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1.
Zh Vopr Neirokhir Im N N Burdenko ; 85(5): 110-115, 2021.
Artigo em Russo | MEDLINE | ID: mdl-34714011

RESUMO

Traumatic brain injury (TBI) affects about 50 million people in the world every year. Posttraumatic epilepsy (PTE) is a significant complication of TBI of any severity. PTE occurs in 20% of patients with TBI. Treatment of patients with PTE is particularly difficult due to obvious tendency towards drug resistance. Currently, there are no validated predictive biomarkers for PTE. Development of a system of validated predictive markers would improve PTE prediction quality and therapeutic approach for these patients. This review is devoted to the current data on the most perspective predictive biomarkers of PTE for clinical practice.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Biomarcadores , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/diagnóstico , Lesões Encefálicas Traumáticas/terapia , Epilepsia Pós-Traumática/diagnóstico , Epilepsia Pós-Traumática/etiologia , Humanos
2.
BMC Neurol ; 21(1): 301, 2021 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-34348691

RESUMO

OBJECTIVES: To summarize the clinical characteristics of post-traumatic epilepsy (PTE), and to identify the factors affecting the latency of PTE after traumatic brain injury (TBI). METHODS: We conducted a retrospective clinical analysis in patients with PTE who visited the outpatient Department of Epilepsy, Beijing Tiantan Hospital from January 2013 to December 2018. The clinical characteristics, including gender, age distribution, seizure type, and latency were summarized. Factors affecting the latency of PTE were evaluated using Kaplan-Meier curves and Cox proportional hazard regression analysis. RESULTS: Complete clinical information was available for 2862 subjects, of which 78.48% were males. The mean age at TBI was 21.4 ± 15.1 years and peaked in the 0 to 12-year-old and 15 to 27-year-old groups. Generalized onset seizure was the most frequent seizure type (72.82% of patients). Approximately 19.95% PTE patients developed drug-resistant epilepsy. The latency of PTE ranged from 8 days to 20 years, with a median of 24.0 (IQR, 5.0-84.0) months. The Kaplan-Meier curves demonstrated that gender, age at TBI, severity of TBI, multiple craniocerebral injuries, post-TBI treatments, acute seizures, and residual disability were associated with PTE latency. The Cox regression model indicated that age ≥ 18 years old, severe TBI with multiple surgical operations, acute seizures, and residual disability were risk factors for shorter PTE latency. CONCLUSIONS: PTE is more common in males than females, and peaked in the 0 to 12-year-old and 15 to 27-year-old groups. Generalized onset seizure was the most common seizure type and 19.95% of participants developed drug-resistant epilepsy. Patients aged ≥18 years old, who suffered severe TBI followed by multiple surgical operations, experienced acute seizures, or with residual disabilities had shorter PTE latency.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Adolescente , Adulto , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/epidemiologia , Criança , Pré-Escolar , Epilepsia Pós-Traumática/epidemiologia , Epilepsia Pós-Traumática/etiologia , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Estudos Retrospectivos , Convulsões , Adulto Jovem
3.
Seizure ; 89: 81-84, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-34023655

RESUMO

PURPOSE: The aim of the current study was to investigate the risk factors for post-traumatic epilepsy (PTE) in a large cohort of patients after severe non-penetrating civilian traumatic brain injury (TBI). METHODS: This was a longitudinal study. All patients with a severe non-penetrating TBI, who were admitted at the neuro-intensive care unit of Shahid Rajaee Trauma Hospital, affiliated with Shiraz University of Medical Sciences, Shiraz, Iran, from 2015 until 2019, were studied. Severe TBI was defined as a Glasgow Coma Scale-Motor score below six. Post-traumatic epilepsy was defined as any seizures that occurred after being discharged from the hospital. RESULTS: In total, 803 patients with severe non-penetrating TBI were studied; 82 patients (10.2%) reported any late post-traumatic seizures (PTSs). A higher Glasgow outcome scale (extended) at discharge was significantly inversely associated with PTE [Odds Ratio (OR)= 0.76, 95% Confidence Interval (CI): 0.65-0.87; p = 0.0001]. Depressed skull fracture (OR= 1.88, 95% CI: 0.92-3.80; p = 0.081), epi­dural hematoma (OR= 1.67, 95% CI: 0.93-2.97; p = 0.083), and sub-dural hematoma (OR= 1.64, 95% CI: 0.96-2.78; p = 0.068) were associated with PTE as trends. CONCLUSION: Our study adds to the literature on the risk of PTE after severe non-penetrating civilian TBI. Our large sample size and also the application of a logistic regression analysis model may suggest that other variables (e.g., depressed skull fracture and intracranial hematoma) are indeed associated with the Glasgow outcome scale (extended) at discharge and that is why they lost their significance in the model.


