Clinically Unsuspected Cerebral Infarction Revealed by Computed Tomography Scanning in Late Onset Epilepsy

The computed tomography (CT) scans of 132 patients with late onset epilepsy were compared with the CT scans of an age- and sex-matched control group. Patients with neurologic symptoms in addition to epilepsy, patients with a definite antecedent cause for epilepsy, and patients with tumours on CT scanning were excluded. Fifteen of the patients with epilepsy, as opposed to two of the controls, had infarcts on their CT scans (p = 0.003 Fisher exact test, two-tailed). In nine of these patients only lacunar infarcts were present. No patient had a history of stroke. We concluded that cerebrovascular disease was the major underlying contributory factor to the development of epilepsy in these patients. Twelve of the 15 patients were aged greater than 60 years, representing 21% of the patients in this age group. There was no difference between the epileptic patients and controls in the presence of clinical features of systemic vascular and cardiac disease. CT scan evidence of cerebral atrophy was as common in the control subjects as in the patients with epilepsy.     

Computed tomographic changes of the brain and clinical outcome of patients with seizures and epilepsy after an ischaemic hemispheric stroke.

It is not well established whether seizures and epilepsy after an ischaemic stroke increase the disability of patients. Seventy-two patients with delayed seizures after a hemispheric infarct (37 with a single seizure and 35 with epilepsy) were included in the study. The modified Rankin scale was used to compare disability of the patients at 1 month after stroke and at 2 weeks after single or the last seizure, in case of epilepsy. The size of the X-ray hypoattenuation zone was compared on computed tomographic (CT) scans, performed in the weeks after the stroke and 1 week after single or repeated seizures. Lesion size was determined by superimposing the CT slices on digital cerebral vascular maps, on which the contours of the infarct area were delineated. The extent of the infarcts was expressed as the percentage fraction of the total surface area of the cerebral hemisphere. Groups with a single seizure and with epilepsy were mutually compared. Infarcts predominated in the parieto-temporal cortical regions. In the overall group the median Rankin score worsened significantly after seizures. The average size of the X-ray hypoattenuation zone was also significantly increased on the CT scans after the seizures, compared with those after stroke, without clear evidence of recent infarction. Mutual comparison of patients with a single seizure episode and of those with epilepsy showed only a trend of more severe disability and of increase in lesion size in the post-stroke epilepsy group. Delayed seizures and epilepsy after ischaemic stroke are accompanied by an increase in lesion size on CT and by worsening of the disability of the patients. This study does not allow to determine whether this is due to stroke recurrence or due to additional damage as a result of the seizures themselves.     

Disappearing CT Lesions in Epilepsy

A striking but reversible computed tomographic (CT) lesion corresponding to seizure activity is reported in a series of 46 epileptic patients. None of these patients had evidence of tuberculosis or cysticercosis, and all were treated with antiepileptic drugs only. Maximal radiological changes occurred in the area of maximal epileptic discharge; however, multiple lesions were seen in three cases. The CT lesion reappeared with recurrence of the ictus in four cases during follow-up, and this, too, disappeared after complete arrest of the seizures. The clinical, CT scan, and other investigatory findings suggest that the seizures may occasionally cause a CT-demonstrable focal abnormality, probably cerebral edema, a consequence of abnormal vascular permeability. Awareness of this radiological entity should avoid misdiagnosis of cerebral tumor, infarction or tuberculoma in patients with seizure disorder.     

CT findings in late-onset epilepsy

We reviewed the CT findings of 387 patients with new-onset seizures after the age of 50. Seizures were generalized in 212 patients, focal in 160, and indeterminant in 15. CT scanning revealed cerebral atrophy in 113 cases, ischemic lesions in 75, cerebral neoplasms in 20, and no abnormality in 177 cases. Tumours were found in only three patients with generalized seizures, and all three had focal neurological deficits at the time of CT diagnosis, while 17 neoplasms were discovered in patients with a focal seizure disorder. The majority of patients with late-onset epilepsy have a normal CT scan with cerebral atrophy being the most common abnormality detected. Cerebral vascular disease appears to be the most frequently identified cause of late-onset epilepsy, while cerebral neoplasms are uncommon.     

