Clinical Neuroscience

[Regulation of water transport in brain oedema]

DÓCZI Tamás, SCHWARCZ Attila, GALLYAS Ferenc, BOGNER Péter, PÁL József, SULYOK Endre, GÖMÖRI Éva, VAJDA Zsolt

OCTOBER 10, 2005

Clinical Neuroscience - 2005;58(09-10)

[The study gives an overview on the regulation of cerebral water content and of brain volume. The molecular mechanisms of the development and resolution of various oedema forms are discussed in detail. The physiological and pathophysiological role of the recently discovered molecular water channel proteins aquaporin-1 (AQP1) and aquaporin-4 (AQP4) as well as the importance of central neuroendocrine regulation by vasopressin and atriopeptin are reviewed based on the relevant literature and personal studies. Quantitative water maps based on the combination of multicompartment- T2, diffusion weighted MRI and T1 studies have proven to be powerful tools for studying new drugs against brain oedema brought about by various neuropathological conditions and for testing their efficacy both in animal experimental and clinical conditions. Non-peptide vasopressin antagonists, atriopeptin agonists and drugs targeting AQP4 are potential new families of oedema-decreasing drugs.]



Further articles in this publication

Clinical Neuroscience

[Frontotemporal dementia - Part III - Clinical diagnosis and treatment]

GALARIOTIS Vasilis, BÓDI Nikoletta, JANKA Zoltán, KÁLMÁN János

[The authors report a comprehensive publication consisting of three parts going into the details of history, prevalence, clinical forms, differential diagnosis, genetics, molecular pathomechanism, and pathology, clinical diagnosis and treatment of frontotemporal dementia (FTD). The third part of the present review focuses on the clinical diagnosis and treatment of FTD. The diagnosis of FTD is problematic even today. Mental status, psychometric testing as well as imaging studies such as PET and SPECT, and laboratory examinations may be helpful in the diagnosis. Unfortunately, bedside tests are generally insensitive to mild dysexecutive deficits. Most of FTDs do not have characteristic laboratory abnormalities or brain atrophy sufficient to set up the diagnosis; these only allow to rule out other disorders and assume the diagnosis of FTD. An effective treatment for FTD is still to be established. The improvement of serotonin metabolism has been proposed as a biological treatment. Recent studies suggest that bromocriptine may improve selective frontal symptoms, but this and the efficacy of other dopaminergic drugs need further evaluation. Drugs that prevent the expression or accumulation of tau seem to be the most promising causal approach. In aphasia behavioral therapy may be attempted. In addition, caregiver management is essential, because as with those of Alzheimer’s dementia patients, they also carry a significant psychosocial stress.]

Clinical Neuroscience

[Ischemic preconditioning in the brain]

NAGY Krisztina, DOMOKI Ferenc, BARI Ferenc

[Stroke-related death is the third most common cause of mortality in Hungary after cardiovascular diseases and cancer. In addition to the unfavourable mortality figures, the consequent development of neurological and psychiatric disorders in stroke patients imposes an enormous burden on the health care system and on the families. Numerous studies are being conducted world wide on the prevention of stroke and other cerebrovascular disorders like chronic hypoperfusion, as well as on acute stroke management and patient rehabilitation issues. As a result, our understanding of the mechanism of hypoxic brain damage steadily increased over the past years and decades which brought along promising achievements both in the field of stroke prevention and therapy. However, these broad-spectrum approaches also made clear that preventing neuronal death and thus reducing neurological damage are complex tasks that cannot be successfully resolved by targeting single mechanisms. Therefore, the development of alternative new drugs and clinically applicable complex neuroprotective strategies is warranted. One of the most promising approaches is to create ischemic tolerance in the brain by using pharmacological preconditioning paradigms. These drugs trigger similar events to those initiated by brief ischemic insults that later can make the cerebral tissue resistant to subsequent otherwise lethal stress (ischemic preco]

Clinical Neuroscience

[Ferenc Katona is 80 years old]


Clinical Neuroscience

[Neurobehavioral assessment in the neonatal period - The impact of Ferenc Katona]

KARMEL Z. Bernard, GARDNER M. Judith

Clinical Neuroscience

[Evolutionary pressure in the development of the unconscious-conscious duality in young children]

ÁDÁM György

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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

[Severe intracranial hypotension in an adolescent with Marfan syndrome. Case report]

