Caspase家族与颞叶癫痫神经元凋亡

颞叶癫痫(temporal lobe epilepsy,TLE)是指与颞叶皮层或颞叶内侧海马等结构发生相关病理改变导致的癫痫,临床主要表现为复杂部分性发作,以海马硬化为典型病理特征.以往研究认为神经元坏死是海马硬化的主要原因,但是近年的研究表明海马硬化可能与神经元的凋亡有关.     

颞叶癫痫患者的心血管功能变化及相关因素分析

目的 分析30例颞叶癫痫患者的临床表现及心血管功能变化,同时测定患者血浆NE、DA、5-HT水平,证实颞叶癫痫患者存在心血管活动变化并探讨其发生机制.方法 详细分析30例颞叶癫痫患者的临床表现、心电图改变及心肌酶学含量变化,同时采用荧光分光光度法检测血浆NE、DA、5-HT含量变化并与非颞叶癫痫患者及正常对照组进行统计学分析.结果 (1)颞叶癫痫患者的临床表现复杂,发作形式多变;30例颞叶癫痫患者18例心电图有改变(60%),CK、LDH颞叶癫痫患者较非颞叶癫痫患者高(P<0.05);非颞叶癫痫患者心肌酶与正常对照组比较无统计学差异(P>0.05).(2)颞叶癫痫患者发作间期血浆NE、5-羟色胺高于非颞叶癫痫组及正常对照组(P<0.05);颞叶癫痫患者血浆DA低于非颞叶癫痫组及正常对照组(P<0.05).结论 颞叶癫痫患者发作形式多样,临床表现复杂,存在心血管功能变化,并与神经递质相关.

Abstract：

Objective To analyze clinical manifestation, the change of cardiovascular function of 30 temporal epilepsy patients, and to determinate the level of norepinephrine, dopamine and 5-HT to verify that temporal epilepsy patients have cardiovascular function change, and to explore the mechanism. Methods To analyze clinical manifestation, electrocardiogram and cardiac creatase of 30 temporal epilepsy patients in detail. Fluorospectrophotometry was used to detect the change of plasma norepinephrine,dopamine and 5-HT. Then a statistical analysis was performed. Results (1) Temporal epilepsy patients'clinical manifestation was complex, seizure pattern was diversified. 18 out of 30 60% temporal epilepsy patients had electrocardiographic change;creatinkinase, lactic dehydrogenase in temporal epilepsy patients are higher than non- temporal epilepsy patient, have statistical difference;but cardiac creatase between non-temporal epilepsy patient and normal control group has no difference;(2) Plasma norepinephrine and 5-HT in temporal epilepsy patients when no seizure were higher than non - temporal epilepsy patient which showed normal control group, had showed statistical difference;dopamine in temporal epilepsy patients were lower than non-temporal epilepsy patient and normal control group, had showed statistical difference. Conclusions Temporal epilepsy patients'have compler clinical manifestation, seizure pattern,and can co-exist with cardiovascular simultaneously function change. Which may bu related to neurotransmitter.     

单侧颞叶癫痫患者双侧大脑半球间的功能协同性研究

目的研究单侧颞叶癫痫患者双侧大脑半球间同伦功能连接的变化。方法纳入左侧颞叶癫痫(left temporal lobe epilepsy,LTLE)21例、右侧颞叶癫痫患者(right temporal lobe epilepsy,RTLE)22例以及正常对照(normal control,NC)20例。采用体素-镜像同伦功能连接(voxel-mirrored homotopic connectivity,VMHC)方法分析数据,计算出各组VMHC改变的脑区。结果与NC组相比较,LTLE组双侧辅助运动区(t=-3.35)、颞中回(t=-3.50)、内侧额上回(t=-3.20)、顶下小叶(t=-3.66)VMHC值降低;双侧角回(t=3.03)、枕下回(t=4.25)、顶上回(t=3.62)VMHC值升高(P0.05,alphasim校正)。与NC组相比较,RTLE组双侧颞中回(t=-4.26)、中央前回(t=-3.29)VMHC值减低;双侧枕下回(t=3.22)、海马旁脑回(t=3.32)和小脑(t=3.50)VMHC值升高(P0.05,alphasim校正)。结论单侧颞叶癫痫患者两侧半球间部分脑区的功能协同性发生了变化。     