Diminished regional cerebral blood flow during the intercritical period in temporal lobe epilepsy

Hemisphere and regional cerebral blood flow (CBF) were determined during interictal periods by intravenous Xenon 133 in 43 patients considered to have "temporal" epilepsy and presenting complex partial attacks with altered consciousness and lateralized EEG anomalies predominant in the temporal region. Brain scans were normal in all cases. Three subgroups were differentiated according to EEG and polygraphic examinations during sleep; temporal epilepsy with left or right EEG anomalies, with asynchronous bilateral EEG anomalies, with alternating labile unilateral EEG anomalies. Measurements of CBF were compared with those of normal subjects (n = 13) of comparable age and with those of epileptic patients with cerebral lesions on CT scan (n = 4). In epileptics with left EEG anomalies CBF was diminished by about 25 p. 100 in the left temporal region and from 15 to 22 p. 100 in other regions of the ipsi- and contralateral hemisphere. In epileptics with right EEG anomalies CBF was diminished by 20 p. 100 in the right temporal region but not on the left. CBF in the third group was comparable to that of normal subjects. In epileptics with abnormal CT scans the reduction in CBF could be correlated with EEG and CT scan findings. Studies were also conducted to determine variations in reactivity to CO2 in the areas with reduced flow, during ictal and interictal periods. Results emphasize the value of CBF measurements for investigation of epileptic foci. The importance of areas of reduced blood flow as a parameter of severity and course is discussed, as well as their pathophysiological significance.     

EEG and CT findings in poststroke epilepsy

The present study was undertaken to assess the diagnostic value of CT in patients with poststroke epilepsy, related to EEG in revealing the factors contributing to the development of epileptic fits. The EEG and CT results were evaluated in 50 patients with poststroke epilepsy and compared with those of 50 patients without epilepsy after stroke. Cortical and extensive lesions involving the cortex were more frequent among patients with poststroke epilepsy. Sparing of certain parts of cerebral cortex was observed within vasogenic lesion. This type of change was only found in the poststroke epilepsy group and may be responsible for development of epileptic fits. It seems that CT has a higher diagnostic value than EEG in evaluating the risk of development of poststroke epilepsy.     

Clinical application of neuroimaging in epilepsy

OBJECTIVE: To evaluate the use of neuroimaging in clinical practice and to assess the prevalence of detected structural abnormalities in epilepsy patients in a clinical set up. METHODS: 919 outpatients were identified and the scan results reviewed. A total of 677 patients had chronic active epilepsy (88 had idiopathic generalised epilepsy (IGE), 588 had localisation related epilepsy, one had symptomatic generalised epilepsy), 57 had a single epileptic seizure, 46 were in remission, and 139 had non-epileptic attacks. RESULTS: 391 patients had no scan (53 patients in this group had IGE, 182 had localisation related epilepsy, one had generalised symptomatic epilepsy, 18 had single epileptic attacks, 21 were in remission, 116 had non-epileptic attacks). Altogether 528 patients had a scan, the results were not available in 33, 163 had x ray computed tomography (CT) only, 178 had standard magnetic resonance imaging (MRI) (slice thickness 5 mm), and 154 had high resolution MRI (including a T1 weighted sequence with 1.5 mm thick slices). Some 252 of 495 scans (51%) were abnormal. Abnormalities were hippocampal sclerosis (n=128), atrophy or non-specific white matter lesions (n=35), vascular abnormalities (n=27), tumours (n=25), brain damage (n=24), malformations of cortical development (n=13). Excluding atrophy and non-specific white matter lesions the prevalence of detected abnormalities was 54% in localisation related epilepsy, 18% in single seizure patients, 16% in epilepsy in remission, and 0% in IGE and non-epileptic attacks. CONCLUSIONS: Abnormalities were detected in more than half of all patients with localisation related epilepsy, and in about one in five patients with single seizures or epilepsy in remission. Many patients had no scan or only CT or standard MRI. The true prevalence of structural abnormalities may be have been higher. Scanning did not add any information in patients with IGE or non-epileptic attacks.     

