AN ANIMAL MODEL EXPLAINS THE ORIGINS OF THE CRANIAL DYSTONIA BENIGN ESSENTIAL BLEPHAROSPASM. Edward J. Schicatano, Michele A. Basso, Craig Evinger. Depts. Neurobiology & Behavior and Ophthalmology, SUNY Stony Brook, Stony Brook, NY, 11794-5230; 2Dept. Psychology, SUNY Stony Brook, Stony Brook, NY 11794.
APStracts 4:0032N, 1997.
ABSTRACT
The current study demonstrates that combining two mild alterations to the rat trigeminal reflex blink system reproduces the symptoms of benign essential blepharospasm, a cranial dystonia characterized by uncontrollable spasms of blinking. The first modification, a small striatal dopamine depletion, reduces the tonic inhibition of trigeminal reflex blink circuits. The second alteration, a slight weakening of the lid closing, orbicularis oculi, muscle, begins an adaptive increase in the drive on trigeminal sensory-motor blink circuits that initiates blepharo- spasm. By themselves, neither of these modifications cause spasms of lid closure, but combined they induce bilateral forceful blinking and spasms of lid closure. A two factor model based on these rodent experiments may explain the development of benign essential blepharospasm in humans. The first factor, a subclinical loss of striatal dopamine, creates a permissive environment within the trigeminal blink circuits. The second factor, an external ophthalmic insult precipitates benign essential blepharospasm. This two factor model may also be applicable to the genesis of other cranial dystonias. 

Received 9 October 1996; accepted in final form 22 January 1997.
APS Manuscript Number J801-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 5 February 1997