液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

液压脑损伤大鼠行为学和脑电图的研究

Objective To investigate the electroencephalogram and ethology in the rat with fluid percussion brain injury and approach its research value in the post traumatic epilepsy. Methods The change of ethology and electroencephalogram of rat in the three months after fluid percussion brain injury were observed and recorded. Results Among the survival 31 rats, there were 11 rats that appeared epilepsy. Epileptic seizure manifestation principally appeared as facial spasm, nod motion, and next limbs convulsion and turnover upspring, et al. The highest epileptic incidence rate appeared in 2 months after lateral fluid percussion brain injury. There were obvious epileptic discharges on the electroencephalogram of epileptic rats and higher wave amplitude and quicker frequency on the lead of 1～5 on the electroencephalogram of some no epileptic rats. Conclusions Post traumatic epilepsy after lateral fluid percussion brain injury in rat is similar with clinical post traumatic epilepsy. It has more research value than the other pest traumatic epileptic animal model.     

Clinical epidemiology of posttraumatic epilepsy in a group of Chinese patients

ObjectiveTo explore the incidence, types of onset, and risk factors of posttraumatic epilepsy (PTE).MethodsThis is a retrospective follow-up study of patients discharged from the Affiliated Hospital of the Medical College of the Chinese People's Armed Police Forces between September 2004 and September 2008 with a diagnosis of traumatic brain injury (TBI).ResultsComplete clinical information was available on 2826 patients. Of the 2826 TBI patients, 141 developed PTE, providing an incidence rate of 5.0%. Twenty-four cases (0.8%) had posttraumatic seizures (PTS), of which 16 (66.7%) continued to experience after the acute phase of their TBI, accounting for 5.0% of the total PTE cases. A total of 125 cases (88.7%) were diagnosed as presenting with late-stage seizures, occurring from 10 days to three years after TBI (93/141 (66.0%) presented within six months after the TBI, 14/141 (9.9%) between six and twelve months, 22/141 (15.7%) between one and two years and only 12/141 (8.5%) between two and three years after the TBI. The severity of PTE was rated mild, medium, and severe in 3.6%, 6.9%, and 17% of the TBI patients. Multiple regression analysis was carried out to identify factors contributing to the risk of developing PTE. Five parameters contributed to the model: Older age, greater severity of brain injury, abnormal neuroimaging, surgical treatment, and early-stage seizures.ConclusionAge, severity of brain injury, neuroimaging results, treatment methods, and early-stage seizures are independent risk factors of PTE.     

Epileptic spasms in paediatric post‐traumatic epilepsy at a tertiary referral centre

Aim. To recognize epileptic spasms (ES) as a seizure type after traumatic brain injury (TBI), accidental or non‐accidental, in infants and children. In the process, we aim to gain some insight into the mechanisms of epileptogenesis in ES. Methods. A retrospective electronic chart review was performed at the Children's Hospital of Michigan from 2002 to 2012. Electronic charts of 321 patients were reviewed for evidence of post‐traumatic epilepsy. Various clinical variables were collected including age at TBI, mechanism of trauma, severity of brain injury, electroencephalography/neuroimaging data, and seizure semiology. Results. Six (12.8%) of the 47 patients diagnosed with post‐traumatic epilepsy (PTE) had ES. Epileptic spasms occurred between two months to two years after TBI. All patients with ES had multiple irritative zones, manifesting as multifocal epileptiform discharges, unilateral or bilateral. Cognitive delay and epileptic encephalopathy were seen in all six patients, five of whom were free of spasms after treatment with vigabatrin or adrenocorticotropic hormone. Conclusion. The risk of PTE is 47/321(14.6%) and the specific risk of ES after TBI is 6/321 (1.8%). The risk of ES appears to be high if the age at which severe TBI occurred was during infancy. Non‐accidental head trauma is a risk factor of epileptic spasms. While posttraumatic epilepsy (not ES) may start 10 years after the head injury, ES starts within two years, according to our small cohort. The pathophysiology of ES is unknown, however, our data support a combination of previously proposed models in which the primary dysfunction is a focal or diffuse cortical abnormality, coupled with its abnormal interaction with the subcortical structures and brainstem at a critical maturation stage.     