Magnetic resonance imaging in partial complex epilepsy

The yield of magnetic resonance (MR) imaging was investigated in 30 patients with partial complex epilepsy, and the results were compared with those of computed tomography (CT). Magnetic resonance imaging and CT disclosed focal cerebral abnormalities in 13 (43%) and eight (26%) patients, respectively. Two additional focal temporal lesions were identified by double-dose CT scanning, increasing the yield of CT to 33%. Magnetic resonance images were abnormal in all patients with focally abnormal CT scans, and in four patients (50%) they defined the extent of the temporolimbic lesions better than did the CT scans. Two of these patients had gliomas. In addition, MR images were focally abnormal in 85% of the patients in whom scalp electroencephalograms showed focal ictal discharges. These data indicate that MR imaging is more informative than CT in partial complex epilepsy.     

中风后癫痫的临床研究

本文报告３６例中风后癫痫发作的临床和ＣＴ资料。通过回顾性病历复习和随访发现，中风后癫痫的发生率占同期住院中风患者的５．２６％，以蛛网膜下腔出血和脑栓塞发生癫痫比率最高，分别为１５％和１２．５％。癫痫发作与ＣＴ所见病灶分布密切相关，皮质病灶较皮质下病灶更易发生病病。癫痫发作可发生于中风后任何时期，但早期癫痫以出血性中风多见，而迟发性癫痫则更多见于脑梗塞患者。     

Regional cerebral blood flow in partial complex epilepsy with and without the presence of lesions

Regional cerebral blood flow (r CBF) was measured by the I.V. 133 Xenon method and use of 27 detectors in 91 patients with complex partial epilepsy in interictal periods (at least 48 h over a complex partial seizure). Some were also examined less than 48 h before or after seizures. All were studied with ictal and interictal electroencephalography (EEG), polysomnography, computed tomography (CT), some had nuclear magnetic resonance scans (MR). The blood flow values were compared with a group of a 20 normal subjects matching for age. A significant decrease of r CBF ranged from 15% to 25% was found in the temporal region in three groups of epileptic patients: with repeated normal CT scans and lateralized EEG abnormalities (N = 46); with cortical atrophy in CT scan (N = 12); with neurosurgical focal lesions on CT and or MR scans glioma, arteriovenous malformation) (N = 10). r CBF was normal or decreased by less than 15% in the other regions of the brain. Patients with repeated normal CT scans and bilateral EEG abnormalities either asynchronous or alternatively observed in the right side or left side on waking EEG or during NREM sleep and REM sleep, did not show reduction in r CBF. In a previous study, r CBF distribution was also found normal during interictal phase in patients with primary generalized epilepsy.(ABSTRACT TRUNCATED AT 250 WORDS)     

A proteomic analysis of pediatric seizure cases associated with astrocytic inclusions

Cerebral hyaline astrocytic inclusions have been observed in a subset of patients with early onset epilepsy, brain structural anomalies, and developmental delay, which indicates that it may represent a unique clinicopathologic entity. To further characterize this condition we use proteomics to investigate differentially expressed proteins in epileptic brain tissue from three pediatric epileptic patients with cerebral hyaline astrocytic inclusions, ranging in age from 5-13 years, and compare to brain tissue from two normal controls. Catalase and carbonic anhydrase I both exhibited increased expression in epileptic brain tissue compared to controls. These findings were confirmed by Western blot analysis. Furthermore, both proteins were localized to astrocytes and in epileptic brain were located within the cerebral hyaline astrocytic inclusions, suggesting a potential role in the generation of this pathologic feature of early onset epilepsy with cerebral hyaline astrocytic inclusions.     

