• Dizziness can be classified into four groups:
  • vertigo (spinning sensation)
  • disequilibrium (feeling of imbalance)
  • light-headedness (sensation of giddiness)
  • presyncope (sensation of feeling faint).
• vertigo may be
  • central (involving the brainstem or cerebellum)
  • peripheral (involving the inner ear). 
• The most common causes of vertigo seen in primary care are
  • benign paroxysmal positional vertigo (BPPV)
  • vestibular neuronitis (VN)
  • Ménière’s disease. 

These peripheral causes of vertigo are benign, and treatment involves reassurance and management of symptoms.

Cause	Description
Peripheral causes
Acute labyrinthitis	Inflammation of the labyrinthine organs caused by viral or bacterial infection
Acute vestibular neuronitis (vestibular neuritis)*	Inflammation of the vestibular nerve, usually caused by viral infection
Benign positional paroxysmal vertigo (benign positional vertigo)	Transient episodes of vertigo caused by stimulation of vestibular sense organs by canalith; affects middle-age and older patients; affects twice as many women as men
Cholesteatoma	Cyst-like lesion filled with keratin debris, most often involving the middle ear and mastoid
Herpes zoster oticus (Ramsay Hunt syndrome)	Vesicular eruption affecting the ear; caused by reactivation of the varicellazoster virus
Ménière’s disease (Ménière’s syndrome, endolymphatic hydrops)	Recurrent episodes of vertigo, hearing loss, tinnitus, or aural fullness caused by increased volume of endolymph in the semicircular canals
Otosclerosis	[ corrected] Abnormal growth of bone in the middle ear, leading to immobilization of the bones of conduction and a conductive hearing loss; this process also may affect the cochlea, leading to tinnitus, vertigo, and sensorineural hearing loss
Perilymphatic fistula	Breach between middle and inner ear often caused by trauma or excessive straining
Central causes
Cerebellopontine angle tumor	Vestibular schwannoma (i.e., acoustic neuroma) as well as infratentorial ependymoma, brainstem glioma, medulloblastoma, or neurofibromatosis
Cerebrovascular disease such as transient ischemic attack or stroke	Arterial occlusion causing cerebral ischemia or infarction, especially if affecting the vertebrobasilar system
Migraine	Episodic headaches, usually unilateral, with throbbing accompanied by other symptoms such as nausea, vomiting, photophobia, or phonophobia; may be preceded by aura
Multiple sclerosis	Demyelinization of white matter in the central nervous system
Other causes
Cervical vertigo	Vertigo triggered by somatosensory input from head and neck movements
Drug-induced vertigo	Adverse reaction to medications
Psychological	Mood, anxiety, somatization, personality, or alcohol abuse disorders

BPPV, Meniere’s Disease, Vestibular Neuritis, and Labyrinthitis:

Condition	Symptoms	Timing	Signs	Etiology	Diagnosis	Treatment
BPPV caused by dislodged otoliths. Brief episodes of vertigo triggered by changes in head position. Diagnosed with the Dix-Hallpike maneuver.	Vertigo triggered by head movement, nausea	Lasts seconds to minutes	Positive Dix-Hallpike test, rotational nystagmus	Displacement of otoconia in semicircular canals	Dix-Hallpike maneuver	Epley maneuver, antihistamines (Meclizine 25-100 mg daily), antiemetics (Ondansetron, Metoclopramide, Promethazine)
Meniere’s Disease believed to be related to abnormal fluid buildup (endolymph) in the inner ear. Possible contributing factors include genetic predisposition, viral infections, autoimmune conditions, allergies, and head trauma.	Vertigo, tinnitus, hearing loss, aural fullness	Lasts 20 minutes to hours	Sensorineural hearing loss, episodic vertigo	Endolymphatic hydrops, idiopathic	Clinical diagnosis, audiometry	Betahistine (16-48 mg/day), thiazide diuretics (25-50 mg/day), salt restriction, avoid alcohol and caffeine
Vestibular Neuritis Often follows a recent upper respiratory tract infection. that affects the vestibular nerve Presents with vertigo that can last days without hearing loss.	Vertigo, nausea, vomiting, balance problems	Lasts days to weeks	Unidirectional horizontal-torsional nystagmus, no hearing loss	Viral infection (e.g., HSV reactivation), inflammation of vestibular nerve	Clinical diagnosis, HINTS exam	Antiemetics (Promethazine 12.5-25 mg every 4-6 hours, Metoclopramide 10 mg TID), antihistamines (Diphenhydramine 25-50 mg every 4-6 hours), vestibular rehab
Labyrinthitis often follows a recent acute otitis media (AOM). Characterized by a prolonged vertigo episode, usually associated with hearing loss and tinnitus on the affected side	Vertigo, nausea, vomiting, hearing loss, tinnitus	Lasts days to weeks	Hearing loss, spontaneous nystagmus	Viral or bacterial infection	Clinical diagnosis, audiometry	Same as vestibular neuritis plus antibiotics if bacterial, vestibular rehabilitation, corticosteroids in some cases if indicated

