Summary

Dizziness is a common and diagnostically challenging complaint that encompasses sensations of vertigo, presyncope, disequilibrium, and lightheadedness. A patient's description of the type of dizziness is often unreliable; a more effective diagnostic approach relies on the TiTrATE framework: Timing, Triggers, And Targeted Examination. The primary goal of the initial evaluation is to differentiate benign peripheral vestibular disorders from dangerous central causes, most notably posterior circulation stroke.

Patients can be categorized into clinical syndromes based on their presentation. Acute Vestibular Syndrome (AVS) involves continuous, spontaneous dizziness lasting days to weeks; the key differential is vestibular neuritis versus stroke, distinguished by the HINTS (Head-Impulse, Nystagmus, Test of Skew) examination. Episodic Vestibular Syndrome (EVS) involves recurrent, transient attacks. If triggered by position changes, the likely diagnosis is Benign Paroxysmal Positional Vertigo (BPPV), confirmed with the Dix-Hallpike maneuver, or orthostatic hypotension. If spontaneous, the differential includes vestibular migraine, Meniere disease, and transient ischemic attack (TIA). Treatment is highly specific to the underlying cause, with many forms of dizziness being manageable or resolving spontaneously.

Etiology

The causes of dizziness are broad and are best categorized by the location of the pathology.

Peripheral Vestibular Disorders (Inner Ear)

• Benign Paroxysmal Positional Vertigo (BPPV): The most common cause of vertigo, resulting from displaced otoconia (canaliths) in the semicircular canals.
• Vestibular Neuritis: Inflammation of the vestibular nerve, presumed to be viral or post-viral. It is termed labyrinthitis if accompanied by hearing loss.
• Meniere Disease: Caused by endolymphatic hydrops (excess fluid in the inner ear).
• Vestibular Schwannoma (Acoustic Neuroma): A benign tumor of the vestibulocochlear nerve (CN VIII).
• Perilymphatic Fistula: An abnormal connection or leak between the inner ear's fluid-filled space (perilymph) and the middle ear, which is typically air-filled. Often secondary to trauma or barotrauma.
• Medication-Induced Ototoxicity: Aminoglycosides are a classic example.

Central Vestibular Disorders (Brainstem & Cerebellum)

• Posterior Circulation Stroke/TIA: Ischemia or hemorrhage affecting the vertebrobasilar system - brainstem or cerebellum. This is the most critical diagnosis to exclude.
• Vertebral Artery Dissection: An important cause of stroke, especially in younger patients. Risk factors include connective tissue disorders like Marfan Syndrome.
• Vestibular Migraine: A common cause of episodic, spontaneous vertigo. Vestibular migraine is thought to be caused by an abnormal activation of the brainstem's vestibular nuclei.
• Multiple Sclerosis: Demyelinating plaques can affect central vestibular pathways.
• Posterior Fossa Tumors: Neoplasms compressing the brainstem or cerebellum.

Systemic, Cardiovascular, and Other Causes

• Orthostatic Hypotension: A common cause of position-triggered lightheadedness (presyncope) commonyl caused by mediation use or volume depletion.
• Cardiac Arrhythmias: Can cause presyncope due to reduced cardiac output leading to reduced cerebral perfusion.
• Anemia or GI Bleeding: Can lead to hypovolemia and orthostasis.
• Hypoglycemia: A key metabolic cause to consider.
• Psychiatric Disorders: Anxiety, panic disorder, and Persistent Postural-Perceptual Dizziness (PPPD) are important non-structural causes.
• Head Trauma/Concussion (Mild Traumatic Brain Injury) and Post-Concussion Syndrome.
• Medication Side Effects: Antihypertensives, antidepressants, and sedatives are common culprits.

Pathophysiology

Dizziness generally arises from a disruption or mismatch in sensory information from the vestibular, visual, and somatosensory (proprioceptive) systems, or from impaired central processing of this information within the brainstem, cerebellum, and higher cortical areas.

