Cerebral Vascular Insufficiency Research Articles

Chronic hypoxia remodels the tumor microenvironment to support glioma stem cell growth

Cerebral organoids co-cultured with patient derived glioma stem cells (GLICOs) are an experimentally tractable research tool useful for investigating the role of the human brain tumor microenvironment in glioblastoma. Here we describe long-term GLICOs, a novel model in which COs are grown from embryonic stem cell cultures containing low levels of GSCs and tumor development is monitored over extended durations (ltGLICOs). Single-cell profiling of ltGLICOs revealed an unexpectedly long latency period prior to GSC expansion, and that normal organoid development was unimpaired by the presence of low numbers of GSCs. However, as organoids age they experience chronic hypoxia and oxidative stress which remodels the tumor microenvironment to promote GSC expansion. Receptor-ligand modelling identified astrocytes, which secreted various pro-tumorigenic ligands including FGF1, as the primary cell type for GSC crosstalk and single-cell multi-omic analysis revealed these astrocytes were under the control of ischemic regulatory networks. Functional validation confirmed hypoxia as a driver of pro-tumorigenic astrocytic ligand secretion and that GSC expansion was accelerated by pharmacological induction of oxidative stress. When controlled for genotype, the close association between glioma aggressiveness and patient age has very few proposed biological explanations. Our findings indicate that age-associated increases in cerebral vascular insufficiency and associated regional chronic cerebral hypoxia may contribute to this phenomenon.

Diabetic ketoacidosis and cognitive impairment in children and adolescents

The aim of the literature review was to highlight modern scientific sources on the formation and clinical manifestations of cognitive impairment in children and adolescents with type 1 diabetes mellitus (DM) after diabetic ketoacidosis (DKA). Type 1 DM is one of the most prevalent endocrine disorders in childhood and adolescence. DKA is the most common acute complication of type 1 DM that may cause cognitive impairment. Cerebral edema is the main cause of cerebral vascular insufficiency in patients with DKA. However, the mechanisms underlying the development of cognitive dysfunction in DKA have not been fully elucidated.The leading hypotheses include development of neuroinflammation, oxidative stress, disruption of neurogenesis, and neurodegeneration. Hypoxic – ischemic injury and changes in the brain neuroanatomy may also cause cognitive dysfunction. Disruption of some brain structures has been reported after DKA episodes, primarily affecting the white matter. Clinical studies in the pediatric population support the presence of a correlation between the severity and frequency of DKA and the severity of cognitive impairment. Cognitive dysfunction in children and adolescents after a DKA episode can manifest through decreased attention, impaired memory and executive function, and reduced IQ. The earliest possible diagnosis of cognitive impairment in pediatric patients with symptoms of DKA in the context of type 1 DM can improve the treatment prognosis for this endocrinopathy.

Chronic Disorders of Cerebral Circulation: a Challenge for the Family Doctor

The article examines modern views on the pathogenesis and clinical manifestations of chronic cerebral ischemia (CCI) and the possibilities of their pharmacotherapy. From this point of view, the requirements for choosing the optimal pharmacological strategy for pathological changes in the brain during ischemia are analyzed. The main goals of the clinical application of the strategy of neuroprotection in general, and in particular the need for a simultaneous effect on the neuronal, neurotransmitter and vascular mechanisms of the development of cognitive and general brain symptoms are considered. The necessity of using membrane-protective, cholinergic and vasotropic type of action is well founded. In this regard, the risks of polypharmacy in such patients and the arguments in favor of prescribing combined drugs were analyzed. The advantages of the innovative domestic combination containing citicoline and ginkgo biloba extract are considered in detail. The mechanisms of action and clinical effects of these components are analyzed with an emphasis on the prospects of their use in general medical practice. Special attention is paid to the justification of new opportunities provided by the synergistic effect of citicoline and ginkgo biloba extract when they are used in the form of a combined dosage form in comparison with monotherapy with these agents. The data on the safety of the use of the specified combination, as well as the scheme of dosage and course regimens, are given. The combination of citicoline + ginkgo biloba extract opens up new opportunities for family doctors in the pharmacotherapy of early cerebral vascular insufficiency symptoms.

Is later-life depression a risk factor for Alzheimer’s disease or a prodromal symptom: a study using post-mortem human brain tissue?

