Ocular dipping movements in an electrocution cardiac arrest survivor

Abstract

Background : Abnormal eye movements can occur in patients with neurological diseases. These have been described in unconscious patients due to anoxic coma and often disappear as the patient regains consciousness. Ocular dipping movements are rarely seen in practice in pediatric patients. Methods : A one year old male patient was brought unconscious with electrocution injury. With resuscitation, he became hemodynamically stable. He could not recognize his mother or respond to visual/auditory stimuli; and had generalized hypertonia. Cranial nerves were normal. He showed abnormal involuntary conjugate vertical saccadic eye movements, consisting of slow downward movement (for 1-2 seconds) followed by a relatively faster return to the primary mid-position. These persisted continuously for 48 hours at irregular intervals of 1-2 seconds. The patient was awake but non-responsive and not interested in surroundings. Results : These eye movements are called ocular dipping (OD) . In a normal person, saccadic movements are meant for stable fixation and are maintained by pause-cell neurons positioned in the pontine raphe. These prevent the occurrence of unwanted saccadic pulses by inhibiting the saccadic premotor burst neurons in the paramedian pontine reticular formation and midbrain. Injury to pause cells leads to extraneous saccades without fixation. It appears that cortical and basal ganglia malfunction causes ocular dipping. OD is mainly seen in anoxic coma and creuztfelt Jacob disease. A 53-year-old man developed ocular dipping following prolonged hypotension.Our patient was in vegetative state with normal respiratory and cardiac function suggesting that major midbrain and medullary centers were intact. Conclusion : The self limiting nature of OD suggests that these are caused by diffuse dysfunction rather than a single structural locus.