Functional neuroanatomical correlates of electrodermalactivity: A positron emission tomographic study

MATS FREDRIKSON,a TOMAS FURMARK,a MARIA TILLFORS OLSSON,aHÅKAN FISCHER,a,b JESPER ANDERSSON,b and BENGT LÅNGSTRÖMb

aDepartment of Psychology, Uppsala University, SwedenbUppsala University PET-Centre Academic Hospital, Sweden

AbstractTo reveal areas in the central nervous system of importance for electrodermal control, regional cerebral blood flow~rCBF! was correlated to nonspecific skin conductance fluctuations ~NSF! during aversive and nonaversive conditions.Participants viewed a TV screen displaying white noise or snake videotapes presented both with and without electricshocks given to the right hand. H2 15O positron emission tomography was used to measure rCBF, and the constantvoltage technique was used to measure NSF from the left hand. Electrodermal activity was positively related to rCBFin the left primary motor cortex ~MI, Brodmann’s Area 4! and bilaterally in the anterior ~Areas 24 and 32! and posteriorcingulate cortex ~Area 23!. Negative relations were observed bilaterally in the secondary visual cortex ~Areas 18 and19! and the right inferior parietal cortex ~Area 39!, with a tendency also for the right insular cortex ~Areas 13, 15, and16!. Because results from lesion and stimulation studies in humans converge with the present imaging results, weconclude that the cingulum and the motor cortex, in addition to the parietal and possibly the insular cortex, form partof one or several distributed neural network~s! involved in electrodermal control. Because these areas also supportanticipation, affect, and locomotion, electrodermal responses seem to reflect cognitively or emotionally mediated motorpreparation.Descriptors: Central nervous system, Brain, Functional neuroanatomy, Autonomic nervous system, Skinconductance response, Neuroimaging

Electrodermal activity ~EDA! is a valid measure of autonomicnervous system activity frequently used to index complex centralnervous system ~CNS! processes such as attention, cognition,learning, and emotion ~see reviews of Boucsein, 1992; Edelberg,1972; Fowles, 1974!. In general, the CNS origin of EDA is de-fined broadly by the experimental protocol rather than specif-ically by functional neuroanatomical knowledge because, at leastin humans, little is known about the CNS underpinnings ofEDA.Studies addressing the neuroanatomical basis of EDA in hu-

mans are few, but lesion, stimulation, and modern brain imagingtechniques have been used occasionally. Raine, Reynolds, andSheard ~1991! found a positive correlation between the amplitudeof the electrodermal orienting response and the size of certainareas in the frontal cortex as assessed with magnetic resonanceimaging. The size of the pons and the left but not the right temporalarea, including the amygdala, were also positively correlated withthe magnitude of the orienting response. However, it is not clear

how individual differences in the size of a given structure relate toindividual differences in function. Therefore, direct measures ormanipulations of brain functions would be more informative.Mangina and Beuzeron-Mangina ~1996! recently reported that

electrodermal responding resulted from intracerebral stimulationof the amygdala, the hippocampus, the anterior cingulate, frontalcortices, and the temporal gyri. Limbic structures were related toipsilateral electrodermal control and cortical areas were related tobilateral electrodermal control. Linden and Berlit ~1995! observedthat stroke patients with brainstem lesions displayed bilateral EDAabnormalities, whereas persons with cortical lesions showed ab-normalities indicative of contralateral control. In several lesionstudies, in which the sites of the lesions were not detailed, right butnot left hemispheric lesions tended to attenuate electrodermal re-actions ~Heilman, Schwartz, & Watson, 1978; Morrow, Vrtunski,Kim, & Boller, 1981; Zoccolotti, Scabini, & Violani, 1982!. In arecent study, Tranel and Damasio ~1994! related focal lesion sitesto skin-conductance orienting responses. Lesions in the ventrome-dial frontal cortex ~right and left!, the right inferior parietal cortex,and the anterior cingulate cortex ~right and left! were associatedwith reduced EDA.Brain imaging studies are of potential value to evaluate how

EDA is dynamically related to central neuronal activity. Usingpositron emission tomography ~PET!, Dawson in a presidentialaddress ~1990! and Hazlett, Dawson, Buchsbaum, and Nuechter-

This work was supported by the Swedish Council for Research in theHumanities and Social Sciences.

