Posts Tagged epileptogenesis

[Abstract + References] Epileptic and Nonepileptic Seizures after Traumatic Brain Injury

Abstract

Representing approximately 5% of epilepsy in the civilian population and up to 50% in certain military populations, posttraumatic epilepsy warrants both increased clinical attention and research considerations. In this chapter, we will discuss the important definitions when considering posttraumatic epilepsy including the timing of posttraumatic seizures and the severity of head injuries. We will also review the epidemiology and risk factors for posttraumatic epilepsy in both the civilian population and the military and will describe the association of head trauma and psychogenic nonepileptic seizures. Our clinical discussion focuses on the timing of posttraumatic seizures, the utility of diagnostic testing, treatment of posttraumatic epilepsy, and outcomes of these patients. In addition, we elucidate potential pathophysiologic mechanisms underlying posttraumatic epilepsy and consider its role as a model for epileptogenesis in current and future research. We highlight the relevant studies in each section and underscore the theme that more research is certainly needed in most areas of posttraumatic epilepsy.

References

  1. 1.
    Caveness WF, Meirowsky AM, Rish BL, Mohr JP, Kistler JP, Dillon JD, et al. The nature of posttraumatic epilepsy. J Neurosurg. 1979;50:545–53.PubMedCrossRefPubMedCentralGoogle Scholar
  2. 2.
    Lowenstein DH. Epilepsy after head injury: an overview. Epilepsia. 2009;50 (Suppl. 2):4–9.CrossRefGoogle Scholar
  3. 3.
    Faul M, Xu L, Wald MM, Coronado VG. Traumatic brain injury in the United States: emergency department visits, hospitalizations and deaths 2002-2006. Atlanta: Centers for Disease Control and Prevention and National Center for Injury Prevention and Control; 2010.CrossRefGoogle Scholar
  4. 4.
    Kovacs SK, Leonessa F, Ling GS. Blast TBI models, neuropathology, and implications for seizure risk. Front Neurol. 2014;5:47.PubMedPubMedCentralCrossRefGoogle Scholar
  5. 5.
    Snell FI, Halter MJ. A signature wound of war. J Psychosoc Nurs Ment Health Serv. 2010:1–7.Google Scholar
  6. 6.
    Zarocostas J. Proliferation of firearms is growing global health problem. Br Med J. 2007;335:470–1.CrossRefGoogle Scholar
  7. 7.
    Agrawal A, Timothy J, Pandit L, Manju M. Post-traumatic epilepsy: an overview. Clin Neurol Neurosurg. 2006;108:433–9.PubMedCrossRefPubMedCentralGoogle Scholar
  8. 8.
    Hauser WA, Annegers JF, Kurland LT. Prevalence of epilepsy in Rochester, Minnesota, 1940-1980. Epilepsia. 1991;31:429–45.CrossRefGoogle Scholar
  9. 9.
    Salazar AM, Jabbari B, Vance SC, Grafman J, Amin D, Dillon JD. Epilepsy after penetrating head injury. I. Clinical correlates: a report of the Vietnam head injury study. Neurology. 1985;35:1406–14.PubMedCrossRefPubMedCentralGoogle Scholar
  10. 10.
    Annegers JF, Coan SP. The risks of epilepsy after traumatic brain injury. Seizure. 2000;9:453–7.PubMedCrossRefPubMedCentralGoogle Scholar
  11. 11.
    Annegers JF, Hauser WA, Coan SP, Rocca WA. A population-based study of seizures after traumatic brain injuries. N Engl J Med. 1998;338:20–4.PubMedCrossRefPubMedCentralGoogle Scholar
  12. 12.
    Ferguson PL, Smith GM, Wannamaker BB, Thurman DJ, Pickelsimer EE, Selassie AW. A population-based study of risk of epilepsy after hospitalization for traumatic brain injury. Epilepsia. 2010;51:891–8.PubMedCrossRefPubMedCentralGoogle Scholar
  13. 13.
    Herman ST. Epilepsy after brain insult: Targeting epileptogenesis. Neurology. 2002;59(Suppl 5):S21–6.PubMedCrossRefPubMedCentralGoogle Scholar
