Clinical Neuroscience

[In memoriam Richter Hugó (1885-1945)]

EMED Alexander

JUNE 02, 2009

Clinical Neuroscience - 2009;62(05-06)

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Clinical Neuroscience

[Datas and facts to the history of the neuro-psychiatry - Szent István Kórház, Budapest (1885-2008)]

FAZEKAS András

Clinical Neuroscience

[Genetics and present therapy options in Parkinson’s disease: a review]

BEREZNAI Benjámin, MOLNÁR Mária Judit

[In the past years, six monogenic forms of Parkinson disease have clearly been associated with this movement disorder. The most frequent forms are LRRK2- and Parkin-associated Parkinson disease. Currently, a genetic diagnosis does not change the therapy, the genes involved in genetic Parkinson disease help to understand the underlying pathophysiologic mechanisms of Parkinson disease. Beside the overview of the molecular-genetic basis, we give a review about genetic testing, pharmacological and other multidisciplinary treatment options.]

Clinical Neuroscience

[Presidential report about the activity of the Hungarian Society of Neurology and Psychiatry 2004-2009]

VÉCSEI László

Clinical Neuroscience

[99-mTc-HMPAO single photon emission computed tomography examinations in genetically determined neurometabolic disorders]

ARANKA László, AMBRUS Edit, VÖRÖS Erika, SVEKUS András, KÓBOR Jenõ, BEREG Edit, PALATKA János, PÁVICS László

[The aim of our study was to determine regional cerebral blood flow (rCBF) abnormalities in different types of enzymopathies. Patients and methods - Among the patients with genetically determined enzymopathies 3 patients had aminoacidopathies, and 11 had different types of encephalopathies, from which 10 had mitochondrial encephalomyopathy (MEMP), and 1 patient had hyperuricaemic encephalopathy. Besides the mentioned 14 patients, 1 had ceroid lipofuscinosis and another patient had tuberous sclerosis. The further distribution of the MEMP patients’ group was the following - 5 patients had MEMP with lactic acidosis, 5 had Leigh’s disease (subacute necrotizing encephalopathy), from which 1 had cytochrome-c-oxidase deficiency (COX). Additionally in all patients were performed cerebral MRI and SPECT examination 10 min. after intravenous administration of 20 Mbq/kg 99 mTc-HMPAO. Results - Fourteen out of 16 SPECT findings were pathologic, showing decreased focal frontal/temporal/temporoparietal cerebral blood perfusion. Aminoacidopathic group - all the 3 patients revealed pathologic signs from the aminoacidopathic patients’ group. Among them the ornithine transcarbamylase (OTC) heterozygous female patient with left-sided hemiparesis caused by hyperammonemic stroke at 10 month-age, showed right sided temporoparietal, occipital and left frontal hypoperfusion, nearly 6 years after the cerebral vascular attack. This finding might be resulted because of diaschisis. Mitochondrial encephalo-myopathic (MEMP) group - all the four patients with MEMP and lactic acidosis showed focal hypoperfusion in the temporal region, while the perfusion was normal in the COX deficient patient and in 2 Leigh’s disease (subacute necrotizing encephalopathy) patients. In the remaining 1 Leigh’s patient frontotemporal hypoperfusion was found. In all patients there were non specific structural abnormalities detected by MRI - cortical and subcortical atrophy, and scattered demyelination foci. In the case of ceroid lipofuscinosis the MRI showed cerebral atrophy and cerebellar hypoplasia, and the SPECT showed right frontal and occipital hypoperfusion, bilateral parietal physiological riping process. The patient with tuberous sclerosis showed bilateral temporo-occipital hypoperfusion. Conclusion - 1. SPECT images demonstrated hypoperfusion rCBF changes in 14 out of all 16 patients. 2. Regional cerebral/cerebellar hypoperfusion was detected by SPECT in mitochondrial encephalomyopathies, with lactate acidosis and aminoacidopathies giving high informative value about the cerebral perfusion.]

Clinical Neuroscience

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SZUPERA Zoltán

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