Heart rate variability and sympathetic skin response in male patients suffering from acute alcohol withdrawal syndrome.
BACKGROUND
Many symptoms of alcohol withdrawal (AW) such as tachycardia or elevated blood pressure might be explained by increased peripheral and central adrenergic activity. In contrast to many neurochemical studies of sympathetic activation during AW, only very few studies investigated autonomic balance using neurophysiological methods.


METHODS
We investigated heart rate variability (HRV) and sympathetic skin response (SSR) in male patients suffering from mild AW syndrome (n = 20, no treatment required) and in patients with moderate to severe AW syndrome (n = 20, clomethiazole treatment) in the acute stage. Sympathovagal influence was quantified using measures of time and frequency domain of HRV as well as modern nonlinear parameters (compression entropy). Furthermore, we obtained latencies and amplitudes of SSR to quantify isolated sympathetic influence. Measures were obtained during the climax of withdrawal symptomatology before treatment, 1 day after climax, and shortly before discharge from hospital. Alcohol withdrawal scores were obtained and correlated to autonomic measures.


RESULTS
Ambulatory blood pressure and AW scores revealed characteristic withdrawal symptoms in both patient groups. Apart from the nonlinear parameter compression entropy, Hc, measures of HRV revealed no sign of autonomic dysfunction in contrast to the significantly increased heart rates at the time of admission. Latencies and amplitudes of SSR did not indicate any increase of sympathetic activity. A negative correlation was found between Hc and mental withdrawal symptoms.


CONCLUSIONS
We show here that classical measures for autonomic nervous system activity such as HRV and SSR are not suitable for describing the autonomic changes seen in acute AW, although a major role for the sympathetic nervous system has been proposed. This might be due to multiple dysregulation of metabolites in AWS or to subtle alcohol-induced damage to neuronal structures, issues that should be addressed in future studies.
Bär
Karl-Jürgen
KJ
Department of Psychiatry, Friedrich-Schiller-University of Jena, Jena, Germany. karl-juergen.Baer@med.uni-jena.de
Boettger
Michael Karl
MK
Neubauer
Rene
R
Grotelüschen
Marei
M
Jochum
Thomas
T
Baier
Vico
V
Sauer
Heinrich
H
Voss
Andreas
A
D000328:Adult; D000430:Alcohol Withdrawal Delirium / Q000503:physiopathology; D001341:Autonomic Nervous System / Q000502:physiology; D002492:Central Nervous System Depressants / Q000009:adverse effects*; D002719:Chlormethiazole / Q000627:therapeutic use; D000431:Ethanol / Q000009:adverse effects*; D018757:GABA Modulators / Q000627:therapeutic use; D005712:Galvanic Skin Response / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017711:Nonlinear Dynamics; D013375:Substance Withdrawal Syndrome / Q000188:drug therapy / Q000503:physiopathology*
D002492:Central Nervous System Depressants; D018757:GABA Modulators; D002719:Chlormethiazole; D000431:Ethanol