Brain Haemorrhage
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Author(s):  
Chon Sum Ong ◽  
Nur Amalina Binti Che Din ◽  
Celine Mien Er Fong ◽  
Amira Nabiha Binti Jamalludin

An accident with a tamping iron made Phineas Gage a historically famous brain-injury survivor. (1) Each year, approximately 1.6 million people sustain traumatic brain injury, leading to 52,000 deaths annually. (2) However, there is limited literature regarding traumatic brain penetration injury that could be found. A 42-year-old male with psychosis forcefully inserted a butter knife through nostril, traversed via sella turcica into posterior corpus callosum in a mental health facility. He was intubated in his local hospital and transferred over to a tertiary hospital for neurosurgical intervention. Radiological imaging showed impingement of knife against the posterior cerebral artery (PCA), multiple brain infarcts, intraventricular, and subarachnoid haemorrhage. The knife was removed after securing the PCA with the collaboration between neurosurgery and interventional radiology team. Sinus repair was immediately performed by the otorhinolaryngologists. External ventricular drain was inserted due to hydrocephalus secondary to brain haemorrhage. He eventually developed ventriculitis leading to sepsis and was treated with multiple antibiotics. The traumatic brain injury led to anterior hypopituitarism and diabetes insipidus which was treated using hormone therapy. He not only survived the fatal brain injury but also regained his Glasgow Coma Scale (GCS) score. This case demonstrates the potential of a multi-disciplinary and specialty approach to achieve outcomes a single specialty team could not. The outcome of a case which was deemed to be a non-survivable brain injury was made different due to the bold decision making, experience and innovative surgical strategy. Future research is needed to better understand and manage brain penetration injury.International Journal of Human and Health Sciences Supplementary Issue-2: 2021 Page: S27


TEM Journal ◽  
2021 ◽  
pp. 1476-1487
Author(s):  
Ahmad Yahya Dawod ◽  
Aniwat Phaphuangwittayakul

It is challenging to establish a significant solution with computer techniques to improve the speed and efficiency of Traumatic Brain Injury (TBI) diagnosis. Several segmentation methods involving diverse precision and a degree of effort have been proposed and detailed within the related literature. Segmentation of Brain image is one of the significant clinical diagnostics implements. This paper proposes a modified (MDRLSE) calculation for haemorrhage segmentation on Computed Tomography (CT) images. The image noise that abdicates the obscured edges is utilized to portray the precise boundary of the haemorrhage region. The proposed segmentation technique achieved an accuracy rate of 97.16%. The technique is implemented using an edge-based involved contour model for image segmentation, providing a simple narrowband to significantly reduce computational costs. The performance results show that it is effective for TBI image segmentation in brain images with various characteristics.


TEM Journal ◽  
2021 ◽  
pp. 1476-1487
Author(s):  
Ahmad Yahya Dawod ◽  
Aniwat Phaphuangwittayakul

It is challenging to establish a significant solution with computer techniques to improve the speed and efficiency of Traumatic Brain Injury (TBI) diagnosis. Several segmentation methods involving diverse precision and a degree of effort have been proposed and detailed within the related literature. Segmentation of Brain image is one of the significant clinical diagnostics implements. This paper proposes a modified (MDRLSE) calculation for haemorrhage segmentation on Computed Tomography (CT) images. The image noise that abdicates the obscured edges is utilized to portray the precise boundary of the haemorrhage region. The proposed segmentation technique achieved an accuracy rate of 97.16%. The technique is implemented using an edge-based involved contour model for image segmentation, providing a simple narrowband to significantly reduce computational costs. The performance results show that it is effective for TBI image segmentation in brain images with various characteristics.


2021 ◽  
Author(s):  
Fancheng Kong ◽  
Li-Qin Lang ◽  
Xia-Ling Zhang ◽  
Ming-Kang Zhong ◽  
Chun-Lai Ma

