PubMed Health⌕ Search

Biomedical subjects

T Dóczi

Publications and source records attributed to T Dóczi.

At least 19 recordsLinked to original sources
PubMed2006

[Microeletrode guided stereotactic pallidotomy and pallido-thalamotomy for treatment of Parkinson's disease].

OBJECTIVE: Authors evaluated the therapeutic effect of the MRI and microelectrodeguided stereotactic pallido- and pallido-thalamotomy in 33 patients with Parkinson's disease (PD), whose symptoms were refractory to pharmacological therapy. MATERIAL AND METHODS: The patients were evaluated according to the internationally standardized rating scales (UPDRS part II, III, Schawb & England, Hoehn & Yahr, and Fahn) at six timepoints: before the operation, and 2 days, 3, 6, 9 and 12 months postoperatively. The patients were divided into 2 groups. Those in group A had relief of all main parkinsonian symptoms after pallidotomy including tremor. The patients in group B had no relief of tremor after pallidotomy. For them the pallidotomy was completed by thalamotomy in the same sitting, which had resulted in cessation of tremor. RESULTS: The following results were obtained by using the UPDRS part III: after pallidotomy "On state" mean: preoperative 51.2, postoperative at 2nd day 29.5 at 3, 6 and 9th month 26, and at 12th month 28.7. "Off state" mean: preoperative 64.3, postoperative at 2nd day 31.6, at 3, 6 and 9th month 26, and at 12th months 30.5. After pallidothalamotomy "On state" mean: preoperative 43.5, postoperative at 2nd day 27.9, at 3rd month 22.9, at 6th month 22.8, and at 9 and 12th month 24.5. "Off state" mean: preoperative 62.6, postoperative at 2nd day 38, at 3rd month 30, at 6th month 31,8 and at 9 and 12th month 33.8. CONCLUSIONS: For those patients, whose tremor was not successfully controlled by pallidotomy, the combined pallido-thalamotomy was effective. The clinical symptomps, according to the rating scales, improved significantly in both groups (student t: P<0.0001), but bilateral lesioning carried higher surgical morbidity.

Brain Mapping↗
PubMed2005

Spectrin breakdown products in the cerebrospinal fluid in severe head injury--preliminary observations.

BACKGROUND: Calcium-induced proteolytic processes are considered key players in the progressive pathobiology of traumatic brain injury (TBI). Activation of calpain and caspases after TBI leads to the cleavage of cytoskeletal proteins such as non-erythroid alpha II-spectrin. Recent reports demonstrate that the levels of spectrin and spectrin breakdown products (SBDPs) are elevated in vitro after mechanical injury, in the cerebrospinal fluid (CSF) and brain tissue following experimental TBI, and in human brain tissue after TBI. METHODS: This study was initiated to detect spectrin and SBDP accumulation in the ventricular CSF of 12 severe TBI-patients with raised intracranial pressure (ICP). Nine patients with non-traumatically elevated ICP and 5 undergoing diagnostic lumbar puncture (LP) served as controls. Intact spectrin and calpain and caspase specific SBDPs in CSF collected once a day over a several day period were assessed via Western blot analysis. Parameters of severity and outcome such as ICP, Glasgow Coma Scale and Glasgow Outcome Scale were also monitored in order to reveal a potential correlation between these CSF markers and clinical parameters. RESULTS: In control patients undergone LP no immunoreactivity was detected. Non-erythroid alpha-II-spectrin and SBDP occurred more frequently and their level was significantly higher in the CSF of TBI patients than in other pathological conditions associated with raised ICP. Those TBI patients followed for several days post-injury revealed a consistent temporal pattern for protein accumulation with the highest level achieved on the 2(nd) -3(rd) days after TBI. CONCLUSION: Elevation of calpain and caspase specific SBDPs is a significant finding in TBI patients indicating that intact brain spectrin- and SBDP-levels are closely associated with the specific neurochemical processes evoked by TBI. The results strongly support the potential utility of these surrogate markers in the clinical monitoring of patients with severe TBI and provide further evidence of the role of calcium-induced, calpain- and caspase-mediated structural proteolysis in TBI.

Adolescent↗
PubMed2004

Fast method for longitudinal relaxation time and water content mapping of the human brain on a clinical MR scanner.

