Vertigo: Causes, Pathophysiology, Differential Diagnosis & Management – Dr. Pothireddy Surendranath Reddy 

Introduction

Vertigo is the false sensation of movement, typically a spinning or rotational feeling, either of oneself or the surroundings. It is one of the most common and distressing symptoms encountered in clinical practice. Though often benign, vertigo may also signal potentially serious pathology, so understanding its causes, underlying mechanisms, differential diagnosis, and management principles is critical.

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In this review, I will discuss:

1. Definition

2. Causes

3. Pathophysiology

4. Differential diagnosis

5. Clinical evaluation

6. Management strategies

7. Prognosis

1. Definition

Vertigo is a subtype of dizziness characterized by the illusion of motion — either that you are moving (e.g., spinning) or that your surroundings are moving. Mayo Clinic+2Mayo Clinic+2

It is distinct from more general “dizziness,” which can mean lightheadedness, imbalance, or presyncope. Mayo Clinic

Vertigo arises when there is a mismatch between sensory inputs (vestibular, visual, somatosensory) or a lesion in the vestibular pathways (inner ear or central nervous system).

2. Causes

The causes of vertigo are heterogeneous. Broadly, they can be classified into peripheral (inner ear) and central (brain) origins, as well as systemic causes that mimic vertigo. NCBI+2WebMD+2

Here are the major causes:

1. Benign Paroxysmal Positional Vertigo (BPPV)

2. Vestibular Neuritis / Labyrinthitis

3. Menière’s Disease

4. Vestibular (Migraine) Migraine

5. Central causes: stroke (especially posterior circulation), demyelinating disease (e.g., multiple sclerosis), brain tumors, cerebellar disorders, drug/toxin-induced vertigo NCBI+1

6. Other systemic causes: orthostatic hypotension, cardiac arrhythmias, dehydration, medications, etc. Mayo Clinic+1

Let’s explore some in greater detail.

2.1 Benign Paroxysmal Positional Vertigo (BPPV)

• This is the most common cause of vertigo. Mayo Clinic

• In BPPV, small calcium carbonate crystals (otoconia) dislodge from the utricle and migrate into one of the semicircular canals (often the posterior canal). Mayo Clinic

• These free-floating particles disturb the endolymph when the head position changes, sending abnormal signals to the brain and provoking vertigo. Mayo Clinic

2.2 Vestibular Neuritis / Labyrinthitis

• Vestibular neuritis is due to inflammation of the vestibular nerve (often viral in origin, e.g., herpes simplex reactivation) PubMed+1

• It causes acute onset of intense, continuous vertigo lasting days, with nystagmus, imbalance, nausea. PubMed

• Labyrinthitis is similar but also involves the cochlear part, so hearing loss or tinnitus may be present.

2.3 Menière’s Disease

• This is characterized by endolymphatic hydrops, i.e., excessive fluid buildup in the inner ear. Mayo Clinic+1

• Patients typically present with episodic vertigo (attacks lasting hours), fluctuating hearing loss, tinnitus, and a feeling of fullness in the ear. Mayo Clinic

• Risk factors / triggers may include high salt intake, caffeine, alcohol, nicotine. Mayo Clinic

2.4 Vestibular Migraine

• Also called migrainous vertigo or vestibular migraine (VM). Medscape+1

• It is among the most common causes of spontaneous episodic vertigo. PubMed+1

• Diagnostic criteria (2021 consensus) require at least 5 episodes of moderate/severe vestibular symptoms lasting 5 minutes to 72 hours, a history of migraine, and migraine features in at least 50% of episodes. PMC

• Other associated symptoms may include nausea, vomiting, motion sickness, auditory symptoms. PMC

2.5 Central Causes

• Lesions in the brainstem or cerebellum can disrupt the vestibular pathways, causing central vertigo. NCBI

• Common etiologies: stroke (posterior circulation), multiple sclerosis, brain tumor, vestibular migraine (already discussed), drug toxicity (e.g., anticonvulsants, aminoglycosides) NCBI