We are thankful to the participants.Address reprint requests to: Mats Fredrikson, Department of Psychol-

ogy, Uppsala University, Box 1225, S-751 42 Uppsala, Sweden. E-mail:mats.fredrikson@itp.uu.se.

Psychophysiology, 35 ~1998!, 179–185. Cambridge University Press. Printed in the USA.Copyright © 1998 Society for Psychophysiological Research

179

lein ~1993! in the full paper reported that schizophrenic patientsclassified as electrodermal nonresponders, as compared with elec-trodermal responders, showed lower absolute total brain metabolicrates at rest and relative ~region0whole brain! lower activity infrontal and hippocampal areas and in the right amygdala. Similarly,we recently observed a positive correlation between regional cere-bral blood flow in the right amygdala and conditioned electroder-mal activity ~Furmark, Fischer,Wik, Larsson, & Fredrikson, 1997!.The animal literature on CNS control of EDA stems from stim-

ulation and lesion studies performed predominantly in cats but alsoin rats and monkeys ~see review by Sequeira & Roy, 1993!. Thereticular formation of the brainstem appears to be the main supra-spinal structure involved in electrodermal control. An inhibitorycenter has been located in the ventromedial reticular formation inthe midbrain, whereas the diencephalic part of the reticular for-mation excite EDA ~Roy, Sequeira, & Delerm, 1993!. Excitatoryinfluences from the hypothalamus and the amygdala have beenreported from several animal preparations ~Davison & Koss, 1975;Lang, Tuovinen, &Valleala, 1964; Yokota, Sato, & Fujimori, 1963!.Also, amygdala lesions in rhesus monkeys ~Bagshaw, Kimble, &Pribram, 1965! and in humans compromise EDA ~Bechara et al.,1995; LaBar, LeDoux, Spencer, & Phelps, 1995!.The role of hippocampus is unclear because findings from an-

imal ~Bagshaw et al., 1965; Edelberg, 1972; Yokota et al., 1963!and human studies ~Hazlett et al., 1993; Knight, 1996; Tranel &Hyman, 1990! are mixed. Data from animal stimulation studiessuggest excitatory thalamic control ~Wang, 1964! and inhibitoryinfluences from the caudate nucleus ~Wang & Brown, 1956!. In thecortex, evidence from stimulation and lesion studies suggest thatthe cingulate gyrus regulates EDA in cats ~Isamat, 1961; Ward,1948!, monkeys ~Showers & Crosby, 1958!, and humans ~Mangi-na & Beuzeron-Mangina, 1996!. Frontal and motor areas are alsoof importance ~Grueninger, Kimble, & Levine, 1965; Langworthy& Richter, 1930; Schwartz, 1937; Wilcott & Bradley, 1970!. Forexample, electrical stimulation of the motor and premotor areas~Brodmann areas 4 and 6! in cats have been reported to elicit EDA~Sequeira & Roy, 1993!. Thus, electrodermal activity seem mod-ulated by one or several neural networks.Following Schliack and Schiffter ~1979!, Boucsein ~1992! pro-

posed that EDA is controlled from three systems differentiallyrelated to arousal, emotion, and locomotion. First, the limbic sys-tem ~the hypothalamus, the anterior thalamus, the cingulate gyrus,the fornix, and the hippocampus!, via hypothalamic thermoregu-latory areas, form an ipsilateral control system involved in thermo-regulation and emotion. A second contralateral system consists ofmotor areas and parts of the basal ganglia involved in locomotion,whereas the third system held to be either ipsi- or contralateralencompasses areas in the reticular formation exercising electro-dermal control associated with basic arousal states.The goal of the present study was to assess the functional

neuroanatomy of EDA by relating nonspecific skin conductancefluctuations ~NSF! to regional cerebral blood flow ~rCBF! mea-sured with PET while participants viewed a TV screen displayingwhite noise and snake videotapes both presented with and withoutelectric shocks. The present analysis is based on data to be pre-sented by Fredrikson, Fischer, Furmark,Wik, andAndersson ~1997!,in which H2 15O methodology was used to measure rCBF withsimultaneous registration of EDAusing the constant voltage method~Venables & Christie, 1973!. To relate NSF ~Boucsein,1992! torCBF, we used a stepwise linear regression model correcting forsubject and stimulation effects, rendering results independent ofthe experimental conditions ~Friston et al., 1995!.