BACKGROUND: Longitudinal relaxation time (T(1)) map generation from human brain slices renders possible the in vivo follow-up of the changes in T(1) values during the course of several pathologies such as stroke, multiple sclerosis, traumatic brain injury etc. T(1) values can be converted to water contents, thus brain oedema reducing therapy can be non-invasively evaluated. The purpose of the study was to work out a fast and simple MRI method to obtain T(1) and water maps of the human brain. METHOD: The T(1) values of Gadolinium solutions with different concentrations were determined by means of MRI methods at a clinical MR scanner operating at 1 Tesla. In order to validate these measurements, T(1) values of the same Gadolinium solutions were also quantified with a relaxometer operating at the same field strength. T(1) and water maps from the brains of healthy volunteers were obtained with an inversion prepared spoiled gradient echo sequence (turbo-FLASH). FINDINGS: The T(1) values of Gadolinium solutions measured with the relaxometer showed a strong correlation (r > 0.999) with those determined with MRI sequences on the whole body scanner. The fastest MRI method to produce T(1) and consequent water maps from human brain was the inversion prepared turbo-FLASH sequence. CONCLUSIONS: The implemented turbo-FLASH method can produce T(1) and water map of a single virtual brain slice within 2 minutes. However, brain tissue containing haemorrhage should be excluded from the measurement due to the large influence of excessive haemoglobin concentration on longitudinal relaxation. The proposed method is available on most of the MR scanners, thus T(1) and water mapping of human brain can be routinely performed.

Adult↗
PubMed2004

Cocaine- and amphetamine-regulated transcript peptide (CART) is a selective marker of rat granule cells and of human mossy cells in the hippocampal dentate gyrus.

Cocaine- and amphetamine-regulated transcript (CART) peptide immunocytochemistry was used to reveal cellular localization in the dentate gyrus and in Ammon's horn of the rat and human hippocampal formations. In the rat dentate gyrus, only granule cells were labeled, whereas in humans, only mossy cells of the hilar region expressed CART peptide immunoreactivity. In the rat, CART-positive granule cells were located at the molecular layer border of the granule cell layer and had no features that would distinguish them from other granule cells. The mossy fiber bundle was labeled in the hilus as well as along the entire CA3 area of Ammon's horn. In the human, CART-immunoreactive mossy cells displayed the characteristic thorny excrescences both on their somata and their main dendrites. Axon collaterals of mossy cells could be seen in the hilus and the main axons formed a dense band in the inner molecular layer of the dentate gyrus, suggesting that mossy cells are the principal source of the associational pathway. Granule cells of the dentate gyrus and pyramidal neurons of the human hippocampal formation were devoid of CART peptide immunoreactivity. A few labeled non-pyramidal cells and a large group of strongly immunostained axons of unknown origin were present in all layers of CA1-3. Granule cells are the main excitatory cell population of the dentate gyrus while mossy cells are in a key position in controlling activity of granule cells. The specific location of CART peptide in the dentate granule cells of rodents and in the mossy cells of the human hippocampus may indicate involvement of neuronal circuitry of the dentate gyrus in the memory-related effects of cocaine and amphetamine. Independently of its functional role, CART peptide can be used as a specific marker of human mossy cells and of the dentate associational pathway. The sensitivity of CART peptide to postmortem autolysis may restrict the use of this marker in surgically removed hippocampi or in human brains removed and fixed shortly after death.

Adult↗
PubMed2004

Comparison of regional vasomotor responses to acetazolamide and CO2 in rabbit cerebrum and cerebellum, measured by a hydrogen clearance method.

