Archive for category Epilepsy
[WEB SITE] Epileptic Disorders – How to diagnose and treat post-stroke seizures and epilepsy – Educational
Stroke is one of the commonest causes of seizures and epilepsy, mainly among the elderly and adults. This seminar paper aims to provide an updated overview of post-stroke seizures and post-stroke epilepsy (PSE) and offers clinical guidance to anyone involved in the treatment of patients with seizures and stroke. The distinction between acute symptomatic seizures occurring within seven days from stroke (early seizures) and unprovoked seizures occurring afterwards (late seizures) is crucial regarding their different risks of recurrence. A single late post-stroke seizure carries a risk of recurrence as high as 71.5% (95% confidence interval: 59.7-81.9) at ten years and is diagnostic of PSE. Several clinical and stroke characteristics are associated with increased risk of post-stroke seizures and PSE. So far, there is no evidence supporting the administration of antiepileptic drugs as primary prevention, and evidence regarding their use in PSE is scarce.
For people with epilepsy, driving is a complex issue. Losing your license, trying to get it reinstated, and deciding whether it’s safe to drive can be frustrating and stressful. Some of us with epilepsy are unable to drive at all. It can help to talk about it with other people going through the same thing.
On MyEpilepsyTeam, the social network and online support group for those living with epilepsy, members talk about a range of personal experiences and struggles. Driving is one of the top 10 topics most discussed.
Here are some question-and-answer threads about driving:
Here are some conversations about driving:
Can you relate?
Have another topic you’d like to discuss or explore? Go to MyEpielpsyTeam today and start the conversation. You’ll be surprised just how many others may share similar stories.
Feel free to ask a question here.
[ARTICLE] Enhancing epilepsy self-management and quality of life for adults with epilepsy with varying social and educational backgrounds using PAUSE to Learn Your Epilepsy – Full Text
•PAUSE is a personalized epilepsy self-management (SM) education program.
•PAUSE was implemented in diverse and mostly underserved adults with epilepsy.
•Self-efficacy, frequency of SM behaviors, and QOL significantly improved over time.
•Personal negative impact of epilepsy significantly reduced over time.
•Greater improvement was seen in those with lower scores at baseline.
People with epilepsy (PWE) come from a wide variety of social backgrounds and educational skillsets, making self-management (SM) education for improving their condition challenging. Here, we evaluated whether a mobile technology-based personalized epilepsy SM education intervention, PAUSE to Learn Your Epilepsy (PAUSE), improves SM measures such as self-efficacy, epilepsy SM behaviors, epilepsy outcome expectations, quality of life (QOL), and personal impact of epilepsy in adults with epilepsy.
Recruitment for the PAUSE study occurred from October 2015 to March 2019. Ninety-one PWE were educated using an Internet-enabled computer tablet application that downloads custom, patient-specific educational programs from Epilepsy.com. Validated self-reported questionnaires were used for outcome measures. Participants were assessed at baseline (T0), the first follow-up at completion of the PWE-paced 8–12-week SM education intervention (T1), and the second follow-up at least 3 months after the first follow-up (T2). Multiple linear regression was used to assess within-subject significant changes in outcome measures between these time points.
The study population was diverse and included individuals with a wide variety of SM educational needs and abilities. The median time for the first follow-up assessment (T1) was approximately 4 months following the baseline (T0) and 8 months following baseline for the second follow-up assessment (T2). Participants showed significant improvement in all SM behaviors, self-efficacy, outcome expectancy, QOL, and personal impact of epilepsy measures from T0 to T1. Participants who scored lower at baseline tended to show greater improvement at T1. Similarly, results showed that participant improvement was sustained in the majority of SM measures from T1 to T2.
This study demonstrated that a mobile technology-based personalized SM intervention is feasible to implement. The results provide evidence that epilepsy SM behavior and practices, QOL, outcome expectation for epilepsy treatment and management, self-efficacy, and outcome expectation and impact of epilepsy significantly improve following a personalized SM education intervention. This underscores a greater need for a pragmatic trial to test the effectiveness of personalized SM education, such as PAUSE to Learn Your Epilepsy, in broader settings specifically for the unique needs of the hard-to-reach and hard-to-treat population of PWE.
Epilepsy, characterized by spontaneous recurrent seizures with unpredictable frequency, is a common and complex neurological disorder that affects the health and quality of life (QOL) of people with epilepsy (PWE) . It is the fourth most common chronic neurological disorder after migraines, Alzheimer’s disease, and Parkinson’s disease in terms of 1-year prevalence per 1000 in the general population . In 2015, approximately 1.2% of American adults reported living with epilepsy; 68.5% had seen a neurologist or epilepsy specialist; 93% were taking antiseizure medication (ASM), and, among those taking medication to control seizures, only 42.4% were seizure-free in the past year . Epilepsy, especially with uncontrolled seizures, poses an immense burden to the people who have it, caregivers, and the society due to a number of factors including associated developmental, cognitive, and psychiatric comorbidities; ASM side effects; higher injury and mortality rates; poorer QOL; and increased financial burden. An estimated 3.0% of global disability-adjusted life years (DALYs) were from neurological disorders in 2010, a quarter of which were from epilepsy; epilepsy was the second-most burdensome chronic neurologic disorder worldwide in terms of DALYs .
Self-management (SM) education has shown to improve SM skills & behaviors and QOL in many chronic diseases including heart disease, diabetes, asthma, and arthritis [5,6]. Barlow defines self-management as an individual’s ability to manage the symptoms, treatments, physical and psychological consequences, and life style changes inherent in living with a chronic condition . However, successful SM requires sufficient knowledge of the condition, its treatment, and necessary skills to perform SM activities. Like other chronic conditions, day-to-day management of epilepsy shifts from healthcare professionals to PWE. Epilepsy care demands active involvement of PWE in keeping up with the health effects of epilepsy and coping with social (e.g., family/friends, stigma, hobbies), health (e.g., seizure response/tracking, comorbidities such as depression/anxiety, sleep, safety, health literacy), employment (e.g., transportation, disability, absenteeism), and economic (e.g., cost of healthcare and medication) challenges. One can only self-manage their disease if they have the tools to do so, including knowledge, access to information relevant to their specific healthcare needs, and the ability to carry out the SM tasks needed for their condition. Evidence shows that many PWE are not knowledgeable about their disorder or often not educated about the risks of epilepsy, injury, and mortality [1,8]. Education needs also vary between individuals and subgroups of PWE. Women, in particular, may seek information on bone health and the effect of ASM on pregnancy or contraception, while older adults’ priorities may relate to fall safety and interactions of ASM with other medications. Existing evidence also reveals that, while patients with chronic diseases are willing to receive SM education materials, perceived information overload (i.e., too much or complex information) negatively influences their usage willingness . Patients with low health literacy are even more susceptible to information overload . The Institute of Medicine recognized SM education gaps for PWE and recommended (Recommendation 9) in its 2012 report, “Epilepsy Across the Spectrum: Promoting Health and Understanding,” to improve and expand educational opportunities for PWE and their families, as well as to ensure that all PWE and their families have access to accurate, clearly communicated educational materials and information .