Assuntos
Epilepsia Pós-Traumática , Epilepsia Pós-Traumática/epidemiologia , Epilepsia Pós-Traumática/etiologia , Escala de Coma de Glasgow , Humanos , Irã (Geográfico)/epidemiologia , Estudos Longitudinais , Fatores de Risco
4.
Seizure ; 90: 9-16, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34052088

RESUMO

Traumatic brain injury (TBI) is defined as a disturbance in brain functioning caused by an external force. The development of post traumatic epilepsy (PTE) is a serious risk associated with TBI. Indeed, other neurological impairments are also common following TBI. In this review, we analyze and discuss the most widely used and best validated rodent models of TBI, with a particular focus on their contribution to the understanding of the PTE development. Furthermore, we explore the importance of these models for the study of other neurobehavioral comorbidities associated with brain injury. The efficient and accurate diagnosis of epilepsy and other neurological comorbidities as a consequence of brain trauma should improve the survival and quality of life of patients after TBI.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Epilepsia , Animais , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/epidemiologia , Modelos Animais de Doenças , Epilepsia/epidemiologia , Epilepsia/etiologia , Epilepsia Pós-Traumática/epidemiologia , Epilepsia Pós-Traumática/etiologia , Humanos , Qualidade de Vida
5.
Seizure ; 88: 36-44, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33812306

RESUMO

OBJECTIVE: We aimed to develop and validate a predictive model of posttraumatic epilepsy (PTE). METHODS: The training cohort was patients registered at West China Hospital and diagnosed as traumatic brain injury (TBI) between January 1, 2011, and December 31, 2017. On the basis of multivariable cox proportional hazards model using a forward stepwise method, the nomogram was generated. We externally validated this instrument in 834 participants from two independent cohorts to assess its performance. RESULTS: The nomogram was built based on the results of multivariable cox proportional hazards regression analysis of 1301patients from West China Hospital. The prevalence of PTE was 12.8% (95% confidence interval [CI], 10.9-14.6%) in training cohort, 10.5% (95% CI, 7.5-13.4%) in the testing 1 cohort, and 6.1% (95% CI, 3.7-8.4%) in the testing 2 cohort. 7 independent predictors of PTE composed the nomogram (sex, time of loss of consciousness, subdural hemorrhage, contusion sites, early posttraumatic seizures, TBI severity, and treatment). The C-index was 0.846 (95% CI, 0.817-0.876), and the corresponding sensitivity and specificity were 0.867 and 0.738. External validations showed good discrimination in overall testing cohorts with a C-index of 0.895 (95% CI, 0.859-0.930), in the testing 1 cohort (C-index 0.897, 95% CI, 0.855-0.938) and testing 2 cohort (C-index, 0.883, 95% CI, 0.814-0.952). Calibration of this model was also good since the calibration plots were close to the ideal line. CONCLUSIONS: This nomogram was developed and validated in a large cohort for individualized prediction of PTE, which can identify individuals at high risk of epilepsy and help us find preventive drugs based on these targeted population.


