Power Spectral Analysis of Slow Modulation of EEG Background Amplitude, Heart Rate, Blood Pressure, and Middle Cerebral Artery Flow Velocity during Head-Up Tilt in Subjects with Postural Tachycardia Syndrome (POTS) and Controls.
Abstract number :
1.138
Submission category :
Year :
2001
Submission ID :
148
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
T.D. Lagerlund, MD, PhD, Neurology, Mayo Clinic, Rochester, MN; P.A. Low, MD, Neurology, Mayo Clinic, Rochester, MN; V. Novak, MD, PhD, Neurology, Ohio State University, Columbus, OH; P. Novak, MD, Neurology, Ohio State University, Columbus, OH; B. McPhee
RATIONALE: Slow ([lt]0.5 Hz) modulation of EEG background amplitude has been previously reported (Novak and Lepicovska, Neuro Report 3(2):189-192, 1992; Novak et al, Neurosci Lett 136(2):213-215, 1992). Slow modulation may have a brainstem autonomic origin because similar frequencies have been recorded from brainstem cardiovascular and respiratory centers in animals. It has been suggested that much of the pathophysiology of postural tachycardia syndrome (POTS) may be brainstem derived. In order to try to link POTS to brainstem pathophysiology, we studied slow modulation of EEG background activity and cardiovascular parameters in subjects with POTS.
METHODS: We simultaneously recorded EEG, blood flow velocity in middle cerebral artery (MCA) using transcranial Doppler, heart rate, respirations, and blood pressure from subjects with POTS and age-matched controls during head-up tilt. Time-frequency analysis of 0.512-s epochs of EEG was performed to determine peak alpha amplitude. Cardiovascular parameters calculated once per heartbeat and EEG amplitudes were resampled at 4 Hz. Spectra calculated by time-frequency analysis using 128 s epochs were divided into 3 bands (ultraslow=0-0.045 Hz, middle=0.045-x Hz, respiratory=x-0.5 Hz) where x is the peak frequency of respiratory spectrum minus 12 times the half width at half maximum of respiratory spectral peak. Peak amplitudes were averaged over pre-tilt and head-up tilt time periods for each patient and control. Grand averages were obtained for the POTS and control groups and compared for pre-tilt and tilt conditions.
RESULTS: EEG modulation was reduced in POTS subjects relative to controls while supine in ultraslow, middle, and respiratory frequency bands. EEG modulation in these bands decreased in controls with head-up tilt but not in POTS subjects. Heart rate modulation in the respiratory frequency band decreased with head-up tilt, and was significantly less in both ultraslow and respiratory frequency bands (but not middle band) in POTS subjects after head-up tilt. Blood pressure modulation (only in middle frequency band) increased with head-up tilt, to a greater degree in POTS subjects. MCA flow velocity modulation in middle and respiratory bands (but not ultraslow band) increased with head-up tilt, to a greater degree in POTS subjects.
CONCLUSIONS: Assuming that altered EEG modulation reflects altered brainstem physiology, the alteration of EEG modulation in POTS subjects supports the hypothesis that brainstem pathophysiology may play a role in POTS.
Support: NIH (P01-NS32352); NIH-GCRC (M01-RR00585); NASA; Mayo Foundation.