外伤性癫痫危险因素的临床分析

目的为外伤性癫痫的早期预防和治疗提供依据。方法回顾性分析356例颅脑损伤病人的临床资料,重点分析外伤性癫痫与颅脑损伤类型,患者年龄、性别以及颅脑损伤严重程度和损伤部位的关系。结果 16岁以下儿童和成人外伤性癫痫发生率分别为16.67%(9/54)和6.62%(20/302),两者相较相差显著(P0.01)。开放性颅脑损伤与闭合性颅脑损伤患者癫痫的发生率分别为29.73%(11/37)和5.64%(18/319),两者相较相差显著(P0.01);脑挫裂伤合并脑内血肿、弥漫性轴索损伤及凹陷性颅骨骨折患者的癫痫发生率分别为16.94%(21/124)、20.51%(8/39)和10.53%(4/38),明显高于CT检查未见颅内明显异常的98例颅脑损伤患者的癫痫发生率1.02%(P0.05)。结论开放性颅脑损伤、脑挫裂伤并脑内血肿、弥漫性轴索损伤、凹陷性颅骨骨折及年龄16岁以下可能是外伤性癫痫的危险因素。     

A population‐based study of risk of epilepsy after hospitalization for traumatic brain injury

Purpose: This study was undertaken to determine the risk of developing posttraumatic epilepsy (PTE) within 3 years after discharge among a population‐based sample of older adolescents and adults hospitalized with traumatic brain injury (TBI) in South Carolina. It also identifies characteristics related to development of PTE within this population. Methods: A stratified random sample of persons aged 15 and older with TBI was selected from the South Carolina nonfederal hospital discharge dataset for four consecutive years. Medical records of recruits were reviewed, and they participated in up to three yearly follow‐up telephone interviews. Results: The cumulative incidence of PTE in the first 3 years after discharge, after adjusting for loss to follow‐up, was 4.4 per 100 persons over 3 years for hospitalized mild TBI, 7.6 for moderate, and 13.6 for severe. Those with severe TBI, posttraumatic seizures prior to discharge, and a history of depression were most at risk for PTE. This higher risk group also included persons with three or more chronic medical conditions at discharge. Discussion: These results raise the possibility that although some of the characteristics related to development of PTE are nonmodifiable, other factors, such as depression, might be altered with intervention. Further research into factors associated with developing PTE could lead to risk‐reducing treatments.     

Predictors and dynamics of posttraumatic epilepsy

Objectives - The goal of our study was to identify clinical, neurophysiological and neuroradiological variables in severe head trauma (SHT) with predictive value for posttraumatic epilepsy (PTE) and to evaluate the influence of each risk factor for the dynamics of epilepsy. Material and methods - We systematically compared 57 PTE patients with 50 age and sex-matched control patients with SHT and no PTE. Mean follow-up was 8 years.
Results - Of all PTE-patients 68.5% had their first seizure within 2 years after the trauma. Significant risk factors for PTE were focal signs in the first examination ( P <0.01), missile injuries ( P <0.01), frontal lesions ( P <0.01), intracerebral hemorrhage ( P <0.01), diffuse contusion ( P <0.01), prolonged posttraumatic amnesia ( P <0.001), depression fracture ( P <0.01) and cortical-subcortical lesions ( P <0.001). The combination of the last 3 variables conferred a particularly high risk for PTE (logistic regression analysis). Combined seizure pattern, high seizure frequency, AED-non-compliance and alcohol abuse predicted poor seizure control.
Conclusion -The risk for PTE is clearly determined by those variables which correlate with the severity, the extent of tissue loss and the penetrating nature of the brain trauma.     

创伤性癫痫的治疗进展

创伤性癫痫(PTE)是指继发于外伤性脑损伤(TBI)的反复出现的自发性癫痫发作。其发病机制复杂,治疗效果不一。本文旨在简要介绍近年来在PTE的动物模型研究,临床治疗方面所取得的进展,以期能够对临床治疗有一定的参考价值。     

Imaging biomarkers of posttraumatic epileptogenesis

Traumatic brain injury (TBI) affects 2.5 million people annually within the United States alone, with over 300 000 severe injuries resulting in emergency room visits and hospital admissions. Severe TBI can result in long‐term disability. Posttraumatic epilepsy (PTE) is one of the most debilitating consequences of TBI, with an estimated incidence that ranges from 2% to 50% based on severity of injury. Conducting studies of PTE poses many challenges, because many subjects with TBI never develop epilepsy, and it can be more than 10 years after TBI before seizures begin. One of the unmet needs in the study of PTE is an accurate biomarker of epileptogenesis, or a panel of biomarkers, which could provide early insights into which TBI patients are most susceptible to PTE, providing an opportunity for prophylactic anticonvulsant therapy and enabling more efficient large‐scale PTE studies. Several recent reviews have provided a comprehensive overview of this subject (Neurobiol Dis, 123, 2019, 3; Neurotherapeutics, 11, 2014, 231). In this review, we describe acute and chronic imaging methods that detect biomarkers for PTE and potential mechanisms of epileptogenesis. We also describe shortcomings in current acquisition methods, analysis, and interpretation that limit ongoing investigations that may be mitigated with advancements in imaging techniques and analysis.     