Methods

ParticipantsSix women with a mean age ~6SD) of 26.8 ~67.3! years ~range,21–41 years! participated. To be included, participants could notmeet any of the criteria specified by DSM-IV ~American Psychi-atric Association, 1994! for specific phobia. None of the partici-pants were excluded on this basis. Persons with previous or currentpsychiatric history or with neurological deficit, somatic disease,chronic use of prescribed medication, or abuse of alcohol or nar-cotics were not included in the study. The study was approved bythe local Ethics Committee and the Radiation Safety Committee ofUppsala University. Informed consent was obtained.

ProcedureParticipants were scanned twice during each of five conditionswith visual stimulation. All visual presentations were displayedon a 11 ! 8.5 cm TV screen about 0.5 m in front of the partici-pant’s eyes. The first and second conditions consisted of visualpresentation of a snake video or white noise, respectively. Thethird and fourth conditions were identical to Conditions 1 and 2,with the addition of the delivery of electric shocks to the righthand. The fifth condition consisted of another presentation of thesnake video without electrical shocks. The order of the examina-tions was such that Conditions 1 and 2 were counterbalanced, aswere Conditions 3 and 4. The condition-specific effects have beenreported by Fredrikson et al. ~1997!, and the effects reported hereare the relations between NSF and rCBF.Eight electric shock stimuli were used during each shock con-

dition. The electrical stimulation consisted of eight 0.5-s electricshocks individually determined to induce “discomfort but not pain”delivered through Beckman Offner Ag0AgCl 0.8-mm-diameterelectrodes applied to the second phalanx of the participant’s rightsecond and third fingers.

Electrodermal RecordingsElectrodermal activity was recorded through Beckman-OffnerAg0AgCl electrodes, 8 mm in diameter and housed in plastic cups,by means of a Hagfors-type constant voltage circuit ~Venables &Christie, 1973!. Isotonic electrode paste served as the electrolyte~0.5% NaCl0100 ml H2O!. The electrodes were fastened with ad-hesive collars to the palmar side of the second phalanx of theparticipant’s left hand. The electrodermal activity was recorded con-tinuously on paper using a Siemens-Elema Mingograph. The NSF~Martin & Rust,1976! exceeding 0.05 mS were counted over 60 sof the initial exposure period corresponding to maximum rCBFactivation and expressed as NSF0min.

Blood Flow RecordingsScanning. Investigations were performed on a GEMS PC2048-

15B scanner ~Holte, Eriksson, & Dahlbom, 1989! that produced15 slices with a 6.5-mm slice spacing and a 6-mm axial and trans-axial resolution. A venous catheter was inserted, and the partici-pants were positioned in the scanner such that the planes wereparallel to a line between the anterior and posterior commissure,where the most basal slice was below the orbita. The participants’heads were fixed in a commercial headholder using a fast harden-ing foam. The lights were dimmed, and participants were allowedto rest for 20 min. A 10-min transmission scan was then performedwith a rotating 68Ge pin source. During the transmission scan, eachparticipant was told that she was to receive the first injection, afterwhich she was given a saline injection. Care was taken to mimic,

180 M. Fredrikson et al.

with regard to the behavior of the injector, an actual emission scanduring this sham injection, which was performed to attenuate anynovelty effects ~Friston, Frith, Liddle, & Frackowiak, 1993!. Foreach emission scan, the injector started the scanning by pressing apedal while simultaneously injecting 600–800 MBq of 15O water.Data were collected in 15 10-s frames following the injection. Eachparticipant had 10 scans during five conditions, with the order ofpresentation partly counterbalanced. After these 10 scans, an addi-tional injection was performed during which the scanner couch wasautomatically translated back and forth between two positions10 cm apart. Data were collected only during one of these positionsand not during the transfer.

