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Induction of Ocular Surface Inflammation and Collection of Involved Tissues

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Published on: August 4, 2022

Animal models for investigating benign essential blepharospasm.

Craig Evinger¹

¹Depts. of Neurobiology & Behavior and Ophthalmology, Stony Brook University, Stony Brook, NY 11794-5230.

Current Neuropharmacology

|July 2, 2013

Summary

Benign essential blepharospasm (BEB) causes involuntary eyelid closure, leading to functional blindness. Animal models suggest abnormal neural circuit interactions are the basis for this focal dystonia.

Keywords:

Basal ganglia blepharospasm blink cerebellum motor adaptation trigeminal.

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Area of Science:

Neurology
Ophthalmology

Background:

Benign essential blepharospasm (BEB) is a focal dystonia affecting 40,000 in the US.
Symptoms include trigeminal hyperexcitability, photophobia, and disabling involuntary eyelid closure.
BEB is thought to arise from genetic predisposition and environmental triggers.

Purpose of the Study:

To investigate the neural basis of BEB.
To explore potential pharmacological treatments for BEB.

Main Methods:

Development of an animal model mimicking BEB's predisposing and triggering factors.
Investigation of abnormal interactions within trigeminal blink circuits, basal ganglia, and cerebellum.

Main Results:

The animal model successfully recreated eyelid spasms characteristic of BEB.
Abnormal interactions among specific neural circuits were identified as the neural basis for BEB.

Conclusions:

Abnormal interactions within trigeminal blink circuits, basal ganglia, and cerebellum are the neural underpinnings of BEB.
Animal models are valuable for studying the pathophysiology and potential treatments for BEB.