• Vestibular Asymmetry: The sensation of vertigo arises from an acute mismatch or asymmetry of inputs from the two vestibular systems. A sudden decrease in firing from one vestibular nerve (e.g., in inflammation caused by vestibular neuritis) is interpreted by the brain as constant head turning, creating an illusion of motion.
• Central lesions disrupt the appropriate processing of these signals, causing a similar effect.  Ischemia (stroke), demyelination (multiple sclerosis), or tumors affecting the vestibular nuclei in the brainstem, the cerebellum, or their interconnecting pathways disrupt the integration and processing of vestibular, visual, and proprioceptive signals. This can lead to vertigo, nystagmus, and postural instability. For example, cerebellar infarction can impair the calibration of the vestibulo-ocular reflex (VOR).
• Canalithiasis (BPPV): In BPPV, dense calcium carbonate crystals (otoconia or canaliths) become dislodged from the utricle and enter a semicircular canal, most commonly the posterior canal. When the head moves into a specific position relative to gravity, these canaliths move within the canal, causing inappropriate stimulation of the canal's sensory hair cells. This sends a powerful, false signal of rotation to the brain that persists until the canaliths settle, explaining the brief, intense, and position-dependent nature of the vertigo.
• Endolymphatic Hydrops (Meniere Disease): This condition is characterized by an increased volume and pressure of endolymph, the fluid within the membranous labyrinth of the inner ear. This "hydrops" is thought to cause distention and intermittent ruptures of the inner ear membranes, leading to a mixing of endolymph and perilymph. This event triggers acute episodes of vertigo, fluctuating sensorineural hearing loss, tinnitus, and aural fullness.
• Cerebral Hypoperfusion (Presyncope): Unlike vertigo, presyncope is not a primary vestibular phenomenon. It results from a transient global reduction in blood flow to the brain, most often from orthostatic hypotension or a cardiac arrhythmia. This decreased perfusion leads to symptoms of lightheadedness, feeling faint, visual graying-out, and, if severe enough, syncope.

Signs and Symptoms

Symptoms

The clinical history, focused on timing and triggers, is the most important diagnostic tool. Patients often have trouble describing their symptoms and will use words interchangeably.

• Vertigo: An illusion of movement of oneself or the environment (e.g., spinning, tilting, rocking). Often indicates vestibular pathology.
• Lightheadedness: A feeling of being about to faint (presyncope), often described as wooziness or disconnectedness. Suggests reduced cerebral perfusion or metabolic causes.
• Gait Instability/Disequilibrium: A sense of imbalance, particularly when walking. Inability to walk unassisted is a major red flag for a central cause.
• Timing:
  • Episodic: Occurs in attacks lasting seconds (BPPV), minutes to hours (Meniere's, vestibular migraine, TIA), or days (vestibular neuritis).
  • Continuous: Persists for days to weeks (AVS - vestibular neuritis vs. stroke).
• Triggers:
  • Triggered by position changes: Lying down, rolling over in bed, or looking up suggests BPPV or orthostatic hypotension.
  • Spontaneous: Occurs at rest without a clear trigger.
  • Specific visual stimuli (e.g., busy patterns, crowds): Can trigger vestibular migraine or PPPD.
• Associated Symptoms
  • Otologic: Hearing loss (unilateral/bilateral, fluctuating/progressive), tinnitus, aural fullness (suggest Ménière's, labyrinthitis, acoustic neuroma).
  • Nausea and Vomiting: Common with acute vertigo from any cause.
• Red Flags
  • The 5 D’s
    • Diplopia - double vision
    • Dysarthria - slurred speech
    • Dysphagia - difficulty swallowing
    • Dysmetria (limb ataxia) - clumsiness
    • Dysphonia - hoarse voice
  • New, severe headache or neck pain
  • Other focal neurological deficit (i.e weakness)

