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Aboriginal, Torres Strait Islander and other First Nations people are advised that this catalogue contains names, recordings and images of deceased people and other content that may be culturally sensitive. Case report, letter to the editor, conference paper, dissertation, personal opinion or commentary. We carried out an electronic literature search to identify relevant studies. The search strings used in each search engine are reported in the Appendix 1.

The selection was done by three reviewers M. In the first stage of the selection process titles were screened to exclude those that were clearly not relevant to the review and then each reviewer read the abstract and full text of the remain articles and selected the relevant ones.

Disagreements between reviewers were resolved through group discussion. Regrettably, availability of information on several issues - sample and diagnosis; study design and protocol; type of EDA assessment; type of data presented in the results etc. The electronic searches identified studies; once duplicates removed records remained of which were excluded because the title clearly had no relevance to the review; records were excluded based on the Abstract; a further 68 studies were excluded because they were not written in English and 41 studies because the full text was not available.

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We assessed the full text of articles and excluded 31 studies at this stage. The main reasons for exclusion were: study population did not match inclusion criteria no primary clinical diagnosis of depression , focus on psychophysiological variables other than EDA e. Seventy-seven studies met all the inclusion criteria and were included in this review.

The selection process is represented in Fig. Although low EDA in depressed patients was first described in [ 32 ], interest in this physiological variable as a marker of depressive disorders occurred mainly between the late s and the s. The studies included in this section are very varied, both regarding sample and EDA variables. For clarity they have been grouped under the following headings: Depressed patients vs. Thorell et al. It has also been reported that depressed patients show marginally faster habituation of the skin resistance orienting response than healthy controls [ 44 , 45 ], although one study [ 35 ] with a lower NOS score than the others 2 vs.

Some researchers looked at age- and gender-related EDA variability. In adolescents [ 46 ] the results were consistent with the notion that EDA is lower in major depressive disorder MDD patients than in control subjects. In contrast SCL was similar in patients with dementia, depressed patients mean age As far as gender is concerned, SCLs were lower in women than in men in both depressed patients and healthy controls [ 47 ]. A study of GSRfound that patients were hyporesponsive because of depressive inhibition in an experimental condition, but failed to find any difference in GSR variables between patients and controls in two rest periods and in a no-response experimental condition [ 48 ].

Unlike most studies in this field Lapierre and Butter reported a higher SCL and higher basal skin resistance in depressed patients than in controls. Other studies reported higher SCLs in depressed subjects than in healthy controls [ 50 , 51 ] and psychiatric controls [ 50 ]. A couple of studies [ 52 , 53 ] failed to find any difference between depressed patients and healthy controls with respect to SCL [ 52 ] and SCR [ 53 ] variables. It should be noted that the Lapierre and Butter study scored 0 on the NOS because of the lack of information about the study design, whereas the other studies [50—52] described above had higher NOS scores 5,4, and 4, respectively.

It has been suggested that in depressed patients level of EDA may be a function of the type of depression. A recent, cross-sectional study offered preliminary evidence that EDA levels may differentiate the phases depressive vs. Lower EDA levels were found in patients with psychomotor retardation or symptoms of inhibition than in agitated depressed patients [ 55 , 56 , 58 ], mean NOS score 4. Moreover, the published research on this issue [ 40 , 58 , 59 , 63 ] is highly heterogeneous with respect to NOS score 2, 5, not applicable, and 1, respectively.

The absence of a SCR was observed in depressed patients with predominance of anxiety symptoms [ 40 ]. However, in view of the significant differences in the methodology and design of the relevant studies and their inconsistent results, the utility of EDA as a means of discrimination between subgroups of depressive patients remains to be demonstrated. Comparisons of EDA in depressed patients and patients with other psychiatric disorders have been performed to ascertain whether EDA can be used as a marker of depressive states.

EDA abnormalities have been described in schizophrenic patients [ 64 ]. Compared with normal controls, both schizophrenic and depressed patients showed high levels of non-response in the habituation series, but schizophrenics - unlike the depressed patients - showed a decrease in SCR non-response to the target tone [ 55 , 65 ]. In contrast Levinson [ 51 ] found no substantial differences between schizophrenic and depressed patients and normal controls with respect to SCR.

Pruneti et al. Have et al. In summary, there have been only six studies comparing depressed patients to other psychiatric patients, and they deal with different disorders, making it hard to draw clear conclusions. The published research using emotional elicitation protocols and other tasks to investigate EDA is highly heterogeneous with respect to sample, EDA variables, task and NOS score range: 3 - 6 , making it very hard to compare studies and to draw unequivocal conclusions.

Other studies found contrasting or mixed results depending on the type of task [ 72 , 73 , 73 , 74 , 75 , 50 ]. For instance, in a standardised mood induction experiment, MDD patients had higher SCRs than controls in the cartoon condition, but not when mood was induced through happy and neutral pictures [ 73 ].

Schneider et al. Rohde and coworkers [ 76 ] studied depressed patients and healthy controls performing a Mindful Breathing Exercise task and found no difference in SCR between the two groups.

