Percutaneous thermal radiofrequency rhizotomy of L2-S1 spinal nerve roots in children with cerebral palsy.

OBJECTIVE: This study presents the results of an evaluation of the effectiveness of percutaneous thermal radiofrequency (RF) ablation of spinal nerve roots to reduce spasticity and improve motor function in children with cerebral palsy (CP). METHODS: A retrospective analysis was conducted on the surgical treatment outcomes of 26 pediatric patients with severe CP (Gross Motor Function Classification System levels IV-V). The assessment protocol included muscle tone assessment using the modified Ashworth scale (MAS), evaluation of passive and active range of motion, gait video recording, and locomotor status evaluation using the Gross Motor Function Measure (GMFM)-88 scale. Thermal RF rhizotomy (ablation of spinal nerve roots) was performed on all patients at the L2-S1 levels at 70°C for 90 seconds. The statistical data analysis was conducted using the t-test and Mann-Whitney U-test. A p value < 0.05 was considered statistically significant. RESULTS: Before the operation, the average level of spasticity in the lower-limb muscles of all patients was 3.0 ± 0.2 according to the MAS. In the early postoperative period, the spasticity level in all examined muscle groups significantly decreased to a mean of 1.14 ± 0.15 (p < 0.001). In the long-term postoperative period, the spasticity level in the examined muscle groups averaged 1.49 ± 0.17 points on the MAS (p < 0.001 compared to baseline, p = 0.0416 compared to the early postoperative period). Despite the marked reduction of spasticity in the lower limbs, no significant change in locomotor status according to the GMFM-88 scale was observed in the selected category of patients. In the long-term period, during the control examination of patients, the GMFM-88 level increased on average by 3.6% ± 1.4% (from 22.2% ± 3.1% to 25.8% ± 3.6%). CONCLUSIONS: The findings of this study offer preliminary yet compelling evidence that RF ablation of spinal nerve roots can lead to a significant and enduring decrease in muscle tone among children with severe spastic CP. Further studies and longer-term data of the impact on functionality and quality of life of patients with CP after spinal root RF ablation are needed.

The Impact of Treadmill Training on Tissue Integrity, Axon Growth, and Astrocyte Modulation.

Spinal cord injury (SCI) presents a complex challenge in neurorehabilitation, demanding innovative therapeutic strategies to facilitate functional recovery. This study investigates the effects of treadmill training on SCI recovery, emphasizing motor function enhancement, neural tissue preservation, and axonal growth. Our research, conducted on a rat model, demonstrates that controlled treadmill exercises significantly improve motor functions post-SCI, as evidenced by improved scores on the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and enhanced electromyography readings. Notably, the training facilitates the preservation of spinal cord tissue, effectively reducing secondary damage and promoting the maintenance of neural fibers in the injured area. A key finding is the significant stimulation of axonal growth around the injury epicenter in trained rats, marked by increased growth-associated protein 43 (GAP43) expression. Despite these advancements, the study notes a limited impact of treadmill training on motoneuron adaptation and highlights minimal changes in the astrocyte and neuron-glial antigen 2 (NG2) response. This suggests that, while treadmill training is instrumental in functional improvements post-SCI, its influence on certain neural cell types and glial populations is constrained.

The Vertebrobasilar Trunk and Its Anatomical Variants: A Microsurgical Anatomical Study.

BACKGROUND: The trunk of the basilar artery has not been included in microanatomy studies. Anatomical variants of the perforant branches of the vertebrobasilar trunk and their relationship with neural structures are very important in surgical approaches. Surgical dissection for the treatment of vascular lesions requires a perfect knowledge of the microsurgical anatomy. METHODS: We conducted a descriptive analysis of 50 brains, which were fixed with formalin at 10% for 2 weeks, and the arterial system was injected with colored latex. After microsurgical dissection, it was divided into three segments: the lower portion went from the anterior spinal artery to the anteroinferior cerebellar artery, the middle segment was raised from the upper limit of the lower portion to the origin of the superior cerebellar artery, and the upper segment ranged from the previous portion until the origin of the posterior cerebral artery. RESULTS: The basilar artery had an average length of 30 mm. The average diameter at its junction with the vertebral arteries was 4.05 mm. The average middle segment was 3.4 mm in diameter and 15.2 mm in length. The diameter of the upper segment was 4.2 mm, and its average length was 3.6 mm. The average number of bulbar arteries was three, and their average diameter was 0. 66 mm. The number of caudal perforator arteries were five on average, with a diameter of 0.32 mm. We found three rare cases of anatomical variants in the vertebra-basilar junction. CONCLUSIONS: The basilar artery emits penetrating branches in its lower, middle, and upper portions. The origin of penetrating branches was single or divided after forming a trunk. However, we observed long branches from perforant arteries.

