Naltrexone-reversible pain suppression in the isolated attacking mouse

Fighting pairs of isolated DBA/2 mice showed a significant increase in tail-flick response latencies independent of whether opponents were losing or winning the combat. The effect lasted less than 10 min in both animals. Elevated pain thresholds were also found in isolates that attacked a nonaggressive conspecific, and were prevented by naltrexone (0.2 mg/kg), while a larger dose (1.0 mg/kg) inhibited the attack behavior. A small increase in pain threshold was observed after exposure of isolates to the test box alone, while isolation per se had no effect on baseline tail-flick latencies. The data demonstrate that endogenous pain suppressing systems are activated during attack and suggest that this opioid-mediated antinociception is a correlate of the isolation syndrome, reflecting enhanced arousal of the attacking animal.     

Anxiety and hypervigilance to cardiopulmonary sensations in non-cardiac chest pain patients with and without psychiatric disorders

We investigated body vigilance, cardiac anxiety, and the mediating role of interoceptive fear on pain in patients with non-cardiac chest pain (NCCP; a syndrome of chest pain in the absence of identifiable organic etiology). Patients were more attentive to cardiac-congruent sensations than cardiac-incongruent sensations (e.g., gastrointestinal, cognitive dyscontrol; p's < .001). Patients with a DSM-IV Axis I anxiety or mood disorder were more body vigilant compared to patients who did not have a disorder (p's < .05). Patients with anxiety disorders were particularly vigilant to and fearful of cardiac sensations relative to patients without anxiety disorders. Latent variable path models examined the extent that interoceptive fear mediated the association between body vigilance and cardiac anxiety on chest pain. Within each model, diagnostic status, body vigilance, and cardiac anxiety were exogenous and predicted interoceptive fear that in turn predicted pain. Separate models examined body vigilance and cardiac anxiety, and both models fit the data well. Findings showed partial mediation for the body vigilance factor, and full mediation for the cardiac anxiety factor. Interoceptive fear played a mediating role in both models. The syndrome of NCCP may persist partly due to conscious hypervigilance to and fear of cardiac-congruent body sensations, particularly among anxious patients.     

The effects of voluntary hyperventilation on patients with chest pain without coronary artery disease

The present investigation was designed to examine panic symptom experience in patients with chest pain of nonorganic etiology, using a hyperventilation provocation procedure. Given the recent focus on panic disorder in patients with nonorganic chest pain, we assessed three indices of physiological arousal, subjective anxiety, and endorsement of DSM-III-R panic symptomatology in response to 3 min of voluntary hyperventilation. Subjects included 23 patients with nonorganic chest pain (CP sample) and matched normal controls (NC sample). The results indicate that hyperventilation produced significant increases in skin conductance, heart rate, and upper trapezious EMG in both CP and NC samples. Despite equivalent levels of physiological arousal and subjective anxiety, the CP sample endorsed a greater number of DSM-III-R panic symptoms relative to the NC sample. Examination of post-hyperventilation symptoms indicated that a greater percentage of the CP sample reported palpitations, nausea, and chest pain when compared with normals. Comparison of CP patients with and without Panic Disorder revealed no significant differences on any measure. The results suggests that hyperventilation plays a role in symptom experience in patients with nonorganic chest pain, although anxiety does not appear central in moderating this effect.     

Quality of Life in Patients with Non-CAD Chest Pain: Associations to Fear of Pain and Psychiatric Disorder Severity

Chest pain in the absence of identified cardiac cause, or non-cardiac chest pain (NCCP), is a common condition that may result in impaired quality of life. Theories of NCCP put forward that patients who react to cardiopulmonary sensations with fear may avoid activities that elicit cardiac sensations. Co-morbid psychiatric disorders, which are prevalent in this population, may predispose individuals to be more vigilant to physiological sensations, including cardiac-related symptoms. The daily impact of avoiding cardiopulmonary cues may limit quality of life. This study examined psychiatric disorders, fear of pain, and quality of life in 30 non-coronary artery disease (CAD) chest pain patients. Psychiatric disorder severity was independently associated with mental health related quality of life and fear of pain was independently associated with physical health related quality of life. This research adds understanding to contributory factors to impaired quality of life among patients with non-CAD chest pain.     