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A couple of studies including elicitation protocols compared depressed patients with a seasonal pattern seasonal affective disorder and healthy controls. When exposed to overcast stimuli [ 77 ] or winter scenes [ 78 ] patients with seasonal affective disorder displayed more frequent SCRs and SCRs of greater magnitude, whereas the opposite pattern was found for sunny stimuli [ 77 ] and there was no disease by stimulus interaction for SCLs [ 77 ].

In short, the heterogeneity of study designs does not allow to draw clear conclusions in this field. Only two studies dealt with this topic and they concerned different hormones, so it is not possible to generalise from the results. Based on the dexamethasone suppression test EDA in depressive patients does not appear to be related to dysfunctions of the hypothalamic-pituitary-adrenal axis. On the other hand, suicide attempters exhibited opposite correlations between EDA and cortisol in plasma and in urine, suggesting that there may be a complex relationship between EDA and cortisol production [ 79 ].

The positive correlations found between basal levels of thyroid hormones and SCL in healthy subjects were absent or reversed in depressed patients [ 80 ]. A cross-sectional study by Weckowicz [ 81 ] found GSR was a near-significant predictor of psychotherapy and drug therapy in depressed patients. Other studies investigating the effects of antidepressant compounds on EDA have found different results, but they cover a range of drugs and the results are mixed.

Of the studies selected for this review, 6 assessed the effects of tricyclic antidepressants imipramine [ 83 , 84 ], amitriptyline [ 85 , 86 , 87 , 88 ] ; 1 a tetracyclic antidepressant maprotiline; [ 83 ] ; 1 a serotonin antagonist and reuptake inhibitor nefazodone; [ 89 ] ; 3 selective serotonin reuptake inhibitors paroxetine; [ 84 ], sertraline; [ 90 ], fluoxetine; [ 91 ] ; 1 a noradrenaline reuptake inhibitor reboxetine; [ 92 ] ; 1 a serotonin-noradrenaline reuptake inhibitor venlafaxine; [ 93 ] ; 1 a reversible inhibitor of monoamine oxidase A moclobemide; [ 94 ] ; and 1 an unspecified antidepressant [ 95 ].

Imipramine-treated patients showed lower EDA than controls [ 84 ]. Regarding amitriptyline, findings were not consistent across studies, spanning from no correlation between the drug plasma level and EDA measures [ 86 ], to lower activation and decreased NS. Reboxetine reduced SCR after multiple dosing [ 92 ], while sertraline, moclobemide and nefazodone-treated patients showed no change in SCR [ 90 , 94 , 89 ]. On the other hand, sertraline-treated patients had lower SCL compared to controls [ 90 ].


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Venlafaxine caused a reduction of EDA measures [ 93 ]. See Tables 1 and 2 for further details. A couple of follow-up studies investigated the temporal stability of EDA. NOS 3. A one-year cross-sectional follow-up study of depressive and depressive-anxious patients found mixed results with respect to the temporal stability of EDA: changes were smallest in stable patients, and greatest in all four labile-activated patients [ 85 ].

The laterality of EDA has also been explored and it has been hypothesised that there is right-hemisphere hyperexcitability in depressive conditions. After the original study by Myslobodsky and Horesh [ 96 ] others reported that EDA levels were lower on the right hand than the left under various experimental conditions, including rest [ 97 ].

Nevertheless, contrasting results were obtained both at rest and during stimulation [ 65 , 98 ], and during different phases of illness, including remission [ 37 , 99 ]. Notably, the first two studies cited in this paragraph had lower NOS scores 3 and 2 than the last four respectively 4, 6, 5, 5 ; the existence of lateral differences in EDA remains to be confirmed. It has been suggested that differences in EDA may be specific to suicidality rather than depression [ ]. Although there has been less research on EDA in individuals exhibiting suicidal behaviour than in people with depression, there is consistent evidence of electrodermal hypoactivity in depressed suicide attempters compared with non-suicidal depressed patients and healthy controls [ 61 , 58 , , ].

Correlations between EDA and the type and level of suicide risk have been suggested. For instance, one study compared patients recently admitted to the hospital because of suicide threats or preoccupations, but with no history of attempts, controls with no history of suicide threats or attempts and no reported suicidal thoughts at the time of data collection and suicide attempters with a history of one or more suicide attempts.

Other studies have assessed SCR habituation in individuals with different patterns of suicidal behaviour. Violent suicide attempters and suicide completers were both found to be fast habituators [ , , ]. The findings on non-violent suicide attempters, patients with suicidal ideation and non-suicidal depressed patients are less clear: one study found that non-violent suicide attempters showed either fast or slow habituation [ ] but another found no differences among these groups violent and non-violent suicide attempters, patients with suicidal ideation, non suicidal patients [ ].

Jandl et al. A study comparing parasuicidal adolescent girls with healthy controls found no differences in EDA variables [ ]. Electrodermal hyporeactivity was strongly associated with high suicide risk. Extremely low electrodermal reactivity had a sensitivity of A further analysis of data from depressive patients by Thorell et al. Recently the protocol for a study involving patients with a primary diagnosis of depression recruited from 15 centres in nine European countries that will test the predictive value of electrodermal hyporeactivity measured with the electrodermal orienting reactivity EDOR test for suicide and suicide attempt has been published.