Several studies have reported contradictory results after examining the efficacy of SM education interventions in improving PWE’s knowledge and understanding of epilepsy and QOL. The Modular Service Package Epilepsy study (MOSES) reported significant improvements in ASM tolerability, epilepsy knowledge, coping with epilepsy, and seizure frequency after 6 months following a 2-day SM education program . Self-management education for people with poorly controlled epilepsy [SMILE (UK)] adapted MOSES for use in the United Kingdom and did not find the 2-day course to be effective in improving QOL or secondary outcome measures (anxiety and depression), after 12 months . Though both MOSES and SMILE were randomized control trials (RCTs), MOSES included all adults with epilepsy whereas SMILE included only adults with chronic epilepsy who had two or more seizures in the prior 12 months. Another RCT compared the effectiveness of a multicomponent SM intervention consisting of five weekly, 2-hour group sessions each followed by a 2-hour group session after three weeks with usual care; they found no difference in measures of self-efficacy, though did find improvements in some epilepsy QOL domains and decreases in measures of ASM side effects . Other studies examining the efficacy of in-person, group-based, online or phone/internet SM interventions, including the Centers for Disease Control and Prevention-supported Managing Epilepsy Well (MEW) network programs, did show improvement in epilepsy SM and QOL [, , , , ].
In addition to existing group-based programs, which require permission to use and specialized training, there is a greater need for patient-centered and patient-specific individualized education interventions for epilepsy SM that are publicly available, cost-effective, and easily disseminated to clinics or in community. The PAUSE to Learn Your Epilepsy (hereafter referred to as “PAUSE”), a MEW network collaboration center, was developed and implemented to address the needs of all PWE, especially those in underserved populations. This program uses publicly available education information from the Epilepsy Foundation (EF) website, epilepsy.com, linked to a mobile technology-based PAUSE application to provide patient-centered personalized epilepsy SM lesson plan to PWE. Detailed information about PAUSE including study design, recruitment, intervention, and assessments has been published previously [19,20]. We reported significantly lower epilepsy SM practices and behaviors among PWE from an underserved population as compared to all PWE. In this paper, we sought to determine whether the PAUSE intervention significantly improves self-efficacy, SM behavior & skills, QOL, personal impact of epilepsy, and epilepsy outcome expectancies over time in adults with epilepsy. We also assessed whether perceived depression symptoms influence longitudinal changes in SM measures following the PAUSE intervention.[…]
June 10, 2020. Source: University Health Network
A new clinical research study has found that a Mozart composition may reduce seizure frequency in patients with epilepsy.
A new clinical research study by Dr. Marjan Rafiee and Dr. Taufik Valiante of the Krembil Brain Institute at Toronto Western Hospital, part of University Health Network, has found that a Mozart composition may reduce seizure frequency in patients with epilepsy.
The results of the research study, “The Rhyme and Rhythm of Music in Epilepsy,” was recently published in the international journal Epilepsia Open. It looks at the effects of the Mozart melody, “Sonata for Two Pianos in D Major, K. 448” on reducing seizures, as compared to another auditory stimulus — a scrambled version of the original Mozart composition, with similar mathematical features, but shuffled randomly and lacking any rhythmicity.
“In the past 15 to 20 years, we have learned a lot about how listening to one of Mozart’s compositions in individuals with epilepsy appears to demonstrate a reduction in seizure frequency,” says Dr. Marjan Rafiee, lead author on the study. “But, one of the questions that still needed to be answered was whether individuals would show a similar reduction in seizure frequency by listening to another auditory stimulus — a control piece — as compared to Mozart.”
The researchers recruited 13 patients to participate in the novel, year-long study. After three months of a baseline period, half of the patients listened to Mozart’s Sonata once daily for three months, then switched to the scrambled version for three months. The others started the intervention by listening to the scrambled version for three months, then switched to daily listening of Mozart.
Patients kept “seizure diaries” to document their seizure frequency during the intervention. Their medications were kept unchanged during the course of the study.
“Our results showed daily listening to the first movement of Mozart K.448 was associated with reducing seizure frequency in adult individuals with epilepsy,” says Dr. Rafiee. “This suggests that daily Mozart listening may be considered as a supplemental therapeutic option to reduce seizures in individuals with epilepsy.”
Epilepsy is the most common serious neurological disorder in the world, affecting approximately 300,000 Canadians and 50 million people worldwide.
Many experience debilitating seizures. The treatment is often one or more anti-seizure medications. But for 30 per cent of patients, the medications are not effective in controlling their seizures.
“As a surgeon, I have the pleasure of seeing individuals benefit from surgery, however I also know well those individuals for whom surgery is not an option, or those who have not benefitted from surgery, so, we are always looking for ways to improve symptom control, and improve quality of life for those with epilepsy,” says Dr. Taufik Valiante, senior author of the study and the Director of the Surgical Epilepsy Program at Krembil Brain Institute at UHN and co-Director of CRANIA.
“Like all research, ours raises a lot of questions that we are excited to continue to answer with further research and support from the epilepsy community.”
While these results are promising, the next step is to conduct larger studies with more patients, over a longer period of time.
- Marjan Rafiee, Kramay Patel, David M. Groppe, Danielle M. Andrade, Eduard Bercovici, Esther Bui, Peter L. Carlen, Aylin Reid, Peter Tai, Donald Weaver, Richard Wennberg, Taufik A. Valiante. Daily listening to Mozart reduces seizures in individuals with epilepsy: A randomized control study. Epilepsia Open, 2020; 5 (2): 285 DOI: 10.1002/epi4.12400
EAN Scientific Panel Neuro-oncology invites you to take part in their survey
Meningeomas and brain tumors may interfere with the ability to drive a vehicle in a number of ways. Seizures, cognitive impairment, motor dysfunction and visual field defects may all impair safe driving. Intracranial tumors are highly heterogenous, ranging from benign meningeomas that nevertheless may cause seizures, to high grade gliomas and brain metastasis. The clinician always considers seizure frequency, compliance and focal deficits when assessing the ability to drive for neurological patients. However, oncological prognosis, risk of recurrence and effects of treatment are factors unique to patients with intracranial tumors. These factors must be evaluated when deciding if or when a patient with a brain tumor or a meningeoma may drive. In addition, different medical professions may differ in awareness of the driving dilemma as well as in practice policy concerning this issue.