  14. 14.
    Christensen J, Pedersen MG, Pedersen CB, Sidenius P, Olse J, Vestergaard M. Long term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study. Lancet. 2009;373:1105–10.PubMedCrossRefPubMedCentralGoogle Scholar
  15. 15.
    Mahler B, Carlsson S, Andersson T, Adelow C, Ahlbom A, Tomson T. Unprovoked seizures after traumatic brain injury: a population-based case-control study. Epilepsia. 2015;56:1438–44.PubMedCrossRefPubMedCentralGoogle Scholar
  16. 16.
    Pugh MJ, Orman JA, Jaramillo CA, Salinsky MC, Eapen BC, Towne AR, et al. The prevalence of epilepsy and association with traumatic brain injury in veterans of the Afghanistan and Iraq wars. J Head Trauma Rehabil. 2014;30:29–37.CrossRefGoogle Scholar
  17. 17.
    Yeh CC, Chen TL, Hu CJ, Chiu WT, Liao CC. Risk of epilepsy after traumatic brain injury: a retrospective population-based cohort study. J Neurol Neurosurg Psychiatry. 2013;84:441–5.PubMedCrossRefPubMedCentralGoogle Scholar
  18. 18.
    Annegers J, Grabow J, Groover R, Laws E, Elveback L, Kurland L. Seizures after head trauma: a population study. Neurology. 1980;30:683–9.PubMedCrossRefPubMedCentralGoogle Scholar
  19. 19.
    Jennett WB, Lewin W. Traumatic epilepsy after closed head injuries. J Neurol Neurosurg Psychiatry. 1960;23:295–301.PubMedPubMedCentralCrossRefGoogle Scholar
  20. 20.
    Angeleri F, Majkowski J, Cacchio G, Sobieszek S, D’Acunto S, Gesuita R, et al. Posttraumatic epilepsy risk factors: one-year prospective study after head injury. Epilepsia. 1999;40:1222–30.PubMedCrossRefPubMedCentralGoogle Scholar
  21. 21.
    Englander J, Bushnik T, Duong TT, Cifu DX, Zafonte R, Wright J, et al. Analyzing risk factors for late post-traumatic seizures: a prospective, multicenter investigation. Arch Phys Med Rehabil. 2003;84:365–73.PubMedCrossRefPubMedCentralGoogle Scholar
  22. 22.
    Asikainen I, Kaste M, Sarna S. Early and late posttraumatic seizure in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia. 1999;40:584–9.PubMedCrossRefPubMedCentralGoogle Scholar
  23. 23.
    Raymont V, Salazar AM, Lipsky R, Goldman D, Tasick G, Grafman J. Correlates of posttraumatic epilepsy 35 years following combat brain injury. Neurology. 2010;75:224–9.PubMedPubMedCentralCrossRefGoogle Scholar
  24. 24.
    Masel BE, Bell RS, Brossart S, Grill RJ, Hayes RL, Levin HS, et al. Galveston brain injury conference 2010: clinical and experimental aspects of blast injury. J Neurotrauma. 2012;29:2143–71.PubMedCrossRefPubMedCentralGoogle Scholar
  25. 25.
    Okie S. Traumatic brain injury in the war zone. N Engl J Med. 2005;352:2043–7.PubMedCrossRefPubMedCentralGoogle Scholar
  26. 26.
    Chase RP, Nevin RL. Population estimates of undocumented incident traumatic brain injuries among combat-deployed US military personnel. J Head Trauma Rehabil. 2015;30(1):E57–64.PubMedCrossRefPubMedCentralGoogle Scholar
  27. 27.
    Brundage JF, Taubman SB, Hunt DJ, Clark LL. Whither the “signature wounds of the war” after the war: estimates of incidence rates and proportions of TBI and PTSD diagnoses attributable to background risk, enhanced ascertainment, and active war zone service, active component, U.S Armed Forces, 2003-2014. Medical Surveillance Monthly Report. 2015;22(2):2–11.PubMedPubMedCentralGoogle Scholar
  28. 28.
    Salinksy M, Evrard C, Storzbach D, Pugh MJ. Psychiatric comorbidity in veterans with psychogenic seizures. Epilepsy Behav. 2012;25:345–9.CrossRefGoogle Scholar
  29. 29.
    Salinksy M, Spencer D, Boudreau E, Ferguson F. Psychogenic nonepileptic seizures in US veterans. Neurology. 2011;77:945–50.CrossRefGoogle Scholar
  30. 30.
    Salinksy M, Storzbach D, Goy E, Evrad C. Traumatic brain injury and psychogenic seizures in veterans. J Head Trauma Rehabil. 2015;30:E65–70.CrossRefGoogle Scholar
  31. 31.
    Chen LL, Baca CB, Choe J, Chen JW, Ayad ME, Cheng EM. Posttraumatic epilepsy in operation enduring freedom/operation Iraqi freedom veterans. Mil Med. 2014;179:492–6.PubMedCrossRefPubMedCentralGoogle Scholar
  32. 32.
    Lee ST, Lui TN. Early seizures after mild closed head injury. J Neurosurg. 1992;76:435–9.PubMedCrossRefPubMedCentralGoogle Scholar
  33. 33.
    Haltiner AM, Temkin NR, Dikmen SS. Risk of seizure recurrence after the first late posttraumatic seizure. Arch Phys Med Rehabil. 1997;78:835–40.PubMedCrossRefPubMedCentralGoogle Scholar
  34. 34.
    Gupta PK, Sayed N, Ding K, Agostini MA, Van Ness PC, Yablon S, et al. Subtypes of post-traumatic epilepsy: clinical, electrophysiological, and imaging features. J Neurotrauma. 2014;31:1439–43.PubMedPubMedCentralCrossRefGoogle Scholar
  35. 35.
    Diaz-Arrastia R, Agostini MA, Madden CJ, Van Ness PC. Posttraumatic epilepsy: the endophenotypes of a human model of epileptogenesis. Epilepsia. 2009;50(Suppl 2):14–20.PubMedCrossRefPubMedCentralGoogle Scholar
  36. 36.
    Jennett B, van de Sande J. EEG prediction of post-traumatic epilepsy. Epilepsia. 1975;16:251–6.PubMedCrossRefGoogle Scholar
  37. 37.
    D’Alessandro R, Tinuper P, Ferrara R, Cortelli P, Pazzaglia P, Sabattini L, et al. CT scan prediction of late post-traumatic epilepsy. J Neurol Neurosurg Psychiatry. 1982;45:1153–5.PubMedPubMedCentralCrossRefGoogle Scholar
  38. 38.
    Thiruppathy SP, Muthukumar N. Mild head injury: revisited. Acta Neurochir (Wein). 2004;146(10):1075–83.CrossRefGoogle Scholar
  39. 39.
    Kumar R, Gupta RK, Husain M, Vatsal DK, Chawla S, Rathore RKS, et al. Magnetization transfer MR imaging in patients with posttraumatic epilepsy. Am J Neuroradiol. 2003;23:218–24.Google Scholar
  40. 40.
    Fox WC, Park MS, Belverud S, Klugh A, Rivet D, Tomlin JM. Contemporary imaging of mild TBI: the journey toward diffusion tensor imaging to assess neuronal damage. Neurol Res. 2013;35:223–32.PubMedCrossRefPubMedCentralGoogle Scholar
  41. 41.
    Hunter JV, Wilde EA, Tong KA, Holshouser BA. Emerging imaging tools for use with traumatic brain injury research. J Neurotrauma. 2012;29:654–71.PubMedPubMedCentralCrossRefGoogle Scholar
  42. 42.
    Immonen R, Kharatishvili I, Grohn O, Pitkanen A. MRI biomarkers for post-traumatic epileptogenesis. J Neurotrauma. 2013;30:1305–9.PubMedPubMedCentralCrossRefGoogle Scholar
  43. 43.
    Temkin NR. Preventing and treating posttraumatic seizures: the human experience. Epilepsia. 2009;50(Suppl. 2):10–3.PubMedCrossRefPubMedCentralGoogle Scholar
  44. 44.
    Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. 1990;323:497–502.PubMedCrossRefPubMedCentralGoogle Scholar
  45. 45.
    Young B, Rapp RP, Norton JA, Haack D, Tibbs PA, Bean JR. Failure of prophylactically administered phenytoin to prevent late post-traumatic seizures. J Neurosurg. 1983;58:236–41.PubMedCrossRefPubMedCentralGoogle Scholar
  46. 46.
    Temkin NR, Dikmen SS, Anderson GD, Wilensky AJ, Holmes MD, Cohen W, et al. Valproate therapy for prevention of posttraumatic seizures: a randomized trial. J Neurosurg. 1999;91:593–600.PubMedCrossRefPubMedCentralGoogle Scholar
  47. 47.
    Chang BS, Lowenstein DH, Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the quality standards Subcommittee of the American Academy of neurology. Neurology. 2003;60(1):10–6.PubMedCrossRefPubMedCentralGoogle Scholar
  48. 48.
    Szaflarski JP, Sangha KS, Lindsell CJ, Shutter LA. Prospective, randomized, single-blinded comparative trial of intravenous levetiracetam versus phenytoin for seizure prophylaxis. Neurocrit Care. 2010;12:165–72.PubMedCrossRefPubMedCentralGoogle Scholar
  49. 49.
    Kwan P, Sander JW. The natural history of epilepsy: an epidemiological view. J Neurol Neurosurg Psychiatry. 2004;75:1376–81.PubMedPubMedCentralCrossRefGoogle Scholar
  50. 50.
    Englot DJ, Rolston JD, Wang DD, Hassnain KH, Gordon CM, Chang EF. Efficacy of vagus nerve stimulation in posttraumatic versus nontraumatic epilepsy. J Neurosurg. 2012;117:970–7.PubMedCrossRefPubMedCentralGoogle Scholar
  51. 51.
    Heck CN, King-Stephens D, Massey AD, Nair DR, Jobst BC, Barkley GL, et al. Two-year seizure reduction in adults with medically intractable partial onset epilepsy treated with responsive neurostimulation: final results of the RNS system pivotal trial. Epilepsia. 2014;55:432–41.PubMedPubMedCentralCrossRefGoogle Scholar
  52. 52.
    Fisher R, Salanova V, Witt T, Worth R, Henry T, Gross R, et al. Electrical stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy. Epilepsia. 2010;51:899–908.PubMedCrossRefPubMedCentralGoogle Scholar
  53. 53.
    Fisher RS, Velasco AL. Electrical brain stimulation for epilepsy. Nat Rev Neurol. 2014;10:261–70.PubMedCrossRefPubMedCentralGoogle Scholar
  54. 54.
    Rao VR, Parko KL. Clinical approach to posttraumatic epilepsy. Semin Neurol. 2015;35:57–63.PubMedCrossRefPubMedCentralGoogle Scholar
  55. 55.
    Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia. 2003;44(suppl 10):11–7.PubMedCrossRefPubMedCentralGoogle Scholar
  56. 56.
    Corkin S, Sullivan EV, Carr FA. Prognostic factors for life expectancy after penetrating head injury. Arch Neurol. 1984;41(9):975–7.PubMedCrossRefPubMedCentralGoogle Scholar
  57. 57.
    Algattas H, Huang JH. Traumatic brain injury pathophysiology and treatments: early, intermediate, and late phases post-injury. Int J Mol Sci. 2013;30:309–41.CrossRefGoogle Scholar
  58. 58.
    Diamond ML, Ritter AC, Failla MD, Boles JA, Conley YP, Kochanek PM, et al. IL-1β associations with posttraumatic epilepsy development: a genetics and biomarker cohort study. Epilepsia. 2015;56:991–1001.PubMedCrossRefPubMedCentralGoogle Scholar
  59. 59.
    Jensen FE. Posttraumatic Epilepsy: Treatable epileptogenesis. Epilepsia. 2009;50(Suppl. 2):1–3.PubMedPubMedCentralGoogle Scholar
  60. 60.
    Prince DA, Parada I, Scalise K, Graber K, Jin X, Shen F. Epilepsy following cortical injury: cellular and molecular mechanisms as targets for potential prophylaxis. Epilepsia. 2009;50(Suppl. 2):30–40.PubMedPubMedCentralCrossRefGoogle Scholar
  61. 61.
    Pitkanen A, Immonen RJ, Grohn OHJ, Kharatishvili I. From traumatic brain injury to posttraumatic epilepsy: what animal models tell us about the process and treatment options. Epilepsia. 2009;50(Suppl. 2):21–9.PubMedCrossRefPubMedCentralGoogle Scholar
  62. 62.
    Kelly KM, Miller ER, Lepsveridze E, Kharlamov E, Mchedlishvili Z. Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact. Epilepsy Res. 2015;117:104–16.PubMedCrossRefPubMedCentralGoogle Scholar
  63. 63.
    Desai BT, Whitman S, Coonley-Hoganson R, Coleman TE, Gabriel G, Dell J. Seizures and civilian head injuries. Epilepsia. 1983;24:289–96.PubMedCrossRefPubMedCentralGoogle Scholar
  64. 64.
    Hahn YS, Fuchs S, Flannery AM, Barthel MJ, McLone DG. Factors influencing posttraumatic seizures in children. Neurosurgery. 1988;22:864–7.PubMedCrossRefPubMedCentralGoogle Scholar

