Verticle Gaze Palsy

Question 1

Vertical Gaze centre

Answer 1

The vertical gaze center, on the other hand, is located in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) in the upper midbrain. The riMLF controls the movement of the eyes vertically, allowing them to move up and down.

The right inset shows the brain-stem pathways for vertical gaze. The region of the riMLF appears to be most important for generating downgaze, whereas the posterior commissure region appears most important for generating upgaze. Vestibular input for vertical gaze arises in the contralateral vestibular nucleus, decussates, and ascends in the MLF to the oculomotor nucleus and the trochlear nucleus.

Vertical gaze does have one center in the cerebral cortex. Diffuse degeneration of the cortex (such as with dementia) can diminish the ability to move the eyes vertically (particularly upward).

Question 2

Vertical Gaze Palsy features

Answer 2

An inability to make a conjugate ocular movement in one direction
This does not cause diplopia since the visual axes remain parallel
By investigating each reflex and conjugate movement in turn, it is possible to establish where a lesion exists

Isolated supranuclear vertical gaze palsies are characterised by preservation of vestibular movement. Bell’s phenomenon, the VOR and caloric nystagmus will generate eye movements into the affected direction of gaze. Large lesions and progressive disease often also affect the adjacent ocular motor nuclei and infranuclear pathways, leading to loss of vestibular movement

Large lesions and progressive diseases may also affect adjacent ocular motor nuclei and infranuclear pathways, leading to loss of vestibular movement

Question 3

Vertical Gaze Palsy where do down gaze deficits and up-gaze deficits arise from?

Answer 3

Down-gaze Deficits:
Arise from bilateral lower center lesions.
Up-gaze Deficits:
Can arise from a unilateral lesion affecting the fibers and nuclei in the posterior commissure.