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Abstract：
OBJECTIVE: The intricate neuroanatomical structure of the cerebellum is of longstanding interest in epilepsy, but has been poorly characterized within the current corticocentric models of this disease. We quantified cross-sectional regional cerebellar lobule volumes using structural magnetic resonance imaging in 1602 adults with epilepsy and 1022 healthy controls across 22 sites from the global ENIGMA-Epilepsy working group.
METHODS: A state-of-the-art deep learning-based approach was employed that parcellates the cerebellum into 28 neuroanatomical subregions. Linear mixed models compared total and regional cerebellar volume in (1) all epilepsies, (2) temporal lobe epilepsy with hippocampal sclerosis (TLE-HS), (3) nonlesional temporal lobe epilepsy, (4) genetic generalized epilepsy, and (5) extratemporal focal epilepsy (ETLE). Relationships were examined for cerebellar volume versus age at seizure onset, duration of epilepsy, phenytoin treatment, and cerebral cortical thickness.
RESULTS: Across all epilepsies, reduced total cerebellar volume was observed (d = .42). Maximum volume loss was observed in the corpus medullare (dmax = .49) and posterior lobe gray matter regions, including bilateral lobules VIIB (dmax = .47), crus I/II (dmax = .39), VIIIA (dmax = .45), and VIIIB (dmax = .40). Earlier age at seizure onset ( η ρ max 2 = .05) and longer epilepsy duration ( η ρ max 2 = .06) correlated with reduced volume in these regions. Findings were most pronounced in TLE-HS and ETLE, with distinct neuroanatomical profiles observed in the posterior lobe. Phenytoin treatment was associated with reduced posterior lobe volume. Cerebellum volume correlated with cerebral cortical thinning more strongly in the epilepsy cohort than in controls.
CONCLUSIONS: We provide robust evidence of deep cerebellar and posterior lobe subregional gray matter volume loss in patients with chronic epilepsy. Volume loss was maximal for posterior subregions implicated in nonmotor functions, relative to motor regions of both the anterior and posterior lobe. Associations between cerebral and cerebellar changes, and variability of neuroanatomical profiles across epilepsy syndromes argue for more precise incorporation of cerebellar subregional damage into neurobiological models of epilepsy.
METHODS: A state-of-the-art deep learning-based approach was employed that parcellates the cerebellum into 28 neuroanatomical subregions. Linear mixed models compared total and regional cerebellar volume in (1) all epilepsies, (2) temporal lobe epilepsy with hippocampal sclerosis (TLE-HS), (3) nonlesional temporal lobe epilepsy, (4) genetic generalized epilepsy, and (5) extratemporal focal epilepsy (ETLE). Relationships were examined for cerebellar volume versus age at seizure onset, duration of epilepsy, phenytoin treatment, and cerebral cortical thickness.
RESULTS: Across all epilepsies, reduced total cerebellar volume was observed (d = .42). Maximum volume loss was observed in the corpus medullare (dmax = .49) and posterior lobe gray matter regions, including bilateral lobules VIIB (dmax = .47), crus I/II (dmax = .39), VIIIA (dmax = .45), and VIIIB (dmax = .40). Earlier age at seizure onset ( η ρ max 2 = .05) and longer epilepsy duration ( η ρ max 2 = .06) correlated with reduced volume in these regions. Findings were most pronounced in TLE-HS and ETLE, with distinct neuroanatomical profiles observed in the posterior lobe. Phenytoin treatment was associated with reduced posterior lobe volume. Cerebellum volume correlated with cerebral cortical thinning more strongly in the epilepsy cohort than in controls.
CONCLUSIONS: We provide robust evidence of deep cerebellar and posterior lobe subregional gray matter volume loss in patients with chronic epilepsy. Volume loss was maximal for posterior subregions implicated in nonmotor functions, relative to motor regions of both the anterior and posterior lobe. Associations between cerebral and cerebellar changes, and variability of neuroanatomical profiles across epilepsy syndromes argue for more precise incorporation of cerebellar subregional damage into neurobiological models of epilepsy.
