Persistent Postural-Perceptual Dizziness (PPPD)

Persistent Postural-Perceptual Dizziness (PPPD) is a long-lasting balance disorder. People feel dizzy, unsteady, or as if they are moving when they are actually still. These symptoms happen most days for at least 3 months. They usually feel worse when you are standing up, when you are moving, or when you are in places with lots of moving or complex visuals (like supermarkets, busy streets, scrolling on a phone, or watching fast videos). PPPD often starts after a vertigo spell, a balance problem, a concussion, a strong migraine phase, a panic attack, or a big illness or stress event, and then it keeps going even after that original trigger improves. PPPD is a functional vestibular disorder: the inner-ear organs and the brain scans may look normal, but the way the brain processes balance and visual information has become overly sensitive and “on guard.” PMCPubMed

Persistent Postural-Perceptual Dizziness (PPPD) is a long-lasting dizziness problem. The dizziness is not a fast spinning feeling like classic vertigo. Instead, it is a constant or near-constant sense of unsteadiness, rocking, swaying, or light-headedness that lasts for at least 3 months. The feelings are usually present most days, can wax and wane, and very often get worse in three everyday situations:

1. When you are upright (standing or walking).

2. When you move, even with gentle movements or when you are moved (for example, in a car).

3. When you look at busy visual scenes (like crowds, supermarket aisles, fast-moving traffic, scrolling screens, or patterned floors).

PPPD often starts after a trigger—for example, an inner ear problem (like BPPV or vestibular neuritis), a migraine flare, a concussion, or a period of intense stress or anxiety. After the trigger calms down or heals, the brain keeps running in a “high-alert balance mode,” and the symptoms persist. Doctors diagnose PPPD using specific criteria created by the Bárány Society (the international vestibular disorders group): persistent non-spinning dizziness or unsteadiness for ≥3 months, present most days, and exacerbated by upright posture, motion, and complex visual stimuli, following a balance-disturbing event, causing distress or impairment, and not better explained by another disorder. PMCPubMed

PPPD is recognized in ICD-11 (the global disease classification) under AB32.0, which helps standardize the diagnosis across countries and clinics. FindACode

A key clinical reminder: PPPD is ruled in by meeting its criteria—it is not only a diagnosis of exclusion. Clinicians should check for and treat triggers and co-existing problems, but the diagnosis stands on its own once the criteria are met. Binasss

---

Why does PPPD happen?

PPPD is a functional vestibular disorder. That means the hardware (ears and brain structures) may be basically intact, but the software—how the brain processes balance and visual information—has gotten stuck in an over-protective pattern.

• After a balance scare (like a big vertigo episode or a concussion), the brain increases visual monitoring and body vigilance.

• This “emergency setting” makes you over-reliant on vision (you watch everything closely) and more sensitive to motion (yours and others’).

• You may also brace your body more, stiffen your posture, and reduce natural head and eye movements.

• Anxiety can reinforce this loop. It is common in PPPD but not required. The anxiety is a result as well as a fuel for the symptoms. PMCSpringerLinkNCBI

In short, PPPD is the brain’s balance network stuck in “safety mode.” The goal in care is to reset it, but here we are focusing on definitions, causes, symptoms, and tests.

People usually describe PPPD as “I feel off,” “as if I’m on a boat,” “swaying,” “rocking,” “foggy,” or “not stable.” They may avoid supermarkets, escalators, busy streets, video games, or scrolling on phones because the visual motion makes them feel worse. They often feel better sitting or lying down, and worse when standing, walking, turning the head, riding in cars, or being in busy visual environments. There may be good hours and bad hours in the same day, especially as fatigue builds up. PMCVestibular Disorders Association

---

Types

PPPD does not have official subtypes like some diseases, but patients and clinicians often talk about practical “types” to guide thinking and testing:

1. Upright-dominant PPPD – main worsening when standing or walking, less when sitting.

2. Motion-dominant PPPD – main worsening with head or body movement, turning, or riding in vehicles.

3. Visually-dominant PPPD – main worsening in busy visual scenes (aisles, traffic, screens, patterns).

4. Mixed PPPD – a common pattern where all three triggers play a role.

5. Post-vestibular PPPD – started after an inner ear problem (e.g., BPPV, vestibular neuritis).

6. Migraine-linked PPPD – symptoms occur in people with migraine; vestibular migraine can be a trigger or comorbidity.

7. Post-concussive PPPD – began after a concussion or mild traumatic brain injury (mTBI).

8. Stress-linked PPPD – began or worsened during intense stress, panic, or health anxiety.

9. Primary PPPD – no clear single trigger is found; the brain’s threat and balance systems slowly shift into PPPD.

10. Fluctuating vs. stable course – some people have big day-to-day swings; others feel a steady level of symptoms.

(These groupings mirror the criteria’s three exacerbators—upright posture, motion, visual complexity—and typical triggers outlined in consensus and reviews.) PMCPubMed

---

Causes

PPPD nearly always starts after something disturbs balance or heightens bodily threat detection. Below are 20 common precipitating events and risk modifiers. Each short paragraph explains the link in simple terms.

1. Benign paroxysmal positional vertigo (BPPV). A sudden spinning spell can scare the balance system. Even after the crystals settle, the brain may stay in high-alert, leaving a lingering PPPD pattern. NCBI

2. Vestibular neuritis or labyrinthitis. An inner ear inflammation causes intense vertigo. The acute event heals, but the learned visual dependence and stiffened posture can persist as PPPD. NCBI

3. Ménière’s disease. Repeated inner ear fluid attacks can condition the brain into a hyper-vigilant balance state between attacks, evolving into PPPD. NCBI

4. Vestibular migraine. Migraine can disrupt sensory integration. The nervous system may become motion and visual-stimulus sensitive, paving the way for PPPD even between migraine flares. ScienceDirectSpringerOpen

5. Concussion or mild traumatic brain injury. After head injury, the brain often over-monitors movement and vision, a pattern that can solidify into PPPD. PMC

6. Panic attack with dizziness. A severe panic episode that includes dizziness can train the brain to link movement/visual input with danger, sustaining PPPD. PMC

7. Period of intense life stress. High stress can heighten body vigilance and balance threat signals; the brain keeps “guard up,” maintaining PPPD symptoms. NCBI

8. Prolonged bed rest or inactivity. Reduced natural head/eye movement can de-train balance reflexes; when activity resumes, the system feels unsafe and overreacts.

9. Visual overload (e.g., screens, VR, scrolling). Heavy visual motion exposure can reinforce visual dependence, keeping the PPPD loop alive. SpringerLink

10. Busy environments (supermarkets, stations, crowds). Repeated discomfort here can build anticipatory anxiety and avoidance, cementing the PPPD cycle. Vestibular Disorders Association

11. Neck strain or whiplash. Cervical proprioception can confuse the balance system; if the brain “doesn’t trust” neck input, it may over-rely on vision and guard posture.

12. Autonomic intolerance (orthostatic problems). Frequent light-headedness on standing can teach the brain to fear upright positions, fueling PPPD-like patterns.

13. Medication side effects (sedatives, stimulants, polypharmacy). Drugs that dull or jitter neural processing can push the brain toward over-monitoring balance.

14. Anemia or low vitamin B12. Systemic fatigue or neuropathy can add instability signals, which the brain may misinterpret as ongoing balance threat.

15. Thyroid disorders. Metabolic speed-ups or slow-downs can worsen light-headedness and anxiety, feeding PPPD vulnerabilities.

16. Chronic pain conditions. Pain fosters body vigilance and reduced movement, promoting stiff posture and balance “guarding.”

17. Poor sleep and fatigue. Tired brains are more visually dependent and less adaptive, which intensifies PPPD sensations through the day.

18. Migraine tendency without clear vestibular migraine. Even without formal vestibular migraine, a migrainous brain is more motion-sensitive. ScienceDirect

19. Motion sickness history. A lifelong motion-sensitive nervous system can be fertile ground for PPPD after a trigger. ScienceDirect

20. No obvious trigger. Sometimes PPPD develops gradually without a single event; the brain slips into over-protective processing of balance inputs. PubMed

Common symptoms of PPPD

1. Non-spinning dizziness. You do not feel like the room is spinning fast. You feel light, floaty, rocking, or swaying.

2. Unsteadiness when upright. Standing still feels unsafe. You may shift your weight, hold onto objects, or avoid lines and open spaces.