via Epileptic and Nonepileptic Seizures after Traumatic Brain Injury | SpringerLink

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[Abstract] No prevention or cure of epilepsy as yet – Invited review

Highlights

  • Approximately 20% of all epilepsy is caused by acute acquired injury such as traumatic brain injury, stroke and CNS infection, with potential to prevent epilepsy
  • No treatment to prevent acquired epilepsy exists; and very few clinical studies have been done during the last 15 years to develop such treatment
  • We review possible reasons for this, possible ways to rectify the situations and note some of the ways currently under way to do so
  • We further review “cures” of epilepsy that occur spontaneously, and after surgical and sometimes medical antiseizure treatments. We note the limited understanding of the mechanisms of such remissions and thus, at present inability to replicate them with targeted therapy

Abstract

Approximately 20% of all epilepsy is caused by acute acquired injury such as traumatic brain injury, stroke and CNS infection. The known onset of the injury which triggers the epileptogenic process, early presentation to medical care, and a latency between the injury and the development of clinical epilepsy present an opportunity to intervene with treatment to prevent epilepsy. No such treatment exists and yet there has been remarkably little clinical research during the last 20 years to try to develop such treatment. We review possible reasons for this, possible ways to rectify the situations and note some of the ways currently under way to do so.

Resective surgical treatment can achieve “cure” in some patients but is sparsely utilized. In certain “self-limiting” syndromes of childhood and adolescence epilepsy remits spontaneously. In a proportion of patients who become seizure free on medications or with dietary treatment, seizure freedom persists when treatment is discontinued. We discuss these situations which can be considered “cures”; and note that at present we have little understanding of mechanism of such cures, and cannot therefore translate them into a treatment paradigm targeting a “cure” of epilepsy.

via No prevention or cure of epilepsy as yet – ScienceDirect

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[Abstract] Big data sharing and analysis to advance research in post-traumatic epilepsy – Review

Highlights

  • We have created the infrastructure for a centralized data repository for multi-modal data.
  • Innovative image and electrophysiology processing methods have been applied.
  • Novel analytic tools are described to study epileptogenesis after traumatic brain injury.

Abstract

We describe the infrastructure and functionality for a centralized preclinical and clinical data repository and analytic platform to support importing heterogeneous multi-modal data, automatically and manually linking data across modalities and sites, and searching content. We have developed and applied innovative image and electrophysiology processing methods to identify candidate biomarkers from MRI, EEG, and multi-modal data. Based on heterogeneous biomarkers, we present novel analytic tools designed to study epileptogenesis in animal model and human with the goal of tracking the probability of developing epilepsy over time.

 

via Big data sharing and analysis to advance research in post-traumatic epilepsy

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[Abstract] Post-stroke epilepsy

Highlights

Post-stroke epilepsy (PSE) is a major complication after stroke.

It is unclear which treatments are most effective in the prevention of recurrence of symptoms, or whether such therapy is needed for primary prevention.

The current understanding of epidemiology, diagnoses, mechanisms, risk factors, and treatments of PSE are covered in this review.

Abstract

Post-stroke epilepsy (PSE) is a common complication after stroke, yet treatment options remain limited. While many physicians prescribe antiepileptic drugs (AED) for secondary prevention of PSE, it is unclear which treatments are most effective in the prevention of recurrence of symptoms, or whether such therapy is needed for primary prevention. This review discusses the current understanding of epidemiology, diagnoses, mechanisms, risk factors, and treatments of PSE.

Source: Post-stroke epilepsy

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[WEB SITE] Researchers Reveal New Possible Cause of Epilepsy – Neuroscience News

A team of researchers from Sanford-Burnham and SUNY Downstate Medical Center has found that deficiencies in hyaluronan, also known as hyaluronic acid or HA, can lead to spontaneous epileptic seizures. HA is a polysaccharide molecule widely distributed throughout connective, epithelial, and neural tissues, including the brain’s extracellular space (ECS). Their findings, published on April 30 in The Journal of Neuroscience, equip scientists with key information that may lead to new therapeutic approaches to epilepsy.

The multicenter study used mice to provide the first evidence of a physiological role for HA in the maintenance of brain ECS volume. It also suggests a potential role in human epilepsy for HA and genes that are involved in hyaluraonan synthesis and degradation.