Clinical studies and reviews that address driving ability in patients with brain tumors are sparse. Most countries do not have national guidelines concerning this issue, and general as well as specific driving legislations vary between countries. In the absence of guidelines or legislation, most clinicians probably prohibit or allow driving on a case-by-case basis, or by adhering to legislation concerning epilepsy or neoplastic disease in general. The use of neuro-psychological evaluation or practical testing is unknown.
The EAN Scientific Panel of neuro-oncology wants to address this issue by performing a survey of national legislations and practice patterns among European neurologists. As a start, we aim to do a survey among the members of the Scientific Panels of Neuro-Oncology and Epilepsy.
The answers will be a guidance for whether there are inconsistences in clinical practice and reason to do a more extensive survey.
Thomas S1, Mehta MP, Kuo JS, Ian Robins H, Khuntia D. Current practices of driving restriction implementation for patients with brain tumors.
J Neurooncol. 2011l;103(3):641-7. doi: 10.1007/s11060-010-0439-7.
Louie AV, D’Souza DP, Palma DA, Bauman GS, Lock M, Fisher B, Patil N, Rodrigues GB.
Curr Oncol. 2012;19(3):e117-22.
Chan E, Louie AV, Hanna M, Bauman GS, Fisher BJ, Palma DA, Rodrigues GB, Sathya A, D’Souza DP.
Curr Oncol. 2013;20(1):e4-e12. doi: 10.3747/co.20.1198
Louie AV, Chan E, Hanna M, Bauman GS, Fisher BJ, Palma DA, Rodrigues GB, Warner A, D’Souza DP. Assessing fitness to drive in brain tumour patients: a grey matter of law, ethics, and medicine. Curr Oncol. 2013;20(2):90-6.
Mansur A1,2, Desimone A2, Vaughan S2, Schweizer TA1,2,3, Das S. To drive or not to drive, that is still the question: current challenges in driving recommendations for patients with brain tumours. J Neurooncol. 2018;137(2):379-385. doi: 10.1007/s11060-017-2727-y.
Most of the patients usually achieve seizure freedom under treatment with antiseizure medications (ASMs). Drug withdrawal in seizure-free patients is still one of the most challenging issues in the management of epilepsy. The decision-making process of whether the treatment should be discontinued must be based on the evaluation of possible long-term side effects of chronic treatment and, on the other hand, the risk of seizure relapse.
This review aims to describe and discuss possible predictors and risk factors for seizure relapse during and after discontinuation, according to the available literature evidence.
The most important risk factors for withdrawal failure are the etiology of the epilepsy syndrome and epilepsy-related factors, worsening or persistence of epileptiform abnormalities on EEG recordings at the time of discontinuation or during drug tapering, and brain MRI abnormalities.
Each single risk factor should be considered together with possible other concurrent predictors.
The decision to withdrawal antiseizure medication in seizure-free patients should be carefully planned and based on the evaluation of predictors. A discontinuation program should include tailored discussion with patients and family members and individualized decision, the taper schedule, and plans for monitoring during and after drug tapering.
Cognitive: deficits often occur in people with epilepsy (PWE). However, in Brazil, PWE might not undergo neurocognitive evaluation due to the low number of validated tests available and lack of multidisciplinary teams in general epilepsy outpatient clinics.
Objective: To correlate Brief Cognitive Battery-Edu (BCB-Edu) scores with epilepsy characteristics of 371 PWE.
Methods: Clinical and cognitive assessment (MMSE, BCB-Edu) of 371 PWE aged >18 years was performed. The clinical aspects of epilepsy were correlated with BCB-Edu data. Cognitive data of PWE were compared against those of 95 healthy individuals (NC), with p-<0.05.
Results: People with epilepsy had lower cognitive performance than individuals in the NC group. Cognitive aspects also differed according to epilepsy characteristics. Predictive factors for impairment in multiple cognitive domains were age and use of more than one antiepileptic drug (logistic regression; R2 Nagelkerke=0.135).
Conclusion: Worse cognitive performance was found in PWE on different domains. There was a relationship between cognitive impairment and the aspects of epilepsy. BCB-Edu proved to be effective as a cognitive assessment screening test for epilepsy in adults. Key words: epilepsy, Brief Cognitive Battery-Edu, cognition[…]
[Abstract + References] Antidepressant effect of vagal nerve stimulation in epilepsy patients: a systematic review
Vagal nerve stimulation (VNS) is an effective palliative therapy in drug-resistant epileptic patients and is also approved as a therapy for treatment-resistant depression. Depression is a frequent comorbidity in epilepsy and it affects the quality of life of patients more than the seizure frequency itself. The aim of this systematic review is to analyze the available literature about the VNS effect on depressive symptoms in epileptic patients.
Material and methods
A comprehensive search of PubMed, Medline, Scopus, and Google Scholar was performed, and results were included up to January 2020. All studies concerning depressive symptom assessment in epileptic patients treated with VNS were included.
Nine studies were included because they fulfilled inclusion criteria. Six out of nine papers reported a positive effect of VNS on depressive symptoms. Eight out of nine studies did not find any correlation between seizure reduction and depressive symptom amelioration, as induced by VNS. Clinical scales for depression, drug regimens, and age of patients were broadly different among the examined studies.
Reviewed studies strongly suggest that VNS ameliorates depressive symptoms in drug-resistant epileptic patients and that the VNS effect on depression is uncorrelated to seizure response. However, more rigorous studies addressing this issue are encouraged.