AIM: Many investigators have proved the usefulness of acetazolamide provocation and the carbon dioxide test for assessment of the local cerebrovascular reactivity by measurement of the regional cerebral blood flow in patients with occlusive cerebrovascular disease. Data originating from a comparison of these two different vasomotor stimuli as concerns the differences in sensitivity to them in various parts of the central nervous system are scarce. Our aim was to compare the cerebral blood flow responses to hypercapnic and acetazolamide stimuli in different brain regions. METHODS: The cerebral blood flow was measured in the cerebrum (cortex and caudate nucleus) and cerebellum (cortex), as measured by a hydrogen clearance method in anaesthetized, artificially ventilated rabbits. RESULTS: In normocapnia, the cerebral blood flow values in the cerebrum and the cerebellum differed significantly. The cerebral blood flow responses to both vasodilatory stimuli were to be significantly higher in the cerebrum than in the cerebellum, but the relative increases, i.e. the mean relative reactivities, were similar in the different regions measured. CONCLUSION: The regional dissimilarity might explain to some extent the different sensitivities of the various brain areas to sudden blood pressure changes (infarction or haemorrhage). The results further suggest that heterogeneity in cerebrovascular reactivity should be considered in the assessment of vasoreactivity in patients with occlusive cerebrovascular disease. Since the comparison of the carbon dioxide and acetazolamide-induced cerebrovascular reactivities revealed a strong linear relationship, it was concluded that acetazolamide provocation is equivalent to the carbon dioxide test in the evaluation of cerebrovascular reactivity.

Acetazolamide↗
PubMed2004

Axosomatic synapses on granule cells are preserved in human non-infiltrating tumour or lesion-related and mesial temporal sclerotic epilepsy, but markedly reduced in tumour-infiltrated dentate gyrus with or without epilepsy.

Granule cells of the human hippocampal dentate gyrus were examined. In controls, granule cells displayed somatic spines and cell nuclei with small infoldings. In addition, the cytoplasm of human granule cells always displayed lipofuscin. Subsurface cisterns of endoplasmic reticulum were frequently observed in the human granule cells. Two types of axosomatic synapses were found; most frequently symmetric and less frequently asymmetric. Many of the axosomatic synapses were isolated by glial processes in tumour or lesion-related epileptic patients, but the ultrastructural characteristics of granule cells were not different from those of the control patients. Large bundles of reactive astroglial fibres appeared regularly in all layers of the dentate gyrus. In tumour infiltrated hippocampi, glial processes dominated the neuropil and the number of perisomatic synapses was markedly reduced. Reduction in the number of perisomatic synapses did not correlate with severity and duration of seizures but did correlate with the malignancy of the tumour. It is suggested that reduction of perisomatic inhibition may not be a characteristic of granule cells in the epileptic human dentate gyrus.

Adolescent↗
PubMed2003

Rare sellar region tumors.

We present three cases of rare intracranial midline tumor in the sellar region, often mimicking pituitary adenomas clinically. We describe their symptoms, radiological and pathomorphological features. The first case is a pituitary adenoma producing growth hormone with ganglion cell differentiation. In addition, a rare intracranial granular cell tumor of sellar region and germinoma of pituitary fossa are also presented. All tumors were resected and histologically analyzed. Their biological behaviour was favorable with a 10-year follow-up demonstrating no recurrent tumor mass.

Adenoma↗
PubMed2002

Fast in vivo water quantification in rat brain oedema based on T(1) measurement at high magnetic field.

BACKGROUND: In vivo water content determination based on magnetic resonance (MR) method is of importance in clinical practice as well as in animal studies to follow up the treatment given in order to reduce brain oedema. The methods proposed in the literature so far are largely time consuming. The aim of this study was to find a fast in vivo water quantification method having real advantage for patients suffering from critical conditions. METHOD: Cold injury was applied to provoke brain oedema in fourteen rats. T(1) values of both the oedematous area and the contralateral normal cortex were determined by two independent methods 24 hours after the cold impact. First, from a series of images recorded by inversion recovery spin echo (IRSE) sequence and then by progressive saturation experiment performed by localised MR spectroscopy using stimulated echo acquisition mode (STEAM). To reduce the acquisition time, a two-element repetition time array was optimised for the STEAM experiment, whereas four inversion times were used for T(1) mapping. Both methods were validated against gel phantoms with known T(1) values. After the MR measurements the animals were sacrificed and the water contents of the regions of interest were determined by gravimetric wet-dry method. FINDINGS: The reciprocals of the in vivo measured T(1) values were correlated with the reciprocals of the brain water contents. STEAM experiment showed stronger correlation (r=0.96) than IRSE (r=0.93). In addition, STEAM provided more accurate T(1) values in the phantom study. Determination of brain water content based on T1 measurement does work also at high magnetic field. Determination of brain water content by Magnetic Resonance Spectroscopy is feasible within 2 minutes. INTERPRETATION: Using the presented fast method, water content can be determined within a couple of minutes in animal experiments as well as in the daily clinical practice.

