Department of Clinical and Experimental Epilepsy, Department of Neuropathology, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Department of Neuroscience, University of Westminster, London, UK.
Acta Neuropathol. 2024 Oct 8;148(1):49. doi: 10.1007/s00401-024-02809-8.
White matter microvascular alterations in temporal lobe epilepsy (TLE) may be relevant to acquired neurodegenerative processes and cognitive impairments associated with this condition. We quantified microvascular changes, myelin, axonal, glial and extracellular-matrix labelling in the gyral core and deep temporal lobe white matter regions in surgical resections from 44 TLE patients with or without hippocampal sclerosis. We compared this pathology data with in vivo pre-operative MRI diffusion measurements in co-registered regions and neuropsychological measures of cognitive impairment and decline. In resections, increased arteriolosclerosis was observed in TLE compared to non-epilepsy controls (greater sclerotic index, p < 0.001), independent of age. Microvascular changes included increased vascular densities in some regions but uniformly reduced mean vascular size (quantified with collagen-4, p < 0.05-0.0001), and increased pericyte coverage of small vessels and capillaries particularly in deep white matter (quantified with platelet-derived growth factor receptorβ and smooth muscle actin, p < 0.01) which was more marked the longer the duration of epilepsy (p < 0.05). We noted increased glial numbers (Olig2, Iba1) but reduced myelin (MAG, PLP) in TLE compared to controls, particularly prominent in deep white matter. Gene expression analysis showed a greater reduction of myelination genes in HS than non-HS cases and with age and correlation with diffusion MRI alterations. Glial densities and vascular size were increased with increased MRI diffusivity and vascular density with white matter abnormality quantified using fixel-based analysis. Increased perivascular space was associated with reduced fractional anisotropy as well as age-accelerated cognitive decline prior to surgery (p < 0.05). In summary, likely acquired microangiopathic changes in TLE, including vascular sclerosis, increased pericyte coverage and reduced small vessel size, may indicate a functional alteration in contractility of small vessels and haemodynamics that could impact on tissue perfusion. These morphological features correlate with white matter diffusion MRI alterations and might explain cognitive decline in TLE.
颞叶癫痫 (TLE) 中的白质微血管改变可能与该疾病相关的获得性神经退行性过程和认知障碍有关。我们定量分析了 44 例 TLE 患者手术切除标本的脑回核心和深部颞叶白质区域的微血管变化、髓鞘、轴突、胶质和细胞外基质标记物,这些患者中有的伴有海马硬化,有的不伴有海马硬化。我们将这些病理数据与术前磁共振成像扩散测量结果在注册区域进行了比较,并对认知障碍和认知能力下降的神经心理学测量结果进行了比较。与非癫痫对照组相比,TLE 患者的小动脉玻璃样变程度增加(硬化指数更大,p<0.001),且与年龄无关。微血管改变包括一些区域的血管密度增加,但平均血管大小均匀减小(用胶原蛋白-4 定量,p<0.05-0.0001),并且小血管和毛细血管的周细胞覆盖增加,特别是在深部白质(用血小板衍生生长因子受体β和平滑肌肌动蛋白定量,p<0.01),癫痫持续时间越长,这种情况越明显(p<0.05)。与对照组相比,TLE 患者的神经胶质数量(Olig2、Iba1)增加,但髓鞘减少(MAG、PLP),在深部白质中更为明显。基因表达分析显示,HS 病例的髓鞘形成基因表达减少程度大于非 HS 病例,且与年龄相关,与磁共振扩散成像改变相关。神经胶质密度和血管大小与磁共振扩散张量成像异常的固定分析中白质异常的血管密度和血管密度增加有关。血管周围间隙增加与各向异性分数降低以及术前与年龄相关的认知加速下降有关(p<0.05)。总之,TLE 中可能发生的获得性微血管病变,包括血管硬化、周细胞覆盖增加和小血管直径减小,可能表明小血管收缩和血液动力学的功能改变,从而影响组织灌注。这些形态特征与白质磁共振扩散成像改变相关,可能解释 TLE 中的认知下降。