PubMed Health⌕ Search

Biomedical subjects

L Vécsei

Publications and source records attributed to L Vécsei.

At least 55 records · Page 3Linked to original sources
PubMed1999

Topical acetylsalicylic acid versus lidocaine for postherpetic neuralgia: results of a double-blind comparative clinical trial.

A double-blind comparative clinical trial was performed with topical aspirin versus lidocaine for the treatment of 40 patients with postherpetic neuralgia. The percentage improvement following topical aspirin application was 72.2 +/- 19.9 S.D., while with lidocaine it was 72.8 +/- 25.3 S.D. These results suggest that the effect of topical treatment with aspirin is as good as that with lidocaine, since there was no significant difference (P = 0.778) between the two drugs in respect of pain reduction and accordingly the topical application of acetylsalicylic acid can be equally recommended.

Adult↗
PubMed1998

[Diagnostic studies of cerebrospinal fluid in patients with multiple sclerosis].

The diagnostic criteria postulated by Poser necessitate clinical and laboratory CSF analysis for establishment of the diagnosis of definitive multiple sclerosis. The present paper reports methods for CSF examinations relating to multiple sclerosis with regard to the examinations suggested by the Charcot Foundation. In the course of CSF analysis, it is important to discriminate between the immunoglobulins present in normal amounts, those synthesized locally in pathological quantities and those penetrating across the damaged blood-CSF barrier. Normally, a parallel assay of CSF and serum specimens is carried out in the course of quantitative and qualitative protein analysis. In 37 patients with clinical multiple sclerosis, we determined the albumin and the immunoglobulin classes IgG, IgA and IgM, using laser nephelometry. An elevated IgG index was found in 76% of the cases, which points to local IgG snythesis and might be proof of the humoral immune response. The albumin quotient, which is suitable for examination of the integrity of the blood-CSF barrier, was within the reference range. Qualitative protein analysis was performed by means of electrophoresis on agarose-gel and isoelectric focusing. Agarose-gel electrophoresis revealed oligoclonal gammopathy in 68%, in contrast with the 91% demonstrated by isoelectric focusing. Comparison of the two kids of qualitative protein analyses indicated that isoelectric focusing was more sensitive for the detection of oligoclonal bands, in support of the literature finding.

Adult↗
PubMed1998

Depletion of calcitonin gene-related peptide from the caudal trigeminal nucleus of the rat after electrical stimulation of the Gasserian ganglion.

Electrical stimulation of the Gasserian ganglion resulted in partial depletion of calcitonin gene-related peptide (CGRP) from ipsilateral central terminals of pseudounipolar primary sensory ganglion cells. Affected terminals exhibit decreased CGRP immunoreactivity as shown by cytophotometric densitometry of the caudal trigeminal nucleus. The decrease in CGRP immunoreactivity is statistically significant only in the medial one-third of the caudal trigeminal nucleus. Since earlier studies have shown that electrical stimulation of the Gasserian ganglion induces first accumulation then depletion of CGRP from perivascular sensory terminals in the dura mater, the present experiments suggest that CGRP is depleted also from central terminals of primary sensory trigeminal neurons, which might be of importance in the pathogenesis of migraine headache.

Animals↗
PubMed1998

Polyneuropathy with endoneurial immune complex deposition as the first manifestation of systemic lupus erythematosus.

A 72-year-old male presented with progressive sensorimotor polyneuropathy. Later weight loss, proteinuria and deteriorating renal function were noted. The electrophysiological examinations revealed extensive, symmetrical demyelinating and axonal polyneuropathy. Frozen sections obtained from sural nerve biopsy sample showed the presence of immune complexes and complements in the walls of the epi- and endoneurial blood vessels, and perineurium suggestive of systemic lupus erythematous (SLE). IgG and Clq deposits were also present along the basement membranes of Schwann cells. The electron microscopy confirmed the presence of immune complex deposition. Diagnosis of SLE was proven by positive serology (anti-nuclear antibodies, anti-Sm, anti-RNP, anti-double-stranded DNA) and renal biopsy showing membranous lupus nephritis with extensive immune complex deposition in the tubular basement membranes. Despite combined immunosuppressive treatment for 10 months, the patient died of complications of generalized immune complex vasculitis. The manifestation of SLE in elderly patients, especially in males, is very rare. Moreover, the polyneuropathy is an unusual initial symptom of SLE. Immune complex deposition in Schwann cell basement membrane probably plays an important role in the pathomechanism of sensorimotor polyneuropathy in SLE.

