In the tectum is located posteriorly and contains the quadrigeminal plate, gray matter, and fiber tracts. Longitudinally, the midbrain has three main parts: the tectum, tegmentum, and basis. The midbrain can be divided into two segments: the tegmentum or ventral portion and the tectum or dorsal portion. 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. Finally, ataxia is caused by compression of the superior cerebellar peduncle. We did not find a reasonable explanation for squint. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. 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. 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. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. 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. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. 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. 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. Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain.
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