Department of Neurology, Royal Prince Alfred Hospital, Missenden Road, Camperdown 2050, Australia; The University of Sydney, Faculty of Medicine and Health, Camperdown 2050, Australia.
Department of Neurology, Royal Prince Alfred Hospital, Missenden Road, Camperdown 2050, Australia; The University of Sydney, Brain and Mind Centre, 94 Mallett Street, Camperdown 2050, Australia.
Epilepsy Behav. 2023 Sep;146:109371. doi: 10.1016/j.yebeh.2023.109371. Epub 2023 Aug 7.
We aimed to (i) compare the clinical, neuropsychological, and neuroimaging characteristics of unprovoked late-onset epilepsy (LOE) patients with cognitive symptoms against probable Alzheimer's disease (AD) patients; (ii) clarify how neurodegeneration and other processes could be implicated in the cognitive symptoms of unprovoked LOE patients; and (iii) characterize the longitudinal trajectory of unprovoked LOE patients with cognitive symptoms.
Twenty-six unprovoked LOE patients with cognitive symptoms and 26 probable AD were retrospectively recruited from epilepsy and memory clinics at a single tertiary referral center. The patients underwent comprehensive clinical, neuropsychological, and Fluorodeoxyglucose PET-CT assessments. All LOE patients had clinical follow-up and a subset of 17 patients had repeat neuropsychological assessments.
At baseline, 18% of LOE patients with cognitive symptoms had dementia-range cognitive impairment and one received a diagnosis of probable AD. Compared with the probable AD group, the LOE group did not perform significantly better in global measures of cognition (total ACE-III), neuropsychological tests for fluency, working memory, language, attention, or executive function, but performed better in naming, memory, and visuospatial ability. The commonest patterns of cognitive impairment in the LOE group were frontal and left temporal, whereas all AD patients exhibited parietotemporal patterns. The AD group had more Fluorodeoxyglucose PET-CT hypometabolism in the parietal and occipital, but not the temporal and frontal lobes. During the 3.0 ± 3.2 years follow-up, improved seizure frequency in the LOE group covaried with improved total ACE-III score, there was no further conversion to probable AD and no group-level cognitive decline.
Unprovoked LOE patients with cognitive symptoms had varying severities of cognitive impairment, and different patterns of cognitive and imaging abnormalities compared with AD patients. They were rarely diagnosed with probable AD at presentation or follow-up. Cognitive outcome in LOE may be related to seizure control. Cerebral small vessel disease may play a role in LOE-associated cognitive impairment.
（i）比较无诱因迟发性癫痫（LOE）伴认知症状患者与可能的阿尔茨海默病（AD）患者的临床、神经心理学和神经影像学特征；（ii）阐明神经退行性变和其他过程如何与无诱因 LOE 患者的认知症状相关；（iii）描述伴认知症状的无诱因 LOE 患者的纵向轨迹。
从一家三级转诊中心的癫痫和记忆诊所回顾性招募了 26 名无诱因 LOE 伴认知症状患者和 26 名可能的 AD 患者。患者接受了全面的临床、神经心理学和氟脱氧葡萄糖 PET-CT 评估。所有 LOE 患者均进行了临床随访，其中 17 名患者进行了重复神经心理学评估。
在基线时，18%的 LOE 伴认知症状患者有痴呆范围的认知障碍，1 名患者被诊断为可能的 AD。与可能的 AD 组相比，LOE 组在总 ACE-III 等整体认知测量、流畅性、工作记忆、语言、注意力或执行功能的神经心理学测试中表现并不显著更好，但在命名、记忆和视觉空间能力方面表现更好。LOE 组最常见的认知障碍模式为额颞叶，而所有 AD 患者表现为顶颞叶模式。AD 组在顶叶和枕叶，而非颞叶和额叶的 Fluorodeoxyglucose PET-CT 代谢率较低。在 3.0±3.2 年的随访期间，LOE 组的癫痫发作频率改善与总 ACE-III 评分改善相关，没有进一步转化为可能的 AD，也没有出现组内认知下降。
无诱因 LOE 伴认知症状患者的认知障碍严重程度不同，与 AD 患者的认知和影像学异常模式不同。他们在就诊或随访时很少被诊断为可能的 AD。LOE 的认知结局可能与癫痫控制有关。脑小血管病可能在 LOE 相关认知障碍中起作用。
