.

Central Causes: When Vertigo Signals Something Serious

Central vertigo accounts for only 5% to 10% of cases in primary care but carries the highest stakes. Posterior circulation ischemia (vertebrobasilar TIA or stroke) is the most urgent diagnosis to exclude. A prospective study of emergency department patients with acute vestibular syndrome found that roughly 3.2% had cerebellar or brainstem infarcts detectable only by MRI, with initial CT missing the majority of these lesions [1].

Red-flag features include: acute onset in a patient over 50 with vascular risk factors, inability to walk without assistance, severe headache, diplopia, dysarthria, dysphagia, facial numbness, or limb weakness. A negative head impulse test (no corrective saccade) in a patient with acute continuous vertigo and nystagmus is paradoxically concerning because it suggests the vestibular nerve is intact, pointing toward a central lesion.

Multiple sclerosis can present with vertigo in 20% of cases, sometimes as the initial symptom. Acoustic neuroma (vestibular schwannoma) causes progressive unilateral hearing loss and mild imbalance rather than true episodic vertigo. Contrast-enhanced MRI of the internal auditory canals is indicated when asymmetric sensorineural hearing loss is identified. The growth rate of untreated vestibular schwannomas averages 1 to 2 mm per year, and small tumors may be managed with observation and serial imaging [14].

Chiari malformation type I can cause positional vertigo and downbeat nystagmus. Cerebellar degeneration from chronic alcohol use, paraneoplastic syndromes, or hereditary ataxias should be considered when vertigo is accompanied by progressive gait instability.

Medication-Induced Vertigo

A substantial number of commonly prescribed medications can cause or worsen vertigo. Aminoglycoside antibiotics (gentamicin, streptomycin) are well-established vestibulotoxins that damage vestibular hair cells, sometimes permanently. Gentamicin-induced bilateral vestibulopathy produces oscillopsia (the illusion that the visual world is bouncing) rather than classic spinning vertigo.

Loop diuretics, particularly at high intravenous doses, carry ototoxic potential. Anticonvulsants (phenytoin, carbamazepine) cause dose-dependent vestibular toxicity manifesting as nystagmus and imbalance. Antihypertensives and alpha-blockers may cause lightheadedness through orthostatic mechanisms rather than true vertigo, but patients often describe both sensations interchangeably.

"A complete medication reconciliation is an essential part of the vertigo evaluation," according to the American Family Physician guideline on dizziness [15]. Patients taking multiple medications with vestibular side effects face compounding risk. Selective serotonin reuptake inhibitors can cause dizziness during initiation and withdrawal. Cisplatin and other platinum-based chemotherapeutics produce both cochlear and vestibular damage that may be irreversible. Whenever a temporal relationship between medication initiation and vertigo onset exists, a trial of dose reduction or substitution is warranted before pursuing extensive vestibular testing.

Persistent Postural-Perceptual Dizziness (PPPD)

PPPD is a relatively new diagnostic entity, codified by the Barany Society in 2017 [16]. It describes a chronic functional vestibular disorder characterized by persistent non-spinning dizziness, unsteadiness, or both, lasting three months or longer. Symptoms worsen with upright posture, active or passive motion, and exposure to complex or moving visual stimuli (grocery store aisles, scrolling screens).

PPPD typically develops after a precipitating event: a vestibular disorder (BPPV, vestibular neuritis), a medical illness, or a psychological stressor. The original trigger resolves, but the brain fails to recalibrate, maintaining a maladaptive state of heightened motion sensitivity.

This is not a diagnosis of exclusion. Diagnostic criteria require all of the following: dizziness present on most days for three or more months, symptoms exacerbated by the three specific triggers listed above, and sufficient functional impairment to warrant clinical attention. PPPD frequently coexists with anxiety and migraine, and each comorbidity should be treated independently.

SSRIs (sertraline 50 to 200 mg, or escitalopram 10 to 20 mg) are the best-studied pharmacologic option, with response rates of approximately 60% to 70% in case series [16]. Vestibular rehabilitation with a habituation-based protocol is considered first-line alongside medication. Cognitive behavioral therapy targeting anxiety-related avoidance behaviors can reduce symptom-driven disability.

Diagnostic Workup: What to Expect

The initial evaluation of vertigo relies primarily on history and physical examination. The timing (episodic vs. continuous), duration (seconds, minutes, hours, days), triggers (positional change, stress, menstrual cycle), and associated symptoms (hearing loss, headache, neurological deficits) narrow the differential more effectively than any single test.

Bedside tests include the Dix-Hallpike and supine roll tests for BPPV, the HINTS battery for acute vestibular syndrome, and a focused neurological exam. Audiometry is essential when hearing loss is reported or suspected.

Videonystagmography (VNG) with caloric testing quantifies vestibular function in each ear independently and is the most widely available objective vestibular test. Vestibular evoked myogenic potentials (VEMPs) assess otolith organ and inferior vestibular nerve function. Rotary chair testing measures the vestibulo-ocular reflex across a range of frequencies.

MRI of the brain with attention to the posterior fossa and internal auditory canals is indicated for suspected central pathology, asymmetric hearing loss, or vestibular symptoms that do not fit a clear peripheral pattern. CT has limited sensitivity for posterior fossa stroke and should not be relied upon to exclude it. The American College of Radiology Appropriateness Criteria rate MRI as "usually appropriate" for vertigo with neurological signs [17].

Blood work is targeted, not routine. Thyroid function, complete blood count, fasting glucose, and vitamin D levels may be checked when clinical suspicion warrants. Routine blood panels have a low diagnostic yield in isolated vertigo.

Treatment Principles Across Vertigo Subtypes

Treatment depends entirely on the underlying cause. Vestibular suppressants (meclizine, dimenhydrinate, benzodiazepines) are appropriate only for acute symptom relief in the first 48 to 72 hours. Prolonged use actually delays central compensation and is discouraged by current guidelines [2].

Vestibular rehabilitation therapy is the single most broadly applicable treatment across nearly all vertigo subtypes. This supervised exercise program promotes central vestibular compensation through gaze stabilization, balance training, and habituation exercises. A Cochrane meta-analysis of 39 RCTs concluded that vestibular rehabilitation is safe and effective for reducing symptoms of unilateral peripheral vestibular dysfunction [8].

For BPPV, the Epley maneuver remains definitive. For vestibular migraine, migraine prophylaxis combined with trigger avoidance is the core strategy. Meniere disease management follows a stepwise approach from salt restriction through intratympanic therapies. PPPD responds to SSRIs and habituation-based rehabilitation. Central causes require cause-specific treatment: anticoagulation for stroke, disease-modifying therapy for MS, or surgical consultation for tumors. The unifying principle across all vertigo subtypes is that early, accurate diagnosis prevents both unnecessary testing and delayed treatment of serious pathology.

Patients presenting with their first episode of severe, continuous vertigo lasting more than 24 hours and any neurological symptom should receive emergent brain MRI with diffusion-weighted imaging to exclude posterior circulation stroke, regardless of CT findings.