Aged↗
PubMed1998

The prevalence of multiple sclerosis in the Hungarian city of Szeged.

OBJECTIVES: The aim of this study was to determine the prevalence of multiple sclerosis in a population in South Hungary. METHODS: The diagnosis was established with the aid of the Poser diagnostic criteria and the degree of physical disability was determined on the Kurtzke expanded disability status scale (EDSS). The present medical state (EDSS score) was determined from outpatient clinical control tests. The prevalence, the average age at onset of the disease and the proportions of the various clinical forms were calculated, and the patients' disability status was estimated. RESULTS: In 1996, the prevalence was 65/100,000, and the incidence from January 1, 1995 through December 31, 1996 was 7/100,000/year. DISCUSSION: During a period of 2 years, the number of diagnosed patients has almost doubled. The disease can be recognized in an early stage with a minimal neurological deficit. The development of the diagnostics necessitates re-examinations with modern diagnostic procedures. During the last 3 years, the general practitioner system has been reorganized, and the working relationships between the clinic and family doctors have developed considerably. A comparison of the present findings with those in other countries with a similar climate revealed very similar prevalence data.

Adult↗
PubMed1998

[Glycolytic enzyme defects and neurodegeneration].

This study was devoted to the continued search for an explanation of the neurodegeneration found in a severely TPI deficient Hungarian patient whose brother with genomically completely identical TPI defect was completely free of neurological disorders. The changes found in the molecular species composition of the major PL subclasses and the decrease in PE plasmalogens explain the earlier round increase in membrane fluidity interfering thereby with the physiological function of membrane enzymes, receptors, signal transduction, protein-protein interactions and vesicle fusion. Plasmalogens have also the capacity to protect against oxidative stress, that is deemed to contribute to neurodegenerative processes. The presence of chronic oxidative stress was well reflected in the decreased levels of GSH and alpha-tocopherol in the affected brothers. Decrease in plasmalogens have been described recently in Zellweger's syndrome, in other peroxisomal neurodegenerative disorders, in demyelinating processes and in Alzheimer's disease. The brain in normal individuals is highly enriched in plasmalogens. The pathological decrease found in TPI deficient lymphocytes will presumably be more pronounced in excitatory tissues. The recently described role of expanding nucleotide triplets in the development of neurodegeneration is suggested to result through the selective binding via their polyglutamine repeats to GAPDH. The role of GAPDH in TPI deficiency may be of crucial help in the elucidation of the development of neurodegeneration, since the enzymatic defect of TPI can be partially bypassed by means of the HMP shunt which generates GAP via GAPDH without the participation of TPI. Considering the results found in TPI deficiency in comparison to the new literary findings in different neurodegenerative diseases the following pathomechanism may be proposed. The protein products of the defective genes due to their abnormal steric structure bind GAPDH in a different manner or in differing quantity than their normal counterparts. The PL composition and the resulting differences in the biophysical properties of the cell membranes have crucial impact on these protein-protein interactions and on the activity of enzymes and membrane transport functions. The plasmalogen decrease impairs the protection against oxidative stress with consecutive worsening of the neurodegenerative process. The final common pathway to neuronal death leads through destabilization of intracellular Ca2+ homeostasis via elevation of intracellular Ca2+ to apoptosis. The most important conclusion is that lipids are not an inert environment of membrane proteins. Unravelling of the pathogenesis of neurodegeneration needs more concerted investigation of the interactions between genetic changes with biophysical and biochemical cell membrane lipid alterations.

Erythrocytes↗
PubMed1997

[Natural killer cell activity in multiple sclerosis patients].

The physical factors are important in the regulation of immunological functions. The primary immunological process maintaining a neuroimmunological disease is influenced by the physical state. In this paper the natural killer activity was demonstrated at 50 patients with definite multiple sclerosis. One fifth of them was depressed. Significantly lower natural killer activity was found in this group unrelated to the disease activity. In the group of patients without depression significantly higher natural killer activity was present in the remission comparing the relapse. Our findings confirmed the frequent appearance of HLA DR2 configuration in multiple sclerosis. HLA differences were not found between the depressed and non-depressed groups. This results concern the role of physical factors in the disease process, but refer to other factors linked to the disease activity.

Adult↗
PubMed1997

Effect of a serotonin agonist (sumatriptan) on the peptidergic innervation of the rat cerebral dura mater and on the expression of c-fos in the caudal trigeminal nucleus in an experimental migraine model.

