Showing papers by "Hua Feng published in 2015"
TL;DR: Norrin protected blood–brain barrier integrity and improved neurological outcome after SAH, and the action of Norrin appeared mediated by Frizzled-4 receptor activation, which promoted &bgr;-catenin nuclear translocation, which then enhanced Occludin, VE-Cadherin, and ZO-1 expression.
Abstract: Background and Purpose— Norrin and its receptor Frizzled-4 have important roles in the blood–brain barrier development. This study is to investigate a potential role and mechanism of Norrin/Frizzled-4 on protecting blood–brain barrier integrity after subarachnoid hemorrhage (SAH). Methods— One hundred and seventy-eight male Sprague–Dawley rats were used. SAH model was induced by endovascular perforation. Frizzled-4 small interfering RNA was injected intracerebroventricularly 48 hours before SAH. Norrin was administrated intracerebroventricularly 3 hours after SAH. SAH grade, neurological scores, brain water content, Evans blue extravasation, western blots, and immunofluorescence were used to study the mechanisms of Norrin and its receptor regulation protein TSPAN12, as well as neurological outcome. Results— Endogenous Norrin and TSPAN12 expression were increased after SAH, and Norrin was colocalized with astrocytes marker glial fibrillary acidic protein in cortex. Exogenous Norrin treatment significantly alleviated neurobehavioral dysfunction, reduced brain water content and Evans blue extravasation, promoted β-catenin nuclear translocation, and increased Occludin, VE-Cadherin, and ZO-1 expressions. These effects were abolished by Frizzled-4 small interfering RNA pretreated before SAH. Conclusions— Norrin protected blood–brain barrier integrity and improved neurological outcome after SAH, and the action of Norrin appeared mediated by Frizzled-4 receptor activation, which promoted β-catenin nuclear translocation, which then enhanced Occludin, VE-Cadherin, and ZO-1 expression. Norrin might have potential to protect blood–brain barrier after SAH.
96 citations
TL;DR: It is found that exposure to 900 MHz EMF radiation for 28 days can significantly impair spatial memory and damage BBB permeability in rat by activating the mkp-1/ERK pathway.
75 citations
TL;DR: It is demonstrated that CB2R stimulation reduced thrombin-induced brain edema and alleviated BBB damage and found that matrix metalloproteinase suppression may be partially involved in these processes.
Abstract: Thrombin mediates the life-threatening cerebral edema and blood-brain barrier (BBB) damage that occurs after intracerebral hemorrhage (ICH). We previously found that the selective cannabinoid receptor 2 (CB2R) agonist JWH-133 reduced brain edema and neurological deficits following germinal matrix hemorrhage (GMH). We explored whether CB2R stimulation ameliorated thrombin-induced brain edema and BBB permeability as well as the possible molecular mechanism involved. A total of 144 Sprague-Dawley (S-D) rats received a thrombin (20 U) injection in the right basal ganglia. JWH-133 (1.5 mg/kg) or SR-144528 (3.0 mg/kg) and vehicle were intraperitoneally (i.p.) injected 1 h after surgery. Brain water content measurement, Evans blue (EB) extravasation, Western blot, and immunofluorescence were used to study the effects of a CB2R agonist 24 h after surgery. The results demonstrated that JWH-133 administration significantly decreased thrombin-induced brain edema and reduced the number of Iba-1-positive microglia. JWH-133 also decreased the number of P44/P42(+)/Iba-1(+) microglia, lowered Evans blue extravasation, and inhibited the elevated matrix metallopeptidase (MMP)-9 and matrix metallopeptidase (MMP)-12 activities. However, a selective CB2R antagonist (SR-144528) reversed these effects. We demonstrated that CB2R stimulation reduced thrombin-induced brain edema and alleviated BBB damage. We also found that matrix metalloproteinase suppression may be partially involved in these processes.
