Parenchymal Brain Injury Research Articles

A challenging decision for emergency physicians: Routine repeat computed brain tomography of the brain in head trauma in infants and neonates.

Head trauma is a leading cause of death and disability. While standard treatment protocols exist for severe head trauma, no clear follow-up standards are available for mild head trauma with positive imaging findings in infants and newborns. Although routine follow-up brain computed tomography (CT) imaging is not recommended for children with moderate and mild head trauma, the necessity for follow-up imaging in infants and newborns remains uncertain. Our study is a retrospective, observational, and descriptive study. Infants under 1 year old presenting to the emergency department with isolated head trauma were reviewed with the approval of the Ethics Committee of Ankara Etlik City Hospital. Inclusion criteria included presentation to the emergency department, undergoing more than one brain CT scan, and sustaining mild head trauma (Glasgow Coma Scale [GCS] >13). Patients with incomplete follow-up data or multiple traumas were excluded. Age, gender, mechanism of trauma, initial and follow-up brain CT findings, hospital admission, and surgical procedures were recorded and analyzed using the SPSS statistical package. Out of 238 screened patients, 154 were included in the study. Of these, 66.9% were male and the average age was 5.99 months. The most common presenting symptom was swelling at the trauma site, observed in 79.2% of cases. The most common mechanism of injury was falling from a height of less than 90 cm, accounting for 85.1% of cases. Pathological progression on follow-up CT was observed in 5.2% of the patients, and only 1.9% required surgical treatment. A total of 34.4% of the patients required hospitalization. Patients with parenchymal brain pathology had a higher rate of pathological progression on follow-up CT and a longer hospital stay. Follow-up CT scans in infants with mild head trauma do not alter patient outcomes except in cases with brain parenchymal pathology. Study data indicated that repeat imaging is not beneficial for isolated skull fractures. Imaging artifacts often necessitated repeated scans, contributing to increased radiation exposure. Unnecessary repeat imaging escalates radiation exposure and healthcare costs. Only a small percentage of patients exhibited progression of intracranial pathology, justifying follow-up imaging solely in the presence of brain parenchymal injury. Larger prospective studies are necessary to confirm these findings.

Characterization of Immune Infiltrates Associated With Radiation Necrosis in the Setting of Brain Metastases Following Stereotactic Radiosurgery and Immunotherapy: A Retrospective Cohort Analysis.

Radiation necrosis (RN) is caused by vascular damage and brain parenchymal injury resulting in inflammation following radiotherapy (RT) for brain metastases. The impact of immunotherapy (IO) on the immune cellular microenvironment in patients' brain metastases is unknown. The objective of this study was to characterize the inflammatory microenvironment in the setting of RN compared to recurrent metastasis and determine whether IO treatment affects the cellular infiltrates. Adult patients with brain metastases from solid tumors who received both systemic IO and RT prior to resection of intracranial lesions were retrospectively analyzed. The resection either showed biopsy-proven RN or recurrent tumor. A group of patients who developed RN and were not on IO was reviewed as well. A total of 18 patients were categorized into one of three groups: necrosis, IO+RT; tumor, IO+RT; and necrosis, RT. Surgical specimens were stained for immune and inflammatory components and reviewed by a neuro-pathologist who remained blinded during the analysis. The presence or absence of lymphocytes, perivascular cuffs, plasma cells, macrophages, and fibrinoid vascular changes was characterized in a semiquantitative manner. The median age was 61.5 years (range 37-82 years). Seventy-seven percent of primary cancers were melanoma. Patients with RN were more likely to exhibit immune infiltrates compared to patients with recurrent metastasis. Limited analysis showed 100% of patients in "necrosis, IO+RT" had quantifiable cell counts; conversely, 83.3% of patients in "tumor, IO+RT" lacked quantifiable cell counts. Additionally, 83.3% of patients in "necrosis, RT" showed immune cells, including lymphocytes, macrophages, plasma cells, and cuffing. The immune microenvironment of brain metastasis following RT and IO showed higher levels of cell infiltrates in the RN setting versus the recurrent tumor setting. Patients who received prior IO compared to those with no IO had similar immune cell infiltrates adjacent to RN. Lower levels of immune cells in tumor recurrence following IO and RT raise the possibility that an environment lacking primed immune cells may decrease the efficacy of IO.

