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Biomedical subjects

V G Amcheslavskiĭ

Publications and source records attributed to V G Amcheslavskiĭ.

At least 19 recordsLinked to original sources
PubMed1997

[The early postoperative period in patients with tumors of the posterior cranial fossa].

The studies carried out during an early postoperative period in patients with posterior fossa tumors were made to analyse the role of the degree and the level of brain stem damages in formation of cerebral reactions. The three groups of cases were selected in accordance with the course of the postoperative period: 1.1-with exitus letalis (irreversible damages); 1.2-rehabilitation in persistent focal damages; 2-restoration with functional safety of brain stem. Differences of the integral cerebral reactions (the state of consciousness, emotional-affective disorders, awakening state) as well as the brain stem syndromes (formation of pathological systems, reciprocal relations between intact and destroyed brain stem structures) and diencephalic-subcortical syndromes were considered.

Adult↗
PubMed1991

[Mechanisms of development of brain edema in neurosurgical pathology].

As many as 120 neurosurgical patients were examined after the excision of hemispheric gliomas, basal and subtentorial tumors. Based on an the computer-aided analysis biochemical and clinical data, attempts have been made to unify the mechanisms responsible for brain edema development in patients with neurosurgical pathology. In the early postoperative period, brain edema occurs in 95% of neurosurgical patients. Edema development, spreading and intensity depend on the site and nature of the primary pathological focus as well as on traumatism of surgical interventions. It is proved that edema is an original, biologically expedient brain response to its injury. This response manifests in hyperhydration of all tissues, with the maximum intensity being concentrated in the focus of injury. Specific (neurogenic neurohumoral) and nonspecific (biochemical, autoimmune, mechanical, and so forth) factors of brain edema development may be distinguished. The differences in the neurogenic and neurohumoral mechanisms by which brain edema develops may be accounted for by the topography of the focus of injury. The closer the pathological focus is to the stem and diencephalic structures, the more remarkable the action of neurogenous and neurohumoral factors and the more distinct the tendency toward edema generalization are. At the diencephalic level of injury, damaged are the structures responsible for central regulation of metabolism and trophicity of nerve cells. The neurogenously precipitated diffuse impairment of permeability of the cells entails their hyperhydration, which marks cellular (cytotoxic) edema. The subtentorial process that affects the vasomotor centre of the stem triggers the neurogenic diffuse alterations in the vascular tone, manifesting in an increase of permeability for water and plasma proteins which is characteristic of vasogenic edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Water↗
PubMedDate not supplied

[Cerebral hemodynamics and metabolism in the acute stage of cerebral aneurysm rupture].

The relationship between lipid peroxidation products and the severity of arterial spasm was studied in 86 patients. For this, the level of radical production, the content of the end lipid peroxidation product malonic dialdehyde and the overall antioxidative activity of lumbar cerebrospinal fluid were determined during 24-hour Doppler monitoring of blood flow in the middle cerebral and internal carotid arteries. Following subarachnoidal hemorrhage, the activation of lipid peroxidation processes was shown to correlate with the severity of arterial spasm and it is likely to contribute to the development of late ischemias. Nimotop used to treat patients with significant arterial spasm caused a reduction in the rate of free radical lipid peroxidation to that characteristic for patients with moderate spasm. The findings suggest that it is expedient of including antioxidants into the combined therapy of patients with acute subarachnoidal hemorrhage.

Acute Disease↗
PubMedDate not supplied

[Nosocomial pneumonia in patients with severe craniocerebral trauma in intensive care units].

Eighty-three patients with severe craniocerebral injuries (CCI) were treated at Institute of Neurosurgery in 1999. Pulmonary infectious complications occurred in 16 of 25 patients with severe CCI. Early nosocomial pneumonia (NP) was diagnosed in 18% and the so-called late NP (associated with artificial ventilation of the lungs) in 35%. Coma longer than 4 days increased the incidence of NP to 62%. The main pathogens of NP are gram-negative aerobic bacteria (61%), the predominant agent being Pseudomonas aeruginosa (18.9%). 76% isolated microorganisms were multiresistant. The most significant risk factors as regards NP in patients with severe CCI were coma combined with bulbar and pseudobulbar disorders.