• Central vertigo often presents with neurological signs (ataxia, dysarthria), and imaging may be required. NCBI

2.6 Systemic / Other Causes

• Conditions like orthostatic hypotension (sudden drop in blood pressure on standing), cardiac arrhythmias, dehydration, anemia, hypoglycemia can produce sensations that mimic vertigo or dizziness. Mayo Clinic+1

• Medication side‑effects (antidepressants, anticonvulsants, sedatives) may contribute. Mayo Clinic

3. Pathophysiology

Understanding vertigo requires understanding how the brain processes balance — integrating inputs from vision, proprioception (somatosensory), and the vestibular system.

3.1 Vestibular Anatomy & Normal Function

• The inner ear contains the vestibular labyrinth, which includes three semicircular canals (sensitive to angular acceleration) and the otolith organs (utricle and saccule) that detect linear acceleration and gravity. Mayo Clinic

• Hair cells in these structures detect movement of the endolymph (fluid) and convert it into neural signals.

• These signals go via the vestibular nerve to the brainstem (vestibular nuclei), cerebellum, and higher centers to maintain posture, ocular reflexes, and spatial orientation.

3.2 Mechanisms Leading to Vertigo

1. Peripheral Mismatch:
   When particles (otoconia) dislodge in BPPV, they abnormally stimulate the semicircular canals during head movement, causing a mismatch in signals. Wikipedia

2. Vestibular Hypofunction:
   In vestibular neuritis, inflammation reduces the firing rate of the affected vestibular nerve, creating an asymmetry between the two sides. The brain receives disproportionate vestibular input, generating vertigo. PubMed

3. Fluid Homeostasis Disturbance:
   In Menière’s disease, endolymphatic hydrops distend the membranous labyrinth, altering the biomechanics of hair cells and their firing, leading to episodic vertigo. Mayo Clinic

4. Neurovascular / Central Processing:
   In central vertigo (e.g., stroke), blood flow disruption in cerebellar or brainstem vestibular nuclei causes altered processing. NCBI
   In vestibular migraine, though pathophysiology is not fully understood, there is evidence of activation of trigeminal-vestibular pathways, central sensory sensitization, and altered brain networks during attacks. PubMed+1

5. Sensory Reorganization / Compensation:
   Over time, the brain can compensate for disrupted peripheral input via neuroplastic changes — central compensation helps reduce vertigo intensity/frequency. Vestibular Disorders Association

4. Differential Diagnosis (DDx)

Because vertigo can arise from many etiologies, a structured differential diagnosis is essential.

Here is a breakdown:

Category

Key Conditions

Distinguishing Features

Peripheral Vertigo

BPPV, Vestibular Neuritis, Menière’s Disease, Labyrinthitis

More common, often associated with ear symptoms (in Menière), triggered by head movements (BPPV), acute onset (neuritis)

Central Vertigo

Stroke (cerebellar/brainstem), Multiple Sclerosis, Tumor, Vestibular Migraine, Drug or Toxicity

Neurological signs (ataxia, dysarthria, diplopia), persistent nystagmus not fatigable, not suppressed by visual fixation, imaging findings NCBI

Systemic / Metabolic

Orthostatic hypotension, Arrhythmias, Hypoglycemia, Dehydration

Features of systemic disease, positional changes, BP fluctuations, labs abnormal

Others

Psychiatric (anxiety), Persistent Postural Perceptual Dizziness (PPPD)

Chronic dizziness, sometimes without clear vestibular lesion; overlap with migraine or anxiety

Special Note on Vestibular Migraine vs Other Causes:
Vestibular migraine needs to be differentiated from BPPV, Menière’s disease, and transient ischemic attacks. According to consensus criteria, it requires recurrent episodes, history of migraine, and exclusion of other vestibular disorders. PMC

5. Clinical Evaluation

A systematic approach helps distinguish among causes.

