Dizziness and Vertigo: Finding the Neurological Cause

The single most important question in any vertigo evaluation is whether the problem originates in the inner ear or in the brain. Peripheral vertigo—caused by conditions such as benign paroxysmal positional vertigo (BPPV), vestibular neuritis, or Ménière’s disease—is far more common and almost always treatable. Central vertigo, arising from the brainstem or cerebellum, is less common but carries serious diagnostic implications including stroke, multiple sclerosis, and cerebellar degeneration.

The problem is that this distinction requires a neurological examination. Most dizzy patients are seen in urgent care or by their primary care physician, given meclizine, and told to follow up if it doesn’t resolve. A 2009 study by Newman-Toker and colleagues published in Academic Emergency Medicine found that stroke was missed in approximately 35% of patients presenting with dizziness to the emergency department when the chief complaint was isolated vertigo without obvious focal deficits. The standard triage approach treats dizziness as a symptom to suppress rather than a sign to decode.

Peripheral vertigo tends to produce intense spinning triggered by head position, with a clear onset and offset. The nystagmus is unidirectional, follows predictable patterns, and fatigues with repeated testing. Central vertigo, by contrast, often presents with less dramatic spinning but more severe imbalance, direction-changing nystagmus, and subtle neurological signs that a non-specialist may not detect. A patient who cannot walk a straight line but whose room isn’t spinning may have a more dangerous problem than the patient who grips the exam table during a Dix-Hallpike maneuver.

Our evaluation begins with the examination itself. Before any imaging is ordered, a careful bedside assessment of eye movements, positional triggers, gait stability, and coordination can distinguish peripheral from central causes with a sensitivity that rivals or exceeds imaging in the acute setting. The HINTS exam (Head Impulse, Nystagmus, Test of Skew), when performed by a neurologist, has been shown to outperform early MRI in identifying posterior circulation stroke presenting as vertigo (Kattah et al., 2009, Stroke).

The reason so many dizzy patients cycle through specialists without improvement is that treatment was started before a diagnosis was made. Meclizine suppresses vestibular input indiscriminately. It may reduce nausea for a few hours, but it does nothing to address the underlying mechanism and can actually delay compensation in vestibular neuritis.

At NGP, treatment follows diagnosis. BPPV patients receive canalith repositioning in the office, which resolves their vertigo in a single session in the majority of cases. Vestibular neuritis patients receive a recovery plan built around vestibular rehabilitation and, where metabolic factors are contributing, targeted IV nutrient support to optimize nerve recovery.

Vestibular migraine patients benefit from the same migraine-specific treatment approach we use for headache patients: trigger identification, preventive pharmacotherapy, and metabolic optimization. For patients with significant migraine burden, our Botox chemodenervation and occipital nerve block protocols reduce both headache frequency and vestibular episodes.

Central vertigo patients require a different trajectory entirely. When imaging reveals a structural lesion, vascular event, or demyelinating disease, we coordinate with neurosurgery, vascular neurology, or neuroimmunology colleagues as indicated. Our clinic serves as the diagnostic entry point: we identify the cause, initiate workup, and ensure the patient reaches the right subspecialty team without delay.