Post traumatic epilepsy （PTE） is a serious complication of traumatic brain injury and a difficult problem in forensic justice practice. In recent years, many biomarkers have been applied to the diagnosis, treatment and prognosis of injuries and diseases. There have been many studies on the biomarkers of PTE in the field of epilepsy. This paper reviews the progress in research on biomarkers of PTE in recent years in order to provide reference for the forensic identification of PTE.
Biomarkers/analysis* ; Brain Injuries, Traumatic/diagnosis* ; Epilepsy/etiology* ; Epilepsy, Post-Traumatic/etiology* ; Humans

Objective To summarize the general characteristics and identification considerations of appraisal of post-traumatic epilepsy （PTE） in forensic clinical expertise. Methods Descriptive statistics were made on the general situations （age and sex）, injury sites, PTE grading, clinical manifestations and blood drug concentrations of 30 cases of PTE. Chi-square test was performed on the differences of sex composition, age group incidences, injury sites, clinical manifestations and PTE grading. Fisher's exact probability method was used to test the differences in clinical manifestations and PTE grading of each site and the differences in PTE grading of different clinical manifestations. Results PTE occurred more frequently among 21 to 40 year olds, more in males than in females, and more frequently in the temporal lobe and frontal lobe. The clinical manifestations were mostly partial seizures and the PTE grading was mostly mild PTE. There were no statistical significance in the differences in distribution of clinical manifestations and PTE grading of injury sites （P>0.05）. The difference in the PTE grading of different clinical manifestations had no statistical significance （P>0.05）. The blood drug concentration of the three identified people did not reach the effective concentration, which affected the final identification opinion. Conclusion In the identification of PTE, in addition to strictly grasping the necessary factors of identification, such as the history of craniocerebral trauma, and epileptic seizures, it is also suggested that attention should be paid to the detection of blood drug concentration. Overall analysis and comprehensive evaluation should be made.
Adult ; Craniocerebral Trauma ; Epilepsy, Post-Traumatic ; Female ; Humans ; Incidence ; Male ; Retrospective Studies ; Young Adult

Post traumatic epilepsy （PTE） refers to the epileptic seizures after traumatic brain injury. Organic damage can be found by imaging examination, and abnormal electroencephalogram can be detected via electroencephalogram examination which has the similar location of the brain injury. PTE has the characteristics of low incidence, absence of case reports, and easy to exaggerate the state of illness, which add difficulties to the forensic identification. This paper reviews the status of epidemiology, pathogenesis, clinical treatment and forensic identification for PTE.
Brain Injuries, Traumatic/physiopathology* ; Electroencephalography ; Epilepsy ; Epilepsy, Post-Traumatic/pathology* ; Forensic Pathology ; Humans ; Incidence

For ictogenesis, initial step is intrinsic bursts of pacemaker neurons and, through exaggerated circuits or networks, the involved neurons become hyperexcitable state. Hypersynchrony of hyperexcitable neurons can induce paroxysmal depolarization shift for developing seizure. The mechanism underlying the development of post-traumatic epilepsy still remains to be elucidated. By traumatic brain injury, breakdown of blood-brain barrier (BBB) may lead network changes, long-lasting epileptiform activity and eventual neurodegeneration. Recently the concept of inflammation and epileptogenesis is widely accepted. In the surgically resected brain tissue from refractory partial epilepsy patients, there are hallmarks of a chronic inflammatory state and, also, via animal experiments, we can find the role of inflammation in the genesis of seizure and epilepsy. Inflammatory mediators (IL-1b, TGF-beta1 and COX-2) are associated with the epileptogenic brain. They can reduce seizure threshold, induce neurodegeneration, neurogenesis, and synaptic plasticity, and also disregulate BBB permeability. The increase in knowledge about a role of inflammation in epileptogenesis may support the use of specific anti-inflammatory drugs for developing disease-modifying treatments that can interfere epileptogenesis.
Animal Experimentation ; Blood-Brain Barrier ; Brain ; Brain Injuries ; Epilepsies, Partial ; Epilepsy ; Epilepsy, Post-Traumatic ; Humans ; Inflammation ; Neurogenesis ; Neurons ; Permeability ; Plastics ; Seizures ; Transforming Growth Factor beta1

