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KMID : 1036520130030010027
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Clinical Neuro-Ophthalmology
2013 Volume.3 No. 1 p.27 ~ p.36
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Supra- and Internuclear Ophthalmoplegia
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Choi Kwang-Dong
Kim Ji-Soo
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Abstract
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Supranuclear eye movement abnormalities result from dysfunctional cerebral, cerebellar, and brainstem afferent connections to the ocular motor nuclei. A clinical hallmark of supranuclear eye movement disorders is disproportionate involvement of saccades. Vestibular eye movements are typically spared. In contrast, nuclear and infranuclear lesions impair saccades, smooth pursuit, and vestibular eye movements equally. Burst neurons for horizontal saccades are located in the pontine paramedian reticular formation (PPRF) and, for vertical saccades, in the midbrain rostral interstitial medial longitudinal fasciculus (riMLF). A PPRF lesion causes slow or absent horizontal saccades, while an riMLF lesion cause slow or absent vertical saccades. Burst inhibition, required to prevent unwanted saccades from degrading vision, is provided by pontine omnipause neurons. The dorsal midbrain (Parinaud’s) syndrome is comprised of a supranuclear upgaze palsy, convergence-retraction nystagmus, Collier’s sign (lid retraction), and pupillary light-near dissociation, which is usually caused by pineal gland lesions and hydrocephalus. Gaze deviation is a common supranuclear process. The frontal eye fields (FEFs) project to the contralateral PPRF. A destructive lesion of the FEFs results in ipsiversive gaze deviation. With an irritative lesion, there is contraversive deviation. “Wrong way eyes” with the patient “looking away” from a destructive lesion may occur from thalamic pathology.
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KEYWORD
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Horizontal gaze palsy, Vertical gaze palsy, Ocular tilt reaction, Eyeball deviation, Ocular motor apraxia
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