

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. Parinaud's may be associated with cranial nerve IV palsy, resulting in “down and out” deviation of the affected eye and often accompanied by a compensatory head tilt to the contralateral side.Understanding Parinaud's Syndrome. We highlight the importance of considering this condition in the context of multiple medications and increased anticholinergic burden. Upper eyelid retraction (Collier's sign) A young woman presented with blurred vision due to anticholinergic syndrome.It has been reported in patients with diabetes mellitus, multiple sclerosis, Wernicke’s encephalopathy, sarcoidosis, tumours, and haemorrhage.1 Although the appearance of pseudo-Argyll Robertson pupil is. Attempts at upward gaze often produce this phenomenon A pseudo-Argyll Robertson pupil is a neurological sign indicating a normal near reflex but the absence of a light reflex (light-near dissociation), a lack of miosis, and pupil irregularity.Pupils respond poorly to light but will constrict with accommodation.This vertical palsy is supranuclear, so a doll’s head maneuver may elevate the eyes, but eventually all upward gaze mechanisms fail.

Physical findings are related to increased ICP in the dorsal midbrain:

Three symptoms and signs (RED flags) for increased ICP may also develop: High grade astrocytomas generally have a much shorter history of these problems prior to presentation. Intermittent headaches related to increased intracranial pressure (ICP).Often non-specific and non-localizing initially.Generally present with a long history of signs and symptoms.
