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Understanding Parinaud’s Syndrome

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’...

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Autores principales: Ortiz, Juan Fernando, Eissa-Garces, Ahmed, Ruxmohan, Samir, Cuenca, Victor, Kaur, Mandeep, Fabara, Stephanie P., Khurana, Mahika, Parwani, Jashank, Paez, Maria, Anwar, Fatima, Tamton, Hyder, Cueva, Wilson
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8615667/
https://www.ncbi.nlm.nih.gov/pubmed/34827468
http://dx.doi.org/10.3390/brainsci11111469
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author Ortiz, Juan Fernando
Eissa-Garces, Ahmed
Ruxmohan, Samir
Cuenca, Victor
Kaur, Mandeep
Fabara, Stephanie P.
Khurana, Mahika
Parwani, Jashank
Paez, Maria
Anwar, Fatima
Tamton, Hyder
Cueva, Wilson
author_facet Ortiz, Juan Fernando
Eissa-Garces, Ahmed
Ruxmohan, Samir
Cuenca, Victor
Kaur, Mandeep
Fabara, Stephanie P.
Khurana, Mahika
Parwani, Jashank
Paez, Maria
Anwar, Fatima
Tamton, Hyder
Cueva, Wilson
author_sort Ortiz, Juan Fernando
collection PubMed
description 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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spelling pubmed-86156672021-11-26 Understanding Parinaud’s Syndrome Ortiz, Juan Fernando Eissa-Garces, Ahmed Ruxmohan, Samir Cuenca, Victor Kaur, Mandeep Fabara, Stephanie P. Khurana, Mahika Parwani, Jashank Paez, Maria Anwar, Fatima Tamton, Hyder Cueva, Wilson Brain Sci Review 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. MDPI 2021-11-06 /pmc/articles/PMC8615667/ /pubmed/34827468 http://dx.doi.org/10.3390/brainsci11111469 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Ortiz, Juan Fernando
Eissa-Garces, Ahmed
Ruxmohan, Samir
Cuenca, Victor
Kaur, Mandeep
Fabara, Stephanie P.
Khurana, Mahika
Parwani, Jashank
Paez, Maria
Anwar, Fatima
Tamton, Hyder
Cueva, Wilson
Understanding Parinaud’s Syndrome
title Understanding Parinaud’s Syndrome
title_full Understanding Parinaud’s Syndrome
title_fullStr Understanding Parinaud’s Syndrome
title_full_unstemmed Understanding Parinaud’s Syndrome
title_short Understanding Parinaud’s Syndrome
title_sort understanding parinaud’s syndrome
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8615667/
https://www.ncbi.nlm.nih.gov/pubmed/34827468
http://dx.doi.org/10.3390/brainsci11111469
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