Assuntos
Epilepsia Pós-Traumática , Epilepsia , China/epidemiologia , Epilepsia/diagnóstico , Epilepsia/epidemiologia , Epilepsia/etiologia , Humanos , Nomogramas , Estudos Retrospectivos
6.
Epilepsia ; 62(6): 1472-1481, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33893636

RESUMO

OBJECTIVE: Traumatic brain injury (TBI) may lead to the disruption of the intestinal barrier (IB), and to the escape of products of commensal gut bacteria, including lipopolysaccharide (LPS), into the bloodstream. We examined whether lateral fluid percussion injury (LFPI) and post-traumatic epilepsy (PTE) are associated with the increased intestinal permeability and endotoxemia, and whether these events in turn are associated with PTE. METHODS: LFPI was delivered to adult male Sprague-Dawley rats. Before, 1 week, and 7 months after LFPI, the IB permeability was examined by measuring plasma concentration of fluorescein isothiocyanate-labeled dextran (FD4) upon its enteral administration. Plasma LPS concentration was measured in the same animals, using enzyme-linked immunosorbent assay. PTE was examined 7 months after LFPI, with use of video-EEG (electroencephalography) monitoring. RESULTS: One week after LFPI, the IB disruption was detected in 14 of 17 and endotoxemia - in 10 of 17 rats, with a strong positive correlation between FD4 and LPS levels, and between plasma levels of each of the analytes and the severity of neuromotor deficit. Seven months after LFPI, IB disruption was detected in 13 of 15 and endotoxemia in 8 of 15 rats, with a strong positive correlation between plasma levels of the two analytes. Five of 15 LFPI rats developed PTE. Plasma levels of both FD4 and LPS were significantly higher in animals with PTE than among the animals without PTE. The analysis of seven rats, which were examined repeatedly at 1 week and at 7 months, confirmed that late IB disruption and endotoxemia were not due to lingering of impairments occurring shortly after LFPI. SIGNIFICANCE: LFPI leads to early and remote disruption of IB and a secondary endotoxemia. Early and late perturbations may occur in different subjects. Early changes reflect the severity of acute post-traumatic motor dysfunction, whereas late changes are associated with PTE.


Assuntos
Lesões Encefálicas Traumáticas/fisiopatologia , Endotoxemia/fisiopatologia , Epilepsia Pós-Traumática/fisiopatologia , Intestinos/fisiopatologia , Animais , Lesões Encefálicas Traumáticas/complicações , Dextranos , Eletroencefalografia , Endotoxemia/etiologia , Epilepsia Pós-Traumática/complicações , Fluoresceína-5-Isotiocianato/análogos & derivados , Lipopolissacarídeos/sangue , Masculino , Permeabilidade , Ratos , Ratos Sprague-Dawley
7.
Epilepsia Open ; 6(1): 181-194, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33681661

RESUMO

Study objectives: Traumatic brain injury (TBI) results in sequelae that include posttraumatic epilepsy (PTE) and sleep-wake disturbances. Here, we sought to determine whether sleep characteristics could predict development of PTE in a model of severe TBI. Methods: Following controlled cortical impact (CCI) or sham injury (craniotomy only), CD-1 mice were implanted with epidural electroencephalography (EEG) and nuchal electromyography (EMG) electrodes. Acute (1st week) and chronic (months 1, 2, or 3) 1-week-long video-EEG recordings were performed after the injury to examine epileptiform activity. High-amplitude interictal events were extracted from EEG using an automated method. After scoring sleep-wake patterns, sleep spindles and EEG delta power were derived from nonrapid eye movement (NREM) sleep epochs. Brain CTs (computerized tomography) were performed in sham and CCI cohorts to quantify the brain lesions. We then employed a no craniotomy (NC) control to perform 1-week-long EEG recordings at week 1 and month 1 after surgery. Results: Posttraumatic seizures were seen in the CCI group only, whereas interictal epileptiform activity was seen in CCI or sham. Sleep-wake disruptions consisted of shorter wake or NREM bout lengths and shorter duration or lower power for spindles in CCI and sham. NREM EEG delta power increased in CCI and sham groups compared with NC though the CCI group with posttraumatic seizures had lower power at a chronic time point compared with those without. Follow-up brain CTs showed a small lesion in the sham injury group suggesting a milder form of TBI that may account for their interictal activity and sleep changes. Significance: In our TBI model, tracking changes in NREM delta power distinguishes between CCI acutely and animals that will eventually develop PTE, but further work is necessary to identify sleep biomarkers of PTE. Employing NC controls together with sham controls should be considered in future TBI studies.


