Hemifacial spasm generally begins as involuntary muscle spasms in the eyelids and then progresses to the entire distribution of the facial nerve. This disease is thought to be due to a compression of the facial nerve at its root entry zone by one of several arteries in the region. The underlying neural mechanisms of the hemifacial spasm are still controversial. Arterial compression of the nerve can modify the facial nerve, facial motoneurons, and the trigeminal nucleus. This proposal investigates the role of each of these modifications in producing the symptoms of hemifacial spasm. Hemifacial spasm patients will used to identify changes in the trigeminal system. An animal model isolating the different mechanisms will be created to characterize the causes of symptom development resulting from motoneuron and trigeminal modifications.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Individual Predoctoral NRSA for M.D./Ph.D. Fellowships (ADAMHA) (F30)
Project #
5F30NS044673-03
Application #
6792045
Study Section
NST-2 Subcommittee (NST)
Program Officer
Gwinn, Katrina
Project Start
2002-08-17
Project End
Budget Start
2004-08-17
Budget End
2005-08-16
Support Year
3
Fiscal Year
2004
Total Cost
$30,502
Indirect Cost
Name
State University New York Stony Brook
Department
Neurosciences
Type
Schools of Medicine
DUNS #
804878247
City
Stony Brook
State
NY
Country
United States
Zip Code
11794
Kassem, Iris S; Evinger, Craig (2006) Asymmetry of blinking. Invest Ophthalmol Vis Sci 47:195-201