Image reconstruction. Data from the first 100 s after arrival ofbolus to the brain were summed in a weighted fashion such thatdata from the initial uptake phase were given a higher weight~Andersson & Schneider, 1997!. Images were reconstructed fromthe weighted summation data following correction for attenuationand scatter by using the transmission scan ~Bergström, Eriksson,Bohm, Blomqvist, & Litton, 1983! and filtered with a 20-mm Han-ning filter. The additional scan, with couch translations, was recon-structed to a 30-slice image set with a 20-cm coverage in axialdirection using contour finding for attenuation correction ~Berg-ström, Litton, Eriksson, Bohm, & Blomqvist, 1982!.

Image registration. The scan with the 20-cm axial coveragewas automatically adapted to a computerized brain atlas ~Anders-son &Thurfjell, 1997; Greitz, Bohm, Holte, & Eriksson, 1991!, andeach of the other emission scans were registered to the scan withfull axial coverage ~Andersson, 1995!. To facilitate communica-tion of results, the Talairach brain ~Talairach & Tournoux, 1988!has been adapted to the Greitz brain, and by using the inverse ofthat transform, Talairach coordinates may be obtained for eachpoint in the Greitz space ~Lennart Thurfjell, personal communica-tion, May 2, 1997!.

Statistical AnalysisData were normalized for global flow by using ratio scaling, inwhich global flow was evaluated for all regions of the brain notaffected by the design, thereby ensuring independence betweenlocal and global flow ~Andersson, in press!. Data were fitted to astatistical model described by

Yijk " u # ti # gj # b~EDAijk $ EDA!

# Eijk !i " 1,2, . . . ,5 ~conditions!j " 1,2, . . . ,6 ~subjects!k " 1,2 ~repeated scans!

~1!

using multiple linear regression ~Friston et al., 1995!, where Yijkdenotes local flow in condition i, subject j, and scan k, u denotesaverage local flow across subjects and conditions, ti denotes ef-fects specific to condition i, gj denotes effects specific to subject j,b denotes the dependence between local flow and EDA, EDAijkdenotes the observed EDA in the scan identified by i, j, and k, andEDA denotes EDA averaged across all scans. Two model fits wereperformed, once including the b term and once excluding the bterm. By relating the variance accounted for by the b term to theresidual variance after fitting the full model, an F statistic describ-ing the effects of EDA was created. The sign-extended square rootof the F statistic yielded a t statistic for the regression versus EDA,

t49 "Zb_ Zb_"

MSbMSE

, ~2!

which was subsequently converted through a probability-preserv-ing transform in which the p values for the t distribution with 49degrees of freedom were calculated and the z scores for those pvalues were written to a z-score map ~Friston, Frith, Liddle, &Frackowiak, 1991!.The significance of the z-score map was assessed at an omnibus

level using the mean square z score ~Worsley, Poline, Vandal, &Friston, 1995!. This test considers the z-score map as a whole andanswers the question as to whether there are one or more regionsin the brain whose blood flow correlates to EDA. By using all theavailable information simultaneously, this test has a high statisticalpower but lacks any localizing power, meaning that the test doesnot supply any information on which specific areas are implied~Friston, Holmes, Poline, Price, & Frith, 1996!. Local testing wasperformed using the spatial extent of connected clusters of voxelswith a z score above 1.96 ~Friston, Worsley, Frackowiak, Mazzi-otta, & Evans, 1994! as the test statistic. This test estimates theprobability of the cluster as a whole but admits no interferences tobe made for the individual pixels within the cluster. The test takesinto account the volume of the tested process and, hence, correctsfor multiple comparisons. The value of 1.96 is lower than the 2.6originally recommended ~Friston et al., 1994! and is motivated bythe use of a different way of estimating global flow ~Andersson, inpress!, thereby avoiding the shift of the z-score distribution thatmight otherwise cause problems when using a low threshold. Fur-thermore, that value is actually higher than the lower level ~1.64!later suggested by Friston et al. ~1996!.By including the task effects ~t! as a confounding factor in the

