איך נראה הפרעות חרדה במכשירי הביופידבק שלנו – שאלות שאני מכין לפרופ' גבירץ. השאלות מבוססות גם על חומרים ממאמרים של פרידמן ושל בורקובק
הנחה ראשונה – חרדה תהיה מלווה בשינויים במדדים של מערכת העצבים המרכזית:
Anxiety is often accompanied by somatic manifestations that suggest marked
changes in autonomic nervous system (ANS) activity, such as rapid heart rate
(HR), shortness of breath, and sweating. These symptoms have frequently been
viewed as signs of increased sympathetic (SNS) activation. This interpretation is in
accord with Cannon's ‘flight-or-fight' model of fear (Cannon, 1929) that is based
upon the assumption of global states of SNS activation.
הנחה שנייה: לא כל הפרעות החרדה יראו בצורה דומה – יתכן שהפרעת הפאניקה תהיה שונה למשל מ OCD או GAD
Among the various forms of anxiety, panic is singularly marked by the rapid
onset of intense somatic symptoms and subjective reports of terror (Barlow, 1988).
The most frequently reported symptom in these cases was
tachycardia. Similarities in symptomology suggest a substantial diagnostic overlap
between NCA and PD (Stampler, 1982).
The scope of biological models of panic has been exceedingly broad. However,
the salience of reports of tachycardia have implicated SNS disturbances since early
investigations of panic syndromes (e.g. Fraser and Wilson, 1918). More contemporary
research has been focused at the level of adrenergic neurotransmitter dysfunctions,
but has not yielded definitive results (e.g. Grunhaus et al., 1981). More global
characterizations have invoked the concept of an autonomic ‘imbalance' in the
direction of sympathetic dominance in pathological anxiety (e.g. Reich, 1982
(original work published in 1939)). Other broad ANS representations include slow
habituation (Lader, 1980), high tonic activation (Roth et al., 1986), and other
sundry ANS dysfunctions (for reviews of ANS models of panic, see Mitchell and
Shapiro, 1991; Friedman and Thayer, in press).
המודל הקלאסי שרובנו גדלנו עליו מזהה חרדה עם פעילות יתר. הרבה מאיתנו שעובדים עם המוליכות החשמלית של העור (EDA) מצפים שחרדה תתבטא ב קו המעיד על תגובתיות רבה. וגם כשאנו רואים לביליות (קו שמשתנה תכופות בתנועות גדולות של שינוי מבלי גרוי חיצוני – יש לנו נטיה להניח שזהו סימן לחרדה.
Classical models have linked anxiety with excess autonomic lability and reactivity (Eysenck, 1970; Costello, 1971). Insuch depictions, the ANS is seen as hyperreactive with chronic fluctuations from a
steady state. These representations are in need of reconsideration in view of the
present state of knowledge of the specificity of ANS regulation of cardiovascular
(CV) function, as is detailed below
It is often held that electrodermal (EDA) lability is a correlate of anxiety (e.g.
Cruz and Larsen, 1995). This notion is supported by oft-cited research that has
found greater spontaneous fluctuations in and diminished habituation of EDA in
anxiety states (for review, see Lader, 1980).
אלא שמחקרים לא תמיד הצליחו לאשש השערה זו – ואפילו יש סימנים שלאביליות של המוליכות החשמלית של העור עשוייה להיות קשורה בקשר הפוך עם חרדה, ושהיא עשויה להיות קשורה ליכולת הסיטואציה טובה.
However, there have been some failures to replicate this relationship (for review, see Katkin, 1975), and
even a negative relationship between EDA lability and state anxiety has been reported
(Kelsey, 1991). In the latter study, EDA labiles also showed more rapid habituation
of cardiac reactivity to stress, which suggests adaptive environmental responsiveness.
Moreover, EDA lability has been found to be associated with superior
performance on perceptual vigilance tasks, efficient allocation of attentional resources,
and enhanced responsivity to changing environmental demands (Surwillo
and Quilter, 1965; Katkin, 1975; Sostek, 1978; Schell et al., 1988). These qualities
are not typically associated with anxiety, which on the contrary, has been linked
with attentional deficits (Mathews, 1990) and poor adaptive responsiveness to the
environment (Neary and Zuckerman, 1976).
ההבנה שדווקא פעילות מופחתת של הEDA קשורה בחרדה נמצאה גם בהפרעת פאניקה וגם בהפרעת חרדה מוכללת. ממצאים אלו יכולים להיות מפורשים כהקטנה בגמישות של המערכת האוטונומית בהפרעות חרדה
Indeed, a diminished range of EDA responding has been found in both panic
and generalized anxiety disorders (Hoehn-Saric et al., 1989, 1991), and were
interpreted as evidence of reduced autonomic flexibility in both groups. This
narrowed range is consistent with reports of decreased EDA orienting responses
in high state anxious individuals (Neary and Zuckerman, 1976), and lower EDA
stress reactivity in clinically anxious women (Goldstein, 1965). In sum, the notion
of excess autonomic lability in anxiety appears to be generally belied by EDA as
well as CV data.
אנו יודעים כי גם במערכת הקרדיווסקולרית ניתן למצוא תמונה דומה. יש הקטנה ב HRV ובטון הוואגאלי (פאראסימפטטי) בהפרעת חרדה מוכללת ובאנשים הנמצאים בדאגה.
גם במדד ה EMG נצפתה תופעה דומה: אנשים בעלי נטייה לחרדה מוכללת הראו מתח שרירים מוגבר בהשוואה לאנשים לא חרדים.
It may be that diminished variability in peripheral physiological responding is
common to various types of clinical anxiety. Reduced HR variability and vagal
tone have been reported in generalized anxiety disorder and worry (Lyonfields et
al., 1995; Thayer et al., 1996a). In addition to a restricted range of EDA, a
reduced range in HR and electromyographic responding have been found in
GAD, and have been interpreted as reflecting a generalized psychophysiological
response rigidity to environmental stimuli (Hoehn-Saric et al., 1989; Hazlett et al.,
1994).
Collectively, these findings led to the present hypothesis that the tachycardia of
panic may be related to poor autonomic HR control as reflected in diminished
HR variability, HF power, and spectral reserve, in contrast to portrayals of
excess autonomic lability in anxiety.