- 1.Chen Z, Brodie MJ, Liew D, Kwan P (2018) Treatment outcomes in patients with newly diagnosed epilepsy treated with established and new antiepileptic drugs a 30-year longitudinal cohort study. JAMA Neurol 75:279–286. https://doi.org/10.1001/jamaneurol.2017.3949Article PubMed Google Scholar
- 2.Spencer S, Huh L (2008) Outcomes of epilepsy surgery in adults and children. Lancet Neurol 7:525–537Article Google Scholar
- 3.De Tisi J, Bell GS, Peacock JL et al (2011) The long-term outcome of adult epilepsy surgery, patterns of seizure remission, and relapse: a cohort study. Lancet 378:1388–1395. https://doi.org/10.1016/S0140-6736(11)60890-8Article PubMed Google Scholar
- 4.Rathore C, Radhakrishnan K (2015) Concept of epilepsy surgery and presurgical evaluation. In: Epileptic disorders
- 5.Benbadis SR, Geller E, Ryvlin P, Schachter S, Wheless J, Doyle W, Vale FL (2018) Putting it all together: options for intractable epilepsy. Epilepsy Behav 88:33–38. https://doi.org/10.1016/j.yebeh.2018.05.030Article Google Scholar
- 6.Ben-Menachem E, Mañon-Espaillat R, Ristanovic R et al (1994) Vagus nerve stimulation for treatment of partial seizures: 1. A controlled study of effect on seizures. Epilepsia 35:616–626. https://doi.org/10.1111/j.1528-1157.1994.tb02482.xCAS Article PubMed Google Scholar
- 7.George R, Salinsky M, Kuzniecky R et al (1994) Vagus nerve stimulation for treatment of partial seizures: 3. Long-term follow-up on first 67 patients exiting a controlled study. Epilepsia. https://doi.org/10.1111/j.1528-1157.1994.tb02484.x
- 8.Elliott RE, Morsi A, Kalhorn SP, Marcus J, Sellin J, Kang M, Silverberg A, Rivera E, Geller E, Carlson C, Devinsky O, Doyle WK (2011) Vagus nerve stimulation in 436 consecutive patients with treatment-resistant epilepsy: long-term outcomes and predictors of response. Epilepsy Behav 20:57–63. https://doi.org/10.1016/j.yebeh.2010.10.017Article PubMed Google Scholar
- 9.Orosz I, McCormick D, Zamponi N, Varadkar S, Feucht M, Parain D, Griens R, Vallée L, Boon P, Rittey C, Jayewardene AK, Bunker M, Arzimanoglou A, Lagae L (2014) Vagus nerve stimulation for drug-resistant epilepsy: a European long-term study up to 24 months in 347 children. Epilepsia 55:1576–1584. https://doi.org/10.1111/epi.12762Article PubMed Google Scholar
- 10.Helmers SL, Wheless JW, Frost M, Gates J, Levisohn P, Tardo C, Conry JA, Yalnizoglu D, Madsen JR (2001) Vagus nerve stimulation therapy in pediatric patients with refractory epilepsy: retrospective study. J Child Neurol 16:843–848. https://doi.org/10.1177/08830738010160111101CAS Article PubMed Google Scholar
- 11.Boylan LS, Flint LA, Labovitz DL, Jackson SC, Starner K, Devinsky O (2004) Depression but not seizure frequency predicts quality of life in treatment-resistant epilepsy. Neurology 62:258–261. https://doi.org/10.1212/01.WNL.0000103282.62353.85CAS Article PubMed Google Scholar
- 12.Kim M, Kim Y-S, Kim D-H, Yang TW, Kwon OY (2018) Major depressive disorder in epilepsy clinics: a meta-analysis. Epilepsy Behav 84:56–69. https://doi.org/10.1016/j.yebeh.2018.04.015Article PubMed Google Scholar
- 13.Ajinkya S, Fox J, Lekoubou A (2020) Trends in prevalence and treatment of depressive symptoms in adult patients with epilepsy in the United States. Epilepsy Behav 105:106973. https://doi.org/10.1016/j.yebeh.2020.106973Article PubMed Google Scholar
- 14.Tombini M, Assenza G, Quintiliani L, Ricci L, Lanzone J, Ulivi M, di Lazzaro V (2020) Depressive symptoms and difficulties in emotion regulation in adult patients with epilepsy: association with quality of life and stigma. Epilepsy Behav 107:107073Article Google Scholar
- 15.Yuan T-F, Li A, Sun X, Arias-Carrión O, Machado S (2016) Vagus nerve stimulation in treating depression: a tale of two stories. Curr Mol Med 16:33–39. https://doi.org/10.2174/1566524016666151222143609CAS Article PubMed Google Scholar
- 16.Harden CL, Pulver MC, Ravdin LD, Nikolov B, Halper JP, Labar DR (2000) A pilot study of mood in epilepsy patients treated with vagus nerve stimulation. Epilepsy Behav 1:93–99. https://doi.org/10.1006/ebeh.2000.0046Article PubMed Google Scholar
- 17.Elger G, Hoppe C, Falkai P, Rush AJ, Elger CE (2000) Vagus nerve stimulation is associated with mood improvements in epilepsy patients. Epilepsy Res 42:203–210. https://doi.org/10.1016/S0920-1211(00)00181-9CAS Article PubMed Google Scholar
- 18.Rush AJ, Marangell LB, Sackeim HA, George MS, Brannan SK, Davis SM, Howland R, Kling MA, Rittberg BR, Burke WJ, Rapaport MH, Zajecka J, Nierenberg AA, Husain MM, Ginsberg D, Cooke RG (2005) Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial. Biol Psychiatry 58:347–354. https://doi.org/10.1016/j.biopsych.2005.05.025Article PubMed Google Scholar
- 19.Rush AJ, George MS, Sackeim HA, Marangell LB, Husain MM, Giller C, Nahas Z, Haines S, Simpson RK Jr, Goodman R (2000) Vagus nerve stimulation (VNS) for treatment-resistant depressions: a multicenter study∗∗See accompanying Editorial, in this issue. Biol Psychiatry 47:276–286. https://doi.org/10.1016/S0006-3223(99)00304-2CAS Article PubMed Google Scholar
- 20.Rush AJ, Sackeim HA, Marangell LB, George MS, Brannan SK, Davis SM, Lavori P, Howland R, Kling MA, Rittberg B, Carpenter L, Ninan P, Moreno F, Schwartz T, Conway C, Burke M, Barry JJ (2005) Effects of 12 months of vagus nerve stimulation in treatment-resistant depression: a naturalistic study. Biol Psychiatry 58:355–363. https://doi.org/10.1016/j.biopsych.2005.05.024Article PubMed Google Scholar
- 21.Liberati A, Altman DG, Tetzlaff J, Mulrow C, Gøtzsche PC, Ioannidis JPA, Clarke M, Devereaux PJ, Kleijnen J, Moher D (2009) The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. J Clin Epidemiol 62:e1–e34. https://doi.org/10.1016/j.jclinepi.2009.06.006Article PubMed Google Scholar
