Persistent pseudobulbar affect secondary to acute disseminated encephalomyelitis

Abstract

Pseudobulbar affect (PBA) is a common complication of central nervous system diseases such as stroke, multiple sclerosis, and other neurological diseases, but it remains under-recognized and under-treated in the clinic. PBA caused by acute disseminated encephalomyelitis (ADEM) has rarely been reported. Here, we report a 30-year-old Chinese woman who has experienced PBA from ADEM for 7 years. The patient's principal manifestations were extreme emotions or tears when she saw, heard, or spoke about sad news or other sad things; the durations of these unmanageable emotions were often less than 30 sec, and they occurred at frequencies that ranged from one to several times a day. Occasionally, she laughed uncontrollably while people were talking despite a lack of funny or sad stimuli in the conversation or the surrounding environment. Thus, her social functioning was impaired. This case indicates that the long-term PBA can occur secondarily to ADEM, and this possibility should be considered clinically to ensure timely identification and treatment.

Keywords: affective lability; central nervous system disease; complication; emotion; involuntary emotional expression disorder; pathological laughter and crying.

Fig. 1

A brain MRI on the 10th day after disease onset: various sized patches of slightly long T1 and slightly long T2 signal intensities scattered across the bilateral parietal gray–white matter junction zones, the subcortical white matter, and the semi-oval center and left cerebellum. Some of these lesions had clear boundaries, and others indicated brain swelling; most of the lesions exhibited small patchy enhancements following the intravenous injection of Gd-DPTA.

Fig. 2

In the 5th week after disease onset, repeated brain MRIs: the original lesion had become more clear, the brain swelling had disappeared, most of the lesions exhibited no enhancement, and individual lesions with mild small patchy enhancements remained present but with significantly reduced signal intensities.

Fig. 3

Brain MRIs 1 year after the disease: the lesion number was similar to that originally observed, but the signal intensities of the lesions had significantly decreased, the boundaries were clear, and lesions exhibited no enhancement.

Fig. 4

Two repeated brain MRIs revealed no new changes. A, B, C, D, E and F were scanned in September 2010. G, H, I, J, K and L were scanned in December 2013.