The supratentorial cerebral dura of the albino rat is equipped with a rich sensory innervation including nociceptive axons and their terminals, which display intense calcitonin gene-related peptide (CGRP) immunoreactivity both in the connective tissue and around blood vessels. Stereotactic electrical stimulation of the trigeminal (Gasserian) ganglion, regarded as an experimental migraine model, induces marked increase and disintegration of club-like perivascular CGRP-immunopositive nerve endings in the dura. Intravenous administration of sumatriptan, prior to electrical stimulation, prevents disintegration of perivascular terminals and induces accumulation of CGRP in terminal and preterminal portions of peripheral sensory axons. Consequently, immunopositive terminals and varicosities increase in size; accumulation of axoplasmic organelles results in a "hollow" appearance of many varicosities. Since sumatriptan exerts its anti-migraine effect by virtue of its agonist action on 5-HT1D receptors, we suggest that sumatriptan prevents the release of CGRP from dural perivascular terminals by an action at 5-HT1D receptors. In the caudal trigeminal nucleus electrical stimulation of the trigeminal ganglion induces, in interneurons, increased expression of the oncoprotein c-fos which is not prevented by intravenous application of sumatriptan. Disparate findings regarding this effect are partly due to the fact that sumatriptan very poorly passes the blood-brain barrier and partly to different experimental paradigms used by different authors.

Animals↗
PubMed1997

[Neurodegeneration: aging and dementia. Etiopathogenic role of electron transport disorders. Therapeutic possibilities].

The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems. The late onset diseases and slow neurodegeneration is connected with excitotoxins and alteration of mitochondrial electron transport chain. In elderly, congenital and acquired defects of mitochondrial complexes cause formation of free radicals. The overstimulation of excitatory amino acid receptors interfere with the cellular energy metabolism and also forming reactive oxygen species. The impaired energy metabolism make neuronal cells vulnerable to the excitotoxic damage. In these ways, excitotoxicity may be the final common pathway of neuronal death in a variety of neurodegenerative diseases. Potential therapeutic strategies would be use receptor antagonist or drugs to bypass energetic defects.

Aged↗
PubMed1997

Amino acid concentrations in cerebrospinal fluid of patients with multiple sclerosis.

As oligodendrocytes have binding sites for excitatory amino acids (glutamate, aspartate, serine, etc.), a role of these molecules in demyelinating disorders is possible. We measured the levels of amino acids in the cerebrospinal fluid (CSF) of patients with multiple sclerosis in comparison with CSF obtained by myelography from patients with lower back pain. There were no significant differences in the CSF concentrations of these amino acids between the two groups. Normal concentrations of excitotoxins do not exclude the role of these molecules in demyelinating disorders.

Adult↗
PubMed1996

Clusterlike headache as a first sign of brain metastases of lung cancer.

We report on a patient with clusterlike headache and multiple brain metastases of lung cancer. Initially, cluster headache was suggested clinically by characteristic symptoms without any focal central nervous system signs. However, magnetic resonance imaging demonstrated multiple brain metastases. It is possible that tumor necrosis factor may have played a role in initiating the clusterlike headache.

Brain Neoplasms↗
PubMed1993

[Ophthalmoplegia in herpes zoster: clinical review based on two case reports].

The authors describe two cases of ophthalmic herpes zoster complicated with ophthalmoplegia. This rare complication developed in the 2nd week after beginning of the disease and it is only slightly influenced by antiviral therapy, but improvement was observed after the administration of corticosteroids. A short overview summarizes the diagnostic possibilities, the therapy and the complication of the disease.

Adrenal Cortex Hormones↗
PubMed1993

[Current data on the pathogenesis of neurodegenerative diseases and some muscular disorders: therapeutic prospectives].

Recent findings suggest that damaged mitochondrial DNA (mtDNA) may play a role in the development of Leber's hereditary optic neuropathy, Huntington's, Parkinson's and Alzheimer's disorders, as well as in that of encephalomyopathies. The mtDNA consist of 16,569 base pair and encodes 13 polypeptides, 2 ribosomal RNAs and 22 transfer RNAs. It is much more injurable than the nuclear DNA (nDNA) and since mtDNA participates in the synthesis of respiratory chain enzymes, therefore, its damage may result in neuronal cell death. The present paper summarizes these novel mechanisms and potential therapeutic strategies with regard to neurological disorders.

Alzheimer Disease↗