Progressive neocortical damage in epilepsy

Our objective was to determine the pattern and extent of generalized and focal neocortical atrophy that develops in patients with epilepsy and the factors associated with such changes. As part of a prospective, longitudinal follow-up study of 122 patients with chronic epilepsy, 68 newly diagnosed patients, and 90 controls, serial magnetic resonance imaging scans were obtained 3.5 years apart. Image subtraction was used to identify diffuse and focal neocortical change that was quantified with a regional brain atlas and a fully automated segmentation algorithm. New focal or generalized neocortical volume losses were identified in 54% of patients with chronic epilepsy, 39% of newly diagnosed patients and 24% of controls. Patients with chronic epilepsy were significantly more likely to develop neocortical atrophy than control subjects. The increased risk of cerebral atrophy in epilepsy was not related to a history of documented seizures. Risk factors for neocortical atrophy were age and multiple antiepileptic drug exposure. Focal and generalized neocortical atrophy commonly develops in chronic epilepsy. Neocortical changes seen in a quarter of our control group over 3.5 years were likely to reflect physiological changes. Our results show that ongoing cerebral atrophy may be widespread and remote from the putative epileptic focus, possibly reflecting extensive networks and interconnections between cortical regions.     

The Syndromic Classification of the International League Against Epilepsy: A Hospital-Based Study from South India

Summary: Purpose: To determine the distribution of various epilepsies and epileptic syndromes in the epileptic population treated in a university hospital in a developing country. Methods: Data concerning 2,531 patients with epilepsy seen between January 1989 and June 1994 were analyzed using the international League Against Epilepsy (ILAE) classification. Results: Of 2,531 cases, 48% fell into ILAE categories 1.3, 3.2, or 4.1 (cryptogenic, without unequivocal generalized or focal seizures; or situation-related seizures, respectively). Localization-related epilepsies (LREs) and epileptic syndromes (1.1, 1.2, 1.3) were found in 1,591 (62.9%) patients; of these patients, symptomatic localization-related epilepsies totaled 62.7%, and idiopathic localization-related epilepsies accounted for only 0.7%. Juvenile myoclonic epilepsy was the most common type of idiopathic generalized epilepsy (IGE), comprising 4.9% of the total study population and 7.7% of patients registered in the epilepsy clinic. A combination of childhood and juvenile absence epilepsies were found in only 0.4% of the total study population. Single computed tomography (CT) enhancing lesion (SCTEL) and focal cerebral calcification (FCC) accounted for 22% of the etiologic factors for localization-related epilepsies. Neurologic deficits were found in 9.5% of patients with SCTEL; none were found with FCC. None of the patients with these lesions had any history of antecedent events that suggested CNS involvement. In patients with localization-related epilepsies with unremarkable clinical data, the proportion of CT scans showing SCTELs was 39 (95% confidence interval [CI], 0.35–0.43) and 0.18 (95% CI, 15–0.21) for FCCs. The proportion for both lesions together was 0.57 (95% CI, 0.53–0.61). Seizures did not recur once the lesion resolved in patients with SCTELs. In patients with FCCs, seizure remission was 71.5% (95% CI, 53.7–85.4) at 3 years. Conclusions: This study illustrates the rarity in one patient population of some of the syndromes and categories described in the ILAE classification. Childhood and juvenile absence epilepsies together formed a small proportion. SCTEL and FCC were important etiologic factors for localization related epilepsies. The epilepsy associated with SCTEL was a form of benign epilepsy; epilepsy associated with FCC had remission rates similar to other remote symptomatic epilepsies. Without neuroimaging evidence, these 2 lesions would have been missed and the patients might have been grouped under cryptogenic localization related epilepsy. For this reason, we emphasize the need for neuroimaging in patients with localization related epilepsies with unremarkable clinical findings, before classification into the cryptogenic category. In the absence of neuroimaging, such patients should be classified as “probably cryptogenic.”     