Assuntos
Lesões Encefálicas Traumáticas/complicações , Modelos Animais de Doenças , Epilepsia Pós-Traumática/etiologia , Transtornos do Sono-Vigília/etiologia , Animais , Encéfalo , Eletroencefalografia , Eletromiografia , Masculino , Camundongos , Tomografia Computadorizada por Raios X , Gravação em Vídeo
8.
Epilepsy Behav ; 116: 107768, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33567399

RESUMO

PURPOSE: We determined burden of caring for patients with post-traumatic epilepsy (PTE) following penetrating traumatic brain injury (TBI) and identified factors predicting higher burden. METHOD: We assessed 331 caregiver-veteran dyads in Phase 2 (136 PTE, 136 non-PTE, and 59 HC dyads), 133 in Phase 4 (47 PTE, 56 non-PTE, and 30 HC dyads) - 30 years later, and 46 dyads in the follow-up study (18 PTE, 19 non-PTE, and 9 HC). Caregiver's burden was measured by Zarit Burden Index and a questionnaire. Veterans completed demographic, mental and physical well-being, quality-of-life, and medical-related information. Caregivers provided information about burden and their assessments of cognitive decline and neuropsychiatric status of the veterans. RESULTS: PTE caregivers perceived significantly more burden than comparison groups at all phases. Bivariate analyses revealed that caregiver distress due to the veteran's neuropsychiatric state including cognitive decline, apathy, and disinhibition and the veteran's characteristics including older age at epilepsy onset and role limitation due to physical problems were associated with higher burden. Finally, we revealed disinhibition distress, and role imitation due to physical problems as the predictors in a model of caregiver burden. CONCLUSION: Elevated PTE caregiver burden is persistent across the life span suggesting that caregivers could benefit from counseling and targeted psychosocial interventions to reduce their burden.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Idoso , Lesões Encefálicas Traumáticas/complicações , Fardo do Cuidador , Cuidadores , Seguimentos , Humanos , Masculino
9.
Epilepsy Behav ; 114(Pt A): 107352, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-32843304

RESUMO

INTRODUCTION: The occurrence rate of posttrauma epilepsy ranges widely from 1% to 30%. Little is known about the underlying epileptogenesis of traumatic brain injury (TBI)-related epilepsy (TRE), because no comparison between TRE and TBI without epilepsy has been performed in terms of neuropathology. Therefore, we postulated that different neuropathological factors may be present between TRE and TBI without epilepsy. The purpose of this study was to clarify differences between TRE and TBI without epilepsy. METHODS: We studied patients who experienced severe head trauma and underwent brain surgery. The age range of the patients was 9-71 years old. Patients with medically resistant epilepsy were included in the Epilepsy group, and patients without epilepsy were included in the nonepilepsy group. Pathological findings, age, sex, and cause of head trauma were statistically compared between these two groups. RESULTS: This study involved 10 patients, nine of whom met the inclusion criteria. Pathological findings for all patients in the Epilepsy group included focal cortical dysplasia (FCD) (p = 0.012). CONCLUSION: The difference between TRE and TBI without epilepsy was underlying FCD in patients with TRE.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Epilepsia , Hemisferectomia , Malformações do Desenvolvimento Cortical , Adolescente , Adulto , Idoso , Lesões Encefálicas Traumáticas/complicações , Criança , Epilepsia/complicações , Epilepsia/cirurgia , Epilepsia Pós-Traumática/etiologia , Humanos , Malformações do Desenvolvimento Cortical/complicações , Malformações do Desenvolvimento Cortical/cirurgia , Pessoa de Meia-Idade , Adulto Jovem
10.
Epilepsy Behav ; 121(Pt B): 107080, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-32317161