model, the resulting relations between rCBF and EDA will bewithin subject and within state. This comparison has importantimplications on the interpretation and specifically the generaliza-tion of the results. Thus, activity in the observed areas correlate tothe EDA in a manner independent of the experimental conditions.Because data are corrected by the least square estimates of the taskeffects rather than by the actual underlying effects, this statementis not perfectly true but will for practical purposes be a relevantapproximation.

Results

EDA measured as nonspecific electrodermal fluctuations had amean ~6SD) value of 1.9 ~61.5!, ranging from 0 to 6 NSF0min.The regression analysis yielded an omnibus p value of .00053, thussupporting a significant relation between electrodermal activityand rCBF. Three rCBF clusters ~1, 2, and 3 in Table 1! had sig-nificant p values ~ ps , .02!, and two clusters ~4 and 5 in Table 1!had borderline significant p values ~ ps , .07!. Significantly pos-itive correlations between EDA and rCBF were observed in themidcingulate cortex ~Brodmann Areas 24, and 32 and Area 23!,with a focus in the left hemisphere extending into the right ~seeTable 1 and Figure 1!. This cluster in the midcingulate also en-compassed the left primary motor cortex ~MI, Area 4!. Negativecorrelations were observed in the second cluster located in theright inferior parietal cortex ~Area 39! and in the right and leftsecondary visual cortex ~Area 19!. Borderline significant correla-tions were observed in Cluster 4, located in the left secondaryvisual cortex ~Area 18!. A borderline significant correlation wasalso evident in the right insular cortex ~Areas 13, 15, and 16!.

Brain networks in electrodermal control 181

Discussion

The goal of the present study was to relate PET measures of rCBFto measures of electrodermal activity. Present ~Boucsein, 1992;Edelberg, 1972; Fowles, 1974! and previous ~Darrow, 1937! mod-els for CNS control of electrodermal activity have pointed out therole of the electrodermal system in thermal regulation, cognition,emotion, and locomotion. We observed correlations between EDA

and CNS activity in structures related to emotion, locomotion,attention, visual perception, and interoception. Neuronal activity inmost ~except frontal! areas reported to be involved in electroder-mal control in the lesion study by Tranel and Damasio ~1994! alsorelated to EDA in the present imaging study.Neural activity of the midcingulate cortex was positively cor-

related with electrodermal activity. This finding is consistent withprevious stimulation and lesion studies in humans ~Mangina &

Table 1. Results for Clusters of Brain Areas Displaying Correlations Between Cerebral Blood Flow andElectrodermal Activity Measured as Nonspecific Electrodermal Fluctuations

Brain areaBrodmannarea x y z

Maximum pixelz value

Clusterp value

Positive CorrelationsCluster 1 .02Anterior cingulate cortex ~si! 32 !5 !11 42 3.55Anterior cingulate cortex ~dx! 32 5 16 48 2.87Anterior cingulate cortex ~si! 24 !22 !17 32 3.21Anterior cingulate cortex ~dx! 24 8 !10 33 2.35Posterior cingulate cortex ~si! 23 !11 !25 32 2.65Posterior cingulate cortex ~dx! 23 14 !37 31 2.40Primary motor cortex ~si! 4 !27 !17 32 3.11

Negative CorrelationsCluster 2 .002Secondary visual cortex ~dx! 19 49 !66 !15 3.49Inferior parietal cortex ~dx! 39 38 !69 0 2.21

Cluster 3 .02Secondary visual cortex ~si! 19 !56 !71 3 2.79

Cluster 4 .06Secondary visual cortex ~si! 18 !26 !97 15 3.00

Cluster 5 .07Insular cortex ~dx! 13,15,16 52 17 !8 3.00

Note: All brain and Brodmann areas included in these clusters are listed. dx " dexter ~right side of the brain!, si " sinister ~leftside of the brain!.