3. Worse with walking. Simple walking increases the sense of motion inside your head. You feel as if the ground moves under your feet.

4. Worse with head or body motion. Turning your head, bending, or riding in a vehicle raises the discomfort.

5. Visual motion sensitivity. Supermarkets, crowds, escalators, scrolling feeds, or fast-cut videos make you feel off balance or sick.

6. Feeling better when sitting or lying. Symptoms ease when you are supported and still, and they return with activity.

7. Brain fog. Thinking and focusing feel slow when dizziness is strong. You may lose your train of thought in busy places.

8. Fatigue. Constant vigilance over balance is exhausting. You feel tired even after simple outings.

9. Tension or anxiety about dizziness. You worry about falling or looking unwell. This is understandable and common in PPPD.

10. Mild nausea. The motion mismatch may cause stomach discomfort, but severe vomiting is less common than in spinning vertigo attacks.

11. Light sensitivity or visual strain. Bright lights, high contrast, or screens increase symptoms.

12. Feeling detached or unreal in busy scenes. Overload from sights and motion can make the world feel odd or distant.

13. Neck and shoulder tightness. Muscles tense to keep you steady, leading to soreness.

14. Avoidance of triggers. You start skipping stores, rides, social events, or driving at night because they set off the dizziness.

15. Fluctuations with stress and sleep. Bad nights, stress, or illness make symptoms worse; restful days make them milder.

Diagnostic tests

PPPD is a clinical diagnosis. That means doctors diagnose it by your story, the pattern of your symptoms, and by excluding other causes with targeted tests. Below are common tests grouped into five categories. The goal is to rule out dangerous or specific diseases and to document which systems are normal or mildly impaired. There is no single “PPPD test.”

A) Physical exam

1. General neurological examination. The doctor checks strength, sensation, reflexes, eye movements, facial muscles, and coordination. A normal neurological exam supports a functional balance problem like PPPD rather than a structural brain disease. Abnormal findings point to other diagnoses that need imaging or specialty care.

2. Gait and stance assessment. The doctor watches how you stand and walk, including turning and stopping. People with PPPD often look careful or stiff, but they usually can walk without frank falls. If there is strong veering, sudden collapse, or one-sided weakness, the doctor looks for other causes.

3. Romberg test and sharpened Romberg. You stand with feet together, first with eyes open then closed; a harder version uses heel-to-toe stance. PPPD may show increased sway, especially with eyes closed, but dramatic loss of balance may suggest other vestibular or neurological problems.

4. Tandem gait (heel-to-toe walking). You walk a straight line placing one foot directly in front of the other. PPPD may make this feel uneasy, but persistent, marked inability can suggest other cerebellar or sensory issues.

B) Manual bedside tests

5. Head impulse (head thrust) test. The clinician turns your head quickly while you fix your gaze on a target. This checks the vestibulo-ocular reflex, which keeps vision steady during head motion. A clear corrective eye movement suggests inner ear weakness; normal results fit PPPD or central causes.

6. Dix-Hallpike maneuver. You are moved from sitting to lying back with the head turned. This provokes positional vertigo if BPPV crystals are loose. A positive result shows classic spinning and nystagmus, which can be treated. If BPPV is ruled out but symptoms persist, PPPD becomes more likely.

7. Supine roll test. Similar to Dix-Hallpike but done lying on your back with head turns to each side. It helps detect horizontal canal BPPV and separates it from persistent non-spinning dizziness.

8. Dynamic visual acuity (bedside). You read an eye chart with head still, then with gentle head turns. A drop in line count with motion suggests a vestibular issue. Normal results with ongoing symptoms lean toward PPPD.

C) Laboratory and pathology tests

9. Complete blood count (CBC). This looks for anemia (low red blood cells) or infection. Severe anemia can cause lightheadedness and must be treated. A normal CBC supports functional causes like PPPD.

10. Metabolic panel and electrolytes. Blood sugar, sodium, potassium, kidney and liver markers are checked. Abnormalities can cause dizziness or weakness. Normal results help exclude medical causes.