RESUMO

A biomarker is a characteristic that can be objectively measured as an indicator of normal biologic processes, pathogenic processes, or responses to an exposure or intervention, including therapeutic interventions. Biomarker modalities include molecular, histologic, radiographic, or physiologic characteristics. To improve the understanding and use of biomarker terminology in biomedical research, clinical practice, and medical product development, the Food and Drug Administration (FDA)-National Institutes of Health (NIH) Joint Leadership Council developed the BEST Resource (Biomarkers, EndpointS, and other Tools). The seven BEST biomarker categories include the following: (a) susceptibility/risk biomarkers, (b) diagnostic biomarkers, (c) monitoring biomarkers, (d) prognostic biomarkers, (e) predictive biomarkers, (f) pharmacodynamic/response biomarkers, and (g) safety biomarkers. We hypothesize some potential overlap between the reported biomarkers of traumatic brain injury (TBI), epilepsy, and posttraumatic epilepsy (PTE). Here, we tested this hypothesis by reviewing studies focusing on biomarker discovery for posttraumatic epileptogenesis and epilepsy. The biomarker modalities reviewed here include plasma/serum and cerebrospinal fluid molecular biomarkers, imaging biomarkers, and electrophysiologic biomarkers. Most of the reported biomarkers have an area under the receiver operating characteristic curve greater than 0.800, suggesting both high sensitivity and high specificity. Our results revealed little overlap in the biomarker candidates between TBI, epilepsy, and PTE. In addition to using single parameters as biomarkers, machine learning approaches have highlighted the potential for utilizing patterns of markers as biomarkers. Although published data suggest the possibility of identifying biomarkers for PTE, we are still in the early phase of the development curve. Many of the seven biomarker categories lack PTE-related biomarkers. Thus, further exploration using proper, statistically powered, and standardized study designs with validation cohorts, and by developing and applying novel analytical methods, is needed for PTE biomarker discovery.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Epilepsia , Biomarcadores , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/diagnóstico , Epilepsia/diagnóstico , Epilepsia/etiologia , Epilepsia Pós-Traumática/diagnóstico , Epilepsia Pós-Traumática/etiologia , Humanos , Curva ROC
11.
Braz. j. med. biol. res ; 54(2): e10656, 2021. graf
Artigo em Inglês | LILACS, Coleciona SUS | ID: biblio-1142583

RESUMO

Research on the prevention of post-traumatic epilepsy (PTE) has seen remarkable advances regarding its physiopathology in recent years. From the search for biomarkers that might be used to indicate individual susceptibility to the development of new animal models and the investigation of new drugs, a great deal of knowledge has been amassed. Various groups have concentrated efforts in generating new animal models of traumatic brain injury (TBI) in an attempt to provide the means to further produce knowledge on the subject. Here we forward the hypothesis that restricting the search of biomarkers and of new drugs to prevent PTE by using only a limited set of TBI models might hamper the understanding of this relevant and yet not preventable medical condition.


Assuntos
Animais , Epilepsia Pós-Traumática/etiologia , Epilepsia Pós-Traumática/prevenção & controle , Modelos Animais de Doenças , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/prevenção & controle , Biomarcadores
12.
Braz J Med Biol Res ; 54(2): e10656, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33331416

RESUMO

Research on the prevention of post-traumatic epilepsy (PTE) has seen remarkable advances regarding its physiopathology in recent years. From the search for biomarkers that might be used to indicate individual susceptibility to the development of new animal models and the investigation of new drugs, a great deal of knowledge has been amassed. Various groups have concentrated efforts in generating new animal models of traumatic brain injury (TBI) in an attempt to provide the means to further produce knowledge on the subject. Here we forward the hypothesis that restricting the search of biomarkers and of new drugs to prevent PTE by using only a limited set of TBI models might hamper the understanding of this relevant and yet not preventable medical condition.