Animals↗
PubMed2001

[Aquaporins in cerebral volume regulation and edema formation].

Regulation of tissue water content and brain volume is of critical importance for the normal functioning of the central nervous system (CNS), which, surrounded by the rigid cranium, is highly sensitive to any increase in the intracranial pressure. Alterations in cerebral water homeostasis and distribution may lead to neuronal and glial swelling known as cytotoxic brain edema, due to accumulation of intracellular water. Although numerous investigations have been performed to elucidate the underlying molecular basis and pathophysiology of brain edema, little is known about the regulation of water transport across the blood-brain barrier and between extra- and intracellular compartments of the brain parenchyma. The discovery and characterization of the aquaporin (AQP) family of membrane water channels provided molecular insight into fundamental processes of water transport across plasma membranes. Two AQPs are expressed abundantly in the mammalian brain: AQP1 in the apical plasma membranes of the cells of choroid plexus in the ventricles, where it has been suggested to participate in the secretion of cerebrospinal fluid and AQP4 in plasma membranes of ependymal cells and astrocytes. The role of AQP4 in the formation of brain oedema was suggested by some recent studies. These findings offer new potentials in brain oedema treatment.

Aquaporins↗
PubMed2001

In vivo water quantification in mouse brain at 9.4 Tesla in a vasogenic edema model.

The aim of our study was to establish a simple in vivo method for water quantification in vasogenic edema, and provide data on imaging of mouse brain at 9.4 Tesla. Apparent T1 and spin density values determined by MRI were found to strongly correlate with the gravimetric water content of mouse brain undergoing cold injury. Using a two-point calibration line between the spin density values for pure water and cortex of mouse brain, as well as the corresponding water contents in vivo, water could be quantified with satisfactory accuracy.

Animals↗
PubMed2001

Effects of centrally administered arginine vasopressin and atrial natriuretic peptide on the development of brain edema in hyponatremic rats.

OBJECTIVE: Centrally released arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) have been shown to participate in brain volume regulation. The aim of the present study was to evaluate the effects of centrally administered AVP and ANP on the time course of development of brain edema in vivo in hyponatremic rats, using diffusion-weighted magnetic resonance imaging. METHODS: We performed intracerebroventricular (ICV) administration of 120 microg AVP, 20 microg ANP, or physiological saline into the right lateral ventricle in 18 rats. Twenty-five minutes after the treatment, we induced systemic hyponatremia by the intraperitoneal administration of 140 mmol/L dextrose solution. Serial diffusion-weighted imaging scans were obtained up to 96 minutes after the start of the hyponatremia. Changes in the brain extra-to intracellular volume fraction ratio were estimated as changes in the apparent diffusion coefficient (ADC). RESULTS: No change in the ADC was observed after the ICV injection of saline or AVP. The onset of hyponatremia induced a rapid and marked ADC reduction in both groups, indicating an increased intracellular space. However, the ADC decrease became significantly more pronounced in the ICV AVP group (83.3+/-4.7% of baseline level, mean +/- standard deviation) than in the saline group (93.7+/-3.3% of baseline, P < 0.001) after 78 minutes of hyponatremia. The ICV injection of ANP induced a prompt ADC increase to 111.5+/-10.0% (P < 0.05) of the baseline level, indicating a rapid reduction in the intracellular compartment. In the initial phase of hyponatremia, the ADC values in the ANP group were consistently higher than those in the saline group, decreasing finally to 86.9+/-9.6% after 96 minutes of hyponatremia. CONCLUSION: Our findings demonstrate the opposite effects of AVP and ANP on the intracellular volume fraction of the brain during the development of cellular brain edema, with an immediate effect on ANP and a delayed effect on AVP. The results emphasize the direct effects of these hormones on the cellular volume regulatory mechanisms in the brain during the development of cerebral edema.

Animals↗
PubMed2001

Brain water and proton magnetic resonance relaxation in preterm and term rabbit pups: their relation to tissue hyaluronan.

