Altered Brain Structure and Function Correlate with Disease Severity and Affective Disorders in Patients with Hemifacial Spasm
Yuan Wang1, Hui Xu1, Chenguang Guo1, and Ming Zhang1

1Department of Medical Imaging, the first affiliated hospital of Xi'an Jiaotong University, Xi'an, China


Hemifacial spasm (HFS) is characterized by unilateral and paroxysmal contraction of orofacial muscles. A group of HFS patients and healthy controls underwent MRI examination and clinical assessment for facial spasm and affective disorders. HFS patients showed thickened left fusiform in cortex along with reduced subcortical volume in the right amygdala. Increased amygdala-driven connections were revealed to the bilateral superior frontal gyrus (SFG) and orbital gyrus (OG), and increased functional connectivity (FC) was detected of fusiform seed to several subregions of frontal lobe. These altered FC changes were associated with certain clinical indices, providing new insight into pathophysiology of the disease.


Hemifacial spasm (HFS) is defined as one of the neuromuscular movement disorders characterized by unilateral, involuntary, and paroxysmal orofacial contractions innervated by the ipsilateral facial nerve. Only one study had assessed the structural and functional alterations of the brain in HFS patients using voxel based morphometry (VBM) and regional homogeneity (ReHo) method until now. Compared to VBM approach, surface-based analysis (SBA) can detect the abnormalities in cortical thickness and areas with subvoxel precision, and resting-state functional connectivity (FC) is used to probe temporal correlations in spontaneous fluctuations across functionally related and structurally distinct brain regions. Therefore, the objectives of this study are as follows: (1) to identify cortical thickness changes in HFS patients and (2) to explore the abnormal functional connectivity derived from these structural alterations compared to healthy controls. Then we aim to investigate the relationship of the structural and functional MRI indices to the clinical variables in HFS group, which may be beneficial to better understand the pathophysiology of this disease.


Thirty HFS patients and 30 age and gender matched healthy volunteers were recruited in this study with three dimensional T1 and functional magnetic resonance imaging (fMRI) acquired on a 3.0T GE scanner. SBA and FC analysis were applied to investigate the differences of structural and resting-state fMRI properties in the whole brain between two groups. After that, correlation analysis was employed between neuroimaging data and severity of facial spasm and neuropsychological disorders in HFS patients, including degrees of facial spasm and scores of Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA).


In comparison to healthy participants, HFS patients showed significant increased cortical thickness in the left fusiform, right supramarginal gyrus, and right parsobitalis region, along with decreased subcortical volume in the right amygdala. Increased amygdala-driven connections were detected to the bilateral superior frontal gyrus (SFG), bilateral orbital gyrus (OG), and left posterior insula (L-PI), together with increased functional connectivity of left fusiform seed to several subregions of the frontal lobe, including the bilateral medial frontal gyrus (MFG), right superior frontal gyrus (SFG) and right anterior cingulate cortex (ACC). Moreover, a few of FC changes mentioned above were associated with the spasm degree and HAMA score in HFS.


Our results firstly demonstrated cortical thickening in the left fusiform in HFS patients than that of the controls. It is established that fusiform plays a key role in face perception. The most consistent and prominent face-selective fMRI activation was located on the lateral part of the fusiform gyrus which was called as the “fusiform face area” or FFA. Given that the enrolled HFS patients underwent chronic and severe facial spasm, most of them were difficult to concentrate on other’s face during social contact. One possible mechanism for adaption to this situation is the compensatory neural reorganization of FFA for the visual fixation difficulty, which may be helpful for patients to identify people in a short period of time.

Moreover, the left fusiform may have altered functional connectivity to medial prefrontal cortex (mPFC) in HFS patients. Based on the current findings that linked the altered fusiform-mPFC functional connectivity to the degree of orofacial spasm and anxiety, we suspect the connection abnormality of the two regions in HFS was partly caused by mimetic muscular contractions and spasm related affective disorders.

Last but not the least, the right amygdala cluster with decreased GMV in patients demonstrated significantly increased connectivity to several subregions of the frontal lobe, such as dorsal lateral prefrontal cortex (DLPFC), dorsal medial prefrontal cortex (DMPFC), and OFC. Besides, the morphological and functional alterations of amygdala may be linked to the spasm triggered visual attentional deficit in patients with HFS, which was supported by bidirectional communication between amygdala and fusiform gyrus during facial information processing. Finally, the correlation analysis showed positive associations of amygdala-frontal connectivity to the degree of facial spasm and anxiety respectively, which may provide an alternative imaging marker for predicting the characteristics of HFS condition.


In conclusion, the present study revealed thickened fusiform cortex and dysfunctional fusiform-mPFC connection in HFS patients. Meanwhile, atrophic right amygdala was detected in patients together with increased functional connectivity of this seed to bilateral DLPFC. Moreover, the altered fusiform-mPFC and amygdala-DLPFC networks were associated with severity of facial spasm and anxiety state, which provide distinct aspect of clues for the evaluation of HFS related disorders.


We thank Dr. Faxiu Bao for their assistance with recruiting patients, as well as Dr. Massieh Moayedi for his advice on functional connectivity analysis. The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


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Cortical thickness comparison in patients with HFS to healthy controls. Differences in cortical thickness between groups were projected onto an average brain template in vertex-wise analysis. Areas with blue color represented increased cortical thickness in patients with HFS (p < 0.001, uncorrected), including the left fusiform, right supramarginal gyrus and right parsobitalis region.

Subcortical volumes in HFS patients compared with healthy controls. Patients merely showed significantly reduced subcortical volume in the right amygdala compared to control group (p < 0.001, uncorrected). L = Left, R = Right.

Increased seed-based functional connectivity following patients with HFS in contrast to healthy controls (p < 0.001, uncorrected). (A) right amygdala-anchored functional connectivity; (B) left fusiform-based functional connectivity. PI = posterior insula; SFG = superior frontal gyrus; MFG = medial frontal gyrus; OG = orbital gyrus; ACC = anterior cingulate cortex; L = Left; R = Right.

The right amygdala-based (A) and left fusiform-based (B) functional connectivity were positively correlated with clinical parameters in patients with HFS, respectively.

Proc. Intl. Soc. Mag. Reson. Med. 27 (2019)