Vertigo and Vestibular Disorders

Mechanical/otoconial

• BPPV: displaced utricular otoconia enter a semicircular canal (posterior >> horizontal > anterior). Idiopathic in most, but head trauma, prolonged supine positioning (dental work, surgery), and prior vestibular neuritis or Ménière disease are recognized precipitants.

Hydropic/pressure

• Ménière disease: endolymphatic hydrops from impaired endolymph resorption; a familial pattern occurs in a minority.
• Perilymphatic fistula / superior semicircular canal dehiscence: barotrauma, straining, or thin temporal bone allows pressure transmission to the labyrinth (Tullio phenomenon — sound-induced vertigo).

Inflammatory/infectious

• Vestibular neuritis and labyrinthitis: presumed post-viral or reactivated herpesvirus inflammation of the vestibular nerve/labyrinth; Ramsay Hunt syndrome (VZV) adds vesicles and facial palsy.
• Suppurative labyrinthitis: direct spread from otitis media, cholesteatoma, or meningitis.
• Autoimmune inner-ear disease and Cogan syndrome: rapidly progressive bilateral audiovestibular loss.

Neoplastic and neurologic

• Vestibular schwannoma at the cerebellopontine angle; bilateral tumors define neurofibromatosis type 2.
• Multiple sclerosis, vestibular migraine, brainstem/cerebellar infarction (posterior circulation, including AICA territory) disrupt central integration.

Toxic

• Ototoxic drugs: aminoglycosides (gentamicin is preferentially vestibulotoxic), cisplatin, loop diuretics, high-dose salicylates.

Modifiable risk factors

• Vascular risk burden — hypertension, diabetes, dyslipidemia, smoking, atrial fibrillation — which drives posterior circulation stroke, the diagnosis examiners hide behind "vertigo" (AHA/ASA stroke guidance).
• Head/neck trauma and cervical manipulation (vertebral artery dissection), ototoxic exposure, sedative and anticholinergic polypharmacy, alcohol, and migraine triggers.
• Vitamin D deficiency has been associated with BPPV recurrence in AAO-HNSF-cited literature; supplementation in deficient patients is reasonable, not universal.

Non-modifiable risk factors

• Age above roughly the fifth decade (BPPV incidence rises steeply), female sex, prior episode of BPPV or vestibular neuritis, osteoporosis, migraine history, and genetic syndromes (NF2, familial Ménière).

• Vestibular apparatus dysfunction (peripheral): The utricle and saccule (detecting linear acceleration) and three semicircular canals (detecting rotational acceleration) maintain tonic firing rates. Peripheral disorders disrupt this balanced tonic activity, causing asymmetric vestibular input to the brainstem vestibular nuclei. This asymmetry generates nystagmus (reflexive eye movements) and vertigo sensation through connections in the cerebellum and brainstem.

• Otolith displacement and endolymphatic fluid dynamics: In benign paroxysmal positional vertigo (BPPV), calcium carbonate crystals (otoconia) detach from the utricle and migrate into semicircular canals. With head movement, gravity causes endolymph flow, stimulating cupulae and generating brief, position-dependent vertigo. In Ménière's disease, endolymphatic hydrops (fluid accumulation) increases pressure in the labyrinth, causing fluctuating symptoms and cochlear involvement.

• Vestibulocochlear nerve damage: Viral labyrinthitis or vestibular neuritis cause inflammation/infection of the eighth cranial nerve or inner ear structures, disrupting afferent vestibular signals. Central compensation mechanisms gradually restore balance over weeks to months but initially produce severe vertigo.

• Central nervous system integration disruption: Brainstem infarction (affecting vestibular nuclei), cerebellar lesions, or posterior circulation stroke disrupt processing of vestibular information. These conditions impair the normal coordination of eye movements, balance reflexes, and spatial orientation, often producing vertigo with focal neurological signs.

• Proprioceptive and visual system compensation failure: Age-related decline in proprioception, visual acuity, or vestibular reserve causes chronic dizziness/imbalance. Medication effects (sedatives, anticonvulsants) or metabolic derangement can impair central compensation mechanisms.

• True vertigo vs. dizziness distinction: Patients report the room "spinning" or themselves "spinning" (rotatory sensation). Associated symptoms include nausea/vomiting, nystagmus, postural instability, and ear fullness. This differs from lightheadedness (presyncope), disequilibrium, or anxiety-related symptoms.