KATP channels are regulators of programmed cell death and targets for the creation of novel drugs against ischemia/reperfusion cardiac injury.

BACKGROUND: The use of percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) is associated with a mortality rate of 5%-7%. It is clear that there is an urgent need to develop new drugs that can effectively prevent cardiac reperfusion injury. ATP-sensitive K+ (KATP ) channel openers (KCOs) can be classified as such drugs. RESULTS: KCOs prevent irreversible ischemia and reperfusion injury of the heart. KATP channel opening promotes inhibition of apoptosis, necroptosis, pyroptosis, and stimulation of autophagy. KCOs prevent the development of cardiac adverse remodeling and improve cardiac contractility in reperfusion. KCOs exhibit antiarrhythmic properties and prevent the appearance of the no-reflow phenomenon in animals with coronary artery occlusion and reperfusion. Diabetes mellitus and a cholesterol-enriched diet abolish the cardioprotective effect of KCOs. Nicorandil, a KCO, attenuates major adverse cardiovascular event and the no-reflow phenomenon, reduces infarct size, and decreases the incidence of ventricular arrhythmias in patients with acute myocardial infarction. CONCLUSION: The cardioprotective effect of KCOs is mediated by the opening of mitochondrial KATP (mitoKATP ) and sarcolemmal KATP (sarcKATP ) channels, triggered free radicals' production, and kinase activation.

Apelin Is a Prototype of Novel Drugs for the Treatment of Acute Myocardial Infarction and Adverse Myocardial Remodeling.

In-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is 5-6%. Consequently, it is necessary to develop fundamentally novel drugs capable of reducing mortality in patients with acute myocardial infarction. Apelins could be the prototype for such drugs. Chronic administration of apelins mitigates adverse myocardial remodeling in animals with myocardial infarction or pressure overload. The cardioprotective effect of apelins is accompanied by blockage of the MPT pore, GSK-3ß, and the activation of PI3-kinase, Akt, ERK1/2, NO-synthase, superoxide dismutase, glutathione peroxidase, matrix metalloproteinase, the epidermal growth factor receptor, Src kinase, the mitoKATP channel, guanylyl cyclase, phospholipase C, protein kinase C, the Na+/H+ exchanger, and the Na+/Ca2+ exchanger. The cardioprotective effect of apelins is associated with the inhibition of apoptosis and ferroptosis. Apelins stimulate the autophagy of cardiomyocytes. Synthetic apelin analogues are prospective compounds for the development of novel cardioprotective drugs.

The Role of Mitochondria-Targeting miRNAs in Intracerebral Hemorrhage.

Non-traumatic intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke, most often occurring between the ages of 45 and 60. Arterial hypertension (AH) is most often the cause of ICH, followed by atherosclerosis, blood diseases, inflammatory changes in cerebral vessels, intoxication and vitamin deficiencies. Cerebral hemorrhage can occur by diapedesis or as a result of a ruptured vessel. AH is difficult to treat, requires surgery and can lead to disability or death. One of the important directions in the study of the pathogenesis of ICH is mitochondrial dysfunction and its regulation. The key role of mitochondrial dysfunction in AH and atherosclerosis, as well as in the development of brain damage after hemorrhage, has been acknowledged. MicroRNAs (miRNAs) are a class of non-coding RNAs (about 18-22 nucleotides) that regulate a variety of biological processes including cell differentiation, proliferation, apoptosis, etc., primarily through gene repression. There is growing evidence to support dysregulated miRNAs in various cardiovascular diseases, including ICH. Further, the realization of miRNAs within mitochondrial compartment has challenged the traditional knowledge of signaling pathways involved in the regulatory network of cardiovascular diseases. However, the role of miRNAs in mitochondrial dysfunction for ICH is still under-appreciated, with comparatively much lesser studies and investigations reported, than those in other cardiovascular diseases. In this review, we summarize the up-to-date findings on the published role miRNAs in mitochondrial function for ICH, and the potential use of miRNAs in clinical settings, such as potential therapeutic targets and non-invasive diagnostic/prognostic biomarker tools.