11. Thyroid function tests. Overactive or underactive thyroid can produce fatigue, anxiety, or lightheadedness. Normal thyroid levels help narrow the diagnosis.

12. Vitamin B12 and folate. Low B12 can cause nerve problems and imbalance. Normal levels reduce the chance that a nutritional deficiency explains symptoms.

D) Electrodiagnostic and specialized vestibular tests

13. Videonystagmography (VNG) or electronystagmography (ENG). These tests record eye movements while you track targets, lie in different positions, or get warm/cool air in the ears (calorics). They identify vestibular weakness or central eye movement problems. PPPD often shows normal or only mild changes.

14. Rotational chair testing. You sit in a chair that gently rotates while eye movements are measured. This evaluates both ears together and central processing. Results can be normal in PPPD but help identify lingering vestibular loss after a trigger like neuritis.

15. Vestibular evoked myogenic potentials (VEMP—cVEMP and oVEMP). These measure reflexes from the otolith organs (saccule and utricle) using sound or vibration. They help detect specific vestibular disorders like superior canal dehiscence. Normal VEMPs support PPPD when symptoms persist.

16. Computerized dynamic posturography (CDP). You stand on a moving platform with changing visual surroundings while your sway is measured. People with PPPD often show “visual dependence” and stiff strategies. CDP patterns can support therapy planning even though they do not “prove” PPPD.

E) Imaging and ear-hearing tests

17. MRI of brain and internal auditory canals. This scan looks for strokes, tumors, demyelination, or other structural issues. A normal MRI helps exclude dangerous causes and supports a functional diagnosis like PPPD.

18. CT of temporal bones (selected cases). This is used when a bony inner ear problem, such as superior canal dehiscence, is suspected. It is not routine for all patients with dizziness but helps when symptoms point that way.

19. Audiometry (hearing test). Hearing levels and speech understanding are checked. Inner ear disorders often have hearing changes. Normal hearing with persistent non-spinning dizziness points more toward PPPD after other causes are ruled out.

20. Otoscopy and tympanometry. Looking in the ear and measuring eardrum movement checks for middle ear fluid or pressure problems. Normal results again push the diagnosis toward PPPD when the clinical pattern fits.

Non-Pharmacological therapies

These are the core of PPPD treatment. They aim to calm oversensitive motion processing, reduce visual dependence, and retrain confidence in movement. Many can be combined.

1. Vestibular Rehabilitation Therapy (VRT)
   What it is: A personalized exercise program with a trained vestibular therapist. It includes gaze-stabilization, balance drills, graded head/body movements, and outdoor/visual exposure tasks.
   Purpose: Reduce dizziness, motion sensitivity, and unsteadiness; restore day-to-day functioning.
   How it works: Repeated, safe exposure teaches your brain to habituate to triggers and recalibrate balance signals. MDPISpringerOpen

2. Cognitive-Behavioral Therapy (CBT) specialized for PPPD
   What it is: Short-term, skills-based therapy to reduce fear of dizziness, avoidance behaviors, and hypervigilance.
   Purpose: Break the fear-avoidance cycle that sustains symptoms.
   How it works: Cognitive reframing + gradual exposure decreases alarm responses to body and visual sensations. RCTs and reviews show added benefit when CBT is combined with standard care. PMCPubMed

3. Graded visual-motion exposure
   What it is: A stepwise plan to face visual triggers (supermarkets, scrolling, traffic) starting from short, easy exposures.
   Purpose: Desensitize visual dependence.
   How it works: Progressive exposure reduces the brain’s over-response to complex visual flow. PubMed

4. Psychoeducation and diagnostic explanation
   What it is: A clear, reassuring conversation about PPPD being real, common, and treatable.
   Purpose: Reduce uncertainty and catastrophic thinking; improve treatment engagement.
   How it works: Understanding the condition lowers anxiety and hypervigilance that amplify symptoms. Vestibular Disorders Association

5. Home balance-confidence training
   What it is: Simple daily drills—standing feet together, semi-tandem, tandem, then unstable surfaces—plus head turns while focused on a target.
   Purpose: Build stability and reduce “wobbliness.”
   How it works: Repeated practice strengthens sensory integration for posture.