The extant literature suggests that suicide attempt with intent to die and completed suicide will be associated with electrodermal hyporeactivity [ 27 ]. The aim of this review is to offer a comprehensive overview of the EDA literature with a view to assessing its potential utility as a biomarker of depressive states and risk of suicidal behaviour, and its potential role in advanced, integrated physiological evaluation systems. Overall, our review of the literature supports the hypothesis that electrodermal hypoactivity is a feature of depression. Nevertheless, considering the number and robustness of studies, EDA seems to be more useful in discriminating depressive patients from healthy controls than from other psychiatric patients.

Moreover, specific EDA features e.

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SCR, habituation rate, etc. Briefly, specific patterns of electrodermal hypoactivity may be a reliable marker of a depressive state at population level, but they should be carefully combined with other physiological and non-physiological indicators when used for preventive and diagnostic purposes. Another area that deserves further investigation is the potential use of EDA to distinguish between subtypes of depression.

At present the evidence suggests that patients with psychomotor retardation, endogenous and psychotic depression show lower EDA values than patients with agitation, non-endogenous and neurotic depression, respectively. It has been hypothesised that electrodermal hypoactivity is a rather stable trait of patients affected by depression, although increases in EDA may indicate euthymia or remission [ 61 , 54 ]. It should be noted that extremely hyporesponsive depressive patients, including suicide attempters and patients with recurrent major depression, may fail to reach the EDA levels of healthy subjects even when in remission [ 54 ].

There is even more debate about the effects of antidepressants on EDA and research has yielded mixed results. In the context of experimental anxiety conditioning tasks some antidepressants blunt EDA in healthy subjects, but the data from depressed patients are not consistent and there is no clear correlation between EDA and clinical improvement.

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As Thorell hypothesised, electrodermal hypoactivity may be a rather stable trait of depressed patients; EDA appears to be only marginally affected by treatment and clinical improvement, and normalisation may not occur until several months - or even years - after clinical recovery [ 61 ]. Moreover, there is only limited evidence in relation to each drug and for most drugs it comes from just one study.

As far as suicidal behaviour is concerned, extreme hyporeactivity has been consistently reported in both suicide attempters and at baseline in subjects who eventually committed suicide during a follow-up period; moreover, hyporeactivity seems to be related to the choice of a violent method for attempted or completed suicide [ , , ]. On this basis it has been hypothesised that extreme electrodermal hypoactivity is a marker of suicidal tendencies in depressed patients, and it appears to be independent of severity of depression [ 61 , ].

Recent studies [ 24 , ] showed that EDA discriminates well between patients who will subsequently commit suicide, make a non-violent suicide attempt or make a violent suicide attempt, but it is less clear that EDA can be used to distinguish individuals with current suicidal ideation from depressed patients who are not currently suicidal.

Opening the « black box » of electrodermal activity in consumer neuroscience research

Nevertheless, it has been suggested that the evidence is sufficient to warrant strict monitoring of both euthymic and depressed patients who are show extreme electrodermal hyporeactivity, even in the absence of suicidal ideation. Obviously close monitoring and adequate antidepressant therapy are even more necessary in hyporeactive patients with suicidal ideation [ 24 ]. Nevertheless, several limitations of this review should be acknowledged. First, as shown by the NOS scores, the quality of several of the included studies is questionable and most are quite old. Definitional inconsistency is also a problem in comparisons of subtypes of depression as there are no standard criteria for distinguishing between, for example, retarded and agitated depression, endogenous and non-endogenous depression or psychotic and neurotic depression.

Furthermore, most studies included patients with various mood disorder diagnoses e. Finally, comorbidity was not always accounted for in comparisons between depression and other pathological conditions. Besides diagnostic issues, over time the EDA assessment methods have changed, leading to inconsistencies. This review offers a more comprehensive assessment of the extant EDA literature than previous ones [ 25 , 26 ] and it corroborates their findings, namely that there are associations between electrodermal hypoactivity and depression and suicidal behaviour.

EDA appears to be a reliable marker, with high sensitivity and specificity, of depressive states, suicidal tendencies and suicidal behaviour [ 24 , 39 , 43 , ]. Nevertheless, further studies are required to validate EDA as an indicator of other clinical features, such as depression subtypes, response to treatment and acute suicide risk. Sudol K, Mann JJ. Biomarkers of suicide attempt behavior: towards a biological model of risk.

Curr Psychiatry Rep. Cognition and the autonomic nervous system: orienting, anticipation, and conditioning. Pandey GN, Dwivedy Y. The neurobiological basis of suicide.

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Int J Psychophysiol. Measuring emotion: behavior, feeling and physiology. In Cognitive Neuroscience of Emotion. Lane and L. New York: Oxford University Press. Boucsein, W. Electrodermal activity 2nd ed. Mechanism of decrease in heart rate by peripheral dopaminergic D2-receptors. Yonsei Med J. Changes in autonomic responsiveness following bilateral amygdalectomy in humans. Neuropsychiatry, Neuropsychol Behav Neurol. Direct electrical stimulation of specific human brain structures and bilateral electrodermal activity.

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