Single-Session Attention Bias Modification Training in Victims of Work-Related Accidents

Individuals who experienced traumatic work-related accidents frequently show cognitive deficits and biased processing of trauma-relevant information, which, in turn, could increase the risk of further accidents. The attention bias modification training (ABMT) is designed to reduce hypervigilance toward and enhance attentional disengagement from threat stimuli. The aim of the present study was to assess whether it is possible to implicitly reduce the attentional bias toward trauma-related stimuli through a single session of ABMT in individuals who experienced a traumatic occupational accident. Nineteen individuals who had experienced a traumatic work-related accident and 11 workers who never experienced a work accident (control group) underwent a preliminary assessment of cognitive performance (executive functions and sustained attention) and an evaluation of the attentional bias toward accident-related pictures by means of a dot-probe task. The results showed that injured workers performed more poorly than controls in tasks of executive functions and concentration abilities. Also, injured workers showed an attentional bias toward trauma reminders (i.e., faster reaction times to probes replacing trauma-related pictures). Injured workers were then randomly allocated to a single-session of ABMT (N = 10) or to an Attention Control Condition (ACC; N = 9). After the training, the dot-probe task was administered again to assess changes in the attentional bias toward trauma-relevant pictures. Injured workers who underwent the ABMT, but not those who underwent the ACC, showed a significant reduction of the attentional bias from pre- to post-training. Overall, these results support previous findings reporting an association between traumatic occupational accidents and cognitive dysfunctions. More importantly, these preliminary findings add to a growing body of evidence suggesting the effectiveness of a short ABMT in reducing the attentional bias after a traumatic workplace accident

Somatic, but not cognitive-affective, symptoms are associated with reduced heart rate variability in individuals with dysphoria

Background: Somatic, but not cognitive-affective, symptoms of depression have been associated with reduced heart rate variability (HRV), and with poor prognosis in cardiovascular patients. However, factors concomitant with cardiovascular diseases may confound the relationship between somatic symptoms of depression and reduced HRV. Therefore, this study examined whether reduced HRV was differentially associated with cognitive-affective and somatic symptoms of depression in medically healthy individuals with and without dysphoria. Methods: Self-reported cognitive-affective and somatic symptoms as measured with the Beck Depression Inventory-II (BDI-II) questionnaire and time and frequency domain parameters of HRV were collected in 62 medically healthy individuals, of whom 25 with and 37 without dysphoria. Results: Somatic, but not cognitive-affective, symptoms of depression were inversely associated with standard deviation of NN intervals (SDNN) (beta = -0.476, p .24). Conclusions: By showing that the relationship between somatic depressive symptoms and reduced HRV extends to medically healthy individuals with dysphoria, the present findings suggest that this association is independent of factors concomitant with cardiovascular diseases. The present study also suggests that individuals with somatic rather than cognitive-affective subsets of depressive symptoms may be at greater risk for developing cardiovascular diseases

Not All Competitions Come to Harm! Competitive Biofeedback to Increase Respiratory Sinus Arrhythmia in Managers

Despite the positive impact on achievement, competition has been associated with elevated psychophysiological activation, potentially leading to a greater risk of cardiovascular diseases. Competitive biofeedback (BF) can be used to highlight the effects of competition on the same physiological responses that are going to be controlled through BF. However, it is still unknown whether competition could enhance the effects of respiratory sinus arrhythmia (RSA)-BF training in improving cardiac vagal control. The present study explored whether competitive RSA-BF could be more effective than non-competitive RSA-BF in increasing RSA in executive managers, who are at higher cardiovascular risk of being commonly exposed to highly competitive conditions. Thirty managers leading outstanding private or public companies were randomly assigned to either a Competition (n = 14) or a Control (n = 16) RSA-BF training lasting five weekly sessions. Managers in the Competition group underwent the RSA-BF in couples and each participant was requested to produce a better performance (i.e., higher RSA) than the paired challenger. After the training, results showed that managers in the Competition group succeeded in increasing cardiac vagal control, as supported by the specific increase in RSA (p < 0.001), the standard deviation of R-R wave intervals (SDNN; p < 0.001), and root mean square of the successive differences between adjacent heartbeats (rMSSD; p < 0.001). A significant increase in the percentage of successive normal sinus beat to beat intervals more than 50 ms (pNN50; p = 0.023; partial eta squared = 0.17), low frequency (p < 0.001; partial eta squared = 0.44), and high frequency power (p = 0.005; partial eta squared = 0.25) emerged independently from the competitive condition. Intriguingly, managers who compete showed the same reduction in resting heart rate (HR; p = 0.003, partial eta squared = 0.28), systolic blood pressure (SBP; p = 0.013, partial eta squared = 0.20), respiration rate (p < 0.001; partial eta squared = 0.46), and skin conductance level (SCL; p = 0.001, partial eta squared = 0.32) as non-competitive participants. Also, the same reduction in social anxiety (p = 0.005; partial eta squared = 0.25), state (p = 0.038, partial eta squared = 0.14) and trait anxiety (p = 0.001, partial eta squared = 0.31), and depressive symptoms (p = 0.023, partial eta squared = 0.17) emerged in the two groups. The present results showed that managers competing for increasing RSA showed a greater improvement in their parasympathetic modulation than non-competing managers. Most importantly, competition did not lead to the classic pattern of increased psychophysiological activation under competitive RSA-BF. Therefore, competition could facilitate the use of self-regulation strategies, especially in highly competitive individuals, to promote adaptive responses to psychological stress