BackgroundDepression and dementia are both common diseases. Although new cases of depression are more common in younger adults, there is a second peak at the age of 50 years suggesting a different pathological process. Late-life depression (LLD) is associated with dementia. However, it remains unclear whether depression represents a dementia prodrome or is a true risk factor for its development.LLD is thought to have a vascular component and this may be a possible link between depression and dementia. We hypothesised that later-life depression is a prodromal manifestation of dementia and would therefore be associated with more AD, and/or ischaemic brain abnormalities that are present in earlier-life depression or in age- and sex-matched controls.MethodsWe assessed post-mortem orbitofrontal cortex and dorsolateral pre-frontal cortex from 145 individuals in 4 groups: 28 18–50-year-olds with depression, 30 older individuals (ages 51–90) with depression, 28 with early AD (Braak tangle stages III–IV) and 57 matched controls (17 early-life, 42 later-life). Levels of Aβ, phospho-tau and α-synuclein were assessed by immunohistochemistry and ELISA. To quantify chronic ischaemia, VEGF, MAG and PLP1 were measured by ELISA. To assess pericyte damage, PDGFRB was measured by ELISA. For blood–brain barrier leakiness, JAM-A, claudin 5 and fibrinogen were measured by ELISA. To quantity endothelial activation, the ratio of ICAM1:collagen IV was assessed by immunohistochemistry.ResultsThere was no evidence of chronic cerebral hypoperfusion or increased Aβ/tau in either depression group. There was also no indication of pericyte damage, increased blood–brain barrier leakiness or endothelial activation in the OFC or DLPFC in the depression groups.ConclusionsContrary to some previous findings, we have not found evidence of impaired vascular function or increased Aβ in LLD. Our study had a relatively small sample size and limitations in the availability of clinical data. These results suggest that depression is a risk factor for dementia rather than an early manifestation of AD or a consequence of cerebral vascular insufficiency.

Neutrophils and their friends.

Neutrophils and their friends.

Speech Therapy as a Component of Comprehensive Rehabilitation of Patients with Acute Impairment of Cerebral Circulation

The article reveals the essence of speech and speech therapy as a component of the rehabilitation process in restoring the health of patients who have suffered acute impairment of cerebral circulation. The concept of cerebral vascular insufficiency was analyzed, which refers to cerebral physiological changes in old age and associated conditions of speech impairment. Vascular diseases of the brain are not only a medical problem, but also a social one: they cause enormous damage to the economy, considering the costs of treatment, medical rehabilitation, and losses in production. The effectiveness of motor recovery after an ischemic stroke in the early recovery period depends largely on timely rehabilitation. Physical exercises have a positive effect on the recovery of the body systems of people who have had an ischemic stroke. The most frequent consequences of stroke in about 40-50% of the total number of patients are disorders of speech function, manifested in the form of aphasia and dysarthria, which are often combined with pathology of other higher mental functions (various types of agnosia and apraxia). Today, speech therapy is practiced by specialists both as a separate method and in combination with other techniques, and is used in individual and group work, including work with patients who have had an acute impairment of cerebral circulation.

No evidence of decreased perfusion or blood‐brain barrier leakiness in later life depression

Depression and dementia are both common diseases. Although new cases of depression are more common in younger adults there is a second peak at the age of 50 years suggesting a different pathological process. Late-life depression (LLD) is associated with dementia. However, it remains unclear whether depression represents a dementia prodrome or is a true risk factor for its development. LLD is thought to have a vascular component and this may be a possible link between depression and dementia. We hypothesised that later-life depression is a prodromal manifestation of dementia and would therefore be associated with more AD, and/or ischaemic brain abnormalities than are present in earlier-life depression or in age- and sex-matched controls.We assessed post-mortem orbitofrontal cortex and dorsolateral pre-frontal cortex from 145 individuals in 4 groups: 28 18-50-year-olds with depression, 30 older individuals (ages 51-90) with depression, 28 with early AD (Braak tangle stages III-IV) and 57 matched controls (17 early-life, 42 later-life). Levels of Aβ, phospho-tau and α-synuclein were assessed by immunohistochemistry and ELISA. To quantify chronic ischaemia, VEGF, MAG and PLP1 were measured by ELISA. To assess pericyte damage, PDGFRB was measured by ELISA. For blood-brain barrier leakiness, JAM-A, claudin 5 and fibrinogen were measured by ELISA and the ratio of ICAM1:collagen IV assessed by immunohistochemistry.There was no evidence of chronic cerebral hypoperfusion or increased Aβ in either depression group. There was also no indication of pericyte damage or increased blood-brain barrier leakiness in the OFC in the depression groups CONCLUSION: Contrary to some previous findings, we have not found evidence of impaired vascular function or increased Aβ in LLD. These results suggest that it is a risk factor for dementia rather than an early manifestation of AD or a consequence of cerebral vascular insufficiency.

