{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T05:52:51Z","timestamp":1770961971576,"version":"3.50.1"},"reference-count":64,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":4451,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1992,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We prospectively examined 11 patients with magnetic resonance imaging\u2013documented infarction in the paramedian thalamopeduncular region, which is supplied by the superior mesencephalic and posterior thalamosubthalamic arteries. Variations in the size and rostral\u2013caudal extent of infarction correlated with the following three clinical patterns: (1) With unilateral paramedian mesencephalic infarction, an ipsilateral third nerve paresis was accompanied by mild contralateral hemiparesis or hemiataxia. Contralateral ptosis and impaired upgaze were observed in two patients; one of them showed additional damage to the posterior commissure. (2) With bilateral infarction in the thalamopeduncular junction, involving the mesencephalic reticular formation, supranuclear vertical gaze defects were accompanied by impaired consciousness or memory, and mild aphasia in some patients. Persistent amnesia was observed only when the dominant anterior nucleus or mamillothalamic tract was damaged. (3) With larger thalamopeduncular infarcts, partial or complete third nerve paresis was combined with supranuclear gaze disturbance and delayed contralateral tremor. An unusual gaze disorder, a variant of the vertical \u201cone\u2010and\u2010a\u2010half syndrome,\u201d occurred with a small strategically placed lesion at the thalamopeduncular junction, best explained by selective damage to supranuclear pathways or partial nuclear involvement. The primary cause of these infarctions was embolism to the basilar apex or local atheroma at the origin of the posterior cerebral artery.<\/jats:p>","DOI":"10.1002\/ana.410320207","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T12:15:45Z","timestamp":1104581745000},"page":"162-171","source":"Crossref","is-referenced-by-count":58,"title":["Paramedian thalamopeduncular infarction: Clinical syndromes and magnetic resonance imaging"],"prefix":"10.1002","volume":"32","author":[{"given":"T. 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