Regulation of autophagy of the heart in ischemia and reperfusion.

Ischemia/reperfusion (I/R) of the heart leads to increased autophagic flux. Preconditioning stimulates autophagic flux by AMPK and PI3-kinase activation and mTOR inhibition. The cardioprotective effect of postconditioning is associated with activation of autophagy and increased activity of NO-synthase and AMPK. Oxidative stress stimulates autophagy in the heart during I/R. Superoxide radicals generated by NADPH-oxidase acts as a trigger for autophagy, possibly due to AMPK activation. There is reason to believe that AMPK, GSK-3ß, PINK1, JNK, hexokinase II, MEK, PKCα, and ERK kinases stimulate autophagy, while mTOR, PKCδ, Akt, and PI3-kinase can inhibit autophagy in the heart during I/R. However, there is evidence that PI3-kinase could stimulate autophagy in ischemic preconditioning of the heart. It was found that transcription factors FoxO1, FoxO3, NF-κB, HIF-1α, TFEB, and Nrf-2 enhance autophagy in the heart in I/R. Transcriptional factors STAT1, STAT3, and p53 inhibit autophagy in I/R. MicroRNAs could stimulate and inhibit autophagy in the heart in I/R. Long noncoding RNAs regulate the viability and autophagy of cardiomyocytes in hypoxia/reoxygenation (H/R). Nitric oxide (NO) donors and endogenous NO could activate autophagy of cardiomyocytes. Activation of heme oxygenase-1 promotes cardiomyocyte tolerance to H/R and enhances autophagy. Hydrogen sulfide increases cardiac tolerance to I/R and inhibits apoptosis and autophagy via mTOR and PI3-kinase activation.

The Effect of Whole Blood and Bone Marrow with the Addition of Pyrimidine-2,4(1h,3h)-dione Thietanyl Derivatives on Free Radical Oxidation.

BACKGROUND: It is relevant to study the general patterns and identify non-specific mechanisms of body protective and adaptive reactions violation, which can lead to the various pathological processes and develop principles for the correction of these disorders. One of the therapy and prevention directions is the search for new medicines. In recent years, new derivatives of pyrimidine bases have been synthesized and studied. Pyrimidine-based medicines have a membrane-stabilizing and immunomodulatory effect and can normalize metabolic disorders and increase the oxidative activity of leukocytes. Disruption of the free radical oxidation processes, the generation of reactive oxygen species and lipid peroxidation, including in whole blood and bone marrow, has gained importance in recent years. METHODS: Each reaction was monitored by thin layer chromatography. 1H, 13C, and 15N NMR spectra were recorded (chemical shifts were expressed as δ-values). We studied the effect of 6-methyl-3-(thietan- 3-yl)pyrimidine-2,4(1H,3H)-dione on the generation of reactive oxygen species (ROS) in the whole blood and bone marrow using the study of whole blood spontaneous and stimulated chemiluminescence (CL). CL methods make it possible to quickly and easily assess the studied material (whole blood, bone marrow) effect on free radical oxidation. Using CL methods, it is possible to reveal the presence of medicines' pro- or antioxidant properties, opening up new possibilities in the search for substances with antioxidant properties and comparing their activity. RESULTS: Alkylation of 6-methylpyrimidine-2,4(1H,3H)-dione by 2-chloromethylthiirane in protic solvents in the presence of alkali leads to the formation of an N-thietane derivative. NMR spectroscopy showed that 6-methylpyrimidine-2,4(1H,3H)-dione was alkylated at position 3. The oxidation reactions of N-(thietan-3-yl)pyrimidine-2,4(1H,3H)-dione were studied, and it was determined that, depending on the excess of the oxidizing agent and the duration of the process, N-(1-oxothietan-3-yl)- or N-(1,1-- dioxothietan-3-yl)pyrimidine-2,4(1H,3H)-diones were formed. The effects of free radical oxidation processes of new biologically active pyrimidine-2,4(1H,3H)-diones were studied. CONCLUSION: New pyrimidine-2,4(1H,3H)-diones increase the general adaptive capabilities of the body and have protective effects in extreme conditions.

Improvement of brain perfusion in patients with chronic brain ischemia at epidural spinal cord electrical stimulation.

