Acute continuous vertigo, with onset over seconds to hours, is a common symptom. It is often associated with nausea, vomiting, gait unsteadiness, head motion intolerance, and nystagmus. The main diagnostic distinction is between central lesions affecting the brainstem/cerebellum, such as potentially life-threatening posterior circulation stroke, and peripheral lesions, such as vestibular neuritis, which affect the vestibulocochlear nerve. Central lesions require further diagnostic evaluation and directed management of the underlying etiology. Vestibular neuritis (also referred to as vestibular neuronitis or, when associated with hearing loss, labyrinthitis) is thought due to idiopathic inflammation of the vestibular nerve, possibly related to a viral infection. Symptoms typically resolve spontaneously over time, and additional diagnostic testing is generally not necessary.

Distinguishing between recurrent episodes of transient vertigo and persistent, continuous vertigo requires careful, focused questioning of the patient. Patients often misunderstand this question and incorrectly report persistent symptoms either because (1) the vertigo recurs every time they move their head or (2) because between discrete attacks of vertigo they retain a vague persistent feeling of ill-defined incomplete recovery. Both these scenarios are common in benign paroxysmal positional vertigo, the most common cause of transient episodic vertigo.

The presence of abnormalities on the general neurologic examination may indicate involvement of brainstem structures outside of the vestibular system. Critically, it should be recognized that the general neurologic examination has poor sensitivity for identifying a central cause of vertigo; it is often normal even in patients with brainstem or cerebellar lesions.

In contrast to the general neurologic examination, a series of specific bedside tests of eye movement (referred to the “HINTS” examination for head impulse-nystagmus-test of skew) is highly sensitive for identification of central causes of vertigo, possibly even more sensitive than brain magnetic resonance imaging. The three components of the “HINTS” examination are (1) the head impulse test (oculocephalic reflex), (2) assessing the direction of horizontal nystagmus, and (3) testing for vertical ocular alignment.

The classic finding in vestibular neuritis is a mixed horizontal/torsional nystagmus that beats away from the affected ear. The direction of this nystagmus remains the same regardless of which direction the eyes move. In contrast, the classic finding of a horizontal cerebellar nystagmus is nystagmus that beats in the direction of gaze, meaning there is right-beating nystagmus when the patient looks to the right and left-beating nystagmus when the patient looks to the left. This “direction changing” nystagmus thus indicates a central lesion is likely present.

The head impulse test assesses the horizontal oculocephalic reflex. To perform a head impulse test, the patient is asked to fixate on a target like the examiner’s nose and the patient’s head is rapidly moved to the right or left. A patient with an intact oculocephalic reflex will reflexively move their eyes in the opposite direction of head movement to maintain fixation. In a patient with an impaired oculocephalic reflex, their eyes will move with their head. To move their eyes back on the target, they will have a catch-up saccade in the opposite direction of the head movement. An abnormal head impulse test suggests an ipsilateral lesion in the horizontal semicircular canal, eighth cranial nerve, or the vestibular nuclei. An abnormal head impulse test is thus usually but not universally indicative of a peripheral lesion, whereas a normal head impulse test suggests a central lesion.

Vertical misalignment of the eyes in the setting of acute vertigo suggests a skew deviation. When the head is tilted in one direction, the eye in the direction of the head tilt must elevate and the contralateral eye must depress to maintain vertical alignment. In addition, both eyes rotate in the opposite direction of the head tilt. An injury to the peripheral or central vestibular pathway can result in a skew deviation in which the eyes are reflexively positioned as if the head is tilted even though the head is not tilted. A skew deviation is usually but not universally indicative of a central lesion.

The combination of normal vertical ocular alignment, direction-fixed nystagmus, and an abnormal head impulse test is considered a “benign” HINTS bedside examination, as it is consistent with a peripheral lesion such as vestibular neuritis.

Treatment of vestibular neuritis consists primarily of supportive care, as symptoms typically improve spontaneously. Patients with acute vestibular neuritis are often markedly uncomfortable due to vertigo, nausea, and vomiting. Benzodiazepines (such as lorazepam) or antihistamines (such as meclizine or dimenhydrinate) can be used for symptomatic relief but should generally only be used for 24–48 hours as longer use may interfere with vestibular recovery. A program of vestibular rehabilitation exercises may be beneficial for some patients. A short-course of corticosteroids is recommended by some experts to speed time to recovery, though no clear benefit has been shown in randomized trials.