5.1 History

• Onset & duration: Is it sudden (neuritis), brief (BPPV), or prolonged (Menière, migraine)?

• Triggers: Head movements, positional changes, food, stress, medications.

• Associated symptoms: Hearing loss, tinnitus, fullness (Menière); headache, photophobia (migraine); neurological features (central).

• Frequency / recurrence: Episodic vs continuous.

• Risk factors: Vascular risk (stroke), migraine history, infection, recent viral illness, medications.

5.2 Physical Examination

• General neurological exam: Look for ataxia, dysarthria, limb weakness, cranial nerve signs.

• Vestibular testing:

  • Dix-Hallpike maneuver: to provoke nystagmus for posterior canal BPPV.

  • Head impulse test (HIT): to assess vestibulo-ocular reflex (abnormal in peripheral hypofunction).

  • Nystagmus observation: Spontaneous, gaze-evoked, direction-changing. Central causes often show non‑fatigable, direction‑changing nystagmus. NCBI+1

• HINTS exam (Head Impulse, Nystagmus, Test of Skew): useful in acute vertigo to distinguish central vs peripheral causes.

5.3 Investigations

• Audiometry: If hearing symptoms (Menière).

• Vestibular function tests: Video-nystagmography (VNG), caloric testing, vestibular-evoked myogenic potentials (VEMPs).

• Imaging: MRI (especially brainstem/cerebellum) if central signs or when stroke is suspected. Important to note: MRI can be falsely negative in the first 48 hours post-stroke; HINTS-positive may still indicate central cause. NCBI

• Laboratory / systemic work-up: BP, orthostatic vitals, blood glucose, ECG, etc.

6. Management

Management of vertigo depends on the cause, acuity, severity, and impact on quality of life.

Here are the key strategies:

6.1 General Principles

• Identify and treat underlying cause.

• Symptomatic relief (vestibular suppressants) in the acute phase.

• Encourage vestibular rehabilitation (central compensation) as soon as feasible.

• Educate patient on safety (risk of falls), lifestyle modifications, and prevention.

6.2 Specific Treatment by Etiology

1. BPPV

   • Canalith repositioning maneuvers (e.g., Epley maneuver) to move otoconia out of the semicircular canal. Mayo Clinic+1

   • In some cases, patients can be taught to perform these maneuvers at home. Mayo Clinic

   • Rarely, surgical options like canal plugging may be considered if maneuvers fail. Mayo Clinic

2. Vestibular Neuritis

   • In acute phase: vestibular suppressants (e.g., antihistamines like meclizine, benzodiazepines) for nausea and severe vertigo. However, these should be used short-term, because prolonged suppression can delay central compensation. AIIMS Rishikesh+2Neuropt+2

   • Once acute symptoms subside: vestibular rehabilitation therapy — gaze stabilization exercises, balance training. Neuropt+1

   • Prognosis good: many patients recover with compensation; per meta-analyses, outcomes are favorable. PubMed

3. Menière’s Disease

   • Lifestyle modifications: low-sodium diet, limit caffeine/alcohol/tobacco. Mayo Clinic

   • Diuretics may be used to reduce endolymphatic pressure. AIIMS Rishikesh

   • During acute attacks: vestibular suppressants, antiemetics, rest.

   • In refractory cases: intratympanic gentamicin (ablative), endolymphatic sac decompression surgery, or other surgical interventions, depending on severity and hearing status.

4. Vestibular Migraine

   • Pharmacologic prophylaxis: based on migraine preventive therapies — beta-blockers, tricyclics, antiepileptics, SNRIs, etc., tailored to patient. Medscape

   • Acute management: antiemetics, vestibular suppressants (short-term), abortive migraine medications.

   • Vestibular rehabilitation: particularly helpful when chronic imbalance or motion sensitivity persists. Medscape

   • Lifestyle modifications: identifying and avoiding triggers (diet, stress, sleep), adaptation strategies.