- 22.Klinkenberg S, van den Bosch CNCJ, Majoie HJM, Aalbers MW, Leenen L, Hendriksen J, Cornips EMJ, Rijkers K, Vles JSH, Aldenkamp AP (2013) Behavioural and cognitive effects during vagus nerve stimulation in children with intractable epilepsy–a randomized controlled trial. Eur J Paediatr Neurol 17:82–90. https://doi.org/10.1016/j.ejpn.2012.07.003Article PubMed Google Scholar
- 23.Ryvlin P, Gilliam FG, Nguyen DK, Colicchio G, Iudice A, Tinuper P, Zamponi N, Aguglia U, Wagner L, Minotti L, Stefan H, Boon P, Sadler M, Benna P, Raman P, Perucca E (2014) The long-term effect of vagus nerve stimulation on quality of life in patients with pharmacoresistant focal epilepsy: the PuLsE (Open Prospective Randomized Long-term Effectiveness) trial. Epilepsia 55:893–900. https://doi.org/10.1111/epi.12611CAS Article PubMed Google Scholar
- 24.Radloff LS (1977) The CES-D Scale. Appl Psychol Meas 1:385–401. https://doi.org/10.1177/014662167700100306Article Google Scholar
- 25.Gilliam FG, Barry JJ, Hermann BP, Meador KJ, Vahle V, Kanner AM (2006) Rapid detection of major depression in epilepsy: a multicentre study. Lancet Neurol 5:399–405. https://doi.org/10.1016/S1474-4422(06)70415-XArticle PubMed Google Scholar
- 26.Klinkenberg S, Majoie HJM, Van Der Heijden MMAA et al (2012) Vagus nerve stimulation has a positive effect on mood in patients with refractory epilepsy. Clin Neurol Neurosurg 114:336–340. https://doi.org/10.1016/j.clineuro.2011.11.016CAS Article PubMed Google Scholar
- 27.Chavel SM, Westerveld M, Spencer S (2003) Long-term outcome of vagus nerve stimulation for refractory partial epilepsy. Epilepsy Behav 4:302–309. https://doi.org/10.1016/S1525-5050(03)00109-4Article PubMed Google Scholar
- 28.Hoppe C, Helmstaedter C, Scherrmann J, Elger CE (2001) Self-reported mood changes following 6 months of vagus nerve stimulation in epilepsy patients. Epilepsy Behav 2:335–342. https://doi.org/10.1006/ebeh.2001.0194CAS Article PubMed Google Scholar
- 29.Hallböök T, Lundgren J, Stjernqvist K, Blennow G, Strömblad LG, Rosén I (2005) Vagus nerve stimulation in 15 children with therapy resistant epilepsy; its impact on cognition, quality of life, behaviour and mood. Seizure 14:504–513. https://doi.org/10.1016/j.seizure.2005.08.007Article PubMed Google Scholar
- 30.Spindler P, Bohlmann K, Straub H-B, Vajkoczy P, Schneider UC (2019) Effects of vagus nerve stimulation on symptoms of depression in patients with difficult-to-treat epilepsy. Seizure 69:77–79. https://doi.org/10.1016/j.seizure.2019.04.001Article PubMed Google Scholar
- 31.Ettinger AB, Weisbrot DM, Nolan EE, Gadow KD, Vitale SA, Andriola MR, Lenn NJ, Novak GP, Hermann BP (1998) Symptoms of depression and anxiety in pediatric epilepsy patients. Epilepsia 39:595–599. https://doi.org/10.1111/j.1528-1157.1998.tb01427.xCAS Article PubMed Google Scholar
- 32.Kerr MP, Mensah S, Besag F, de Toffol B, Ettinger A, Kanemoto K, Kanner A, Kemp S, Krishnamoorthy E, LaFrance WC Jr, Mula M, Schmitz B, van Elst L, Trollor J, Wilson SJ, International League of Epilepsy (ILAE) Commission on the Neuropsychiatric Aspects of Epilepsy (2011) International consensus clinical practice statements for the treatment of neuropsychiatric conditions associated with epilepsy. Epilepsia 52:2133–2138. https://doi.org/10.1111/j.1528-1167.2011.03276.xArticle PubMed Google Scholar
- 33.Tombini M, Assenza G, Quintiliani L, Ricci L, Lanzone J, de Mojà R, Ulivi M, di Lazzaro V (2019) Epilepsy-associated stigma from the perspective of people with epilepsy and the community in Italy. Epilepsy Behav 98:66–72. https://doi.org/10.1016/j.yebeh.2019.06.026Article PubMed Google Scholar
- 34.Dussaule C, Bouilleret V (2018) Psychiatric effects of antiepileptic drugs in adults. Gériatrie Psychol Neuropsychiatr du Viellissement 16:181–188. https://doi.org/10.1684/pnv.2018.0733Article Google Scholar
- 35.Pisani LR, Nikanorova M, Landmark CJ, Johannessen SI, Pisani F (2018) Specific patient features affect antiepileptic drug therapy decisions: focus on gender, age, and psychiatric comorbidities. Curr Pharm Des 23:5639–5648. https://doi.org/10.2174/1381612823666170926103631CAS Article Google Scholar
- 36.Assenza G, Lanzone J, Dubbioso R et al (2020) Thalamic and cortical hyperexcitability in juvenile myoclonic epilepsy. Clin Neurophysiol
- 37.Pellegrino G, Mecarelli O, Pulitano P, Tombini M, Ricci L, Lanzone J, Brienza M, Davassi C, di Lazzaro V, Assenza G (2018) Eslicarbazepine acetate modulates EEG activity and connectivity in focal epilepsy. Front Neurol 9. https://doi.org/10.3389/fneur.2018.01054
- 38.Rolle CE, Fonzo GA, Wu W, Toll R, Jha MK, Cooper C, Chin-Fatt C, Pizzagalli DA, Trombello JM, Deckersbach T, Fava M, Weissman MM, Trivedi MH, Etkin A (2020) Cortical connectivity moderators of antidepressant vs placebo treatment response in major depressive disorder. JAMA Psychiatry 94305:397. https://doi.org/10.1001/jamapsychiatry.2019.3867Article Google Scholar
- 39.Vecchio F, Miraglia F, Curcio G, Della Marca G, Vollono C, Mazzucchi E, Bramanti P, Rossini PM (2015) Cortical connectivity in fronto-temporal focal epilepsy from EEG analysis: a study via graph theory. Clin Neurophysiol 126:1108–1116. https://doi.org/10.1016/j.clinph.2014.09.019Article PubMed Google Scholar
- 40.Vecchio F, Miraglia F, Curcio G, Altavilla R, Scrascia F, Giambattistelli F, Quattrocchi CC, Bramanti P, Vernieri F, Rossini PM (2015) Cortical brain connectivity evaluated by graph theory in dementia: a correlation study between functional and structural data. J Alzheimers Dis 45:745–756. https://doi.org/10.3233/JAD-142484Article PubMed Google Scholar
- 41.Parker CS, Clayden JD, Cardoso MJ, Rodionov R, Duncan JS, Scott C, Diehl B, Ourselin S (2018) Structural and effective connectivity in focal epilepsy. NeuroImage Clin 17:943–952. https://doi.org/10.1016/j.nicl.2017.12.020Article PubMed Google Scholar
