Hungarian Radiology

[Jenő Forrai's intellectual heritage]


AUGUST 20, 2003

Hungarian Radiology - 2003;77(04)



Further articles in this publication

Hungarian Radiology

[Event Schedule of the Society of Hungarian Radiologists, 2003]

Hungarian Radiology

[The congress of ESGAR was a success in Budapest]


Hungarian Radiology

[Professional and legal responsibility of a medical physicist]


Hungarian Radiology

[In memoriam Sándor Holbok]


Hungarian Radiology

[Placebo effect]


All articles in the issue

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Clinical Neuroscience

[Early onset dementias: Case studies]

MERKLI Hajnalka, PÁL Endre, GÁTI István, KOSZTOLÁNYI Péter, KÖVÉR Ferenc

[Introduction - Dementia is a decline of intellectual abilities. The etiology of dementia syndrome is diverse. The authors describe three patients with early-onset dementia. Case reports - The first patient was a 44 years old male with mild gait, body ataxia, memory loss, slowness and apathy. Investigations proved AIDS dementia syndrome. In the second case of a 37 years old female patient, herpes simplex encephalitis was suspected due to sudden onset of speech arrest and to brain MRI and CSF findings. Her symptoms improved during antiviral treatment but later progressive dementia developed. CSF serological tests proved the presence of neurolues-dementia paralytica. The third patient was a 38-years-old female. Neurological examination was performed because of progressive memory loss, changed behaviour and impaired attention. Neuropsychological test showed severe dementia. Metachromatic leukodystrophy was proven by decreased arylsulfatase activity. Conclusions - It is not easy to recognize the early symptoms of dementia. In these cases, besides detailed history, neurological examination and neuropsychological tests, brain MRI and cerebral spinal fluid serological tests were indispensable for a correct diagnosis, especially in the young patients.]

Clinical Neuroscience


SISKA Éva, NEUWIRTH Magdolna, REBECCA Gooding, MOLNÁR Mária Judit

[The congenital cataracts facial dysmorphism neuropathy (CCFDN) syndrome (OMIM 604168) is a recently described autosomal recessive developmental disorder. It is almost completely restricted to an endogamous group of the European Vlax Roma population, called the Rudari. The CCFDN syndrome is a complex phenotype involving multiple systems, characterized by facial dysmorphism, congenital cataracts, microcorneae, delayed early motor and intellectual development, hypogonadotrop hypogonadism, hypomyelination of the peripheral nervous system, and serious complications related to general anaesthesia. This disorder is caused by a homozygous mutation of the carboxy-terminal domain phosphatase 1 (CTDP1) gene, localized to the 18q23 region. Authors present one genetically identified case in a large Roma family. The case documents that the CCFDN mutation is present also in the Hungarian Roma population. Underlie of antropomorphological data the authors presume that the CCFDN mutation reached Hungary as a result of emigration of Vlax Gypsies in the 18th century. The paper calls attention to the fact that molecular genetic diagnostics can replace invasive methods and makes possible the identification of heterozygotes without clinical symptoms. The introduction of the genetic screening enables us to perform genetic counselling and prevention in this high-risk population.]

Lege Artis Medicinae

[Our Intellectual Heritage Vince Varró: Géza Hetényi – an Intellectual Successor of the Korányis]


Hungarian Immunology

[Our archaic heritage: the innate immunity. The cellular immunity of Drosophila]

ANDÓ István, LAURINYECZ Barbara, NAGY István, MÁRKUS Róbert, FLORENTINA Rus, VÁCZI Balázs, ZSÁMBOKI János, FEHÉR László, ELISABETH Gateff, DAN Hultmark, KURUCZ Éva

[Authors describe the essentials of the cellular immunity of Drosophila. They describe the Drosophila CD system, the main blood cell lineages and a blood cell differentiation model based on the expression of the CD antigens.]

Clinical Neuroscience

[Neuroprotection in brain ischemia - doubts and hopes]


[In ischaemic stroke the two major potential therapeutic strategies are aimed at either improving cerebral blood flow or directly interacting with the cytotoxic cascade - a large body of evidence gained from animal studies is in support of them. In clinical trials direct neuroprotection by blocking the neurotoxic cascade remained ineffective, although there are several clinical trials still in progress. We summarize the experimental data and present the results of clinical trials and also discuss why so many drugs, which were effective in animal studies, failed in human trials. It is emphasized, that 1. in most animal studies the reduction of infarct size, i.e. the amount of saved penumbral tissue, was the outcome measure, whereas neurological function remained unassessed; 2. the recovery of intellectual performance and higher cortical functions are of major importance in the future quality of life in stroke victims; however, it is impossible to examine these parameters appropriately in animal studies; 3. in many clinical trials the patient population was rather heterogenous and low in number, the study protocol was not optimal and the critical analysis of the subacute and chronic phase was lacking or insufficient. We present the major experimental stroke models, discuss their similarities, differencies and limitations as compared to the human pathophysiological processes. The pitfalls of extrapolating data from animal studies to clinical practice are also summarized. The complex network of functional and morphological intercellular connections, the long timescale of neurotoxic and reparative events and the lessons learned from clinical trials suggest, that the use of drug combinations (therapeutic cocktails) targeting multiple steps of the neurotoxic cascade would hopefully result in more effective treatment of ischaemic stroke. Strategies to facilitate brain plasticity and regeneration is an additional promising tool to enhance recovery in brain ischaemia.]