Does concomitance of Hashimoto's disease and type 1 diabetes affect diabetes control and development of its complications?

IntroductionAutoimmune diseases concomitant with diabetes may complicate the treatment and adversely affect the prognosis. The most common is Hashimoto’s disease (HD). We compared diabetes control and prevalence of chronic complications in type 1 diabetes patients differing in the coexistence of HD.Material and methodsMedical records of 188 type 1 diabetics were analysed. Hashimoto’s disease was diagnosed based on medical history, as well as determination of the levels of thyroid peroxidase antibodies, hormones and ultrasound examination. Statistical analysis was performed using Statistica 10PL.ResultsHD was diagnosed in 43 (23%) patients. The mean HbA1c was 8.8 ±1.5% in the group with HD, and 9 ±1.6% in the group without HD (ns). The prevalence of diabetes complications was similar in both groups: ischaemic heart disease was diagnosed in 19% of patients with HD and 19% without HD, cerebral vascular insufficiency – 8% and 7%, peripheral neuropathy – 14% and 12%, sensory polyneuropathy – 47% and 46%, diabetic foot – 7% and 8%, Charcot osteoarthropathy – 7% and 2%, cardiovascular neuropathy – 21% and 28%, neuropathy of the gastrointestinal tract – 5% and 6%, nephropathy – 12% and 19%, retinopathy – 42% and 43%, and cataract in 28% and 19%, respectively. Impaired hypoglycaemia perception was rarer in the group with HD: 9% vs. 25% (p ≈ 0.04).ConclusionsHashimoto’s disease does not significantly affect the level of type 1 diabetes control or the development of its complications. Only autonomic neuropathy in the form of impaired awareness of hypoglycaemia is rarer in patients with that thyroiditis.

Neurologic Manifestations of COVID-19 in Children: Emerging Pathophysiologic Insights.

The COVID-19 pandemic has affected mortality and morbidity across all ages, including children. Neurologic manifestations of coronavirus disease 2019, ranging from headaches to cerebrovascular stroke, may involve the CNS or peripheral nervous system. Neurologic involvement is also noted in the multisystem inflammatory syndrome in children, a pediatric condition that occurs weeks after infection with severe acute respiratory syndrome coronavirus 2, the virus that causes COVID-19. Knowledge about mechanisms of neurologic disease and immunologic response to severe acute respiratory syndrome coronavirus 2 is scarce but rapidly growing. Here, we concisely review experimental and clinical data relevant to pathophysiologic hypotheses regarding neurologic manifestations of coronavirus disease 2019. We highlight important knowledge gaps in differences between adults and children in their response to coronavirus disease 2019.

Pathophysiological mechanisms of neurological disorders in experimental animals exposed to vibration

The review presents an analysis of literature on the study of nervous system changes in experimental animals exposed to vibration. The hypoxic type of cellular metabolism against the background of vibration is the result of vascular mechanoreceptors stimulation and spasm of blood vessels as well as intravascular pressure phase fluctuations and impaired blood and lymph outflow. Hemodynamic disorders and microangiopathy in the central nervous system can reach the level of cerebral vascular impairment and capillary-trophic insufficiency of the brain. Changes in calcium homeostasis at the cellular and tissue levels is a key mechanism of neuronal destruction occurring alongside with impaired blood supply to the nervous tissue in patients with vibrational disease. Long-term exposure to vibration results in reduced tissue respiration in the brain structures of experimental animals, that is most pronounced in the cortex and leads to a pathological change of spontaneous electrical activity of brain structures. Acute vibration stress stimulated the synthesis and excretion of serotonin not only in the hippocampus and hypothalamus but also in the cerebellum, which explains the disturbances of the oculomotor reactions observed in vibration exposure in the control system of the vertical vestibular ocular reflex. A decrease in the total number of neurons as well as an increase in the number of astroglia cells against the background of paravascular tissue edema were revealed against the background of changes in neurotransmitters levels. An increase in the concentration of the biomarker of structural and functional damage to brain tissue specific protein S-100B accompanies the development of professional sensorineural hearing loss and dysfunction of cerebral level vegetative regulation.