Reduced heart rate variability is associated with vulnerability to depression

Background: Heart rate variability (HRV) mirrors cardiac autonomic modulation, an index of well-being. Reduced HRV has been reported in depression, but few studies investigated HRV in individuals at-risk of or remitted from a full-blown depressive episode. The present study aimed at examining whether reduced HRV could be a potential indicator of vulnerability to depression. Methods: Self-reported psychological measures and three-minute resting-state ECG were collected in two at-risk populations [group with dysphoria (n = 27), group with past depression (n = 16)] and in a control group (n = 25). Time- and frequency-domain HRV parameters were computed. Analysis of covariance was conducted to detect between-groups differences for each measure. Results: Standard Deviation of Normal to Normal intervals (SDNN) and High Frequency (HF) power of HRV were found to be reduced both in individuals with dysphoria and in those with past depression as compared with controls. Whereas psychological measures did not significantly differ among individuals with past depression and controls, HRV was capable of discriminating between the two groups. Limitations: Past depression was assessed retrospectively with self-reported information. The inclusion of a group with depression would provide an overview about HRV during the illness course. Conclusions: The findings suggest that reduced HRV is likely to be implicated in the risk of developing full-blown depression, rather than being a mere correlate of current depressive state. The results suggest that HRV may improve clinicians\u2019 ability to early identify people at risk for depression who can benefit from targeted prevention by psychiatric and psychological interventions

Assessment of linear and nonlinear/complex heartbeat dynamics in subclinical depression (dysphoria)

Objective: Depression is one of the leading causes of disability worldwide. Most previous studies have focused on major depression, and studies on subclinical depression, such as those on so-called dysphoria, have been overlooked. Indeed, dysphoria is associated with a high prevalence of somatic disorders, and a reduction of quality of life and life expectancy. In current clinical practice, dysphoria is assessed using psychometric questionnaires and structured interviews only, without taking into account objective pathophysiological indices. To address this problem, in this study we investigated heartbeat linear and nonlinear dynamics to derive objective autonomic nervous system biomarkers of dysphoria. Approach: Sixty undergraduate students participated in the study: according to clinical evaluation, 24 of them were dysphoric. Extensive group-wise statistics was performed to characterize the pathological and control groups. Moreover, a recursive feature elimination algorithm based on a K-NN classifier was carried out for the automatic recognition of dysphoria at a single-subject level. Main results: The results showed that the most significant group-wise differences referred to increased heartbeat complexity (particularly for fractal dimension, sample entropy and recurrence plot analysis) with regards to the healthy controls, confirming dysfunctional nonlinear sympatho-vagal dynamics in mood disorders. Furthermore, a balanced accuracy of 79.17% was achieved in automatically distinguishing dysphoric patients from controls, with the most informative power attributed to nonlinear, spectral and polyspectral quantifiers of cardiovascular variability. Significance: This study experimentally supports the assessment of dysphoria as a defined clinical condition with specific characteristics which are different both from healthy, fully euthymic controls and from full-blown major depression

The moderating role of depressive symptoms in the association between heart rate variability and cognitive performance in cardiac patients

