1993 Volume 96 Issue 3 Pages 444-456,547
Autonomic nervous function in 68 vertiginous patients and 33 controls was studied using power spectral analysis of heart rate variability.
First, a system was developed which computes the power spectral density (PSD) of beat-tobeat heart intervals using a continuous non-invasive finger blood pressure recording obtained with the FINAPRESS device. A fast-Fourier transform algorithm was used to compute the PSD. In frequencies up to 0.5Hz, the PSD of heart rate variability contains three major components: a low frequency (P1), a middle frequency (P2) and a high frequency (P3). Each component was normalized by dividing the absolute values by total power (T), and then used as an index of each component.
Second, the effects of passive tilt, respiratory frequency and specific pharmacological sympathetic or parasympathetic blockade on the indices of these components were evaluated in the control group.
The following results were obtained.
1. During passive tilt, the normalized power of P2 was increased, whereas that of P3 was decreased.
2. The peak frequency of P3 was consistent with the frequency of respiration.
3. Sympathetic blockade decreased the normalized power of P2, whereas parasympathetic blockade decreased the normalized power of P3.
From these results, I concluded that the normalized power of P2 and P3 are quantitative markers of sympathetic and vagal nervous activities, respectively.
Third, the results of spectral analysis in patients were compared with those in controls.
The following characteristics of autonomis nervous function in vertiginous patients were noted.
1. The normalized power of P3 in patients was lower than that in controls, suggesting that parasympathetic nervous activity at rest was suppressed in patients.
2. The increase of normalized power of P2with passive tilt was suppressed in patients, suggesting suppression of sympathetic response to passive tilt.
3. In patients with Meniere's disease, during the active period of vertigo attacks, the normalized power of P2, which is an index of sympathetic activity, was higher than that in the intervals between vertigo attacks.
Fourth, with caloric stimulation in the control group, an increase of the normalized power of P2was observed during or after the stimulation, which suggests that vestibular stimulation increases sympathetic activity.
I therefore suggest the following:
1. Decreased parasympathetic activity and suppression of sympathetic response were present in the vertiginous patients.
2. Sympathetic activity was increased by vertigo attacks in the patients with Meniere's disease.