- 42.Saletu B, Anderer P, Saletu-Zyhlarz GM (2010) EEG topography and tomography (LORETA) in diagnosis and pharmacotherapy of depression. Clin EEG Neurosci 41:203–210CAS Article Google Scholar
- 43.Zhdanov A, Atluri S, Wong W, Vaghei Y, Daskalakis ZJ, Blumberger DM, Frey BN, Giacobbe P, Lam RW, Milev R, Mueller DJ, Turecki G, Parikh SV, Rotzinger S, Soares CN, Brenner CA, Vila-Rodriguez F, McAndrews MP, Kleffner K, Alonso-Prieto E, Arnott SR, Foster JA, Strother SC, Uher R, Kennedy SH, Farzan F (2020) Use of machine learning for predicting escitalopram treatment outcome from electroencephalography recordings in adult patients with depression. JAMA Netw Open 3:e1918377–e1918377Article Google Scholar
- 44.Romero-Osorio Ó, Gil-Tamayo S, Nariño D, Rosselli D (2018) Changes in sleep patterns after vagus nerve stimulation, deep brain stimulation or epilepsy surgery: systematic review of the literature. Seizure 56:4–8. https://doi.org/10.1016/j.seizure.2018.01.022Article PubMed Google Scholar
- 45.Murray BJ, Matheson JK, Scammell TE (2001) Effects of vagus nerve stimulation on respiration during sleep. Neurology 57:1523–1524CAS Article Google Scholar
- 46.Benca RM, Obermeyer WH, Thisted RA, Gillin JC (1992) Sleep and psychiatric disorders: a meta-analysis. Arch Gen Psychiatry 49:651–668CAS Article Google Scholar
- 47.Wu JC, Bunney WE (1990) The biological basis of an antidepressant response to sleep deprivation and relapse: review and hypothesis. Am J Psychiatry
- 48.Tononi G, Cirelli C (2012) Time to be SHY? Some comments on sleep and synaptic homeostasis. Neural Plast 2012:1–12. https://doi.org/10.1155/2012/415250Article Google Scholar
- 49.Assenza G, Pellegrino G, Tombini M, di Pino G, di Lazzaro V (2013) Delta waves increase after cortical plasticity induction during wakefulness. Clin Neurophysiol 124:e71–e72. https://doi.org/10.1016/j.clinph.2014.09.029Article Google Scholar
- 50.Assenza G, Di Lazzaro V (2015) A useful electroencephalography (EEG) marker of brain plasticity: delta waves. Neural Regen Res 10:1216–1217. https://doi.org/10.4103/1673-5374.162698Article PubMed Google Scholar
- 51.Wolf E, Kuhn M, Normann C, Mainberger F, Maier JG, Maywald S, Bredl A, Klöppel S, Biber K, van Calker D, Riemann D, Sterr A, Nissen C (2016) Synaptic plasticity model of therapeutic sleep deprivation in major depression. Sleep Med Rev 30:53–62Article Google Scholar
- 52.Sanacora G, Zarate CA, Krystal JH, Manji HK (2008) Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders. Nat Rev Drug Discov 7:426–437CAS Article Google Scholar
- 53.Di Pino G, Pellegrino G, Capone F et al (2016) Val66Met BDNF polymorphism implies a different way to recover from stroke rather than a worse overall recoverability. Neurorehabil Neural Repair 30:3–8. https://doi.org/10.1177/1545968315583721Article PubMed Google Scholar
- 54.Sen S, Duman R, Sanacora G (2008) Serum brain-derived neurotrophic factor, depression, and antidepressant medications: meta-analyses and implications. Biol Psychiatry 64:527–532CAS Article Google Scholar
- 55.Goldschmied JR, Gehrman P (2019) An integrated model of slow-wave activity and neuroplasticity impairments in major depressive disorder. Curr Psychiatry Rep 21:30Article Google Scholar
- 56.O’Leary OF, Ogbonnaya ES, Felice D et al (2018) The vagus nerve modulates BDNF expression and neurogenesis in the hippocampus. Eur Neuropsychopharmacol 28:307–316. https://doi.org/10.1016/j.euroneuro.2017.12.004CAS Article PubMed Google Scholar
- 57.Lang UE, Bajbouj M, Gallinat J, Hellweg R (2006) Brain-derived neurotrophic factor serum concentrations in depressive patients during vagus nerve stimulation and repetitive transcranial magnetic stimulation. Psychopharmacology 187:56–59. https://doi.org/10.1007/s00213-006-0399-yCAS Article PubMed Google Scholar
- 58.Hays SA, Rennaker RL, Kilgard MP (2013) Targeting plasticity with vagus nerve stimulation to treat neurological disease. Progress in brain research. Elsevier, In, pp 275–299Google Scholar
- 59.Capone F, Assenza G, Di Pino G et al (2015) The effect of transcutaneous vagus nerve stimulation on cortical excitability. J Neural Transm 122:679–685. https://doi.org/10.1007/s00702-014-1299-7Article PubMed Google Scholar
- 60.Kimberley TJ, Prudente CN, Engineer ND, Pierce D, Tarver B, Cramer SC, Dickie DA, Dawson J (2019) Study protocol for a pivotal randomised study assessing vagus nerve stimulation during rehabilitation for improved upper limb motor function after stroke. Eur Stroke J 4:363–377Article Google Scholar
[ARTICLE] Prediction of the Recurrence Risk in Patients With Epilepsy After the Withdrawal of Antiepileptic Drugs – Full Text PDF
Many seizure-free patients who consider withdrawing from antiepileptic drugs (AEDs) hope to discontinue treatment to avoid adverse effects. However, withdrawal has certain risks that are difficult to predict. In this study, we performed a literature review, summarized the causes of significant variability in the risk of postwithdrawal recurrent seizures, and reviewed study data on the age at onset, cause, types of seizures, epilepsy syndrome, magnetic resonance imaging (MRI) abnormalities, epilepsy surgery, and withdrawal outcomes of patients with epilepsy. Many factors are associated with recurrent seizures after AED withdrawal. For patients who are seizure-free after treatment, the role of an electroencephalogram (EEG) alone in ensuring safe withdrawal is limited. A series of prediction models for the postwithdrawal recurrence risk have incorporated various potentially important factors in a comprehensive analysis. We focused on the populations of studies investigating five risk prediction models and analyzed the predictive variables and recommended applications of each model, aiming to provide a reference for personalized withdrawal for patients with epilepsy in clinical practice.