While epilepsy is one of the most common neurological disorders—affecting approximately 1 percent of the population worldwide—it is one of the least understood. It is characterized by recurrent spontaneous seizures caused by the abnormal firing of neurons. Although epilepsy treatment is available and effective for about 70 percent of cases, a substantial number of patients could benefit from a new therapeutic approach.

Epilepsy is a brain disorder that causes seizures that disturb brain activity. Credit Sanford-Burnham Medical Research Institute.

“Hyaluronan is widely known as a key structural component of cartilage and important for maintaining healthy cartilage. Curiously, it has been recognized that the adult brain also contains a lot of hyaluronan, but little is known about what hyaluronan does in the brain,” said Yu Yamaguchi, M.D., Ph.D., professor in our Human Genetics Program.

“This is the first study that demonstrates the important role of this unique molecule for normal functioning of the brain, and that its deficiency may be a cause of epileptic disorders. A better understanding of how hyaluronan regulates brain function could lead to new treatment approaches for epilepsy,” Yamaguchi added.

The extracellular matrix of the brain has a unique molecular composition. Earlier studies focused on the role of matrix molecules in cell adhesion and axon pathfinding during neural development. In recent years, increasing attention has been focused on the roles of these molecules in the regulation of physiological functions in the adult brain.

In this study, the investigators examined the role of HA using mutant mice deficient in each of the three hyaluronan synthase genes (Has1, Has2, Has3).

“We showed that Has-mutant mice develop spontaneous epileptic seizures, indicating that HA is functionally involved in the regulation of neuronal excitability. Our study revealed that deficiency of HA results in a reduction in the volume of the brain’s ECS, leading to spontaneous epileptiform activity in hippocampal CA1 pyramidal neurons,” said Sabina Hrabetova, M.D., Ph.D., associate professor in the Department of Cell Biology at SUNY.

“We believe that this study not only addresses one of the longstanding questions concerning the in-vivo role of matrix molecules in the brain, but also has broad appeal to epilepsy research in general,” said Katherine Perkins, Ph.D., associate professor in the Department of Physiology and Pharmacology at SUNY.

“More specifically, it should stimulate researchers in the epilepsy field because our study reveals a novel, non-synaptic mechanism of epileptogenesis. The fact that our research can lead to new anti-epileptic therapies based on the preservation of hyaluronan adds further significance for the broader biomedical community and the public,” the authors added.

NOTES ABOUT THIS EPILEPSY RESEARCH

Contact: Susan Gammon, Ph.D. – Sanford-Burnham Medical Research Institute
Source: Sanford-Burnham Medical Research Institute press release
Image Source: The image is adapted from the Sanford-Burnham Medical Research Institute press release
Original Research: Abstract for “Hyaluronan Deficiency Due to Has3 Knock-Out Causes Altered Neuronal Activity and Seizures via Reduction in Brain Extracellular Space” by Amaia M. Arranz, Katherine L. Perkins, Fumitoshi Irie, David P. Lewis, Jan Hrabe, Fanrong Xiao, Naoki Itano, Koji Kimata, Sabina Hrabetova, and Yu Yamaguchi in Journal of Neuroscience. Published online April 30 2014 doi:10.1523/JNEUROSCI.3458-13.2014

Source: Researchers Reveal New Possible Cause of Epilepsy – Neuroscience News

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[Abstract] Prognostic models for predicting posttraumatic seizures during acute hospitalization, and at 1 and 2 years following traumatic brain injury – Epilepsia

Epilepsia. 2016 Jul 19. doi: 10.1111/epi.13470. [Epub ahead of print]