Objective: Increasing life expectancy and aging of the population is accompanied by a steady increase in the number of elderly patients with chronic cerebral ischemia and age-related cognitive impairment associated with cerebral hypoperfusion and microangiopathy. The aim of this study was to identify long-term changes in cerebral blood flow (CBF) in patients with chronic cerebral ischemia at the epidural electrical stimulation of the spinal cord (SCS). Materials and methods: Changes in cerebral blood flow were studied according to CT perfusion in 59 patients (aged 55-78 years) with vertebrogenic pain syndromes and chronic cerebral ischemia during epidural electrical stimulation of the spinal cord at the cervical (C3-C5) and lower thoracic (Th9-Th10) levels. Results: In all patients, on the 5th day of trial SCS, an increase in cerebral blood flow by from 58.6 ± 1.13 ml/100 ml/min to 64.8 ± 1.21 ml/100 ml/min (p < 0.01) with stimulation at the Th9-Th10 level and from 58.8 ± 1.12 ml/100 ml/min to 68.2 ± 1.42 ml/100 ml/min (p < 0, 01) with stimulation at the C3-C5 level. These changes in brain perfusion were preserved during the follow-up examination 1 year after the implantation of chronic SCS system. The greatest increase in CBF was registered in the frontotemporal regions, subcortical structures and white matter of the brain. Changes in cerebral perfusion did not correlate with the degree of reduction in the severity of the accompanying pain syndrome. The change in CBF in the control group (32 patients) in all periods was not statistically significant. Conclusion: Our results show that SCS is accompanied by a persistent improvement in brain perfusion, which may be potentially useful for developing methods for reducing age-related vascular disorders in the elderly.

Pharmacological Approaches to Limit Ischemic and Reperfusion Injuries of the Heart: Analysis of Experimental and Clinical Data on P2Y12 Receptor Antagonists.

Ischemic and reperfusion injuries of the heart underlie the pathogenesis of acute myocardial infarction (AMI) and sudden cardiac death. The mortality rate is still high and is 5-7% in patients with ST-segment elevation myocardial infarction. The review is devoted to pharmacological approaches to limitation of ischemic and reperfusion injuries of the heart. The article analyzes experimental evidence and the clinical data on the effects of P2Y12 receptor antagonists on the heart's tolerance to ischemia/reperfusion in animals with coronary artery occlusion and reperfusion and also in patients with AMI. Chronic administration of ticagrelor prevented adverse remodeling of the heart. There is evidence that sphingosine-1-phosphate is the molecule that mediates the infarct-reducing effect of P2Y12 receptor antagonists. It was discussed a role of adenosine in the cardioprotective effect of ticagrelor.

Long non-coding RNAs as biomarkers and therapeutic targets for ischemic stroke.

Background: The problem of ischemic stroke (IS) has become increasingly important in recent years, as it ranks first in the structure of disability and mortality, crowding out other vascular diseases. In this regard, the study of this pathology and the search for new therapeutic and diagnostic tools remains an urgent problem of modern medical science and practice. Long non-coding RNAs (lncRNAs)-based therapeutics and diagnostic tools offer a very attractive area of study. Therefore, this systematic review aims at summarizing current knowledge on promising lncRNAs as biomarkers and therapeutic targets for IS exploring original articles and literature reviews on in vivo, in vitro and ex vivo experiments. Methods: The current systematic review was performed according to PRISMA guidelines. PubMed, MEDLINE and Google Scholar databases were comprehensively explored to perform the article search. Results: 34 eligible studies were included and analyzed: 25 focused on lncRNAs-based therapeutics and 9 on lncRNAs-based diagnosis. We found 31 different lncRNAs tested as potential therapeutic and diagnostic molecules in cells and animal model experiments. Among all founded lncRNA-based therapeutics and non-invasive diagnostic tools, nuclear enriched abundant transcript 1 (NEAT1) emerged to be the most investigated and proposed as a potential molecule for IS diagnosis and treatment. Conclusions: Our analysis provides a snapshot of the current scenario regarding the lncRNAs as therapeutic molecules and biomarkers in IS. Different lncRNAs are differently expressed in IS, and some of them can be further evaluated as therapeutic targets and biomarkers for early diagnosis and prognosis or treatment response. However, despite many efforts, none of the selected studies go beyond preclinical studies, and their translation into clinical practice seems to be very premature.

MicroRNAs-mediated regulation of glucose transporter (GLUT) expression in glioblastoma.

