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T Dóczi

Publications and source records attributed to T Dóczi.

72 records · Page 4Linked to original sources
PubMed1986

Blood-brain barrier damage during the acute stage of subarachnoid hemorrhage, as exemplified by a new animal model.

Models have been devised and characterized in the laboratory rat for studying the neuropathology of subarachnoid hemorrhage. Several ways of injecting blood via different routes have been tried; cortical subarachnoid administration is the most reproducible suitable model. The location of injected blood was detected in histological sections. In this rat model for subarachnoid hemorrhage, the arterial blood pressure and the intracranial pressure did not elevate significantly, and the influence of major ischemic components in the development of brain edema could also be ruled out. Measurements performed on the water, electrolyte, and albumin contents of brain tissue have clearly indicated that the brain edema developing in the acute stage of rat experimental subarachnoid hemorrhage could be classified as having a primarily vasogenic component as well. These findings may have implications in the treatment of subarachnoid hemorrhage.

Acute Disease↗
PubMed1985

The pathogenetic and prognostic significance of blood-brain barrier damage at the acute stage of aneurysmal subarachnoid haemorrhage. Clinical and experimental studies.

In a retrospective study, pathological tissue enhancement was found in nearly two fifths of patients with acute SAH on contrast-enhanced cranial computed tomography. By means of absorption measurements with the region of interest technique over the basal ganglia, it was proved indirectly that pathological tissue enhancement should be brought about not only by hyperaemia, i.e., a blood volume increase, but also by extravasation of the contrast material, i.e., blood-brain barrier (BBB) disruption. A similar conclusion was drawn from the retrospective isotope brain scintigraphy study. It was further established that, although the pathological contrast enhancement was most obvious in the cortex, and particularly in the neighbourhood of the subarachnoid spaces, the phenomenon is probably widespread throughout the brain. Patients with abnormal enhancement are likely to be in less favourable clinical grades, have a high incidence of marked or diffuse spasm, have a poorer outcome independent of surgical or conservative treatment, and develop cerebral infarction more frequently. Systemic arterial hypertension was associated with an increased incidence of abnormal enhancement. Pathological tissue contrast enhancement or isotope accumulation in the first few days of SAH may serve as prognostic signs indicative of the late development of vasospasm and ischaemia. As ischaemic disruption of the capillary system is not prominent in the initial days following any stroke, vasoactive substances arising from the breakdown of the blood clot should play important part in the BBB damage in the acute stage of SAH. The "cortical SAH" model developed in the animal experiments ensured a constant subarachnoid blood volume with minimal local brain damage. The intracranial pressure and mean arterial blood pressure did not change significantly, and perfusion defects did not arise. Thus, this model proved suitable for studying the influence on the BBB of vasoactive blood breakdown products (responsible for arterial spasm) without the accompanying effects of pathological conditions such as raised intracranial pressure, systemic hypertension, non-reflow phenomena, which also disrupt the BBB. Measurements on the water, electrolyte, albumin contents of brain tissue, as well as the immunohistochemical localization of albumin, clearly indicated that the brain oedema developing at the acute stage of experimental SAH could be classified as having a primary vasogenic component in addition to the cytotoxic component. This increased capillary permeability was found to be brought about by opening of tight junctions and pinocytosis in the endothelial cells. The pathological capillary permeabilit

Adolescent↗
PubMed1984

Involvement of vasopressin in brain edema formation: further evidence obtained from the Brattleboro diabetes insipidus rat with experimental subarachnoid hemorrhage.

