A new study has shed light on how behavioral variant frontotemporal dementia (bvFTD) disrupts empathy processing, with the help of advanced imaging techniques that have revealed significant disturbances in the brain regions responsible for understanding and reacting to others’ pain. The research was published in JAMA Network Open.
Empathy is the capacity of an individual to perceive, be sensitive to, and care about the emotional state of others. Multiple regions in the brain play a role in empathy, such as mirror neurons, the anterior insular and medial prefrontal cortices, the amygdala, the basal ganglia, the anterior cingulate cortex, and the orbitofrontal cortex.
Loss of empathy is a defining characteristic of bvFTD. Those affected may show a lack of concern for others and an inability to respond to the needs of their loved ones. In severe instances, bvFTD can even lead to morally questionable behaviors that can undermine their ability to build and maintain relationships. Previous studies have indicated that the lack of empathy in bvFTD stems from the impaired functioning of frontoinsular and temporal neuronal structures that are crucial for processing social information. Moreover, bvFTD has been shown to directly impact the ventromedial prefrontal cortex, which is mainly responsible for regulating complex emotions, controlling impulsive behaviors, and making moral judgments.
In this study, 28 patients with bvFTD were compared to an equal number of individuals with normal cognitive function in a classic case-control study. The patients and controls had similar median ages, 66.7 and 67.6 years respectively, and comparable educational attainment distributions.
The study was conducted across three centers in Stockholm, Sweden. The Interpersonal Reactivity Index (IRI) was employed to evaluate empathy by measuring its cognitive and affective aspects. Task-based functional magnetic resonance imaging (fMRI) was used to track any alterations in brain activity among both the controls and the patients.
Subtraction techniques were utilized to remove the blood oxygen level-dependent (BOLD) signal at baseline from the signal in the pain condition. This enabled the researchers to isolate the brain responses related to empathy for pain (EFP).
Two regions of interest (ROIs) were chosen: one based on a meta-analysis of areas commonly reported to be activated during EFP and the other based on the activation pattern seen in controls during EFP (CA-ROI). The CA-ROI was used to explore associations with empathy-related responses as it exhibited normal activation patterns in this task.
Compared to controls, where the blood oxygen level-dependent (BOLD) signal during EFP was increased in 12 areas, it was only increased in two areas among bvFTD patients. The BOLD signal was decreased under the ROI related to affective empathy, with an average change during EFP of about 21% for controls versus -1.3% for patients. However, no reduction in the BOLD signal was observed under the cognitive empathy ROI.
The EPF-BOLD signal in the CA-ROI was increased in control participants who reported a higher self-perception of empathic feelings in the IRI. Among bvFTD patients, the signal for EPF was positively correlated with the informants’ ratings of the patients’ empathic concerns. That is, according to others, the higher this signal, the more likely the patient was to have empathic feelings.
The fMRI findings from this task-based study on empathy for pain in bvFTD cases demonstrated reduced responses in the brain regions that are vital for processing empathic feelings. This alteration reflects an early consequence of the various changes in neuronal structure and function that occur in bvFTD. The magnitude of empathy-related neural activity was correlated with the patients’ ability to experience empathy, as judged by those living with the affected patients.
However, the current study had some limitations. Multiple devices were used for fMRI, which might have introduced variability in the results. Additionally, the study included patients with both sporadic and genetic bvFTD, and the bvFTD diagnoses were clinical, lacking neuropathological confirmation.
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