66 citations
TL;DR: It is shown that ICH/IVH caused more significant chronic hydrocephalus and iron accumulation than primary IVH alone and intracerebral hematoma plays a vital role in persistent iron overload and aggravated Hydrocephalus after ICH /IVH.
Abstract: Background and Purpose—The intraventricular hemorrhage (IVH) secondary to intracerebral hemorrhage (ICH) was reported to be relevant to a higher incidence of hydrocephalus, which would result in poorer outcomes for patients with ICH. However, the mechanisms responsible for this relationship remain poorly characterized. Thus, this study was designed to further explore the development and progression of hydrocephalus after secondary IVH. Methods—Autologous blood injection model was induced to mimic ICH with ventricular extension (ICH/IVH) or primary IVH in Sprague-Dawley rats. Magnetic resonance imaging, Morris water maze, brain water content, Evans blue extravasation, immunohistochemistry staining, Western blot, iron determination, and electron microscopy were used in these rats. Then, deferoxamine treatment was used to clarify the involvement of iron in the development of hydrocephalus. Results—Despite the injection of equivalent blood volumes, ICH/IVH resulted in more significant ventricular dilation, ep...
63 citations
TL;DR: The present ICH with the ventricular extension rat model features characteristics of both ICH and IVH rat models, which could be used for extending the pathophysiological understanding of post-hemorrhagic chronic hydrocephalus and perihematomal tissue damage.
Abstract: Primary spontaneous intracerebral hemorrhage (ICH) with secondary intraventricular hemorrhage (IVH) is an important clinical problem of which little is known. IVH and hydrocephalus are independent predictors of poor outcome in ICH. The aims of this study were, therefore, to establish a rat model of ICH with ventricular extension and investigate the occurrence of post-hemorrhagic chronic hydrocephalus and perihematomal tissue injury. Based on our previous rat model of IVH, we adjusted the injection coordinates and 200 μl autologous blood was stereotaxically infused into the right striatum (coordinates: 0.2 mm posterior, 2.2 mm lateral, and 5.0 mm depth to the bregma). At 24 h post-infusion, the rats produced reproducible hematoma and ventricle expansion, which closely mimics the ICH with ventricular extension in humans. Hematoma consequences and perihematomal tissue injury were evaluated on the acute phase. At 4 weeks, ventricular dilatation, brain tissue loss, hippocampus volume, and cortical thickness were measured with magnetic resonance imaging and neurocognitive function was assessed using the Morris water maze test. With blood infusion, the animals demonstrated brain edema, blood-brain barrier breakdown, and marked perihematomal tissue injury on the acute phase. At 4 weeks, the T2 images showed remarkable hydrocephalus and tissue loss, and the Morris water maze test revealed neurocognitive deficits. The present ICH with the ventricular extension rat model features characteristics of both ICH and IVH rat models, which could be used for extending our pathophysiological understanding of post-hemorrhagic chronic hydrocephalus and perihematomal tissue damage.
58 citations
TL;DR: PO-induced preferred differentiation into neurons and oligodendrocytes is a potential paradigm for NSPCs-based therapies, and the ERK signaling pathway was involving in this process.
Abstract: Neural stem/progenitor cells (NSPCs) replacement therapies are the most attractive strategies to restore an injured brain. Key challenges of such therapies are enriching NSPCs and directing them differentiation into specific neural cell types. Here, three biomaterial substrates Poly-L-ornithine (PO), Poly-L-lysine (PLL) and fibronectin (FN) were investigated for their effects on proliferation and differentiation of rat NSPCs, and the underlying mechanisms were also explored. The results showed PO significantly increased NSPCs proliferation and induced preferred differentiation, compared with PLL and FN. Checking protein markers of several neural cell subtypes, it is showed PO significantly induced NSPCs expressing Doublecortin (DCX) and Olig2, one for neuroblasts and young neurons and the other for young oligodendrocytes. It is suggested the ERK signaling pathway was involving in this process because an ERK antagonist U0126 could inhibit PO's effects mentioned above, as well as an ERK pathway agonist Ceramide C6 could enhance them. Given that both neurons and oligodendrocytes are the most vulnerable cells in many neurological diseases, PO-induced preferred differentiation into neurons and oligodendrocytes is a potential paradigm for NSPCs-based therapies.
