The skin is the largest organ in the human body. The skin mirrors attentional, defensive, and problem-solving processes through tonic and phasic electrodermal activity that depend on eccrine sweat glands. Electrodermal level (EDL) is a tonic measure that indexes the baseline value. Electrodermal response (EDR) is a phasic measure that refers to change from baseline value. Electrodermal biofeedback is used to treat hyperhidrosis (excessive sweating), in psychotherapy to monitor unconscious processes, and in stress management.

This unit discusses Descriptions of most commonly employed biofeedback modalities: Electrodermal activity (III-A 2) and Structure and function of the autonomic nervous system (V-A 3).
Students completing this unit will be able to discuss:

  1. Descriptions of most commonly employed biofeedback modalities: Electrodermal activity
    A. Characteristic signals
  2. Physiological mechanisms underlying commonly employed biofeedback modalities, including electrodermal activity

EDA is measured using three methods: conductance, resistance, and potential. Both conductance and resistance are measured exosomatically (from outside the body) by passing an electric current through the skin.

Level is a tonic measure of electrodermal activity that quantifies the average amplitude over a specified period of time. Response is a phasic measure of electrodermal activity that represents a spontaneous or stimulus-elicited change in sweat gland activity.

Conductance indexes how easily current passes through the skin and is measured as skin conductance level (SCL) and skin conductance response (SCR).



Below is a BioGraph Infiniti skin conductance display.

Resistance (the reciprocal of conductance) is also called galvanic skin response (GSR) and reflects opposition to current movement and is measured as skin resistance level (SRL) and skin resistance response (SRR).


Skin potential is monitored endosomatically (from within the body) by detecting voltage differences between two electrodes on the skin surface. Skin potential is measured as skin potential level (SPL) and skin potential response (SPR).


The protective skin boundary consists of the epidermis (outer layer), dermis (inner layer), and hypodermis. The epidermis is comprised by five layers (stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum germinativum). The dermis contains blood and lymph vessels, smooth muscle, and sebaceous and sweat glands. The secretory portion of sweat glands is located in the hypodermis. This region consists of connective tissue below the dermis containing blood and lymph vessels.


Caption: The skin cross-section here seen comes from a microscopic section of human skin, showing in a high level of detail and resolution the different layers of the skin with their relationships to each other. Cut-away areas of the model allow for easy identification of layers and how they interrelate in this image. An eccrine sweat gland is depicted on the right side.

Skin contains apocrine and eccrine sweat glands. Apocrine sweat glands usually open into hair follicles and are mainly distributed in the armpits and genital region. Apocrine sweat glands produce sweat odor and distress can expel sweat from their tubules.

Eccrine sweat glands are distributed across the body except for areas like the lip margins, outer ear, clitoris, and glans penis. They are densest on the palms and soles of the feet. A square inch of palmar surface may contain about 3,000 sweat glands (Jacob & Francone, 1970). Cadaver studies indicate that the entire body may contain from 2-5 million sweat glands (Fowles, 1986).

Eccrine sweat glands are mainly concerned with thermoregulation (temperature control) through evaporative cooling. While all eccrine sweat glands respond to emotion and temperature, palmar and plantar sweat glands appear more responsive to emotional stimuli because of higher density (about 1,000 glands per cm2, compared with 100-200 per cm2 on the trunk and limbs). Palmar sweating seems specialized for grasping objects, increasing tactile sensitivity, and protecting skin from damage (Hugdahl, 1995).

An eccrine sweat gland consists of a secretory portion and sweat duct. The secretory portion, that produces sweat, consists of coils arranged in a ball .3-.4 mm in diameter. These coils are lined by myoepithelial cells that resemble smooth muscle cells. Myoepithelial cells may help produce spontaneous electrodermal activity. They are influenced by norepinephrine, and possibly, by epinephrine circulating as a hormone in the blood. The sweat duct is a long tube that excretes sweat through a pore at the epidermis.

Eccrine sweat glands are mainly innervated by sympathetic cholinergic fibers. Unmyelinated cholinergic fibers are densest around the secretory portion, but a few lie close to the duct. Researchers have also found nearby adrenergic fibers. Neurotransmitters like VIP may complement ACh and NE (Shields et al., 1987).

The sympathetic nervous system primarily controls EDA. This view is supported by the strong correlation between sympathetic action potentials and skin conductance responses (SCRs) at normal room temperature (Wallin, 1981). Increased sympathetic nervous system activation results in greater sweating from the palms.

Sympathetic fibers release acetylcholine (ACh) to trigger sweating. ACh binds to the secretory portion allowing calcium ions to enter and stimulate sweating by acting as a second messenger. The role of noradrenergic fibers in sweating remains unclear (Fowles, 1986). Human sweat begins as plasma-like precursor sweat. The sweat duct reabsorbs sodium chloride as sweat passes through.

Why is ACh released to trigger sweating instead of norepinephrine, which is the postsynaptic transmitter throughout the sympathetic nervous system?

The substitution of ACh for NE makes sense when we remember that ACh typically controls exocrine glands (glands that secrete into ducts). Eccrine sweat glands are also exocrine glands. They secrete sweat into ducts that open on the skin surface.

Interestingly, the sympathetic motor neurons innervating eccrine sweat glands are actually programmed to secrete norepinephrine, but are instructed by the sweat glands to release ACh, instead.

The sweat circuit model proposes that EDA is a function of sweat duct filling and action by a selective membrane in the epidermis. Edelberg (1972) proposed that duct-filling produces SCRs, while both duct-filling and the selective membrane control response recovery.

Normally, sweat glands are filled to the Malpighian layer. The standing level of sweat in the duct determines tonic (slowly changing) EDA values measured by skin conductance level, skin potential level, and skin resistance level.

