Pathological laughter as prodromal manifestation of transient ischemic attacks--case report and brief review

Abstract

Background: Based on a case report, the authors reviewed the data about involuntary emotional expression disorder (IEED). IEED includes the syndromes of pathological laughing and crying (PLC) and emotional lability (EL). PLC is a rare disorder of emotional expression characterized by relatively uncontrollable episodes of laughter and crying or both that do not have an apparent motivating stimulus.

Case presentation: Authors report the case of a 59-year-old man who presented with recurrent episodes of PLC of approximately 2 min duration, consisting of accelerated breathing, emission of guttural, snoring sounds, frowning of the eyebrows, followed by laughter accompanied by motor restlessness of all four limbs. PLC episodes preceded left carotid transient ischemic attacks (TIA's) manifested by reversible aphasia and right hemiparesis. Electroencephalography performed during PLC episodes revealed no spike-wave activity. Brain magnetic resonance imaging showed lacunar infarcts in the left lenticulo-capsulo-thalamic area and multiple round lesions in the cortical-subcortical and in the deep white matter of frontal-parietal-occipital lobes bilaterally, with T2 hyperintensity, T1 isointensity and no diffusion changes. The episodes were interpreted as transient ischemic attacks although gelastic seizures could not be excluded. The etiological investigations revealed unstable plaques on the left carotid artery bulb and the aortic arch and a degenerative mitral valve stenosis. The patient was treated first with antiplatelet therapy and antiepileptic drugs but PLC stopped only after anticoagulation was started. During follow-up the patient continued to have left carotid and vertebrobasilar TIA's being on oral anticoagulation. The patient became asymptomatic only after mitral valve replacement was performed.

Conclusions: This case illustrates the difficulty distinguishing between gelastic epilepsy and TIA's in cases of PLC episodes and discuss the neuroanatomic bases and pathophysiology of this rare condition.

Fig. 1

EEG performed during PLC episodes showed no spike wave activity only slow waves on the derivations on the right side

Fig. 2

A, B Polygonal left side area intra- and supranuclear hyperintense T2, hypointense with hyperintense periphery on FLAIR images, which interface pyramidal fibers in the posterior arm of internal capsule leeding to Wallerian degeneration of them - left lateral pontine dots that apare hyperintense on T2 and FLAIR images, without restricted diffusion

Fig. 3

Paraventricular left temporal poligonal area with reduced dimensions between exams - area of ischemia in the subacute stage - hyperintense on T2 and FLAIR, hypointense on T1 without restricted diffusion

Fig. 4

A, B Video EEG during awake state and during sleep without spike-waves anomalies but with some slow waves especially on the right side during sleep