The molecular mechanisms behind aneurysmal subarachnoid haemorrhage (aSAH) are still poorly understood. Expression patterns of miRNAs may help elucidate the post-transcriptional gene expression in aSAH. Here, we evaluate the global miRNAs expression profile (miRnome) of patients with aSAH to identify potential biomarkers. We collected 33 peripheral blood samples (27 patients with cerebral aneurysm, collected 7 to 10 days after the haemorrhage, when usually is the cerebral vasospasm risk peak, and six controls). Then, were performed small RNA sequencing using an Illumina Next Generation Sequencing (NGS) platform. Differential expression analysis identified eight differentially expressed miRNAs. Among them, three were identified being up-regulated, and five down-regulated. miR-486-5p was the most abundant expressed and is associated with poor neurological admission status. In silico miRNA gene target prediction showed 148 genes associated with at least two differentially expressed miRNAs. Among these, THBS1 and VEGFA, known to be related to thrombospondin and vascular endothelial growth factor. Moreover, MYC gene was found to be regulated by four miRNAs, suggesting an important role in aneurysmal subarachnoid haemorrhage. Additionally, 15 novel miRNAs were predicted being expressed only in aSAH, suggesting possible involvement in aneurysm pathogenesis. These findings may help the identification of novel biomarkers of clinical interest.
Tumours of the Central Nervous System (CNS) are an important cause of mortality from cancer. Epidemiological data on neoplams affecting the CNS are scarce in Brazil, especially in the Amazon region. The study aims at describing the histopathological profile of CNS tumours cases at a high-complexity referral cancer center. This study has described a 17-year-series profile of CNS tumours, registered at a high-complexity referral cancer center in Pará state, from January 1997 until July 2014 in the Brazilian Amazon Region. Data was gathered from histopathology reports kept in the hospital’s cancer registry and 949 cases of CNS tumours were analyzed. The most common histopathology were neuroepithelial tumours (approx. 40%) and meningioma was the most frequent especific tumor histologic subtype (22.2%). Neuroepithelial tumours were more frequent in patients with ages ranging from less than a year to 19 years, whereas metastatic tumours were prevalent in patients over 40 years of age. It was not found temporal trends during the studied period. The knowledge of these tumours profile is valuable for the understanding of cancer epidemiology in the region, since its prevalence is currently underreported and more awareness on the disease is needed.
The aneurysmal subarachnoid hemorrhage is a major public health problem described as a sudden drastic event with no warning symptoms and high morbidity and mortality rates. The role of the endothelial isoform of nitric oxide synthase gene polymorphism in intracranial aneurysms (IAs) is still a matter of controversy with divergent findings among European, American, and Asian populations. Our study purposed to test the association between intracranial aneurysms formation and nitric oxide gene polymorphisms through a systematic review and meta-analysis. Systematic search on Medline, Lilacs, and EMBASE was performed. The primary search resulted in 139 papers, out of which 9 met our inclusion criteria after a full text analysis. The dominant T786C model found a significant association with IA (OR 1.22, 95 % CI 1.04-1.44, p = 0.01), so did studies of the recessive T786C model (OR 0.37, 95 % CI 0.30-0.45, p < 0.0001) but with opposite effect. Our findings support the presence of the T786C polymorphism as a predictor for the development of intracranial aneurysm in the cerebral vascular system. More studies are necessary in order to elucidate the pathways of the endothelial nitric oxide synthase (eNOS) in cerebrovascular diseases and in defining how different allelic combinations of the eNOS gene single-nucleotide polymorphism (SNP) could favor this pathological process.
Background: There are no studies describing the cerebral hemodynamic patterns that can occur in traumatic brain injury (TBI) patients following decompressive craniectomy (DC). Such data have potentially clinical importance for guiding the treatment. The objective of this study was to investigate the postoperative cerebral hemodynamic patterns, using transcranial Doppler (TCD) ultrasonography, in patients who underwent DC. The relationship between the cerebral circulatory patterns and the patients' outcome was also analyzed. Methods: Nineteen TBI patients with uncontrolled brain swelling were prospectively studied. Cerebral blood circulation was evaluated by TCD ultrasonography. Patients and their cerebral hemispheres were categorized based on TCD-hemodynamic patterns. The data were correlated with neurological status, midline shift on CT scan, and Glasgow outcome scale scores at 6 months after injury. Results: Different cerebral hemodynamic patterns were observed. One patient (5.3%) presented with cerebral oligoemia, 4 patients (21%) with cerebral hyperemia, and 3 patients (15.8%) with cerebral vasospasm. One patient (5.3%) had hyperemia in one cerebral hemisphere and vasospasm in the other hemisphere. Ten patients (52.6%) had nonspecific circulatory pattern. Abnormal TCD-circulatory patterns were found in 9 patients (47.4%). There was no association between TCD-cerebral hemodynamic findings and outcome. Conclusion: There is a wide heterogeneity of postoperative cerebral hemodynamic findings among TBI patients who underwent DC, including hemodynamic heterogeneity between their cerebral hemispheres. DC was proved to be effective for the treatment of cerebral oligoemia. Our data support the concept of heterogeneous nature of the pathophysiology of the TBI and suggest that DC as the sole treatment modality is insufficient.
Acute liver failure, also known as fulminant hepatic failure (FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. Cerebral edema and intracranial hypertension are common causes of mortality in patients with FHF. The management of patients who present acute liver failure starts with determining the cause and an initial evaluation of prognosis. Regardless of whether or not patients are listed for liver transplantation, they should still be monitored for recovery, death, or transplantation. In the past, neuromonitoring was restricted to serial clinical neurologic examination and, in some cases, intracranial pressure monitoring. Over the years, this monitoring has proven insufficient, as brain abnormalities were detected at late and irreversible stages. The need for real-time monitoring of brain functions to favor prompt treatment and avert irreversible brain injuries led to the concepts of multimodal monitoring and neurophysiological decision support. New monitoring techniques, such as brain tissue oxygen tension, continuous electroencephalogram, transcranial Doppler, and cerebral microdialysis, have been developed. These techniques enable early diagnosis of brain hemodynamic, electrical, and biochemical changes, allow brain anatomical and physiological monitoring-guided therapy, and have improved patient survival rates. The purpose of this review is to discuss the multimodality methods available for monitoring patients with FHF in the neurocritical care setting.
Acute liver failure, also known as fulminant hepatic failure (FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. This is an uncommon, but not rare, condition with approximately 2,000 cases annually in the United States and a mortality rate ranging from 50% to 90%, despite intensive care therapy 1,2 . Cerebral edema leading to intracranial hypertension complicates approximately 50% to 80% of patients with severe FHF (grade III or IV coma), in whom it is the leading cause of death 2,3,4 . Brain edema in FHF patients is a relatively recent concept. In a 1944 report of 125 autopsies of military patients who had died from a condition he called fatal hepatitis (previously referred to as idiopathic acute yellow atrophy of the liver), Lucké 5 noted little alteration in the brain except for edema, but did not describe cerebral herniation. The first reports of brain edema and cerebral herniation as complications of FHF only emerged in the 1980s 6,7 . It is also noteworthy that brain edema and intracranial hypertension are not recognized common features of chronic liver failure, despite some case reports and small series 8,9 . The recent recognition of brain edema in FHF patients could be due to the advances in FHF patient care. Previously, FHF patients were dying from early hepatocellular insufficiency complications, mainly hemorrhage or sepsis ABSTRACTIntracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.Keywords: hepatic insufficiency; intracranial hypertension; brain edema. RESUMOO edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.Palavras-chave: insuficiência hepatica; hipertenção intracraniana; edema encefálico.
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