Assuntos
Lesões Encefálicas Traumáticas , Modelos Animais de Doenças , Epilepsia Pós-Traumática , Animais , Biomarcadores , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/prevenção & controle , Epilepsia Pós-Traumática/etiologia , Epilepsia Pós-Traumática/prevenção & controle
13.
Epilepsia ; 61(9): 2035-2052, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32786029

RESUMO

OBJECTIVE: To identify postinjury physiologic, behavioral, and cognitive biomarkers for posttraumatic epilepsy to enrich study populations for long-term antiepileptogenesis studies. METHODS: The EPITARGET cohort with behavioral follow-up and 1-month 24/7 video-electroencephalography (vEEG) monitoring included 115 adult male Sprague-Dawley rats with lateral fluid-percussion-induced traumatic brain injury (TBI), 23 sham-operated controls, and 13 naive rats. Animals underwent assessment of somatomotor performance (composite neuroscore), anxiety-like behavior (elevated plus maze, open field), spatial memory (Morris water maze), and depression-like behavior (Porsolt forced swim, sucrose preference). Impact force, postimpact apnea time, postimpact seizure-like behavior, and body weight were monitored. RESULTS: TBI rats were impaired in the composite neuroscore (P < .001) on days (D) 2-14 and in the spatial memory test (P < .001) on D35-39 post-TBI. Differences in the elevated plus-maze (D28 and D126) and in the open field (D29 and D127) between TBI rats and controls were meager. No differences were observed in the Porsolt forced swim and sucrose preference tests as compared with sham-operated controls. Epilepsy developed in 27% of rats by the end of the sixth month. None of the behavioral or cognitive outcome measures discriminated rats with or without epilepsy. The receiver-operating characteristic analysis indicated that a decrease in body weight between D0 and D4 differentiated TBI rats with epilepsy from TBI rats without epilepsy (48% sensitivity, 83% specificity, area under the curve [AUC] 0.679, confidence interval [CI] 95% 0.56-0.80, P < .01). A 16% body weight decrease during D0-D4 could be used as a biomarker to enrich the study population from 27% (observed) to 50%. SIGNIFICANCE: Single behavioral and cognitive outcome measures showed no power as prognostic/diagnostic biomarkers for posttraumatic epilepsy. A reduction in body weight during the first postinjury week showed some prognostic value for posttraumatic epileptogenesis and could serve as a subacute measure for selectively enriching the study population for long-term preclinical biomarker and therapy discovery studies of posttraumatic epileptogenesis.


Assuntos
Ansiedade/fisiopatologia , Apneia/fisiopatologia , Lesões Encefálicas Traumáticas/fisiopatologia , Depressão/fisiopatologia , Epilepsia Pós-Traumática/epidemiologia , Convulsões/fisiopatologia , Memória Espacial/fisiologia , Perda de Peso/fisiologia , Animais , Ansiedade/psicologia , Comportamento Animal , Peso Corporal , Encéfalo/fisiopatologia , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/patologia , Lesões Encefálicas Traumáticas/psicologia , Depressão/psicologia , Modelos Animais de Doenças , Eletroencefalografia , Teste de Labirinto em Cruz Elevado , Epilepsia Pós-Traumática/etiologia , Teste do Labirinto Aquático de Morris , Teste de Campo Aberto , Prognóstico , Curva ROC , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley
16.
J Neurol Neurosurg Psychiatry ; 91(11): 1154-1157, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32848013

RESUMO

BACKGROUND: Traumatic brain injury (TBI) causes early seizures and is the leading cause of post-traumatic epilepsy. We prospectively assessed structural imaging biomarkers differentiating patients who develop seizures secondary to TBI from patients who do not. DESIGN: Multicentre prospective cohort study starting in 2018. Imaging data are acquired around day 14 post-injury, detection of seizure events occurred early (within 1 week) and late (up to 90 days post-TBI). RESULTS: From a sample of 96 patients surviving moderate-to-severe TBI, we performed shape analysis of local volume deficits in subcortical areas (analysable sample: 57 patients; 35 no seizure, 14 early, 8 late) and cortical ribbon thinning (analysable sample: 46 patients; 29 no seizure, 10 early, 7 late). Right hippocampal volume deficit and inferior temporal cortex thinning demonstrated a significant effect across groups. Additionally, the degree of left frontal and temporal pole thinning, and clinical score at the time of the MRI, could differentiate patients experiencing early seizures from patients not experiencing them with 89% accuracy. CONCLUSIONS AND RELEVANCE: Although this is an initial report, these data show that specific areas of localised volume deficit, as visible on routine imaging data, are associated with the emergence of seizures after TBI.


