ArticleCurrent neuropharmacology2013
Animal models for investigating benign essential blepharospasm.
Article in Current neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Deep brain stimulation for Meige syndrome.Surgical neurology international · 2025Article
- The pathogenesis of blepharospasm.Frontiers in neurology · 2023Review
- Blink index as a response predictor of blepharospasm to botulinum neurotoxin-A treatment.Brain and behavior · 2021Article
- Blepharospasm, Oromandibular Dystonia, and Meige Syndrome: Clinical and Genetic Update.Frontiers in neurology · 2021Review
- Treatment of Blepharospasm/Hemifacial Spasm.Current treatment options in neurology · 2017Review
- A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm.Frontiers in computational neuroscience · 2017Article
- Blepharospasm: Update on Epidemiology, Clinical Aspects, and Pathophysiology.Frontiers in neurology · 2016Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The focal dystonia benign essential blepharospasm (BEB) affects as many as 40,000 individuals in the United States. This dystonia is characterized by trigeminal hyperexcitability, photophobia, and most disabling of the symptoms, involuntary spasms of lid closure that can produce functional blindness. Like many focal dystonias, BEB appears to develop from the interaction between a predisposing condition and an environmental trigger. The primary treatment for blepharospasm is to weaken the eyelid-closing orbicularis oculi muscle to reduce lid spasms. There are several animal models of blepharospasm that recreate the spasms of lid closure in order to investigate pharmacological treatments to prevent spasms of lid closure. One animal model attempts to mimic the predisposing condition and environmental trigger that give rise to BEB. This model indicates that abnormal interactions among trigeminal blink circuits, basal ganglia, and the cerebellum are the neural basis for BEB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.