Aim: 

The lower brain stem neurotransmitter dysfunction is suggested as possible neurobiological basis of panic disorder (PD). We supposed the changes in visual-oculomotor integration which can support the above suggestion.

Methods: 

The electrooculographic recordings of gaze refixation accuracy, the gain of the optokinetic nystagmus (OKN), the EEG potentials related to the gaze refixations and the P300 wave triggered by voluntary blocking the reflexive gaze refixations were analysed in PD outpatients at least 1 year after the last panic attack. The patients were working regularly without taking a specific medication.

Results: 

The greater interindividual variability of the OKN gain as well as its decrease in relation to increased velocity of moving visual stimuli was found in PD patients. Moreover, their gaze refixations were significantly more inaccurate as compared to 5% inaccuracy in healthy controls. In PD patients the gaze refixation related potentials over the frontal eye fields were of longer duration and when recorded over the parietal eye fields the longer preparation for gaze refixation and attenuated correlates of the oculomotor muscle units at the onset of the gaze refixation were found.

Conclusions: 

The results confirm suggested disordered early processing of sensory stimuli in PD. Since the changes persist after successive treatment they point to the considerable fluctuation of the overall activation level in neuronal loops participating in oculomotor circuits. The OKN and gaze refixations with their central correlates are proposed as a part of the battery of electrophysiological diagnostic tests in PD.