Posttraumatic headache (PTH) is one of several complications of traumatic brain injury (TBI). PTH usually resolving within the first 3 months, although a minority develop chronic headaches. PTH remains among the most controversial headache topics to its propensity for chronicity and often associated additional cognitive, behavioral, and somatic problems. Sufficient psychological or neurobiological markers for PTH do no exist, thus treatment can be very challenging and should always be multidisciplinary to make every reasonable effort in preventing the development of chronic pain. Posttraumatic seizure or epilepsy (PTE) is defined as a recurrent seizure disorder due to traumatic brain injury. PTE can be divided into three groups: immediate, early and late seizures. Immediate and early seizures are provoked seizures, whereas late seizure is unprovoked seizure. The effects of antiepileptic drugs (AED) in patients with TBI must be assessed separately in terms of prevention and control of provoked seizures and prevention of subsequent unprovoked seizures. Routine preventive AEDs are not indicated for patients with TBI and the effects are controversy.
Anticonvulsants ; Brain ; Brain Injuries ; Chronic Pain ; Epilepsy ; Headache ; Headache Disorders ; Humans ; Post-Traumatic Headache ; Seizures

PURPOSE: Post-traumatic seizures (PTS) are well-recognized complications from head injuries and children are particularly more vulnerable to them. The aim of this study was to investigate the clinical characteristics of PTS in children and the findings of several diagnostic tools and to determine the role of prophylactic anticonvulsants. METHODS: We retrospectively reviewed the medical records of patient under 18 years of age who presented with seizures after traumatic brain injuries. Data analyzed included patient's demographics, clinical presentations, radiological and electroencephalographic findings, management and outcomes. RESULTS: Thirty one patients with PTS were included in the study and consisted of 13 males and 18 females. A mean age of the accident was 3.2 years (4 months-6.8 years) and a mean duration of follow-up was 26.0 months (12 months-54 months). Twenty one patients (67.7%) developed seizures within 24 hours after injury. Focal radiological findings were observed in 83.8% and described as subdural or epidural hematoma (25.8%), intraparenchymal hemorrhage (19.3%) and intracerebral parenchymal lesions (51.6%). Electroecephalographic findings included background abnormalities in 32.2% and interictal epileptiform discharges in 45.1%. All patients were treated with anticonvulsants for a certain period of time and a mean duration of treatment was 12.5 weeks (4-40 weeks). Eight patients (25.8%) developed subsequent seizures during follow-up period and 2 patients (6.5%) were diagnosed afterward with post-traumatic epilepsy. CONCLUSION: PTS generally take a benign clinical course, but subsequent seizures including epileptic seizures can occur in minor proportion. In these cases, radiological and electroencephalographic findings are helpful in prediction of clinical course of PTS.
Anticonvulsants ; Brain Injuries ; Child ; Craniocerebral Trauma ; Demography ; Epilepsy ; Epilepsy, Post-Traumatic ; Female ; Follow-Up Studies ; Hematoma ; Hemorrhage ; Humans ; Male ; Medical Records ; Retrospective Studies ; Seizures

OBJECTIVETo observe the quality of life in patients with post-traumatic epilepsy and discuss the influencing factors.

METHODSWe assessed 105 patients with post-traumatic epilepsy and 100 healthy people as control using Quality of Life Scale-31 (QOL-31), Self-rating Depressing Scale (SDS) and Self-rating Anxiety Scale (SAS), and conducted retrospective analysis on the depression, anxiety, site of trauma, control of seizure, EEG and therapeutic compliance.

RESULTSPatients with post-traumatic epilepsy scored much lower than the control group on QOL-31 (P less than 0.01), but higher than the control group on SDS and SAS (P less than 0.01). Multiple regression analysis indicated that major influencing factors on the quality of life were anxiety, therapeutic compliance, depression, poor control of epileptic seizure and site of trauma.

CONCLUSIONSThe quality of life in patients with post-traumatic epilepsy has significantly declined. Doctors should pay attention to psychological and mental problems of patients with epilepsy, such as depression and anxiety, enhancing therapeutic compliance and controlling epileptic seizure, which are the keys to improving prognosis.