Rising sweat levels produce phasic (rapidly changing) EDA values measured by skin conductance response, skin potential response, and skin resistance level.

EDA response recovery (return to tonic levels) is due to gradual sweat diffusion through the duct wall into the stratum corneum (Edelberg, 1972). The contribution of a selective membrane to active reabsorption remains unclear (Fowles, 1986).

Edelberg (1972) described the long, tubular sweat ducts as resistors (which can assume varying values) wired in parallel. Even when we are exposed to a loud sound, not all sweat glands are active at the same time. Further, an individual sweat gland's activity falls on a continuum. Since sweat column height (resistor value) reflects the degree of activity, the higher sweat rises, the larger the response amplitudes.

Edelberg (1993) revised his explanation of the rapid shift from conductance to resistance in the sweat circuit model with his poral valve model. Since the existence of a reabsorption membrane has never been confirmed, he proposed a simpler mechanical explanation. Initially, the sweat duct is empty and the pore at the skin surface is closed (A). Sweat secretion rises in the duct, increasing skin conductance, and the pore remains closed (B). Sweat fills the duct to capacity until pressure forces the poral valve open, producing maximum skin conductance (C). Loss of sweat to the skin surface reduces the intraductal pressure needed to keep the poral valve open, causing it to close and conductance to rapidly decline (D).


Hugdahl (1995) proposed that locomotor, orienting-activating, and thermoregulatory systems centrally control electrodermal activity.

The locomotor system (premotor cortex, pyramidal tract, and brainstem) hydrates the soles of the feet and palms of the hands to increase running speed and hand dexterity.

The orienting-arousal system (lateral frontal cortex, amygdala and hippocampus, and reticular formation) produces sweating to protect the skin from injury in situations demanding focused attention (e.g., novel stimuli) or vigilance for threats.

The thermoregulatory system (anterior hypothalamus) produces cold sweating during trauma, in which increased sweating is accompanied by constriction of peripheral blood vessels, and increased electrodermal activity in the hands and digits.

Boucsein (1992) proposed that electrodermal activity in the hand is centrally controlled by ipsilateral and contralateral systems. The ipsilateral system involves the cingulate gyrus, anterior thalamus, and hypothalamus. This system expresses limbic system (LS) activity through control of thermoregulatory areas in the hypothalamus, and mediates the affective and emotional contribution to electrodermal activity. The contralateral system expresses activity in the lateral prefrontal cortex (i.e., premotor cortex) and the basal ganglia or BG (i.e., caudate nucleus and putamen), and mediates electrodermal activity during cognition, orienting, and locomotion.

The controversy over the role of both brain hemispheres in electrodermal activity continues, due in part to confounding sensorimotor with cognitive and emotional tasks. Research by Davidson, Fedio, Smith, and colleagues (1992) suggests different roles for the left and right brain hemispheres in control of arousal, and orientation and habituation, and supports the view that the contralateral pathways responsible for bilateral differences in electrodermal activity are excitatory.

Temperature influences electrodermal activity since the primary function of eccrine sweat glands is to regulate body temperature. Gender differences in skin conductance level and reactivity may disappear when researchers control for a subject's most reactive hand (Roman et al., 1989). Boucsein (1992) reported lower skin conductance levels for black subjects than whites, possibly due to fewer sweat glands in dark skin. EDA declines with aging. Finally, muscle relaxants reduce electrodermal activity.

Skin potential response (SPR) can exhibit a monophasic negative or positive waveform, biphasic waveform (negative, then positive), or triphasic waveform (negative, positive, then negative). The classic pattern is biphasic (Stern, Ray, & Quigley, 2001).


Monophasic negative SPRs are associated with slow recovery times. This pattern may be part of a defensive reaction (sweat reduces abrasive injury).

Biphasic SPRs (negative then positive) involve a rapid return to baseline. This pattern reflects the rapid sweat reabsorption seen in goal-directed behavior. Moisture is reduced to improve manipulation by the digits (Edelberg, 1970).

Skin potential may provide more information than skin conductance. Edelberg (1973) argued that skin potential contains an epidermal component, absent in skin conductance, in addition to a shared sweat gland component. While SPRs require sweat gland activity, SPLs are still seen when sweat gland activity is blocked with atropine (Venables & Martin, 1967).

What does electrodermal activity mean cognitively? Katkin (1975) argued that electrodermal activity is a personality variable that reflects allocation of attention and information processing.

Researchers have divided subjects into labiles and stabiles to describe personality differences in electrodermal variability. Labiles show higher resting SCLs and larger SCRs, and more rapid responses to stimuli and return to resting levels than stabiles. These differences support the view that labiles better respond to changing environmental demands and better allocate attentional resources to environmental events (Schell, Dawson, & Filion, 1988).

Now that you have completed this module, describe the difference between level and response, exosomatic and endosomatic measurements, and labiles and stabiles. Summarize the main reasons for palmar sweating.

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Cacioppo, J. T., & Tassinary, L. G. (Eds.). (1990). Principles of psychophysiology. New York: Cambridge University Press.

Edelberg, R. (1993). Electrodermal mechanism: A critique of the two-effector hypothesis and a proposed replacement. In J. C. Roy, W. Boucsein, D. C. Fowles, and J. H. Gruzelier (Eds.), Progress in electrodermal research, pp. 7-30. New York: Plenum Press.

Hugdahl, K. (1995). Psychophysiology: The mind-body perspective. Cambridge, MA: Harvard University Press.

M. S. Schwartz, & F. Andrasik (Eds.). (2003). Biofeedback: A practitioner's guide (3rd ed.). New York: The Guilford Press.

Stern, R. M., Ray, W. J., & Quigley, K. S. (2001). Psychophysiological recording (2nd ed.). New York: Oxford University Press.

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