人参皂甙Rd对颞叶癫大鼠学习记忆能力及海马5-HT表达的影响

目的研究人参皂甙Rd对氯化锂-匹罗卡品点燃颞叶癫(temporal lobe epilepsy,TLE)大鼠学习记忆能力及海马5-HT表达的干预作用。方法建立氯化锂-匹罗卡品点燃颞叶癫大鼠模型,将30只造模成功的颞叶癫大鼠随机分为TLE组(生理盐水10ml/kg腹腔注射,15只)及GSRd干预组(人参皂甙Rd2mg/kg腹腔注射,15只),另选15只大鼠作为正常对照组;采用Morris水迷宫及免疫组化染色分别检测各组大鼠学习记忆能力及海马5-HT表达水平。结果与正常对照组比较,TLE组大鼠学习记忆能力下降,海马5-HT表达明显减少(P0.05);与TLE组比较,GSRd干预组可显著提高大鼠学习记忆能力及海马5-HT的表达水平(P0.05)。结论人参皂甙Rd可能通过增加海马5-HT的表达来提高颞叶癫大鼠学习记忆能力。     

颞叶癫痫手术方式选择及侧裂静脉的保护

颞叶癫痫（temporal lobe epilepsy,TLE）是成人和青少年最常见的难治性癫痫。国内外诸多研究显示,手术治疗TLE的疗效明显优于药物治疗。本文回顾性分析成都363医院2009年6月至2011年6月,采用单侧颞叶切除术治疗的35例颞叶癫痫患者。     

颞叶癫痫认知下降特点及其相关因素分析

目的:比较颞叶癫痫海马硬化者和非海马硬化者之间认知的差别,并分析颞叶癫痫患者认知下降的相关性因素。方法:收集110例颞叶癫痫患者临床资料,包括发病年龄、病程、发作情况;用修订韦氏记忆和韦氏智力量表来评价患者的记忆和智力水平;总结手术后患者的病理资料以确定患者是否伴有海马硬化。结果:伴有海马硬化颞叶癫痫患者的长期记忆和总记忆商分别为37．4±10．0,81．8±19．1;非海马硬化颞叶癫痫患者的长期记忆和总记忆商分别为42．0±8．2,88．3±13．4,伴有海马硬化颞叶癫痫患者的长期记忆和总记忆商显著低于非海马硬化颞叶癫痫患者的长期记忆和总记忆商(P值分别为0．01和0．049)。左侧起源与右侧起源的颞叶癫痫患者的语言智商分别为88．9±9．8和95．0±11．4,二者相比有显著性差异(P=0．013<0．05)。颞叶癫痫患者的总记忆商与癫痫病程呈负相关(r=-0．256,P=0．007<0．01),操作智商与癫痫发作频率呈负相关(r=-0．206,P=0．031<0．05),总智商与教育程度呈正相关(r=0．189,P=0．048<0．05)。结论:海马硬化的颞叶癫痫患者比非海马硬化的颞叶癫痫患者具有更差的长期记忆和总记忆商,左侧起源的颞叶癫痫患者比右侧起源的颞叶癫痫患者语言智商损伤更明显。颞叶癫痫患者病程越长其记忆商越差;癫痫发作越频繁其操作智商越差;教育对保护颞叶癫痫患者的智能有一定的作用。     

双侧颞叶癫痫的外科治疗策略

单侧颞叶癫痫(Unilateral temporal lobe epilepsy,UTLE)是最适合外科手术的对象之一,手术疗效已得到肯定。但是仍有部分颞叶癫痫患者术后发作控制不理想,可能与致痫灶为双侧颞叶起源或颞叶附加癫痫综合征等因素相关。其中双侧颞叶癫痫(Bilateral temporal lobe epilepsy,BTLE)是临床治疗的难题,常常药物疗效差,而又不被建议外科治疗。然而,目前BTLE的诊断标准、发病率、以及外科治疗策略等方面仍不明确。文章对BTLE的临床概念、发生率、形成机制、临床特点、诊断依据、神经心理学检查及外科手术策略进行分析、探讨。结果显示,基于头皮发作间期、发作期脑电图(EEG)判定BTLE并不可靠,经过颅内电极发作期EEG记录后,部分患者可以诊断为UTLE,接受手术切除后,效果满意;部分患者的颅内EEG记录显示癫痫发作具有明显的偏侧倾向,也可以考虑切除性手术。高频(EEG)监测、神经影像学检查及神经心理学检查对BTLE的诊断和治疗策略也有重要意义。     

