Biomedical subjects

James L Abelson

Publications and source records attributed to James L Abelson.

16 recordsLinked to original sources

PubMed2007

HPA axis activity in patients with panic disorder: review and synthesis of four studies.

Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis may play a role in panic disorder. HPA studies in patients with panic disorder, however, have produced inconsistent results. Seeking to understand the inconsistencies, we reexamined endocrine data from four studies of patients with panic disorder, in light of animal data highlighting the salience of novelty, control, and social support to HPA axis activity. Patients with panic disorder were studied (1) at rest over a full circadian cycle, (2) before and after activation by a panicogenic respiratory stimulant (doxapram) that does not directly stimulate the HPA axis, and (3) before and after a cholecystokinin B (CCK-B) agonist that is panicogenic and does directly stimulate the HPA axis. Patients with panic disorder had elevated overnight cortisol levels, which correlated with sleep disruption. ACTH and cortisol levels were higher in a challenge paradigm (doxapram) than in a resting state study, and paradigm-related ACTH secretion was exaggerated in patients with panic disorder. Panic itself could be elicited without HPA axis activation. Patients with panic disorder showed an exaggerated ACTH response to pentagastrin stimulation, but this response was normalized by prior exposure to the experimental context or psychological preparation to reduce novelty and enhance sense of control. Novelty is one of a number of contextual cues known from animal work to activate the HPA axis. The HPA axis abnormalities seen in patients with panic disorder in the four experiments reviewed here might all be due to exaggerated HPA axis reactivity to novelty cues. Most of the published panic/HPA literature is consistent with the hypothesis that HPA axis dysregulation in panic is due to hypersensitivity to contextual cues. This hypothesis requires experimental testing.

Adolescent↗

PubMed2006

Medial frontal cortex activity and loss-related responses to errors.

Making an error elicits activity from brain regions that monitor performance, especially the medial frontal cortex (MFC). However, uncertainty exists about whether the posterior or anterior/rostral MFC processes errors and to what degree affective responses to errors are mediated in the MFC, specifically the rostral anterior cingulate cortex (rACC). To test the hypothesis that rACC mediates a type of affective response, we conceptualized affect in response to an error as a reaction to loss and amplified this response with a monetary penalty. While subjects performed a cognitive interference task during functional magnetic resonance imaging, hemodynamic activity in the rACC was significantly greater when subjects lost money as a result of an error compared with errors that did not lead to monetary loss. A significant interaction between the incentive conditions and error events demonstrated that the effect was not merely attributable to working harder to win (or not lose) money, although an effect of motivation was noted in the mid-MFC. Activation foci also occurred in similar regions of the posterior MFC for error and interference processing, which were not modulated by the incentive conditions. However, at the level of the individual subject, substantial functional variability occurred along the MFC during error processing, including foci in the rostral/anterior extent of the MFC not appearing in the group analysis. The findings support the hypothesis that the rostral extent of the MFC (rACC) processes loss-related responses to errors, and individual differences may account for some of the reported variation of error-related foci in the MFC.

Adult↗

PubMed2006

Videoconferencing-based cognitive-behavioral therapy for obsessive-compulsive disorder.

Obsessive-compulsive disorder (OCD) is a prevalent, chronic and disabling anxiety disorder. Despite the efficacy and strength of pharmacologic interventions for OCD, medications are not always well accepted or effective, making an efficacious psychosocial alternative especially attractive. Cognitive-behavioral therapy (CBT) has been established as an effective treatment for adult OCD, yet access to such treatment is limited, especially in rural areas. Technological advances allow for therapy to be provided in a real-time format over a videoconferencing network. This method allows therapists to provide state-of-the-art treatment to patients who would not otherwise have access to it. This paper presents three cases of OCD successfully treated via videoconferencing CBT. The presence of OCD was established via structured clinical interview and clinician-rated outcome measures were completed by evaluators blinded to the method of treatment. A multiple baseline across individuals design was used to support the internal validity of the CBT outcome data. Patient ratings of therapeutic alliance were high across all three cases. Information gathered from qualitative interviews post-treatment confirmed quantitative measures finding high levels of patient satisfaction. This pilot study suggests that videoconferencing-based CBT is a promising method to bring appropriate treatment to thousands who live far distances from well-trained therapists.

Adult↗

PubMed2006

Increased psychiatric morbidity after abdominal aortic surgery: risk factors for stress-related disorders.

