Abstract

We used resting-state functional magnetic resonance imaging to investigate the global spontaneous neural activity involved in pathological laughing and crying after stroke. Twelve pathological laughing and crying patients with isolated pontine infarction were included, along with 12 age- and gender-matched acute isolated pontine infarction patients without pathological laughing and crying, and 12 age- and gender-matched healthy controls. We examined both the amplitude of low-frequency fluctuation and the regional homogeneity in order to comprehensively evaluate the intrinsic activity in patients with post-stroke pathological laughing and crying. In the post-stroke pathological laughing and crying group, changes in these measures were observed mainly in components of the default mode network (medial prefrontal cortex/anterior cingulate cortex, middle temporal gyrus, inferior temporal gyrus, superior frontal gyrus, middle frontal gyrus and inferior parietal lobule), sensorimotor network (supplementary motor area, precentral gyrus and paracentral lobule), affective network (medial prefrontal cortex/anterior cingulate cortex, parahippocampal gyrus, middle temporal gyrus and inferior temporal gyrus) and cerebellar lobes (cerebellum posterior lobe). We therefore speculate that when disinhibition of the volitional system is lost, increased activation of the emotional system causes pathological laughing and crying.

Highlights

  • Neurological maladies may cause pathological laughing and crying (PLC), a dramatic syndrome characterized by the abnormal expression of emotions [1,2,3]

  • In the post-stroke pathological laughing and crying (PSPLC) group, bilateral paramedian basal lesions were observed in four patients, while bilateral paramedian basal–tegmental lesions were observed in six patients

  • As far as we know, this study was the first to use resting-state functional magnetic resonance imaging (rs-fMRI) to investigate the potential alterations of brain function in vivo in individuals with PSPLC

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Summary

Introduction

Neurological maladies may cause pathological laughing and crying (PLC), a dramatic syndrome characterized by the abnormal expression of emotions [1,2,3]. The prevalence of PLC in cerebrovascular disease is 11–34%, the existing data are limited [4]. Patients with this disorder will suddenly begin to laugh or cry, often in episodes that are incongruous with the emotions they are feeling [5]. Patients’ quality of life may be markedly reduced by PLC, due to the humiliating nature of certain outbursts (for instance, the patient may laugh during a funeral). People with this disorder often limit their social engagement [5]

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