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[Unusual pathological ocular movement caused by dysfunction of the saccade generation mechanism]
1Department of Neurology, Faculty of Medicine, Kyushu University.
Abstract:
We describe a patient with abnormal ocular movement, probably due to dysfunction of saccade generation mechanism in the lower pons involving the omnipause neuron and a feed-back circuit. A 26-year-old man had fever, mild headache and sore throat for a few days and also noted unstable gait and diplopia. These symptoms subsided, but he noticed oscillopsia about 2 months later. On admission in our hospital, the neurological examination revealed no abnormalities except for abnormal eye movements, which were induced by voluntary or involuntary ocular movement and lasted for a few minutes. The abnormal ocular movement was irregular in direction, amplitude and rhythmicity, and the voluntary and involuntary ocular movements could not be elicited during the period of this abnormal ocular movement. The abnormal ocular movement completely disappeared for about 1 hour by intravenous injection of TRH. At this time bilateral mild abducens palsy was demonstrated by EOG examination. The abnormal ocular movement in this patient, which has nerve been reported in the literature, was considered to be due to a disinhibition of excitatory burst neuron (EBN) caused by the dysfunction of omnipause neuron, and possibly due to a delay of feed-back information of saccade to the EBN.
Insights
This study details a rare case of abnormal ocular movements in a patient, likely caused by issues with the saccade generation mechanism in the pons. Treatment with TRH temporarily resolved these unusual eye movements.
Area of Science:
- Neuroscience
- Ophthalmology
Background:
- Saccade generation is crucial for rapid eye movements.
- Dysfunction in the pontine saccade generation mechanism can lead to abnormal ocular motility.
Observation:
- A patient presented with transient, irregular abnormal ocular movements after initial symptoms of fever and headache.
- These movements, characterized by oscillopsia and inability to perform voluntary saccades, were temporarily resolved by intravenous TRH.
- Electrooculography revealed bilateral mild abducens palsy during the episodes.
Findings:
- The abnormal ocular movements are hypothesized to result from disinhibition of excitatory burst neurons (EBNs).
- This disinhibition is likely due to a dysfunction of the omnipause neuron and a potential delay in saccadic feedback circuits.
- This specific presentation of abnormal ocular movement has not been previously reported in medical literature.
Implications:
- This case highlights a novel mechanism of abnormal ocular movement possibly linked to pontine circuitry.
- Understanding the role of omnipause neurons and feedback circuits in saccade generation is critical.
- Further research into TRH's effect on such neurological conditions may offer new therapeutic avenues.