Biological Psychiatry - Vol. 2

By Hugo D'Haenen; J.A. Den Boer et al. | Go to book overview

XVIII–6
Psychophysiology of Mood Disorders

Silvana Galderisi


INTRODUCTION

Mood disorders are markedly heterogeneous with respect to signs, symptoms, course, response to therapeutic interventions and outcome. Attempts at reducing heterogeneity by subgrouping subjects on the basis of clinical aspects is a valuable strategy; however, the scarce impact on everyday practice of most clinical subtypes underscores its limitation. External validation of clinical subtypes (demonstrating that they are characterized by different psychophysiological patterns) has been an important goal of psychophysiological research in mood disorders. Several other conceptual strategies can be identified throughout the reviewed literature: the search for trait or state markers, the attempt at clarifying pathogenetic mechanisms of the observed dysfunctions, and the identification of early predictors of course, outcome or response to different therapeutic interventions.

On the whole, however, the field has suffered from the lack of unifying hypotheses and systematic research, which is reflected in the fact that relevant reviews, including the present one, are organized according to the different techniques applied in the investigations. Moreover, evaluation and comparison of different findings is often hampered by poor characterization of studied populations with respect to relevant or confounding variables such as symptoms, clinical subtypes, medication (or other therapeutic intervention) history, or substance abuse or dependence.

This chapter is organized in two main sections, peripheral and central measures, each including several subsections dealing with specific measures or techniques.

As previous excellent reviews of the topic are available (Goodwin and Jamison, 1990; Henriques and Davidson, 1989; Zahn, 1986), an attempt has been made to cover the relevant literature with particular attention to more recent findings. Furthermore, since some readers might be unfamiliar with specific technical issues, when deemed appropriate a brief definition and description of the psychophysiological measures or techniques discussed in the section is provided.


PERIPHERAL PSYCHOPHYSIOLOGICAL INDICES
IN RESEARCH ON MOOD DISORDERS

Disturbances of several physiological functions, such as sleep, appetite, sexual drive, sweat secretion and chronobiological rhythms, are commonly found in mood disorders and indicate a dysregulation of the autonomous system in affected subjects. Despite the large number of studies focusing on autonomic measures, much remains to be done to characterize this dysregulation. Investigations based on die concomitant evaluation of several autonomic parameters are promising; their integration with central measures, as well as witii neuroendocrine and neurochemical measures, may contribute greatly to progress in this field of research.


Electrodermal Activity

Electrodermal activity (EDA) has been largely investigated as a measure of tonic and phasic arousal. Different variables can be evaluated, including the skin conductance level (SCL; the tonic level, generally measured after a resting period, before the first stimulus presentation), the spontaneous skin conductance responses (SSCRs; nonspecific fluctuations of activity independent of external stimuli), the skin conductance orienting responses (SCORs; related to external stimuli) and habituation (reduction in response to repeated stimulation). For each of these indices the eventual asymmetry pattern can be assessed.

Low baseline EDA has been frequently found in depressed patients when compared with healthy subjects. Such a reduction has been observed for both SCL and SCORs (Dawson et al., 1977, 1985; Iacono et al., 1983; 1984; Schnur et al., 1995; Storrie et al., 1981; Ward et al., 1983; Zahn, 1986). Negative or discrepant findings have also been reported: Toone et al. (1981) found no difference between unmedicated subjects with depression and healthy comparison subjects; Albus et al. (1982) found higher SCL in drug-free depressed patients as compared with controls; Levinson (1991) reported higher SCL and a trend toward more SSCRs in a group of depressed patients (including schizoaffective depressed subjects), and interpreted the finding as me result of a hyperarousal condition. Faster habituation of the SCOR has been demonstrated in depressive patients (Frith et al., 1982; Thorell, 1987). However, findings have been inconsistent (Miquel et al., 1999; Storrie et al., 1981). Methodological issues might partly account for the observed discrepancies, while the confounding role of clinical heterogeneity in tested populations is not strongly supported by available findings. In fact, the reduction of EDA activity and reactivity in subjects with mood disorders appears rather independent of subjects' clinical characteristics. Low SCL has been found in both medicated and unmedicated depressed subjects (Iacono et al., 1983; Storrie et al., 1981; Thorell et al., 1987; Ward and Doerr, 1986), in unipolar and bipolar patients (Williams et al., 1985) and in acutely ill depressed and manic patients, as well as after clinical recovery associated with antidepressant treatment or electroconvulsive therapy (Dawson et al., 1977; Storrie et al., 1981), in both suppressors and nonsuppressors to the dexamethasone suppression test (DST) (Williams et al., 1985), and in subclinically depressed versus non-depressed college students (Gehricke and Shapiro, 2001). However, EDA reduction seems to be even more pronounced in endogenous patients and in patients with symptoms of inhibition (Dawson et al., 1977; Lader and Wing, 1969; Thorell et al., 1987; Williams et al., 1985).

EDA stability across different clinical subtypes of affective disorders has prompted research on its potential diagnostic utility. Reduced SCL as a diagnostic index of depression was investigated by several authors (Dawson et al., 1985; Iacono et al., 1983; Ward

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