Bilateral vestibulopathy in elderly patients

Balance disorders and recurring falls are the most frequent causes of medical treatment in old age. Chronic cerebral vascular insufficiency is considered to be the cause of instability in most of these cases, and its role in the development of postural instability in old age is likely to be greatly overrated. At the same time, the role of chronic peripheral vestibular disorders, by contrast, is underestimated. The emergence in recent years of sensitive, specific and, at the same time, relatively accessible methods of diagnosing peripheral vestibulopathies has led to a much more frequent diagnosis of peripheral vestibulopathies, and their role in the development of postural instability in elderly patients is being revisited. This review considers current approaches to the diagnosis and treatment of bilateral vestibulopathy.

Analysis of Volatile Constituents of Ginkgo Leaf

Ginkgo biloba L. (Ginkgoaceae) is one of the oldest trees on earth. The medicinal use of its seeds and leaves has been a tradition for thousands of years. The standardized extract (known as EGb 761) contains several biologically active components, among them are terpenes and flavonoid glycosides that are responsible for the pharmacological activities of Ginkgonis folium. According to European Union herbal monographs (EUHM), the leaves of Ginkgo are recommended for the treatment of dementia, cerebral vascular insufficiency, and disorders of the peripheral circulation. The aim of our work was to analyze volatile constituents of Ginkgo leaf. Leaves of 3 Ginkgo trees were analyzed; 2 of which grow in the Medicinal Plants Garden (young trees A and B) and 1 at the Botanical Garden (old tree C) in Bratislava. The leaves were collected in 2014. The essential oil was isolated and quantified using hydrodistillation according to European Pharmacopoeia (Ph. Eur.) The volatile constituents of Ginkgonis folium were evaluated qualitatively and quantitatively using gas chromatography-mass spectrometry (GC-MS) and gas chromatography with flame ionization detection (GC-FID). We identified 16 constituents of the leaves of tree A, 18 in tree B, and 14 in tree C. The volatiles of the 3 trees differ in the respective amounts of monoterpenoids, hydrocarbons, fatty acids, and their methyl esters. The following constituents were identified in all of the 3 trees in largest percentage: hexahydrofarnesyl acetone (23.6%, 16.0%, and 27.7%), α-linolenic acid methyl ester (14.8%, 20.7%, and 15.1%), and pentacosane (22.2%, 22.4%, and 21.9%). Other identified compounds include the monoterpenes ( E)- α-ionone and ( E)- β-ionone.

Selection of Patients with Resistant Arterial Hypertension for the Catheter-Based Renal Sympathetic Denervation

elaboration of algorithm for selection of patients with resistant arterial hypertension (AH) for Catheter-Based RenalSympathetic Denervation (CBRSD). We examined 284 patients with resistant AH. On stage 1 we excluded mostfrequent causes of secondary AH. In 247 patients (86.9 %) we established secondary character of AH, in 37 patients (13.1 %) AH wasfound to be essential. On stage 2 patients with essential AH were given 3-5 component hypotensive therapy. At the background of thistherapy we conducted 24‑hour ambulatory blood pressure monitoring (ABPM). CBRSD procedure was considered indicated if accordingto ABPM average 24‑hour blood pressure (BP) was above 150 and 100 mm Hg, and 24‑hour elevated BP load exceeded 60 %.In 13 of 37 patients (35 %) BP level satisfied these conditions. For CBRSD we used high frequency generator. Ablation was performedusing the Symplicity Catheter. Results were assessed in 1, 2, 9, 12, and 28 months. Target BP level at the background of minimaldoses of hypotensive drugs was achieved in 11 patients (85 %), what was confirmed by ABPM data. Levels of mean 24-4 hour systolicand diastolic BP significantly decreased from 173.9±14.9 to 143±21.3, р<0.05, and from 108.2±8.7 to 91.4±13.8 mm Hg., р<0.05,respectively. Index of elevated systolic BP time decreased from 78.2±14.6 to 49.8±29.6 %, р<0.05. Best effect was achieved in patients with AH duration before the procedure less than 7 years. None of the patients had episodes of cerebral vascular insufficiency or heart failure progression. While determining indications to bilateral CBRSD one should be governed by such criteria as exclusion of symptomatic AH and objective proofs of AH resistance (according to ABPM at the background of hypotensive therapy).