56 citations
TL;DR: expression of RAGE and its ligand high-mobility group protein B1 were increased at 12 hours after ICH, along with blood–brain barrier permeability and perihematomal nerve fiber injury, and RAGE signaling is involved in blood– brain barrier and white matter fiber damage after I CH.
Abstract: Background and Purpose— To determine whether the receptor for advanced glycation end-products (RAGE) plays a role in early brain injury from intracerebral hemorrhage (ICH), RAGE expression and activation after injury were examined in a rat model of ICH with or without administration of a RAGE-specific antagonist (FPS-ZM1). Methods— Autologous arterial blood was injected into the basal ganglia of rats to induce ICH. The motor function of the rats was examined, and water content was detected after euthanization. Blood–brain barrier permeability was determined by Evans blue staining and colloidal gold nanoparticle tracers. Nerve fiber injury in white matter was determined by diffusion tensor imaging analysis, and the expression of target genes was analyzed by Western blotting and quantitative reverse transcription polymerase chain reaction. FPS-ZM1 was administered by intraperitoneal injection. Results— Expression of RAGE and its ligand high-mobility group protein B1 were increased at 12 hours after ICH, along with blood–brain barrier permeability and perihematomal nerve fiber injury. RAGE and nuclear factor-κB p65 upregulation were also observed when FeCl 2 was infused into the basal ganglia at 24 hours. FPS-ZM1 administration resulted in significant improvements of blood–brain barrier damage, brain edema, motor dysfunction, and nerve fiber injury, and the expression of RAGE, nuclear factor-κB p65, proinflammatory mediators interleukin 1β, interleukin-6, interleukin-8R, cyclooxygenase-2, inducible nitric oxide synthase, and matrix metallopeptidase-9 was attenuated. Moreover, decreases in claudin-5 and occludin expression were partially recovered. FPS-ZM1 also reversed FeCl 2 -induced RAGE and nuclear factor-κB p65 upregulation. Conclusions— RAGE signaling is involved in blood–brain barrier and white matter fiber damage after ICH, the initiation of which is associated with iron. RAGE antagonists represent a novel therapeutic intervention to prevent early brain injury after ICH.
54 citations
TL;DR: Iron may be the key stimulus that activates the Wnt signaling pathway and regulates subarachnoid fibrosis after cerebral hemorrhage, and that DFX may be a candidate for preventing PHCH in patients with IVH.
53 citations
TL;DR: It is found that iron plays a role in brain injury following GMH and that minocycline reduces iron overload afterGMH and iron-induced brain injury in vivo.
52 citations
TL;DR: With the evidence presented in this review, future clinical management of acutely brain injured patients will expand to include the recirculation concept, establishing a harmony between arterial and venous systems, in addition to the established recanalization and reperfusion strategies.
47 citations
TL;DR: Cilostazol, alone or in combination with aspirin, significantly reduces stroke recurrence, poststroke intracranial hemorrhage, and extracranial bleeding in patients with a prior ischemic stroke as compared with other antiplatelet therapies.