Russell A. Reeves; Richard Gorniak.Author Information
A seizure is a transient occurrence of abnormal excessive or synchronous neuronal activity in the brain. Seizures manifest in different ways based on the anatomic regions of hyperactive neuronal activity. For example, patients may develop focal symptoms due to abnormal activity in the temporal lobe, whereas global signs represent widespread aberrant neuronal activity. Seizures may initially manifest as focal symptoms with subsequent generalization to the remaining cortex. Furthermore, patients may or may not lose consciousness during a seizure, depending on whether or not the limbic structures and brainstem are involved.
Seizure activity in the brain can be caused by numerous anatomic abnormalities such as tumors, infection, inflammatory/autoimmune processes, vascular malformations, stroke, trauma, cortical malformations/dysplasias, gray matter heterotopias, mesial temporal sclerosis, encephaloceles or other acquired or developmental abnormalities. Patients may have seizures due to medical factors such as metabolic derangement, withdrawal, hyperthermia, or toxins as well. However, patients may also suffer from recurrent seizures without known underlying etiology. Patients with at least two unprovoked seizures separated by at least 24 hours may be diagnosed with epilepsy.
Seizure management relies on the treatment of the underlying etiology and/or anti-seizure drug therapy, and, for most patients, part of the evaluation for the underlying cause requires diagnostic workup with imaging. Various diagnostic imaging modalities may be used for patients with recurrent seizures, many adding complementary information for the care of these patients. Furthermore, diagnostic imaging can provide information that localizes epileptogenic lesions in patients with refractory epilepsy that require surgical intervention, potentially obviating the need for invasive electroencephalography (EEG). As such, understanding the uses and limitations of each modality is of critical importance for the treatment of these patients.Go to:
Seizures can manifest as a result of a wide variety of anatomic abnormalities within the brain as well as toxic or metabolic derangements. Anatomic abnormalities that result in seizures can be located nearly anywhere within the brain, though usually involve the neocortex or mesial temporal region, particularly the hippocampi. Because of this, imaging is typically employed to adequately scrutinize all structures of the brain with careful attention directed towards the hippocampi.
The hippocampi are situated within the medial aspect of the temporal lobes bilaterally and occupy the medial floor of the lateral ventricles. They are a core limbic structure, responsible for learning and memory formation. The hippocampus is composed of two distinct gray matter structures known as the cornu ammonis and the dentate gyrus. Anterior to posterior it is divided into the head, body, and tail segments. On coronal imaging, the hippocampal head is characterized by digitations which give its superior surface an undulating contour. The hippocampal body can be recognized by its “jelly roll” or “swiss roll” appearance of the interlocking dentate gyrus, Ammon horn, and intervening strata. White matter tracts from the hippocampus traverse its superior surface, forming the alveus, which condenses into bundles called fimbria, which continue posteriorly as the fornix. The fornix terminates just off of midline within the mamillary body; this white matter tract plays a vital role in the Papez circuit. Adjacent to the head of the hippocampus lies the amygdala and entorhinal cortex.
Hippocampal sulcus remnant cysts and incomplete hippocampal inversion are developmental variants in the hippocampus, which should not be confused with pathology.
The bilateral and symmetric nature of the hippocampi allows for direct comparison during imaging. Unilateral abnormalities may shed light on the underlying etiology of a patient’s refractory epilepsy. However, gross abnormalities of the hippocampi may be bilateral in up to 10% of cases. Additionally, hippocampal lesions can be associated with extra hippocampal epileptogenic lesions. Proper identification of hippocampal abnormalities is critical for patients with medically refractory epilepsy, as surgical resection of the epileptogenic focus is the standard treatment for these patients. Go to:
Plain radiography represents the earliest form of diagnostic imaging. X-rays are used to generate image contrast based on differences in tissue attenuation. Because the soft tissues of the brain exhibit similar attenuation characteristics, the use of plain radiographs to evaluate for structural lesions within the brain is extremely limited. As such, plain radiographs play no role in the diagnostic workup for patients suffering from seizures. Go to:
Computed tomography (CT) utilizes helically acquired x-rays and postprocessing techniques to generate cross-sectional images. Modern CT scanners receive x-ray attenuation data in a nearly isotropic manner, which allows the generation of voxels that can be reconstructed in coronal, sagittal, and three-dimensional formats. As with the limitations of plain radiographs, the brain soft tissues are poorly evaluated on routine CT examinations because the attenuation characteristics of the brain soft tissues and many pathologies are similar. Iodinated intravenous contrast can highlight the vascular structures of the brain or areas of enhancement. Seizure activity may result in increased cortical enhancement due to increased cortical perfusion but is typically an unanticipated observation in patients that are not suspected of seizures rather than a sought out diagnostic finding. As such, CT plays a limited role in the imaging workup of patients considering epilepsy surgery.Go to:
Magnetic resonance imaging (MRI) is the preferred diagnostic modality for patients with seizures. MRI offers excellent signal-to-noise and contrast within the brain. Seizures that are attributed to known metabolic arrangements may not necessarily require further diagnostic studies; however, nearly every patient that suffers from an unexplained seizure should undergo an MRI to evaluate for underlying structural brain abnormalities. Virtually any MRI can be used to assess for mass lesions within the brain, but high field strength scanners, more than 1.5 Tesla, should be used for evaluating patients with epilepsy when possible. Specialized imaging protocols have been developed which optimize subtle signal intensity alterations and anatomic abnormalities within the hippocampi. This is particularly critical for patients undergoing evaluation for surgical management of intractable epilepsy, as small abnormalities within the hippocampi may be undetectable without specialized techniques.
