Motor cortical excitability following repetitive transcranial magnetic stimulation in patients with Alzheimer’s dementia

الملخص EN

Introduction : In Alzheimer’s disease (AD), transcranial magnetic stimulation (TMS) studies have shown abnormalities of motor cortical excitability, but the exact nature of deficits and its importance are not known.

Objectives : The aim of the stud) was to establish how different mechanisms interact to promote motor system hyperexcitability in AD in relation to cognitive function and clinical features and to investigate the effect of rTMS on the excitability of the motor cortex.

Material and methods : 45 AD patients and 37 healthy normal volunteers matched for age and sex were included in the study.

Neurological evaluation, Minimental State Examination (MMSE).

And Clinical Dementia Rating (CDR).

were conducted for each participant.

Neurophysiological evaluations were performed before and after rTMS for all patients including resting and active motor thresholds (RMT and AMT), motor evoked potential (MEP), cortical silent period (CSP) and transcallosal inhibition (TCI).

Results : As expected, AD patients showed a significant reduction in RMT, and AMT.

shortening of MEP latency, prolonged both CSP and TCI.

There is a significant negative correlation between duration of illness on one hand and RMT & AMT.

The more deterioration of cognitive function associated with more increase cortical excitability (reduced RMT & AM T) in AD patients.

Also there were a positive association between the hyper-excitability of the cortex and extra-pyramidal manifestation and primitive reflexes.

Significant shortening of both CSP and TCI in patients receiving 20 HZ in comparison to those received 1 HZ and sham rTMS.

No significant changes in RMT.

And AMT after application of rTMS.

Conclusion : AD associated with hyper-excitability of the motor cortex.

These changes were correlated with duration of illness and MMSE.

Twenty Hertz rTMS can produce a long lasting change in cortical excitability in AD patients through shortening of CSP and TCI.