Abstract: Background Antiplatelet therapy is recommended for patients who have experienced ischemic stroke. We performed a meta-analysis to compare the efficacy and safety of cilostazol with other antiplatelet therapies in patients with ischemic stroke. Methods PubMed, EMBASE, MEDLINE, and the Cochrane Library were searched for randomized controlled trials published in English from May 1999 to May 2013. Clinical outcomes were compared by pooled and meta-regression analyses. Results Nine studies involving 6328 patients satisfied our inclusion criteria. Stroke recurrence (including hemorrhagic and ischemic) with cilostazol use was 5.3% (157) versus 8.3% (248) in control group (risk ratio .63 [.52-.76], 95% confidence interval [CI]). Poststroke intracranial hemorrhage was .5% (16) with cilostazol versus 1.6% (46) in control group (risk ratio .36 [.21-.63], 95% CI). Poststroke extracranial bleeding complications occurred in 2.4% (66) of the patients taking cilostazol versus 3.9% (108) in control group (risk ratio .62 [.46-.83], 95% CI). No significant difference in cerebrovascular events (nonfatal stroke, intracranial hemorrhage, and transient ischemic attack) was found between the cilostazol group (8.2%, 246) versus control group (12.0%, 360; risk ratio .71 [.50-1.01], 95% CI). In addition, the cilostazol therapy brought about a nonsignificant reduction of cardiac adverse events (heart failure, myocardial infarction, and angina pectoris) comparing with control groups, with 3.8% (99) of the cilostazol group versus 4.7% (123) of control group (risk ratio, .81 [.62-1.04], 95% CI). Conclusions Cilostazol, alone or in combination with aspirin, significantly reduces stroke recurrence, poststroke intracranial hemorrhage, and extracranial bleeding in patients with a prior ischemic stroke as compared with other antiplatelet therapies.
TL;DR: The results suggest that PTEN inhibited by BPV(pic) plays a neuroprotective role in SAH pathophysiology, possibly by alterations in glutamate AMPA receptor subunits.
TL;DR: MFGE8 could alleviate neurologic damage in early brain injury after SAH via anti-inflammation and anti-apoptosis effects and may serve as a promising therapeutic target for future management of SAH patients.
TL;DR: Estrogen appears to exert a protective effect on spinal motor neurons following OGD, via G PR30, and the PI3K/Akt pathway may be one of those involved in the estrogen-related antiapoptotic effects mediated by GPR30.
Abstract: Spinal cord injury (SCI) may result in severe dysfunction of motor neurons. G-protein-coupled receptor 30 (GPR30) expression in the motor neurons of the ventral horn of the spinal cord mediates neuroprotection through estrogen signaling. The present study explored the antiapoptotic effect of estrogen, mediated by GPR30 following SCI, and the mechanisms underlying this effect. Spinal motor neurons from rats were cultured in vitro in order to establish cell models of oxygen and glucose deprivation (OGD). The effects of estrogen, the estrogen agonist, G1, and the estrogen inhibitor, G15, on motor neurons were observed using MTT assays. The effects of E2, G1 and G15 on spinal motor neuron apoptosis following OGD, were detected using flow cytometry. The role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) inhibitor, LY294002, was also determined using flow cytometry. Rat SCI models were established. E2, G1 and E2+LY294002 were administered in vivo. Motor function was scored at 3, 7, 14, 21 and 28 d following injury, using Basso-Beattie-Bresnahan (BBB) standards. Cell activity in the estrogen and G1 groups was higher than that in the solvent group, whereas cell activity in the E2+G15 group was lower than that in the E2 group (P<0.05). Following OGD, the proportion of apoptotic cells significantly increased (P<0.05). The proportion in the estrogen group was significantly lower than that in the solvent group, whereas the proportion of apoptotic cells in the E2+G15 and E2+LY294002 groups was higher than that in the E2 group (P<0.05). Treatment with E2 and G1 led to upregulation of P-Akt expression in normal cells and post-OGD cells. The BBB scores of rats in the E2 and G1 groups were higher than those in the placebo group (P<0.05). The BBB scores of the E2+LY294002 group were lower than those of the E2 group (P<0.05). Estrogen thus appears to exert a protective effect on spinal motor neurons following OGD, via GPR30. The PI3K/Akt pathway may be one of those involved in the estrogen-related antiapoptotic effects mediated by GPR30.
TL;DR: It is concluded that DA plays a critical role in post-TBI depression, and that amantadine shows its potential value in anti-depression treatment for TBI.