True nystagmus and vertigo will never last longer than a couple of weeks if caused by a peripheral lesion because compensation occurs; such is not true for a central lesion.

History

• associated neurological symptoms such as weakness, dysarthria, sensory changes, ataxia or confusion – consider central causes, such as cerebrovascular accidents (CVAs), tumours and multiple sclerosis 
• check for Risk factors for vascular disease
  • smoking, diabetes
  • obesity
  • hypertension
  • hypercholesterolaemia
• symptoms of nausea, vomiting and hearing loss more associated with Peripheral pathology
• triggered by a
  • change in the position of the head
  • recent upper respiratory tract infection (URTI)
  • stress
  • Loud noises (called Tullio phenomenon)
  • Medications, including frusemide, salicylates and antihypertensive agents
• Trauma – Perilymphatic fistula should be considered if there is a history of recent head injury.
• hearing loss and Vertigo
  • seen in labyrithitis and Ménière’s disease
  • No hearing loss – seen in benign paroxysmal positional vertigo (BPPV) and vestibular neuronitis (VN)

Duration of Symptoms

Duration of episode	Suggested diagnosis
A few seconds	Peripheral cause: unilateral loss of vestibular function; late stages of acute vestibular neuronitis; late stages of Ménière’s disease
Several seconds to a few minutes	Benign paroxysmal positional vertigo; perilymphatic fistula
Several minutes to one hour	Posterior transient ischemic attack; perilymphatic fistula
Hours	Ménière’s disease; perilymphatic fistula from trauma or surgery; migraine; acoustic neuroma
Days	Early acute vestibular neuronitis*; stroke; migraine; multiple sclerosis
Weeks	Psychogenic (constant vertigo lasting weeks without improvement)

Provoking Factors

Provoking factor	Suggested diagnosis
Changes in head position	Acute labyrinthitisbenign positional paroxysmal vertigocerebellopontine angle tumormultiple sclerosisperilymphatic fistula
Spontaneous episodes (i.e., no consistent provoking factors)	Acute vestibular neuronitiscerebrovascular disease (stroke or transient ischemic attack)Ménière’s diseasemigrainemultiple sclerosis
Recent upper respiratory viral illness	Acute vestibular neuronitis
Stress	Psychiatric or psychological causesmigraine
Immunosuppression (e.g., immunosuppressive medications, advanced age, stress)	Herpes zoster oticus
Changes in ear pressure, head trauma, excessive straining, loud noises	Perilymphatic fistula

Associated Symptoms

Symptom	Suggested diagnosis
Aural fullness	Acoustic neuromaMénière’s disease
Ear or mastoid pain	Acoustic neuromaacute middle ear disease (e.g., otitis media, herpes zoster oticus)
Facial weakness	Acoustic neuromaherpes zoster oticus
Focal neurologic findings	Cerebellopontine angle tumor; cerebrovascular disease; multiple sclerosis (especially findings not explained by single neurologic lesion)
Headache	Acoustic neuroma; migraine
Hearing loss	Ménière’s disease; perilymphatic fistula; acoustic neuroma; cholesteatoma; otosclerosis; transient ischemic attack or stroke involving anterior inferior cerebellar artery; herpes zoster oticus
Imbalance	Acute vestibular neuronitis (usually moderate); cerebellopontine angle tumor (usually severe)
Nystagmus	Peripheral or central vertigo
Phonophobia, photophobia	Migraine
Tinnitus	Acute labyrinthitis; acoustic neuroma; Ménière’s disease

