<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2019-001_s_001"><h3>Introduction.</h3><p>So far, cardiac sympathetic dysfunction, demonstrated in pharmacoresistant epilepsy patients with ictal bradycardia or asystole by I-123 metaiodobenzylguanidine (I-123 MIBG) imaging has been attributed to repeated occurrence of seizure activity.</p></sec><sec id="j_joepi-2019-001_s_002"><h3>Aim.</h3><p>Discussion of the mechanisms of cardiac sympathetic dysfunction associated with ictal asystole under consideration of a case with new onset epilepsy.</p></sec><sec id="j_joepi-2019-001_s_003"><h3>Materials and methods.</h3><p>We describe the occurrence of a cardiac asystole during a complex-partial seizure in an antiepileptic-drug-naïve patient with new-onset symptomatic epilepsy.</p></sec><sec id="j_joepi-2019-001_s_004"><h3>Results.</h3><p>MIBG imaging showed reduced tracer accumulation in cardiac sympathetic nerve endings in this patient with right parietotemporal glioblastoma.</p></sec><sec id="j_joepi-2019-001_s_005"><h3>Discussion and Conclusion.</h3><p>To our knowledge, this is the first report of impaired cardiac sympathetic function in new-onset symptomatic epilepsy without antiepileptic drug treatment. MIBG imaging should be considered in patients with ictal bradycardia or asystole.</p></sec></abstract>

Ictal asystole with reduced cardiac sympathetic function in new-onset symptomatic epilepsy

<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2019-002_s_001"><h3>Introduction</h3><p>In 2014, a group of Polish epilepsy experts published recommendations for antiepileptic drug (AED) use in adults with epilepsy. Selection of AEDs was based on the registration and reimbursement status in Poland, evidence of efficacy, and the personal views and experiences of the epilepsy practitioners.</p></sec><sec id="j_joepi-2019-002_s_002"><h3>Method</h3><p>In 2018 previous recommendations were reviewed by the ad hoc group consisting of the authors of the original paper and additional epilepsy experts. As a result of joint work and reaching a consensus, an updated version of these recommendations has been prepared.</p></sec><sec id="j_joepi-2019-002_s_003"><h3>Discussion and recommendations</h3><p>This update focuses on the epileptic seizure type treatment recommendations for initial monotherapy and add-on treatment in adult patients. Some new relevant aspects of treatment with AEDs are addressed, including information on the safety of valproic acid (VPA) in women of childbearing potential.</p></sec></abstract>

Recommendations of the Polish Society of Epileptology for the treatment of epileptic seizure in adult patients in Poland: an update

<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2019-003_s_001"><h3>Background.</h3><p>The concept of rational polytherapy implies using a combination of antiepileptic drugs with synergistic effect, which in turn, may result in additive or reduced toxicity. This concept is not consensually accepted.</p></sec><sec id="j_joepi-2019-003_s_002"><h3>Aim.</h3><p>To present evidence in favour and against rational polytherapy.</p></sec><sec id="j_joepi-2019-003_s_003"><h3>Methods.</h3><p>Narrative literature review on PubMed and Medline databases using the following terms: epilepsy treatment, rational therapy/polytherapy, supraadditive treatment, drug-resistant epilepsy treatment. Cited references within selected articles were also evaluated.</p></sec><sec id="j_joepi-2019-003_s_004"><h3>Results.</h3><p>Against rational therapy is the evidence of clinical efficacy of the use of antiepileptic drugs with the same mechanism of action and without increased side-effects. Rational therapy may fail because while the addition of one antiepileptic drug to others with the same or different mechanisms of action leads to additive therapeutic efficacy, it also leads to more side effects. The evidence for the robust, unique, true synergism found between valproate and lamotrigine is questionable because the two drugs together may lead to complex pharmacokinetic interactions jeopardizing a consistent interpretation of the data. Data from studies with antiepileptic drugs with multiple mechanisms of action may be questionable because the same mechanism of action might not be responsible for drug efficacy or toxicity in different patients. Favouring rational therapy is the evidence that genetic animal models of seizures and drug-related neurotoxicity are ideal to evaluate the efficacy and toxicity of drug combinations, and that the most successful experimental combination of two antiepileptic drugs would be the one with a single mechanism of action and the other with a multiple mechanism of action.</p></sec><sec id="j_joepi-2019-003_s_005"><h3>Conclusion.</h3><p>Rational therapy is a sub-optimal, but worth being attempted strategy for the use of antiepileptic drugs in combination.</p></sec></abstract>

Rational polytherapy: Myth or reality?