The radiology and cerebral vascular insufficiency subject-A case report and literature review

Magnetic Resonance (MR) uses many exam of medical image field. In this case report, we found an interesting case. We did not call it as patient because she did not present any symptoms, thus we call it as subject. Natural cerebral vascular deficiency was seldom to be reported due to subject does not present any obvious symptoms when subject is health or young. Hope that this case report would increase we know more about the congenital part cerebral vascular deficiency. A 36 y old female, who come to our hospital for advanced medical health examination. On the regular radiology exam, the MRI showed she has a congenital part cerebral vascular deficiency on December in 2013. In general, main cerebral artery deficiency would cause some impact on physiological, however, its seemly does not affect her in daily or intelligent working, or we still not know would it affect to human. This case report showed a young women persistent hypoglossal artery was missing. We should continuous follow the subject by regular medical health examination. For her, we can prevent further congenital caused injuries. It also added a rare case of Taiwanese in medical imaging academic field.

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

Acute cerebral ischemia is a manifestation of cerebral vascular insufficiency and has a high mortality. However, the therapy for acute cerebral ischemia is still limited. This study aimed to investigate the effect of microRNA-381 (miR-381) on the repair of nerve injury in rats with acute cerebral ischemia after cerebral lymphatic blockage (CLB) by targeting leucine-rich repeat C4 protein (LRRC4) through the Stromal cell-derived factor-1/CXC chemokine receptor-4 signaling pathway. Rat models of CLB and middle cerebral artery occlusion (MCAO) were established, and 56 Wistar rats were divided into sham, MCAO, CLB + MCAO, CLB + MCAO + miR-381 inhibitor, CLB + MCAO + miR-381 mimic, CLB + MCAO + AMD3100 and CLB + MCAO + miR-381 mimic + AMD3100 groups. Modified neurological severity score (mNSS was used to determine nerve injury, TTC staining to measure infarction volume, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and flow cytometry to evaluate cell apoptosis, immunofluorescence to measure BrdU-positive cell number, enzyme-linked immunosorbent assay (ELISA) to determine contents of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), nerve growth factor (NGF) and neurite outgrowth inhibitor -A (Nogo-A), Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting to evaluate expression of miR-381, LRRC4, SDF-1, CXCR4, pERK, Slit2 and vascular endothelial growth factor (VEGF). LRRC4 was a target gene of miR-381. Compared with the results in the CLB + MCAO group, mNSS, infarction volume, apoptosis rate and TNF-α, IL-1β, IL-6 and Nogo-A contents as well as LRRC4 expression in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups were increased (those in the CLB + MCAO + AMD3100 group > those in the CLB + MCAO + miR-381 mimic + AMD3100 group), while BrdU-positive cell number, contents of NGF and IL-10, and expression of SDF-1, CXCR4, pERK, Slit2 and VEGF in brain tissues were decreased (those in the CLB + MCAO + AMD3100 group < those in the CLB + MCAO + miR-381 mimic + AMD3100 group). The results in the CLB + MCAO + mimic group were opposite of those in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups. Taken together, we concluded that up-regulation of miR-381 promoted nerve injury repair in acute cerebral ischemia rats after CLB by negatively regulating LRRC4 through activating the SDF-1/CXCR4 signaling pathway.

Cerebral infarctions in vertebrobasilar artery atherosclerosis

to obtain more specific information on the morphology and pathogenesis of cerebral infarctions occurring in vertebrobasilar artery (VBA) atherosclerosis. Macro- and microscopic investigations of the brain, its arterial system, and heart were conducted in 69 autopsy cases with infarctions located in the vertebrobasilar system (VBS) in atherosclerosis. 69 cases were found to have 206 VBA infarctions of various extent and locations. The detected infarctions were single and multiple in 27 and 42 cases, respectively. The detected infarctions included extensive (n=7), large (n=9), medium (n=63), small deep (lacunar) (n=97), and small superficial (n=30). The brain stem showed lacunar infarctions most frequently (76% of the infarctions at this site). Medium and small infarctions were identified at the same frequency in the cerebral hemispheres and cerebellum. The occurrence of 94% of the extensive and large infarctions was ascertained to be pathogenetically associated with atherothrombotic occlusion of the intracranial arteries in the VBS. 76% of the small infarctions occurred through the mechanism of cerebral vascular insufficiency in tandem atherostenosis of VBAs in conjunction with an additional decrease in cerebral blood flow under the influence of an extracerebral factor (coronary heart disease). Medium infarctions were approximately equifrequently due to the two aforementioned causes and, in some cases, to cardiogenic thromboembolism of VBAs. Infarctions were multiple in most cases; while recent large atherothrombotic infarctions were frequently concurrent with small organized infarctions resulting from tandem atherostenosis of VBAs. This investigation could establish the relationship between the site, extent, and pathogenetic factors of infarctions in the VBA bed in atherosclerosis, as well as the prognostic value of small infarctions as predictors for severe ischemic stroke.

