برتری جانبی افتراقی اضطراب خصلتی و ترس و وحشت خصلتی : ارتباط پتانسیل برانگیخته
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33321||1998||24 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Personality and Individual Differences, Volume 26, Issue 2, 11 January 1998, Pages 333–356
There is an ongoing debate on whether the terms anxiety and fear denote distinct states. Brain imaging studies suggest they may indeed be dissociable and are differentially lateralized. A study of 54 normal college students successfully found doubly dissociable electrophysiological correlates of trait anxiety and fearfulness that had the predicted laterality. Trait anxious participants displayed a left-lateralized visual N1 (localized to the temporo-parietal junction) whereas trait fearful participants presented a right-lateralized P1r (localized to the superior parietal region). These findings support the proposal that trait anxiety and trait fearfulness are distinct personality dimensions with distinctive patterns of laterality.
Trait anxiety is an individual difference variable that has attracted particular experimental interest. Studies have found a wide array of behavioral differences in the high trait anxious, including narrowed attention, heightened automatic responses and bias towards threatening stimuli. For clinicians, it throws light on neurotic disorders. For personality psychologists, it is related to two of the major self-report personality dimensions (neuroticism and introversion). For emotion researchers, it is the chronic expression of one of the better studied emotions. For all this interest, trait anxiety remains poorly understood. One problem plaguing researchers has been multiplying constructs with uncertain interrelationships (e.g. anxiety, fear, worry, emotionality, arousal, etc.). A related issue is that these instruments are typically all moderately intercorrelated, leaving issues of discriminant and convergent validity clouded. Two common measures that particularly call for examination are the Spielberger State-Trait Anxiety Inventory (STAI) and the Fear Survey Schedule (FSS). The STAI (Spielberger, 1983) is the most commonly used instrument for measuring anxiety in experiments. Experimenters have found it particularly attractive because it yields scores for both state anxiety and trait anxiety. The latter section asks raters the self-descriptiveness of such phrases as “I lack self-confidence”. The FSS (Wolpe and Lang, 1964) was developed in the context of behavioral therapy of fear disorders, particularly phobias. It assesses how much the rater fears a wide variety of stimuli compiled from clinical experience (e.g. suffocating, angry people, blood). Several versions have been developed with differing numbers of items but are largely similar. Studies typically rely on just one or the other measure, depending on which has been customary for that line of inquiry. While these two measures are clearly related, it is unclear in what manner. It could be argued that they both measure the same construct; the two typically correlate in the range of about 0.27 to 0.60 (Hersen, 1973). Measurement specific variance (due to the different question formats) could be responsible for the divergence between the two measures. Alternatively, they could measure distinct constructs. Some clinicians (Barlow, 1988; Öhman, 1993) have argued that neurotic pathologies fall into two distinct groups, those of anxiety (e.g. generalized anxiety disorder, obsessive–compulsive disorder) and of fear (e.g. phobia, post-traumatic stress disorder, panic disorder). Barlow describes anxiety as a system of associated thoughts, memories and autonomic responses whereas fear is a primitive emergency response. Öhman makes a similar argument, making the additional proposal that fear is set off by preconscious feature detectors whereas anxiety can be set off by either preconscious significance evaluators or postconscious expectancy systems. It is therefore possible that the FSS and the STAI may measure the trait expression or susceptibility to these two states. The moderate correlation could arise from co-occurrence or common measurement error (like acquiescence bias). It is not yet clear from these theories how this putative dichotomy could be tested. Inspired by clinical observations, some behavioral neuroscience researchers have proposed biological systems that could underlie these two states. An influential formulation (Gray, 1982; Gray and McNaughton, 1996) suggests that the septo-hippocampal system acts as a comparator, detecting unexpected events. In such cases a behavioral inhibition system (BIS) is activated which halts current motor programs, increases arousal and triggers orienting to the unexpected event. Anxiety would represent chronic activation of this system. Panic (what might also be called fear) is suggested to be the activation of a fight/flight system centered on the central gray and triggered by the amygdala (Gray, 1987). While the anxiety system is well defined, the eliciting conditions and behavioral concomitants of the fear system remains rather vague and so it would be difficult to empirically distinguish them, particularly since both are proposed to produce physiological arousal. The most promising proposal of anxiety and fear that lends itself to experimental tests is that anxiety (anxious anticipation) may be left-lateralized and fear (anxious arousal) right-lateralized (Heller et al., 1995). Many cerebral blood flow studies have found that anxiety disorders involve greater left frontal region activation (Johanson et al., 1986; Baxter et al., 1987; Swedo et al., 1989; Johanson et al., 1992; Rubin et al., 1992; Breiter et al., 1996), although one report found left anterior orbital but right orbital