Competitive fighting in the rat.

Competitive fighting was obtained in pairs of like-sexed laboratory rats by placing a single piece of food into the food hopper following 48 hr. of food deprivation. The fighting was characterized by offensive sideways posture, full aggressive posture, and bite and kick attack. Tests were conducted at 110-120 days of age on pairs of animals that had been housed together since weaning. Fighting was more frequent in pairs consisting of nonlittermates than in pairs of littermates, and it was equally frequent in male and female pairings. Probability of fighting was enhanced by prior experience with food deprivation, and attack was most often initiated by the heavier animal of the pair.     

Health care utilisation in patients with non-cardiac chest pain: A longitudinal analysis of chest pain,anxiety and interoceptive fear

Chest pain can be a frightening experience that leads many to seek medical evaluation. The symptom results in costly health care utilisation. Over half of patients referred for cardiac evaluations of chest pain do not obtain definitive medical explanations for their symptoms; these cases are described as non-cardiac chest pain (NCCP). Some patients with NCCP are not reassured after being informed their chest pain is non-cardiac in origin and seek repeated medical evaluation. Co-morbid anxiety and mood disorders often coexist with NCCP and are associated with health care utilisation. The current study examined chest pain, general anxiety, interoceptive fear and health care utilisation in a sample of 196 chest pain patients near the time of cardiac evaluation (Time 1), and 70 of these patients one year later (Time 2). Results indicate that anxiety and interoceptive fear were significantly associated with health care utilisation at Time 1, and only interoceptive fear (at Time 1) predicted health care utilisation at Time 2. This study develops research in this area by examining the relation of anxiety and health care utilisation longitudinally in patients with NCCP.     

Understanding Chest Pain: What Every Psychologist Should Know

Chest pain is one of the most frequent presenting complaints in Emergency Rooms and other medical settings. A considerable number of these patients do not have significant coronary artery disease. This led to plausible alternative explanations for these presenting symptoms and these patients tend to have unremarkable cardiac outcomes. Nevertheless, many studies have also documented that symptoms and related disability persist in the face of reassurances about benign cardiac status. Given the implied threat of chest pain (e.g., myocardial infarction) and the presence of chest pain symptoms in other noncardiac conditions (including anxiety and panic), it is not surprising that many of these patients present with considerable emotional distress. Consequently, chest pain symptoms represent diagnostic and treatment dilemmas for physicians and psychologists alike. The extent to which cardiac and noncardiac factors contribute to all forms of chest pain remains unknown. The function of this review is to provide mental health professionals with a primer on relevant clinical issues in chronic chest pain. We examine several common medical and psychiatric causes of chronic chest pain and selectively review (1) the relevant medical and psychiatric diagnostic and treatment considerations for chest pain and (2) the hypothetical biobehavioral mechanisms relevant to psychological intervention, (3) while expanding on existing conceptual models for understanding chest pain, and (4) offering some suggestions for future research.     

反复胸闷胸痛伴心理精神障碍的诊疗进展

近年来,临床中关于反复胸闷胸痛患者的较高误诊率引起了广大医务工作者的重视,此类患者伴有的心理精神障碍往往被忽视,得不到合理的治疗,预后较差.本文主要讨论关于反复胸闷胸痛患者病因的鉴别、心理精神障碍引起胸闷胸痛的机制、胸闷胸痛与心理精神障碍的关系、“双心”医学诊疗模式以及反复胸闷胸痛的治疗进展,通过增强临床医生对“双心”医学的认识降低胸闷胸痛患者的误诊率、漏诊率,减少过度治疗,通过心血管医学和心理干预联合治疗,改善心血管疾病患者的预后、降低死亡率.     