From the immune system to mood disorders especially induced by Toxoplasma gondii: CD4+ T cell as a bridge.

Toxoplasma gondii (T. gondii), a ubiquitous and obligatory intracellular protozoa, not only alters peripheral immune status, but crosses the blood-brain barrier to trigger brain parenchymal injury and central neuroinflammation to establish latent cerebral infection in humans and other vertebrates. Recent findings underscore the strong correlation between alterations in the peripheral and central immune environment and mood disorders. Th17 and Th1 cells are important pro-inflammatory cells that can drive the pathology of mood disorders by promoting neuroinflammation. As opposed to Th17 and Th1, regulatory T cells have inhibitory inflammatory and neuroprotective functions that can ameliorate mood disorders. T. gondii induces neuroinflammation, which can be mediated by CD4+ T cells (such as Tregs, Th17, Th1, and Th2). Though the pathophysiology and treatment of mood disorder have been currently studied, emerging evidence points to unique role of CD4+ T cells in mood disorder, especially those caused by T. gondii infection. In this review, we explore some recent studies that extend our understanding of the relationship between mood disorders and T. gondii.

EphA4/EphrinB2 signaling mediates pericyte-induced transient glia limitans formation as a secondary protective barrier after subarachnoid hemorrhage in mice

BackgroundMost patients with subarachnoid hemorrhage (SAH) do not exhibit brain parenchymal injury upon imaging but present significant blood–brain barrier (BBB) disruption and secondary neurological deficits. The aim of this study was to investigate whether stressed astrocytes act as a secondary barrier to exert a protective effect after SAH and to investigate the mechanism of glial limitan formation. MethodsA total of 204 adult male C57BL/6 mice and an endovascular perforation SAH model were employed. The spatiotemporal characteristics of glial limitan formation after SAH were determined by immunofluorescence staining and transmission electron microscopy. The molecular mechanisms by which pericytes regulate glia limitans formation were analyzed using polymerase chain reaction, Western blotting, immunofluorescence staining and ELISA in a pericyte-astrocyte contact coculture system. The findings were validated ex vivo and in vivo using lentiviruses and inhibitors. Finally, pericytes were targeted to regulate glial limitan formation, and the effect of the glia limitans on secondary brain injury after SAH was evaluated by flow cytometry and analysis of neurological function. ResultsStress-induced glial limitan formation occurred 1 day after SAH and markedly subsided 3 days after ictus. Pericytes regulated astrocyte glia limitan formation via EphA4/EphrinB2 signaling, inhibited inflammatory cell infiltration and altered neurological function. ConclusionsAstrocyte-derived glia limitans serve as a secondary protective barrier following BBB disruption after SAH in mice, and pericytes can regulate glial limitan formation and alter neurological function via EphA4/EphrinB2 signaling. Strategies for maintaining this secondary protective barrier may be novel treatment approaches for alleviating early brain injury after SAH.

Cranial defect and pneumocephalus are associated with significant postneurosurgical positional brain shift: evaluation using upright computed tomography

