A study aimed to better understand SOM using infrared oculography. They examined and recorded five patients with SOM.
Binocular infrared oculography showed that in primary gaze, all patients exhibited torsional oscillations, which worsened in infraduction and abduction and improved in supraduction and adduction. Saccades showed increased downward saccade amplitudes but normal peak velocities. During fixation in primary gaze, removal of target led to extorsion and supraduction, unmasking underlying superior oblique weakness.
This data suggest both weakness and activity-dependent hyperactivity of the trochlear motor unit, supporting a model of injury followed by aberrant regeneration 1).
Abhinav et al., describe a first reported case of chronic disabling SOM in association with a cerebellopontine angle arachnoid cyst, who had a gradual and eventually complete symptomatic resolution 8 months following cyst marsupialisation. Among other aetiologies, SOM may therefore be due to abnormal CSF flow dynamics resulting in structural compromise of the nerve 2).