Open AccessUnraveling the mysteries of the midbrain – A case report
Author(s) -
Adonai Alencar Rufino,
Beatriz Girão Portela,
Alan Alves de Lima Cidrão,
Deborah Moreira Rangel,
Vitor Araújo Marinho
Publication year - 2021
Language(s) - English
Resource type - Conference proceedings
DOI - 10.5327/1516-3180.623
Subject(s) - midbrain , oculomotor nucleus , anatomy , context (archaeology) , psychology , gaze , medial longitudinal fasciculus , decussation , eye movement , palsy , nystagmus , oculomotor nerve , medicine , neuroscience , audiology , central nervous system , biology , paleontology , alternative medicine , pathology , psychoanalysis
Context: The rostral midbrain and thalamomesencephalic junction are the supranuclear premotor control of vertical eye movements, and is supplied by the posterior thalamo-subthalamic paramedian artery originated from P1 segment of posterior cerebral artery. Case report: A 51-year-old man presented with sudden speech difficulties, dizziness and dyplopia, associated with moderate intensity headache. Neuroophthalmological examination revealed incomplete ptosis of the right eye, with mydriatic pupil, poorly reactive to light. No eye movements were present on attempted upward gaze. On attempted downward gaze, depression of the left eye was observed but with absent saccades. Lateral gaze to the right was intact, while attempted gaze deviation to the left revealed adduction deficit of the right eye with incomplete abduction of the left eye without nystagmus. Convergence was absent. He exhibited left hemiataxia with left hypoestesia. MRI showed acute right paramedian thalamic and mesencephalic stroke. Conclusions: About the vertical one and a half syndrome, it was suggested damage in the pathway to contralateral downgaze neurons before its decussation with the unilateral interstitial nucleus of Cajal. As for the contralateral lateral rectus palsy we infer that this patient’s abduction deficit was due to pseudo-abducens palsy, with several mechanisms that could explain abduction deficits associated with upgaze palsy. Claude’s syndrome is usually explained by a lesion of oculomotor nerve fascicle and the superior cerebellar peduncle, affecting cerebellothalamic connections.