不同术式选择对颞叶癫痫患者术后记忆功能影响的初步探讨

目的探讨不同术式选择对颞叶癫痫患者术后记忆功能的影响。方法 2009~2013年共248例海马硬化性颞叶癫痫患者在我院接受手术治疗,其中83例行标准前颞叶切除术(anterior temporal lobectomy,ATL),165例行选择性海马杏仁核切除术(selective amygdalohippocampectomy,SAH)。患者在术前、术后3个月及术后两年分别接受临床记忆功能评估。结果 ATL组和SAH组优势半球侧手术的患者临床记忆商数(memory quotient,MQ)在术后3个月(74.5±16.2,75.6±19.5)均有明显下降(P0.05),术后两年(75.1±14.1,76.1±17.6)略有恢复但仍然显著低于术前(82.9±15.8,83.2±21.2)(P0.05),其中SAH组术后3个月及术后两年相较术前MQ的减低程度都小于ATL组(7.6 vs.8.4;7.1 vs.7.8);ATL组和SAH组非优势半球侧手术的患者术后3个月的MQ(87.2±15.1,88.1±16.9)均高于术前(85.5±13.5,85.3±19.7),但无统计学意义,至术后两年时,两组患者的MQ(92.8±12.7,93.7±17.1)对比术前都有了显著的改善(P0.05),其中SAH组患者的改善幅度较ATL组略大(8.4 vs.7.3)。结论相比于ATL,SAH可能更有利于保护海马硬化性颞叶癫痫患者的术后记忆功能。     

神经干细胞与颞叶癫

流行病学调查资料显示，癫痫在我国的患病率约为十万分之7。以此推算，我国癫痫的患病人数约为900万，其中约75％～80％的病人可以用药物控制。即使如此，仍然有约20％-25％的患者无法用药物控制发作而成为难治性癫痫。颞叶癫痫（temporal lobe epilepsy，TLE）是难治性癫痫中最常见的一种类型，是指那些起源于颞叶的有简单部分性发作、复杂部分性发作或继发全身性发作特征的一类癫痫，约占难治性癫痫总数的60％左右。研究显示，颞叶癫痫患者中约65％-70％存在一侧海马硬化，即海马神经元脱失和胶质增生。尽管对海马和杏仁核行选择性切除可使一部分病人得以痊愈，但手术本身有一定的危险性，可引起偏瘫、偏盲、记忆损害等，且对双侧海马硬化的患者不宜作双侧切除。     

T2 hyperintense signal in patients with temporal lobe epilepsy with MRI signs of hippocampal sclerosis and in patients with temporal lobe epilepsy with normal MRI