Epidemiology of Posttraumatic Epilepsy: A Critical Review

Summary:  Problem: Traumatic brain injury (TBI) is a major cause of epilepsy. We need to understand its frequency and its contribution to the total spectrum of the convulsive disorders.
Methods: A review of selected articles dealing with epilepsy after brain trauma was undertaken.
Results: The number of epidemiologic studies of posttraumatic seizures has increased substantially over the past 40–50 years, offering steadily increasing knowledge of the frequency, natural history, and risk factors of this well-recognized complication of TBI. In general, the incidence of posttraumatic seizures varies with the time period after injury and population age range under study, as well as the spectrum of severity of the inciting injuries, and has been reported to be anywhere from 4 to 53%. As high as 86% of patients with one seizure after TBI will have a second in the next 2 years. Longer-term remission rates of 25–40% have been reported. Significant risk factors for the development of seizures in the first week after injury include acute intracerebral hematoma (especially subdural hematoma), younger age, increased injury severity, and chronic alcoholism. Significant risk factors for the development of seizures >1 week after TBI include seizures within the first week, acute intra-cerebral hematoma (especially subdural hematoma), brain contusion, increased injury severity, and age >65 years at the time of injury.
Conclusions: Epilepsy is a frequent consequence of brain injury in both civilian and military populations. We understand some factors associated with its development, but there remain many unanswered questions.     

From traumatic brain injury to posttraumatic epilepsy: What animal models tell us about the process and treatment options

A large number of animal models of traumatic brain injury (TBI) are already available for studies on mechanisms and experimental treatments of TBI. Immediate and early seizures have been described in many of these models with focal or mixed type (both gray and white matter damage) injury. Recent long-term video-electroencephalography (EEG) monitoring studies have demonstrated that TBI produced by lateral fluid-percussion injury in rats results in the development of late seizures, that is, epilepsy. These animals develop hippocampal alterations that are well described in status epilepticus–induced spontaneous seizure models and human posttraumatic epilepsy (PTE). In addition, these rats have damage ipsilaterally in the cortical injury site and thalamus. Although studies in the trauma field provide a large amount of information about the molecular and cellular alterations corresponding to the immediate and early phases of PTE, chronic studies relevant to the epileptogenesis phase are sparse. Moreover, despite the multiple preclinical pharmacologic and cell therapy trials, there is no information available describing whether these therapeutic approaches aimed at improving posttraumatic recovery would also affect the development of lowered seizure threshold and epilepsy. To make progress, there is an obvious need for information exchange between the trauma and epilepsy fields. In addition, the inclusion of epilepsy as an outcome measure in preclinical trials aiming at improving somatomotor and cognitive recovery after TBI would provide valuable information about possible new avenues for antiepileptogenic interventions and disease modification after TBI.     

The risks of epilepsy after traumatic brain injury.

The aim of this study is to present the incidence of traumatic brain injury (TBI) and identify those characteristics of brain injuries that are associated with the development of seizures. We identified 5984 episodes of TBI (loss of consciousness, post-traumatic amnesia, or skull fracture) in Olmsted County, Minnesota, from 1935 to 1984. Of these, 4541 were followed for seizure. Injuries were classified as mild (loss of consciousness or amnesia less than 30 minutes), moderate (loss of consciousness 30 minutes to 1 day or a skull fracture), or severe (loss of consciousness of more than 1 day, subdural hematoma, or brain contusion). The incidence of TBI in the period from 1975 to 84 peaked at 800 per 100 000 in males aged 15-24. The relative risk of seizures was 1.5 (95 percent confidence interval 1.0-2.2) after mild injuries, but with no increase after 5 years; 2.9 (95 percent confidence interval 1.9-4.1) after moderate injuries; and 17.2 (95 percent confidence interval 12.3-23.6) after severe injuries. Significant risk factors were brain contusion with subdural hematoma, skull fracture, loss of consciousness or amnesia of 1 day or more, and age over 65 years. We conclude that TBI is a major public health problem and contributes to the occurrence of seizures and epilepsy.