Objectives: To investigate the electrophysiologic mechanism of cataplexy, the authors measured motor evoked potential (MEP) and H-reflex during asymptomatic, cataplectic and post-cataplectic periods in a narcolepsy patient.
Methods: For MEP recording,...
Objectives: To investigate the electrophysiologic mechanism of cataplexy, the authors measured motor evoked potential (MEP) and H-reflex during asymptomatic, cataplectic and post-cataplectic periods in a narcolepsy patient.
Methods: For MEP recording, transcranial magnetic stimulation (TMS) was applied to the right and left hemispheres using a Magstim 200 stimulator and a figure of 8-shaped coil. MEP amplitudes in resting state were measured at stimulus intensities of 120 and 150% of resting motor threshold (rMT). H-reflex was elicited by electrical stimuli on a tibial nerve.
Results: rMT at baseline was 43% in the right and 39% in the left hemisphere. Mean MEP amplitude at baseline was 1.15 mV at a stimulation intensity of 120% rMT and 1.77 mV at 150% rMT. During a cataplectic episode, MEP amplitude abruptly decreased to 0.15 mV at 120% rMT and 0.18 mV at 150% rMT when the patient began to feel facial weakness and experience difficulty talking; subsequently no MEP was evoked during loss of whole body muscle tone. H-reflexes were well elicited during asymptomatic periods (mean amplitude: 2.55 mV at 10.0 mA) whereas H-reflex amplitude abruptly decreased and then disappeared after a cataplectic attack started.
Conclusion: Suppression of both MEP and H-reflex during cataplexy indicates that postsynaptic spinal motor neuron inhibition is the main pathomechanism underlying cataplexy.