<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2019-004_s_001"><h3>Introduction</h3><p>It is estimated that 30% of people with epilepsy continue to have seizures despite treatment. The approval of many new antiseizure drugs during the past two decades has not substantially reduced the proportion of patients with medically refractory disease. Patients need new treatments. Many families choose to try alternative therapy options. An abundance of preclinical evidence and anecdotal human data support the use of cannabinoids in the treatment of epilepsy.</p></sec><sec id="j_joepi-2019-004_s_002"><h3>Aim.</h3><p>The present review paper aims to present the current state of knowledge regarding the effectiveness and safety of cannabinoids in the treatment of epilepsy.</p></sec><sec id="j_joepi-2019-004_s_003"><h3>Material and methods</h3><p>This review covers the most relevant and recent papers identified using the Pub-Med database.</p></sec><sec id="j_joepi-2019-004_s_004"><h3>Results and discussion</h3><p>Cannabidiol has shown anticonvulsant activity in many acute animal models of seizures. Recently three well controlled randomized trails focused on the potential usefulness of cannabinoids in the treatment of epilepsy have been published. Based on these publications, the US Food and Drug Administration approved in 2018 a purified, plant-derived cannabinoid for the treatment of seizures in patients with Dravet syndrome and Lennox-Gastaut syndrome.</p></sec><sec id="j_joepi-2019-004_s_005"><h3>Conclusion.</h3><p>An abundance of preclinical evidence and anecdotal human data support the use of cannabinoids in the treatment of epilepsy. Recently purified, plant-derived cannabinoid was approved for the treatment of seizures in patients with Dravet syndrome and Lennox-Gastaut. Additional data are needed to determine the long-term efficacy and safety of cannabidiol for severe epilepsy syndromes</p></sec></abstract>

Cannabinoids in the treatment of epilepsy – an updated review

<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2019-005_s_001"><h3>Background.</h3><p>The role of neurobiological and immunity variables in the genesis of psychopathological syndromes in patients with partial epilepsy is not properly understood. It concerns also the role of handedness.</p></sec><sec id="j_joepi-2019-005_s_002"><h3>Aim</h3><p>The study was carried out in order to find the influence of clinical (neurobiological) and immune variables on co-morbid psychopathological syndromes in patients with epilepsy separately for right-handers and left-handers.</p></sec><sec id="j_joepi-2019-005_s_003"><h3>Material and Methods.</h3><p>Ninety two (92) patients with epilepsy were recruited into the study. Among the studied patients were 85 right-handers and 7 left-handers. The data on frequency of each seizure semiotics, the assessment of seizures severity and the length of remission were used as main basic clinical variables. Assessment of psychopathological status of patients has been performed by using of Symptom Check List-90 (SCL-90). The amounts of different lymphocytes clusters also were calculated. The product moment correlation analysis was used to find the possible relationships separately for right-handers and left-handers.</p></sec><sec id="j_joepi-2019-005_s_004"><h3>Results.</h3><p>In the right-handers group only significant correlation between the focal motor seizure frequency and value of Hostility construct of SCL-90 scale (r = 0.284, p = 0.045), and between the total count of T-lymphocytes and expression of Psychoticism, SCL-90 (r =−0.271, p = 0.049). In the left-handers group stochastically significant correlations between focal seizures with impaired awareness (FSIA), focal to bilateral tonic-clonic seizures (FBTCS) and National Hospital Seizure Severity Scale (NHS3) score with 5 SCL-90 constructs were revealed. The regulatory index (CD4/CD8 ratio) correlates positively with Obsessions (r = 0.780, p = 0.039); Interpersonal sensitivity (r = 0.80, p = 0.031); Depression (r = 0.834, p = 0.02); Aggression (r = 0.926, p = 0.003); Paranoid ideations (r = 0.873, p = 0.01) and Psychoticism (r = 0.913, p = 0.004).</p></sec><sec id="j_joepi-2019-005_s_005"><h3>Conclusion.</h3><p>Neurobiological and immune variables determine the psychopathological constructs strictly in left-handers.</p></sec></abstract>

The influence of clinical and immune variables on psychopathological syndromes in partial epilepsies in relation to handedness

<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2019-006_s_001"><h3>Background.</h3><p>Glucose transporter type 1 deficiency syndrome (GLUT1-DS) is a treatable metabolic disorder caused by mutation in the <italic>SLC2A1</italic> gene. The functional deficiency of the GLUT1 protein leads to impaired glucose transport into the brain, resulting in a spectrum of neurological phenotypes. The most severe classic phenotype comprises infantile-onset epileptic encephalopathy associated with delayed development, acquired microcephaly, motor coordination disturbances, and spasticity. The less severe clinical features, such as paroxysmal exercise-induced dystonia with or without epileptic seizures, are also observed.</p></sec><sec id="j_joepi-2019-006_s_002"><h3>Aim.</h3><p>Hypothesis, that one possible treatment option entails intrathecal injection of glucose.</p></sec><sec id="j_joepi-2019-006_s_003"><h3>Material and Methods.</h3><p>We describe a woman, who was diagnosed as having epilepsy and treated for years with different antiepileptic drugs with no clinical effect. She had only two generalized tonic clonic seizures in her life. The patient suffered from increasing frequency of the paroxysmal involuntary movements of lower limbs, leading to gait disturbances and falls, which were misdiagnosed as epileptic seizures. The jerks of the head and limbs were observed from the first months of her life. The symptoms were provoked by stress and exertion. Additionally, mild intellectual disability was noted during her growth.</p></sec><sec id="j_joepi-2019-006_s_004"><h3>Results.</h3><p>Glucose concentrations in cerebrospinal fluid were low. The <italic>SLC2A1</italic> gene analysis resulted in the identification of a heterozygous missense mutation p.Arg333Trp. identification. The diagnosis of GLUT1-DS was confirmed.</p></sec><sec id="j_joepi-2019-006_s_005"><h3>Conclusion.</h3><p>Delayed diagnosis resulted in many problems with the acceptance of the ketogenic diet, which is considered the treatment of choice in GLUT1 deficiency syndromes. To our knowledge, this is the first case report of GLUT1-DS diagnosis occurring in adulthood and published in Poland.</p></sec></abstract>