BackgroundIncreased MRI T2 signal is commonly present not only in the hippocampus but also in other temporal structures of patients with temporal lobe epilepsy (TLE), and it is associated with histological abnormalities related to the epileptogenic lesion.ObjectiveThis study aimed to verify the distribution of T2 increased signal in temporal lobe structures and its correlations with clinical characteristics of TLE patients with (TLE-HS) or without (TLE-NL) MRI signs of hippocampal sclerosis.MethodsWe selected 203 consecutive patients: 124 with TLE-HS and 79 with TLE-NL. Healthy controls (N = 59) were used as a comparison group/comparative group. T2 multiecho images obtained via a 3-T MRI were evaluated with in-house software. T2 signal decays were computed from five original echoes in regions of interest in the hippocampus, amygdala, and white matter of the anterior temporal lobe. Values higher than 2 standard deviations from the mean of controls were considered as abnormal.ResultsT2 signal increase was observed in the hippocampus in 78% of patients with TLE-HS and in 17% of patients with TLE-NL; in the amygdala in 13% of patients with TLE-HS and in 14% of patients with TLE-NL; and in the temporal lobe white matter in 22% of patients with TLE-HS and in 8% of patients with TLE-NL. Group analysis demonstrated a significant difference in the distribution of the T2 relaxation times of the hippocampus (ANOVA, p < 0.0001), amygdala (p = 0.003), and temporal lobe white matter (p < 0.0001) ipsilateral to the epileptogenic zone for patients with TLE-HS compared with controls but only for the amygdala (p = 0.029) and temporal lobe white matter (ANOVA, p = 0.025) for patients with TLE-NL compared with controls. The average signal from the hippocampus ipsilateral to the epileptogenic zone was significantly higher in patients with no family history of epilepsy (two-sample T-test, p = 0.005).ConclusionIncreased T2 signal occurs in different temporal structures of patients with TLE-HS and in patients with TLE-NL. The hippocampal hyperintense signal is more pronounced in patients without family history of epilepsy and is influenced by earlier seizure onset. These changes in T2 signal may be associated with structural abnormalities related to the epileptogenic zone or to the nature of the initial precipitating injury in patients with TLE.     

Hippocampal and amygdaloid damage in partial epilepsy: a cross-sectional MRI study of 241 patients

Patients with drug-refractory temporal lobe epilepsy (TLE) often have hippocampal and amygdaloid damage. The present study investigated the factors associated with the occurrence and severity of damage in patients with partial epilepsy. Magnetic resonance imaging was used to measure the volumes of the hippocampus and the amygdala in 241 patients with different durations of epilepsy. We also investigated the association of damage with the location of seizure focus and clinical factors (age at onset of seizures, lifetime seizure number and medical history of complex febrile convulsions, intracranial infection or status epilepticus) with regression analysis. We found that high lifetime seizure number (P<0.05), history of complex febrile convulsions (P<0.01), and age < or = 5 years at the time of the first seizure (P<0.01) were significant risk factors for reduced hippocampal volume in TLE patients. The severity of amygdaloid damage did not differ between TLE patients with different durations of epilepsy or seizure frequency, but complex febrile convulsions (P<0.05) and intracranial infection (P<0.05) were associated with amygdaloid damage. In patients with extratemporal or unclassified partial epilepsy, the hippocampal and amygdaloid volumes did not differ when patients with different durations of epilepsy were compared with controls. The present findings indicate that a high seizure number, the occurrence of complex febrile convulsions, and an early onset of seizures contribute to hippocampal volume reduction in patients with TLE. The data provided have important implications with regard to early and effective management and seizure control in vulnerable patients.     

Volumetric Changes in Hippocampal Subregions and Memory Performance in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

In the present study we explored the different patterns of volumetric atrophy in hippocampal subregions of patients with left and right mesial temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). Meanwhile, the memory impairment patterns in Chinese-speaking TLE-HS patients and potential influencing factors were also determined. TLE-HS patients (21 left and 17 right) and 21 healthy controls were recruited to complete T2-weighted imaging and verbal/nonverbal memory assessment. The results showed that both left and right TLE-HS patients had overall reduced hippocampal subregion volumes on the sclerotic side, and cornu ammonis sectors (CA1) exhibited maximum atrophy. The verbal memory of left TLE-HS patients was significantly impaired (P < 0.001) and was not associated with the volumes of the left hippocampal subregions. Verbal or nonverbal memory impairment was not found in the patients with right TLE-HS. These results suggested that the atrophy of hippocampal subregion volumes cannot account for the verbal memory impairment, which might be related to the functional network.     