Physical Examination Findings

• HINTS Examination (for Acute Vestibular Syndrome):
  • Head Impulse: Assesses VOR.  An abnormal test (corrective saccade present) is reassuring, suggesting a peripheral lesion. A normal test (no corrective saccade) is highly concerning for a central lesion (stroke).
  • Nystagmus: Fast-phase alternating (direction-changing) nystagmus suggests a central cause.
  • Test of Skew: The presence of vertical skew deviation upon alternate cover testing is a specific sign of a central (brainstem) lesion.
  • "INFARCT" mnemonic for a central cause: Impulse Normal, Fast-phase Alternating, Refixation on Cover Test.
• Nystagmus: The characteristics of nystagmus are crucial for differentiating central from peripheral causes.
  • Peripheral Nystagmus: Typically unidirectional (fast phase beats in the same direction regardless of gaze), horizontal or torsional, suppressed by visual fixation, and fatigable.
  • Central Nystagmus: Can be direction-changing (gaze-evoked), purely vertical or torsional, not suppressed by fixation, and non-fatigable.
• Provocative Maneuvers
  • Dix-Hallpike Maneuver (for Triggered Episodic Vertigo): Provokes transient vertigo (usualyl <30-60 seconds) and a characteristic upbeat-torsional nystagmus in posterior canal BPPV a few seconds after moving the patient from sitting to supine with head turned 45° and extended 20°.
  • Supine Roll Test: To diagnose horizontal canal BPPV.
• Gait Assessment: Severe truncal ataxia or the inability to stand or walk without support is a powerful indicator of a central (cerebellar) lesion.
• Orthostatic Vital Signs: A drop in systolic BP ≥20 mmHg or diastolic BP ≥10 mmHg within 3 minutes of standing is diagnostic of orthostatic hypotension.

Diagnostic Workup

The diagnostic approach should be guided by the clinical syndrome identified through the history. Categorizing dizziness based on Timing, Triggers, and Targeted Examination (TiTrATE) can be very helpful.

1. Categorize the Patient: Using timing and triggers, place the patient into one of three syndromes:
   • Acute Vestibular Syndrome (AVS): Continuous dizziness for days.
   • Triggered Episodic Vestibular Syndrome (EVS): Brief, triggered episodes.
   • Spontaneous Episodic Vestibular Syndrome (EVS): Transient, unprovoked episodes.
2. Perform Targeted Examination:
   • AVS: Perform the HINTS exam. A single "dangerous" finding (normal head impulse, direction-changing nystagmus, or skew deviation) warrants an urgent workup for stroke.
   • Triggered EVS: Perform the Dix-Hallpike maneuver to test for BPPV. Check orthostatic vital signs.
   • Spontaneous EVS: The physical exam is often normal between episodes. Focus on a thorough neurologic and cardiovascular exam.
3. Ancillary Testing:
   • Neuroimaging:
     • Non-contrast Head CT: Often the initial imaging in the emergency department for acute, severe dizziness, particularly if intracranial hemorrhage is suspected. However, it has low sensitivity for acute ischemic stroke (especially in the posterior fossa) and non-hemorrhagic central lesions.
     • MRI with diffusion-weighted imaging (DWI) is the test of choice for suspected central causes (stroke, tumor, MS). CT is insensitive for acute posterior fossa ischemia. Be aware that even DWI MRI can be falsely negative in up to 20% of posterior circulation strokes in the first 24-48 hours. The HINTS exam can be more sensitive than early imaging.
     • Magnetic Resonance Angiography (MRA) or CT Angiography (CTA) of the head and neck: To evaluate for vascular lesions such as arterial dissection, stenosis, or aneurysms if clinically suspected.
   • Laboratory Studies: Generally not indicated for isolated vertigo. CBC (anemia), BMP (electrolytes, hypoglycemia), and glucose in patients with non-vertiginous dizziness, presyncope, or systemic symptoms.
   • ECG: Essential for patients with presyncope or suspected arrhythmia.
   • Audiometry: Indicated for patients with suspected Meniere disease or any unilateral hearing loss to characterize its nature and severity.

Treatment

Treatment for dizziness is directed at the underlying etiology. Life-threatening conditions require immediate, specific interventions (e.g., thrombolysis/thrombectomy for stroke, reperfusion for ACS, anticoagulation for PE).

