Vestibular Disorders & Dizziness: The Functional Approach
Dizziness is one of the most common complaints in medicine and one of the most poorly managed. Patients describe it in a dozen different ways — spinning, floating, swaying, lightheaded, off-balance, drunk feeling, rocking on a boat.
Vestibular Disorders & Dizziness: The Functional Approach
The World Is Not Spinning — Your Brain Is Confused
Dizziness is one of the most common complaints in medicine and one of the most poorly managed. Patients describe it in a dozen different ways — spinning, floating, swaying, lightheaded, off-balance, drunk feeling, rocking on a boat. Conventional medicine tends to prescribe meclizine (an antihistamine vestibular suppressant) and send them home. This is like treating a fire alarm by removing the batteries.
The vestibular system is a masterpiece of biological engineering. It tells your brain where your head is in space, how fast it is moving, and in what direction — and it does this continuously, unconsciously, and with remarkable precision. When it breaks down, the consequences are not just physical. Vestibular dysfunction causes anxiety, cognitive impairment, fatigue, and a profound sense of disorientation that affects every dimension of life.
Understanding the anatomy, identifying the specific disorder, and applying targeted rehabilitation is the path forward.
Vestibular Anatomy: The Inner Compass
The vestibular apparatus sits within the temporal bone, adjacent to the cochlea, in a structure called the labyrinth.
Three semicircular canals — anterior (superior), posterior, and horizontal (lateral) — detect rotational head movement (angular acceleration). Each canal is oriented in a different plane, together covering all three axes of rotation. Inside each canal, a swelling called the ampulla contains the cupula — a gelatinous structure that deflects when fluid (endolymph) moves in response to head rotation. This deflection bends hair cells, generating electrical signals.
Otolith organs — the utricle and saccule — detect linear acceleration and gravity. The utricle is oriented horizontally (detects forward/backward/side-to-side movement). The saccule is oriented vertically (detects up/down movement). Both contain a gelatinous membrane studded with calcium carbonate crystals (otoconia) that shift with gravity and acceleration, bending the underlying hair cells.
Vestibular nerve (cranial nerve VIII, vestibular division) carries signals from the canals and otoliths to the vestibular nuclei in the brainstem (four nuclei: medial, lateral, superior, inferior). From there, information is distributed to:
- Oculomotor nuclei — for the vestibulo-ocular reflex (stabilizing vision during head movement)
- Spinal cord — for the vestibulospinal reflex (postural control)
- Cerebellum (flocculonodular lobe) — for calibration and error correction
- Thalamus and cortex — for conscious perception of movement and spatial orientation
- Autonomic centers — which is why vestibular dysfunction causes nausea, sweating, and heart rate changes
BPPV: Crystals Out of Place
Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder, affecting roughly 2.4% of the population at some point. It is also the most satisfying to treat — because it can often be cured in a single visit.
Mechanism
Those calcium carbonate crystals (otoconia) in the utricle can become dislodged — by head trauma, infection, age-related degeneration, or sometimes spontaneously. When loose crystals migrate into one of the semicircular canals (most commonly the posterior canal), they create false signals of rotation whenever the head moves into certain positions. The brain receives contradictory information — the eyes and proprioceptors say you are still, but the vestibular system says you are spinning. The result is brief, intense vertigo triggered by specific head positions.
Canalithiasis (free-floating crystals in the canal) produces brief episodes lasting under a minute. Cupulolithiasis (crystals adhered to the cupula) produces longer-lasting positional vertigo.
Diagnosis
Dix-Hallpike test — the gold standard for posterior canal BPPV. The patient sits upright, the clinician turns the head 45 degrees to one side, then rapidly lays the patient back with the head hanging below the table edge. A positive test produces a burst of upbeat, torsional nystagmus after a brief latency (2-5 seconds), lasting 10-30 seconds, with subjective vertigo. The nystagmus direction tells you which ear and which canal.
Supine roll test — for horizontal canal BPPV. The patient lies supine and the head is turned 90 degrees to each side. Direction-changing horizontal nystagmus indicates horizontal canal involvement. Geotropic nystagmus (beating toward the ground) suggests canalithiasis. Apogeotropic nystagmus (beating away from the ground) suggests cupulolithiasis or anterior arm involvement.
