Compassion fatigue among oncologists: the role of grief, sense of failure, and exposure to suffering and death.

PURPOSE: Oncologists cope with unique work characteristics that increase their risk of developing compassion fatigue-that is, burnout and secondary traumatic stress-and can result in reduced capacity and interest in being empathetic to the suffering of others (Stamm B. The concise ProQOL manual, 2010). At the same time, oncologists can experience compassion satisfaction-that is, the positive aspects of caring. This study explored the associations of compassion fatigue and compassion satisfaction with oncologists' grief and sense of failure beyond their reported exposure to suffering and death. METHODS: Seventy-four oncologists completed self-administered questionnaires examining compassion fatigue, compassion satisfaction, grief, exposure to suffering and death, and sense of failure. RESULTS: The oncologists reported that they face the loss of approximately 50% of their patients, and that their patients suffer from profound emotional and physical pain. High levels of compassion fatigue and grief, and moderate levels of sense of failure, were reported. Findings showed a lack of association between exposure to suffering and death and compassion fatigue and satisfaction. However, grief and sense of failure were found to predict both aspects of compassion fatigue: secondary traumatic stress (p < 0.001, p < 0.003, respectively) and burnout (p < 0.002, p < 0.025, respectively). CONCLUSIONS: These results highlight the importance of the oncologists' subjective experiences of grief and sense of failure, beyond their reports of exposure to suffering and death, in terms of their levels of compassion fatigue. Implications of these findings include the need to develop interventions for oncologists that will allow them to acknowledge, process, and overcome negative experiences of failure and grief.

Grief over patients, compassion fatigue, and the role of social acknowledgment among psycho-oncologists.

OBJECTIVE: Compassion fatigue-that is, secondary traumatic stress (STS) and burnout-is a traumatic emotional state experienced by health care providers and expressed in a reduced capacity to be interested in and empathic to the suffering of others. Compassion fatigue may be related to grief over patients' loss. We examined the relation between grief and compassion fatigue among psycho-oncologists while exploring the impact of social acknowledgment on this association. We hypothesized that social acknowledgment would moderate the relation between grief and compassion fatigue. METHODS: Participants were 60 Israeli psycho-oncologists in a cross-sectional study. Measures consisted of a demographic questionnaire, the Texas Revised Inventory of Grief-Present, the Social Acknowledgment questionnaire, and the Professional Quality of Life Questionnaire. RESULTS: The participants reported relatively high levels of grief and high levels of compassion fatigue. Grief and compassion fatigue were significantly positively associated (STS: r = 0.41, p < 0.01; Burnout: r = 0.45, p < 0.01). A k-means cluster analysis based on social acknowledgment and grief yielded three meaningful clusters: High Grief-Low Social Acknowledgment; Medium Grief-High Social Acknowledgment; and Low Grief-Medium Social Acknowledgment. Levels of STS in the first cluster were significantly higher in comparison to levels of STS in each of the other clusters (F = 6.22, p < 0.01). CONCLUSIONS: Psycho-oncologists experience patient loss as part of their daily work. In response, they may develop grief reactions. This grief, when it is not perceived by them as being socially acknowledged, may result in high levels of STS: a phenomenon with undesirable personal and professional implications.

Neuromodulation of reinforced skill learning reveals the causal function of prefrontal cortex.

Accumulating evidence has suggested functional interactions between prefrontal cortex (PFC) and dissociable large-scale networks. However, how these networks interact in the human brain to enable complex behaviors is not well-understood. Here, using a combination of behavioral, brain stimulation and neuroimaging paradigms, we tested the hypothesis that human PFC is required for successful reinforced skill formation. We additionally tested the extent to which PFC-dependent skill formation is related to intrinsic functional communication with this region. We report that inhibitory noninvasive transcranial magnetic stimulation over lateral PFC, a hub region with a diverse connectivity profile, causally modulated effective reinforcement-based motor skill acquisition. Furthermore, PFC-dependent skill formation was strongly related to the strength of functional connectivity between the PFC and regions in the sensorimotor network. These results point to the involvement of lateral PFC in the neural architecture that underlies the acquisition of complex skills, and suggest that, in relation to skill acquisition, this region may be involved in functional interactions with sensorimotor networks.

Memory reactivation improves visual perception.

Human perception thresholds can improve through learning. Here we report findings challenging the fundamental 'practice makes perfect' basis of procedural learning theory, showing that brief reactivations of encoded visual memories are sufficient to improve perceptual discrimination thresholds. Learning was comparable to standard practice-induced learning and was not due to short training per se, nor to an epiphenomenon of primed retrieval enhancement. The results demonstrate that basic perceptual functions can be substantially improved by memory reactivation, supporting a new account of perceptual learning dynamics.

Reward disrupts reactivated human skill memory.

Accumulating evidence across species and memory domains shows that when an existing memory is reactivated, it becomes susceptible to modifications. However, the potential role of reward signals in these mechanisms underlying human memory dynamics is unknown. Leaning on a wealth of findings on the role of reward in reinforcing memory, we tested the impact of reinforcing a skill memory trace with monetary reward following memory reactivation, on strengthening of the memory trace. Reinforcing reactivated memories did not strengthen the memory, but rather led to disruption of the memory trace, breaking down the link between memory reactivation and subsequent memory strength. Statistical modeling further revealed a strong mediating role for memory reactivation in linking between memory encoding and subsequent memory strength only when the memory was replayed without reinforcement. We suggest that, rather than reinforcing the existing memory trace, reward creates a competing memory trace, impairing expression of the original reward-free memory. This mechanism sheds light on the processes underlying skill acquisition, having wide translational implications.