Assuntos
Contusão Encefálica/diagnóstico por imagem , Hemorragia Encefálica Traumática/diagnóstico por imagem , Afinamento Cortical Cerebral/diagnóstico por imagem , Epilepsia Pós-Traumática/diagnóstico por imagem , Lobo Frontal/diagnóstico por imagem , Hipocampo/diagnóstico por imagem , Lobo Temporal/diagnóstico por imagem , Adulto , Contusão Encefálica/complicações , Hemorragia Encefálica Traumática/complicações , Lesões Encefálicas Traumáticas/diagnóstico por imagem , Regras de Decisão Clínica , Biologia Computacional , Eletroencefalografia , Epilepsia Pós-Traumática/epidemiologia , Epilepsia Pós-Traumática/etiologia , Feminino , Lobo Frontal/patologia , Escala de Coma de Glasgow , Hipocampo/patologia , Humanos , Processamento de Imagem Assistida por Computador , Modelos Logísticos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Tamanho do Órgão , Estudos Prospectivos , Lobo Temporal/patologia , Fatores de Tempo , Adulto Jovem
17.
Fa Yi Xue Za Zhi ; 36(3): 365-368, 2020 Jun.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-32705851

RESUMO

Abstract: 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.


Assuntos
Biomarcadores , Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Epilepsia , Biomarcadores/análise , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/diagnóstico , Epilepsia/diagnóstico , Epilepsia/etiologia , Epilepsia Pós-Traumática/diagnóstico , Epilepsia Pós-Traumática/etiologia , Humanos
18.
Med Sci Monit ; 26: e923919, 2020 Jul 20.
Artigo em Inglês | MEDLINE | ID: mdl-32687486

RESUMO

BACKGROUND Post-traumatic epilepsy (PTE) is a common type of acquired epilepsies secondary to traumatic brain injury (TBI), accounting for approximately 10-25% of patients. The present study evaluated activity of PP-4-one against mTOR signaling activation in a rat model of FeCl2-induced post-traumatic epilepsy. MATERIAL AND METHODS Epilepsy in rats was induced by injecting 10 µl FeCl2 (concentration 100 mM) at a uniform rate of 1 µl/minute. The iNOS expression was detected using a Leica microscope connected to a digital camera system. Reverse transcription polymerase chain reaction (RT­PCR) was used for determination of NR1 mRNA expression. RESULTS The post-traumatic epilepsy induced neuronal degeneration in the hippocampus and frontal cortex of the rats. Treatment with PP-4-one prevented neuronal degeneration in the hippocampus and frontal cortex in rats with post-traumatic epilepsy. The data revealed markedly higher levels of p-mTOR and p-P70S6K in rat hippocampal tissues after induction of traumatic epilepsy. Treatment of post-traumatic epilepsy rats with PP-4-one significantly suppressed p-mTOR and p-P70S6K expression, and PP-4-one treatment reduced epileptic brain injury in the rats with post-traumatic epilepsy. CONCLUSIONS PP-4-one exhibits an anti-epileptogenic effect in the rat model of PTE by inhibiting behavioral seizures through suppression of iNOS and astrocytic proliferation. Moreover, PP-4-one treatment suppressed NR1 expression and targeted the mTOR pathway in PTE-induced rats. Thus, PP-4-one shows promise as a novel and effective therapeutic agent for treatment of epilepsy induced by PTE.