Brain water accumulation (1.2%) with an accompanying increase in the sodium content was observed in Wistar rats as early as 1 hour after experimental subarachnoid hemorrhage (SAH). After 6 and 24 hours, the water content was 1.3 and 1.4%, respectively, higher than that of control animals. In contrast, in Brattleboro diabetes insipidus rats the content of brain water and electrolytes had not changed significantly 1 hour after the administration of blood into the subarachnoid space. Increased brain water and sodium and a normal potassium content, indicative of a vasogenic type of brain edema, were seen at 6 hours after SAH. In these animals, known to be devoid of vasopressin, the increase in brain water 24 hours after SAH was 2.6%, compared with 1.4% for Wistar rats with SAH. It is suggested that the lack of vasopressin could alter the course of brain edema formation after experimental SAH in Brattleboro diabetes insipidus rats. It is hypothesized that vasopressin, by regulating the water permeability of the brain capillaries, the choroid plexus, and the cerebrospinal fluid absorption structures, plays an important role in controlling the brain fluid and electrolyte balance during the course of SAH.

Animals↗
PubMed1984

5-hydroxytryptamine injected intraventricularly fails to influence the brain water content.

Measurement of the content of brain water and electrolytes after the intraventricular administration of 5-hydroxytryptamine in rats, with and without exposure to osmotic stress, failed to show water accumulation in the brain parenchyma. It is suggested that elevation of serotonin in the cerebrospinal fluid--resembling pathological situations such as subarachnoid hemorrhage--does not play a primary role in brain edema formation.

Animals↗
PubMed1983

Disturbances of cerebrospinal fluid circulation during the acute stage of subarachnoid hemorrhage.

Radioisotope cisternography was performed and the erythrocyte and hemoglobin contents of the cerebrospinal fluid (CSF) were determined within the first 4 days after subarachnoid hemorrhage in 42 patients. The clinical condition of the patients was related to the severity of the CSF circulation disturbances. Thirty-five patients had some degree of disturbance of CSF flow, and only 2 of the 42 patients had normal flow. In 5 cases the cisternograms were inconclusive. The severity of CSF circulation disturbances correlated well with clinical condition. No relationship was found between the number of erythrocytes in the CSF and the development of CSF circulation disturbances. The CSF erythrocyte content did not correlate with the clinical condition. It is suggested that flow disturbances of the CSF during the acute stage of subarachnoid hemorrhage might play an important role in the pathomechanism of the disease.

Adolescent↗
PubMed1982

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after head injury.

The authors report a review of 1808 patients admitted for the treatment of craniocerebral injuries. Eighty-four (4.6%) developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Two types of SIADH (severe and mild) were defined on the basis of laboratory findings and clinical signs. SIADH occurred in 0.6% of the patients with mild head injury, 10.6% of those with moderate head injury, and 4.7% of the patients with severe head injury. Regular measurements of serum electrolytes, osmolality, and urinary sodium depletion should be made during the treatment of patients suffering from head trauma because unexpected clinical deterioration may often have a reversible cause: SIADH.

Adolescent↗
PubMed1982

Brain water accumulation after the central administration of vasopressin.

The intraventricular administration of vasopressin or DDAVP (desmopressin acetate) increased the brain water content from 78.2% to 79.2-79.5%. This was achieved without an accompanying water load. The applied water load alone did not increase the water content of the brain. There was no significant difference in the water content of the brain between animals treated with intraventricular vasopressin and intravenous water load and animals receiving only intraventricular vasopressin. The water content of the olfactory bulbs of the control animals was 3.8% higher than that of the hemispheres. While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% subsequent to the intraventricular administration of DDAVP. Measurement of the brain electrolyte content was not conclusive as to the mechanism of water permeability changes. The possible mechanism is discussed. Although no tissue or cerebrospinal fluid concentrations of vasopressin enabling comparison with clinical pathological conditions have been measured, it is suggested that increased secretion of vasopressin into the cerebrospinal fluid in conditions such as subarachnoid hemorrhage or intracranial hypertension of various origins might play a role in edema formation.

Animals↗
PubMed1982

[The syndrome of "inappropriate" antidiuretin secretion associated with a subarachnoid hemorrhage from a ruptured aneurysm].