• Specific Treatments for Common Causes of Dizziness:
  • Benign Paroxysmal Positional Vertigo (BPPV):
    • Canalith Repositioning Maneuvers (CRMs): Highly effective.
      • Epley maneuver: For posterior canal BPPV (most common).
      • Semont maneuver: Alternative for posterior canal BPPV and cupulolithiasis (otoliths attached to the cupula)
      • Lempert (BBQ roll) maneuver or Gufoni maneuver: For horizontal canal BPPV.
    • Vitamin D Supplementation: For patients with documented low levels, may reduce BPPV recurrence.
    • Medications (vestibular suppressants): Generally not recommended for BPPV as they do not address the underlying mechanism and may delay recovery.
  • Vestibular Neuritis/Labyrinthitis:
    • Corticosteroids: E.g., Prednisone 60 mg daily with a taper over 10-14 days, if initiated within 72 hours of symptom onset. Evidence supporting significant benefit is moderate, but commonly used.
    • Symptomatic Relief (short-term, 1-3 days):
      • Antiemetics: Ondansetron 4-8 mg PO/IV q8h PRN.
      • Vestibular Suppressants: Meclizine 25-50 mg PO q6-8h PRN; Diazepam 2-5 mg PO q8-12h PRN. Use sparingly to avoid hindering central compensation.
    • Vestibular Rehabilitation Therapy (VRT): Crucial for promoting long-term recovery and central compensation.
  • Ménière's Disease:
    • Lifestyle Modifications: Low-salt diet (<1.5-2 g/day ), avoidance of caffeine, alcohol, and stress.
    • Diuretics: E.g., Hydrochlorothiazide 25 mg with Triamterene 37.5 mg daily.
    • Acute Attack Management: Vestibular suppressants, antiemetics (as for vestibular neuritis).
    • Intratympanic Therapies (for refractory symptoms):
      • Corticosteroids (e.g., dexamethasone) injection.
      • Gentamicin injection (ablative, risk of hearing loss).
    • Surgery: Endolymphatic sac procedures, vestibular nerve section, or labyrinthectomy for severe, intractable cases.
  • Vestibular Migraine:
    • Acute Treatment: Similar to migraine headaches: NSAIDs, triptans (e.g., sumatriptan 50-100 mg PO), CGRP antagonists. Antiemetics and short-term vestibular suppressants may be helpful.
    • Prophylactic Treatment (for frequent/severe attacks): Beta-blockers (e.g., propranolol 40-160 mg/day in divided doses), calcium channel blockers (verapamil), TCAs (e.g., nortriptyline 10-75 mg QHS), SNRIs (e.g., venlafaxine XR 37.5-150 mg daily), topiramate, CGRP monoclonal antibodies.
    • Lifestyle Modifications: Identify and avoid migraine triggers (dietary, sleep, stress).
  • Persistent Postural-Perceptual Dizziness (PPPD):
    • Vestibular Rehabilitation Therapy (VRT): Core treatment focusing on habituation and desensitization.
    • SSRIs or SNRIs: E.g., Sertraline (start 25-50 mg/day, titrate to 100-200 mg/day) or Venlafaxine XR.
    • Cognitive Behavioral Therapy (CBT).
  • Orthostatic Hypotension:
    • Non-pharmacologic: Increased fluid (2-3 L/day) and salt intake, compression stockings, abdominal binders, raising head of bed at night, slow positional changes, counter-pressure maneuvers (e.g., leg crossing).
    • Pharmacologic:
      • Fludrocortisone: 0.1-0.3 mg PO daily (monitor for hypokalemia, edema).
      • Midodrine: 2.5-10 mg PO TID (taken during daytime hours).
      • Droxidopa: For neurogenic orthostatic hypotension.
• General Symptomatic Relief for Acute Vertigo (Short-Term Use):
  • Antihistamines: Meclizine (25-50 mg PO q6-8h PRN), Dimenhydrinate (50 mg PO q4-6h PRN).
  • Benzodiazepines: Diazepam (2-5 mg PO q8-12h PRN), Lorazepam (0.5-1 mg PO q8-12h PRN). Use sparingly due to sedation, risk of dependence, and potential to impair central compensation if used long-term.
  • Antiemetics: Ondansetron (4-8 mg PO/SL/IV q8h PRN), Promethazine (12.5-25 mg PO/IM/PR q4-6h PRN).
• Vestibular Rehabilitation Therapy (VRT):
  • An exercise-based program designed to promote central nervous system compensation for vestibular deficits. Includes exercises for gaze stability (e.g., VOR adaptation), habituation to provocative movements, balance training, and conditioning.
  • Indications: Unilateral or bilateral vestibular hypofunction, BPPV (residual dizziness after CRMs), PPPD, post-concussion dizziness, stable central vestibular disorders.
• Fall Prevention Strategies: Essential for patients with significant dizziness, especially older adults. Includes home safety assessment, appropriate footwear, use of assistive devices if needed.