Psychosis in epilepsy patients and other chronic medically ill patients and the role of cerebral pathology in the onset of psychosis: A clinical epidemiological study

BACKGROUND: In a 3-year epidemiological survey (N=2623) prevalence of psychosis in epilepsy patients as compared with other chronic medically ill patients is assessed. AIM: To explore the role of cerebral pathology as compared to the role of chronic burden of disease in the onset of psychosis. METHOD: One thousand seven hundred fifty two patients with chronic medical disorders admitted to an Academic Hospital and 901 patients with epilepsy admitted to a tertiary care epilepsy clinic were assessed by CIDI, MINI and clinical psychiatric interview in a two stage screening survey. Medical files were searched for MRI scans about cerebral pathology. Poisson regression analysis was performed to estimate the relative risk for psychosis in both groups. RESULTS: In total, 52 patients with prevalent psychosis were found: 49 (5.4%) in the epilepsy clinic and 3 (0.17%) in the Academic Hospital. Age range (18-88), mean age (42) and gender distribution (equal) were similar in both samples. RR is 8.37 (2.74, 25.52). In 16 of the 49 epilepsy patients, cerebral pathology existed with mainly temporal and frontal localisation and of childhood-onset vascular or infectious origin. CONCLUSIONS: This finding suggests that in the onset of psychosis in epilepsy patients, the role of cerebral pathology, especially localized left temporal and frontal, is of strong etiological importance. The following epilepsy endophenotypes should be explored as factors in vulnerability for psychosis as well: frequent and severe epileptic activity; and psychotic reactions to certain AEDs, such as Topiramate and Lamotrigine. Burden of disease does not seem to play an important role.     

Computed tomography in patients with transient ischaemic attacks: when is a transient ischaemic attack not a transient ischaemic attack but a stroke?

Summary In a prospective community-based study, 184 patients with transient ischaemic attacks (TIAs) were identified from a study population of about 105,000 between 1981 and 1986. Computed tomography (CT) was attempted in all those with cerebral ischaemic attacks (n=152, 83%); patients with amaurosis fugax only (n=32, 27%) were not scanned routinely. Scans were obtained in 120 (79%) of those with cerebral attacks and 12 (38%) of those with amaurosis fugax. The scans were reported by a neuroradiologist who was blinded to the patients' clinical features. Of 120 (27% :95% confidence interval 19–35) scans in patients with cerebral attacks, 32 showed a focal area of hypodensity or cortical loss, but in only 14 (12% :95% confidence interval 6–18) was this in an area of the brain appropriate to the patients' symptoms. There were no significant differences in the clinical features, the duration of attacks or the prognosis (i.e, risk of death, stroke or myocardial infarction) of patients with and without ischaemic lesions on CT. It is concluded that patients with clinically definite TIAs who have a presumed ischaemic and appropriately sited lesion on CT should not be re-classified as having had a stroke.     

颅内结构性病变继发癫痫62例临床分析

目的 总结颅内结构性病变与继发性癫痫的关系并提出手术方法。方法 对62例颅内结构性病变继发癫痫患者的临床资料进行回顾性分析。结果 本组病历以AVM最多见，其次是颅脑肿瘤；癫痫发作为唯一主诉症状，其临床的发作形式与其性质和部位有关。结论 CT及MRI是诊断颅内结构性病变的重要方法；综合治疗该类病变是可能的有效途径。     

Late onset epileptic seizures A retrospective study of 250 patients

A retrospective study of 250 patients with late-onset epilepsy was carried out. The ages ranged from 22 to 88. The seizures were partial in 104 patients and generalized in 146. The neurological examination was abnormal in 41 patients and normal in 209. The EEG studies and CT scan revealed abnormalities in 76.5% and 50.8% respectively. The most frequent CT scan findings were diffuse atrophy (19.2%), tumors (16.4%) and cerebral infarct (8.8%). The clinical parameters which best predicted the CT scan abnormalities were an abnormal neurological examination and simple partial seizures. In seven of the 45 patients with space-occupying lesions, the clinical examination and EEG were normal. The etiology of the convulsions was established in 201 patients, the most frequent cause being chronic alcoholism (62 cases), tumors (41 cases), postischemic vascular epilepsy (33 cases) and postraumatic epilepsy (28 cases). We conclude that a CT scan is essential in the assessment of patients with epileptic convulsions of late onset, even when the EEG and clinical examination are normal.     

