Clinical Neuroscience


JANUARY 30, 2012

Clinical Neuroscience - 2012;65(01-02)



Further articles in this publication

Clinical Neuroscience


RAJNA Péter, TAJTI János

Clinical Neuroscience

[Depression in neuropsychiatric diseases]


[Depression is frequently observed together with neurological disorders. Moreover this connection is bidirectional in the case of several neurological disorders, as depression can be either a comorbide syndrome or also a risk factor of them. Neurobiological background of depression involves neuroanatomical structures, their interconnected networks, disturbances of neurotransmitters, neurohormonal, neuroimmunological and neurotrophic changes, genetic background. Disfunction of these systems also plays a role in the pathogenesis of comorbid depression of neurological disorders. Interactions and clinical aspects of biological factors involved in the pathogenesis of depression in dementias, Parkinson’s disease, cerebrovascular disorders and epilepsy are discussed further. Depression as a result of neurobiological factors responsible for both neurological and psychiatric consequencies of these disorders, are often atypical as a clinical manifestation, however chracteristic for the particular neurological disorder. Evaluation of the biological backgound and clinical features of depression in neurological disorders makes the complex neuropsychiatric approach of these disorders possible.]

Clinical Neuroscience

[The clinical relevance of 1p19q codeletion of oligodendrogliomas at the Department of Neurosurgery in Debrecen]

KLEKNER Álmos, FEKETE Gábor, RENCSI Márta, MÉHES Gábor, SZABÓ Péter, BOGNÁR László

[Object - To determine the clinical relevance of 1p19q codeletion in case of patients treated between 2006 and 2008 with oligodendroglial tumor at the Department of Neurosurgery, University of Debrecen. Questions - Beside the traditional morphological investigations, methods of rapidly developing molecular pathology are also available for routine diagnostic procedures. Numerous studies confirm that the codeletion of the 1p and 19q alleles has a clinical relevance regarding the sensitivity for chemotherapy. In this study the connection between the 1p19q codeletion and clinical parameters was tested to evaluate the prognostic role of this genetic alteration in neurosurgical patients. Methods, clinical data - In the present study experiences about the clinical relevance of 1p19 codeletion is summarized. Between 2006 and 2008, 28 patients with brain tumor containing oligodendroglial component was tested for 1p19q codeletion. The result of the analysis was compared with clinical data such as tumor localization, extent of resection, histological grade, presence of astrocyte component, time of first recurrence, age and gender. Furthermore, the potency of 1p19q codeletion as a prognostic factor for chemosensitivity by analyzing the data of patients who underwent different treatment protocols was also evaluated. Results - Our results suggest that 1p19q codeletion can be valued as a positive prognostic factor, which is concordant with the results available in the literature. We also found positive correlation with oligodendroglial component, recurrence free survival of grade III tumors, sensitivity to chemoand radiotherapy, and inverse correlation with histological grade and age was detected. Conclusion - Though the 1p19q codeletion is currently not the part of the routine patient management, based on our study we found it appropriate for clinical use as a prognostic factor, and its predictive role in establishing oncotherapy can be also discussed.]

Clinical Neuroscience

[The validation of the hungarian version of the Dimensional Yale-Brown Obsessive-Compulsive Scale]

HARSÁNYI András, CSIGÓ Katalin, RAJKAI Csaba, DÖME László, DEMETER Gyula, RACSMÁNY Mihály

[Background - The Obsessive-Compulsive disorder (OCD) has a complex phenotype, which can be summarized by using a few consistent and temporally stable symptom dimensions. The dimensional approach derived from the systematic factor analytic studies of OCD symptoms. In 2006, a new psychometric scale was created by M.C. Rosario-Campos and her colleague, the Dimensional Yale- Brown Obsessive-Compulsive Scale (DY-BOCS). This scale measures the presence and severity of obsessive-compulsive (OC) symptoms within six distinct dimensions. The Hungarian translation of the test and preliminary results were published in 2009. Purpose - The objective of this recent study was two folded: on one hand, our goal was to validate the Hungarian version of the DY-BOCS on a larger sample size. On the other hand, we wanted to publish our results gained by the Hungarian version of the test in English. Methods - We assessed 30 Hungarian patients diagnosed with OCD by DSM-IV. Reliability and validity of the expert and of the self-report were estimated. Results - Self-report and expert ratings were highly correlated. The global DY-BOCS score was well correlated with the total Yale-Brown Obsessive-Compulsive Scale score. The internal validity of the symptom dimensions and the global severity score were high. Divergent validity was also good. Conclusion - These results indicate that the Hungarian version of the DY-BOCS is a reliable and valid clinical tool.]

Clinical Neuroscience

[Mutation analysis of alpha-galactosidase A gene in Hungarian Fabry patients]

LÁSZLÓ Aranka, TÖRÖK László, RAFFAI Sarolta, TÖRÖK Éva, SALLAY Éva, ENDREFFY Emőke, MORVAI László, AMSTEL Ploos Van JK

[Aim was to detect the mutations of alpha-galactosidase A gene in two Hungarian Fabry patients. Methods - Mutation analysis was performed by polymerase chain reaction (PCR) sequencing of the seven exons and adjacent introns of the alpha-galactosidase A gene. Results - Case 1. (19 y. male patient) Mutation analysis was done for alpha-galactosidase gene, a missence mutation has been identified in the 5th exon, the aspartic acid at codon 266 has been substituted by a tyrosine (notation D266Y) due to a G-T transversion at position 10287 of the alpha GAL-A gene. Case 2. (28 y. male Fabry patient) The GAL-A mutation has been proven to be R220X mutation in exon 5 of the alpha-galactosidase A gene.]

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