Associated with Hearing Loss

Diagnosis	Characteristics of hearing loss
Acoustic neuroma	Progressive, unilateral, sensorineural
Cholesteatoma	Progressive, unilateral, conductive
Herpes zoster oticus (i.e., Ramsay Hunt syndrome)	Subacute to acute onset, unilateral
Ménière’s disease	Sensorineural, initially fluctuating, initially affecting lower frequencies; later in course: progressive, affecting higher frequencies
Otosclerosis	Progressive, conductive
Perilymphatic fistula	Progressive, unilateral
Transient ischemic attack or stroke involving anterior inferior cerebellar artery or internal auditory artery	Sudden onset, unilateral

Peripheral vs. Central Causes of Vertigo

Feature	Peripheral vertigo	Central vertigo
Nystagmus	Combined horizontal and torsional; inhibited by fixation of eyes onto object; fades after a few days; does not change direction with gaze to either side	Purely vertical, horizontal, or torsional; not inhibited by fixation of eyes onto object; may last weeks to months; may change direction with gaze towards fast phase of nystagmus
Imbalance	Mild to moderate; able to walk	Severe; unable to stand still or walk
Nausea, vomiting	May be severe	Varies
Hearing loss, tinnitus	Common	Rare
Nonauditory neurologic symptoms	Rare	Common
Latency following provocative diagnostic maneuver	Longer (up to 20 seconds)	Shorter (up to 5 seconds)

Physical examination

• Ear examination:
  • visualise the tympanic membranes
    • look for vesicles that can be seen in a Herpes zoster infection
    • retraction pockets as seen in cholesteotoma.
  • hearing assessment
• Neurological examination:
  • Gait
  • Balance
  • Coordination
  • Romberg’s sign
  • heel-toe test
• Eye examination:
  • nystagmus and papilledema. 
  • Nystagmus is quick, jerky, involuntary movements of the eye.
    • Vertical nystagmus is only seen if the cause is central
    • Nystagmus due to central causes may be horizontal, rotational or vertical, and does not disappear on fixing the gaze.
    • Nystagmus in the peripheral type disappears with fixation of the gaze.
  • Cardiovascular examination:
    • Pulse
    • blood pressure
    • heart rate and rhythm 
  • Carotid examination

Dix−Hallpike manoeuvre

• The patient sits at the edge of the bed and the examiner turns the patient’s head 30–45 degrees to the side being tested. 
• The patient needs to keep their eyes open and focus on a stable point, and then quickly lie supine and hyperextend the neck. 
• Horizontal nystagmus denotes a positive test. This test can induce vertigo, so patients should be warned about this before the test is performed

Orthostatic blood pressure testing 

• A drop in the systolic blood pressure by more than 20 mm/Hg from a lying down to standing position is significant for a postural drop. 
• This is seen in patients who are dehydrated or who present with autonomic dysfunction.
• Autonomic dysfunction can occur acutely and be driven by vertigo.

HINTs Exam

• is a screening tool for distinguishing a central cause of vertigo from an acute peripheral vestibulopathy (APV), such as vestibular neuritis
• Normal neurological exam cannot accurately exclude a central process
• 10% of patients with a cerebellar infarct, usually in the medial branch of the PICA, will have isolated vertigo without other associated deficit.
• In the HiNTs exam derivation paper, only 51% of those with a central process causing vertigo had a neurological sign on exam
• A positive HINTS exam has been reported to have a high sensitivity and specificity for the presence of a central cause of vertigo
• HINTS is comprised of three core components:
  • head impulse test
  • evaluation of nystagmus
  • test of skew