TL;DR: The results suggest that functional connectivity density mapping may provide a useful means to assess PD-related neurodegeneration and to study the pathophysiology of PD.
TL;DR: The characteristics, regulation pathways and functions ofpericyte are reviewed, the evolving new pathophysiological roles of pericyte that are implicated in early brain injury after SAH are summarized and understanding is improved in order to explore potential novel therapeutic options for patients with SAH.
TL;DR: It is concluded that brainstem-cerebellar circuit plays an essential role in DEC while the amygdala modulates this process, and that the medial prefrontal cortex as a candidate is involved in the extra-ceebellar mechanism underlying delay eyeblink conditioning (DEC) in mice.
TL;DR: Findings suggest that activation of the endocannabinoid system might attenuate inflammation-induced secondary brain injury after GMH in rats by reducing microglia accumulation through a mechanism involving ERK dephosphorylation.
TL;DR: Rat recombinant progranulin alleviated neuronal death via sortilin 1-mediated and Akt-related antiapoptosis pathway and may have potentials to ameliorate early brain injury for subarachnoid hemorrhage patients.
Abstract: Objectives:Progranulin has been reported to have neuroprotective actions in cultured neurons. This study investigated the effect of recombinant rat progranulin on early brain injury after subarachnoid hemorrhage.Design:Controlled in vivo laboratory study.Setting:Animal research laboratory.Subjects:T
TL;DR: This study provides the first evidence that administration of VPA enhances the neurogenic potential of NSPCs after SCI and reveals the therapeutic value of delayed treatment of Vpa to SCI.
Abstract: Although the adult spinal cord contains a population of multipotent neural stem/precursor cells (NSPCs) exhibiting the potential to replace neurons, endogenous neurogenesis is very limited after spinal cord injury (SCI) because the activated NSPCs primarily differentiate into astrocytes rather than neurons. Valproic acid (VPA), a histone deacetylase inhibitor, exerts multiple pharmacological effects including fate regulation of stem cells. In this study, we cultured adult spinal NSPCs from chronic compressive SCI rats and treated with VPA. In spite of inhibiting the proliferation and arresting in the G0/G1 phase of NSPCs, VPA markedly promoted neuronal differentiation (β-tubulin III(+) cells) as well as decreased astrocytic differentiation (GFAP(+) cells). Cell cycle regulator p21(Cip/WAF1) and proneural genes Ngn2 and NeuroD1 were increased in the two processes respectively. In vivo, to minimize the possible inhibitory effects of VPA to the proliferation of NSPCs as well as avoid other neuroprotections of VPA in acute phase of SCI, we carried out a delayed intraperitoneal injection of VPA (150 mg/kg/12 h) to SCI rats from day 15 to day 22 after injury. Both of the newborn neuron marker doublecortin and the mature neuron marker neuron-specific nuclear protein were significantly enhanced after VPA treatment in the epicenter and adjacent segments of the injured spinal cord. Although the impaired corticospinal tracks had not significantly improved, Basso-Beattie-Bresnahan scores in VPA treatment group were better than control. Our study provide the first evidence that administration of VPA enhances the neurogenic potential of NSPCs after SCI and reveal the therapeutic value of delayed treatment of VPA to SCI.
TL;DR: It is founded that the Ephedra sinica extract alleviated the blood-brain barrier disruption and brain edema, eventually improved neurological functions after SAH in rats, and suggested complement C3 inhibition by theEphedra Sinica extract may be a protective factor against early brain injury afterSAH.
TL;DR: OPN plays an important role in the neuroprotection elicited by HBO-PC, and preconditioning with HBO promoted expression of OPN, which reduced the expression of interleukin (IL)-1β/nuclear factor-κ-gene binding and augmented protein kinase B (Akt).