   • Psychotherapy: for associated anxiety, motion sickness, symptom persistence. According to vestibular‑migraine guideline resources, therapeutics also target psychological comorbidity. Vestibular Disorders Association

5. Central Vertigo

   • Stroke: If acute posterior circulation stroke, management as per stroke protocol (e.g., thrombolysis if within window, supportive care). NCBI

   • Multiple sclerosis: Treat with disease-modifying therapy, symptomatic treatment.

   • Tumors: Neurosurgical / oncological management as appropriate.

   • Drug-induced: Remove or reduce offending agent if possible.

   • Throughout: vestibular rehabilitation to enhance compensation.

6.3 Supportive Measures

• Fall risk mitigation: ensure good lighting, remove tripping hazards, may use cane if needed. Mayo Clinic

• Patient education: explain the benign nature (if so), reassure during acute attacks, give home exercises.

• Consider psychological support: many patients develop anxiety around vertigo; vestibular disorders are often associated with psychological comorbidity. Vestibular Disorders Association

6.4 Medication Summary (based on Standard Treatment Guidelines)

According to AIIMS (Rishikesh) Standard Treatment Guidelines: AIIMS Rishikesh

• Antihistamines: Meclizine, Dimenhydrinate

• Benzodiazepines: Diazepam, Clonazepam

• Anticholinergics: Scopolamine (patch, for motion sickness)

• Diuretics + low-sodium diet (for Menière)

• Antimigraine agents (for vestibular migraine)

• SSRIs for psychosomatic vertigo

7. Prognosis and Follow-Up

• Many causes of vertigo (like BPPV and vestibular neuritis) have good prognosis if diagnosed and managed appropriately.

• Central causes’ prognosis depends on the underlying disease (e.g., stroke, tumor).

• Vestibular rehabilitation plays a critical role: patients who actively perform gaze stabilization and balance exercises typically compensate better.

• Recurrence: BPPV can recur, so patients should be educated about self‑maneuvers.

• Chronic dizziness (e.g., from vestibular migraine) may require long-term management, including lifestyle changes, prophylactic meds, and therapy.

Summary (Key Points)

1. Vertigo is a false sensation of movement and arises from mismatched or abnormal vestibular input.

2. Causes are broadly peripheral (inner ear), central (brain), or systemic.

3. The most common causes include BPPV, vestibular neuritis, Menière’s disease, and vestibular migraine.

4. A careful history, vestibular examination (including Dix-Hallpike, HIT, HINTS), and appropriate investigations (audiometry, imaging) are vital to diagnosis.

5. Management is cause-specific: repositioning maneuvers for BPPV, vestibular rehab for neuritis, preventive therapy for migraine, etc.

6. Supportive care, patient education, and fall prevention are essential.

7. Many patients recover well, especially with early diagnosis and rehabilitation.

References & Further Reading

• Mayo Clinic — BPPV: Symptoms & causes. Mayo Clinic

• Mayo Clinic — Dizziness: Diagnosis & treatment. Mayo Clinic+1

• Menière’s Disease – Mayo Clinic. Mayo Clinic

• Vestibular Neuritis – PubMed review. PubMed

• Vestibular Migraine – Diagnostic criteria (Barány Society / IHS). PMC

• Vestibular Migraine – Medscape overview. Medscape

• Central Vertigo – StatPearls. NCBI

• Vestibular Disorders Association – Pathophysiology & treatment. Vestibular Disorders Association

• AIIMS Rishikesh Standard Treatment Guidelines, CNS diseases (vertigo section). AIIMS Rishikesh

Reference;

https://my.clevelandclinic.org/health/symptoms/21769-vertigo

https://www.webmd.com/brain/vertigo-symptoms-causes-treatment

https://en.wikipedia.org/wiki/Vertigo

https://www.ncbi.nlm.nih.gov/books/NBK482356

https://medlineplus.gov/ency/article/001432.htm

https://www.healthline.com/health/vertigo

https://www.mayoclinic.org/diseases-conditions/vertigo/symptoms-causes/syc-20370055