Pearls

Epidemiology and General Information

• Dizziness accounts for approximately 3-4% of all emergency department visits.
• In ambulatory settings, the causes of dizziness are distributed roughly as: 40% peripheral vestibular dysfunction, 10% central brainstem/cerebellar lesion, 15% psychiatric disorders, and 25% other causes like presyncope or disequilibrium.
• Benign Paroxysmal Positional Vertigo (BPPV) is the single most common cause of vertigo, especially in older adults.
• The prevalence of dizziness increases significantly with age; in older adults, dizziness is often multifactorial, involving sensory deficits, polypharmacy, and cardiovascular disease.

Pathophysiology

• The fundamental mechanism of true vertigo is an asymmetry in vestibular inputs between the right and left sides, whether the disruption is peripheral or central.
• Benign paroxysmal positional vertigo (BPPV) results from otoconia (calcium carbonate crystals) dislodged from the utricle (canalithiasis) migrating into a semicircular canal (most often posterior), causing aberrant endolymphatic flow and cupular deflection with specific head movements relative to gravity. The sensation stops when the otoconia settle, hence the episodes are shortlived.
• The HINTS exam differentiates central from peripheral causes in acute vestibular syndrome by exploiting pathophysiological distinctions: an abnormal head impulse typically points to peripheral vestibular nerve dysfunction, whereas a normal head impulse, direction-changing nystagmus, or skew deviation strongly suggests central pathology like a brainstem or cerebellar stroke.
• Persistent postural-perceptual dizziness (PPPD) is characterized by maladaptive central processing of vestibular, visual, and somatosensory information, often leading to heightened visual dependence and anxiety about motion, frequently after an acute vestibular event or period of stress.
• Alcohol intoxication causes vertigo by creating a density difference between the endolymph and the cupula in the semicircular canals, making them sensitive to gravity.

Etiology and Risk Factors

• Medication side effects are a frequent and reversible cause of dizziness; always perform a thorough medication review, especially for antihypertensives, sedatives, and anticholinergics.
• Vertebral artery dissection is a critical cause of posterior circulation stroke to consider in young patients presenting with dizziness, often associated with neck pain or recent trauma. Conditions that predispose younger patients to this include connective tissue disorders like Ehlers-Danlos syndrome, Marfan syndrome, and fibromuscular dysplasia.
• Low vitamin D levels are a recognized risk factor for the recurrence of BPPV. Supplementation has been shown to decrease the rate of recurrence.