From heart attacks to melanoma: do common sense models of somatization influence symptom interpretation for female victims?

Common sense models regarding gender and stress influenced how laypeople responded to information about symptoms in 3 experiments. In Study 1, medical intervention was perceived to be less important for female targets reporting chest pain and stressful events than for male targets experiencing identical symptoms and stressors. In addition, chest pain was less likely to be attributed to cardiac causes for female targets. This gender-based stress-discounting effect was replicated for symptoms of gallstones and melanoma in Study 2, where participants again were less likely to recommend medical care for female than for male targets. Recognition memory for information about a somatizing target was tested in Study 3; results suggested that laypeople hold stereotypes associating somatization with female gender. The authors' findings provide insight into the naive theories that shape symptom interpretation and self-referral behavior.     

Simone Weil’s Passion Mysticism: The Paradox of Chronic Pain and the Transformation of the Cross

Simone Weil’s theology is deeply connected to her experiences with chronic pain. Pain is paradoxical in that it is an essentially private phenomenon yet it simultaneously demands to be shared with another. Weil’s life and thought exemplify both aspects of this paradox, demonstrating how her pain alienated her from her own body and from others, and how her thought found full expression as she attempted to share experiences with pain. Weil’s experience of pain was transformed in her passion mysticism, the deep connection she felt with the crucified Christ. In this connection, the most unbearable aspect of her pain, the threat, which it presented to her very self through annihilation, was absorbed into the cross and transformed by God’s love. While this did not necessarily diminish Weil’s pain, the meaning it had for her as a person was transformed through an encounter with Christ crucified, in which she experienced God’s suffering along with her.     

Place avoidance learning and stress-induced analgesia in the attacked mouse: role of endogenous opioids

In this study, mechanisms of pain inhibition (tail-flick test) and memory (place avoidance paradigm) were investigated in attacked, DBA/2 and C57BL/6, mice. During training, exposure of test animals to 10 or 30 bites by an aggressive, isolated ICR mouse situated in the dark half of a bright/dark conditioning box induced a significantly higher social conflict analgesia in DBA than in C57 mice. Naltrexone (0.5 and 2.0 mg/kg) reduced this response in DBA mice that received 30, but not 10, bites and was ineffective in C57 mice. This points to different, opioid versus naltrexone-insensitive nonopioid, analgesic mechanisms. During place choice testing in the same box 24 h later, DBA mice that had received 30, but not 10, bites showed a significant, naltrexone-reversible, avoidance of the attack place. No place avoidance learning was observed in C57 mice. The data provided unequivocal evidence that place avoidance learning was a result of associative conditioning, in that neither pairing nor social conflict per se significantly changed the preference for the dark side seen in experimentally naive DBA mice. Antagonism of place avoidance conditioning was observed regardless of whether testing was carried out in the drugged or undrugged state, excluding possible state-dependent effects as an explanation for the naltrexone-induced impairment. Individual correlational analysis in saline-injected, attacked DBA mice revealed a negative relationship between the analgesic state immediately after training and the avoidance of attack place during testing. In summary, the results suggest strain-dependent analgesic and learning mechanisms and indicate that endogenous opioids released in attacked DBA mice support pain inhibition and modulate the memorization of attack place by their analgesic effects, as well as by mechanisms independent of pain inhibitory systems.     

Unexplained chest pain: a review of psychological conceptualizations and treatment efficacy

This review critically considers psychological theories and models used to understand unexplained chest pain, and efficacy of treatment strategies. It discusses the strengths and limitations of current perspectives, and highlights implications for future research and interventions. A comprehensive range of literature examining unexplained chest pain, and published over the last three decades, was thus reviewed finding that, although unexplained chest pain has been examined as a psychological phenomenon for over 100 years, explanatory models have emerged only in the last two decades. Neither psychophysiological nor psychodynamic models have been significantly advanced. Only cognitive-behavioural models have been explicitly derived to explain and manage the condition, and require further refinement to address conceptual and methodological limitations. Studies assessing treatment efficacy suggest cognitive-behavioural therapy as a first-line therapy, but have failed to establish whether the approach is acceptable and effective in routine care. Comprehensive psychological understanding of unexplained chest pain, and its management, is therefore developing but is far from complete. Cognitive-behavioural interventions show promise but are likely to be enhanced by greater theoretical clarity and understanding of resistance to their implementation.     

