It has less commonly been associated with spasm of accommodation on attempted upward gaze, pseudoabducens palsy (also known as thalamic esotropia) or slower movements of the abducting eye than the adducting eye during horizontal saccades, see-saw nystagmus and associated ocular motility deficits including skew deviation, oculomotor nerve palsy, trochlear nerve palsy and internuclear ophthalmoplegia. Causes
Parinauds syndrome results from injury, either direct or compressive, to the dorsal midbrain. 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. Classically, it has been associated with three major groups:

Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome. Women in their 20s-30s with multiple sclerosis
Older patients following stroke of the upper brainstemHowever, 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. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome. Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilsons disease, kernicterus, and barbiturate overdose. Diagnosis
Diagnosis can be made via combination of physical exam, particularly deficits of the relevant cranial nerves. Confirmation can be made via imaging, such as CT scan or MRI. Treatment
Treatment is primarily directed towards etiology of the dorsal midbrain syndrome.
For unilocular GOCs with minimal tissue deterioration, "enucleation, curettage, and marsupialization" is a suitable treatment plan. Notably, the performance of enucleation or curettage as the primary action is linked to an incomplete extraction of the GOC and is only recommended to the less invasive lesions. Multilocular GOCs require a more invasive procedure such as "peripheral ostectomy, marginal resection, or partial jaw resection". GOCs associated with a more severe structural damage are encouraged to undergo marsupialization as either an initial or supplementary surgery. The frequency of reappearance is likely due to the lingering cystic tissue structures that remain after the performance of curettage. The incorporation of a "dredging method i.e. repetition of enucleation and curettage" is also suggested until the remnants of the GOC diminishes for certain. The treatment ensures scar tissue is removed to promote the successful reconstruction of osseous material for jaw preservation. Alongside the main treatments, bone allograft application, cryosurgery, and apicoectomy are available but have not been consistently recommended. Though Carnoys solution, the chloroform-free version, is recommended with the treatment as it degenerates the majority of the damaged dental lamina. The most effective type of treatment remains unknown due to the lack of detailed data from reported cases. Post-treatment protocols
Follow-up appointments are necessary after the removal of the GOC as there is a high chance of remission, which may be exacerbated in cases dealing with "cortical plate perforation". The GOC has a significant remission rate of 21 to 55% that can potentially develop during the period of 0.5 to 7 years post-surgery.