Adolescent↗
PubMedDate not supplied

[Principles of intensive care during the acute period of severe craniocerebral trauma in children].

Prospective analysis of the course of severe craniocerebral injury (CCI) in 37 children showed that the results of treatment depended on methods of intensive care. In children the outcome of CCI depends primarily on adequacy of maintaining effective cerebral bloodflow during the acute period of CCI irrespective of the terms and etiological factors of coma. Adequate cerebral perfusion pressure is attained with osmodiuretics, saluretics, and hemodynamic therapy. Hyperventilation is justified in cases with coma developing within 2 h after the injury; it should not lead to long (more than 1 h) decrease of PaCO2 below 28 mm Hg. The authors emphasize that every delayed decrease of consciousness after the injury should be thoroughly analyzed in order to rule out intracranial complications (epi/subdural and intracerebrai hematomas) in no more than 6 h, which is the maximal time allowed for decision making. Use of unapproved medical methods and drugs in children during acute period of severe CCI is ineffective and even hazardous, because it distracts the physician's attention to negligible details of treatment; in addition many of such drugs have side effects.

Acute Disease↗
PubMedDate not supplied

[Involvement of thyroid hormones in mental recovery following severe craniocerebral trauma].

To study a role of thyroid hormones in the recovery of mental performance, 71 patients (60 males, 11 females) aged 7 to 66 years (mean age 32.7 +/- 3.5) with severe brain injury (TBI). According to the stage of mental recovery (1--none; 2--elementary acts; 3--verbal contact; 4--spatial orientation; 5--intellectual and mnestic processes and emotional and personality traits), the study was divided into 5 series. Immunoradiometric assay of thyroid hormones (T3 and T4) and their free fractions (FT3 and FT4), thyroid-stimulating hormone (TSH), thyroxine-binding globulin (TBG), and prolactin (P) revealed significant alterations in thyroid metabolism at stages 1 to 4, which appeared as low T3 syndrome. The thyrotropin-releasing hormone (TRH) test made in study series 3 to 5 suggests that the patients have neuroendocrine dysfunctions at the mentioned recovery stages of mental functions of the brain. There was a close relationship of clinical parameters (mental time course) to alterations in the thyroid status and metabolism and to morphological impairments of brain tissues in their traumatic damage, which is evidenced by a correlation of the levels of blood and spinal fluid markers (neurone-specific enolase--NSE and protein S-100) of brain injury with psychopathological disorders (r = -0.96 and -0.6, respectively; p < 0.05) and by the assessment of TBI outcomes (r = -0.65 and -0.62, respectively; p < 0.05). Thus, the findings clinically confirm the neurotransmitter role of thyroid hormones at the stages of mental recovery. In addition, the results show that measurement of blood T3, FT3, TSH, T4, TBH, and NSE should be included into neurochemical monitoring in SBI as prognostically significant criteria. They also may serve as a basis for timely correction of thyroid metabolism.

Adolescent↗
PubMedDate not supplied

[Problems in brain protection].

The main aim of intensive care in acute head injury and in the postoperative period is to prevent, detect, and revert a secondary neuronal injury. To maintain the optimum systemic and cerebrovascular functions can substantially promote this aim achievement. There are some new neuroprotective interventions that are currently under investigation. Although the major focus of recent cerebral protection researches has been on the development of receptor-specific drugs, this effort has resulted in better outcomes. At present, patients are well served by using more traditional techniques to prevent and treat cerebral ischemic events. Initial therapy should include interventions to improve cerebral perfusion and the oxygen-carrying capacity of blood. Once this is accomplished, measures should be made to monitor blood glucose concentrations and to treat fever. General anesthetic choice may be of great importance in monitoring intracranial pressure and seizure activity. However, if direct cerebral protection is desired, a barbiturate should be the anesthetic of choice. All these measures should increase the chance of patients to neurologically recover following hypoxia and ischemia.

Blood Glucose↗
PubMedDate not supplied

[Cerebral low T3 syndrome].