Treatment
Epley maneuver (canalith repositioning procedure) — for posterior canal BPPV. A specific sequence of head positions that uses gravity to guide the loose crystals out of the posterior canal and back into the utricle. Success rate: 80-90% in a single treatment. Some patients require 2-3 sessions.
Semont maneuver — an alternative for posterior canal BPPV. A rapid side-to-side movement designed to fling the crystals out of the canal. More vigorous than the Epley, sometimes preferred when the Epley fails.
Barbecue roll (Lempert maneuver) — for horizontal canal BPPV. A 360-degree roll toward the unaffected ear, performed in 90-degree increments.
Recurrence: BPPV recurs in approximately 50% of patients within 5 years. Vitamin D deficiency (see below) and osteoporosis increase recurrence risk.
Vestibular Neuritis and Labyrinthitis
Vestibular neuritis is acute inflammation of the vestibular nerve — typically viral (herpes simplex type 1 is the suspected agent in most cases, based on autopsy studies by Arbusow et al.). Labyrinthitis includes cochlear involvement, so hearing loss and tinnitus accompany the vertigo.
Presentation: Sudden onset of severe, sustained vertigo lasting days, with nausea and vomiting. Nystagmus beats away from the affected ear (fast phase contralateral). The acute phase is brutal — patients cannot stand or walk.
Acute management: Vestibular suppressants (meclizine, diazepam, ondansetron for nausea) for the first 48-72 hours only. Corticosteroids (methylprednisolone taper) within the first 72 hours may improve vestibular function recovery (Strupp et al. 2004). Valacyclovir has been studied but the evidence for adding it to steroids is mixed.
The critical point: Vestibular suppressants must be stopped after 2-3 days. They interfere with vestibular compensation — the brain’s natural process of recalibrating to the new asymmetric vestibular input. Patients who remain on meclizine chronically never compensate and remain dizzy indefinitely. This is one of the most common iatrogenic errors in vestibular medicine.
Vestibular rehabilitation — the primary treatment. Gaze stabilization exercises (VOR training), habituation exercises, and balance retraining. The brain has remarkable capacity to compensate for unilateral vestibular loss — but only if it is challenged to do so. Without rehabilitation, many patients develop chronic uncompensated vestibulopathy.
Meniere’s Disease
Meniere’s disease is defined by episodic attacks of vertigo (lasting 20 minutes to 12 hours), fluctuating low-frequency hearing loss, tinnitus, and aural fullness — caused by endolymphatic hydrops (excess fluid pressure in the endolymphatic compartment of the inner ear).
The conventional approach: low-sodium diet (<1500-2000 mg/day to reduce fluid retention), diuretics (hydrochlorothiazide or acetazolamide), betahistine (widely used in Europe, less so in the US), and in refractory cases, intratympanic gentamicin (which destroys vestibular hair cells to stop vertigo — effective but destructive) or endolymphatic sac surgery. The Meniett device delivers intermittent low-pressure pulses through a tympanostomy tube to decompress the endolymph.
The Functional Approach
Standard Meniere’s management often misses the upstream drivers:
Food sensitivities — beyond sodium. Patients with Meniere’s frequently have IgG-mediated food sensitivities (not IgE allergies). Wheat, dairy, and eggs are common triggers. An elimination diet with structured reintroduction can reduce attack frequency dramatically.
Autoimmune inner ear disease — Meniere’s may have an autoimmune component in a subset of patients. Anti-HSP70 antibodies, elevated ESR, response to corticosteroids — these suggest immune-mediated pathology. Check ANA, ESR, complement, and consider a steroid trial.
Cervical spine dysfunction — the vertebral arteries pass through the transverse foramina of the cervical vertebrae. Upper cervical dysfunction can impair blood flow to the vertebrobasilar system, which supplies the inner ear. Manual therapy to the upper cervical spine has been reported to improve Meniere’s symptoms in case series.
TMJ dysfunction — the temporomandibular joint shares innervation with the tensor tympani and tensor veli palatini muscles. TMJ dysfunction can affect Eustachian tube function and alter middle ear pressure, potentially influencing endolymphatic dynamics. A dental/TMJ evaluation is warranted.
