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A 52-year-old man, with metastatic melanoma deposits in the frontal lobes bilaterally (figure 1A), developed acute headache and impaired voluntary eye movements in all directions of gaze. On examination (supplementary online video), voluntary saccades were severely hypometric, and smooth pursuit was absent. However, ductions were full with vestibular stimulation, and quick phases of vestibular nystagmus were intact. He was occasionally able to make saccades to visual and auditory stimuli, but these movements were hypometric and made with increased latency. CT of the brain showed intraparenchymal haemorrhages within the frontal lobes bilaterally, at the sites of the metastases (figure 1B).
The patient's ocular motor findings were consistent with acquired ocular motor apraxia (OMA), which is characterised by loss of voluntary eye movements with preserved reflex eye movements.1 In this patient, OMA was due to lesions involving both frontal eye fields, which lie in the caudal middle frontal gyrus and control all voluntary eye movements, including saccades, smooth pursuit and vergence.1–3 The frontal eye fields receive input from the parietal eye field, supplementary eye field and prefrontal cortex.1 ,2 The parietal eye field is mainly responsible for reflexive saccades to novel stimuli,4 which were relatively intact in our patient because this area was spared. Although the frontal and parietal eye fields have specific saccadic functions, the eye fields have complementary roles in saccade generation such that only bilateral lesions to both the frontal and parietal eye fields will cause persistent OMA.5 Our patient regained some voluntary saccadic initiation several days following presentation, likely due to preservation of the parietal eye fields. However, he succumbed to his disease soon after.
Competing interests None.
Patient consent Obtained.
Ethics approval Ethics approval was provided by Single case reported, consent obtained.
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