OBJECTIVE: Research on surgical outcomes has focused on technical results and physical morbidity. However, postoperative psychiatric complications are common and can undermine functional results. High rates of posttraumatic stress disorder and major depressive disorder have been documented after cardiac events or surgery. These complications are also expected after abdominal aortic surgery, but their incidence and relevant risk factors in this population have not been documented. METHODS: We examined the development of posttraumatic stress and depressive symptoms in patients with aortic aneurysms or occlusive disease, comparing surgical with nonsurgical patients and predicting that surgery and a prolonged intensive care stay would contribute to the development of psychiatric morbidity. A consecutive sample of vascular surgery patients (n = 109) was recruited 6 months to 2 years after surgery. Data were analyzed by using group comparisons, regression, and path analyses. RESULTS: Rates of objectively determined postoperative psychiatric morbidity were extremely high (32%). Surgical patients were more than four times more likely to develop psychiatric disorders (odds ratio, 4.8; P = .02). Being younger, having increased preoperative blood pressure, and being intubated at the end of surgery were linked to greater rates of psychiatric morbidity (P < .05), but a longer intensive care stay was not. CONCLUSIONS: New-onset psychiatric symptoms are common after abdominal aortic surgery, and preoperative and surgical factors were more predictive than postoperative complications and stress, as reflected in intensive care unit stays. Prospective examination of vulnerability in this model could identify risk factors for stress-related psychiatric morbidity and help improve surgical outcomes.

Adult↗

PubMed2005

Deep brain stimulation for refractory obsessive-compulsive disorder.

BACKGROUND: Neurosurgery (anterior capsulotomy) has been beneficial to many patients with debilitating, refractory obsessive-compulsive disorder (OCD), but the irreversibility of the procedure is an important limitation to its use. Nondestructive, electrical stimulation (deep brain stimulation; DBS) has proven an effective alternative to ablative surgery for neurological indications, suggesting potential utility in place of capsulotomy for OCD. METHODS: The effects of DBS for OCD were examined in four patients in a short-term, blinded, on-off design and long-term, open follow-up. The patients had incapacitating illness, refractory to standard treatments. Hardware developed for movement disorder treatment was surgically implanted, with leads placed bilaterally in the anterior limbs of their internal capsules. Patients received stimulation in a randomized "on-off" sequence of four 3-week blocks. Ongoing, open stimulation was continued in consenting patients after the controlled trial. RESULTS: Patients tolerated DBS well. Dramatic benefits to mood, anxiety, and OCD symptoms were seen in one patient during blinded study and open, long-term follow-up. A second patient showed moderate benefit during open follow-up. CONCLUSIONS: It appears that DBS has potential value for treating refractory psychiatric disorders, but additional development work is needed before the procedure is utilized outside of carefully controlled research protocols.

Adult↗

PubMed2005

Error-related hyperactivity of the anterior cingulate cortex in obsessive-compulsive disorder.

BACKGROUND: Hyperactivity of the anterior cingulate cortex (ACC) in patients with obsessive-compulsive disorder (OCD) has been shown to increase with symptom provocation and to normalize with treatment-induced symptom reduction. Although the functional significance of anterior cingulate involvement in OCD remains unknown, electrophysiological evidence has linked this region to error-processing abnormalities in patients with OCD. In this functional magnetic resonance imaging (fMRI) study, we sought to further localize error-processing differences within the ACC of OCD patients compared with healthy subjects. METHODS: Event-related fMRI data were collected for eight OCD patients and seven healthy subjects during the performance of a simple cognitive task designed to elicit errors but not OCD symptoms. RESULTS: Both OCD patients and healthy subjects demonstrated dorsal ACC activation during error commission. The OCD patients exhibited significantly greater error-related activation of the rostral ACC than comparison subjects. Activity in this region was positively correlated with symptom severity in the patients. CONCLUSIONS: Error-processing abnormalities within the rostral anterior cingulate occur in the absence of symptom expression in patients with OCD.

Adult↗

PubMed2005

Cognitive modulation of the endocrine stress response to a pharmacological challenge in normal and panic disorder subjects.