The authors studied the time course of changes in the parameters of the cerebral thyronergic system (total and free triiodthyronine (T3) and thyroxin (T4), thyroxine-binding globulin (TBG), thyroid-stimulating hormone (TSH) by radioimmunoassay (Immunotech, Czechia; CIS, France), proinflammatory cytokine of TNF-alpha by enzyme immunoassay (Innogenetic, Belgium) in the blood and cerebrospinal fluid (CSF) in 59 patients (37 males and 22 females whose age ranged from 21 to 64 years) in acute subarachnoidal hemorrhage due to arterial aneurysmal rupture. On admission, the condition of 47 (79.7%) was rated as grades III-VI according to the Hunt-Hess scale, which was responsible for high mortality rates (33.89% in the assessment of outcomes according to the Glasgow outcome scale). The causes of death were ischemic and hemorrhagic insults, edema of the brain, cerebral stem wedging. Laboratory findings were analyzed in relation to the clinical condition of patients, outcomes, and the degree of secondary vasospasm assessed by Doppler transcranial study by the average blood flow velocity in the middle cerebral artery. They revealed a significant depression of thyroidal metabolism with developed the total low T3 syndrome just before surgical treatment in patients with deterioration in the early postoperative period. The significant correlations found by the authors between the decreased blood T3 and TSH levels and 1) the severity of neurological disorders; 2) the degree of vasospasm, and 3) the outcome of disease, as well as negative correlations of elevated TNF-alpha levels not only in the blood, but also in CSF with the content of CT3, CT4 and with the severity of neurological symptomatology are indicative of the development of isolated syndrome in the brain, which is characterized by specific thyroidal metabolic disorders, which the author propose to call the cerebral low T3 syndrome (by taking into account the presence of the autonomic systems of thyroidal homeostatic provision).

Adult↗
PubMedDate not supplied

[Differential approach to the application of hyperventilation in acute period of severe brain injury in relation to cerebral circulation].

Seventeen patients with severe brain injury (Glasgow-8 Coma Scale 3-8 scores) complicated by traumatic subarachnoidal hemorrhage and severe cerebral hemodynamic disorders (hyperemia, vasospasm) were examined. Hyperventilation was performed in different phases of cerebral circulation under multiparametrical monitoring (intracranial pressure, cerebral perfusion pressure, jugular oximetry, Doppler study using the carotid compression test). The use of hyperventilation to eliminate intracranial hypertension in victims with brain hyperemia was shown to make cerebral circulation consistent with brain tissue oxygen demands and to improve the autoregulatory reserve of cerebral vessels. The application of hyperventilation to eliminate intracranial hypertension in vasospasm leads to a temporary reduction in intracranial pressure, but simultaneously causes cerebral circulatory changes that do not correspond to cerebral oxygen demands, as well as lowered cerebral perfusion pressure, which increases a risk for ischemic brain tissue lesion. This requires a strict rationale for the use of hyperventilation and for multiparametrical monitoring of cerebral functions, which includes jugular oximetry, Doppler transcranial study, and measurement of intracranial pressure throughout the hyperventilation period in order to prevent secondary brain lesion.

Adolescent↗
PubMedDate not supplied

[Cerebral circulatory autoregulation as a guide for controlling the parameters of assisted ventilation in acute severe brain injury].

The paper presents the results of cerebral circulation (CC) in 17 ventilated patients with severe brain injury in its acute phase. All the patients developed traumatic subarachnoidal hemorrhage, which was accompanied with angiospasm in the majority of cases. Doppler transcranial study (DTCS) was performed, by using the carotid compression test; the findings correlated with paCO2 and CV parameters. A dynamic study was performed every two days starting from their admission to an intensive care unit to the recovery from coma or normalization of CC parameters. The dilation and constriction components of the CC reserve were assessed from the results of this test and continued to be controlled during therapy. Thus, this paper shows the possibility of goal-oriented correction of CC autoregulation and optimization by selecting the parameters of assisted ventilation and by changing paCO2 under the guidance of Doppler transcranial study.

Adolescent↗
PubMedDate not supplied

[The intercentral relations of cortical bioelectrical activity in the human brain after surgical interventions on brain stem formations].

