Summary:Purpose: A controversy currently exists regarding the significance of dissociation and conversion in the pathogenesis of pseudoepileptic seizures. After the abolition of the term "hysterical neurosis" from the current diagnostic systems, these seizures were diagnosed as either Dissociative Disorders (ICD-10) or in the DSM IV as Somatoform disorder, most often of conversion type. Recent studies of patients with Dissociative Disorders found that most patients also had conversion symptoms.Methods: In the present study, 60 patients of an outpatient clinic for epilepsy were assessed for the presence of dissociative symptoms and general psychopathologic symptoms by using the German version of the Dissociative Experience Scale (DES) and the Symptom Check List (SCL-90-R).Results: The patients with pseudoepileptic seizures showed a significantly higher incidence of dissociation (p < 0.0098) and general psychopathologic symptoms (p < 0.0083). Depression, anxiety, and obsession were dominating psychopathologic symptoms in all patients.Conclusions: The significantly higher incidence of dissociation in the patients with pseudoepileptic seizures suggests dissociation in the pathogenesis of these seizures.
In patients with epilepsy, previously not satisfactorily treated with CBZ or OXC, conversion to TPM may result in an improvement in seizure control as well as in quality of life.
Epilepsy and long QT-syndromeCase reportn Abstract In a Kurdish female patient, an idiopathic long QTsyndrome (LQTS) was diagnosed after twenty years of symptoms. Within two generations of her extended family, there were fifteen afflicted members. With this case, we present an uncommon occurrence of a seizure disorder with syncope and epileptic seizures from LQTS. A newly discovered mutation of the KCNQ1-protein seems to be responsible for the combined appearance of symptoms from cardiac arrhythmias and epileptic seizures. We discuss the literature with regard to the complex differential diagnosis of LQTS with syncope implied loss of consciousness and postural tone, syncopal myoclonus and grand mal seizures.
gegenfiber haben eine Reihe anderer Autoren, vor Allem Emmerich 1, 9 ferner Bonome z und in den letzten Jahren RSmer 3 das Serum als ein baktericides erkl~irt. Ihnen schliesst sich Weichselbaum in seiner im Jahre 1904 ersehienenen Monographie 4 an. Dagegen ist yon Issaeff s in einer in Metsehnikoff's Laboratorium entstandenen Arbeit die Ansieht begrfindet worden, dass das Serum weder eine baktericide , noch eine antitoxisehe Wirkung besitzt, sondern dass es die Leukoeyten derart stimutirt, class sie die Infectionserreger durch Phagocytose vernichten. Diese Hypothese, der sich mehrere sp~itere Autoren ansehlossen, ist dutch Denys Schiller Mennes 6 und dutch Hub er ~, auf deren Versuche wir noch zurfickkommen, aufgenommen und erg{inzt worden. Hinsichtlich der Streptokokken-Immunitiit wurden analoge Anschauungen vertreten und auch bier sowohl Antitoxin wie bakterieide Kriifte supponirt, ohne dass eine Einigung der Anschauungen zu Stande gekommen whre. Noch mehr abet als bei den Pneumokokken wurde auf die cellul~iren Vorg~inge Gewieht gelegt: insbesondere hat Border s auf Grund ausgedehnter Versuehe die immunisirende Wirkung des Serums ausschliesslich auf Phagoeytose zurfickgeffthrt. Bereits vorher waren jedoch dutch Denys in Gemeinschaft mit seinen Schfilera Leclef und Marchand 9 die phagocytKren Vorg~nge, die sich bei der Immunitiit gegen Streptokokken abspielen, beschrieben and durch eine ganz neuartige Methodik n~iher analysirt worden: diese Beobachmngen haben dann den Ausgangspunkt ffir unsere Untersuchungen abgegeben. Auoh die Mehrzahl der spateren Beobachter hat sich der An.~icht geniihert, dass man zur Erklarung der Streptokokkenimmunit~t ohne die Annahme der Mitwirkung cellul~rer Einflfisse nieht auskommt. Wir verweisen insbesondere auf die Ausffihrungen fiber die Theorie der Wirkung des Strel)tokokkenserums yon Aronson lo Meyer11, Miehaelis 1~,
Epileptology in medical educationn Abstract Neurology and especially epileptology is taught insufficiently in common medical schools in Germany. Problem based learning and the direct contact to the patient opens emotionally access for students to learn and understand the field of epileptology. We present a student's visit in an outpatient clinic followed by a seminar. Since 1983 this method of teaching has been used to improve the lack of knowledge and skills mentioned in the German Epilepsy Report '98.
Mutations in several genes encoding ion channels can cause the long-QT (LQT) syndrome with cardiac arrhythmias, syncope and sudden death. Recently, mutations in some of these genes were also identified to cause epileptic seizures in these patients, and the sudden unexplained death in epilepsy (SUDEP) was considered to be the pathologic overlap between the two clinical conditions. For LQT-associated KCNQ1 mutations, only few investigations reported the coincidence of cardiac dysfunction and epileptic seizures. Clinical, electrophysiological and genetic characterization of a large pedigree ( n = 241 family members) with LQT syndrome caused by a 12-base-pair duplication in exon 8 of the KCNQ1 gene duplicating four amino acids in the carboxyterminal KCNQ1 domain ( KCNQ1 dup12; p.R360_Q361dupQKQR, NM_000218.2, hg19). Electrophysiological recordings revealed no substantial KCNQ1-like currents. The mutation did not exhibit a dominant negative effect on wild-type KCNQ1 channel function. Most likely, the mutant protein was not functionally expressed and thus not incorporated into a heteromeric channel tetramer. Many LQT family members suffered from syncopes or developed sudden death, often after physical activity. Of 26 family members with LQT, seizures were present in 14 (LQTplus seizure trait). Molecular genetic analyses confirmed a causative role of the novel KCNQ1 dup12 mutation for the LQT trait and revealed a strong link also with the LQTplus seizure trait. Genome-wide parametric multipoint linkage analyses identified a second strong genetic modifier locus for the LQTplus seizure trait in the chromosomal region 10p14. The linkage results suggest a two-locus inheritance model for the LQTplus seizure trait in which both the KCNQ1 dup12 mutation and the 10p14 risk haplotype are necessary for the occurrence of LQT-associated seizures. The data strongly support emerging concepts that KCNQ1 mutations may increase the risk of epilepsy, but additional genetic modifiers are necessary for the clinical manifestation of epileptic seizures.
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