ROSDY Beáta, KOLLÁR Katalin, MÓSER Judit, VÁRALLYAY György, KORDÁS Mariann

[Spontaneous intracranial hypotension is a rare complication of connective tissue disorders. One of them is Marfan syndrome. It predisposes the patient to meningeal diverticula. Possibly after minor unrecognised head trauma or secondary to Valsalva manoeuvre cerebrospinal fluid leak from meningeal diverticula can happen. It causes postural headache. We describe a 15 year old adolescent female newly diagnosed with Marfan syndrome, who presented with intractable postural headache. Our patient's brain MRI showed bilateral frontal subdural effusion, narrow ventricles, downward displacement of the brainstem, enlarged cervical venous plexi, dural ectasias and wide nerve root sleeves. Radionuclide cisternography demonstrated CSF leaks at multiple sites. She could not be treated conservatively, but was successfully treated by epidural saline injections. Control brain and cervical MRI confirmed her healing, too. At the two and half year follow up visit, she was completely well. So we recommend this easiest technic to use before epidural autolog blood patches.]

Clinical Neuroscience

[Neurological and psychiatrical prospects of apathy]


[During his long practice as head physician of a neurological and psychiatrical department with over 100 beds performed the examination and department of more than a hundred thousand patients. Based on the acquired experience and the data of the most recent literature he treats every aspect of the apathy syndrome. He emphasizes the multidisciplinary approach during both establishing the causes and the examination and treatment of patients. In order to clarify the diagnosis consultations with other disciplines must be used as well as the the knowledge provided by the now essential CT, MRI, PET, SPECT. The author discusses the international therapeutical possibilities and practice after the recently alredy possible exact diagnosis.]

Clinical Neuroscience

[Posterior ischaemic optic neuropathy]

BOÓR Krisztina, KOVÁCS Krisztina, RÓZSA Anikó, PÁNCZÉL Gyula, SZILVÁSSY Ildikó, GÁCS Gyula

[Here one case report of the posterior ischaemic optic neuropathy, a rare and underdiagnosed form of the non arteritic ischaemic optic neuropathy is presented, to underline the value of the MRI in the diagnosis. The ischaemic optic neuropathy is the infarction of the optic nerve. Depending on the affected segment of optic nerve (optic nerve head or retrobulbar segment) two subclasses exist: the anterior (AION) and the posterior (PION) ischaemic optic neuropathy. Ischaemic optic neuropathy characterized by sudden, painless, mononuclear loss of vision, and/or visual field defect, that is accompanied by a diagnostic picture of the optic disc fundus only in the case of the AION. The diagnosis of the PION is based on a diagnosis of exclusion described by Hayreh in 1981. The macular and retinal laesions, the etiological role of toxic agent, the compression and the inflammation of the optic nerve all have to be excluded. The differential diagnosis between the PION and the retrobulbar neuritis is more difficult. Nowadays, in addition to the case history and the clinical data the diagnosis of the PION could be confirmed with help of VEP (visual evoked potential) and MRI. In the case of an old woman who had a sudden, painless visual loss of left eye we confirmed the diagnosis of PION with MRI which was presumed after had excluding other etiological factors.]

Lege Artis Medicinae


SZÁNTÓ Antónia, VEISZ Richárd, KRENÁCS László, CSIKI Zoltán, GRIGER Zoltán, ZEHER Margit

[INTRODUCTION - Takayasu’s arteritis is an idiopathic inflammatory disease of the great elastic arteries, mainly of the aorta and its primary branches. It primarily affects young women. CASE REPORT - A 20-year-old woman presented with general inflammatory symptoms that had begun 3 to 4 months before. Earlier she underwent a biopsy from a mass on the neck thought to be a lymph node, which on histopathological examination turned out to be a non-necrosing granulomatosis in the wall of a large artery. Based on this finding as well as on the presence of fever, weight loss, carotid murmur, anaemia, elevated platelet count, increased sedimentation rate, the lack of pulse and the findings of imaging examinations, Takayasu’s arteritis was diagnosed. Treatment was started with high-dose steroid monotherapy, which resulted in clinical and laboratory remission after a short time. The imaging findings (neck soft tissue sonogram and MRI) also showed improvement, however, a moderate but definite disease activity was still present, thus steroid treatment was supplemented with azathioprin. CONCLUSION - It is important to follow the disease both clinically and with imaging techniques for an early recognition of the need for changing or adjusting the treatment.]