This study compared group cognitive-behavioral therapy (12-week trial), surface electromyographic biofeedback (12-week trial), and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Subjects were 78 women randomly assigned to one of three treatment conditions and assessed at pretreatment, posttreatment and 6-month follow-up via gynecological examinations, structured interviews and standard questionnaires pertaining to pain (Pain Rating Index and Sensory scale of the McGill Pain Questionnaire, vestibular pain index, pain during intercourse), sexual function (Sexual History Form, frequency of intercourse, Information subscale of the Derogatis Sexual Functioning Inventory), and psychological adjustment (Brief Symptom Inventory). As compared with pretreatment, study completers of all treatment groups reported statistically significant reductions on pain measures at posttreatment and 6-month follow-up, although the vestibulectomy group was significantly more successful than the two other groups. However, the apparent superiority of vestibulectomy needs to be interpreted with caution since seven women who had been assigned to this condition did not go ahead with the intervention. All three groups significantly improved on measures of psychological adjustment and sexual function from pretreatment to 6-month follow-up. Intent-to-treat analysis supported the general pattern of results of analysis by-treatment-received. Findings suggest that women with dyspareunia can benefit from both medical and behavioral interventions.

No abstract

Vulvar vestibulitis can be reliably diagnosed in women with dyspareunia. Pain is limited to the vulvar vestibule and can be rated and described in a consistent fashion by these women. Erythema does not appear to be a useful diagnostic criterion.

A single exposure to a severe stressor (either cold swim or inescapable shock) impairs subsequent performance in a shuttle avoidance-escape task (1), a deficit attributed to reduction in brain noradrenergic activity produced by these stressors. In the present paper, two experiments are described which examine how repeated exposure to such stressors affects (a) shuttle avoidance-escape performance (Experiment 1), and (b) aspects of brain norepinephrine metabolism (Experiment 2). Experiment 1 showed that, whereas subjects receiving the single exposure to cold swim or shock showed a large avoidance-escape deficit, subjects that received repeated exposure to these stressors for 14 days performed similarly to the control group that received no stressor. Experiment 2 showed that, whereas subjects that received one session of the inescapable shock stressor showed a lower level of norepinephrine in hypothalamus and cortex than did subjects that received no shock, subjects that received repeated exposure to inescapable shock or cold swim showed neurochemical "habituation." Subjects that received repeated shock showed elevated tyrosine hydroxylase activity and no depletion of norepinephrine level, and both repeated shock and cold swim caused a decrease in uptake of 3H-norepinephrine by slices of cortex in vitro. Thus, it is concluded that the behavioral and neurochemical changes that were observed after the stressful conditions studied are consistent with the hypothesis that changes in avoidance-escape responding following exposure to these stressful events are due to changes in brain noradrenergic activity.

If animals receive inescapable electric shocks, their subsequent avoidanceescape learning is poor. This phenomenon, which can be called the interference effect, was studied in four experiments. Experiment 1 demonstrated that, depending on the parameters of the inescapable shock used, there exists a transitory effect and a separable, more permanent, long-term interference effect. Experiments 2 and 3 investigated the long-term effect, showing that it (a) required inescapable shocks of at least 5 sec duration in order to develop and (b) was still evident 1 week after such inescapable shock. It is suggested that, whereas the transient effect is produced by a short-lived neurochemical change, the long-term effect is mediated by a learned response. Consistent with this differentiation, Experiment 4 showed that the interference effect measured 30 min. after inescapable shock did not occur when animals had been repeatedly exposed to the type of inescapable shock that produced the transitory effect, whereas the interference effect measured 72 hr. after inescapable shock became more pronounced when animals had been repeatedly exposed to the type of inescapable shock that produced the long-term deficit. Aspects of the data suggest that learned helplessness is not the basis of the long-term interference phenomenon.Deficits in avoidance-escape learning after uncontrollable, but not after controllable, electric shocks were reported by Overmier and Seligman (1967) and Seligman and Maier (1967) in dogs. To account for the interference with avoidance-escape behavior that followed inescapable shock (hereafter referred to as the interference effect), these investigators proposed that the animals had learned to be "helpless." According to this

This article presents three experiments that explore whether inescapable shock of long duration and moderate intensity (LoShk) produces an avoidance-escape deficit (called an interference effect) by causing animals to learn to respond less actively or by causing them to learn to be "helpless."The first experiment showed that if animals given LoShk were subsequently tested in an avoidance-escape "nosing" response that required little motor activity, they learned and performed better than no-shock controls. The second experiment verified that the same LoShk treatment that led to this better performance in the first experiment would indeed interfere with subsequent avoidance-escape acquisition in those test situations that have previously been used to demonstrate the interference effect, that is, the three-response lever press, two-response shuttle, and single-response barrier jump. Finally, in the third experiment, using triplets in the classical avoidance-escape, yoked, and control animal paradigm, it was shown that yoked animals performed more poorly than either avoidance-escape or control animals on a subsequent three-response lever-press task but performed better on the nosing avoidanceescape task that required little movement. The results are interpreted as being compatible with the idea that animals acquire the tendency to be inactive as a result of exposure to long-duration, moderate-intensity, inescapable shock. The results are seen as incompatible with the idea that animals learn "helplessness," that is, not to associate behavior with its consequences, as a result of exposure to such shock.In a preceding article , it was shown that what is called the "interference effect," that is, the disruption of avoidance-escape behavior by prior exposure to inescapable shock, occurs in at least two different ways. The first type of interference effect follows a single session of high-intensity, inescapable shock, and this deficit dissipates relatively rapidly over time. It is our contention that the original work done on the interference effect (Overmier & Selig-

II.

This paper attempts to show that severely stressful conditions can lead to a deficit in avoidance-escape responding by reducing noradrenergic activity in the brain. It is argued that this stress-induced neurochemical change explains more adequately an avoidance-excape deficit seen previously in dogs after severe inescapable shock than does the "learned helplessness" explanation originally offered for this effect. A series of six experiments are described that test the stress-neurochemical change explanation, which is called the "motor activation deficit" hypothesis. The first experiment showed that a brief exposure to cold swim, which reduced central noradrenergic activity but did not induce "learned helplessness," produced an avoidance-escape deficit similar to that observed after inescapable shock in the original "learned helplessness" studies. Subsequent experiments demonstrated that the deficit induced by cold swim was also similar to the original deficit in that it too dissipated with the passage of time and was reduced by pretraining animals in the correct response. Further experiments then showed that the deficit induced by cold swim was (a) aggravated by raising the height of the barrier between compartments in the shuttle box, and (b) did not occur if the avoidance-escape task used required little motor activity, both of the findings being predicted by the "motor activation deficit" hypothesis. Finally, an avoidance-escape deficit was produced by inescapable shock, and it was found that this stressor likewise did not impair avoidance-escape responding if the task required little skeletal activity, a result not predicted by the "learned helplessness" hypothesis. The paper concludes by discussing how the results presented in this paper, as well as in succeeding papers, support the "motor activation deficit" explanation for certain avoidance-escape deficits, defining the cases to which the explanation applies and discussing the neurotransmitters involved.