Fishman Commentary: In many patients, dry eye disease present with a neuropathic component, which I refer to as the “trigeminal ganglion pain continuum.” In this paper, the authors show that changes at the synaptic level in the brainstem occur in dry eye disease.
- * Patients with dry eye have an abnormal enhancement of excitability in blink reflex circuits.
- * The abnormalities were present in both, primary and secondary dry eye syndromes.
- * The abnormal sensorimotor integration may be due to sensitization due to excessive sensory input
- aDepartment of Neurology, Cerrahpasa Medical Faculty, I.U.C, Istanbul, Turkey
- bDepartment of Ophtalmology, Cerrahpasa Medical Faculty, I.U.C, Istanbul, Turkey
- cIDIBAPS (Institut d’Investigació August Pi i Sunyer), Barcelona, Spain
We hypothesized that there may be changes in sensory integration pathways in patients with dry eye. To confront this issue, we analyzed blink reflex (BR), prepulse modulation (PPM) of BR, and excitability recovery of BR to paired stimuli in 17 experimental subjects with dry eye syndrome.
We included 17 experimental subjects, 8 with primary and 9 with secondary, dry eye syndrome. We also examined a control group of 14 age and gender matched control subjects. After clinical evaluation, we recorded BR, PPM of BR (at 50 and 100 ms intervals) and BR percentage recovery to paired stimulation (at 300 and 500 ms intervals).
None of the patients had any spasm activity. Experimental subjects had significantly larger R2 and R2c AUCs, significantly greater excitability recovery at 300 ms interval and significantly reduced R2 and R2c prepulse inhibition, in comparison to control subjects. Experimental subjects with primary dry eye syndrome had higher number of spontaneous blinks than experimental subjects with secondary dry eye syndrome (54.0 ± 10.3 for primary dry eye and 43.5 ± 13.3 secondary dry eye).