About signs and symptoms: Can semiotics expand the view of clinical medicine?

Semiotics, the theory of sign and meaning, may help physicians complement the project of interpreting signs and symptoms into diagnoses. A sign stands for something. We communicate indirectly through signs, and make sense of our world by interpreting signs into meaning. Thus, through association and inference, we transform flowers into love, Othello into jealousy, and chest pain into heart attack. Medical semiotics is part of general semiotics, which means the study of life of signs within society. With special reference to a case story, elements from general semiotics, together with two theoreticians of equal importance, the Swiss linguist Ferdinand de Saussure and the American logician Charles Sanders Peirce, are presented. Two different modes of understanding clinical medicine are contrasted to illustrate the external link between what we believe or suggest, on the one hand, and the external reality on the other hand.     

Cardiophobia: a paradigmatic behavioural model of heart-focused anxiety and non-anginal chest pain.

Cardiophobia is defined as an anxiety disorder of persons characterized by repeated complaints of chest pain, heart palpitations, and other somatic sensations accompanied by fears of having a heart attack and of dying. Persons with cardiophobia focus attention on their heart when experiencing stress and arousal, perceive its function in a phobic manner, and continue to believe that they suffer from an organic heart problem despite repeated negative medical tests. In order to reduce anxiety, they seek continuous reassurance, make excessive use of medical facilities, and avoid activities believed to elicit symptoms. The relationship of cardiophobia to illness phobia, health anxiety, and panic disorder is discussed. An integrative psychobiological model of cardiophobia is presented which includes previous learning conditions relating to experiences of separation and cardiac disease; deficient and inappropriate behavioural repertoires which constitute a psychological vulnerability for cardiophobic problems; negative life events, stressors, and conflicts in the person's present situation that trigger and contribute to the symptoms; current affective, cognitive, and behavioural symptoms and their stimulus properties; and genetic and acquired biological vulnerability factors. Finally, recommendations for the treatment of cardiophobia are derived from the model and areas of future research are outlined.     

Importance of tactile and olfactory cues to the inhibition of the grasshopper mouse's attack through toxicosis

This study examined the effect that toxicosis paired with the presence of a distinctive texture had on the inhibition of the grasshopper mouse's predatory attack. The first experiment measured the context in which tactile cues would be most effective by presenting prey with various combinations of added stimuli. The combination of distinctive tactile, olfactory, and gustatory cues produced the longest lasting inhibition. Because certain manipulations also had an unintended weak odor associated with them, the second experiment measured the importance of a weak or strong odor to inhibition of a mouse's attack. A combination of strong odor and distinctive texture paired with toxicosis inhibited an attack more effectively than a weak odor and a similar texture. In a third experiment, toxicosis was paired with an acraea moth caterpillar which has a highly distinctive texture. This produced the longest lasting inhibition of mouse's attack observed thus far. The ecological significance of a combination of a distinctive texture and odor to the inhibition of the grasshopper mouse's attack is discussed.     