OBJECTIVE: Posttraumatic seizures (PTS) are well-recognized acute and chronic complications of traumatic brain injury (TBI). Risk factors have been identified,but considerable variability in who develops PTS remains. Existing PTS prognostic models are not widely adopted for clinical use and do not reflect current trends in injury, diagnosis, or care. We aimed to develop and internally validate preliminary prognostic regression models to predict PTS during acute care hospitalization, and at year 1 and year 2 postinjury.METHODS: Prognostic models predicting PTS during acute care hospitalization and year 1 and year 2 post-injury were developed using a recent (2011-2014) cohort from the TBI Model Systems National Database. Potential PTS predictors were selected based on previous literature and biologic plausibility. Bivariable logistic regression identified variables with a p-value < 0.20 that were used to fit initial prognostic models. Multivariable logistic regression modeling with backward-stepwise elimination was used to determine reduced prognostic models andto internally validate using 1,000 bootstrap samples. Fit statistics were calculated, correcting for overfitting (optimism).RESULTS: The prognostic models identified sex, craniotomy, contusion load, and pre-injury limitation in learning/remembering/concentrating as significant PTS predictors during acute hospitalization. Significant predictors of PTS at year 1 were subdural hematoma (SDH), contusion load, craniotomy, craniectomy, seizure during acute hospitalization, duration of posttraumatic amnesia, preinjury mental health treatment/psychiatric hospitalization, and preinjury incarceration. Year 2 significant predictors were similar to those of year 1: SDH, intraparenchymal fragment, craniotomy, craniectomy, seizure during acute hospitalization, and preinjury incarceration. Corrected concordance (C) statistics were 0.599, 0.747,and 0.716 for acute hospitalization, year 1, and year 2 models, respectively.SIGNIFICANCE: The prognostic model for PTS during acute hospitalization did not discriminate well. Year 1 and year 2 models showed fair to good predictive validity for PTS. Cranial surgery, although medically necessary, requires ongoing research regarding potential benefits of increased monitoring for signs of epileptogenesis, PTS prophylaxis, and/or rehabilitation/social support. Future studies should externally validate models and determine clinical utility.

Source: Traumatic Brain Injury Resource Guide – Research Reports – Prognostic models for predicting posttraumatic seizures during acute hospitalization, and at 1 and 2 years following traumatic brain injury

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[WEB SITE] Study explores development of epilepsy after brain injury – Health News

27/05/2015 10:15:00

Scientists at Newcastle University will carry out a pioneering study to look at the development of epilepsy following a serious brain injury.

Epilepsy can be triggered after traumatic brain damage such as a stroke, head trauma and some infections, yet no-one knows why some people go on to develop the life-threatening condition and others do not.

A team at Newcastle University has now been awarded more than £147,000 from leading charity, Epilepsy Research UK, to study epileptogenesis – a term used to describe how epilepsy arises after an injury to the brain.

Epileptogenesis involves a long and complex cascade of events, and what little is known about it mainly focuses on the latter stages, as seizures start to occur. Identifying what happens at the beginning, however, could lead to important breakthroughs and, ultimately, treatments to stop the serious condition developing.

The two-year project is being led by Dr Andrew Trevelyan, from Newcastle University’s Institute of Neuroscience, and it is one of only nine schemes nationwide in 2015 to receive a grant from the charity.

Dr Trevelyan (pictured) said: “We are delighted that Epilepsy Research UK are continuing to support our work.  Several years ago they provided me with the fellowship that helped to start my research group at Newcastle University, and which now includes eight people working full-time trying to understand what goes wrong during an epileptic seizure. That work led to key insights into how we identify from where in the brain the seizures arise.

“Now we want to understand how epilepsy might develop after an injury to the brain. This is a huge clinical problem because following such injuries, which include head trauma, strokes and some kinds of infection, there is a high risk of developing epilepsy.  But we cannot identify which people are at most risk, and even we could do so, we have no drugs to help them. What we need is the equivalent of the ‘morning after’ pill, to give people who have had a head injury or infection.”

Continue —>  Health News – Study explores development of epilepsy after brain injury.

 

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[WEB SITE] Clinical Approach to Posttraumatic Epilepsy

Abstract

Traumatic brain injury (TBI) is one of the most common causes of acquired epilepsy, and posttraumatic epilepsy (PTE) results in significant somatic and psychosocial morbidity. The risk of developing PTE relates directly to TBI severity, but the latency to first seizure can be decades after the inciting trauma. Given this “silent period,” much work has focused on identification of molecular and radiographic biomarkers for risk stratification and on development of therapies to prevent epileptogenesis. Clinical management requires vigilant neurologic surveillance and recognition of the heterogeneous endophenotypes associated with PTE. Appropriate treatment of patients who have or are at risk for seizures varies as a function of time after TBI, and the clinician’s armamentarium includes an ever-expanding diversity of pharmacological and surgical options. Most recently, neuromodulation with implantable devices has emerged as a promising therapeutic strategy for some patients with refractory PTE. Here, we review the epidemiology, diagnostic considerations, and treatment options for PTE and develop a roadmap for providers encountering this challenging clinical entity.

more –> Clinical Approach to Posttraumatic Epilepsy.

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