Acute partial transverse myelitis with normal cerebral magnetic resonance imaging: transition rate to clinically definite multiple sclerosis

OBJECTIVE: To determine the long-term risk of developing clinically definite multiple sclerosis (CDMS) in patients with acute partial transverse myelitis (APTM) and normal cerebral magnetic resonance imaging (MRI) scans. METHODS: We retrospectively studied 30 consecutive patients with clinical evidence of APTM. Patients with symmetric severe acute transverse myelitis were considered to have complete transverse myelitis and were excluded. All patients underwent spinal and cerebral MRIs, 13 underwent cerebrospinal fluid analysis and 11 patients underwent evoked potential studies. Various other studies were performed to assess for connective tissue disease and causes of APTM other than demyelinating disease. RESULTS: After an average follow-up of 61 months, all laboratory and clinical evidence, including relapse history, indicated that three patients developed lesions on cerebral MRI and could be classified as CDMS by either Poser criteria (two patients) or MacDonald criteria (one patient). Relapses limited to the spinal cord seen clinically were seen in 14/30 (46.6%) patients. Oligoclonal bands were seen in 8/13 (62%) patients; one patient transitioned to CDMS. Unifocal lesions of the cord were seen in 19/30 (63%) patients, multifocal lesions were seen in 8/30 (27%) and 3/30 (10%) had negative MRIs. The three patients who converted to CDMS did so within five years of the onset of myelitis. CONCLUSION: APTM with normal cerebral MRI had a low rate of conversion to CDMS in this long-term study. To date, there have been only a few follow-up studies that have addressed this issue.     

癫痫起始区和“病灶”之间解剖关系的探讨

目的探讨癫痫起始区（EOZ）和脑内“病灶”间的解剖关系。方法回顾性分析2007年11月-2009年11月手术治疗的358例癫痫患者的临床资料。其中22例经头颅MRI证实脑内有“病灶”,经头皮脑电图和颅内电极脑电图确定了EOZ的患者纳入本研究。测量EOZ和“病灶”间距离,定义其解剖关系为重叠（相距〈5mm）、相邻（〈20mm）、远离（〉20mm）。术后对“病灶”行病理学检查。结果EOZ与脑内“病灶”重叠者4例、相邻者13例、远离者5例。病理学结果示,解剖关系为重叠或相邻者多为血管性病变和颅内肿瘤等患者,远离者多为脑发育不良和脑软化坏死等患者。结论“病灶”的病理性质是影响其和EOZ解剖关系的主要因素,“病灶”所处脑区及癫痫病程的影响不确定（P〈0．01）。     

Transient ischaemic attacks are associated with increased rates of global cerebral atrophy

OBJECTIVES: To determine whether patients presenting with a first transient ischaemic attack (TIA) subsequently show increased rates of brain atrophy compared with age matched controls; and to assess potential risk factors for brain atrophy in this group. METHODS: 60 patients with a first, isolated TIA and 26 age and sex matched controls were recruited. None had evidence of cognitive impairment. Vascular risk factors were treated appropriately. All subjects had volumetric imaging at the start of the study and one year later, when they were clinically reassessed. TIA patients also had serial dual echo brain imaging. Rates of whole brain atrophy were calculated from the registered volumetric scans, as was the incidence of new ischaemic lesions. In the TIA group, the degree of white matter disease was assessed. Atrophy rates and blood pressure were compared between patients and controls. RESULTS: 22 patients (37%) developed new "clinically silent" infarcts during follow up. The mean (SD) annualised percentage atrophy rate in the TIA group was significantly higher than in the controls, at 0.82 (0.39)% v 0.33 (0.3)% (p < 0.0001). In the TIA group, diastolic blood pressure (p = 0.004) and white matter disease severity (p < 0.001) were correlated with cerebral atrophy rate. Increased white matter disease was found in patients in whom new ischaemic lesions developed (p < 0.001). CONCLUSIONS: Patients presenting with a first TIA have excess global brain atrophy compared with age matched controls over the subsequent year. Increased atrophy rates following a TIA may be directly or indirectly related to increasing white matter disease and diastolic hypertension. Future studies should assess whether this atrophy inevitably leads to cognitive decline, and whether aggressive treatment of risk factors for cerebrovascular disease (particularly hypertension) after a TIA can influence outcome.