Vertigo and Dizziness in Pokhara: ENT Causes, Diagnosis and Treatment
Dizziness is one of the most common symptoms in general medical practice, yet it is also one of the most diagnostically imprecise — because patients use the word “dizziness” to describe several entirely different sensations, each with different causes and treatments. Correctly classifying the type of dizziness is the first and most important step, because the management of vertigo is completely different from the management of presyncope, and treating the wrong diagnosis with the wrong intervention is ineffective at best and dangerous at worst.
What Is the Difference Between Vertigo, Presyncope and Disequilibrium?
Vertigo is the illusion of movement — the sense that either the person or their surroundings are spinning or moving when they are stationary. It is caused by asymmetric input to the brain from the vestibular (balance) system. Most causes of vertigo are ENT (inner ear or vestibular nerve) in origin, though central nervous system causes (brain) also occur.
Presyncope is the sensation of nearly fainting — lightheadedness, greyness of vision, feeling that consciousness is about to be lost. It is caused by reduced cerebral blood flow, typically from cardiac, cardiovascular, or autonomic causes (low blood pressure on standing — orthostatic hypotension). It is not an ENT problem.
Disequilibrium is a sense of unsteadiness or poor balance, without a spinning sensation. It is most commonly caused by cerebellar or brainstem disease, proprioceptive impairment (peripheral neuropathy), or multisensory impairment in older patients.
Distinguishing which of these the patient is experiencing is the first clinical task, and it is accomplished by careful history-taking — asking the patient to describe the sensation without using the word “dizzy” if possible.
What Is BPPV and Why Is It the Most Common Cause of Vertigo?
Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo, accounting for approximately 20–30% of all vertigo presentations. It is caused by displacement of otoconia — tiny calcium carbonate crystals that normally sit on a membrane in the inner ear — into one of the semicircular canals. When the head is moved, these free-floating crystals create inappropriate fluid movement in the canal, generating a false signal of rotation.
The key features of BPPV are: brief episodes of vertigo (typically 10–30 seconds) triggered by specific head positions — lying down, rolling over in bed, looking up, or bending forward. The vertigo is intense but brief. There is no hearing loss or tinnitus.
The Dix-Hallpike test is the diagnostic test for posterior canal BPPV (the most common variant). The examiner moves the patient from sitting to lying with the head turned 45 degrees to one side and hyperextended over the edge of the examination table. A positive test produces characteristic rotatory nystagmus (rapid involuntary eye movement) after a brief latency. The nystagmus fatigues with repeated testing.
BPPV is not dangerous. It resolves spontaneously in many patients within weeks, but the most efficient treatment is the Epley canalith repositioning manoeuvre — a specific sequence of head movements performed by the clinician over approximately 5 minutes. Efficacy is approximately 80% for posterior canal BPPV after a single treatment session, rising further with repeat treatment. This procedure is performed at A&B International Hospital’s ENT clinic.
What Is Meniere’s Disease?
Meniere’s disease is a disorder of the inner ear caused by endolymphatic hydrops — abnormal accumulation of endolymph fluid in the membranous labyrinth. This produces a classic tetrad of symptoms: episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus (usually low-pitched, like a roaring or humming), and a sense of fullness in the affected ear.
Unlike BPPV, Meniere’s attacks are not triggered by head position and last significantly longer. The hearing loss is distinctive — it affects low frequencies initially, which is opposite to the high-frequency loss of most other sensorineural conditions. Over time, hearing loss can become permanent.
Management aims to reduce attack frequency and prevent progressive hearing loss. Low-salt diet and diuretic therapy (acetazolamide or hydrochlorothiazide) reduce endolymphatic pressure. Betahistine is widely used for its vestibular and microvascular effects. During acute attacks, vestibular sedatives (prochlorperazine) provide symptomatic relief. In refractory cases, intratympanic gentamicin (which ablates vestibular function in the affected ear) or surgery is considered.
What Is Vestibular Neuritis?
Vestibular neuritis is inflammation of the vestibular nerve, usually following a viral illness. It produces a single, severe prolonged episode of vertigo lasting days, accompanied by nausea and vomiting, without hearing loss (which distinguishes it from labyrinthitis, where cochlear involvement produces both vertigo and hearing loss).
The patient typically presents unable to walk without assistance, with continuous rotatory vertigo and severe nausea. Nystagmus is present on examination. The head impulse test is positive — the brain cannot compensate for the sudden rotational stimulus from the affected side.
Treatment is supportive: vestibular sedatives for the acute phase (prochlorperazine, meclizine), steroids if given early, and vestibular rehabilitation exercises (Cawthorne-Cooksey exercises or formal vestibular physiotherapy) to accelerate central compensation. Most patients recover significantly over 6–12 weeks.
When Does Vertigo Indicate a Central Cause Requiring Brain Imaging?
Central causes of vertigo — brainstem stroke, cerebellar stroke, vestibular schwannoma (acoustic neuroma), or multiple sclerosis — require urgent or expedited investigation. Features that distinguish central from peripheral vertigo and should prompt brain imaging include:
Vertigo without a clear positional trigger and with prominent imbalance out of proportion to the vertigo intensity. New onset of severe vertigo in a patient with stroke risk factors — particularly older patients with hypertension, diabetes, or known vascular disease. Vertigo accompanied by other neurological symptoms: double vision, slurred speech, weakness or numbness in the face or limbs, difficulty swallowing. Hearing loss that is sudden and severe (rather than fluctuating). Headache accompanying the vertigo.
The HINTS examination (Head Impulse test, Nystagmus pattern, Test of Skew) performed by an experienced clinician is more sensitive than CT scan in differentiating central from peripheral acute vertigo. Where any doubt exists, MRI of the posterior fossa is the definitive investigation.
What About Altitude-Related Dizziness in Pokhara Trekkers?
Trekkers passing through Pokhara who are ascending to altitude commonly present with symptoms that may overlap with vestibular pathology. Acute mountain sickness (AMS) produces headache, nausea, and lightheadedness above 2,500 m. High-altitude cerebral oedema (HACE) in severe cases produces ataxia and altered consciousness and is a medical emergency requiring immediate descent and dexamethasone.
These altitude-related conditions do not cause true rotatory vertigo and are not treated with Epley or betahistine. They require descent and appropriate altitude sickness management.
A&B International Hospital
Pokhara-02, Bindhyaabasini Way to Sarangkot
Phone: +977 061-412512
Website: abinthospital.com
If you are experiencing episodes of spinning vertigo, particularly when changing head position, or prolonged vertigo with hearing changes, an ENT consultation at A&B International Hospital will provide accurate diagnosis and, for BPPV, immediate treatment. ECHS polycards accepted.
