هراس از خون و عنکبوت هراسی: دو هراس خاص با مدولاسیون های مختلف اتونوم قلبی

Cardiac reactions to two fear-related and one control film were compared in individuals high in spider or blood/injury fear. Twelve subjects in each phobic group were selected on the basis of their scores in the Spider or Mutilation Questionnaires and a semi-structured interview. Cardiac responses and self-reported affective ratings to the films were investigated. Sympathetic and parasympathetic cardiac influences were indexed by T-wave amplitude and respiratory sinus arrhythmia measured during film viewing. Basal parasympathetic cardiac control was also assessed during a paced breathing task. Results indicate differential autonomic modulation of cardiac responses for blood and spider phobics. Although each group reacted with marked cardiac activation to its feared stimulus, a sympathetic increase followed by withdrawal over time was found in blood phobics. Greater vagal tone at rest was present in blood phobics compared with spider phobics.

Specific phobia is defined as a marked, persistent and unreasonable fear evoked by the presence or anticipation of clearly discernible objects or situations. Typically, the extreme anxiety reaction induced by exposure to the fear-related stimulus leads to avoidance behavior which significantly interferes with the individual's functioning (American Psychiatric Association, 1994). The somatic and autonomic changes associated with this non-adaptive emotional reaction play a considerable role in assessment of the disorder and treatment outcomes (Lang, 1971 and Hugdahl, 1989). As an extreme fear response, phobia involves a marked global increase in sympathetic activity, together with the subjective experience of heightened arousal. These psychophysiological changes are consistent with general mobilization for avoidance or escape behavior. In particular, in response to threat, heart rate is expected to increase, so that cardiac acceleration has frequently been employed as an index of the defense reaction or rejection of stimulation in normal subjects (Graham and Clifton, 1966 and Turpin, 1986), as well as a measure of fearfulness of the phobic object in phobic patients (Sartory, 1986 and Hugdahl, 1989). Indeed, a strong positive linear relationship between HR changes and subjective fear ratings has been found at intense fear levels (Sartory et al., 1977). Animal phobia (especially toward spiders or snakes) has often been considered in the literature as a prototypical specific phobia. There is considerable evidence that this category of phobic individuals shows increased sympathetic activity both during exposure to the phobic stimulus and during phobic imagery (e.g. Lang et al., 1970, Prigatano and Johnson, 1974 and Fredrikson, 1981). Autonomic changes include heart rate and blood pressure increases, cephalic and peripheral vasoconstriction associated with increases in skeletal muscle blood flow, and augmented phasic and tonic electrodermal activity. Self-report measures indicate high subjective tension, whereas behavioral variables, as indexed by viewing times of phobic pictures (Hamm et al., 1997) or by in vivo behavioral tests (Prigatano and Johnson, 1974) suggest a marked tendency for avoidance/withdrawal. Most studies exploring the psychophysiological response patterns in animal phobics have employed slides as phobic objects (Prigatano and Johnson, 1974, Geer, 1966, Hare and Blevings, 1975 and Hamm et al., 1997), whereas tonic visual stimulations (e.g. films or videotapes) have rarely been used (Fredrikson et al., 1995). For both stimulus conditions, the resulting autonomic response pattern is consistent with a defense response and supports clear aversive motivational disposition. In striking contrast with this typical reaction in animal phobics, a different, unique psychophysiological response to the feared stimulus is often observed in blood–injection–injury phobia. Blood phobics directly or indirectly exposed to blood, injuries or wound situations, typically display a diphasic cardiovascular response pattern. A first phase, involving heart rate and blood pressure increases, is immediately followed by a marked and dramatic drop in both variables. This response occurs to various extents and may eventually lead to emotional fainting (vasovagal syncope) due to the considerable reduction in cerebral blood flow (Graham et al., 1961, Öst et al., 1984, Kleinknecht, 1988 and Steptoe and Wardle, 1988). Studies employing film stimuli or in vivo presentations of the phobic object indicate that the diphasic autonomic pattern is reliably displayed across time (Graham et al., 1961, Öst et al., 1984 and Steptoe and Wardle, 1988). Significant increases in heart