lateralization (Nordahl et al., 1989). This generalization has to be limited by the repeated finding that treatment improvements are correlated most with right hemisphere deactivation (Buchsbaum et al., 1987; Baxter et al., 1992; Swedo et al., 1992), resulting in suggestions that obsessive–compulsive disorder (OCD) at least is more related to right hemisphere mechanisms. In view of the other studies, it seems more plausible that the left hemisphere is more involved in the anxiety process and the right hemisphere is more involved in the immediate recovery process. Fear disorders (phobic responses and panic), on the other hand, generally involve right hemisphere activity (Reiman et al., 1984; Stewart et al., 1988; O'Carroll et al., 1993, although bilateral activation has also been reported (Fredrikson et al., 1993). Additionally, OCD patients reporting feelings of panic during the recording session showed greater right prefrontal activation (Swedo et al., 1989), although this activation also correlated with state anxiety scores, as measured by the State-Trait Anxiety Inventory (Spielberger, 1983). None of these reports involve the temporal pole regions that were reported activated in response to lactate-induced panic attack (Reiman et al., 1989a) and shock threat (Reiman et al., 1989b) and were later attributed to jaw muscle artifact (Drevets et al., 1992). Finally, of 15 epileptic patients who experienced ictal fear (the sudden experience of fear without apparent cause, thought to be due to the abnormal burst of activity from the epileptic foci), 13 were found to have seizures originating in the right temporal lobe (Hermann et al., 1992). There is also some supporting behavioral evidence for lateralization. OCD patients have been repeatedly found to be impaired at right hemisphere visuo-spatial tasks while being normal or better at verbal tasks (Boone et al., 1991; Zielinski et al., 1991; Aronowitz et al., 1994). It is unclear whether other putative anxiety disorders also display such signs of lateralized bias. Another possible link between fear and the right hemisphere is the finding that arousal produces a tunnelvision effect, focusing attention and causing peripheral cues to be neglected (Easterbrook, 1959). This effect is said to affect both spatial attention, slowing responses to peripheral locations, and problem-solving, causing secondary information to be ignored. More recent work concerning spatial attention has suggested that arousal focuses attention on the most relevant locations, only directing attention to the center when it is confounded with relevance (Cornsweet, 1969; Geen, 1980). One difficulty with this formulation is that it predicts that anxiety (as a source of arousal) should promote improved task focus (Eysenck, 1982). Evidence suggests rather that anxiety may cause increased distractibility (Deffenbacher, 1978) and lowered processing efficiency (Eysenck and Eysenck, 1985). These studies have not sought to make any distinction between anxiety and fear so it is quite possible that this effect is more characteristic of fear, accounting for this contradiction. There is reason to think that the Easterbrook effect may reflect right-lateralized processes and fear in particular. Experiments with animal models suggest that the norepinephrine (NE) arousal system mediates narrowing attention to relevant cues (Minor et al., 1984; Selden et al., 1990), much as the Easterbrook effect is said to do. There is some evidence that this arousal system is in turn right-lateralized (Tucker and Williamson, 1984). For example, lesions of the frontal pole of the right hemisphere, but not the left hemisphere, can produce depletion of cortical NE (since the NE tract curves over the front of the cortex, lesions at this point can block the supply to the entire neocortex) (Pearlson and Robinson, 1981). NE has been implicated in the alerting functions of the right parietal (Posner and Petersen, 1990), an area that has also been implicated in visual selective attention (Corbetta et al., 1993). Finally, NE has been particularly implicated in fear disorders. NE is abnormally high (Butler et al., 1992) and abnormally regulated (Charney and Heninger, 1986) in panic patients. It has also been demonstrated that there is an extensive connection between somatic defense reactions (as found in panic attacks) and tonic activity in the locus coeruleus, which originates the bulk of the NE system (Svensson, 1987). It is not proposed that anxiety and fear involve global lateralized activity but only some functions within each hemisphere. Indeed, a substantial case has been built with EEG studies that the prefrontal regions show a different pattern of lateralization of affect with positive mood correlating with left hemisphere activation and negative mood with right hemisphere activation (Davidson, 1984; Fox, 1991; Wheeler et al., 1993), although a case has been made for the opposite as well (Tucker and Williamson, 1984). These findings have been shown for both state and trait differences. A more recent study with PET has shown a complementary picture (Dolski et al., 1996). On the other hand, such EEG measures have yielded mixed results for anxiety with one study reporting left frontal activity for worriers (Carter et al., 1986) while another reported no such lateralization for trait anxiety (Tomarken and Davidson, 1994). It should be emphasized that this account is not meant to be a reductionistic one, that anxiety and fear are defined solely by the activation of these systems. Psychopathologies in particular are the result of complex interactions of many levels and so the primary question is whether there are natural dividing lines, especially at the neural systems level where brain imaging methods can be informative.