摘要：
目的：小脑复杂的神经解剖结构对癫痫有长期的兴趣，但在目前的皮质中心模型中，这种疾病的特征很少。我们使用结构磁共振成像对全球ENIGMA-癫痫工作组22个地点的1602名成人癫痫患者和1022名健康对照者的横截面区域小脑小叶体积进行了量化。
方法：采用了最先进的基于深度学习的方法，将小脑分成28个神经解剖亚区域。线性混合模型比较了（1）所有癫痫中的总小脑体积和区域小脑体积，(2)颞叶癫痫伴海马硬化(TLE-HS),（3）非病灶性颞叶癫痫，(4)遗传性全身性癫痫,和（5）颞外局灶性癫痫（ETLE）。在癫痫发作时检查小脑体积与年龄的关系，癫痫的持续时间，苯妥英治疗,和大脑皮层厚度.
结果：在所有癫痫患者中，观察到小脑总体积减少（d=0.42）。在髓质体（dmax=0.49）和后叶灰质区域观察到最大体积损失，包括双侧小叶VIIB（dmax=0.47），短肢I/II(dmax=.39)，VIIIA(dmax=.45)，和VIIIB(dmax=.40)。癫痫发作时年龄较早(ηρmax2$$\\eta{\\mathit{\\mathsf{\\rho}}_{\\mathsf{max}}^{\\mathsf{2}}$$$=.05)和持续时间较长(ηρmax2$\\\eta{\\mathit\06\mathsf{\n}与{\结果在TLE-HS和ETLE中最为明显，在后叶观察到不同的神经解剖学轮廓。苯妥英治疗与后叶体积减少有关。与对照组相比，癫痫队列中的小脑体积与大脑皮层变薄的相关性更强。
结论：我们提供了慢性癫痫患者小脑深和后叶次区域灰质体积损失的有力证据。涉及非运动功能的后部亚区域的体积损失最大，相对于前叶和后叶的运动区域。大脑和小脑变化之间的关联，癫痫综合征的神经解剖学特征和变异性表明，小脑次区域损伤更精确地纳入癫痫的神经生物学模型。
方法：采用了最先进的基于深度学习的方法，将小脑分成28个神经解剖亚区域。线性混合模型比较了（1）所有癫痫中的总小脑体积和区域小脑体积，(2)颞叶癫痫伴海马硬化(TLE-HS),（3）非病灶性颞叶癫痫，(4)遗传性全身性癫痫,和（5）颞外局灶性癫痫（ETLE）。在癫痫发作时检查小脑体积与年龄的关系，癫痫的持续时间，苯妥英治疗,和大脑皮层厚度.
结果：在所有癫痫患者中，观察到小脑总体积减少（d=0.42）。在髓质体（dmax=0.49）和后叶灰质区域观察到最大体积损失，包括双侧小叶VIIB（dmax=0.47），短肢I/II(dmax=.39)，VIIIA(dmax=.45)，和VIIIB(dmax=.40)。癫痫发作时年龄较早(ηρmax2$$\\eta{\\mathit{\\mathsf{\\rho}}_{\\mathsf{max}}^{\\mathsf{2}}$$$=.05)和持续时间较长(ηρmax2$\\\eta{\\mathit\06\mathsf{\n}与{\结果在TLE-HS和ETLE中最为明显，在后叶观察到不同的神经解剖学轮廓。苯妥英治疗与后叶体积减少有关。与对照组相比，癫痫队列中的小脑体积与大脑皮层变薄的相关性更强。
结论：我们提供了慢性癫痫患者小脑深和后叶次区域灰质体积损失的有力证据。涉及非运动功能的后部亚区域的体积损失最大，相对于前叶和后叶的运动区域。大脑和小脑变化之间的关联，癫痫综合征的神经解剖学特征和变异性表明，小脑次区域损伤更精确地纳入癫痫的神经生物学模型。