In a patient with subarachnoid haemorrhage due to the rupture of an Arteria-communicans-anterior aneurysm, hyperadiuretinism developed which could be diagnosed by laboratory examinations. The pathological condition was removed by a reduction of the daily supply of liquids. The lesson that can be learned from this case is that in the treatment of patients with subarachnoid haemorrhages a systematic control of the serum sodium level, the sodium excretion an the osmolality of the serum and the urine is important.

Humans↗
PubMed1981

Syndrome of inappropriate secretion of antidiuretic hormone after subarachnoid hemorrhage.

The authors report a review of 290 patients admitted for the treatment of subarachnoid hemorrhage. Twenty-seven (9.3%) patients developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The diagnosis was established by means of daily laboratory investigations (serum electrolytes and osmolality; urine sodium and osmolality; and fluid balance). The patients were divided into two groups (severe and mild SIADH) on the basis of clinical symptoms and signs and laboratory findings. High values of urine osmolality and sodium concentration in patients with low values of serum osmolality and sodium concentration were demonstrated. Thirteen (4.5%) patients had severe and 14 (4.8%) patients had mild SIADH. The source of bleeding was not discovered in 14 patients (4.8%). Nearly 10% of the patients with an aneurysm on the anterior communicating artery developed SIADH. Fluid therapy for these patients is described, and the treatment of SIADH is discussed.

Adolescent↗
PubMedDate not supplied

Increased vulnerability of the blood-brain barrier to experimental subarachnoid hemorrhage in spontaneously hypertensive rats.

The influence of chronic arterial hypertension upon the permeability to albumin of the cerebral capillaries, i.e. the blood-brain barrier, was studied in normotensive Wistar and spontaneously hypertensive Wistar rats with experimental subarachnoid hemorrhage. The blood-brain barrier permeability to albumin was assessed quantitatively by spectrophotometric determination of Evans blue extravasation. Subarachnoid hemorrhage was produced by injecting autologous blood into the cortical subarachnoid space. A significant increase of Evans blue albumin extravasation was found in the spontaneously hypertensive rats with subarachnoid hemorrhage as compared with normotensive animals suffering from subarachnoid hemorrhage. Subarachnoid hemorrhage in this model alone caused a significant Evans blue extravasation, whereas sham-operation did not. These findings emphasize the necessity for effective attempts to reduce the leakage of the capillary system in the early stage of subarachnoid hemorrhage.

Albumins↗
PubMedDate not supplied

[Stereotactic thalamotomy for Parkinsonian and others types of tremor. Experiences of thalamic multiunit burst activity by means of semimicroelectrode].

INTRODUCTION: Better understanding of the basic mechanism of disorders of movement, together with improvements in surgery and electrophysiological techniques have led to a resurge of interest in the surgical treatment of patients with tremor. Ventrolateral thalamotomy has been considered to be an alternative neurosurgical treatment for disabled persons including those with drug-resistant Parkinson s disease and other types of tremor. PATIENTS AND METHODS: Thirty four of 47 patients had Parkinson s disease (n= 23), essential tremor (n= 4), multiple sclerosis (n= 5), olivopontocerebellar lesion (n= 1) and posttraumatic tremor (n= 1) and did not show satisfactory improvement after drug treatment. The lesions were made in the thalamic nucleus. In 26 patients simultaneous recordings were made of nerve activity in the thalamus and of burst activity. RESULTS: In 23% of the cases the appropriate site for the final lesion could not be determined in accordance with electrostimulation of the empirical objective. In these patients the objective was determined after observation of the electrophysiological activity localized to the burst activity seen during the operation. The patients were followed-up for 6-24 months (average 12 months); 88% of them had no tremor or moderate contralateral tremor. The patients were assessed on a modified Fahn scale. Average scoring fell from a preoperative evaluation of 73.8 points to 34.0 after three months; 30.7 after six months, 32.0 after 9 months, 37.1 after 12 months and 35.2 points after 18 months. CONCLUSION: Of 47 thalamotomies done, 13 (29%) were successful and 5 (10%) maintained their original state, but no cases became worse or had serious complications.

Corpus Striatum↗