ReviewBrain sciences2021
Understanding Parinaud's Syndrome.
Review in Brain sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Brainstem infarct from cervical vertebral artery dissection presenting as a transient Parinaud syndrome.American journal of ophthalmology case reports · 2025Article
- Convergence Retraction Nystagmus Secondary to Central Nervous System Disseminated Coccidioides Immitis Infection in a Dog.Veterinary medicine and science · 2025Article
- The diagnostic significance of pupillary reflex pathways: insights from classical examination and advanced pupillometry.Frontiers in neuroscience · 2025Review
- Nystagmus in Clinical Practice: From Diagnosis to Treatment-A Comprehensive Review.Clinical ophthalmology (Auckland, N.Z.) · 2025Review
- Parinaud's syndrome: a stroke chameleon.Internal and emergency medicine · 2024Article
- When Pediatric Headaches Are Not Benign-Eye Findings.Children (Basel, Switzerland) · 2023Article
- Diagnosis and Management of Pineal Germinoma: From Eye to Brain.Eye and brain · 2023Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parinaud's syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud's syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud's main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier's sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud's syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud's syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.
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