Figure 1. Transaxial ~A!, sagittal ~B!, and coronal ~C! images visualizing significant positive correlations between regional cerebralblood flow and nonspecific electrodermal fluctuations in the anterior and posterior cingulate cortex and in the primary motor cortex.Top is anterior in the transaxial images, left is dexter ~right side of the brain! in the transaxial and coronal images, and left is anteriorin the sagittal image. Neural activation displayed correspond to Brodmann Areas 4 ~MI!, 23, 24, and 32.

182 M. Fredrikson et al.

Beuzeron-Mangina, 1996; Tranel & Damasio, 1994!. Tranel andDamasio ~1994! reported that individuals with bilateral anteriorcingulate lesions had compromised or had no EDA responses, andMangina and Beuzeron-Mangina ~1996! reported that intracerebralstimulation of the anterior cingulate cortex resulted in electroder-mal reactions, thus supporting a prominent role for the anteriorcingulate in electrodermal control. The connectivity pattern in thepresent study was lateralized to the left but extended into the righthemisphere. In general, the correlative pattern was lateralized tothe left for the anterior cingulate and the primary motor cortex andlateralized to the right for the inferior parietal and insular cortices.The interpretation of this pattern is not clear. This pattern maysupport lateralized control, but we measured EDA only on theparticipants’ left hands and therefore we cannot evaluate measuredlaterality properly. In addition, electric shocks were always givenon the participant’s right hand and therefore we cannot evaluatestimulated laterality in detail. Finally, although the focus of thecluster, for example in the anterior cingulate cortex, was in the lefthemisphere, the cluster extended into the right hemisphere sup-porting incomplete lateralization.The anterior cingulum forms part of an attentional system ~for

a review, see Cabeza & Nyberg, 1997! that executes control overendocrine and autonomic functions, including electrodermal activ-ity ~cf. Devinsky, Morrell, & Vogt, 1995, for a review!. Activity inthis area relates to emotional control in depression ~Drevets et al.,1997!, pain affect ~Rainville, Duncan, Price, Carrier, & Bushnell,1997!, anticipation ~Murtha, Chertkow, Beauregard, Dixon, &Evans, 1996!, and anticipatory electrodermal responses ~Bechara,Damasio, Tranel, & Damasio, 1997! when choosing adverse re-sponse options. Blood flow in the anterior and posterior cingulatehas also been found to display a left-sided increase as a function ofclassical conditioning, indicating that the cingulum could serve asa sensory–sensory interface integrating, for example, visual andtactile nocioceptive information ~Fredrikson,Wik, Fischer, &Anders-son, 1995!.Data from the present study support that activity in the mid-

cingulate is associated with electrodermal control. This finding isconsistent with results in animals demonstrating activation of Area24 as related to autonomic adjustments during classical condition-ing ~Devinsky et al., 1995!. The cingulate cortex is reciprocallyconnected with most sensory cortices, projects heavily to the peri-acqueductal gray, and via the insula the cingulate cortex connectsto somatosensory areas ~Devinsky et al., 1995!. Given this inte-grative capacity, we ~Fredrikson et al., 1995! have previously ar-gued that activity of the anterior cingulate cortex integrates at leastsome aspects of affect and attention. If so, these aspects seem en-coded in the close vicinity of electrodermal control.Neural activity in the primary motor cortex ~MI, Area 4! was

positively correlated with electrodermal activity. The localizationgenerally fits with the anatomical representation of the hand ~Ka-washima et al., 1995!. Thus, data support models linking the elec-trodermal response to motor activity. Although locomotion was notpart of the study requirements because movements were restrictedin the PET scanner, areas in the brain exercising motor controlrelated to electrodermal activity. In support of Darrow’s ~1937!claim, the motor system seems inherently wired into the electro-dermal control system ~see also Boucsein, 1992; Edelberg, 1972;Fowles, 1974!.Activity in the secondary visual cortex ~Right Area 19 and Left

