![]() This vertical palsy is supranuclear, so doll’s head maneuver should elevate the eyes, but eventually all upward gaze mechanisms fail. Paralysis of upgaze: Downward gaze is usually preserved. Parinaud’s Syndrome is a cluster of abnormalities of eye movement and pupil dysfunction, characterized by: Parinaud’s syndrome, includes multiple clinical signs, with the most prominent being paralysis of upward gaze. This case demonstrates the imaging features of tumefactive venous infarction in SIH and highlights the risk of misinterpretation as a neoplasm with potentially catastrophic consequences 7). However, this patient underwent a brainstem biopsy, which in retrospect may have been avoidable. ![]() The patient was ultimately diagnosed with tumefactive venous infarction secondary to SIH. Isolated Oculomotor Nerve Nucleus Infarct 5).Ī case of longstanding, undiagnosed spontaneous intracranial hypotension (SIH) with an acute presentation of Parinaud’s syndrome, in whom serial imaging demonstrated development of a midbrain mass. Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson’s disease, kernicterus, and barbiturate overdose. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome. Older patients following stroke of the upper brainstem However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. ![]() A video demonstrates a convergence-retraction nystagmus on upgaze and failure of accommodation, and her brain imaging confirms a corresponding pre-tectal contrast enhancing T2 hyperintense lesion suggestive of demyelination 4). Women in their 20s-30s with multiple sclerosis.Ī 26 year old Pakistani lady with first presentation of a demyelinating event, presenting as Parinaud’s syndrome. ![]() Pineal region tumor: Pinealoma (intracranial germinomas) are the most common lesion producing this syndrome). Gradual benign loss of upgaze in senescence.Ĭlassically, it has been associated with three major groups: Stroke or brainstem hemorrhage in the upper part. Finally, ataxia is caused by compression of the superior cerebellar peduncle.Parinaud’s Syndrome results from injury, which compresses the the quadrigeminal plate at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF), specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.Ī dilated suprapineal recess can compress the mesencephalic tectum, due to hydrocephalus. 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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