ated with pathologic tearfulness: GM volume reduction and aberrantly increased rsALFF in the left fusiform gyrus, reduced rsALFF in the right inferior parietal lobule, and reduced rsFC between the right hippocampus and the right middle frontal gyrus. While activations in all of these regions have been repeatedly shown in self-face processing,^[@R49],[@R50]^ the aberrantly increased rsFC and rsALFF in patients with pathologic tearfulness require further investigation, as they may reflect compensatory or maladaptive mechanisms.

Our study describes a novel disorder of emotion regulation following aLE that is characterized by residual pathologic tearfulness, is not related to low mood or cognitive impairment, and is associated with specific abnormalities within networks supporting emotion regulation. Clinicians need to be aware of the potential for such symptoms to develop after aLE and of the distress they can cause. Furthermore, pathologic tearfulness offers a useful neuropsychological model for exploring the neural mechanisms of emotion regulation and may provide insight into the breakdown of these mechanisms across a wide range of neurologic conditions. This will inform the development and refinement of behavioral and pharmaceutical interventions.

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The authors thank the participants of this study.

Study funding
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C.R.B. is supported by a Medical Research Council Clinician Scientist Fellowship (MR/K010395/1). S.R.I. is supported by the Wellcome Trust (104079/Z/14/Z), the UCB--Oxford University Alliance, BMA Research Grants--Vera Down grant (2013) and Margaret Temple (2017), Epilepsy Research UK (P1201), and the Fulbright UK--US commission (MS Society Research Award). The research was funded/supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Departm