Patients with medically intractable partial complex epilepsy are most commonly affected by mesial temporal sclerosis (MTS). MRI is essential in identifying MTS, as it has characteristic findings of volume loss and increased T2/FLAIR signal intensity due to hippocampal neuronal cell death and gliosis. There may also be associated atrophy within the ipsilateral amygdala, entorhinal cortex, fornix, or mammillary body. Identifying these subtle differences requires the acquisition of a 1 mm isotropic series with T1 weighting and FLAIR. Reconstructions must be performed perpendicular to the plane of the hippocampi to allow adequate side-to-side comparison. A coronal T2-weighted series should also be obtained with 2 mm slices and sub-mm in-plane resolution to allow both side-to-side comparisons of the hippocampi as well as to delineate the typical internal architecture. These sequences are also useful in detecting focal cortical dysplasias, gray matter heterotopias, and small encephaloceles.
Intravenous contrast may improve the utility of MRI depending on the clinical circumstances. Gadolinium-based contrast agents act to increase the T1 signal, highlighting vascular structures and blood-brain barrier abnormalities. A common approach to patients with seizures is to perform non-enhanced MRI sequences initially and only to administer contrast if the nonenhanced study requires further investigation. That said, patients with intractable epilepsy undergoing evaluation for possible surgical treatment do not routinely require intravenous contrast. Finally, it should be noted that MRI does not require the use of ionizing radiation, where this is a necessary consequence of CT imaging.
Although MRI can be useful for the detection of underlying structural lesions, MRI can also be used to evaluate brain physiology. In patients being evaluated for surgical resection, functional MRI (fMRI) is useful in identifying the language laterality and can, in many instances, replace the invasive Wada test.Go to:
Ultrasound utilizes high-frequency sound waves to generate diagnostic images. The advantage of ultrasound is that no ionizing radiation is required for its use. Unfortunately, calcified structures such as the bones of the calvarium preclude adequate sound transmission for an ultrasound to be useful in diagnostic imaging of the brain. As such, ultrasound plays no role in the evaluation of patients with seizures.Go to:
Nuclear imaging plays an adjunctive role in seizure imaging. Due to its technical limitations, nuclear studies are not considered to be first-line imaging modalities for patients with seizures. However, there are circumstances where nuclear imaging studies add complementary information to that of traditional cross-sectional imaging such as MRI.
Positron emission tomography with fluorodeoxyglucose (FDG-PET) allows for metabolic imaging within the brain. The fluorodeoxyglucose is actively taken up by neuronal cells, in an activation-dependent distribution. Thus, FDG uptake is increased in parts of the brain during a seizure, and conversely, uptake is decreased within the seizure focus interictally. These temporal factors contribute significant limitations to FDG-PET imaging, making it technically challenging to obtain the images either during a seizure or immediately after. Furthermore, PET imaging has low resolution compared to CT and MRI, with a resolution limit of approximately 1 cm. Because of this limitation, FDG-PET imaging is often co-registered with either CT or MRI data to provide useful colocalization between the foci of metabolic abnormality and anatomic structures. However, in patients with suspected temporal lobe epilepsy, interictal FDG-PET is frequently useful in seizure localization, especially in patients with normal MRI scans.
Single-photon emission CT (SPECT) produces images through the use of radioisotope production of gamma rays. These radioisotopes are linked to parent molecules, known as radiopharmaceuticals. Radiopharmaceuticals such as Tc99m-HMPAO do not cross the blood-brain barrier and act as perfusion agents within the brain. Through rapid intravenous administration of a radiopharmaceutical within 90 seconds of seizure onset, regions of increased perfusion within the brain can be identified, which correspond to the seizure focus. Similarly, postictal administration results in decreased cerebral blood flow in the epileptogenic center. Subtracting ictal and interictal SPECT studies with coregistration to an MRI (SISCOM) improves the utility of SPECT imaging. However, radiopharmaceutical administration within 90 seconds of seizure onset is technically challenging, limiting the utility of SPECT imaging. This modality is most commonly used when conventional MRI imaging, electroencephalograms, and other adjunct tests are equivocal in seizure focus localization.Go to:
As described previously, both CT and magnetic resonance angiography are uncommonly performed in patients with seizure disorders. A notable exception includes patients who are suspected of having underlying ischemic or vascular disease within the head or neck. Outside of these narrow indications, cross-sectional angiography is seldomly performed during the routine seizure workup. Additionally, more invasive tests such as catheter-based angiography may be used for further delineation of vascular pathology but are rarely required. Before surgical interventions, vascular imaging may be warranted, but this is dependent on the individual clinical scenario.Go to:
Before the advent of modern CT and MRI scanners, patient positioning was of critical importance to obtain accurate and useful diagnostic images. However, modern scanners can acquire data in an isotropic fashion, which permits post imaging processing and reconstruction. Prior to this technical development, adjusting for differences in patient positioning was not easily performed. Nearly all studies are performed supine with the patient lying in a comfortable position. This is particularly relevant for MRI studies since image quality is significantly degraded with even small patient movements; as such, ensuring that a patient can maintain a particular position long enough for image acquisition is of considerable technical importance. Similar principles also apply to FDG-PET and SPECT imaging studies.Go to:
Gaining a full understanding of the various imaging modalities for patients who suffer from seizures is of critical importance. Nearly one-third of patients with epilepsy will not achieve remission with antiepileptic medications alone, and many patients will have underlying anatomic abnormalities that may offer a surgical cure. Specialized MRI protocols are necessary to thoroughly scrutinize the hippocampi, as many of these patients will develop or demonstrate mesial temporal sclerosis. More subtle abnormalities, such as focal cortical dysplasias, require advanced postprocessing techniques and expert neuroradiologists for a full evaluation. Patients with structural lesions concordant with seizure localization on EEG should receive a preoperative fMRI to map regions of eloquent neocortex. In cases where no anatomic lesion is identified on MRI, FDG-PET may offer complementary information, revealing areas of hypometabolism or help guide the placement of intracranial EEG electrodes. Finally, if PET fails to aid localization, ictal, and interictal SPECT imaging can be performed to evaluate dynamic changes in cerebral perfusion, helping direct the placement of intracranial EEG electrodes for definitive localization of an epileptogenic focus. Further advanced imaging equipment and techniques are under development and available at a limited number of institutions, including the use of 7T MRI. This increased field strength offers an opportunity to detect even more subtle lesions, potentially increasing overall imaging sensitivity and providing curative surgery to a greater proportion of patients. Advanced neuroimaging will continue to play an evolving role in the surgical management of patients with medication-refractory epilepsy. Go to:
To access free multiple choice questions on this topic, click here.