Electrodermal Activity as a Predictor of Schizophrenic Relapse

Abstract

Electrodermal activity and self-report of affect were recorded from schizophrenic patients with their relative absent and present, at index admission and on two subsequent occasions after discharge. It was hypothesised that it would be possible to discriminate at index admission patients who relapsed in the subsequent 2-year period from those who remained well, and that these differences would be stable over time and independent of illness episode. The former hypothesis was supported in part, but not the second. The results did not support electrodermal hyperactivity as a stable, enduring vulnerability marker.

Electrodermal predictors of functional outcome and negative symptoms in schizophrenia

“…These studies examining electrodermal activity while at rest and in response to nontask orienting stimuli or simple task stimuli are consistent with findings obtained when activity has been recorded while patients were socially interacting with relatives. Sturgeon, Turpin, Kuipers, Berkowitz, and Leff (1984) and Tarrier and Barrowclough (1989) reported that higher levels of electrodermal activity were associated with greater relapse rates over a 9‐month and 2‐year period, respectively.…”

Psychophysiological prodromal signs of schizophrenic relapse: A pilot study

“…One easily measured physiological sign of stress is increased electrodermal activity (EDA). EDA is controlled by the sympathetic nervous system (SNS) (Dawson et al, 2007), is known to increase in response to psychosocial stressors considered key in psychotic relapse in schizophrenia (Tarrier et al, 1979; Tarrier & Barrowclough, 1989), and has been found to increase during exacerbation of symptoms (Dawson et al, 1994). …”

The interaction of electrodermal activity and expressed emotion in predicting symptoms in recent‐onset schizophrenia

“…Heightened SNS activity, often indexed by (EDA), is frequently found in schizophrenia patients (e.g., Dawson & Nuechterlein, 1984; Dawson et al, 1994), and is related to longer hospital stays poor symptomatic and functional outcomes (Schell et al, 2005; Tarrier & Barrowclough, 1989). It is possible that stressors induce SNS activation, which then impairs cognitive processing and causes patients to further misinterpret stimuli and to interact with the environment in ways that contribute to a return of symptoms (Dawson & Nuechterlein, 1984; Nuechterlein et al, 1992a; 1992b).…”

“…The finding that high EE predicts psychotic relapse is well replicated (Wearden et al, 2000). The relationship between living in a high-EE family and poor outcome may be due to the stressful nature of living in such an environment—a relationship that may be mediated by heightened SNS activation on the part of the patient (Nuechterlein & Dawson, 1984; Tarrier & Barrowclough, 1989). Indeed, higher levels of EDA are observed in patients whose families express high EE (e.g., Tarrier et al, 1979).…”