Abstract: Neurosurgical operations may result in surgical injury which would lead to postoperative neurological deficits. Hyperbaric oxygen preconditioning (HBO-PC) may be beneficial for such people. However, the exact mechanism underlying HBO-PC is not well known yet. The aim of this study is to explore the role of osteopontin (OPN) in HBO-PC-induced neuroprotection. The study consisted of two experiments. In experiment 1, Sprague Dawley (SD) rats were divided into four groups: sham group, HBO-PC sham group, stroke group, and HBO-PC group (HBO-PC + stroke). The animals in the second experiment were randomly assigned to one of two groups: OPN small interfering (siRNA) group (HBO-PC + stroke + OPN siRNA) and control siRNA group (HBO-PC + stroke + negative control siRNA). Neurological outcome in HBO-PC group was better than that of stroke group. After OPN siRNA was administered, neurological function aggravated compared with control siRNA group. Brain morphology and structure seen by light microscopy was diminished in stroke group and OPN siRNA group, while fewer pathological injuries occurred in HBO-PC and control siRNA group. The infarct volume in HBO-PC group was the lowest, followed by OPN siRNA group and stroke group, respectively. Preconditioning with HBO promoted expression of OPN, which reduced the expression of interleukin (IL)-1β/nuclear factor-κ-gene binding (NFκB) and augmented protein kinase B (Akt). OPN siRNA reversed these changes. OPN plays an important role in the neuroprotection elicited by HBO-PC. Pretreatment with HBO may be beneficial for people going to undertake brain surgery.
TL;DR: A potential clinical utility for CB2R agonists as a potential therapy to reduce neurological injury and improve patient outcomes after GMH is suggested.
TL;DR: The data suggested a more serious disturbance of tissue oxygenation and cerebral metabolism in the acute stage after ICH at high altitude, perhaps through a mechanism involving the amelioration of the derangement of cerebral oxygenations and metabolism following high-altitude ICH.
Abstract: Introduction
Intracerebral hemorrhage (ICH) at high altitude is not well understood to date. This study investigates the effects of high altitude on ICH, and examines the acute neuroprotection of hyperbaric oxygen (HBO) therapy against high-altitude ICH.
TL;DR: It is shown in rats that optogenetic activation of the right caudal mPFC pyramidal neurons as a CS is sufficient to support the acquisition of delay eyeblink conditioning (DEC), and the associative memory was not stably expressed during the initial period of daily conditioning session even after the CR acquisition reached the asymptotic level.
Abstract: It is generally accepted that the associative learning occurs when a behaviorally neutral conditioned stimulus (CS) is paired with an aversive unconditioned stimulus (US) in close temporal proximity. Eyeblink conditioning (EBC) is a simple form of associative learning for motor responses. Specific activation of a population of cells may be an effective and sufficient CS for establishing EBC. However, there has been no direct evidence to support this hypothesis. Here, we show in rats that optogenetic activation of the right caudal mPFC pyramidal neurons as a CS is sufficient to support the acquisition of delay eyeblink conditioning (DEC). Interestingly, the associative memory was not stably expressed during the initial period of daily conditioning session even after the CR acquisition reached the asymptotic level. Finally, the intensity and consistency of the CS were found to be crucial factors in regulating the retrieval of the associative memory. These results may be of importance in understanding the neural cellular mechanisms underlying associative learning and the mechanisms underlying retrieval process of memory.
TL;DR: The results indicate that axon regeneration may be promoted by modified physical and biochemical characteristics of intra- and extracellular architecture in glial scar tissues in rats, which could potentially help to understand better the composition ofglial scar in central nervous system injury.
TL;DR: It is suggested that endovascular treatment is relatively safe and technically feasible in most patients with PcomA aneurysms in the presence of fetal PCA using multiple strategies.