6. Walking program with head turns
   What it is: Daily walks, starting short and slow, adding gentle head movements and uneven surfaces as tolerated.
   Purpose: Restore automatic gait-balance coupling.
   How it works: Encourages central compensation while staying safe and graded.

7. Breathing and autonomic calming (paced breathing, box breathing)
   Purpose: Lower the fight-or-flight arousal that fuels dizziness.
   How it works: Slow exhalation lengthens vagal tone and decreases bodily “alarm” sensations that the brain misreads as imbalance.

8. Mindfulness/acceptance-based strategies
   Purpose: Reduce reactivity to dizziness sensations.
   How it works: Non-judgmental attention retrains the brain to notice but not chase internal sensations, weakening the symptom loop.

9. Sleep optimization
   Purpose: Improve neuro-sensory stability and mood resilience.
   How it works: Consistent bed/wake times, light exposure in the morning, and reducing late-night screens support vestibular compensation.

10. Hydration and steady fueling
    Purpose: Avoid orthostatic dips and irritability that can amplify symptoms.
    How it works: Fluids and regular meals help maintain blood pressure and brain energy.

11. Screen and visual ergonomics
    Purpose: Ease visual flow stress from monitors/phones.
    How it works: Larger fonts, reduced scroll speed, frequent micro-breaks, and fewer overlapping windows decrease complex visual load.

12. Task pacing and activity planning
    Purpose: Prevent boom-and-bust cycles.
    How it works: Break tasks into predictable blocks with planned rests to build tolerance without flare-ups.

13. Tai Chi or Qigong
    Purpose: Improve dynamic balance and calm the nervous system.
    How it works: Slow, mindful shifting of weight challenges vestibular integration gently.

14. Yoga (balance-focused, slow flow)
    Purpose: Improve postural control and breath regulation.
    How it works: Combines graded balance challenges with parasympathetic activation.

15. Strength and core training (gentle, progressive)
    Purpose: Support posture and reduce fatigue that magnifies dizziness.
    How it works: Strong legs and core reduce sway and reinforce movement confidence.

16. Vision therapy elements in rehab (when indicated)
    Purpose: Address abnormal optokinetic/visual motion sensitivity.
    How it works: Carefully dosed optokinetic and tracking tasks help re-normalize visual-vestibular interaction, usually inside VRT.

17. Virtual-reality–assisted exposure (specialist-guided)
    Purpose: Practice complex visual scenes safely.
    How it works: Controlled VR visual flow provides graded desensitization. (Adjunctive; evidence evolving.) MDPI

18. Return-to-work/school accommodations
    Purpose: Keep life moving while recovering.
    How it works: Adjust lighting, reduce multitasking, allow short visual breaks, and gradually increase demands—prevents avoidance patterns from “sticking.”

19. Community or online support groups
    Purpose: Reduce isolation, normalize the experience, and share coping tactics.
    How it works: Social learning lowers fear and improves adherence.

20. Neuromodulation (research/adjunct only)
    What it is: Techniques like repetitive transcranial magnetic stimulation (rTMS) are being studied for refractory cases.
    Purpose: Potentially calm overactive cortical networks linked to dizziness perception.
    How it works: Magnetic pulses modulate excitability in motion-processing areas. Current evidence is preliminary; not first-line. PMC

---

Medicines used in PPPD

Important: Medicines are helpers, not stand-alone cures. The strongest evidence today supports CBT + VRT, with medicines used to reduce symptom intensity and treat anxiety/migraine comorbidities. High-quality placebo-controlled trials for many drugs are still limited, so doctors tailor therapy to the person in front of them. PMC

For each medicine below, doses are typical adult ranges—not personal advice. Always discuss with your clinician.