Only few studies have assessed brain shift caused by positional change. This study aimed to identify factors correlated with a large postneurosurgical positional brain shift (PBS). Sixty-seven patients who underwent neurosurgical procedures had upright computed tomography (CT) scan using settings similar to those of conventional supine CT. The presence of a clinically significant PBS, defined as a brain shift of ≥ 5 mm caused by positional change, was evaluated. The clinical and radiological findings were investigated to identify factors associated with a larger PBS. As a result, twenty-one patients had a clinically significant PBS. The univariate analysis showed that supratentorial lesion location, intra-axial lesion type, craniectomy procedure, and residual intracranial air were the predictors of PBS. Based on the multivariate analysis, craniectomy procedure (p < 0.001) and residual intracranial air volume (p = 0.004) were the predictors of PBS. In a sub-analysis of post-craniectomy patients, PBS was larger in patients with supratentorial craniectomy site and parenchymal brain injury. A large craniectomy area and long interval from craniectomy were correlated with the extent of PBS. In conclusion, patients who undergo craniectomy and those with residual intracranial air can present with a large PBS. In post-craniectomy patients, the predisposing factors of a large PBS are supratentorial craniectomy, presence of parenchymal injury, large skull defect area, and long interval from craniectomy. These findings can contribute to safe mobilization among postneurosurgical patients and the risk assessment of sinking skin flap syndrome.

C.1 Cerebral venous sinus thrombosis in preterm infants

Background: Previous studies of neonatal cerebral venous sinus thrombosis (CVST) have focused on term infants, and studies of preterm infants are lacking. In this study, we examined the clinical and radiological features, treatment and outcome of CVST in preterm infants. Methods: This was a retrospective cohort study of preterm infants (gestational age &lt;37 weeks) with radiologically confirmed CVST. All MRI/MRV and CT/CTV scans were re-reviewed. Clinical and radiological data were analysed using descriptive statistics, ANOVA and chi-square tests. Results: A total of 26 preterm infants with CVST were included. Of these, 65% were late preterm, 27% very preterm and 8% extreme preterm. Most (73%) were symptomatic at presentation with seizures or abnormal exam. Transverse (85%) and superior sagittal (42%) sinus were common sites of thrombosis. Parenchymal brain injury was predominantly periventricular (35%) and deep white matter (31%) in location. Intraventricular hemorrhage occurred in 46%. Most infants (69%) were treated with anticoagulation. None of the treated infants had hemorrhagic complications. Outcome at follow-up ranged from no impairment (50%), mild impairment (25%) and severe impairment (25%). Conclusions: Preterm infants with CVST are often symptomatic and have white matter brain lesions. Anticoagulation treatment of preterm CVST appeared to be safe and was not associated with hemorrhagic complications.

Cerebral Venous Sinus Thrombosis in Preterm Infants.

Neonatal cerebral venous sinus thrombosis (CVST) can lead to brain injury and neurodevelopmental impairments. Previous studies of neonatal CVST have focused on term infants, and studies of preterm infants are lacking. In this study, we examined the clinical and radiological features, treatment and outcome of CVST in preterm infants. This was a retrospective, consecutive cohort study of preterm infants (gestational age <37 weeks) with radiologically confirmed CVST. All magnetic resonance imaging/MRV and CT/CTV scans were re-reviewed to study thrombus characteristics and pattern of brain injury. Outcome was assessed by the validated pediatric stroke outcome measure at the most recent clinic visit. Twenty-six preterm infants with CVST were studied. Of these, 65% were moderate-late preterm (32-37 weeks), 27% very preterm (28-32 weeks), and 8% extreme preterm (<28 weeks). Most (73%) were symptomatic at presentation with seizures or abnormal exam. Transverse (85%) and superior sagittal (42%) sinuses were common sites of thrombosis. Parenchymal brain injury was predominantly periventricular (35%) and deep white matter (31%) in location. Intraventricular hemorrhage occurred in 46%. Most infants (69%) were treated with anticoagulation. No treated infant (including eleven with pretreatment hemorrhage) had new or worsening post-treatment hemorrhage. Outcomes ranged from no deficits (50%), mild-moderate (25%), and severe (25%) impairment. In our sample of preterm infants with CVST, more than one-quarter were asymptomatic. White matter brain lesions predominated and one-half had neurological deficits at follow-up. Anticoagulation of preterm CVST in this small cohort appeared to be safe. Larger studies of preterm CVST are needed.