MULTIMODAL NEUROPROTECTIVE THERAPY OF COMORBID PATIENTS WITH CHRONIC CEREBRAL ISCHEMIA

The article reviews the etiological factors and pathophysiological mechanisms by which the cerebral vascular insufficiency develops and advances. It presents the main directions in the treatment of such patients including the combined use of polymodal drugs with neuroprotective, metabolic and vascular effects.

Endovascular treatments for posterior cerebral artery aneurysms and vascular insufficiency of fetal-type circulation after parent artery occlusion

We present a retrospective analysis of endovascular treatments for posterior cerebral artery (PCA) aneurysms and discuss the susceptibility of a fetal-type PCA to vascular insufficiency after parent artery occlusion. Among 1207 aneurysms treated with endovascular therapy between March 1997 and March 2013 in our institution, 10 patients (0.8%) presented PCA aneurysms. The principal strategy was to employ selective coil embolization for the aneurysm. However, in certain cases of fusiform or dissecting aneurysms, we performed parent artery occlusion with coils. Clinical and radiological data were collected from hospital charts and evaluated retrospectively. The mean age was 52.7±15.6years (range, 12–65years). Five patients (50%) were admitted with a subarachnoid hemorrhage, and one patient presented with slowly developing paralysis. The remaining four patients were diagnosed incidentally. Five patients underwent selective coil embolization, and five patients underwent parent artery occlusion. All endovascular therapies were successfully performed. However, two patients in the parent artery occlusion group suffered cerebral infarction, and both patients exhibited a fetal-type PCA. The remaining three patients in the parent artery occlusion group exhibited an adult-type PCA and did not suffer a cerebral infarction. Endovascular treatment with either selective coil embolization or parent artery occlusion is safe and effective as the long as the anatomical type of the PCA is considered. Patients with a fetal-type PCA may develop vascular insufficiency upon parent artery occlusion. Neurosurgeons should attempt to preserve the parent artery using a flow-diverting stent or stent-assisted technique for a fetal-type PCA aneurysm.

Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study

Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smooth muscle cells, gelatinases degrading elastin (matrix metalloproteinases 2 and 9 (MMP2 and MMP9) and tissue inhibitors of matrix metalloproteinases 1 and 2 (TIMP1 and TIMP2) on formalin-fixed surgical samples with the methods of immunohistochemistry and confocal laser scanning microscopy. Results: We revealed the fragmentation of elastic fibers (100% of patients) and some reduction of smooth muscle cells (p 0.05). Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors.

THE COURSE OF CEREBRAL VASCULAR INSUFFICIENCY IN PATHOLOGIC TORTUOSITY OF CAROTID ARTERIES, ITS ROLE IN INDICATIONS FOR SURGICAL TREATMENT

The article describes the effect of pathologic tortuosity of carotid arteries on cerebral circulation, variants of the course of vascular cerebral insufficiency and clinical manifestations, their role in indication for surgical treatment. The pathologic tortuosity of carotid arteries is revealed by the clinical picture of vascular cerebral insufficiency in carotid and/or vertebrobasilar basins. The work assesses the role of spiral computed tomography with contrasting and magnetic resonance imaging in the verification of signs of episodes of focal neurologic deficiency in patients with the tortuosity of carotid arteries and the potential for application of transcranial Doppler for evaluation of cerebral blood flow disorders in different variants of cerebral vascular insufficiency. The article covers the problems of analysis of the received data for indication for surgical treatment for the tortuous internal carotid artery and presents the long-term results of the surgical treatment of the patients with tortuosity of carotid artery (dynamics of neurological symptoms and the absence of cerebral infarction on the area of the surgery).