1. Sertraline (SSRI)
   Dose & timing: Start 25–50 mg daily; usual 50–200 mg daily; once daily, morning or evening.
   Purpose: Reduce chronic dizziness intensity, anxiety, and hypervigilance; improves function—especially with CBT.
   How it works: Increases serotonin signaling, which calms alarm circuits and may reduce visual-motion sensitivity.
   Evidence: Open-label data and a randomized study show benefit; combining with CBT improves outcomes and may allow lower medication doses.
   Common side effects: Nausea, sleep change, headache, sexual side effects—often ease after 4–6 weeks. PubMedPMCSemantic Scholar

2. Paroxetine (SSRI)
   Dose & timing: 10–40 mg daily.
   Purpose: Similar to sertraline for PPPD with anxiety features.
   Mechanism: Serotonin reuptake inhibition.
   Side effects: Drowsiness, weight gain, sexual side effects; taper slowly to prevent withdrawal. ScienceDirect

3. Fluoxetine (SSRI)
   Dose & timing: 10–40 mg daily; long half-life.
   Purpose/Mechanism: As above; sometimes chosen when smoother tapering is desired.
   Side effects: Activation, insomnia, GI upset. PMC

4. Escitalopram (SSRI)
   Dose & timing: 5–20 mg daily.
   Purpose: Well-tolerated option for anxiety-dizziness loops.
   Side effects: Nausea, headache; generally fewer drug interactions (still review with clinician).

5. Venlafaxine (SNRI)
   Dose & timing: Start 37.5 mg daily; usual 75–150 mg daily (sometimes higher); once daily with food.
   Purpose: Helpful when migraine or depression co-exists; some clinical series report ≥50% improvement in many patients.
   Mechanism: Boosts serotonin and norepinephrine; can reduce central sensitivity and help migraine prevention.
   Side effects: Nausea, increased sweating, blood pressure rise at higher doses; avoid abrupt stops due to withdrawal. PubMedPMC

6. Duloxetine (SNRI)
   Dose & timing: 30–120 mg daily.
   Purpose: Consider when pain symptoms or anxiety are prominent.
   Side effects: Nausea, dry mouth, sleep change. (Evidence in PPPD is extrapolated from anxiety/chronic dizziness management.) PMC

7. Amitriptyline or Nortriptyline (TCA)
   Dose & timing: Start 10 mg at night; usual 10–50 mg nightly.
   Purpose: Useful when vestibular migraine overlaps with PPPD; may also aid sleep.
   Mechanism: Modulates serotonergic/noradrenergic pathways and pain processing.
   Side effects: Dry mouth, constipation, drowsiness; start low and go slow. Oxford Academic

8. Propranolol (β-blocker) for migraine-overlap
   Dose & timing: 20–120 mg per day in divided doses.
   Purpose: Migraine prevention when vestibular migraine co-exists; indirectly reduces dizziness flares in those patients.
   Side effects: Fatigue, low blood pressure/heart rate; not for uncontrolled asthma. Oxford Academic

9. Verapamil (calcium-channel blocker) for migraine-overlap
   Dose & timing: Common preventive range 120–240 mg/day in divided doses (specialist-guided).
   Purpose: Alternative migraine prevention; sometimes used in vestibular migraine.
   Side effects: Constipation, low blood pressure, swelling. Vestibular Disorders Association

10. Short-term vestibular suppressants (e.g., meclizine) or benzodiazepines (e.g., clonazepam)—limited role
    Use: Short bursts only for acute vertigo spells—not for chronic PPPD—because they slow compensation and can cause dependence or sedation.
    Side effects: Drowsiness, falls, memory effects (benzodiazepines). Discuss very carefully with your doctor. SpringerLink

Cochrane review found no placebo-controlled RCTs yet that prove SSRIs/SNRIs work for PPPD, even though many clinics see benefit when medications are combined with CBT and VRT. That’s why a personalized, multimodal plan is recommended. PMC

---

Dietary molecular supplements

PPPD itself has no specific vitamin cure. Supplements are sometimes used to support migraine overlap, sleep, or stress regulation, which can indirectly calm PPPD. Always review interactions with your clinician.

1. Magnesium (e.g., citrate or glycinate) — 200–400 mg elemental/day.
   Supports migraine prevention and calms neuromuscular excitability; may ease sensory hyper-responsiveness.

2. Riboflavin (Vitamin B2) — 200–400 mg/day.
   Classic migraine supplement; supports mitochondrial energy handling in neurons.

3. Coenzyme Q10 — 100–300 mg/day with food.
   Mitochondrial support; sometimes combined with riboflavin for migraine overlap.

