Related Experiment Videos
Blink reflex discloses CNS dysfunction in neurologically asymptomatic patients with systemic sclerosis
Roberto Casale1, Giuseppe Frazzitta, Cira Fundarò
1Department of RRF and Service of Clinical Neurophysiology, Salvatore Maugeri Foundation, IRCCS Rehabilitation Institute of Montescano, Via per Montescano, 27040 Montescano, Italy.
Summary
Systemic sclerosis (SSc) patients without neurological symptoms showed delayed R2 blink reflex responses, indicating central nervous system involvement. This suggests subcortical white matter dysfunction, possibly from microvascular lesions, in early-stage SSc.
Area of Science:
- Neurology
- Immunology
- Neurophysiology
Background:
- Systemic sclerosis (SSc) is an autoimmune disease affecting connective tissues.
- Nervous system involvement can occur in SSc, but is often subtle in early stages.
- Trigeminal nerve and brainstem function are key indicators of neurological health.
Purpose of the Study:
- To investigate trigeminal nerve, brainstem, and brain function in neurologically asymptomatic SSc patients.
- To identify subclinical nervous system involvement in early SSc.
- To differentiate central vs. peripheral nervous system dysfunction in SSc.
Main Methods:
- Electromyography (EMG) was used to record blink reflex R1 and R2 components.
- 35 SSc patients without cranial nerve impairment and 20 controls were studied.
- SSc patient data included disease classification, duration, autoantibodies, and skin score.
Main Results:
- No SSc patients exhibited abnormal R1 blink reflex responses.
- Six SSc patients (18%) demonstrated delayed R2 blink reflex responses.
- No correlation was found between R2 latency and clinical or laboratory SSc parameters.
Conclusions:
- Asymptomatic SSc patients can have selective R2 blink reflex abnormalities, unlike symptomatic patients with R1/R2 issues.
- The R2 delay suggests central nervous system dysfunction, potentially affecting medullary polysynaptic circuits or cortico-reticular pathways.
- Suprasegmental dysfunction, possibly due to microvascular lesions in the subcortical white matter, is implicated in asymptomatic SSc patients.