1. Head Impulse Test

• Position of the Tester: Sitting directly in front of the patient.
• Position of the Subject: Sitting with eyes fixed on the examiner’s nose or a distant target.
• Precautions: Ensure the patient has no neck issues (e.g., vertebrobasilar insufficiency) and that their neck range of motion is adequate for testing.
• Instructions for the Subject: The patient should maintain focus on the examiner’s nose or a target during the procedure without closing their eyes prematurely.
• Examiner Action:
  • Gently turn the patient’s head to one side and then quickly move it back to the center.
  • Positive Test (Peripheral Etiology): If the patient has a significant lag, followed by a corrective saccade (a quick eye movement to re-fixate on the target), the test is positive, indicating a likely peripheral cause of vertigo.
    • If corrective saccades are observed on only one side, this reinforces a peripheral cause.
  • Negative Test (Concerning for Central Etiology): If there is no corrective saccade and the eyes remain fixed on the target during head movement, this may suggest a central cause.
  • Comparison: Perform the test on both sides, noting any asymmetry. A positive test on only one side generally suggests a peripheral etiology, while corrective saccades in both directions or in the vertical plane are concerning for a central cause.

2. Nystagmus Assessment

• Procedure:
  • Observe the patient’s primary gaze with eyes looking straight ahead.
  • Then ask the patient to look to the left and right, avoiding any fixation point (this minimizes suppression of nystagmus).
• Interpretation:
  • Unidirectional Nystagmus (Peripheral Origin): Nystagmus that consistently beats in the same direction regardless of gaze direction is more likely peripheral and less concerning.
  • Bidirectional or Vertical Nystagmus (Central Origin):
    • Bidirectional Gaze-Evoked Nystagmus: The nystagmus changes direction depending on gaze direction (beats toward the side the patient is looking). This finding is highly specific for central causes, particularly stroke.
    • Vertical Nystagmus: Nystagmus with a vertical component, especially when it doesn’t fatigue or is direction-changing, is highly suggestive of a central etiology

3. Test of Skew

• Procedure:
  • Ask the patient to focus on your nose.
  • Cover one eye and then quickly uncover it while covering the opposite eye, observing the uncovered eye for any corrective movement.
  • Repeat this maneuver with the other eye.
• Interpretation:
  • Abnormal Skew (Central Origin): If there is any vertical or diagonal corrective movement of the uncovered eye, this suggests a central cause of vertigo. This finding is also often associated with vertical diplopia.

Distinguishing peripheral vs central vertigo using the HINTS examination

	Peripheral	Central
Head impulse test	Abnormal	Normal
Nystagmus	None or unidirectional	Bidirectional or vertical
Test of skew	No vertical skew	Vertical skew

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Benign Paroxysmal Positional Vertigo (BPPV)

• most common cause for episodic vertigo
• acute attacks of transient vertigo initiated by certain head positions lasting seconds to minutes, accompanied by nystagmus that fatigues on repeated testing
• It is caused by an accumulation of calcium crystals in the posterior semicircular canal. 
• These crystals affect the movement of the endolymph in the semicircular canals, which causes vertigo
• may occur following a
  • head injury
  • viral infection (URTI)
  • degenerative disease
  • idiopathic
• diagnosed by history and positive Dix-Hallpike manoeuvre 
• Management
  • Assess patients with BPPV for factors that modify management
    • impaired mobility or balance
    • central nervous system disorders
    • lack of home support
    • increased risk for falling
  • Non-Pharm
    • Educate patients regarding
      • reassure patient that process resolves spontaneously in weeks to months
      • the impact of BPPV on their safety
      • the potential for disease recurrence
      • the importance of follow-up
    • Particle repositioning maneuvers
      • Epley’s manoeuvre or Brandt-Daroff exercises
  • Pharm
    • drugs to suppress the vestibular system may provide minimal relief for some patients
    • it does not solve the problem
    • it only masks the problem
  • Symptomatic treatment
    • persistent nausea and vomiting may require IV hydration and antiemetics e.g. prochlorperazine

Epley maneuver

• (A) Patient sits on the examination table, with eyes open and head turned 45 degrees to the right
• (B) The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table
• (C)The physician turns the patient’s head 90 degrees to the left side. The patient remains in this position for 30 seconds
• (D) The physician turns the patient’s head an additional 90 degrees to the left while the patient rotates his or her body 90 degrees in the same direction. The patient remains in this position for 30 seconds
• (E) The patient sits up on the left side of the examination table.
• The procedure may be repeated on either side until the patient experiences relief of symptoms