Epilepsy, Post-Traumatic ; psychology ; Humans ; Quality of Life ; Regression Analysis ; Retrospective Studies

Development of myoclonus can manifest as a side effect of antiepileptic drugs in subjects with preexisting epilepsy, post-traumatic brain injury, encephalopathy, or focal and multifocal brain lesions. A 69-year-old male showed new onset severe myoclonus and confusion two days after taking 1200 mg gabapentin. The patient had end-stage renal disease secondary to type 2 diabetes and was receiving hemodialysis twice a week. After increasing hemodialysis to three times a week and discontinuing gabapentin, myoclonus spontaneously resolved. Here we report the first case of myoclonus in a Korean subject with diabetic renal failure. We recommend caution in the administration of gabapentin for diabetic subjects with renal disease.
Aged ; Amines ; Anticonvulsants ; Brain ; Brain Injuries ; Cyclohexanecarboxylic Acids ; Diabetic Neuropathies ; Epilepsy, Post-Traumatic ; gamma-Aminobutyric Acid ; Humans ; Kidney Failure, Chronic ; Male ; Myoclonus ; Renal Dialysis ; Renal Insufficiency

OBJECTIVETo assess the preventive effect of sodium valproate on early posttraumatic seizures in traumatic brain injury (TBI) patients.

METHODSThe retrospective study was based on 159 patients with TBI treated at Department of Neurosurgery, Nanjing General Hospital of Nanjing Command enrolled between January 1, 2008 and December 31, 2009. The in-hospital section of the retrospectively collected database includes information on age, sex, initial Glasgow Coma Score (GCS), results of CT scanning, operation, usage of sodium valproate, seizures in the first week after injury and outcome.

RESULTSSeven patients (4.4%) showed early posttraumatic seizures. Although the incidence was zero in patients who received sodium valproate treatment, the difference between the treatment and control groups was not statistically significant. Of the 87 severe TBI patients (GCS 3-8), 6 patients in the control group (6.9%) suffered from early seizures during the first week after TBI and no patient who received preventive therapy suffered from seizures. The difference between the treatment and the control groups was still not statistically significant. Of the 72 mild and moderate TBI patients (GCS 9-15), only 1 patient in the control group suffered from seizures and no patient in the treatment group suffered.

CONCLUSIONSAlthough the results suggest that the study is not sufficiently powerful to detect a clinically important difference in the seizure rates between the treatment and control groups, sodium valproate is effective in decreasing the risk of early posttraumatic seizures in severe TBI patients. Further prospective studies are recommended.

Adolescent ; Adult ; Aged ; Anticonvulsants ; therapeutic use ; Brain Injuries ; complications ; Epilepsy, Post-Traumatic ; prevention & control ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Valproic Acid ; therapeutic use

OBJECTIVE: To investigate the value of ubiquitin(Ub) and ubiquitin-activating enzymel(UbE1) for the appraisement of post traumatic epilepsy (PTE). METHODS: Fifteen specimens from human epileptic temporal cortex originating from PTE were collected as the PTE group. Fifteen specimens from non-PTE were collected as the non-PTE group. Meanwhile, 15 normal cerebral cortex specimens from people dead from acute traffic accident were collected as the control groups. Observe morphology changes of each group with HE, then with immunohistochemistry of Ub and UbE1. RESULTS: Compared to the control group, morphology changes of neuron quantity reduction, neuron denaturation and so on were observed both in the PTE group and the non-PTE group under HE, especially in the PTE group. Ub and UbE1 mainly expressed in the nucleus and cytoplasm of the neurons in epilepsy spot without extracellular expression. The expression of Ub and UbE1 is PTE group > non-PTE group > control group (P < 0.05). CONCLUSIONS The neuron denaturation are one of the main pathology changes of epilepsy, and it is more obvious in the PTE group. Immunohistochemistry of Ub and UbE1 may be more helpful to distinguish PTE and non-PTE than HE staining.
Case-Control Studies ; Cell Count ; Cell Nucleus/metabolism* ; Craniocerebral Trauma/complications* ; Epilepsy/pathology* ; Epilepsy, Post-Traumatic/pathology* ; Forensic Pathology ; Humans ; Immunohistochemistry ; Neurons/pathology* ; Staining and Labeling ; Ubiquitin/metabolism* ; Ubiquitin-Activating Enzymes/metabolism*