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 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.
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Authors | E J Schicatano, M A Basso, C Evinger |
Journal | Journal of neurophysiology
(J Neurophysiol)
Vol. 77
Issue 5
Pg. 2842-6
(May 1997)
ISSN: 0022-3077 [Print] United States |
PMID | 9163399
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
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Topics |
- Animals
- Basal Ganglia
(physiology)
- Blepharospasm
(physiopathology)
- Blinking
(physiology)
- Disease Models, Animal
- Dominance, Cerebral
(physiology)
- Dopamine
(physiology)
- Dystonia
(physiopathology)
- Electromyography
- Male
- Nerve Net
(physiopathology)
- Neural Inhibition
(physiology)
- Rats
- Rats, Sprague-Dawley
- Signal Processing, Computer-Assisted
- Trigeminal Nerve
(physiopathology)
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