4. Omega-3 fatty acids (EPA/DHA) — 1–2 g/day combined EPA+DHA.
   Anti-inflammatory effects; may improve general brain health and mood.

5. Vitamin D3 — dose individualized (often 1000–2000 IU/day, check levels).
   Low vitamin D is common and replacement supports neuromuscular function.

6. B-complex including B6 and B12 — label dose.
   Supports nerve health and energy metabolism; correct deficiencies if present.

7. L-theanine — 100–200 mg up to twice daily.
   Promotes calm alertness; may reduce anxiety-driven symptom spikes.

8. Melatonin — 1–3 mg 1–2 hours before bed.
   Improves sleep timing, which stabilizes symptoms.

9. Ginger extract — 250–500 mg as needed.
   May reduce nausea in motion sensitivity.

10. Electrolyte solution on high-symptom days — per label.
    Helps maintain blood volume when upright sensitivity is high.

(These are general, adjunctive ideas; strong PPPD-specific trials are limited. Prioritize VRT + CBT; use supplements thoughtfully.)

---

Regenerative / stem-cell drugs

There are no approved immune-booster, regenerative, or stem-cell drugs for PPPD. PPPD is a functional vestibular-brain processing disorder, not an immune deficiency or a tissue-loss condition. Listing “stem-cell drugs” for PPPD would be inaccurate and unsafe. The most evidence-based plan remains education + VRT + CBT, with carefully chosen SSRIs/SNRIs when needed. Research on neuromodulation (like rTMS) is ongoing but remains adjunct/experimental. If you see “regenerative” or “stem cell” advertisements for PPPD, approach them with caution and discuss with a specialist first. PMC+1

---

Surgeries

PPPD has no surgical treatment. Surgery is only considered if there’s a different, structural vestibular problem that triggered symptoms and still needs fixing (for example, a perilymph fistula repair, superior canal dehiscence repair, Menière’s procedures like endolymphatic sac surgery, or, very rarely, vestibular nerve section/labyrinthectomy for severe unilateral attacks). Even then, PPPD can persist after surgery, so the main tools are still VRT + CBT + targeted meds. If someone suggests surgery for PPPD itself, seek a second opinion.

Procedures (for underlying conditions only, not PPPD itself):

1. Perilymph fistula repair – closes abnormal hole between middle and inner ear to stop pressure-triggered vertigo.

2. Superior canal dehiscence (SCD) plugging/resurfacing – covers a bony opening causing sound/pressure-induced vertigo.

3. Endolymphatic sac decompression/shunt (Menière’s) – reduces inner-ear fluid pressure in selected cases.

4. Intratympanic gentamicin (Menière’s, selected severe cases) – weakens overactive vestibular input to reduce attacks.

5. Vestibular nerve section or labyrinthectomy (rare, last resort) – disables one inner ear to stop intractable attacks.

---

Prevention strategies

1. Seek early rehab after a vertigo, concussion, or strong migraine episode—don’t wait months. Early action lowers the risk of persistent symptoms. SpringerOpen

2. Keep moving in small, safe steps. Gentle, daily movement prevents the brain from “locking in” avoidance.

3. Practice visual-motion exposure in a graded way—short supermarket visits, slow scrolling, short public-transport rides—then build up.

4. Protect sleep (regular schedule, morning light, quiet/dark bedroom).

5. Manage stress (breathing, mindfulness, brief restorative breaks).

6. Limit long-term vestibular suppressants or daily benzodiazepines. They hinder compensation unless used briefly for acute crises. SpringerLink

7. Treat comorbid migraine/anxiety/depression because these can amplify PPPD. Oxford Academic

8. Stay hydrated and fuel regularly.

9. Use screen ergonomics: larger text, steady scrolling, frequent pauses.

10. Work with a vestibular therapist for a personalized, progressive plan. MDPI

---

When to see a doctor urgently versus routinely

• Urgent, same-day care or emergency: sudden severe headache or “worst ever,” new weakness/numbness on one side, trouble speaking, new double vision, chest pain, fainting, sudden hearing loss, or a high-speed head injury.

