A6 Vestibular and Acoustic Balance Dysfunction

Topic

When the head turns, its angular acceleration acts upon the semicircular canals of the inner ear, which function like a hydraulic gyroscope. Each canal contains a closed loop of endolymph that, due to inertia, tends to lag behind the canal's movement when the head begins to turn. This difference creates a relative flow of endolymph that persists as long as the angular acceleration continues and ceases when the head stops accelerating, even if it keeps turning at a constant speed.

The endolymph flow pushes against the cupula, a gelatinous structure spanning the narrowest part of the semicircular canal. The cupula deforms in response to the force of the flow, bending the vestibular hair cells embedded within it. The greater the flow produced by angular acceleration, the greater the deformation of the cupula and the displacement of these cells.

The bending of the hair cells alters the firing rate of the vestibular nerve: movement in one direction increases activity above the baseline level, while movement in the opposite direction decreases it. At rest, both vestibular nerves exhibit similar baseline rates; consequently, the brain detects no difference between the two sides and perceives no rotation. During actual angular acceleration, however, the semicircular canals on both sides respond in opposite ways: the firing rate of one vestibular nerve increases while that of the opposite side decreases.

The brain interprets the difference between the two nerves as an asymmetry in firing rates. Under normal conditions, this asymmetry arises from angular acceleration and is interpreted as head movement. Vertigo occurs when a similar asymmetry arises in the absence of actual angular acceleration. Since the brain cannot independently distinguish whether the difference stems from a genuine turn or a vestibular system disturbance, it interprets the signal as movement, creating the sensation that the head or the surroundings are spinning, even though the head remains stationary. A common cause of this abnormal signal is dislodged otoconia. These tiny crystals normally remain fixed in another region of the inner ear but can break loose and enter a semicircular canal. When the head's position changes relative to gravity, the otoconia shift within the canal even in the absence of actual rotation. Their movement drags the endolymph along, creating an abnormal flow that deforms the cupula in a manner similar to angular acceleration. Consequently, a temporary asymmetry arises between the firing rates of the two vestibular nerves, and the brain interprets this signal as rotation. The episode recurs whenever the person assumes positions that trigger the otoconia to shift again within the affected canal.

Vestibular asymmetry can also result from more permanent damage to one of the vestibular nerves; therefore, corrective approaches depend on the underlying cause. Repositioning maneuvers employ a calculated sequence of head positions, using gravity to move the dislodged otoconia out of the semicircular canal where they had become trapped. Once their movement within the canal ceases, the abnormal endolymph flow stops, and symmetry between the vestibular signals is restored.

Vestibular rehabilitation works differently. It does not directly alter the semicircular canals or the endolymph; instead, it fosters brain adaptation to a persistent asymmetry between the two vestibular nerves. Through this process, the brain gradually learns not to interpret a stable difference between the signals from the two sides as evidence of actual rotation. Thus, even if the asymmetry does not disappear completely, its perceptual manifestation as vertigo—when the head is not turning—is reduced.

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