Anxiety: A Common but Multifaceted Condition 17
ley, 2000). All of these peripheral physiological responses are associated with arousal
but cause various perceptible symptoms such as trembling, shaking, hot and cold spells,
heart palpitations, dry mouth, sweating, shortness of breath, chest pain or pressure, and
muscle tension (see Barlow, 2002).
The role of PNS excitation, which causes a conservation of certain physiological
responses, has not been as well researched in anxiety. The PNS is involved in symp-
toms like tonic immobility, drop in blood pressure, and fainting, which are a type of
“conservation- withdrawal” response strategy (Friedman & Thayer, 1998). The effects
of PNS stimulation include decreased heart rate and force of contraction, constricted
pupils, relaxed abdominal muscles, and constriction of the lungs (Bradley, 2000). More-
over, research on heart rate variability in panic attacks indicates that the cardiovascular
activity associated with anxiety should not be seen simply in terms of excessive SNS
activation but also reduced compensatory PNS excitation. Thus the PNS probably plays
a greater role in anxiety than previously considered.
Barlow (2002) concluded that one of the most robust and enduring findings in
the past 50 years of psychophysiological research is that chronically anxious individu-
als exhibit a persistently elevated autonomic arousal level often in the absence of an
anxiety- producing situation. For example, Cuthbert et al. (2003) reported significantly
elevated heart rate base levels for panic and specific phobias but not social phobia or
posttraumatic stress disorder (PTSD) groups. Other researchers, however, have linked
anxiety (or neuroticism) to excess autonomic lability and reactivity rather than to endur-
ing tonic levels of activation (Costello, 1971; Eysenck, 1979). Craske (2003) proposed
that heightened cardiovascular reactivity might be a predisposing factor for panic dis-
order such that a tendency to experience intense and acute autonomic activation could
increase the salience and therefore threat attributed to bodily sensations.
Empirical support for autonomic differences between anxious and nonanxious con-
trols in response to stressful or threatening stimuli has not been consistently obtained
across studies (Barlow, 2002). Freidman and Thayer (1998) also noted that psychophysi-
ological findings of reduced heart rate and electrodermal variability challenge the view
that anxiety is characterized by excessive autonomic lability and reactivity. Neverthe-
less, anxious individuals do show a slower decline in their physiological response to
stressors (i.e., slow habituation), but this is probably due to their higher initial baseline
arousal level (Barlow, 2002). In addition Lang and colleagues found greater physiologi-
cal arousal to fear- relevant imagery in snake phobic individuals, but reactivity was less
evident in those with panic (Cuthbert et al., 2003; Lang, 1979; Lang, Levin, Miller, &
Kozak, 1983). Together these results suggest that heightened physiological reactivity
to fear stimuli may be greatest in specific phobic conditions but less evident in other
anxiety states like panic disorder or PTSD. However, a heightened basal arousal level
and slower habituation rate might be seen more consistently across various anxiety dis-
orders, thereby providing the physiological basis for chronically anxious individuals to
misinterpret their persistent state of hyperarousal as evidence of an anticipated threat
or danger.
Recent psychophysiological research suggests that individuals with chronic anxi-
ety exhibit diminished autonomic flexibility in response to stressors (Noyes & Hoehn-
Saric, 1998). This is characterized by a weak but sustained response to stressors, indi-
cating a poor habituation trajectory. In a study of heart rate reactivity under baseline,
relaxation, and worry conditions, Thayer, Friedman, and Borkovec (1996) found that