Clinical Presentation and Diagnosis

• The patient's subjective description of dizziness (e.g., "spinning," "lightheaded," "off-balance") is less diagnostically reliable than a focused inquiry into the timing, triggers, and associated symptoms (TiTrATE) of the episodes.
• Trigger vs. Exacerbation: A critical distinction is whether head movement triggers dizziness that is otherwise absent at rest (suggesting an episodic issue like BPPV), or if it exacerbates continuous, ongoing dizziness (suggesting an acute vestibular syndrome like vestibular neuritis or stroke).
• In a patient with Acute Vestibular Syndrome, the HINTS exam is more sensitive for stroke than an initial (first 24-48 hours) MRI scan when performed by trained professionals.
• The "Normal" Head Impulse Test: In a patient with an acute vestibular syndrome, a normal head impulse test (no corrective saccade) is a highly concerning sign for a central cause like a stroke. An abnormal test (with a corrective saccade) points towards a peripheral cause like vestibular neuritis.
• Different semicircular canals involved in BPPV produce distinct types of nystagmus during the Dix-Hallpike test. Posterior Canal (most common): Upbeating and torsional nystagmus. Horizontal Canal: Horizontal nystagmus that can be geotropic (beating toward the ground) or apogeotropic (beating away from the ground), diagnosed with a supine roll test. Anterior Canal (rare): Downbeating nystagmus with a minor torsional component.
• Observing Skew Deviation: When performing the test of skew (cover-uncover test), the key is to look for a vertical correction of the uncovered eye. The presence of skew deviation increases the odds of a stroke or other central cause by approximately 20-fold.
• Spontaneous Nystagmus in BPPV: The presence of spontaneous nystagmus (nystagmus when the patient is sitting still and looking straight ahead) is not a typical feature of BPPV and should raise suspicion for another cause, such as vestibular neuritis or stroke.
• The 5 D’s are red flag neurological signs/symptoms that often present in tandem with vertigo in central etiologies like bainstem or cerebellar stroke. They include Diplopia - double vision, Dysarthria - slurred speech, Dysphagia - difficulty swallowing, Dysmetria (limb ataxia) - clumsiness, and Dysphonia - hoarse voice
• Vomiting can be a very prominent, and sometimes overlooked, symptom of a cerebellar stroke.
• Inability to stand or walk unassisted is a major red flag for a central (cerebellar) cause of vertigo, even in the absence of other focal neurologic deficits.
• Associated otologic symptoms including hearing loss, tinnitus, and aural fullness may suggest Meniere’s, labyrinthitis, and acoustic neuromas. While typically pointing to a peripheral cause, auditory symptoms can also be a sign of a stroke involving the anterior inferior cerebellar artery (AICA).
• Otolithic Crisis of Tumarkin: A rare manifestation of Meniere's disease where patients experience sudden, violent drop attacks without any loss of consciousness.
• A normal non-contrast head CT scan does not exclude an acute ischemic stroke, particularly in the posterior fossa or within the initial few hours of symptom onset; MRI with DWI is far more sensitive for ischemia.
• The Dix-Hallpike maneuver is the diagnostic gold standard for posterior canal BPPV; a positive test elicits transient (typically <60 seconds), torsional, upbeating nystagmus that appears after a brief latency and fatigues with repetition.

Treatment

• Vestibular suppressant medications (e.g., meclizine, benzodiazepines) should only be used for short-term (≤3 days) symptomatic relief in acute vestibular neuritis or Meniere's disease. Prolonged use impedes central compensation and recovery.
• The Epley maneuver is highly effective for posterior canal BPPV, with success rates approaching 90-100% after one or two treatments. It is considered first-line treatment and is preferred over medications.
• Meniere's Disease Treatment: While salt restriction and diuretics are common recommendations, there is limited high-quality evidence to support their effectiveness.
• Vestibular Neuritis and Steroids: The use of corticosteroids is common but not definitively proven to improve long-term outcomes. If used, they should be started within 3 days of symptom onset. A suggested regimen involves a slow taper of methylprednisolone over several weeks.
• Vestibular Migraine: Triptans are generally contraindicated for basilar migraines due to the theoretical risk of vasoconstriction and stroke.
• Vestibular rehabilitation therapy (VRT) is a cornerstone of management for chronic dizziness due to vestibular hypofunction, PPPD, and post-concussion syndrome, utilizing exercises to improve gaze stability, balance, and habituation to motion. It trains the brain to compensate for vestibular deficits.

Complications

• Dizziness is a major risk factor for falls and fall-related injuries, particularly in the elderly. These can include fractures, subdural hematomas, prolonged hospitalizations, and loss of independence.
• Posterior circulation strokes are frequently misdiagnosed as benign peripheral vertigo, leading to significant morbidity and mortality. An estimated 35% of such strokes are initially missed.
• Chronic dizziness, as seen in Persistent Postural-Perceptual Dizziness (PPPD), can lead to significant functional impairment, anxiety, and a reduced quality of life.