CONTEXT: The hypothalamic-pituitary-adrenal (HPA) axis may mediate the deleterious effects of stress on health. It is sensitive to cognitive and emotional aspects of organism-environment interactions, such as familiarity, control, and social support. Scientific study of how such factors moderate human HPA axis activity has been limited. Their relevance to HPA axis disturbances in psychiatric patients is largely unexplored. OBJECTIVE: To determine whether cognitive manipulation can alter HPA axis activity in laboratory studies and whether patients with panic disorder are differentially sensitive to the manipulated factors. DESIGN: Pharmacological activation paradigm (cholecystokinin-B agonist pentagastrin) by which we examined symptom and endocrine effects on subjects randomly assigned to a standard introduction or a cognitive intervention. SETTING: Clinical research center. PARTICIPANTS: Recruited from university clinic and newspaper advertisements. Fourteen patients with panic disorder and 14 controls, individually matched for age and sex. Intervention Half of each group received a 9-minute cognitive intervention designed to reduce novelty, increase cognitive coping, and provide a sense of control. MAIN OUTCOME MEASURES: Corticotropin (ACTH) and cortisol levels. RESULTS: The cognitive intervention significantly reduced cortisol (P = .02) and ACTH (P = .01) levels, despite pentagastrin's robust stimulation of both hormones (P<.001). The intervention effect was evident in patients and controls, who did not differ in basal HPA axis activity or response to pentagastrin. They did differ in panic symptom responses, which were unaffected by the intervention, and in ACTH effects of the intervention. Patients' exaggerated anxiety responses to pentagastrin were normalized by the intervention. CONCLUSIONS: Cognitive/emotional manipulation can substantially modulate HPA axis responses to pharmacological activation in humans, and HPA disturbances in panic disorder may be secondary to manipulable cognitive/emotional sensitivities. Further study of such factors as novelty, control, and coping may help clarify the origins of HPA axis disturbance in psychiatric disorders and the mediators linking psychosocial stress to disease.

Adaptation, Psychological↗

PubMed2005

Twenty-four hour growth hormone secretion in patients with panic disorder.

BACKGROUND: Patients with panic disorder have blunted growth hormone (GH) responses to clonidine, suggesting subsensitivity of post-synaptic alpha(2)-adrenoreceptors, presumably in response to excessive central noradrenergic outflow. However, basal levels of GH release over a full circadian cycle have not been examined in panic. Reduced basal GH release would suggest an overall hypo-active GH system rather than a specific alpha-adrenergic abnormality. METHODS: To determine whether panic patients show reduced basal GH secretion, 20 patients and 12 healthy controls were studied. Blood samples were drawn every 15 min for 24 h and plasma was assayed for GH. Patients were restudied during successful treatment with alprazolam. Groups were compared on overnight and daytime GH secretion and circadian patterns of release. RESULTS: Patients showed normal levels on all measures of GH release. Treatment may have reduced nocturnal GH release slightly, but treated patients still did not differ from controls. The normal predominance of sleep over waking GH secretion was seen in both groups. CONCLUSIONS: Panic patients, in contrast to depressed patients, have normal somatotrophic axis activity when measured in a resting state over a full circadian cycle. GH dysregulation may only be evident in these patients in activation paradigms and has been most consistently demonstrated by challenges with the alpha(2)-noradrenergic agonist, clonidine.

Adult↗

PubMed2005

Interaction of brain noradrenergic system and the hypothalamic-pituitary-adrenal (HPA) axis in man.

BACKGROUND: Numerous interactions between the brainstem locus coeruleus system and the HPA axis have been shown in experimental animals. This relationship is less well characterized in humans and little is known about the influence of psychiatric disorders, which disturb one of these systems, on this relationship. METHODS: Untreated subjects with pure MDD (n = 13), MDD with comorbid anxiety disorders (n = 17), and pure anxiety disorders (n = 15) were recruited by advertising. Age and sex matched control subjects were recruited for each subject with a psychiatric diagnosis (n = 45). All subjects underwent a social stressor, the Trier Social Stress Test (TSST), and blood was collected for ACTH assay. These same subjects also underwent a clonidine challenge study for assessment of growth hormone release as a marker of tonic noradrenergic activation. RESULTS: Examining log transformed area under the curve response for each hormone, a significant negative relationship (simple regression) was observed between systems in normal subjects. This relationship was preserved in anxiety subjects. However, both pure depressed and comorbid depressed and anxiety subjects demonstrated disruption of this relationship. CONCLUSIONS: Under normal circumstances, noradrenergic systems can influence the magnitude of the HPA axis response to stress. However, in subjects with major depression, HPA axis activation appears autonomous of noradrenergic influence.

Adrenocorticotropic Hormone↗

PubMed2004

Anxious and depressive disorders and their comorbidity: effect on central nervous system noradrenergic function.