Abstract: Posterior communicating artery (PcomA) aneurysms in the presence of the fetal variant of posterior cerebral artery (PCA) often pose technical challenges for endovascular treatment because of a greater potential for ischemic injury with the fetal PCA compromise. The purpose of this study was to assess the feasibility and results of endovascular treatment for these lesions. We retrospectively reviewed our experience and results of endovascular treatments for a series of nine consecutive patients with PcomA aneurysms occurring at the origin of fetal PCAs at the Department of Neurosurgery of Southwest Hospital, Chongqing, China, between June 2011 and June 2014. Depending on the angiographic findings, location and shape of the aneurysms, various therapeutic strategies were used including coiling by single or double microcatheter, balloon remodeling technique, and single or Y-stenting technique. Overall, fetal PCA was preserved patent in all cases, and complete or near complete occlusion was achieved in 8/9 cases. There was no procedure-related morbidity or mortality. With the exception of one patient who died of pneumonia 6 weeks after treatment, no clinical evidence of neurologic deterioration and hemorrhagic complication was seen during the follow-up period in the remaining 8 patients. Our experience suggests that endovascular treatment is relatively safe and technically feasible in most patients with PcomA aneurysms in the presence of fetal PCA using multiple strategies.
TL;DR: The results demonstrated the feasibility of correctly lateralizing the epileptic foci by using full frequency adaptive directed transfer function to scalp EEG interictal spike activity.
Abstract: Purpose The purpose of this work was to find an objective and quantitative method for epileptic foci lateralization that may aid and support the decision made by the usually chosen lateralizing criteria. Methods A frequency-derived causal analysis method, full frequency adaptive directed transfer function, was applied to the interictal scalp EEG data collected from 2 groups of total 30 epileptic patients. Group A included 15 refractory epileptic patients who had undergone an epileptic surgery; group B consisted of 15 outpatient epileptic patients who had a seizure type of generalized tonic-clonic seizure. All patients had no abnormalities detected in their routine brain MRI examinations. The methodology that leads to the lateralization is based on several processing steps: interictal spikes selection, full frequency adaptive directed transfer function analysis, significant causal connections extraction, and then lateralization. Results Ninety-six of 104 spikes' sources lateralized by full frequency adaptive directed transfer function were consistent with their corresponding surgery side in group A, with the accuracy of 92.31%. Ninety-seven of 101 spikes' sources were lateralized correctly in group B, according to technicians' judgments from ictal scalp video-EEG recordings, with the accuracy of 96.04%. Conclusions The results demonstrated the feasibility of correctly lateralizing the epileptic foci by using full frequency adaptive directed transfer function to scalp EEG interictal spike activity.
TL;DR: blast wave can pass through the skull to directly injure brain tissue and the results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure.
Abstract: Purpose We once reported blast-induced traumatic brain injury (bTBI) in confined space. Here, bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene. Methods The goats were placed at 2, 4, 6 and 8 m far from explosion center. Trinitrotoluene (TNT) was used as the source of the blast wave and the pressure at each distance was recorded. The systemic physiology, electroencephalogram, serum level of S-100beta, and neuron specific enolase (NSE) were determined pre and post the exposure. Neuroanatomy and neuropathology were observed 4 h after the exposure. Results Simple blast waveforms were recorded with parameters of 702.8 kPa-0.442 ms, 148.4 kPa-2.503 ms, 73.9 kPa-3.233 ms, and 41.9 kPa-5.898 ms at 2, 4, 6 and 8 m respectively. Encephalic blast overpressure was on the first time recorded in the literature by us at 104.2 kPa-0.60 ms at 2 m, where mortality and burn rate were 44% and 44%. Gross examination showed that bTBI was mainly manifested as congestive expansion of blood vessels and subarachnoid hemorrhage, which had a total incidence of 25% and 19% in 36 goats. Microscopical observation found that the main pathohistological changes were enlarged perivascular space (21/36, 58%), small hemorrhages (9/36, 25%), vascular dilatation and congestion (8/36, 22%), and less subarachnoid hemorrhage (2/36, 6%). After explosion, serum levels of S-100β and NSE were elevated, and EEG changed into slow frequency with declined amplitude. The results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure. Conclusion Blast wave can pass through the skull to directly injure brain tissue.