The present study was performed to investigate simultaneously total brain water, T1 and T2 relaxation times, and hyaluronan (HA) in fetal and neonatal rabbits. Attempts were also made to establish the relationship of HA to total brain water and to T2-derived motionally distinct water fractions, since HA is known to bind water and to limit tissue water mobility. Experiments were carried out in fetal Pannon white rabbit pups at gestational ages of 25, 27, 29, and 31 days and at a postnatal age of 4 days. The brain tissue water content (desiccation method), T1 and T2 relaxation times (H1-NMR method), and HA concentration (radioassay HA 50) were measured, and free and bound water fractions were calculated by using multicomponent fits of the T2 relaxation curves. Compared with values in newborn pups, water and HA contents were found to be highly elevated in the preterm brain and decreased markedly during early postnatal life. The trends and time courses of T1 and T2 relaxation times proved to be similar, but the postnatal decrease in T2 was preceded by a significant decline in late gestation. Maturity-related changes occurred in the T2 relaxation derived bound water fraction which amounted to 4-19% of brain water. The bound water fraction appeared to be independent of total brain water and HA concentration, and HA is, therefore, unlikely to be the only factor controlling brain water mobility. The clear dissociation of bound water fraction from total water suggests restructuring of brain water during the perinatal period.

Animals↗
PubMed2001

Subluxation of a lumbar vertebra in a patient with Marfan syndrome. Case report.

Marfan syndrome is a hereditary disorder of the connective tissue that, in its most classic form, includes cardiovascular, ocular, and skeletal features. The neurological problems associated with the disease are mainly caused by intracranial vascular abnormalities and spinal meningeal defects, but other neurological manifestations are rarely present. Scoliosis, a skeletal manifestation of the syndrome, occurs frequently, but its onset, natural history, and radiological characteristics differ from those of the idiopathic form. Scoliosis in a patient with Marfan syndrome seldom accompanies other spinal deformities. In this article the authors describe the case of a patient with Marfan syndrome and scoliosis in whom lumbar subluxation occurred. This rare deformity, diagnosed on three-dimensional computerized tomography scanning, has not been reported previously in association with Marfan syndrome. Its development can be explained in terms of the theory of progressive rotatory dislocation. The morphological characteristics, clinical features, and surgical treatment of the deformity are presented.

Adolescent↗
PubMed2000

Increased aquaporin-4 immunoreactivity in rat brain in response to systemic hyponatremia.

The present study was undertaken to assess whether the protein and mRNA expression levels of the glial water channel aquaporin-4 (AQP4) undergo downregulation and whether there is a subcellular redistribution of AQP4 protein in rat brain in response to systemic hyponatremia and brain edema. Systemic hyponatremia was induced for 4 or 48 h by combined administration of hypotonic dextrose i.p. and 8-deamino-arginine vasopressin (dDAVP) s.c. Semiquantitative immunoblotting of membrane enriched fractions showed significantly increased immunoreactivity to 164 +/- 12% (n = 6) and 153 +/- 12% (n = 6) of control levels in brain after 4 or 48 h of systemic hyponatremia, respectively. Similarly, immunoblots of cerebellar samples revealed an increase in AQP4 immunoreactivity to 136 +/- 6% (n = 6) and 218 +/- 44% (n = 6) of control levels, after 4 or 48 h of hyponatremia. In contrast, AQP4 mRNA levels were unchanged after 4 h of severe hyponatremia (104 +/- 14% of control levels; n = 17), indicating that there are no changes in AQP4 expression in response to systemic hypoosmolarity. Immunocytochemistry and high-resolution immunogold electron microscopy revealed highly polarized labeling of AQP4 in astrocyte end-feet surrounding capillaries and forming the glia limitans. This pattern of labeling was not changed whereas an increased labeling intensity of AQP4 could be observed in response to hyponatremia. In conclusion, hyponatremia causes a pronounced and rapid increase in AQP4 immunoreactivity that is not accompanied by any increase in AQP4 mRNA expression. The increased AQP4 immunosignal may reflect secondary conformational modifications of AQP4 protein, leading to enhanced antibody binding. This post-translational modification of AQP4 may participate in the adaptation of cerebral tissue to systemic hyponatremia.

Animals↗