Assuntos
Epilepsia Pós-Traumática/tratamento farmacológico , Pirazóis/química , Pirazóis/farmacologia , Piridinas/química , Piridinas/farmacologia , Animais , Anticonvulsivantes/farmacologia , Astrócitos/metabolismo , Encéfalo/metabolismo , Lesões Encefálicas , Lesões Encefálicas Traumáticas , Modelos Animais de Doenças , Epilepsia/tratamento farmacológico , Epilepsia/metabolismo , Epilepsia Pós-Traumática/metabolismo , Lobo Frontal/metabolismo , Hipocampo/metabolismo , Masculino , Ratos , Ratos Sprague-Dawley , Proteínas Quinases S6 Ribossômicas 70-kDa/efeitos dos fármacos , Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo , Convulsões , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo
19.
ACS Chem Neurosci ; 11(13): 1900-1908, 2020 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-32479057

RESUMO

Post-traumatic epilepsy (PTE) is one of the detrimental outcomes of traumatic brain injury (TBI), resulting in recurrent seizures that impact daily life. However, the pathological relationship between PTE and TBI remains unclear, and commonly prescribed antiepileptic drugs (AED) are ineffective against PTE. Fortunately, emerging research implicates neuroinflammation, particularly, tumor necrosis factor-α (TNF-α), as the key mediator for PTE development. Thus, this review aims to examine the available literature regarding the role of TNF-α in PTE pathology and, subsequently, evaluate TNF-α as a possible target for its treatment. A comprehensive literature search was conducted on four databases including PubMed, CINAHL, Embase, and Scopus. Articles with relevance in investigating TNF-α expression in PTE were considered in this review. Critical evaluation of four articles that met the inclusion criteria suggests a proportional relationship between TNF-α expression and seizure susceptibilit and that neutralization or suppression of TNF-α release results in reduced susceptibility to seizures. In conclusion, this review elucidates the importance of TNF-α expression in epileptogenesis postinjury and urges future research to focus more on clinical studies involving TNF-α, which may provide clearer insight into PTE prevention, therefore improving the lives of PTE patients.


Assuntos
Lesões Encefálicas Traumáticas , Epilepsia Pós-Traumática , Anticonvulsivantes/uso terapêutico , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/tratamento farmacológico , Epilepsia Pós-Traumática/tratamento farmacológico , Epilepsia Pós-Traumática/etiologia , Humanos , Convulsões/tratamento farmacológico , Convulsões/etiologia , Fator de Necrose Tumoral alfa
20.
Brain Inj ; 34(7): 889-894, 2020 06 06.
Artigo em Inglês | MEDLINE | ID: mdl-32506958

RESUMO

Objective: To estimate national frequency of posttraumatic epilepsy (PTE) after severe traumatic brain injury (TBI) and assess injury severity (Glasgow Coma Scale (GCS) and posttraumatic amnesia (PTA)) as prognostic factors for PTE. METHODS: Data on patients ≥18 years surviving severe TBI 2004-2016 were retrieved from the Danish Head Trauma Database (n = 1010). The cumulative incidence proportion (CIP) was estimated using death as competing event. The association between injury severity and PTE was assessed using multivariable competing risk regressions. RESULTS: CIP of PTE 28 days and one year post-TBI was 6.8% (95% confidence interval (CI) 5.4-8.5) and 18.5% (95% CI 16.1-21.1%), respectively. Injury severity was not associated with PTE within 28 days post-TBI but indicated higher PTE-rates in less severely injured patients. PTA-duration >70 days was associated with PTE 29-365 days post-TBI (Adjusted sub-hazard ratio 4.23 (95% CI 1.79-9.99)). GCS was not associated with PTE 29-365 days post-TBI. CONCLUSION: The PTE frequency was higher compared to previous estimates. Increasing injury severity was associated with PTE 29-365 days post-TBI when measured with PTA, but not with GCS. Though nonsignificant, the increased PTE-risk within 28 days in lower severity suggests an underdiagnosing of PTE.


Assuntos
Lesões Encefálicas Traumáticas , Traumatismos Craniocerebrais , Epilepsia Pós-Traumática , Epilepsia , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/epidemiologia , Epilepsia Pós-Traumática/epidemiologia , Epilepsia Pós-Traumática/etiologia , Escala de Coma de Glasgow , Humanos
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