Current knowledge about the role of microRNAs (miRNAs) in tumor glucose metabolism is growing, and a number of studies regularly confirm the impact miRNAs can have on glucose metabolism reprogramming in tumors. However, there remains a lack of understanding of the broader perspective on the role of miRNAs in energy reprogramming in glioblastoma. An important role in the metabolism of glucose is played by carrier proteins that ensure its transmembrane movement. Carrier proteins in mammalian cells are glucose transporters (GLUTs). In total, 12 types of GLUTs are distinguished, differing in localization, affinity for glucose and ability to regulate. The fact of increased consumption of glucose in tumors compared to non-proliferating normal tissues is known. Tumor cells need glucose to ensure their survival and growth, so the type of transport proteins like GLUT are critical for them. Previous studies have shown that GLUT-1 and GLUT-3 may play an important role in the development of some types of malignant tumors, including glioblastoma. In addition, there is evidence of how GLUT-1 and GLUT-3 expression is regulated by miRNAs in glioblastoma. Thus, the aim of this study is to highlight the role of specific miRNAs in modulating GLUT levels in order to take into account the use of miRNAs expression modulators as a useful strategy to increase the sensitivity of glioblastoma to current therapies.

Modern aspects of the use of natural polyphenols in tumor prevention and therapy.

Polyphenols are secondary plant metabolites or organic compounds synthesized by them. In other words, these are molecules that are found in plants. Due to the wide variety of polyphenols and the plants in which they are found, these compounds are divided according to the source of origin, the function of the polyphenols, and their chemical structure; where the main ones are flavonoids. All the beneficial properties of polyphenols have not yet been studied, since this group of substances is very extensive and diverse. However, most polyphenols are known to be powerful antioxidants and have anti-inflammatory effects. Polyphenols help fight cell damage caused by free radicals and immune system components. In particular, polyphenols are credited with a preventive effect that helps protect the body from certain forms of cancer. The onset and progression of tumors may be related directly to oxidative stress, or inflammation. These processes can increase the amount of DNA damage and lead to loss of control over cell division. A number of studies have shown that oxidative stress uncontrolled by antioxidants or an uncontrolled and prolonged inflammatory process increases the risk of developing sarcoma, melanoma, and breast, lung, liver, and prostate cancer. Therefore, a more in-depth study of the effect of polyphenolic compounds on certain signaling pathways that determine the complex cascade of oncogenesis is a promising direction in the search for new methods for the prevention and treatment of tumors.

Functions of the bone morphogenetic protein signaling pathway through non-coding RNAs.

Bone morphogenetic proteins (BMPs) are proteins of the transforming growth factor-ß (TGF-ß) family, which plays an important role in the formation of skeletal and cartilage tissue and their regeneration. BMPs play a key role in the formation of new blood vessels and promote the migration, proliferation, and differentiation of mesenchymal stem cells (MSCs) into chondroblasts and osteoblasts. It is known that malfunction of BMPs signaling can cause a disease state. Epigenetic regulation of expression plays a key role in the control of many cellular processes. Important participants in this regulation are non-coding RNAs (ncRNAs), which are RNA molecules that are not translated into proteins. The best known of these are microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). In addition, the results of many studies make it possible to establish an unambiguous functional relationship between these ncRNAs. Being involved in the regulation of a large number of target genes responsible for the life of the cell, miRNAs, lncRNAs, and circRNAs are essential for the normal development and functioning of the body, and the violation of their functions accompanies the development of many pathophysiological processes including oncogenesis. In the present review, we discuss different insights into the regulation of BMPs signaling pathway by miRNAs, lncRNAs and circRNAs governed.

Circulating miRNAs as Diagnostic and Prognostic Biomarkers in High-Grade Gliomas.