Peri-ictal bed leaving in temporal lobe epilepsy: incidence and lateralizing value

We analyzed peri-ictal bed leaving (PBL) symptoms in 105 patients with temporal lobe epilepsy (TLE). All patients were classified as Engel I at the 2-year follow-up visit. Histopathological examination revealed hippocampal sclerosis (TLE-HS) in 64 patients and other lesions in 38 patients (TLE-other); 3 patients had no lesions. We reviewed 412 seizures. PBL was defined as lateralized leaving of the bed occurring during the seizure or up to 3 minutes after the end of the seizure. PBL was observed in 28 of 105 patients (26.7%), and in 45 of 412 seizures (10.9%). PBL occurred more frequently in patients with TLE-HS than in patients with TLE-other (32.8% vs 17.1%, P=0.058). PBL was ipsilateral to the seizure onset in 71.4% of patients and 71.2% of seizures (P=0.012 and P<0.001). In patients with TLE-HS, PBL was ipsilateral to seizure onset in 76.2% of patients and 81.2% of seizures (P=0.008 and P<0.001). In patients with TLE-other, PBL was ipsilateral to seizure onset in 42.8% of patients and 46.1% of seizures. There were no differences in the incidence and lateralizing value between patients with right-sided and those with left-sided TLE. PBL is a relatively frequent peri-ictal sign in patients with TLE. The side of PBL in patients with TLE-HS lateralizes the seizure onset to the ipsilateral temporal lobe.     

伴海马硬化的颞叶癫痫药物治疗的预后因素分析

目的回顾性研究药物治疗伴海马硬化的颞叶癫痫(TLE-HS)的有效性,分析预测药物治疗效果的相关预后因素,以早期识别药物难治性癫痫,筛查手术候选者。方法 190例颞叶癫痫患者MRI证实伴海马硬化,药物治疗至少随访2年或以实施手术为观察终点。根据观察终点是否发作分为有效组和耐药组。采用χ2检验和t检验对两组在年龄、性别、癫痫家族史、早期突发损伤因素(包括热性惊厥、颅内感染、脑创伤、围生期损伤)、起病年龄、病程、癫痫持续状态、认知功能障碍、精神异常、发作类型、发作频率、是否存在先兆,发作间期脑电图异常放电的单双侧性、MRI海马硬化出现的侧别、药物方案(单药、联合)等方面进行比较。并进一步将有统计学意义的参数,采用二分类Logistic回归分析方法进行药物治疗预后因素的相关分析。结果 190例TLE-HS,有效组54例,耐药组136例,其中手术51例。进行两组的一般人口学资料(年龄、性别、起病年龄、病程)统计学处理,P值分别为0.35,0.29,0.44,0.00。病程差异有统计学意义。两组间在早期促发因素(出生史、热性惊厥史、脑炎史、脑创伤史)方面比较差异有统计学意义(P值分别为0.99,0.17,0.38,0.90)。两组在其他相关病史(癫痫持续状态、家族史、认知障碍、精神障碍)方面比较(P值分别为0.34,0.93,0.72,0.70)差异无统计学意义。在癫痫发作频率和发作先兆方面两组间差异无统计学意义(P=0.01,0.04),而发作类型和间期脑电图痫样放电特点方面两组间差异无统计学意义(P=0.34,0.88)。两组在MRI海马硬化出现在左右侧或双侧的情况比较(P=0.43)差异无统计学意义。有效组39例为单药治疗,15例为联合治疗。耐药组单药治疗者46例,联合治疗者90例。两组间的药物治疗方案差异有统计学意义(P=0.00)。病程和药物治疗方案与药物治疗预后间差异有统计学意义(P=0.01,0.00),但病程与预后之间无关联(OR=1.09),药物治疗方案是药物治疗预后不良的危险因素(OR=4.92)。结论 28.4%的TLE-HS药物治疗2年以上无发作。病程长,发作每月多于4次,存在先兆,多药联合治疗的患者可能更容易耐药。其中多药联合治疗是预测TLE-HS药物治疗效果不佳的独立危险因素。     

Brain diffusion during hyperventilation: diffusion-weighted MR-monitoring in patients with temporal lobe epilepsy and in healthy volunteers

