{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T04:52:02Z","timestamp":1789620722883,"version":"build-2803163510"},"reference-count":19,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1997,5,1]]},"abstract":"<jats:p> Schicatano, Edward J., Michele A. Basso, and Craig Evinger. Animal model explains the origins of the cranial dystonia benign essential blepharospasm. J. Neurophysiol. 77: 2842\u20132846, 1997. 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 blepharospasm. By themselves, neither of these modifications causes 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. <\/jats:p>","DOI":"10.1152\/jn.1997.77.5.2842","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T00:59:24Z","timestamp":1514163564000},"page":"2842-2846","source":"Crossref","is-referenced-by-count":155,"title":["Animal Model Explains the Origins of the Cranial Dystonia Benign Essential Blepharospasm"],"prefix":"10.1152","volume":"77","author":[{"given":"Edward J.","family":"Schicatano","sequence":"first","affiliation":[{"name":"Departments of Neurobiology and Behavior and Ophthalmology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michele A.","family":"Basso","sequence":"additional","affiliation":[{"name":"Department of Psychology, State University of New York at Stony Brook, Stony Brook, New York 11794-5230"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig","family":"Evinger","sequence":"additional","affiliation":[{"name":"Departments of Neurobiology and Behavior and Ophthalmology and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-22-07318.1996"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-22-07308.1996"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00230472"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/108.3.593"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.47.2.508"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/mds.870090210"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/eye.1988.79"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00229040"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF00247600"},{"key":"B10","first-page":"1404","volume":"21","author":"Evinger C.","year":"1995","journal-title":"Soc. 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