Abstract BackgroundDrug-resistant epilepsy (DRE) is a chronic condition derived from spontaneous changes and regulatory effects in the epileptic brain. DNA methylation, an inheritable but reversible epigenetic change, may participate in this complicated regulatory network. As demethylation factors, ten-eleven translocation (TET) family members have become a focus in recent studies of neurological disorders. Thus, we aimed to unravel their role in DRE and their function related to the possible refractory factor ABCB1 in a blood-brain barrier (BBB) model.MethodsWe quantified and localized TET1, TET2 and 5-hydroxymethylcytosine (5-hmC) in the temporal lobe cortex of DRE patients (n = 27) and traumatic brain haemorrhage controls (n = 10) by immunochemical staining. TET2 and ABCB1 expression patterns were determined in the temporal cortex and isolated brain capillaries of DRE patients using immunohistological detection and Western blot analysis, respectively. A BBB model constructed with hCMEC/D3 cells was used to verify the demethylation and regulatory effects of TET2 on ABCB1.ResultsTET2 expression was significantly increased in the temporal cortical tissue of DRE patients with or without hippocampal sclerosis (HS) compared to control patients, while TET1 and 5-hmC showed differences in expression. We also discovered that the vascular endothelium of DRE patients has a strong affinity for TET2. ABCB1 and TET2 have identical densities in the DRE temporal cortex, and they both have evidently higher expression in the vascular endothelium from the neocortex of DRE patients. In the BBB, TET2 depletion can cause attenuated expression and function of ABCB1, as well as a pattern of higher methylation in CpG islands of the ABCB1 promoter.ConclusionsThrough a cohort study performed on the temporal cortex and brain vessels of DRE patients, we identified a novel epigenetic marker, TET2. Data from experiments in a BBB model suggest that TET2 has a specific regulatory effect on ABCB1, which may serve as a potential mechanism and target in DRE and requires further research.


PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246678
Author(s):  
Keiko Ikeda ◽  
Adriana A. Tienda ◽  
Fiona E. Harrison ◽  
Kiyoshi Kawakami

Na+,K+-ATPase is a crucial protein responsible for maintaining the electrochemical gradients across the cell membrane. The Na+,K+-ATPase is comprised of catalytic α, β, and γ subunits. In adult brains, the α3 subunit, encoded by ATP1A3, is predominantly expressed in neurons, whereas the α2 subunit, encoded by ATP1A2, is expressed in glial cells. In foetal brains, the α2 is expressed in neurons as well. Mutations in α subunits cause a variety of neurologic disorders. Notably, the onset of symptoms in ATP1A2- and ATP1A3-related neurologic disorders is usually triggered by physiological or psychological stressors. To gain insight into the distinct roles of the α2 and α3 subunits in the developing foetal brain, whose developmental dysfunction may be a predisposing factor of neurologic disorders, we compared the phenotypes of mouse foetuses with double homozygous knockout of Atp1a2 and Atp1a3 (α2α3-dKO) to those with single knockout. The brain haemorrhage phenotype of α2α3-dKO was similar to that of homozygous knockout of the gene encoding ascorbic acid (ASC or vitamin C) transporter, SVCT2. The α2α3-dKO brain showed significantly decreased level of ASC compared with the wild-type (WT) and single knockout. We found that the ASC content in the basal ganglia and cerebellum was significantly lower in the adult Atp1a3 heterozygous knockout mouse (α3-HT) than in the WT. Interestingly, we observed a significant decrease in the ASC level in the basal ganglia and cerebellum of α3-HT in the peripartum period, during which mice are under physiological stress. These observations indicate that the α2 and α3 subunits independently contribute to the ASC level in the foetal brain and that the α3 subunit contributes to ASC transport in the adult basal ganglia and cerebellum. We propose that decreases in ASC levels may affect neural network development and are linked to the pathophysiology of ATP1A2- and ATP1A3-related neurologic disorders.


2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098772
Author(s):  
Tian-Jiao Zhang ◽  
Zhen Shen ◽  
Min Li ◽  
Jing Zhu ◽  
Yue-Bo Li ◽  
...  

Choriocarcinoma is a highly malignant gynaecological tumour. This disease becomes life-threatening once brain haemorrhage or brain herniation occurs. Timely and accurate brain surgery can gain treatment time for patients that have a large number of cerebral haemorrhages and/or brain herniation. This current report describes a case of choriocarcinoma secondary to a hydatidiform mole in a 55-year-old woman that presented with neurological symptoms. Following admission to hospital, computed tomography examination found that lung and brain metastases were accompanied by cerebral haemorrhage. Cerebral hernia occurred during induction chemotherapy treatment and emergency surgery was performed. The patient recovered after individual chemotherapy and rehabilitation treatment. Patients with a very high risk of choriocarcinoma with brain metastasis should be referred to a comprehensive medical centre. Necessary surgical treatment and individualized chemotherapy can reduce the mortality of patients with choriocarcinoma brain metastasis.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Conti ◽  
I.C Bogazzi ◽  
M Mazzucchelli ◽  
A Covelli ◽  
D Molesti ◽  
...  

