Recovery function of and effects of hyperventilation on somatosensory evoked high-frequency oscillation in Parkinson's disease and myoclonus epilepsy

• Published in: Neuroscience research Vol. 46; no. 4; pp. 485 - 492
• Main Authors: Mochizuki, Hitoshi, Machii, Katsuyuki, Terao, Yasuo, Furubayashi, Toshiaki, Hanajima, Ritsuko, Enomoto, Hiroyuki, Uesugi, Haruo, Shiio, Yasushi, Kamakura, Keiko, Kanazawa, Ichiro, Ugawa, Yoshikazu
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 01.08.2003
• Subjects: Adult; Aged; Electric Stimulation; Electroencephalography; Epilepsies, Myoclonic - physiopathology; Evoked Potentials, Somatosensory - physiology; High-Frequency Ventilation - methods; Humans; Hyperventilation; Hyperventilation - physiopathology; Median Nerve; Middle Aged; Myoclonus epilepsy; Neural Inhibition - physiology; Parkinson Disease - physiopathology; Parkinson's disease; Recovery function; Recovery of Function - physiology; Somatosensory evoked potential; Time Factors; Parkinson's disease; Recovery function; Somatosensory evoked potential; Myoclonus epilepsy; Hyperventilation
• ISSN: 0168-0102; 1872-8111
• DOI: 10.1016/S0168-0102(03)00129-9

To evaluate recovery function of and effects of hyperventilation (HV) on high-frequency oscillations (HFOs) of median nerve somatosensory evoked potential (SEP), we recorded SEPs in 8 Parkinson's disease (PD) patients with enlarged HFOs, 4 myoclonus epilepsy (ME) patients and 10 healthy volunteers ( N). SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Responses were amplified with filters set at 0.5 and 3000 Hz. HFOs were obtained by digitally filtering raw SEPs from 500 to 1000 Hz. We measured amplitudes of the N20 onset–peak (N20o–p), N20 peak–P25 peak (N20p–P25p), P25 peak–N33 peak (P25p–N33p), the early (1st–2nd) and late (3rd) HFOs. For the recovery function study, paired-pulse stimuli at various interstimulus intervals (20, 50, 100, 150, 200 and 300 ms) were given. To investigate effects of HV, amplitudes of several components of SEPs recorded after HV were compared with those before HV. In PD and ME, the N20o–p recovery curve showed significantly less suppression as compared with those of N. The P25p–N33p recovery curve of ME showed longer suppression than those of N and PD. There were no significant differences in the early or late HFOs recovery curves among three groups. At the dysinhibited state after HV, the late HFO was reduced in association with a significant enlargement of the N20p–P25p amplitude in normal subjects. This suggests that the late HFOs should reflect bursts of inhibitory interneurons. In the ME patients, the early HFOs significantly decreased by HV. The pattern in ME patients may be explained by a kind of compensation for already enhanced SEPs (giant SEP) in the dysinhibited situation. We conclude that (1) Giant HFOs are normally regulated by inhibitory neuronal systems involving in paired stimulation SEP. (2) The late HFOs must reflect bursts of GABAergic inhibitory interneurons.