• Peripheral vertigo characteristics: Vertigo is severe, episodic, and often accompanied by unilateral hearing loss or tinnitus (especially Ménière's disease). Nystagmus is rotatory or horizontal, beats away from the affected ear, and fatigues with repeated head movement (suppressed by visual fixation). Romberg test is often abnormal with eyes closed.

• Benign Paroxysmal Positional Vertigo (BPPV) presentation: Brief episodes (10-60 seconds) of severe vertigo triggered by specific head positions (turning in bed, looking up, tilting head backward). Dix-Hallpike maneuver reproduces symptoms with upbeating/rotatory nystagmus. Episodes cluster in episodes lasting days to weeks, then remit spontaneously.

• Vestibular neuritis/labyrinthitis: Acute onset of severe vertigo, often preceded by viral illness. Unilateral hearing loss absent (distinguishes from labyrinthitis). Horizontal nystagmus with symptom beat away from affected side. Severe for 3-5 days, then gradually improves over weeks with central compensation.

• Ménière's disease triad: Episodic vertigo (20 minutes to hours), fluctuating unilateral hearing loss, and tinnitus/ear fullness. Vertigo attacks are unpredictable and severely disabling. Between attacks, patients may be asymptomatic or have chronic tinnitus/hearing impairment.

• Central vertigo red flags: Vertigo with focal neurological signs (ataxia out of proportion, cranial nerve deficits, weakness, sensory loss, dysarthria). Constant rather than episodic presentation. Nystagmus that does not fatigue, changes direction with gaze, or is purely vertical/torsional. Headache, fever, or recent head trauma.

• Acute Stroke (posterior circulation): Vertigo with ipsilateral facial numbness, contralateral body numbness/weakness, diplopia, dysarthria, or ataxia (VOMIT mnemonic: Vertigo, Oscillopsia, nystagmus, Myosis, Ipsilateral facial loss). Can present without hearing loss.

• Clinical history and nystagmus examination: Characterize vertigo onset (sudden vs. gradual), duration (seconds to minutes vs. hours vs. constant), triggers, and associated symptoms. Perform Dix-Hallpike maneuver (head extended 20° below horizontal with 45° rotation) to elicit BPPV. Perform Romberg test (eyes closed, feet together) and tandem walking. Assess nystagmus direction, type (rotatory vs. horizontal), fatigability, and whether fixation suppresses it. Unilateral nystagmus suggests peripheral; vertical or bidirectional nystagmus suggests central.

• Hallpike and supine roll tests: Dix-Hallpike is most sensitive/specific for posterior canal BPPV; supine roll test for horizontal canal BPPV. Positive test shows nystagmus onset after 1-5 second latency, lasting <60 seconds, with symptom reproduction and fatigue with repetition (hallmark of BPPV).

• Weber and Rinne tuning fork tests: Assess for conductive vs. sensorineural hearing loss. Weber lateralizing to affected ear suggests sensorineural loss (Ménière's disease or labyrinthitis with cochlear involvement). Normal hearing tests favor vestibular neuritis or central causes.

• Head impulse test (Halmagyi test): Patient fixes gaze on examiner's nose while examiner moves head side to side. Normal (corrective saccade absent): peripheral vestibular loss. Abnormal (corrective saccade present to refixate): suggests brainstem/cerebellar pathology or acute peripheral loss.

• Caloric testing and videonystagmography: Warm and cold water irrigation of external auditory canal stimulates vestibular system. Reduced response (hypoactive) on affected side suggests peripheral loss. Used to quantify and lateralize peripheral vestibular dysfunction. Videonystagmography (VNG) infrared recording objectively measures nystagmus characteristics.

• Vestibular-evoked myogenic potential (VEMP): Tests saccular (cVEMP) and utricular (oVEMP) function via EMG response to loud clicks or vibration. Abnormal VEMP may indicate otolith dysfunction in Ménière's disease or superior canal dehiscence syndrome.

• MRI and neuroimaging: Indicated for vertigo with central features (focal neurological signs, atypical nystagmus, progressive symptoms, abnormal head impulse test). MRI with diffusion-weighted imaging (DWI) detects acute brainstem/cerebellar infarction. MRI with constructive interference steady-state (CISS) sequences visualize eighth cranial nerve (excludes schwannoma) and evaluates inner ear anatomy.

• Audiometry: Pure-tone and speech audiometry quantify hearing loss. Sensorineural pattern with low-frequency involvement suggests Ménière's disease. Normal audiometry with vertigo suggests vestibular neuritis or BPPV.

• Electrocochleography: Measures electrical potentials of inner ear. Elevated summating potential-to-action potential ratio suggests endolymphatic hydrops (Ménière's disease).