BACKGROUND: Although comorbidity of anxiety with depression is common, investigations of physiologic abnormalities related specifically to comorbidity are rare. This study examined relationships of DSM-IV-defined depression, anxiety, and their comorbidity to noradrenergic function measured by blunting of the growth hormone (GH) response to the alpha2 adrenoreceptor agonist (and imidazoline receptor agent) clonidine and by blood pressure and symptom responses. METHODS: Fifteen subjects with pure social anxiety or panic disorder, 15 with pure major depression, and 18 with both depression and anxiety were compared with healthy control subjects matched for age and gender. Other factors known to affect GH (weight, menstrual status, prior antidepressant, or other drug exposure) were controlled. RESULTS: Anxiety produced GH blunting, but depression was associated with normal GH responses. The comorbid state did not affect results beyond the impact of anxiety. Preclonidine stress-related GH elevations were observed, to the greatest degree in anxious subjects. Relevant symptom, but not blood pressure, changes were significantly associated with blunting. CONCLUSIONS: With use of pure depression and anxiety groups and careful control of other factors known to affect GH, these results demonstrate central nervous system noradrenergic dysfunction in anxiety disorders. In contrast to less rigorously controlled studies, noradrenergic function in depression was normal.

Adrenergic alpha-Agonists↗

PubMed2004

Effect of comorbid anxiety disorders on the hypothalamic-pituitary-adrenal axis response to a social stressor in major depression.

BACKGROUND: Major depressive disorder (MDD) is often complicated by anxiety symptoms, and anxiety disorders occur in approximately 30% of mood cases. This study examined the influence of anxiety comorbidity on the hypothalamic-pituitary-adrenal (HPA) axis response to stress in patients with MDD. METHODS: Untreated subjects with pure MDD (n = 15), MDD with comorbid anxiety disorders (n = 18), and pure anxiety disorders (n = 15) were recruited by advertising. Age- and gender-matched control subjects were recruited for each subject with a psychiatric diagnosis (n = 48). All subjects underwent a social stressor, the Trier Social Stress Test (TSST), and blood was collected for adrenocorticotropic hormone (ACTH) and cortisol assay. RESULTS: When all depressed patients (n = 33) were compared with their matched control subjects (n = 33), they showed a significantly greater ACTH response to the stressor; however, this exaggerated ACTH response was exclusively due to the depressed group with comorbid anxiety disorders. A similar but nonsignificant effect was observed in the cortisol response. Subjects with pure mood or pure anxiety disorders showed normal ACTH and cortisol responses to the TSST. All patient groups showed similar levels of TSST-induced anxiety. CONCLUSIONS: Comorbid anxiety disorders might play a role in the increased activation of the HPA axis observed in patients with major depression.

Adrenocorticotropic Hormone↗

PubMed2004

Effect of repeat exposure on neuroendocrine and symptom responses to pentagastrin.

The cholecystokinin (CCK-B) agonist pentagastrin stimulates dose-dependent release of adrenocorticotropin (ACTH) and cortisol in humans, likely via direct pharmacological action at pituitary CCK-B receptors. Pentagastrin also produces side effects, however, which may be experienced as novel or anxiety arousing and could contribute to ACTH release. Available data suggest that pentagastrin's activation of the hypothalamic-pituitary-adrenal (HPA) axis is unrelated to anxiety symptoms themselves, but novelty effects have not been examined in this model and do strongly activate this system in animals. To further explore the impact of novelty and anxiety symptoms on HPA responses, pentagastrin was administered twice to 12 subjects (six male, six female) under single-blind conditions. Repeat pentagastrin injection was associated with a slight habituation in the magnitude of symptom and HPA axis responses, but robust HPA and symptom responses were seen following both injections. No relationships were found between anxiety symptoms and HPA activity and the modest symptomatic and neuroendocrine habituation appeared to occur independently. Pentagastrin may release ACTH and cortisol through direct pharmacological action, perhaps enhanced on first exposure by psychologically mediated novelty effects. Novelty, per se, is not likely the primary mediator of the HPA response. This model may be useful for further study of cognitive-emotional modulators of HPA axis activity.

Adrenocorticotropic Hormone↗

PubMed2004

Effects of propranolol on symptom and endocrine responses to pentagastrin.