Abstract TMP95: Cerebral Sinovenous Thrombosis In Preterm Infants

Introduction: Neonatal cerebral sinovenous thrombosis (CSVT) can lead to brain injury and long-term neurodevelopmental impairments. Previous studies of neonatal CSVT have primarily focused on term infants, and studies of preterm infants are lacking. In this study, we examined the clinical and radiological features, treatment and outcome of CSVT in preterm infants. Methods: This was a retrospective, consecutive cohort study of preterm infants (gestational age &lt;37 weeks) with radiologically confirmed CSVT. All MRI/MRV and CT/CTV scans were re-reviewed to study thrombus characteristics and the pattern of brain injury. Clinical and radiological data were analysed using descriptive statistics, ANOVA and chi-square tests. Outcome was assessed by the validated Pediatric Stroke Outcome Measure (PSOM). Results: A total of 26 preterm infants with CSVT were included. Of these, 65% were late preterm, 27% very preterm and 8% extreme preterm. Most (73%) were symptomatic at presentation with seizures or abnormal exam. Transverse (85%) and superior sagittal (42%) sinus were most common sites of thrombosis. Parenchymal brain injury was predominantly periventricular (35%) and deep white matter (31%) in location. Intraventricular hemorrhage occurred in 46%. Most infants (69%) were treated with anticoagulation. None of the treated infants had hemorrhagic complications. Outcome at follow-up ranged from no impairment (39%), mild impairment (19%) and severe impairment (19%). Conclusions: Preterm infants with CSVT are often symptomatic and have white matter brain lesions at presentation. Anticoagulation treatment of preterm CSVT in this small cohort appeared to be safe. Further larger studies and treatment.

Spontaneous Calvarial Infarction with Epidural Hematoma and Subgaleal Hemorrhage in a Teenager with Sickle Cell SS Disease and Glucose-6-Phosphate Dehydrogenase Deficiency

Introduction:Sequelae of sickle cell disease (SCD) are often the result of vaso-occlusion (VOC) related to the dysmorphic shape of sickled red blood cells (RBC). Bone infarction occurs commonly in patients with sickle cell, most notably in long bones and axial skeleton. Infarct occurs much less frequently in the bones of the skull. Calvarial bone infarct results in MRI findings of T2 hyperintensity in areas of bone marrow edema with associated swelling or hemorrhage. Symptomatic headaches in children with SCD are more likely to be due to severe underlying cerebral pathologies than in those children without SCD. When evaluating a child with SCD presenting with headache, it is important to consider calvarial infarct.Case Description:A 15 year old male with a history of sickle cell disease (type SS) and G6PD deficiency presented with chief complaints of headache and swelling over the left parietal region of the skull for two days with associated left sided visual disturbance. He denied head trauma or seizure-like activity. Upon presentation he was febrile with tachycardia and a normal neurological exam. CT scan of his head was significant for a left subgaleal hemorrhage and bilateral epidural midline and left parietal fluid collections consistent with bone marrow infarcts and associated subacute epidural hematomas, without evidence of brain parenchymal injury or sinus venous thrombosis. A follow up MRI obtained during hospitalization indicated that the left subgaleal hematoma remained stable with breakdown of subgaleal blood products. The patient was treated primarily with supportive care including hydration, packed red blood cell transfusions and pain management. He did not require neurosurgical intervention. His hospital course was complicated by VOC, sickle cell hepatopathy and acute chest syndrome.Discussion:Rarely, cranial VOC has resulted in epidural hematoma. In this case, calvarial infarct with unilateral headache, acute vision loss and acute cranial swelling resulted in subgaleal hemorrhage. This clinically significant finding results from bleeding between the periosteum and scalp galea aponeurosis, which may lead to hypovolemic shock. Calvarial infarcts should be considered on the differential in sickle cell disease patients presenting with a headache as prompt diagnosis can improve morbidity outcomes. DisclosuresNo relevant conflicts of interest to declare.

