Peripheral versus Central Vestibular Disorders Characteristics

Peripheral versus Central Vestibular Disorders Characteristics

What distinguishes peripheral from central causes of vestibular dysfunction? 

Most patients with peripheral vestibular dysfunction have more severe vertiginous symptoms, while those with central nervous system etiology usually do not have severe vertigo.

Patients with peripheral vertigo may have short episodes, lasting seconds (benign positional vertigo), minutes (Ménière’s disease), or hours (vestibular neuritis).

Auditory symptoms (hearing loss, tinnitus, and aural fullness) are more frequently associated with peripheral vestibular disease.

Position changes associated with vertigo are more often related to peripheral causes. Central causes of vestibular dysfunction have a more variable presentation, which may be described as tilting to one side, or nonspecific lightheadedness or clumsiness.

Associated symptoms of diplopia, such as dysphasia, dysarthria, hemiparesis, cephalgia, seizures, memory loss, or sensory findings, suggest central etiology. In central vestibular dysfunction, the nystagmus is usually more prominent than symptoms and may be disconjugate.

Visual fixation suppresses peripheral nystagmus and increases amplitude of the central nystagmus.

Peripheral versus Central Vestibular Disorders Characteristics

PeripheralCentralBothNotes
Alexander’s lawNo Alexander’s lawVertigo
Visual suppression at least partlyNo visual suppressionDisequilibrium
Positional, classical D–HNot positionalNausea
Normal saccades, pursuit, OKNPossible abnormal saccades, pursuit, OKNHearing loss
Possible: hoarseness, difficulty swallowing, mixed sensory loss characteristic of lateral medullary syndromeSudden onset of symptoms
Minor skew deviationLarge skew deviation
No gaze-evoked nystagmusGaze-evoked nystagmus is present
Possible impaired C-VEMPPossible impaired O-VEMPDetails still unclear in this new area
Bithermal caloric weaknessNo caloric weaknessIf rotatory chair is impaired and caloric weakness is not present the problem may still be peripheral
Rotatory chair VOR decreased gain but intact phasesRotatory chair decreased gain and abnormal phasesBoth caloric impairment and rotatory impairment may be present in either central or peripheral

D–H , Dix–Hallpike; OKN , optokinetic nystagmus; C-VEMP , cervical vestibular evoked myogenic potentials; O-VEMP , ocular evoked myogenic potentials; VOR , vestibulo-ocular reflex.

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