E. Lee Murray, MD
OVERVIEW
Hospital neurology consultation in the field of neuro-otology is usually for the following scenarios:
Most central causes of these symptoms are usually associated with other clinical findings that eclipse these complaints. The role of the neurologist is to ensure that neurologic causes are considered and to promote appropriate ENT evaluation and treatment as needed.
VESTIBULOPATHIES
Vestibulopathies are common, with the idiopathic variety being the most common diagnosis. Here we consider primary vestibulopathies; also considered in the differential diagnosis are central causes. In general, central causes are less likely to produce sustained nystagmus and are more likely to have associated nonvestibular symptoms. Diagnoses to be considered may be multiple sclerosis, stroke, brainstem tumor, and infections affecting the brainstem. Vestibulopathies include:
•Benign paroxysmal positional vertigo
◦Episodes of vertigo and nystagmus with change in head position or specific head position, especially turning or bending over
◦Diagnosed by clinical exam with maneuvers discussed below
◦Imaging often not needed especially with classic presentation and examination
◦Treated by repositioning maneuvers, as discussed below. Medical treatment may include antihistamines, benzodiazepines, and/or antiemetics.
◦While most causes of vestibulopathy are idiopathic, head trauma can cause vestibular symptoms by injury directly to the labyrinth or CN 8. Hearing loss is common.
◦Episodes of vertigo with tinnitus and ultimately hearing loss
◦Diagnosis is by clinical exam. MRI may be necessary to evaluate for acoustic nerve lesion but often is not needed with classic presentation.
◦Treatment of acute attacks is with antihistamines, benzodiazepines, and/or antiemetics. Prevention of attacks with diuretics and diet is often prescribed but limited in established efficacy
◦Progressive hearing loss often with vertigo that may be positional. Distinguished from many other causes by the conductive nature of the hearing loss.
◦Diagnosis is clinical with the conductive loss. Differentiation from Ménière disease is most important.
◦Treatment is often with surgery.
Regardless of cause, some of the most effective agents for vertigo include antihistamines, anticholinergics, benzodiazepines, and antiemetics. Some representative individual agents include:
Benign Paroxysmal Positional Vertigo
Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo but is an uncommon cause of hospital admission; but because this can occur in patients with vascular risk factors, admission sometimes occurs for rapid evaluation and treatment. Patients often reports gait difficulty so posterior circulation stroke is often considered in the differential diagnosis.1
PRESENTATION is with abrupt onset of vertigo with change in head position. Symptoms are often noted on waking, especially with sitting up or turning over in bed. Symptoms often abate within 30 secs or less, and symptoms are minimal if the head is still.
DIAGNOSIS is suspected with positional vertigo in the absence of other neurologic symptoms. Differential diagnosis includes stroke, demyelinating disease, and intoxication. Dix-Hallpike maneuvers are diagnostic for many patients. If there is still any doubt or if the maneuvers are inconclusive, then magnetic resonance imaging (MRI) of the brain is appropriate to look for infarction or other structural or inflammatory lesion. MR angiography (MRA) or computed tomography angiography (CTA) may not be needed if no vascular changes are seen on the MRI, but small posterior circulation infarctions may be missed on MRI.
MANAGEMENT usually includes vestibular rehab and medications for vertigo such as meclizine and benzodiazepines, which are often of only modest effectiveness. The Epley canalith repositioning procedure is curative for many patients,2 but symptoms may recur.
Vestibular Neuropathy
Vestibular neuropathy is a dysfunction of the vestibular system giving symptoms related to incongruent signals from the vestibular apparatuses. The cause is idiopathic in most patients, but some etiologies that have been implicated include HSV-13 and trauma. This category might have been labeled vestibular neuronitis, but since there is not documentation of an inflammatory component for most patients, the present term is preferred.
PRESENTATION is typically with vertigo that is often severe, lasting for hours or days. Symptoms increase with head movement but are always present during the episode and do not have the degree of exacerbation with movement that would be expected with BPPV. Nausea and vomiting are common. Exam shows nystagmus with the fast phase away from the affected side, although the nystagmus may only be visible with provocation. Gait is often impaired but appendicular coordination is normal.
DIAGNOSIS is suggested by vertigo with more of a steady symptomatology than BPPV. Gait ataxia and nystagmus are supportive. The Hallpike maneuver is especially helpful for patients who do not have characteristic nystagmus on examination.
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