Midbrain-hypothalamic interrelationships in the control of aggressive behavior

Previous studies have suggested an involvement of the midbrain ventral tegmental area in the biting attack upon a rat elicited by electrical stimulation of the lateral hypothalamus in cats. In order assess further the relationship between these two regions, 12 cats were implanted with attack-eliciting electrodes in both the lateral hypothalamus and the midbrain ventral tegmental area. Following a lesion of the midbrain attack site, attack previously elicited from hypothalamic electrodes ipsilateral to the lesion was eliminated or significantly reduced in frequency. The attack elicited from electrodes in the hypothalamus contralateral to the lesion was unaffected. Midbrain lesions made at sites from which attack was never elicited had no effect on hypothalamically elicited attack. The midbrain lesion in some cases eliminated only certain components of the total attack pattern; for example, the approach of a cat to the rat frequently remained present while the bite was absent. Additionally, it was found that the attack elicited from rostral hypothalamic electrodes was disrupted to a greater degree by a single midbrain lesion than the attack elicited from more caudal hypothalamic electrodes. These finding are discussed in terms of the neural system mediating this form of aggressive behavior in cats.     

Chest pain without coronary artery disease: An exploratory comparison with panic disorder

Recent reports have indicated similarities between patients with persistent chest pain of nonorganic origin and patients with panic disorder. In order to explore this association further, we administered a structured interview and three self-report measures (State-Trait Inventory, Beck Depression Inventory, and SCL90-R) to three subject groups: (1) a sample with persistent chest pain (CP; n=14) who had been screened and found to have normal coronary arteries, (2) a sample of patients with panic disorder (PD; n=14), and (3) a sample of matched normals (n=14). CP patients were considered to be free of coronary artery disease (CAD) following normal cardiac catheterization and/or normal thallium stress tests and were not diagnosed initially with panic disorder. PD patients were diagnosed with a standardized psychiatric interview and were free of organic causes of panic. Using an exploratory data analytic approach, the results indicated that both CP and PD samples reported increased levels of state and trait anxiety (p <.0001), depression (p <.01), and somatization (p <.0001) compared with normals. CP patients differed from PD patients in their less frequent use of anxiolytic medication (p <.01) and lower levels of reported panic anxiety and phobic avoidance (p <.0001). These data suggest that persistent chest pain in the absence of CAD shares some features with panic disorder, yet differs from panic in key ways as well. The results are discussed in light of the role of anxiety in contributing to symptom labeling.This research was supported by Grant 86G-491 from the American Heart Association, Texas Affiliate, to J.G.B. H.T. is the recipient of USPHS Research Career Development Award K04-HL-0122246.     

The pain-aggression relationship and its expression in naturalistic settings

Relationships between environmental events and aggression are briefly reviewed. Response-independent pain is a fundamental antecedent environmental cause of attack. Aggression-contingent pain decrease causes further attack strengthening, while pain increase following aggression can decrease attack and foster escape and avoidance behavior. Recent experiments that have questioned the pain-aggression relation and proposed, in the alternative, a pain-defense relationship are discussed. It is argued that this contradiction results from observational difficulties in naturalistic settings, discordance between field and laboratory terminology, substitution of behavioral taxonomy in the place of functional analysis, incomplete understanding of previous findings, and an absence of essential experimental control observations.     

Stress Induced Oral Behaviors and Facial Pain

Facial pain is frequently associated with environmental stress and emotional distress. One hypothetical mechanism by which stress is translated into pain is through stress induced motor function (e.g., teeth clenching, grinding, nail biting). Existent data partially supports these stress-hyperactivity models although they have also come under theoretical and empirical attack. The purpose of this study was to examine the relationship between oral behaviors and pain in an analog sample of facial pain sufferers and student controls. Subjects engaged in a controlled clenching task and reported on subjective facial pain intensity and unpleasantness at 5 specified times over the subsequent 48 hours. A one-way ANCOVA indicated group differences in self reported oral habits (p < .05) with the facial pain group reporting great frequency of oral habits. Two repeated measures ANCOVAs (i.e., pain intensity and pain unpleasantness), controlling for baseline pain ratings, indicated a between groups effect with facial pain sufferers experiencing significantly greater pain over the 48 hours postexperiment (p < .05). This study supports a hyperactivity model of facial pain and provides clues about relevant factors in facial pain development.