Sigma–1 receptor activation alleviates blood–brain barrier disruption post cerebral ischemia stroke by stimulating the GDNF–GFRα1–RET pathway

Blood–brain barrier (BBB) disruption is one of the most important pathological manifestations of ischemic stroke. Reducing BBB collapse is effective in alleviating brain parenchymal injury and cognitive dysfunction. Our previous study reported that Sigma–1 receptor (Sig–1R) activation in cerebral microvascular endothelial cells (CMECs) ameliorated BBB impairment, but the detailed mechanism remains unclear. In this study, we investigated Sig–1R activation as a BBB integrity promoter via many post ischemic stroke pathways. Sig–1R activation in BBB–associated astrocytes can increase glia–derived neurotrophic factor (GDNF) secretion in bilateral common carotid artery occlusion (BCCAO) mice. Upregulated GDNF activates its receptors in CMECs to promote BBB integrity, and activated Sig–1R in CMECs facilitates this process. In vitro experiments have found that Sig–1R activation in CMECs promotes the interaction between the GDNF α1 receptor and transduction rearrangement gene, increasing PI3K–AKT–junction protein signaling pathway expression. Sig–1R activation could be an effective therapeutic method for preventing BBB damage in ischemic stroke and other neurological conditions.

The dimensions of white matter injury in preterm neonates

White matter injury (WMI) represents a frequent form of parenchymal brain injury in preterm neonates. Several dimensions of WMI are recognized, with distinct neuropathologic features involving a combination of destructive and maturational anomalies. Hypoxia-ischemia is the main mechanism leading to WMI and adverse white matter development, which result from injury to the oligodendrocyte precursor cells. Inflammation might act as a potentiator for WMI. A combination of hypoxia-ischemia and inflammation is frequent in several neonatal comorbidities such as postnatal infections, NEC and bronchopulmonary dysplasia, all known contributors to WMI. White matter injury is an important predictor of adverse neurodevelopmental outcomes. When WMI is detected on neonatal brain imaging, a detailed characterization of the injury (pattern of injury, severity and location) may enhance the ability to predict outcomes. This clinically-oriented review will provide an overview of the pathophysiology and imaging diagnosis of the multiple dimensions of WMI, will explore the association between postnatal complications and WMI, and will provide guidance on the signification of white matter anomalies for motor and cognitive development.

β-1, 3-galactosyltransferase 2 ameliorates focal ischemic cerebral injury by maintaining blood-brain barrier integrity

Blood–brain barrier (BBB) damage at the early stage of ischemic stroke is a vital cause of brain parenchymal injury. The mechanism of BBB disruption has been intensively investigated, but still not fully understood. β-1, 3-galactosyltransferase 2 (B3galt2) is expressed in the brain, but its role in the pathogenesis of cerebral ischemia remains unknown. In this study, we investigated the role of B3galt2 in cerebral ischemia in mice. Focal cerebral ischemia was induced in mice by middle cerebral artery occlusion (MCAO). B3galt2 protein levels were determined in microvessels which were isolated from ischemic brain at 12, 24 and 72 h after MCAO. Mice were administered lentiviral vectors encoding B3galt2 (LV- B3galt2) or recombinant transforming growth factor-β1 (r-TGF-β1) by intracerebroventricular injection. We assessed infarct volume and neurologic deficits on days 1, 3, and 14 after MCAO, blood–brain barrier (BBB) integrity at 12 and 24 h after MCAO, and the levels of TGF-β1, TGF-βR(Ⅱ) and p-Smad2/3 at 24 and 72 h after MCAO. Our results indicated that B3galt2 was expressed in brain microvascular endothelial cells and increased in the ischemic microvessels. Overexpression of B3galt2 by LV- B3galt2 administration reduced infarct volume and improved functional outcome after cerebral ischemia. Moreover, the neuroprotective effects were associated with preventing BBB damage. Compared with wild-type (WT) mice, heterozygous B3galt2 knockout (B3galt2−/+) mice not only showed severe BBB damage, neurologic functional deficits, but also showed reduced expression of TGF-β1, TGF-βR(Ⅱ) and p-Smad2/3 in microvessels after cerebral ischemia. Pre-administration of r-TGF-β1 reduced BBB damage, and improved the neurological outcomes in both WT mice and B3galt2−/+ mice after cerebral ischemia. Our results suggested B3galt2 protected against ischemic stroke in mice, and the underlying mechanism might include TGF-β signaling pathway in brain microvascular endothelial cells.