Glucose transporter type 1 deficiency syndrome (GLUT1-DS) – delayed diagnosis and treatment. A case report

In memoriam

AHEAD OF PRINT

Volume 32 (2024): Issue 1 (May 2024)

Volume 31 (2023): Issue 1 (November 2023)

Volume 29 (2021): Issue 1 (July 2021)

Volume 28 (2020): Issue 1 (December 2020)

Volume 27 (2019): Issue 1 (February 2019)

Volume 26 (2018): Issue 1-2 (June 2018)

Volume 25 (2017): Issue 1-2 (December 2017)

Volume 24 (2016): Issue 2 (December 2016)

Volume 24 (2016): Issue 1 (June 2016)

Volume 23 (2015): Issue 2 (December 2015)

Volume 23 (2015): Issue 1 (June 2015)

Volume 22 (2014): Issue 2 (December 2014)

Volume 22 (2014): Issue 1 (June 2014)

Volume 21 (2013): Issue 2 (December 2013)

Volume 21 (2013): Issue 1 (June 2013)

Journal of Epileptology

 The Journal of Epileptology – published since 2013 - is an international, open access peer reviewed scientific journal that publishes articles of clinical and experimental epilepsy.   The following categories of epilepsy related topics are accepted for publications: medical hypotheses, basic research, clinical research, reviews and special reports, product investigation, diagnostic and medical technology, case reports, letters to Editor, reports from international and local activities.   The aim of the journal is to widen the international community of readers, research and clinicians interested in various aspects of epilepsy and disseminate interdisciplinary knowledge in all fields related to epilepsy.   The Journal of Epileptology is owned by the Foundation of Epileptology which was established in 1993 by Professor Jerzy Majkowski. The Foundation of Epileptology is the first non-governmental organization in Poland whose priority is to improve the quality of life of persons with epilepsy by improving the diagnostic and therapeutic skills of doctors and by shaping a positive attitude to epilepsy among the public. The Foundation, led by this idea, brings together physicians, psychologists, scientists and academics, social activists and other people who wish to contribute to the development of epileptology and thus provide medical assistance to persons with epilepsy.     About Society   The Foundation of Epileptology was established in 1993 by Professor Jerzy Majkowski who also founded the Department of Neurology and Epileptology at the Medical Centre for Postgraduate Education (CMKP) in 1988. The Foundation of Epileptology is the first non-governmental organisation in Poland to have as its priority the improvement of quality of life of epileptic patients by means of furthering doctors' diagnostic and therapeutic mastery and developing a positive approach to epilepsy among the general public. The Foundation, led by this idea, attracts physicians, psychologists, researchers and academics, social activists and other persons who wish to contribute to the development of epileptology and thereby bring medical assistance to people suffering from epilepsy. The Foundation of Epileptology was registered in the Foundation Register of the District Court for the Municipality of Warsaw on 16 March 1993 and thereby acquired legal status. The Founder appointed the Foundation Council and the Foundation Executive Committee.   The Foundation of Epileptology co-operates with the Polish Society of Epileptology, the Warsaw-based Society for Victims of Epilepsy and their Friends "Calm Head" (Spokojna Głowa) and other domestic and foreign organisations with similar goals. The Foundation of Epileptology is a member of the European Epilepsy Academy (EUREPA) and Professor Majkowski is co-organiser and member of the first Executive Committee and is now a member of the EUREPA Research Advisory Committee. The Executive Committee of the Polish Society of Epileptology shares its headquarters with the Epilepsy Foundationv   Archiving   The archiving of issues published from 2013 to 2017 will occur, and thus all issues published in the current form of the Journal will become available on-line. However, the issues published quarterly under the journal’s earlier name of Epileptologia during 1993 to 2012 will be successively attached and published on journal’s website www.journal-epileptology.com.   Sciendo archives the contents of this journal in Portico - digital long-term preservation service of scholarly books, journals and collections.   Plagiarism Policy   The editorial board is participating in a growing community of Similarity Check System's users in order to ensure that the content published is original and trustworthy. Similarity Check is a medium that allows for comprehensive manuscripts screening, aimed to eliminate plagiarism and provide a high standard and quality peer-review process. 