Hyperventilation (HV) can be used to provoke epileptiform activity and occasionally seizures in generalised and in focal epilepsies. Based on the hypothesis that HV might alter brain diffusion in the epileptogenic areas of patients with temporal lobe epilepsy (TLE), we examined these alterations using quantitative diffusion MR imaging (DI) in four patients with TLE and unilateral hippocampal sclerosis (TLE-HS) and six patients with TLE without hippocampal sclerosis (TLE-pure), and in 10 healthy volunteers. Brain diffusion was measured at baseline and immediately after 4 min of HV. In all patients with TLE HV was repeated two times, 4 min each, followed by subsequent DI. The apparent diffusion coefficient (ADC) was quantified in predefined regions of interest. In controls, the ADC did not differ between baseline and HV and between right and left side. Compared to controls TLE-HS patients showed significantly higher ADC at baseline in the hippocampus of the ictogenic side (111+/-13 vs. 87.5+/-4.26 x 10(-5) mm(2)/s, P=0.029). During HV ADC decreased significantly in the ictogenic hippocampus compared to controls (-17.3+/-7.1 vs. -3.34+/-8.7, P=0.004). In TLE-pure patients ADC of the ictogenic hippocampus was higher than in normals (99.3+/-14.2 vs. 87.5+/-4.26 x 10(-5) mm(2)/s, P=0.031) but there was no significant decrease during HV. Serial HV did not further enhance this decrease. No significant HV-induced changes were seen in other brain areas. In conclusion, our results show that HV can induce dynamic changes of brain diffusion in patients with sclerotic hippocampi but not in non-sclerotic hippocampi. These findings may be utilized for lateralisation of the epileptogenic hippocampus during presurgical evaluation of TLE.     

Entorhinal cortex MRI assessment in temporal,extratemporal, and idiopathic generalized epilepsy

PURPOSE: We previously showed a reduction in the volume of the entorhinal cortex (EC) ipsilateral to the seizure focus in patients with intractable temporal lobe epilepsy (TLE). The purpose of this study was to examine the specificity of EC atrophy in epilepsy. METHODS: We performed volumetric measurement of the EC on high-resolution magnetic resonance imaging (MRI) in patients with TLE (n = 70), extratemporal lobe epilepsy (ETE; n = 18), and idiopathic generalized epilepsy (IGE; n = 20). EC volumes of epilepsy patients were compared with those of 48 age- and sex-matched normal controls. Within the TLE group, 63 patients were selected prospectively with hippocampal atrophy ipsilateral to the seizure focus. The remaining seven patients were chosen retrospectively based on normal volumetric MRI of the hippocampus and amygdale, as well as normal histopathologic examination of the resected tissue. RESULTS: Compared with normal controls, EC volume was smaller ipsilateral but not contralateral to the seizure focus in patients with TLE (p < 0.001). No difference in the EC volumes ipsilateral and contralateral to the seizure focus was seen in patients with ETE and IGE compared with normal controls. The individual analysis showed that the EC was atrophic in 73% of TLE patients with hippocampal atrophy. Three of the seven TLE patients with normal volumetric MRI of the hippocampus and amygdala and normal histopathologic examination had EC atrophy ipsilateral to the seizure focus. In no patient with ETE or IGE was the EC found to be atrophic. CONCLUSIONS: EC atrophy ipsilateral to the seizure focus appears to be specific to mesial temporal lobe structural damage associated with TLE.     

Decreased hippocampal volume on MRI is associated with increased extracellular glutamate in epilepsy patients

Purpose: Temporal lobe epilepsy (TLE) is associated with smaller hippocampal volume and with elevated extracellular (EC) glutamate levels. We investigated the relationship between the hippocampal volume and glutamate in refractory TLE patients.
Methods: We used quantitative MRI volumetrics to measure the hippocampal volume and zero-flow microdialysis to measure the interictal glutamate, glutamine, and GABA levels in the epileptogenic hippocampus of 17 patients with medication-resistant epilepsy undergoing intracranial EEG evaluation. The relationships between hippocampal volume, neurochemical levels, and relevant clinical factors were examined.
Results: Increased EC glutamate in the epileptogenic hippocampus was significantly related to smaller ipsilateral (R²= 0.75, p < 0.0001), but not contralateral hippocampal volume when controlled for glutamine and GABA levels, and for clinical factors known to influence hippocampal volume. Glutamate in the atrophic hippocampus was significantly higher (p = 0.008, n = 9), with the threshold for hippocampal atrophy estimated as 5 μM. GABA and glutamine levels in the atrophic and nonatrophic hippocampus were comparable. Decreased hippocampal volume was related to higher seizure frequency (p = 0.008), but not to disease duration or febrile seizure history. None of these clinical factors were related to the neurochemical levels.
Conclusions: We provide evidence for a significant association between increased EC glutamate and decreased ipsilateral epileptogenic hippocampal volume in TLE. Future work will be needed to determine whether the increase in glutamate has a causal relationship with hippocampal atrophy, or whether another, yet unknown factor results in both. This work has implications for the understanding and treatment of epilepsy as well as other neurodegenerative disorders associated with hippocampal atrophy.     

