Saccadic Palsy Research Articles

Conjugate eye deviation: Localization of hemispheric lesions

Conjugate eye deviation (CED) is generally attributed to a lesion of the frontal eye fields or its subcortical projections leading to a contralateral saccadic palsy. This theory is mainly based on experimental studies. However, clinical studies yield rather conflicting results as to the localizing value of this sign. The authors therefore performed a prospective study of 74 patients with CED caused by a hemispheric lesion. The diagnosis and site of the lesion was based on CT-scan and/or autopsy findings. In all but two patients the sign was caused by a stroke. The results of the study can be summarized as follows1. The area of the frontal eye fields is not damaged in most patients with CED, rather, the inferior parietal lobule is involved.2. One exclusive location of the lesion responsible for CED is unlikely.3. CED can probably result from a lesion at different sites within the circuit formed by inferior parietal lobule-frontal eye fields-superior colliculus and pontine reticular formation, predominantly...

Hypothetical explanation of selective saccadic palsy caused by pontine lesion.

Recent clinical neuropathologic reports are inconsistent with previous models of how pontine neural circuits generate saccadic eye movements. We present a hypothetical explanation of these and other clinical and experimental findings based on a new model that accurately predicts the eye signs in pontine lesions.

Palsy of upward and downward saccadic, pursuit, and vestibular movements with a unilateral midbrain lesion

Upward and downward gaze palsy was measured by a magnetic search coil technique and correlated with neuropathologic findings in a patient with a unilateral midbrain infarct. Oculography demonstrated (1) saccadic palsy above primary position and slow, limited vertical saccades below; (2) low-gain, restricted vertical pursuit; and (3) low-gain, abnormal phase lead, and restricted range of the vertical vestibulo-ocular reflex (VOR). Bidirectional palsy of vertical saccades is attributed to unilateral loss of burst cells in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and interruption of burst cell fibers from the opposite riMLF. Pathways mediating vertical pursuit and integration of the vertical VOR also traversed the infarct, which included the interstitial nucleus of Cajal.