Chronic infection — there are case reports and small studies linking Meniere’s to chronic Lyme disease (Borrelia burgdorferi is known to affect cranial nerves) and reactivated herpes viruses. A thorough infectious workup is appropriate, especially when Meniere’s presentation is atypical.
Migraine overlap — vestibular migraine and Meniere’s can coexist or mimic each other. If there is a personal or family history of migraine, the migraine pathway should be addressed simultaneously.
Vestibular Migraine
Vestibular migraine is the second most common cause of recurrent vertigo and the most common cause of spontaneous episodic vertigo. It affects roughly 1% of the population and is significantly underdiagnosed.
The concept is threshold theory — the migrainous brain has a lower threshold for sensory processing overload. When the threshold is exceeded by accumulated triggers (hormonal shifts, stress, sleep deprivation, dietary triggers, weather changes, sensory overload), the brainstem and thalamic circuits that process vestibular input malfunction, producing vertigo, dizziness, motion sensitivity, and disequilibrium. Headache may or may not accompany the vestibular symptoms — in fact, up to 30% of vestibular migraine episodes occur without headache.
Management: trigger identification and avoidance, magnesium (400-600 mg daily as glycinate or threonate — effective for migraine prevention), CoQ10 (300 mg daily — Sandor 2005 trial), riboflavin (400 mg daily — Schoenen 1998), feverfew, butterbur. Vestibular rehabilitation is uniquely effective because it raises the vestibular threshold — the brain becomes less reactive to vestibular input. For frequent episodes: preventive medications (nortriptyline, venlafaxine, topiramate) or CGRP inhibitors (erenumab, fremanezumab).
PPPD: The Anxious Vestibular Brain
Persistent Postural-Perceptual Dizziness (PPPD) — formerly called chronic subjective dizziness — is a functional vestibular disorder characterized by persistent non-spinning dizziness, unsteadiness, and hypersensitivity to motion (self-motion and visual motion) lasting more than 3 months.
PPPD typically begins after an acute vestibular event (BPPV, vestibular neuritis, concussion, panic attack) that resolves, but the brain fails to recalibrate. The vestibular processing networks remain in a hypervigilant state — constantly monitoring for the threat that has already passed. There is a strong overlap with anxiety, but PPPD is not simply anxiety. It is a maladaptive neuroplastic response — the brain has learned to be dizzy.
Treatment triad: Vestibular rehabilitation (habituation and desensitization), cognitive behavioral therapy (addressing the fear-avoidance cycle that perpetuates the condition), and for some patients, SSRIs or SNRIs (sertraline 50-200 mg or venlafaxine 75-150 mg — which modulate the serotonergic circuits involved in vestibular processing, not just mood). The combination is more effective than any single intervention.
Cervicogenic Dizziness
The cervical spine contains dense proprioceptive receptors — particularly in the upper cervical segments (C1-C3) and the deep suboccipital muscles. These receptors feed directly into the vestibular nuclei. When cervical proprioception is disrupted — by muscle spasm, joint dysfunction, whiplash injury, or chronic postural strain — the brain receives conflicting information about head position, producing dizziness.
Cervicogenic dizziness is a diagnosis of exclusion — vestibular causes must be ruled out first. Clues: dizziness provoked by neck movement or sustained neck postures, associated neck pain or stiffness, history of whiplash or cervical injury, resolution with cervical treatment.
Treatment: upper cervical manual therapy, suboccipital muscle release, cervical proprioceptive retraining (joint position error testing and correction, laser-guided head repositioning), and postural correction.
Mal de Debarquement Syndrome
MdDS is a rare but debilitating condition — a persistent sensation of rocking, swaying, or bobbing, typically triggered by prolonged exposure to passive motion (cruise ship, airplane, car trip). The sensation improves with passive motion (driving) and worsens at rest. It can last months to years.
The mechanism appears to involve the velocity storage integrator in the vestibular nuclei becoming “stuck” on the pattern of passive motion. Dai and colleagues at Mount Sinai developed a promising treatment using full-field optokinetic stimulation tuned to the patient’s specific rocking frequency. Conventional vestibular rehabilitation has limited effectiveness for MdDS. Benzodiazepines (clonazepam) provide symptomatic relief but are not curative.