Hippocampal atrophy in temporal lobe epilepsy: the 'generator' and 'receiver'

Bonilha L, Halford JJ, Morgan PS, Edwards JC. Hippocampal atrophy in temporal lobe epilepsy: the ‘generator’ and ‘receiver’.
Acta Neurol Scand: 2012: 125: 105–110.
© 2011 John Wiley & Sons A/S. Objective – Some patients with unilateral medial temporal lobe epilepsy (MTLE) display bilateral hippocampal atrophy on MRI, even though seizures originate in only one hippocampus. The correct identification of the epileptogenic hippocampus (the ‘generator’) vs the non‐epileptogenic (the ‘receiver’) may lead to better surgical planning and results. Materials and Methods – We studied 14 patients with MTLE (eight left and six right) who became seizure free after unilateral hippocampal resection, with hippocampal sclerosis confirmed by histology. Hippocampal tridimensional morphometry was performed comparing patients and healthy controls employing a voxel‐wise Wilcoxon test. Results were corrected for multiple comparisons with the application of a False Discovery Rate (FDR)‐corrected threshold for q < 0.05. Results – Patients with MTLE showed atrophy involving the ipsilateral hippocampus and the contralateral hippocampus, more pronouncedly within the ipsilateral hippocampus in the anterior–inferior aspect of the hippocampal head (left MTLE, left hippocampus x = ?28, y = ?16, z = ?24, Z = 3.6; right MTLE, right hippocampus x = 22, y = ?11, z = ?27, Z = 2.9). On the contralateral hippocampus, the atrophy was more noticeable in the posterior head and body areas. Conclusion – The epileptogenic hippocampal atrophy has an anatomically distinct pattern compared with the contralateral hippocampus. This information may help guide the presurgical assessment of MTLE.     

Everyday memory impairment in patients with temporal lobe epilepsy caused by hippocampal sclerosis

ObjectivePatients with temporal lobe epilepsy caused by hippocampal sclerosis (TLE-HS) have episodic memory impairment. Memory has rarely been evaluated using an ecologic measure, even though performance on these tests is more related to patients' memory complaints. We aimed to measure everyday memory of patients with TLE-HS to age- and gender-matched controls.MethodsWe evaluated 31 patients with TLE-HS and 34 healthy controls, without epilepsy and psychiatric disorders, using the Rivermead Behavioral Memory Test (RBMT), Visual Reproduction (WMS-III) and Logical Memory (WMS-III). We evaluated the impact of clinical variables such as the age of onset, epilepsy duration, AED use, history of status epilepticus, and seizure frequency on everyday memory. Statistical analyses were performed using MANCOVA with years of education as a confounding factor.ResultsPatients showed worse performance than controls on traditional memory tests and in the overall score of RBMT. Patients had more difficulties to recall names, a hidden belonging, to deliver a message, object recognition, to remember a story full of details, a previously presented short route, and in time and space orientation. Clinical epilepsy variables were not associated with RBMT performance. Memory span and working memory were correlated with worse performance on RBMT.SignificancePatients with TLE-HS demonstrated deficits in everyday memory functions. A standard neuropsychological battery, designed to assess episodic memory, would not evaluate these impairments. Impairment in recalling names, routes, stories, messages, and space/time disorientation can adversely impact social adaptation, and we must consider these ecologic measures with greater attention in the neuropsychological evaluation of patients with memory complaints.