Abstract

Purpose: Understand the pathophysiology of the signs and symptoms of Parinaud’s syndrome

Methods:We did an advances search strategy and a MeSH subheading search strategy using the terms. We included only studies conducted in humans in the last 25 years, written in English language

Results: After applying the inclusion/exclusion criteria wegathered25 papers for the discussion of the paper.

Conclusion: Parinaud's syndrome's main symptoms are diplopia, blurry vision, visual field defects, ptosis, squint, and ataxia. Diplopia is caused mainly due to involvement of the IV nerve. Blurry vision is related to accommodation problems, while the visual field defects are thought to be a consequence of chronic papilledema that causes optic neuropathy. The ptosis in Parinaud's syndrome is caused by damage of the oculomotor nerve. We did not find a good explanation forsquint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.

Parinaud's syndrome's main signs are Upward gaze paralysis, upper eyelid retraction, convergence/retraction nystagmus (CRN), and pseudo-Argyl Robertson pupils. Two nuclei are involved in the upward gaze palsy, riMLF and Cajal's. When downgaze is compromised, there is an involvement of the posterior commissure or pretectal area. Collier's sign occurs when there is damaged of the posterior commissure. The posterior commissure controls the saccade's speed have and inhibited the eyelid upgaze. CRN is a vergence anomaly, not a saccadic anomaly. CRN arises from a dysfunction of rostral interstitial nuclei of the riMLF and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the supranuclear fibers' lack of inhibition. External compression of the posterior commissure causes the pseudo-Argyl Robertson pupils. Pseudo-Argyl Robertson pupils conserved some response to light because there is an additional pupillary light response pathway that involves attention to a conscious bright dark stimulus.