Intravenous injections of CCK-B agonists, such as pentagastrin, produce symptoms of panic and potent activation of the human hypothalamic-pituitary-adrenal (HPA) axis. It is unclear whether these psychological and endocrine effects are mediated by similar or independent processes. Independence is supported by prior evidence that beta-adrenergic receptor blockade attenuates cardiovascular and symptom but not vasopressin responses to CCK-4. To further explore associations between somatic, emotional and endocrine responses to CCK-B agents, and potential beta-adrenergic mediating mechanisms, symptom and endocrine responses to pentagastrin were examined after propranolol pre-treatment. Cardiovascular, symptom, and endocrine (ACTH, cortisol, epinephrine) responses to pentagastrin were measured in 16 healthy adult subjects randomly assigned to receive propranolol or placebo pre-treatment. Propranolol significantly blocked the normal cardiac acceleration produced by pentagastrin, but did not reduce panic symptom or anxiety effects. It delayed and perhaps enhanced the cortisol response. No relationship between HPA and symptom responses following pentagastrin could be detected, though pre-pentagastrin cortisol was inversely related to post-injection panic symptom intensity. Endocrine, cardiovascular and symptom responses to pentagastrin appear to be separately mediated, as they did not change in concert in response to propranolol pre-treatment, nor were they correlated with one another. The results are consistent with the presence of inhibitory beta-adrenergic mediation of the HPA axis in humans. They support the hypothesis that the HPA response to pentagastrin is not secondary to the psychological stress of its side effects.

Adrenergic beta-Antagonists↗

PubMed2003

The buffering effects of active coping on the relationship between SES and cortisol among African American young adults.

Cortisol levels have consistently been related to socioeconomic status (SES). Possible moderators for this relationship are coping styles that are known to moderate relationships between cardiovascular factors and SES. The authors examined whether coping style moderated a relationship between resting cortisol levels and various measures of SES in a sample of urban, African American young adults. Those scoring low on coping style had high cortisol levels if they were currently students or unemployed. This effect, however, differed for men and women. The authors suggest that coping style may play an adaptive role regarding salivary cortisol measures in young adults when they are students or unemployed. Active coping may help protect against stress among young African American adults.

Adaptation, Psychological↗

PubMedDate not supplied

Salivary cortisol response during exposure treatment in driving phobics.

OBJECTIVE: Extensive research on the hypothalamic-pituitary-adrenal (HPA) axis response to stress has not clarified whether that axis is activated by phobic anxiety. We addressed this issue by measuring cortisol in situational phobics during exposure treatment. METHODS: Salivary cortisol was measured in 11 driving phobics before and during three exposure sessions involving driving on crowded limited-access highways and compared with levels measured in 13 healthy controls before and during two sessions of driving on the same highways. For each subject, data collected in the same time period on a comparison nondriving day served as an individual baseline from which cortisol response scores were calculated. RESULTS: Cortisol levels of driving phobics and controls did not differ on the comparison day. Phobics also had normal cortisol response scores on awakening on the mornings of the exposures but these were already increased 1 hour before coming to the treatment sessions. Phobics had significantly greater cortisol response scores during driving exposure and during quiet sitting periods before and afterward. These greater responses generally paralleled increases in self-reported anxiety. At the first exposure session, effect sizes for differences in cortisol response scores between the two groups were large. Initial exposure to driving in the first session evoked the largest responses. CONCLUSION: The data demonstrate that the HPA axis can be strongly activated by exposure to, and anticipation of, a phobic situation.

Adrenal Cortex↗

PubMedDate not supplied

The development of persistent pain and psychological morbidity after motor vehicle collision: integrating the potential role of stress response systems into a biopsychosocial model.

OBJECTIVES: Persistent pain and psychological sequelae are common after motor vehicle collision (MVC), but their etiology remains poorly understood. Such common sequelae include whiplash-associated disorders (WAD), fibromyalgia, and posttraumatic stress disorder (PTSD). Increasing evidence suggests that these disorders share overlapping epidemiologic and clinical features. A model is proposed in which central neurobiological systems, including physiologic systems and neuroanatomical structures involved in the stress response, are an important substrate for the development of all 3 disorders and interact with psychosocial and other factors to influence chronic symptom development. METHODS: Epidemiologic and clinical characteristics regarding the development of these disorders after MVC are reviewed. Evidence suggesting a role for stress response systems in the development of these disorders is presented. RESULTS: Contemporary evidence supports a model of chronic symptom development that incorporates the potential for interactions between past experience, acute stress responses to trauma, post-MVC behavior, and cognitive/psychosocial consequences to alter activity within brain regions which process pain and to result in persistent pain, as well as psychological sequelae, after MVC. Such a model incorporates factors identified in prior biopsychosocial theories and places them in the landscape of our rapidly developing understanding of stress systems and CNS pain-modulating pathways. CONCLUSION: New models are needed to stimulate deeper examination of the interacting influences of initial tissue damage, acute pain, psychosocial contingencies, and central stress pathways during chronic symptom development after MVC. Deeper understanding could contribute to improved treatment approaches to reduce the immense personal and societal burdens of common trauma-related disorders.

Accidents, Traffic↗