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The natural history of brainstem ocular motility disorders due to vascular pathology
Published in Jan-Tjeerd de Faber, 28th European Strabismological Association Meeting, 2020
Four of our patients had a third palsy. Two patients had a nuclear third nerve palsy, one patient had a complete left third nerve palsy and limited movement in the right eye corresponding to contralateral superior rectus involvement and the second patient had a complete right third nerve palsy with a contralateral superior division third nerve palsy. The bilateral defect is due to the anatomy of the nucleus and its fibres. The fibres for superior rectus function pass through the contralateral superior rectus subnucleus without synapse and innervate the contralateral superior rectus (Bienfang 1975). Therefore lesions in this region cause ipsilateral third nerve palsies and contralateral superior rectus weakness. Levator function is under bilateral control at the level of the third nerve nuclei due to the bilateral organisation of the caudal central subnucleus that supplies the levator muscle (Leigh & Zee 1991) and therefore can result in bilateral ptosis. Two patients had a fascicular lesion resulting in a third nerve palsy without pupil involvement but also with a vertical gaze palsy. Fascicular lesions can give additional signs such as hemiplegia, central Horner’s syndrome and intention tremor, e.g. Weber’s syndrome, Benedikt’s syndrome and Claude’s syndrome.
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Claude Syndrome Ipsilateral paralysis of the third and fourth nerves with contralateral hemianesthesia, due to compression of the arterial supply to the inferior nucleus ruber (red nucleus) by mesencephalic lesions. First described by French neurologist, Henri C.J. Claude (1869–1945) of Paris in 1912.
Brain regions, lesions, and stroke syndromes
Published in Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees, Stroke in Practice, 2017
Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees
Claude’s syndrome. Named after French psychiatrist and neurologist Henri Claude; is produced by paramedian upper midbrain and cerebro-thalamic connection infarction; manifests with ipsilateral CN III palsy and contralateral cerebellar signs.
Isolated Ocular Motor Nerve Palsies
Published in Journal of Binocular Vision and Ocular Motility, 2018
Stacy L. Pineles, Federico G. Velez
Given the anatomy of the third nerve, there are several coexistent symptoms that should be sought on history and examination in order to localize the lesion and guide work-up. Lesions of the oculomotor nucleus can result in bilateral ptosis (due to a shared LPS nucleus), contralateral or bilateral SR palsy (due to the crossing fibers of the SR nucleus), ipsilateral mydriasis and ipsilateral inferior rectus, medial rectus, and inferior oblique palsies. Although this clinical scenario is fairly classic for a nuclear lesion, there is variability in the possible presentation, and a nuclear third nerve palsy may also be mimicked by a fascicular lesion.11 Fascicular CNIII palsies are often associated with obvious neurological symptoms due to the adjacent structures in the brainstem. In children and adults with CNIII palsies, the following symptoms should be sought to evaluate for brainstem syndromes: contralateral ataxia (Claude syndrome), contralateral hemiparesis (Weber syndrome), and contralateral tremor (Benedikt syndrome). Despite the proximal location, fascicular CNIII palsies can present with superior or inferior divisional involvement given the topographical arrangement of the nerve fibers. Rarely, nuclear and fascicular lesions can result in an isolated muscle palsy, although isolated muscle palsies should also prompt consideration of other diagnostic entities.