Association of traumatic brain injury with late life neuropathological outcomes in a community‐based cohort

AbstractBackgroundDespite extensive interest in risk for dementia following traumatic brain injury (TBI), there is scant research on neuropathological outcomes among community‐dwelling elders with TBI exposure. We previously reported an association of TBI resulting in loss of consciousness (LOC) with microinfarcts and Lewy body pathology, but TBI exposure data were limited to a single self‐report question. With expanded ascertainment data from medical records and structured interview on lifetime TBI exposure, we conducted a comprehensive investigation of neuropathological associations of TBI in a large autopsy cohort.Method780 older adults from the Adult Changes in Thought (ACT) study underwent brain autopsy (Table 1). Participants were members of Kaiser Permanente Washington who completed biennial clinic visits including self‐reported head trauma with LOC exposure. These data were supplemented with medical record abstraction, and, for 244 people, with structured interviews, increasing the sensitivity for TBI‐LOC in that sample from 16% to 20% (see Figure 1). Neuropathology outcomes included neurofibrillary tangle distribution (Braak), neuritic plaque density, Lewy body distribution, vascular pathology, hippocampal sclerosis, and cerebral cortical atrophy. Exposures of interest included TBI with or without LOC. We used Poisson regressions with robust standard errors adjusted for age, sex, education, and APOε4 genotype, weighted back to the full cohort (n=5546; Table 2) in a bootstrapping procedure accounting for errors in estimating weights.ResultTBI with LOC was associated with increased cortical atrophy (Table 3). In those with the structured interview (including TBI without LOC), the neuropathological associations of TBI were attenuated; no outcomes were statistically significant (Table 4). These findings apply to the full ACT cohort, not just people with TBI data in the autopsy sample.ConclusionCerebral cortical atrophy results from chronic brain parenchymal injury, potentially including vascular brain injury and tauopathy. Understanding mechanisms underlying associations of TBI with microvascular brain injury and pathological tau are poorly understood; future studies deploying new techniques to better quantify these lesions and differentiate between TBI‐related, age‐related, and ADRD‐related pathways are needed.

Serial changes in serum phosphorylated neurofilament and value for prediction of clinical outcome after traumatic brain injury.

Background: Phosphorylated neurofilament heavy subunit (pNF-H) is a constituent protein of the nerve axon, which leaks into the peripheral blood in various central nervous disorders. This study examined the time course of pNF-H value up to 1 month after injury and investigated the correlation with clinical outcome.Methods: Serum pNF-H concentration was measured on admission, and at 24 h, 72 h, 1 week, 2 weeks, and 1 month after injury in 20 patients, 15 males and 5 females aged 35–68 years (mean 52 years), with traumatic brain injury (TBI) transported to our hospital between April 2016 and March 2017. The clinical outcome at discharge was evaluated by Glasgow Outcome Scale.Results: The pNF-H value showed no increase in patients without brain parenchymal injury, but pNF-H value increased depending on the severity of brain damage. pNF-H value peaked at 2 weeks after injury. Two patients with peak value exceeding 10,000 unit had very severe injury and died during hospitalization. Peak pNF-H value was 3210 ± 1073 unit in 12 patients with good outcome and 9884 ± 2353 unit in 8 patients with poor outcome (P = 0.0119).Conclusion: Serum pNF-H level tended to increase and peak at 2 weeks after injury, and the peak pNF-H value was correlated with clinical outcome after TBI. The temporal profile of blood pNF-H seems to be useful to predict the clinical outcome after TBI.

