One of the early PET studies to investigate sensory motor processing found a specific change in how the brain responds to a vibration stimulus on the hand. The same abnormal processing also was found in a group of people with blepharospasm, providing further evidence for the similarity of brain mechanisms in different types of dystonia, whether affecting the hand or the face. Preliminary evidence also suggests that this brain response may recover with administration of a drug called levodopa, that most likely has its site of action deep in the brain in the basal ganglia. The suggestion that the basal ganglia are involved in dystonia in general and blepharospasm in particular is supported by several other lines of evidence. First, there is a reduction in dopamine receptor function in this area in people with blepharospasm.
Dopamine is a chemical messenger that transmits signals between nerve cells.
The specific spot that dopamine attaches to on the receiving nerve cell is called a receptor. Measurements of dopamine receptors are also reduced to this same degree in an animal model of dystonia. This animal model provides a number of opportunities for further investigation of the mechanisms underlying blepharospasm. Interestingly, another completely different animal model of eyelid squeezing has been developed by Craig Evinger in New York. He demonstrated that a deficiency of dopamine in the striatum is an important factor in the development of blepharospasm-like movements.