Abstract Objective To search for rates of major bleeding events in patients (pts) with age ≥80 or ≥90 years (y.) with ongoing anticoagulants referred to hospital. Methods Patients complaining any bleeding events were submitted to propensity score matching for major bleeding and stratified according to age ≥80 or ≥90 y. and warfarin or direct oral anticoagulants (DOACs). Setting A General Hospital, northwest Tuscany, five-year survey, 385,650 visits; catchment area 197,722 inhabitants, of whom 18,373 on warfarin and 14,808 on DOACs. Out of DOACs, dabigatran and rivaroxaban were available in the catchment area since 5 y., apixaban 4 y. and edoxaban 3 y; 5,553 pts received rivaroxaban, 4,602 dabigatran, 3,147 apixaban and 1,506 edoxaban. Endpoint Primary endpoint was one-week death, and incidence of major bleeding. Results Out of 7,474 pts considered, 2504 (33.5%) pts were older than 80 y., of whom 518 (6.8%) were older than 90 y; they were enrolled in the study. Overall, 253 (10.1%) showed history of stroke/TIA, 578 (22.9%) atrial fibrillation, 277 (11.1%) cancer, 177 (7.0%) congestive heart failure, 33 (1.3%) pulmonary thromboembolism. Of these 7,474 pts 1,040 (41.5%) showed major bleeding: 621 (24.8%) were gastrointestinal of which 258 (10.3%) of the upper tract and 363 (14.5%) of the lower tract; 794 (31.7%) were brain haemorrhage; the remaining patients showed other bleeding. Overall, 435 (5.8%) pts needed reversal anticoagulation, 325 (4.4%) red blood cell pack, and 2879 (38.5%) admission. Eventually, 127 pts have been readmitted to the hospital for ischemic stroke and 499 for new bleeding event. CHA2D2VASc-score was 2.5±1.5 and Charlston Comorbidity Index was 3.4±2.3. Out of 2,504 patients older than 80 y., 367 (14,7%) received anticoagulants (including heparin) of which 134 (5.4%) received warfarin versus 63 (2.5%) DOACs (p<0.001); 24 dabigatran, 19 rivaroxaban, 17 apixaban, and 3 edoxaban. Overall 88 (3.5%) needed reversal anticoagulation, 128 pts (5.1%) red blood cell pack, and 825 (32.9%) pts admission. One-week mortality rate as follows: anticoagulants 35 (1.4%) versus DOACs 6 (0.2%), p<0.001; dabigatran 0, rivaroxaban 2, apixaban 2, edoxaban 2. Out of 518 patients older than 90 y., 98 (18.9%) received anticoagulants (including heparin) of whom 44 (8.5%) received warfarin; 11 (2.1%) DOACs (p<0.001); 4 dabigatran, 2 rivaroxaban, 4 apixaban, and 1 edoxaban. Overall 24 (4.6%) needed reversal anticoagulation, 50 (9.7%) red blood cell pack, and 203 (39.2%) admission. One-week mortality rate as follows: anticoagulants 10 (1.9%) versus DOACs 1 (0.2%), p<0.001; dabigatran 0, rivaroxaban 0, apixaban 1 (0.2%), edoxaban 0. Conclusion Patients of 80 y. and even 90 y. or older, with ongoing warfarin, showed higher percentage of major bleeding events and mortality rate versus DOACs. Within DOACs, edoxaban was more likely to show lower rate of major bleeding events, without differences in death rate. Funding Acknowledgement Type of funding source: None


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Natasha Ting Lee ◽  
Carly Selan ◽  
Joanne S. J. Chia ◽  
Sharelle A. Sturgeon ◽  
David K. Wright ◽  
...  

Abstract Stroke is caused by obstructed blood flow (ischaemia) or unrestricted bleeding in the brain (haemorrhage). Global brain ischaemia occurs after restricted cerebral blood flow e.g. during cardiac arrest. Following ischaemic injury, restoration of blood flow causes ischaemia–reperfusion (I/R) injury which worsens outcome. Secondary injury mechanisms after any stroke are similar, and encompass inflammation, endothelial dysfunction, blood–brain barrier (BBB) damage and apoptosis. We developed a new model of transient global forebrain I/R injury (dual carotid artery ligation; DCAL) and compared the manifestations of this injury with those in a conventional I/R injury model (middle-cerebral artery occlusion; MCAo) and with intracerebral haemorrhage (ICH; collagenase model). MRI revealed that DCAL produced smaller bilateral lesions predominantly localised to the striatum, whereas MCAo produced larger focal corticostriatal lesions. After global forebrain ischaemia mice had worse overall neurological scores, although quantitative locomotor assessment showed MCAo and ICH had significantly worsened mobility. BBB breakdown was highest in the DCAL model while apoptotic activity was highest after ICH. VCAM-1 upregulation was specific to ischaemic models only. Differential transcriptional upregulation of pro-inflammatory chemokines and cytokines and TLRs was seen in the three models. Our findings offer a unique insight into the similarities and differences in how biological processes are regulated after different types of stroke. They also establish a platform for analysis of therapies such as endothelial protective and anti-inflammatory agents that can be applied to all types of stroke.


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