Introduction: Coronary heart disease (CHD) is strongly associated with cognitive impairment, which is a core feature of depression, highly prevalent in patients with CHD. Interestingly, patients with CHD and individuals with depression display reduced heart rate variability (HRV), which proxies a complex network integrating autonomic and attentional systems. This study investigated the moderating role of depressive symptoms in the relation between reduced HRV and cognitive performance in patients with CHD. Method: The sample included 274 patients with CHD (mean [standard deviation] age = 62 [9.5] years; 13 % women) admitted to cardiac rehabilitation units. Visual attention and task switching were assessed through the Trail Making Test (TMT). Depressive symptoms were assessed with the Beck Depression Inventory-II (BDI-II). Resting electrocardiographic recordings were collected to compute HRV indices. Results: Patients with more severe depressive symptoms displayed an inverse association between HRV and cognitive performance (TMT-A: b = -0.08, p = .022; TMTB: b = -0.07, p = .042), whereas patients with milder depressive symptoms showed no significant association (TMT-A: b = -0.00, p = .90; TMTB: b = -0.02, p = .44). Conclusions: Depressive symptoms may strengthen the relation between reduced HRV and poorer cognitive performance in cardiac patients. The presence of depressive symptoms may signal the dysfunction of a network subserving autonomic and cognitive function

Pain-related somatosensory evoked potentials and functional brain magnetic resonance in the evaluation of neurologic recovery after cardiac arrest: a case study of three patients

This case series investigates whether painful electrical stimulation increases the early prognostic value of both somatosensory-evoked potentials and functional magnetic resonance imaging in comatose patients after cardiac arrest. Three single cases with hypoxic-ischemic encephalopathy were considered. A neurophysiological evaluation with an electroencephalogram and somatosensory-evoked potentials during increased electrical stimulation in both median nerves was performed within five days of cardiac arrest. Each patient also underwent a functional magnetic resonance imaging evaluation with the same neurophysiological protocol one month after cardiac arrest. One patient, who completely recovered, showed a middle latency component at a high intensity of stimulation and the activation of all brain areas involved in cerebral pain processing. One patient in a minimally conscious state only showed the cortical somatosensory response and the activation of the primary somatosensory cortex. The last patient, who was in a vegetative state, did not show primary somatosensory evoked potentials; only the activation of subcortical brain areas occurred. These preliminary findings suggest that the pain-related somatosensory evoked potentials performed to increase the prognosis of comatose patients after cardiac arrest are associated with regional brain activity showed by functional magnetic resonance imaging during median nerves electrical stimulation. More importantly, this cases report also suggests that somatosensory evoked potentials and functional magnetic resonance imaging during painful electrical stimulation may be sensitive and complementary methods to predict the neurological outcome in the acute phase of coma. Thus, pain-related somatosensory-evoked potentials may be a reliable and a cost-effective tool for planning the early diagnostic evaluation of comatose patients

Psychobiological mechanisms underlying cognitive decline in cardiac surgery patients