Area 18! and in the right inferior parietal cortex ~Area 39! wasnegatively correlated with EDA. Tranel and Damasio ~1994! re-ported that parietal, specifically right parietal, but not occipital

lesions attenuated EDA. Thus, lesion and imaging data convergein supporting a functional role for the right parietal cortex in elec-trodermal control. Previous data suggested that occipital lesionsgenerally do not affect EDA ~Tranel & Damasio, 1994!. Hence,associations between occipital activity and EDA are more likely toreflect an indirect rather than a direct impact on EDA.Raine et al. ~1991!, in a between-subjects study, reported that

larger areas in the left but not the right temporal cortex wereassociated with increased skin conductance activity. Because weobserved negative correlations between electrodermal activity andbrain blood flow in parts of the right insular cortex ~located in theanterior temporal cortex!, structural factors are most likely notassociated with functional neuroanatomy in any straightforwardmanner. However, most likely our areas were not identical to thoseof Raine et al. ~1991!, and electrodermal reactions were not iden-tically measured. Also, between- and within-subjects designs wereused, respectively. The insular cortex is involved in visceral sen-sation and internal interoception ~Aziz et al., 1997!. The negativerelation between neural activity in this area and electrodermal ac-tivity may index an electrodermal feedback control mechanism.Because neuroanatomical connections support a close link betweenthe anterior cingulate and the insular cortex ~Devinsky et al., 1995!,it is likely that those areas could form an integrated network in EDAcontrol.Because task-specific aspects were statistically controlled for in

the present study, results seem to generalize beyond the presentprotocol. However, the regression approach used in the presentstudy only reveals covariation between the central and autonomicnervous system, and we have no indication that areas correlatedwith electrodermal activity are causally related to electrodermalcontrol. If brain activation is causally related to electrodermalcontrol, positive correlations are likely to mirror excitatory influ-ences, whereas negative correlations are likely to index inhibitoryinfluences. Furthermore, we cannot disentangle indirect control, forexample, resulting from emotional arousal, from more direct in-fluences. Stimulation studies performed in animals and humanshave indicated that the thresholds for the elicitation of EDA differin various brain regions ~Sequeira & Roy, 1993!. An argumentcould be construed that those areas in which EDA is elicited at alower threshold are more likely to be involved in direct control,whereas those brain regions with relatively higher thresholds con-trol EDAmore indirectly. Stimulation studies using this logic haveimplicated that the reticular formation, the hypothalamic-limbicsystem including the anterior cingulate cortex and the motor area,are involved in electrodermal control ~cf. Boucsein, 1992!.Because of a restricted field of view of 10 cm, we only sampled

rCBF data from cortical and central structures but not from thereticular formation. Activation in several brain areas were relatedto EDA, but we could not confirm the involvement of the amyg-dala, the hypothalamus, or the thalamus in directing EDA or rep-licate the pattern of changes observed in schizophrenic personsreported by Dawson ~1990! and Hazlett et al. ~1993!. The reasonsfor this lack of confirmation could be manifold. Hazlett et al. ~1993!used uncorrected statistics and a between-group median split ap-proach, making false positives more likely than false negatives. Weused a within-subjects design and statistics corrected for multiplecomparisons, making the reverse true ~i.e., false negatives weremorelikely than false positives!. They studied the resting state, whereaswe studied activated states. They observed schizophrenic individ-uals, whereas we observed normal healthy control participants. Theymeasured EDAand brain activity on separate occasions, whereas weperformed simultaneous measures. They used glucose metabolism

Brain networks in electrodermal control 183

for a more extended period, whereas we measured blood flow fora brief period. In addition, we studied only women, and this re-striction to one gender may limit the generalizability. Any of thesestudy differences could contribute to differences in results.The present study, in general agreement with stimulation and

lesion studies performed in humans and animals, confirms that

activity in brain fields related to affect, anticipation, attention,autonomic control, and locomotion are associated with EDA. Interms of Boucsein’s ~1992! model, we observed covariation be-tween EDA and rCBF in the emotional and locomotor controlsystems, whereas data are silent on the third reticular system be-cause of the limited field of view.

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~Received May 13, 1997; Accepted September 25, 1997!

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