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Updated: Jun 26, 2026

Utilizing Transcranial Magnetic Stimulation to Study the Human Neuromuscular System
Published on: January 20, 2012
Preliminary observations in cortical excitability changes using transcranial magnetic stimulation (TMS), it's
R S Shaik1, V H Ganaraja1, A Bhattacharya1
1Department of Neurology, National Institute of Mental Health & Neurosciences, Bangalore, 560029, India.
Background:
Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing central nervous system disease most commonly associated with aquaporin-4 antibodies (AQP4-Ab) and Myelin oligodendrocyte glycoprotein (MOG) antibodies. These demyelinating disorders influence cortical excitability, which has been studied using advanced imaging techniques and transcranial magnetic stimulation (TMS) in our study.
Methods:
This is a prospective study of 30 subjects. Ten subjects, each of AQP4, MOGAD, and dual seronegative (SN)-NMOSD, were recruited and compared to 30 healthy controls. All the subjects underwent TMS and MRI with diffusion tensor imaging (DTI). Resting motor threshold (RMT), central motor conduction time (CMCT), ipsilateral (ISP) and contralateral silent period (cSP), short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were the TMS parameters assessed. Fractional anisotropy (FA) and axial diffusivity (AD) were the DTI parameters studied. DTI findings were correlated with the TMS parameters.
Results:
The study cohort had a male-to-female ratio of (M: F) = 13:17. RMT was highest in the AQP4-Ab subgroup (40.2 ± 11.9%) compared to SN NMOSD (36.2 ± 4.6%) and MOGAD (34.5 ± 6.7%). CMCT was maximum prolonged in subjects with MOGAD (9.6 ± 1.9 msec). The cSP was reduced in MOGAD (79.9 ± 36.3msec). SICI was lowest in the AQP4-Ab subgroup (1.27 ± 1.12) and was preserved in the MOGAD subgroup (0.88 ± 0.55). The DTI data demonstrated statistically significant, reduced FA and AD in AQP4-Ab and SN NMOSD subjects.
Conclusion:
This is the first study that looked at the cortical excitability changes in the three subgroups of NMOSD. It has been observed that AQP4 NMOSD and SN NMOSD had a severe form of demyelinating disease compared to MOGAD.
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