Individualized Perioperative Blood Pressure Management for Adult Moyamoya Disease: Experience from 186 Consecutive Procedures

BackgroundIn adult patients with moyamoya disease (MMD) underwent combined revascularization, cerebral infarction during the acute postoperative phase is common and can lead to neurological dysfunction after revascularization in MMD patients. The aim of this study was to share the experience of individualized perioperative blood pressure (BP) management for adult MMD patients in one single center. MethodsWe retrospectively reviewed 144 adult patients with MMD who underwent 186 procedures of combined revascularization at our institution from March 2013 to July 2019. Clinical features and outcomes were analyzed, in particular regarding cerebral infarction and hyperperfusion syndrome (HPS). All of the patients received individualized management perioperatively, especially about the blood pressure management according to the characteristics of moyamoya disease. ResultsPostoperative cerebral infarction and HPS within 14 days after revascularization were recorded. Cerebral infarction occurred in four (2.1%) procedures among four patients. No patients suffered from a malignant cerebral infarction and only one patient had permanent neurological deficits. The incidence of HPS was 10.8% and no one presented with intracranial hemorrhage. All of the symptoms were reversible without any brain parenchymal injury. ConclusionsOur findings suggest that we can decrease the incidence and extent of cerebral infarction in adult MMD patients following combined revascularization by individualized perioperative BP management.

Correlation of Initial Computed Tomography Findings with Outcomes of Patients with Acute Subdural Hematoma: A Prospective Study

Abstract Introduction In modern emergency service systems, patients are often treated with sedation, intubation, and ventilation at the accident site. But neurosurgical assessment before all these emergency services is important. Thus, this study was designed to investigate the relationships between various parameters of initial CT scan findings and the outcomes of the patients. Methodology A total of 56 adult patients of traumatic acute subdural hematoma (SDH) whose computed tomography (CT) scan was performed within 8 hours of injury were recruited. The patients with prolonged hypotension, open head injury or depressed skull fracture, bilateral side acute SDH, or contusions/hematoma/extradural hematoma on the contralateral side were excluded. Six separate CT findings were analyzed and recorded, including hematoma, midline shift, subarachnoid hemorrhage (SAH), presence of basal cistern obliteration (BCO), intraparenchymal hematoma/contusion in the same hemisphere, and presence of effacement of the sulcal spaces, and were followed up for three months for outcome analysis. Results The overall mortality and functional recovery rate were 27 and 50%, respectively. The patients with obliterated basal cisterns and the presence of underlying SAH in patients with acute SDH had statistically significant poorer outcomes as compared with others. However, the extent of midline shift, SDH thickness, and the presence of underlying contusions and sulcal effacement on initial CT scan showed no statistically significant correlation with patients’ outcomes. Conclusions BCO and presence of subarchnoid hemorrhage underlying acute SDH on the earliest scan in head injury patients signify the severity of brain parenchymal injury. Along with the initial Glasgow Coma Scale score after resuscitation, these two factors should be considered as the most significant ones for predicting the outcomes in traumatic acute SDH patients.

Understanding multifactorial brain changes in type 2 diabetes: a biomarker perspective.

People with type 2 diabetes are at an increased risk of cognitive impairment and dementia (including Alzheimer's disease), as well as subtle forms of cognitive dysfunction. Current diabetes guidelines recommend screening for cognitive impairment in groups at high risk and providing guidance for diabetes management in patients with diabetes and cognitive impairment. Yet, no disease-modifying treatment is available and important questions remain about the mechanisms underlying diabetes-associated cognitive dysfunction. These mechanisms are likely to be multifactorial and different for subtle and more severe forms of diabetes-associated cognitive dysfunction. Over the past years, research on dementia, brain ageing, diabetes, and vascular disease has identified novel biomarkers of specific dementia aetiologies, brain parenchymal injury, and cerebral blood flow and metabolism. These markers shed light on the processes underlying diabetes-associated cognitive dysfunction, have clear applications in current research and increasingly in clinical diagnosis, and might ultimately guide targeted treatment.