• BPPV—Canalith repositioning maneuvers (first-line, definitive): Epley maneuver for posterior canal

Disease-related

• Falls, hip fracture, and head injury: loss of the vestibulo-ocular and vestibulospinal reflexes in an older patient; signaled by a positive Romberg with eyes closed, tandem-gait failure, and recurrent unexplained falls. The most common real-world morbidity of BPPV.
• **Tumarkin otolithic crisis (drop attack)**: abrupt otolithic discharge in advanced Ménière disease causes a sudden fall without loss of consciousness or postictal state — the finding that separates it from syncope and seizure.
• Progressive sensorineural hearing loss: repeated hydropic injury flattens the audiogram from the classic low-frequency pattern to global loss.
• Suppurative labyrinthitis with meningitis — an emergency. Fever, headache, meningismus, or vertigo arising from a draining ear or cholesteatoma mandates urgent imaging, CSF evaluation, and IV antibiotics per IDSA bacterial meningitis guidance; healed suppurative labyrinthitis may ossify the cochlea, narrowing the window for cochlear implantation.
• Missed cerebellar or brainstem infarction — the highest-stakes emergency. Cerebellar infarct edema peaks days later and compresses the fourth ventricle, producing obtundation, hydrocephalus, and tonsillar herniation; AHA/ASA guidance supports early neurosurgical involvement for suboccipital decompression.
• Persistent postural-perceptual dizziness: maladaptive central compensation after any acute vestibular insult, producing chronic non-spinning dizziness worsened by motion and visual patterns.

Treatment-related

• Vestibular suppressants (antihistamine/anticholinergic meclizine, benzodiazepines): blunt central compensation and prolong recovery; in elders they cause sedation, delirium, and falls. AAO-HNSF explicitly recommends against routine vestibular suppressants for BPPV.
• Antidopaminergic antiemetics (prochlorperazine, promethazine, metoclopramide): dystonia, akathisia, and QT prolongation.
• Canalith repositioning: transient nausea/vomiting and canal conversion — new horizontal-canal nystagmus on supine roll test; caution with cervical stenosis or unstable cervical spine.
• Intratympanic gentamicin, labyrinthectomy, or vestibular nerve section for refractory Ménière: intended ablation risks ipsilateral deafness and, if bilateral vestibular loss occurs, oscillopsia and gait ataxia in the dark.
• Diuretics used in Ménière: hypokalemia and hyponatremia.

• Duration and trigger sort the differential faster than any test: seconds with positional change = BPPV; minutes to hours with hearing loss/tinnitus/aural fullness = Ménière; days of continuous vertigo after a viral prodrome = vestibular neuritis (labyrinthitis if hearing is lost); minutes with headache, photophobia, and no hearing loss = vestibular migraine, the most common cause of recurrent spontaneous vertigo.
• **Dix-Hallpike producing latent, fatigable, upbeating-torsional nystagmus toward the dependent ear is diagnostic of posterior-canal BPPV**. The single best next step is the Epley maneuver — not imaging, not meclizine. AAO-HNSF recommends against routine radiographic imaging or vestibular testing when the history and Dix-Hallpike are classic.
• HINTS is the exam-favorite tool in acute vestibular syndrome, and its logic is counterintuitive: a normal head impulse test (no corrective saccade), direction-changing nystagmus, or a positive test of skew points central and demands MRI with DWI. An abnormal head impulse with a corrective saccade indicates peripheral loss. HINTS applies only to continuous vertigo with nystagmus, never to episodic positional vertigo.
• A normal early MRI does not exclude posterior circulation stroke — DWI can be falsely negative in the first hours in the brainstem; the exam outranks the scan, and repeat imaging is warranted.
• Vertical or purely torsional nystagmus, nystagmus unsuppressed by visual fixation, severe truncal ataxia, and inability to sit unsupported are central until proven otherwise.
• Sudden sensorineural hearing loss with vertigo is an otologic emergency: AAO-HNSF supports prompt audiometry and corticosteroids; think AICA infarct if brainstem signs accompany it.
• Progressive unilateral SNHL with tinnitus, poor speech discrimination, and a diminished corneal reflex = vestibular schwannoma; bilateral tumors mean NF2. Order MRI with gadolinium of the internal auditory canals.
• Common distractor: prescribing scheduled meclizine or a benzodiazepine. They are for the first 24–48 hours of severe acute vertigo only, since they delay central compensation; vestibular rehabilitation is the durable answer.