Objectives: miR-181a/b and miR-410 downregulation and miR-155 upregulation has been shown to play important roles in the oncogenesis and progression of gliomas including high-grade gliomas. However, the potential role of plasma miR-181a/b, miR-410 and miR-155 in the diagnosis and prognosis of high-grade gliomas remains poorly known. Methods: We retrieved published articles from the PubMed, the Cochrane Central Register of Controlled Trials, and Web of Science database and obtained different sets of data on microRNAs (miRNAs) expression profiling in glioma and highlighted the most frequently dysregulated miRNAs and their gene-targets (PDCD4, WNT5A, MET, and EGFR) in high-grade gliomas. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was carried out to measure the pre- and postoperative plasma levels of miR-181a/b, miR-410 and miR-155 in 114 Grade 3-4 glioma patients, 77 Grade 1-2 glioma patients and 85 healthy volunteers as control group. The diagnostic and prognostic value of circulating miR-181a/b, miR-410 and miR-155 as biomarker was estimated by the Receiver Operating Characteristic (ROC) curve and the area under the curve (AUC) and Kaplan-Meier analysis. Results: We found a plasma miRNA signature including three downexpressed miRNAs and one overexpressed (miR-181a, miR-181b and miR-410; miR-155) in high-grade glioma patients in comparison with low-grade glioma patients control group. The ROC curve AUC of these four circulating miRNAs were ≥ 0.75 for high-grade glioma patients in before and after surgery. Higher circulating miR-155 and lower miR-181a/b and miR-410 expression is associated with clinical data, clinic pathological variables, worse overall survival (OS) of patients and negative correlated with potential gene-targets expression. Moreover, Kaplan-Meier analysis showed that miR-181a/b, miR-410 and miR-155 were independent predictors of OS in high-grade glioma patients. Conclusions: Our data, for the first time, demonstrated that circulating miR-181a/b, miR-410 and miR-155 could be a useful diagnostic and prognostic non-invasive biomarkers in high-grade gliomas.

Endoscopic third ventriculostomy in patients younger than 2 years: outcome analysis of 41 hydrocephalus cases.

OBJECT: The object of this study was to analyze the outcome of endoscopic third ventriculostomy (ETV) in patients under 2 years of age and investigate factors related to ETV success or failure in this patient population. METHODS: The authors reviewed their experience in using endoscopic third ventriculostomy (ETV) in the treatment of 41 hydrocephalus patients younger than 2 years. The mean duration of follow-up was 45 months. The relationship between ETV efficacy and the following variables was analyzed: cause of hydrocephalus, level of CSF occlusion, primary versus secondary ETV, type of surgical procedure, head circumference, patient age at ETV, patient age at first manifestation of hydrocephalus, and anatomical features of the ventricle. Success of ETV was assessed based on the results of neurological examination and postoperative imaging during the follow-up period. RESULTS: The authors performed 32 primary ETVs and 10 secondary ETVs (ETV after hydrocephalus surgery) in 41 patients (a second ETV was performed in 1 patient). The success rates of primary and secondary ETV were 75.8 and 55.6%, respectively (no significant difference, p = 0.15). The ETV was clinically and radiologically successful in 30 (71.4%) of 42 procedures during a mean (+/- SD) follow-up period of 45.0 +/- 4.8 months (range 12-127 months). A negative relationship was found between success of ETV and the thickness of the floor of the third ventricle (the most effective procedures were those in which the floor of the ventricle was thinnest [p < 0.05]). There was a highly significant correlation between ETV success and prolapse of the ventricle floor (p < 0.001). Also, there was an inverse relationship between ventricle floor thickness and the width of the third ventricle (p < 0.005). In our group of patients there was significant correlation between ETV success and patient age at onset of hydrocephalus (the most effective procedures were in patients in whom signs of hydrocephalus first occurred after 1 month of age [p = 0.02]). CONCLUSIONS: Endoscopic third ventriculostomy was successful in 71.4% of procedures in children younger than 2 years and in 75.0% of procedures in infants. Success of ETV in children younger than 2 years depends not on the age of the patient or cause of hydrocephalus but on the thickness of the floor of the third ventricle and the patient's age at first manifestation of hydrocephalus.

Microsurgical study of the interpeduncular cistern and its communication with adjoining cisterns.

OBJECTIVE: Investigating the structure, contents, location, and borders of interpeduncular cistern and its communications with adjoining cisterns. MATERIALS AND METHODS: Microsurgical anatomy of the interpeduncular cistern was studied in 14 adult cadaver brains, using a surgical microscope(x3 to x40 magnification). RESULTS: The interpeduncular cistern was divided into two portions: superficial (free) and deep (vascular). The superior wall of interpeduncular cistern was separated into the hypothalamic and mesencephalic part. It has communication with ambient, prepontine, carotid, cerebellopontine, oculomotor, and crural cisterns. CONCLUSION: The interpeduncular cistern is a compound bulk structure. This classification is necessary for the quantitative and qualitative study of the interpeduncular anatomy. Also, it is necessary to neurosurgeons for the guiding line in this region.