Rocca Maria A, Agosta Federica, Colombo Bruno, Mezzapesa Domenico M, Falini Andrea, Comi Giancarlo, Filippi Massimo
Neuroimaging Research Unit, Scientific Institute and University Ospedale San Raffaele, Milan, Italy.
Hum Brain Mapp. 2007 May;28(5):373-82. doi: 10.1002/hbm.20279.
If fatigue in multiple sclerosis (MS) is related to an abnormal activation of the sensorimotor brain network, the activity of such a network should vary with varying fatigue. We studied 22 patients treated with interferon beta 1a (IFNbeta-1a; Avonex, Biogen, Cambridge, MA) with no fatigue (10) and with reversible fatigue (12). fMRI examinations were performed: 1) the same day of IFNbeta-1a injection (no fatigue; entry), 2) the day after IFNbeta-1a injection (fatigue; time 1), and 3) 4 days after IFNbeta-1a injection (no fatigue; time 2). Patients performed a simple motor task with the right, clinically unaffected hand. At time 1, compared with entry and time 2, MS patients with reversible fatigue showed an increased activation of the thalamus bilaterally. In MS patients without fatigue thalamus was more activated at entry than at time 1. In both groups at entry the primary SMC and the SMA were more activated than at times 1 and 2. At entry and time 1, when compared to patients with reversible fatigue, those without showed increased activations of the SII. Conversely, patients with reversible fatigue had increased activations of the thalamus and of several regions of the frontal lobes. An abnormal recruitment of the fronto-thalamic circuitry is associated with IFNbeta-1a-induced fatigue in MS patients.
如果多发性硬化症（MS）中的疲劳与感觉运动脑网络的异常激活有关，那么这样一个网络的活动应该会随着疲劳程度的变化而变化。我们研究了22例接受干扰素β-1a（IFNβ-1a；安万特，百健公司，马萨诸塞州剑桥）治疗的患者，其中无疲劳的患者10例，有可逆性疲劳的患者12例。进行了功能磁共振成像（fMRI）检查：1）在IFNβ-1a注射当天（无疲劳；入组时），2）在IFNβ-1a注射后一天（疲劳；时间1），以及3）在IFNβ-1a注射后4天（无疲劳；时间2）。患者用临床上未受影响的右手执行一项简单的运动任务。在时间1时，与入组时和时间2相比，有可逆性疲劳的MS患者双侧丘脑的激活增加。在无疲劳的MS患者中，丘脑在入组时比在时间1时更活跃。在两组中，入组时初级感觉运动皮层（SMC）和辅助运动区（SMA）比在时间1和时间2时更活跃。在入组时和时间1时，与有可逆性疲劳的患者相比，无疲劳的患者次级躯体感觉皮层（SII）的激活增加。相反，有可逆性疲劳的患者丘脑和额叶几个区域的激活增加。额-丘脑回路的异常募集与IFNβ-1a诱导的MS患者疲劳有关。