Technological advances over the past four decades have decreased the major complications or mortality in cardiac surgery. However, a significant number of patients suffer from adverse neurological and cognitive outcomes which, in turn, remain an important cause of postoperative morbidity and are responsible for an increasing proportion of perioperative deaths. Adverse neurological and cognitive outcomes after cardiac surgery are the result of multiple preoperative and/or intraoperative factors. While demographic, biomedical, and psychological disorders (e.g., anxiety and depression) represent preoperative variables associated with postoperative adverse outcomes, intraoperative cerebral hypoperfusion, microembolization and neuroinflammation that are related to cardiopulmonary bypass also represent a major cause of impairment after surgery. Despite a growing interest in adverse psychological outcomes after cardiac surgery, the psychobiological mechanisms underlying postoperative cognitive decline have to be investigated yet. In this dissertation, four studies are described, that were meant to examine cognitive decline and depression after cardiac surgery and some psychobiological mechanisms underlying the afore-mentioned phenomena. The main aim of Experiment I was to provide further evidence about the preoperative relationships among anxiety, depression, cognitive dysfunctions and risk-stratification scores, namely the Stroke Index and European System for Cardiac Operative Risk Evaluation, in patients undergoing cardiac surgery. It was found that both the risk-stratification scores showed significant correlations with cognitive performance, whereas only the European System for Cardiac Operative Risk Evaluation was significantly associated also with anxiety and depression. The main goal of Experiment II and III was to investigate the hemodynamic cerebral factors underlying cognitive decline after cardiac surgery. Experiment II was designed to examine whether cerebral hypoperfusion may represent a predictor of cognitive decline in patients undergone cardiac surgery after controlling for common demographic and biomedical risk factors. Experiment II showed that hypoperfusion in the left middle cerebral artery selectively predicted the incidence of cognitive decline after surgery, whereas blood flow velocity in the right middle cerebral artery was unrelated to postoperative cognitive decline. Hence, cardiac surgery patients with reduced left cerebral blood flow velocity preoperatively are at greater risk for postoperative cognitive decline. Left cerebral hypoperfusion may also represent an independent predictor of cognitive decline in cardiac surgery patients. Experiment III was designed to determine the effects of lateralization and type of microembolization on postoperative cognitive decline in patients who had undergone heart valve surgery. Experiment III showed that microembolization in the left middle cerebral artery significantly correlated with early and late (i.e., 3-month follow-up) postoperative cognitive decline, while microembolization in the right middle cerebral artery was unrelated to early and late cognitive decline. Moreover, an association between solid microemboli with early but not late postoperative cognitive decline was noted. In contrast, gaseous microembolization was related to both early and late cognitive decline. Given the relevant role played by depression as a risk factor for postoperative adverse clinical and cognitive outcomes, the main aim of the Experiment IV was to examine, postoperatively, whether electroencephalographic activity could reflect the influence of depression during an emotional imagery task requiring the subject being involved in a cognitive task (retrieval and imagery), which is emotionally laden. There was no difference between groups in resting electroencephalographic activity, whereas patients with depression showed a significant reduced frontal theta power during the emotional imagery task compared to those without depression. Also, a significant correlation was selectively found between frontal theta power and emotional reappraisal. Taken together these experiments provide a better understanding of the psychological and physiological mechanisms underlying postoperative cognitive decline and depression in cardiac surgery patients. In conclusion, the present thesis suggests the need for including preoperative and postoperative evaluation of cognitive and affective status as well as objective hemodynamic and/or electroencephalographic measures to accurately predict and/or treat patient’s dysfunctional psychological outcomes after cardiac surgeryLe innovazioni tecnologiche conseguite nella seconda metà del XX secolo hanno ridotto le complicazioni maggiori e la mortalità nei pazienti sottoposti a cardiochirurgia. Nonostante gli evidenti benefici clinici nella pratica medica, un numero significativo di pazienti presenta disfunzioni neurologiche e/o psicologiche nel periodo postoperatorio che, a loro volta, sono responsabili per l’incremento della mortalità perioperatoria e della morbidità postoperatoria. Tali disfunzioni neurologiche e cognitive in seguito a cardiochirurgia sono il risultato di diversi fattori preoperatori e/o intraoperatori. Mentre le variabili demografiche, biomediche e psicologiche (tra cui ansia e depressione) rappresentano importati fattori preoperatori associati allo stato di salute postoperatorio, l’ipoperfusione cerebrale, l’embolizzazione e/o i processi neuroinfiammatori associati al bypass cardiopolmonare durante la chirurgia rappresentano fattori di rischio intraoperatori per le disfunzioni neurologiche e cognitive postoperatorie. Sebbene vi sia un sempre crescente interesse nello studio delle disfunzioni psicologiche in seguito a cardiochirurgia, i meccanismi psicobiologici sottostanti il declino cognitivo postoperatorio devono ancora essere indagati. Perciò, nella presente tesi sono descritti quattro studi che, per prima cosa, avevano lo scopo di indagare l’entità del declino cognitivo e della depressione in seguito a cardiochirurgia e, in secondo luogo, miravano ad identificare alcuni fattori di stampo psicobiologico coinvolti nel declino cognitivo e depressione postoperatori. L’Esperimento I mirava, come scopo principale, a fornire nuove evidenze circa la relazione, nel periodo preoperatorio, tra ansia, depressione, disfunzioni cognitive e punteggi di rischio biomedico (lo Stroke Index e l’European System for Cardiac Operative Risk Evaluation) in pazienti in attesa di intervento cardiochirurgico. I risultati del presente studio hanno indicato che, mentre entrambi i punteggi di rischio biomedico erano associati allo stato cognitivo preoperatorio dei pazienti cardiochirurgici, solo l’European System for Cardiac Operative Risk Evaluation teneva in considerazione anche i fattori di rischio associati all’ansia e depressione. Lo scopo principale degli Esperimenti II e III era indagare l’associazione fra fattori emodinamici cerebrali perioperatori e disfunzioni cognitive in seguito a cardiochirurgia. L’Esperimento II è stato disegnato per indagare se l’ipoperfusione cerebrale preoperatoria potesse essere un predittore di declino cognitivo postoperatorio nei pazienti sottoposti a cardiochirurgia, anche dopo aver controllato per i più comuni fattori di rischio demografici e biomedici. L’Esperimento II ha mostrato che l’incidenza del declino cognitivo si associava selettivamente all’ipoperfusione nell’arteria cerebrale media sinistra, mentre la velocità di flusso ematico nell’arteria cerebrale media destra non correlava con il declino cognitivo postoperatorio. L’ipoperfusione cerebrale sinistra, quindi, sembra rappresentare un fattore di rischio indipendente per il declino cognitivo in pazienti sottoposti a cardiochirurgia. L’Esperimento III è stato disegnato per determinare il ruolo dell’asimmetria e della natura della microembolizzazione intraoperatoria sul declino cognitivo postoperatorio in pazienti sottoposti a chirurgia valvolare. L’Esperimento III ha mostrato che la microembolizzazione intraoperatoria nell’arteria cerebrale media sinistra correlava significativamente sia con il declino cognitivo nell’immediato postoperatorio (alle dimissioni) che a distanza nel tempo (a 3 mesi dall’intervento chirurgico), mentre gli eventi embolici nell’arteria cerebrale media destra non erano associati né al declino cognitivo immediato né a distanza nel tempo. Inoltre, i microemboli solidi correlavano significativamente con il declino cognitivo immediato ma non al follow-up di 3 mesi. Al contrario, è stata riscontrata un’associazione significativa tra gli eventi microembolici gassosi ed il declino cognitivo immediato e a 3 mesi di distanza dall’intervento chirurgico. Dato il ruolo rilevante giocato dalla depressione come fattore di rischio per le disfunzioni cognitive postoperatorie, lo scopo principale dell’Esperimento IV è stato quello di indagare, nel periodo postoperatorio, se e come la depressione potesse influenzare l’attività elettroencefalografica durante un compito di imagery emozionale, il quale, a sua volta, implica sia un’elaborazione di tipo cognitivo che emozionale. Sebbene nessuna differenza tra i gruppi sia stata riscontrata nell’attività elettroencefalografica a riposo, rispetto ai controlli non depressi, si osservava nei pazienti depressi una ridotta attività theta frontale durante il compito di imagery emozionale. Inoltre, una ridotta ampiezza della theta frontale si associava selettivamente a disregolazione emozionale (ridotta capacità di reappraisal). Questi esperimenti, considerati nel loro insieme, forniscono una migliore e più approfondita comprensione dei meccanismi psicologici e fisiologici sottostanti il fenomeno del declino cognitivo e depressione postoperatori in pazienti cardiochirurgici. In conclusione, la presente tesi suggerisce la possibilità di includere sia una valutazione cognitiva e affettiva pre e postoperatoria che misure emodinamiche e/o elettroencefalografiche oggettive in grado di predire e/o facilitare il trattamento delle disfunzioni psicologiche postoperatorie nei pazienti sottoposti a cardiochirurgi

