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Dortmund, Germany

Episodes that resemble seizures but are not epileptic are mostly psychogenic seizures. They are often misdiagnosed for far too long. Many characteristics raise the suspicion of psychogenic seizures such as situational beginning, firm closing of the eyelids, asynchronous movements, shaking of the head, closed mouth, lack of cyanosis, rapid reorientation and a change of seizure symptoms during time. EEG recording during a seizure enables to reliably distinguish between epileptic and psychogenic seizures. Interictal EEG recordings however may give false-positive findings (epileptiform discharges, although no epilepsy is present) or give false-negative findings (normal EEG despite epilepsy). There is good evidence that the way in which a patient spontaneously reports his attacks, provides crucial evidence for the distinction psychogenic vs. epileptic seizure. Patients with epileptic seizures try to describe the attack as accurate as possible. They want to understand how it came about and want to reconstruct the seizure onset. Psychogenic seizures are caused by repressed subconscious conflicts and fears. The patient therefore provides descriptions of surrounding factors but not the seizure itself. Mainly external circumstances are reported, negations are frequent. Activities with which is tried to stop the seizure are hardly ever spontaneously mentioned. To make these differences in the spontaneous description evident it is essential to conduct the history taking in a way, which instead of leading the patient, offers him sufficient space to describe what is important to him. Source

The development of the EEG during childhood takes place in a typical, but individually variable way. The period of EEG maturation lasts from the 16th Week of gestation into early adulthood and undergoes, both during wakefulness and sleep, characteristic phases with typical EEG patterns, which differ to some extent from those of mature adult EEGs. This article will provide an overview of the maturation of EEG background activity and, as far as they are known, of their normal variants in the course of childhood. In the immature EEG of the preterm infant, the EEG-patterns of conventional EEG-recordings are compared to those of amplitude-integrated EEGs. In the EEG of later childhood, typical patterns of maturation are demonstrated and the main pathologic differential diagnoses of these signs of normal brain-development are mentioned. © 2012. Source

Zacharias R.,Campus Management | Schmidt M.,Campus Management | Kny J.,Campus Management | Sifringer M.,Campus Management | And 5 more authors.
Brain Research | Year: 2010

Exposure to Gamma-aminobutyric-acid (GABA)A-receptor agonists and N-Methyl-d-Aspartate (NMDA)-antagonists has been demonstrated to induce neurodegeneration in newborn rats. Exogenous erythropoietin (EPO) protects against NMDA antagonist-mediated neuronal death. In this study we evaluated whether EPO is also effective in limiting neurodegeneration of the GABAA-mimetic agent propofol in newborn rats. 6 day old rats were randomized to one of four groups and treated with intraperitoneal applications of 3 × 30 mg/kg propofol at 0, 90 and 180 min, propofol in combination with 5000 IU/kg rEPO, propofol in combination with 20,000 IU/kg rEPO or sham injections of PÄD II solution as controls. After 24 h, brains of the animals were histopathologically examined and a summation score of degenerated cells was calculated for every brain. Propofol increased neuronal degeneration scores from 16,090 ± 4336 to 28,860 ± 6569 (p < 0.01). This effect was completely abolished by low-dose rEPO (14,270 ± 4542, p < 0.001 versus propofol only; p > 0.05 versus controls). In contrast, high-dose rEPO was not protective (23 930 ± 8896, p > 0.05 versus propofol only). Propofol may cause neuronal death in newborn rat brains, which is prevented by low-dose rEPO but not high-dose rEPO. © 2010 Elsevier B.V. All rights reserved. Source

Pauli S.,University of Gottingen | Schmidt T.,University of Gottingen | Funke R.,Sozialpadiatrisches Zentrum | Zoll B.,University of Gottingen | And 4 more authors.
European Journal of Medical Genetics | Year: 2012

We report on monochorionic diamniotic male twins discordant for the trisomy 12p syndrome. Trisomy 12p mosaicism with a supernumerary der(12)(pter > q12) was detected in approximately 50% of lymphocytes in both children. Fluorescence in situ hybridisation (FISH) revealed a high grade mosaicism of approximately 77% trisomy 12p cells in buccal smear and 85% in hair follicles in the affected twin, while in the normal developing brother an additional 12p chromosome fragment could not be detected in those tissues. Instead, in 3% of buccal smear and hair follicle cells a minute supernumerary marker chromosome comprising central portions of chromosome 12 was observed. Trisomy 12p mosaicism, confined to the lymphocytes of the unaffected twin, may be due to prenatal twin-to-twin transfusion, explaining the conspicuously discordant clinical phenotype. We discuss the possible sequence of events leading to the cytogenetic findings and compare the clinical phenotype presented in the affected twin with other cases of trisomy 12p and tetrasomy 12p (Pallister-Killian syndrome). © 2012 Elsevier Masson SAS. Source

Schulte E.C.,TU Munich | Schulte E.C.,Helmholtz Center Munich | Claussen M.C.,TU Munich | Jochim A.,TU Munich | And 14 more authors.
Movement Disorders | Year: 2013

Background: Recently, mutations in an open-reading frame on chromosome 19 (C19orf12) were identified as a novel genetic factor in neurodegeneration with brain iron accumulation (NBIA). Because of the mitochondrial localization of the derived protein, this variant is referred to as mitochondrial membrane protein-associated neurodegeneration with brain iron accumulation (MPAN). Methods/Results: We describe the clinical phenotype and MRI of 3 newly identified individuals with MPAN due to either previously reported or novel homozygous or compound heterozygous genetic alterations in C19orf12. Conclusions: MPAN is characterized by a juvenile-onset, slowly progressive phenotype with predominant lower limb spasticity, generalized dystonia, and cognitive impairment. Typical additional features include axonal motor neuropathy and atrophy of the optic nerve. MRI showed iron deposition in the globus pallidus and substantia nigra without the eye-of-the-tiger sign, which is typical for PKAN, the most frequent form of NBIA. © 2012 Movement Disorder Society Copyright © 2012 Movement Disorders Society 28 2 February 2013 10.1002/mds.25256 Brief Report Brief Reports Copyright © 2012 Movement Disorders Society. Source

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