rate and blood pressure followed by pronounced decreases were observed in blood donors during venipuncture by Graham et al. (1961). After cardiac acceleration, marked deceleration and even fainting occurred in 5-min or even 30-min film presentation (Öst et al., 1984 and Steptoe and Wardle, 1988), whereas no significant HR decrease was found by Lumley and Melamed (1992) who employed 1-min scenes. When slides were used as phobic stimuli (6 or 10 s in duration), overall cardiac acceleration emerged in high-fear subjects, and no reliable diphasic pattern was observed. Interestingly, a strong cardiac acceleration was apparent only in the first trial block and was followed by a deceleration in the later blocks (Klorman et al., 1977 and Hamm et al., 1997). Although these data consistently suggest that the autonomic dysfunctions (and eventually fainting) require tonic stimulations to be fully displayed, a specific detection of the temporal boundaries of the beginning and completion of the diphasic cardiac reaction is lacking, also considering the extreme variability found between individuals who eventually faint (Graham et al., 1961). Such a puzzling autonomic phenomenon characterizing blood phobia as compared to other specific phobias, calls for both physiological and psychological interpretations. Engel (1978) suggested that this autonomic pattern is the result of circulatory preparation for action (namely, flight) in the face of threat when avoidance, in fact, is not possible. Increased muscle blood flow, produced by vasodilation in skeletal muscles and mediated by sympathetic vasomotor nerves, would persist in the face of decreased muscle tone and marked drops in blood pressure and cardiac output. These conflicting physiological responses would reflect the activation of both sympathetic (‘flight–fight’) and parasympathetic (‘conservation–withdrawal’) emergency systems, simultaneously or in rapid alternation. A psychological condition of unresolvable uncertainty, as to whether overt action or inhibition is the most appropriate response to an overwhelming threat, would parallel the above-mentioned cardiovascular instability (Engel, 1978). An overcompensatory parasympathetic rebound to an hyperdynamic sympathetic response to threat is the alternative interpretation proposed by Graham et al. (1961). The first phase of the cardiac reaction would be a reflection of anxiety, involving a marked increase in sympathetic activity. The second phase would reflect the intervention of antagonistic parasympathetic reflex mechanisms, acting to prevent the heart rate and blood pressure from rising without control. The cessation of anxiety and the sudden withdrawal of the intense sympathetic stimulation would leave the vagal reflexes unopposed, leading to an exaggerated parasympathetic activation. Based on these and on other similar interpretations (e.g. Sledge, 1978 and Vingerhoets, 1984), it is clear that the notion of disruption of the autonomic balance, as well as the complex sympathetic/parasympathetic interrelationship, seems to play a central role in blood phobia. Moreover, the selective association of fainting with blood phobics rather than with other phobic individuals and the peculiarity of the cardiovascular symptoms support the hypothesis of autonomic specificity (Connolly et al., 1976 and Friedman et al., 1993). Basal autonomic dysfunction, specifically a parasympathetic predominance in cardiac chronotropic control, has been hypothesized to be present in blood phobics. Angrilli et al. (1997) showed larger respiratory sinus arrhythmia (RSA) at rest (an index of cardiac vagal activity) in blood phobics as compared with non-phobic controls. Friedman and Thayer (1998) recently reported a higher cardiac vagal tone in blood phobics compared with nonclinical panickers, even though the highest levels were found in control subjects, whereas Steptoe and Wardle (1988) reported no reliable difference between blood phobics and healthy participants in intrinsic parasympathetic control of the heart. These inconsistent findings may be partly due to the different methods used for subject selection and quantification of the dependent measure (e.g. clinical vs. nonclinical samples; time-domain vs. frequency-domain indices of cardiac autonomic control). In association with the evidence that individual differences in fear do modulate the autonomic response pattern to the phobic stimulus, a large number of studies indicate that a prevailing HR deceleration is observed to the sight of blood-related stimuli even in non-fearful, unselected subjects (Klorman et al., 1977, Gross and Levenson, 1993, Lang et al., 1993 and Palomba et al., 2000), suggesting a stimulus-response specificity. In line with