Early indicators of vulnerability to depression: The role of rumination and heart rate variability

Background: Despite the evidence of increased levels of rumination and reduced heart rate variability (HRV) in depression, whether these measures can be considered early indicators of vulnerability to depression has yet to be investigated. Therefore, the present study aimed to investigate both levels of rumination and resting HRV in individuals with familial risk for depression that is the most reliable risk factor for the disorder. Methods: Rumination and vagally-mediated HRV were assessed using the Ruminative Response Scale and a smartphone-based photoelectric volumetric pulse wave assay, respectively, in 25 individuals who had family history of depression (but did not report current depressive symptoms), 15 individuals who reported depressive symptoms (but had no family history of depression), and 25 controls (without depressive symptoms and family history of depression). Results: Individuals with depressive symptoms and those with a family history of depression were characterized by higher levels of rumination and lower cardiac vagal control than controls. Limitations: Given the small sample size, this study should be used to design larger confirmatory studies; the cross-sectional nature of the study does not allow discussing the results in terms of cause-effect relationships. Conclusions: Our findings suggested that individuals at risk of developing depression, also in absence of depressive symptoms, are defined by defective self-regulation capacity that may lead to future depression episodes. Increased ruminative thoughts and reduced HRV may represent early indicators of vulnerability to depression. Effective prevention programs designed to reduce rumination and/or increase HRV may reduce the risk of developing a full-blown depressive episode