In the process of dynamic study of cortical bioelectrical activity and indices of its intercentral interaction in 52 neurosurgical patients with focal lesion on the brainstem level, the dependence was shown of the CNS reactions to the operative intervention on the character and degree of damage. Variants were described of compensatory neurodynamic reconstructions of electrical processes in observations with transient, stable and irreversible pathological foci of brainstem localization.

Adaptation, Physiological↗
PubMedDate not supplied

[Computed tomography in the diagnosis of complications in the early postoperative period in patients with tumors of the posterior cranial fossa].

The authors analyse the results of clinico-CT studies in complicated course of the early postoperative period in 104 patients (87 adults and 17 children) with tumors of the posterior cranial fossa (PCF). According to the histological structure and predominant topography of the neoplasm, the cases were divided into 46 extracerebral parastem tumors (meningiomas, neurinomas, chordomas, cholesteatomas) among which 24 extended supratentorially and 22 to Blumenbach's clivus; 23 gliomas of the cerebellum and fourth ventricle; 16 primary gliomas of the stem; 19 other new growths (hemangioblastomas, hamartomas, choroid papillomas, germinomas). A common factor was coexistence of the main complicating condition--circulatory disorder in the stem with edema and dislocation of the stem, disturbed spatial relations between the PCF structures. Dynamic CT studies allowed the authors to differentiate 3 main variants of pathological changes differing in the character of cerebral circulatory disorders: 1st--a wide zone of reduced density in the brain stem; the extent of this zone in the orocaudal direction and its relation to the diameter of the stem (dorsal, ventral, lateral parts) varied; 2nd--combination of zones of reduced density in the stem and cerebellum with hemorrhagic inclusions--multiple "punctate" inclusions or in the form of blood clots; 3rd--in mosaic pattern of the ischemic foci in the stem and cerebellum there was a prevalence of hemorrhages in the form of multiple small extravasations of blood at different levels of the stem, in the subcortical parts, blood clots in the seat of the tumor, hemotamponade of the brain ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Intensive therapy in syndromes of disorders of cerebral blood circulation in the bed of the anterior cerebral arteries following the removal of middle basal tumors].

255 patients have been examined in the early postoperative period after the removal of tumors located in diencephalic and sella turcica regions. The early postoperative period was complicated by circulation disturbances in the vascular bed of the anterior cerebral or anterior communicative arteries. The clinical pattern, CT scans and morphological data were analysed. Three principal clinical syndromes of the postoperative period were lined out: 1) extrapyramidal-diencephalic syndrome; 2) extrapyramidal-capsular syndrome; 3) frontal-corpocallosal syndrome. The reason for these syndromes was the occlusion of the anterior cerebral and anterior communicative arteries or their branches. The diencephalic syndrome had poor prognosis. The postoperative therapy included hormones. It was necessary to prevent the onset of adrenal insufficiency and diabetes insipidus. The differential diagnosis of thrombosis and vasospasm was of great importance. In case of vasospasm, such medicines as sermion, redergine and nimodipine had a strong therapeutic effect. In vascular thrombosis these medicines were ineffective. Systemic approach to circulation disturbances seems of utmost importance for the analysis of postoperative complications.

Adolescent↗
PubMedDate not supplied

[Brain edema as a cause of critical states in neurosurgical patients].

The results of the studies in 120 patients after resection of tumours located in cranial fossa (40 cases), basal-diencephalic area (45 cases), hemispheres (35 cases) have shown the role of brain edema in the onset of critical conditions after neurosurgery (with consideration of a new concept concerning the mechanisms of brain edema development). It has been demonstrated that brain edema at its early stages is a biologically expedient adaptation response to any damage and is manifested in hyperhydration of all the tissues, most marked in the affected focus. Specific (neurogenic, neurohumoral) and non-specific (biochemical, autoimmune, mechanical, etc.) factors of brain edema onset have been identified. It turned out that the location of the affected focus determines the differences in neurogenic and neurohumoral mechanisms of the edema onset. The nearer the affected focus to the stem and diencephalic structures, the more marked the effect of neurogenic and neurohumoral factors and the more distinct the tendency towards edema generalization. Brain edema may be a cause of critical conditions and lethal outcomes only when it leads to dislocation and strangulation of them brain structures, and disturbances of brain metabolism and blood flow.

Brain Edema↗