In the dorsal midbrain (Parinaud's) syndrome, the classic triad includes upgaze palsy, convergence-retraction nystagmus, and light-near dissociation. The neural substrate for convergence-retraction nystagmus is:

• A Damage to the medial rectus subnuclei of CN III causing synchronous bilateral medial rectus palsy
• B Interruption of the posterior commissure fibers carrying upgaze signals from the interstitial nucleus of Cajal
• C Lesion of the rostral interstitial nucleus of the MLF (riMLF) affecting vertical saccade generation
• D Disinhibition of convergence neurons in the midbrain reticular formation causing co-contraction of all extraocular muscles on attempted upgaze ✓

Explanation

Convergence-retraction nystagmus in Parinaud's syndrome occurs on attempted upgaze when there is disinhibition of midbrain convergence burst neurons. Normally, these neurons are inhibited during upgaze. In dorsal midbrain lesions, this inhibition is lost, causing co-contraction of all extraocular muscles (especially the medial recti) on attempted upward saccades. This produces quick convergent movements of the eyes with simultaneous globe retraction into the orbit (due to co-contraction of all recti pulling the globe posteriorly). Elicited by upward optokinetic tape, the convergence-retraction response is pathognomonic of dorsal midbrain dysfunction from pinealoma, hydrocephalus, or periaqueductal lesions.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

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Written and medically reviewed by the StethoPrep medical team.