these data, it has been hypothesized that some autonomic/constitutional specificity may predispose individuals who are extreme in this stimulus-specific cardiac response toward developing blood phobia (Connolly et al., 1976 and Friedman et al., 1993). In a previous study (Palomba et al., 2000), a complex, mixed autonomic response pattern has been shown in normal subjects passively exposed to a film-clip depicting a thoracic operation. HR slowing (by itself indexing either augmented parasympathetic activation, or reduced sympathetic activation, or both), was associated with increased T-wave amplitude (TWA) and skin conductance levels (indicating decreased β-adrenergic and increased cholinergic sympathetic activity, respectively). One explanation for such a mixed autonomic pattern was that blood stimulus induced a multiple affect state made up by disgust, surprise, fear and other emotional states. This is in line with the psychological conditions of conflict and uncertainty in blood phobics as the critical determinants of fainting (Engel, 1978). The autonomic response pattern reliably developed across the 2′12″ of film presentation, and clearly differentiated the surgery film from a threatening scene, the latter inducing cardiac acceleration throughout the film presentation. Moreover, the observed HR decrease to the surgery scene was found to be accentuated in individuals high in parasympathetic cardiac control measured at rest, indicating that basal differences in vagal tone influenced the cardiac emotional response to this specific stimulus condition. The present study was designed to extend the previous work and investigate the cardiac response induced by the sight of blood in individuals high in blood/injury fear, with a special reference to the role of the complex sympathetic/parasympathetic interrelationship in determining the emerging emotional response. In particular, it was hypothesized that blood phobics would show a diphasic cardiac reaction in the face of the feared stimulus. In order to investigate the autonomic basis of the expected cardiac response pattern, two measures of autonomic influences on the heart were employed: TWA and RSA. The former is considered to be inversely related to myocardial β-adrenergic sympathetic activity (Furedy and Heslegrave, 1983 and Rau, 1991), whereas the latter has been widely proposed as a non-invasive index of parasympathetic cardiac control (McCabe et al., 1984 and Grossman and Svebak, 1987). During the first, acceleratory phase the sympathetic cardiac control was expected to be augmented. Accordingly, TWA was expected to be reduced. The role played by each of the autonomic branches in the second phase of the response is less clearcut. Therefore, either a withdrawal of sympathetic activity (increased TWA) associated with increased parasympathetic activity (increased RSA) or a conflicting activation of both systems (decreased TWA and increased RSA), simultaneously or in rapid alternation, were hypothesized during the second phase. The second related issue concerns the autonomic basal predisposition which could be associated with blood phobia. It was hypothesized that blood phobics would have greater intrinsic parasympathetic control of the heart, as compared with other specific phobics, and that this difference could be related to their specific autonomic cardiac response pattern. This prediction was tested by measuring RSA during a paced respiration task before the experimental session as an index of vagal tone at rest. It was interesting to assess within a single study the resting cardiac autonomic control and the autonomic reactions in blood phobics and spider phobics during exposure to both fear-related and fear-unrelated material. Indeed, in the literature, direct, systematic comparison of blood with other specific phobics has largely been neglected. Spider phobia, a prototypical animal phobia, was thus selected as a control phobic condition. A coherent increase in heart rate accompanied by TWA decrease was hypothesized for spider phobics in the face of the feared stimulus. Few studies have addressed the comparison between blood and animal phobics (e.g. Hamm et al., 1997), but neither employing tonic stimulations nor including measures of cardiac autonomic control. Two film clips were selected as phobic stimuli for each type of specific phobia. Based on our previous study (Palomba et al., 2000), film stimuli lasting 2 min and 12 s were employed in order to obtain continued exposure and to allow temporal examination of the development of the autonomic responses. Subjective and cardiac autonomic responses were investigated to evaluate differences between the two phobic groups in responding to fear-related stimuli.