Bilateral Facial Nerve Palsy following Head Injury: A Report of Two Uncommon Cases

AbstractBilateral facial nerve palsy (FNP) following head injury without any brain parenchymal injury or brain stem injury is quite an uncommon presentation. We came across two baffling cases of head trauma in which the patients developed simultaneous bilateral lower motor FNPs without any significant findings in initial brain scans which would suggest the pathophysiology for such a condition. Both the cases were found to be having longitudinal fractures of the temporal bone leading to injury of the facial nerves bilaterally. After conservative management, both the cases showed appreciable neurological improvement on follow-up. Hence, although bilateral FNP can be a diagnostic dilemma, it is quite possible to precisely localize the site of injury and successfully treat it.

The Concordance of Optic Nerve Sheath Diameter Measurements with the Clinical Course in Children with Traumatic Head Injury

Intracranial pressure (ICP) monitoring is of profound importance concerning prognosis and treatment among children with traumatic brain injury (TBI). Measurements of the optic nerve sheath diameter (ONSD) are one of the methods recommended for ICP monitoring. In this study, we aimed to evaluate the correlation of ONSD change in brain computed tomography (CT) with pediatric Glasgow Coma Score (pGCS) in the follow-up of pediatric cases with TBI, and also to evaluate the usability of the ONSD, which is the indicator of ICP. The data of 921 pediatric patients who were admitted to the emergency department with head injury between January 2016 and January 2018 were retrospectively evaluated in this study. Age, gender, trauma type, brain CT finding, pGCS, type of intracranial hemorrhage (ICH), and isolated skull fracture (ISF) were investigated. The patients were evaluated in three groups based on CT findings: (i) patients with parenchymal brain injury, (ii) patients with ISF, and (iii) patients with normal brain CT results. The measurements of ONSD were performed using CT. Whether the ONSD measurement results of the patients were compatible with the clinical data was investigated. The median age of the patients was 36 months (interquartile range [IQR] = 64) and 64.2% were male. The ONSD values and pGCSs of the patients with parenchymal injury were found to be significantly higher than patients with ISF and normal brain CT findings (p<0.05). The pGCSs showed a significant negative correlation with the first and second measurement results of ONSD (p<0.05). In groups undergoing control brain CT, ONSD levels in the second brain CT were found to be significantly high (p<0.05). In the clinical follow-up, ONSD measurements are reliable and significant parameters when evaluated with brain CT findings and pGCSs. We think that repeated ONSD measurements will be useful in determining possible adverse effects of secondary injury, as well as in determining the severity of the trauma during admission.

Clinical Relevance of Seizure in Pediatric Patients with Isolated Acute Subdural Hematoma without Parenchymal Brain Injury.

Isolated acute subdural hematoma (aSDH) in pediatric patients is rare, but it has a major impact on outcome. The purpose of this study was to determine incidence, seizure risk factors, and the outcome of pediatric patients with aSDH. Within a 10-year period (2007-2016), 10 children with aSDH were identified. Baseline characteristics and these parameters were analyzed: pediatric Glasgow Coma Scale (pGCS) score at admission and 24 hours after the operation, hematoma volume/side, and midline shift. Functional outcome was assessed at 3-month follow-up using the King's Outcome Scale for Childhood Head Injury score. Three subgroups were identified depending on age and etiology: birth-associated, nontraumatic, and traumatic aSDH. The overall incidence of seizures was 60%, and an even higher rate (75%) was observed in children < 1 month of age. Of those patients, two (67%) developed late seizures. Significant predictors for seizures were low pGCS score at admission (p = 0.03) and 24 hours after surgery (p = 0.03) as well as increased midline shift (p = 0.02). Patients with seizures tended to have an unfavorable outcome. Pediatric patients with aSDH are at high risk for seizures, particularly if the pGCS score is low at admission/24 hours after the operation and midline shows a shift. Determining seizure-prone pediatric patients may facilitate early antiepileptic treatment and promote better clinical outcomes.