• Soon (within days to weeks): dizziness lasting >3 months, repeated near-falls, major impact on work/school, new or worsening anxiety or depression, or if you’re unsure whether you have PPPD, vestibular migraine, BPPV, Menière’s disease, or something else.

• Anytime: before starting, stopping, or changing medications or supplements; if you’re pregnant or have heart rhythm, liver, kidney, or psychiatric conditions.

---

What to eat—and what to limit

PPPD does not have a special “PPPD diet.” These tips help stabilize energy, hydration, and migraine overlap (if present).

Helpful to eat/drink

1. Water and electrolyte fluids across the day.

2. Regular meals with lean protein and complex carbs to prevent dips that can worsen dizziness.

3. Magnesium-rich foods (leafy greens, nuts, beans).

4. Omega-3 sources (fish like salmon, sardines; walnuts).

5. Colorful fruits/vegetables for antioxidants that support brain health.

Consider limiting (especially if migraine-prone)

1. Excess caffeine (can increase jitteriness for some; others tolerate small amounts).
2. Alcohol, especially red wine (can trigger dizziness or migraine in some).
3. Highly processed foods high in salt/MSG in people who notice sensitivity.
4. Tyramine-rich aged foods (aged cheeses, cured meats) if they trigger migraine for you.
5. Big, late-night meals that disturb sleep.

---

Frequently Asked Questions

1. Is PPPD “all in my head”?
   PPPD is real. It’s a functional vestibular disorder—your hardware looks okay, but your brain’s processing of motion/visual/body signals is over-sensitive. The good news: processing can be retrained. PubMed

2. Can PPPD be cured?
   Many people significantly improve with VRT + CBT, sometimes plus a carefully chosen medicine. Recovery is not overnight; it’s usually steady, graded progress. PMCMDPI

3. Why did mine start after a vertigo attack or illness?
   A strong trigger can push the balance system into a protective, hyper-vigilant mode. For some, that response doesn’t turn off without retraining. PMC

4. What’s the difference between PPPD and BPPV?
   BPPV causes brief spinning vertigo triggered by head position changes due to loose crystals in the inner ear. PPPD causes non-spinning dizziness most days for months and is worse with standing, motion, and busy visuals. (They can occur together, and PPPD can persist after BPPV is treated.) PMC

5. How is PPPD different from vestibular migraine?
   Vestibular migraine is a migraine disorder with episodic vestibular attacks. PPPD is chronic daily dizziness. They often overlap; treating migraine can help PPPD in those patients. PMCOxford Academic

6. Will meclizine fix PPPD?
   No. Long-term use can slow recovery. It’s sometimes used briefly for acute vertigo, but not for chronic PPPD. SpringerLink

7. Are antidepressants just for mood?
   In PPPD they’re used to reduce dizziness sensitivity, treat anxiety/migraine overlap, and support rehab. Evidence suggests benefit in practice, but high-quality placebo-controlled trials are still limited. PMC

8. Is CBT just “talk therapy”?
   It’s skills-based training that changes how your brain responds to dizziness signals. When added to standard care, it improves outcomes. PMC

9. How long until I feel better?
   Many feel first improvements in weeks, with steady gains over months when doing VRT/CBT consistently. Timelines vary.

10. Is exercise safe?
    Yes—graded movement is essential. Start small, keep it safe, and build up with your therapist.

11. Can I drive?
    If you feel visually overwhelmed or unsteady, avoid driving until symptoms are better controlled. Ask your clinician for guidance.

12. Do I need brain scans?
    Often not, if history and exam fit PPPD and other causes are excluded. Scans can be normal in PPPD. Your doctor decides based on red flags.

13. Does blue-light blocking help?
    What helps most is limiting complex visual motion and using screen ergonomics. Some people like blue-light filters for comfort; results vary.

14. Is neuromodulation (like rTMS) ready?
    Not yet as standard care. Early studies are promising but preliminary; it’s an adjunct for difficult cases under specialist care. PMC

15. What’s the single most important thing I can do today?
    Start a gentle, daily movement habit and planned visual-motion exposure, and ask for referral to vestibular therapy. Add CBT skills to calm the alarm system. MDPI

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 21, 2025.