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.
Highlights
In Parinaud’s syndrome or dorsal midbrain syndrome, the two structures that are mainly and causally involved in the symptomatology are the midbrain and the pineal gland.The midbrain can be divided into two segments: the tegmentum or ventral portion and the tectum or dorsal portion
We start with a brief discussion of the differential diagnosis of Parinaud’s syndrome and its main etiologies, and we proceed to review the pathophysiology of the sign and symptoms of the disease
A lesion in the inhibitory nuclei of the posterior commissure nucleus of the posterior commissure (nPC) decreases the M group’s inhibition, which increases the excitatory output to the central caudal nuclear (CCN) [26]
Summary
In Parinaud’s syndrome or dorsal midbrain syndrome, the two structures that are mainly and causally involved in the symptomatology are the midbrain and the pineal gland. In the tectum is located posteriorly and contains the quadrigeminal plate, gray matter, and fiber tracts [1]. The oculomotor nucleus is located more ventrally than the trochlear nucleus [1] It can be divided by the superior and inferior colliculus [2]. The pineal gland is surrounded by stromal cells [3] It is bordered ventrally by the midbrain and quadrigeminal plate, posteriorly by the splenium of the corpus callosum, rostrally by the third ventricle, and caudally by the vermis of the cerebellum [5]. This study covers the differential diagnosis and the etiologies of Parinaud’s syndrome, follow by a review of the pathophysiology of the signs and symptoms of Parinaud’s syndrome
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