Nutritional Support for Vestibular Health
Magnesium — 400-600 mg daily (glycinate, threonate, or taurate). Magnesium reduces neuronal excitability, supports vestibular compensation, and prevents migraine — relevant in vestibular migraine. Deficiency is common and undertested (serum magnesium is a poor marker; RBC magnesium is better).
Ginkgo biloba — Cesarani et al. (1998) showed that EGb 761 extract (standardized ginkgo) improved vestibular compensation after unilateral vestibulopathy. The mechanism involves increased microcirculation in the inner ear and central vestibular structures, plus antioxidant protection. Dose: 120-240 mg daily of standardized extract.
Vitamin D — Jeong et al. (2020) published in Neurology that vitamin D supplementation (combined with calcium) significantly reduced BPPV recurrence in patients with low vitamin D levels. The proposed mechanism: vitamin D is essential for calcium metabolism, and the otoconia are calcium carbonate crystals. Deficient vitamin D may lead to otoconia demineralization and fragmentation, predisposing to BPPV. Target: serum 25-OH vitamin D 40-60 ng/mL.
CoQ10 — 200-300 mg daily. Supports mitochondrial function in the metabolically active vestibular hair cells. Particularly relevant in vestibular migraine.
B vitamins — B12 deficiency can cause vestibular dysfunction. Methylcobalamin 1000-5000 mcg sublingual. B6 (P5P) is a cofactor for neurotransmitter synthesis in the vestibular nuclei.
Omega-3 fatty acids — 2-3 grams EPA/DHA daily. Anti-inflammatory, supports neuronal membrane integrity in vestibular pathways.
Vestibular Rehabilitation Exercises
Vestibular rehabilitation is the treatment for vestibular disorders, not a supplementary add-on. It works by driving neuroplastic compensation — forcing the brain to recalibrate its processing of vestibular information.
VOR Training (Gaze Stabilization)
VOR x1: Hold a business card at arm’s length. Read the text while turning the head side to side (or up and down), keeping the card stationary. Start slowly, increase speed as tolerated. The goal is to maintain clear vision during head movement. 1-2 minutes per direction, 3-5 times daily.
VOR x2: Move the card in the opposite direction as the head. This doubles the VOR demand. Progress to this after VOR x1 is comfortable.
Habituation Exercises
Identify the 3-5 positions or movements that most provoke dizziness (Shepard and Telian protocol). Perform each movement 3-5 times, 2-3 times daily. The intensity of dizziness should gradually decrease over days to weeks. This is graded exposure — the brain learns that the stimulus is not dangerous and recalibrates its response.
Balance Progression
Progress through increasingly challenging conditions:
- Feet apart, firm surface, eyes open (baseline)
- Feet together, firm surface, eyes open
- Feet together, firm surface, eyes closed
- Tandem stance (heel-to-toe), eyes open
- Single leg stance, eyes open
- All above on foam surface
- Add head movements during balance tasks
- Add cognitive tasks (counting backward, conversation) during balance
Optokinetic Training
Exposure to full-field optokinetic stimulation (a rotating drum with stripes, or a video of a moving visual scene) challenges the brain’s ability to resolve vestibular-visual conflict. This is particularly useful in PPPD and visual vestibular mismatch. Start with 30-60 seconds and progress gradually — this stimulus can be intensely provocative initially.
The Integration
Dizziness is never just an ear problem. It is a brain problem — a failure of the brain to accurately integrate information from the vestibular apparatus, the eyes, and the body’s proprioceptors. The functional approach asks: which specific component is failing, why is it failing, and what does the brain need to compensate?
Sometimes the answer is a 30-second Epley maneuver. Sometimes it is months of vestibular rehabilitation. Sometimes it is identifying a food sensitivity driving vestibular migraine, correcting vitamin D deficiency to prevent BPPV recurrence, or treating upper cervical dysfunction that has been mistaken for an inner ear problem.
When the ground beneath you feels unstable, the instinct is to stop moving. But the vestibular brain heals through calibrated challenge — through carefully dosed movement that forces it to recalculate, recalibrate, and rewire.
What is your brain really telling you when the world starts to tilt?