Vestibular (Peripheral) Vertigo
The pathophysiology of vestibular vertigo can be difficult to understand, so lets start at the beginning. The semicircular canals and the ampulla detect rotations movements. The utricle and the saccule detect changes in head position relative to gravity. This is achieved via the otolithic membrane within them as shown in the video below.
BPPV
If otolith debris migrates in to the semicircular canal it can either adhere to the cupula (cupulolithiasis) or lies within the canal (canalalithiasis) which causes inappropriate deflection of the cupula. This is demonstrated in the following video.
As such BPPV is caused by hyperfunction, as opposed to the other causes of vestibular vertigo which are the result of vestibular hypofunction. This is relevant clinically as the nystagmus provoked by BPPV will result in the fast phase being towards the affected ear.
Nystagmus
Nystagmus from a vestibular cause follow a set of rules:
- Direction of nystagmus remains the same regardless of direction of gaze
- Intensity of nystagmus reduces with fixation
- Usually a mixed torsional (rotational) and horizontal nystagmus
- Abide by Alexander’s Law “the intensity of the nystagmus increases when the eye moves in the direction of the fast-phase
Alexander’s Law is demonstrated in the following video:
