Acquired ocular motor apraxia: A clinico-pathological study

Abstract

Acquired ocular motor apraxia is characterized by the inability to initiate intentional saccades. Saccades evoked by vestibular stimulation are present. Bilateral lesions involving the frontal and parietal cortex are hypothesized. The number of clinico-pathological studies is small; lesions are usually extensive.

Case report: A 73-year-old woman was reanimated after a cardiac arrest. She rapidly recovered. Consciousness was normal. There was no limb paralysis. Facial and eyelid movements were normal, spontaneous and on command. Pupillary light reflex was present. The eyes were in the midline position and immobile. Intentional saccades, to command and visually guided, were absent in the horizontal and vertical planes. Sporadically, saccade on command elicited a head movement associated with a slow vestibular eye movement in the opposite direction. Smooth pursuit was absent in all directions. Optokinetic stimulation provoked no eye movements. Oculocephalic movements were present. Cold water irrigation of one ear provoked a tonic deviation of both eyes to the irrigated side with irregular small corrective saccades to the other side. The patient died 30 days after the appearance of the eye movement disorder.

Autopsy findings: The brainstem was normal, especially the collicular area. Circumscribed areas of pseudo-laminar necrosis were present in the superior bank of the left inferior frontal sulcus (middle frontal gyrus), immediately anterior to the precentral gyrus and in the upper and lower banks of the left intra-parietal sulcus, involving the angular gyrus. The left frontal lesion was 7 mm long in the coronal plane and was seen on only one section, with slices taken every 5 mm. The left parietal lesion had a length of 15 mm in the coronal plane and was seen on two consecutive sections. On the right side cortical micro-infarctions were seen in the same areas. The lesions are compatible with 30-day-old ischemia and are interpreted as border zone infarcts after systemic hypotension.

Our case is very similar to the case reported by Pierrot-Deseilligny et al.¹ in which the lesions were visualized by MRI. Small lesions as observed in our case are rare and are important for location of the human cortical areas involved in the control of saccades. Our findings confirm that small bilateral lesions in the posterior part of the middle frontal gyrus (frontal eye field) and in the posterior parietal lobule can completely abolish intentional saccades and smooth pursuit eye movements.

Key Words:

• acquired oculomotor apraxia
• bilateral frontoparietal lesions