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Meniere’s Disease (Endolymphatic Hydrops)

• Pathophysiology: Meniere’s disease is believed to result from excess fluid (endolymph) in the cochlear and vestibular structures, which disrupts inner ear function and eventually affects the semicircular canals.
• Epidemiology: Most commonly affects individuals aged 40-60.
• Key Features:
  • Vertigo: Episodes lasting minutes to hours; over time, vertigo attacks may diminish, leaving hearing loss as the primary issue.
  • Fluctuating Hearing Loss: In early stages, hearing may normalize between attacks; later stages often result in permanent, unilateral, low-frequency hearing loss, with bilateral loss potentially developing over time.
  • Tinnitus: Persistent ringing or buzzing, often fluctuating in intensity.
  • Aural Fullness: A sensation of pressure or fullness in the affected ear.
  • Drop Attacks (Tumarkin Crises): Sudden falls without warning, potentially associated with nausea and vomiting.
• Course: Early in the disease, hearing returns to normal between attacks, but in later stages, there may be permanent, fluctuating low-frequency hearing loss and persistent tinnitus.
• Triggers: Stress and other factors may precipitate attacks, which often occur in clusters and can be debilitating.
• Diagnostic Test: Pure tone audiometry is the most valuable test to assess sensorineural hearing loss.
• Management:
  • Acute Management:
    • Bedrest
    • IV antiemetics
    • Antivertigo medications (e.g., Serc/betahistine)
    • Low molecular weight dextrans
  • Long-Term Management:
    • Medical: Low-salt diet and potassium-sparing diuretics (e.g., triamterene, amiloride)
    • Local Treatment: Gentamicin injection to ablate vestibular function in severe cases
    • Surgical: Selective vestibular neurectomy or transtympanic labyrinthectomy; however, the disease may recur in the opposite ear.

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Recurrent Vestibulopathy

• Epidemiology: Typically affects individuals aged 30-50, with equal incidence in men and women.
• Features:
  • Episodic vertigo lasting minutes to hours.
  • No hearing loss, tinnitus, or neurological deficits.
• Etiology: Uncertain, but may be linked to trauma, viral infections, or deafferentation of cranial nerve VIII.
• Management: Symptomatic treatment; most cases eventually go into remission.

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Vestibular Neuronitis

• Pathophysiology: Inflammation of the vestibular nerve, often following a viral upper respiratory infection or herpes zoster. The inflammation is thought to be immune-mediated following a viral illness.
• Epidemiology: Commonly affects middle-aged adults and may occur in clusters during respiratory infection outbreaks.
• Clinical Presentation:
  • Sudden onset of vertigo
  • Inability to stand or walk
  • Nausea and vomiting
  • Persistent balance problems
• Symptoms: Typically constant, lasting 2-3 days, followed by gradual recovery (distinguishing it from episodic conditions like BPPV or Meniere’s disease). Patients may experience prolonged unsteadiness for months after an attack.
• Differential Diagnosis: No hearing loss or tinnitus (hearing loss suggests labyrinthitis instead).
• Management:
  • Acute Phase (first 24–72 hours): Bed rest and antiemetics.
  • Reassurance: Symptoms improve over time, though full recovery may take weeks to months.

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Labyrinthitis

• Pathophysiology: Labyrinthitis is inflammation of the inner ear structures (bony and membranous labyrinth). It may follow middle ear infections, which can spread to the inner ear.
• Course: Symptoms may last days to weeks and often follow a viral infection.
• Clinical Presentation:
  • Sudden onset of vertigo
  • Unilateral hearing loss
  • Nausea and vomiting
  • Tinnitus, often described as whistling
  • Typically no fever or pain.
• Key Differentiating Feature: Hearing loss (uncommon in BPPV) is the primary distinguishing factor between labyrinthitis and other types of peripheral vertigo.
• Management:
  • Viral Labyrinthitis: Usually self-limiting; supportive care may be sufficient.
  • Suppurative Labyrinthitis: Requires urgent medical attention, especially if associated with a middle ear infection. Treatment includes:
    • Emergency drainage of otitis media and IV antibiotics
    • Possible mastoidectomy in severe cases
    • Watch for complications like meningeal extension or inner ear destruction.