Early-stage microvascular alterations of a new model of controlled cortical traumatic brain injury: 3D morphological analysis using scanning electron microscopy and corrosion casting

Sangiorgi, S.; Benedictis, Alessandro De; Protasoni, Marina; Manelli, A.; Reguzzoni, Marcella; Cividini, Andrea; Dell’Orbo, Carlo; Tomei, G.; Balbi, Sergio

doi:10.3171/2012.11.jns12627

Cited by 49 publications

(34 citation statements)

References 28 publications

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“…Abnormal endothelial cells have large cytoplasmic vacuoles as well as pinocytotic vesicles . Using a corrosion casting technique and scanning electron microscopy (SEM), Sangiorgi et al (2013) describe microvascular injury similar to that found in human tissue by Rodriguez-Baeza et al (2003) While the human study involved convenience samples with tissue collected between 1 and 20 days after TBI, the cerebral vasculature in the rodent study was cast at 2 time points after CCI, 3 and 12 h. At 3 h, changes in morphology and vascular architecture are seen primarily in medium-sized and capillary vessels. Focal swelling of perforating vessels, widening of intercellular junctions and structural changes of endothelial cells are also observed.…”

Section: Preclinical Studies Of Acute Changesmentioning

confidence: 98%

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Cerebral Vascular Injury in Traumatic Brain Injury

Kenney

Amyot

Haber

et al. 2016

Experimental Neurology

228

176

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Traumatic cerebral vascular injury (TCVI) is a very frequent, if not universal, feature after traumatic brain injury (TBI). It is likely responsible, at least in part, for functional deficits and TBI-related chronic disability. Because there are multiple pharmacologic and non-pharmacologic therapies that promote vascular health, TCVI is an attractive target for therapeutic intervention after TBI. The cerebral microvasculature is a component of the neurovascular unit (NVU) coupling neuronal metabolism with local cerebral blood flow. The NVU participates in the pathogenesis of TBI, either directly from physical trauma or as part of the cascade of secondary injury that occurs after TBI. Pathologically, there is extensive cerebral microvascular injury in humans and experimental animal, identified with either conventional light microscopy or ultrastructural examination. It is seen in acute and chronic TBI, and even described in chronic traumatic encephalopathy (CTE). Non-invasive, physiologic measures of cerebral microvascular function show dysfunction after TBI in humans and experimental animal models of TBI. These include imaging sequences (MRI-ASL), Transcranial Doppler (TCD), and Near InfraRed Spectroscopy (NIRS). Understanding the pathophysiology of TCVI, a relatively under-studied component of TBI, has promise for the development of novel therapies for TBI.

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Section: Preclinical Studies Of Acute Changesmentioning

confidence: 98%

“…The predominant findings are abnormal vessels with focal constriction and distal caliber reduction in the subcortical microvasculature adjacent to the subcortical white matter. These are thought to reflect cytotoxic edema from secondary brain injury (Sangiorgi et al, 2013).…”

Section: Preclinical Studies Of Acute Changesmentioning

confidence: 99%

Cerebral Vascular Injury in Traumatic Brain Injury

Kenney

Amyot

Haber

et al. 2016

Experimental Neurology

228

176

View full text Add to dashboard Cite

show abstract

“…[11][12][13] Traumatic axonal injury (TAI) is purported to be one of the most common pathological substrates in TBI and an important cause of persistent postconcussive symptoms. 14 TAI occurs on a spectrum from mild to severe and induces pathologies ranging from focal disruption of axons to complete neuronal degradation.…”

Section: Introductionmentioning

confidence: 99%

Trauma-Specific Brain Abnormalities in Suspected Mild Traumatic Brain Injury Patients Identified in the First 48 Hours after Injury: A Blinded Magnetic Resonance Imaging Comparative Study Including Suspected Acute Minor Stroke Patients

Ricciardi

Bokkers

Butman

et al. 2017

Journal of Neurotrauma

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We assessed the utility of a brief MRI protocol, appropriate for the acute setting, to detect acute traumatic brain injury (TBI) in patients with suspected mild TBI (mTBI) and distinguish traumatic from nontraumatic brain injury by comparing trauma with nontrauma patients. Twenty-two patients with suspected mTBI were included in this exploratory study over a period of 9 months. Median time from injury to MR scanning was 5.4 h (interquartile range 3.6-15.3). To determine the specificity of certain findings for TBI, 61 patients presenting with suspected minor acute stroke were included as a comparative group using the same MRI methods. A selected series of MRI sequences (diffusion-weighted imaging, fluid attenuated inversion recovery [FLAIR], and T2* weighted) were independently evaluated by two neuroradiologists blinded to clinical diagnosis, for presence of specific findings. In a separate session, all cases in which at least one MRI sequence above was positive were classified as TBI, stroke, or indeterminate. Intracranial MRI abnormalities were observed in 47 (57%) of the 83 studied patients. Based on findings on MRI, 12 (55%) of 22 suspected mTBI patients were classified as having traumatic injury. Nine (47%) of the 19 suspected mTBI patients with a negative CT had findings on MRI. Abnormalities on MRI consistent with trauma were observed most frequently on postcontrast FLAIR (83%) and T2*-weighted (58%) sequences. We demonstrated the ability of a fast MRI protocol to identify trauma-related abnormalities not seen on CT, and differentiate acute trauma from nonspecific chronic disease in a blinded cohort of mTBI patients.

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“…Recently, it has been clearly shown that TBI causes significant changes in pial and parenchymal vessels altering their morphology and function (Sangiorgi et al 2013). Thus, the primary injury caused by a head trauma affects pial vessels that are origins of perforating vessels.…”

Section: Introductionmentioning

confidence: 99%

Ablation of matrix metalloproteinase-9 gene decreases cerebrovascular permeability and fibrinogen deposition post traumatic brain injury in mice

et al. 2014

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Traumatic brain injury (TBI) is accompanied with enhanced matrix metalloproteinase-9 (MMP-9) activity and elevated levels of plasma fibrinogen (Fg), which is a known inflammatory agent. Activation of MMP-9 and increase in blood content of Fg (i.e. hyperfibrinogenemia, HFg) both contribute to cerebrovascular disorders leading to blood brain barrier disruption. It is well-known that activation of MMP-9 contributes to vascular permeability. It has been shown that at an elevated level (i.e. HFg) Fg disrupts blood brain barrier. However, mechanisms of their actions during TBI are not known. Mild TBI was induced in wild type (WT, C57BL/6J) and MMP-9 gene knockout (Mmp9−/−) homozygous, mice. Pial venular permeability to fluorescein isothiocyanate-conjugated bovine serum albumin (FITC-BSA) in pericontusional area was observed 14 days after injury. Mice memory was tested with a novel object recognition test. Increased expression of Fg endothelial receptor intercellular adhesion protein-1 and formation of caveolae were associated with enhanced activity of MMP-9 causing an increase in pial venular permeability. As a result, an enhanced deposition of Fg and cellular prion protein (PrPC) were found in pericontusional area. These changes were attenuated in Mmp9−/− mice and were associated with lesser loss of short-term memory in these mice than in WT mice. Our data suggest that mild TBI-induced increased cerebrovascular permeability enhances deposition of Fg-PrPC and loss of memory, which is ameliorated in the absence of MMP-9 activity. Thus, targeting MMP-9 activity and blood level of Fg can be a possible therapeutic remedy to diminish vasculo-neuronal damage after TBI.

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Early-stage microvascular alterations of a new model of controlled cortical traumatic brain injury: 3D morphological analysis using scanning electron microscopy and corrosion casting

Cited by 49 publications

References 28 publications

Cerebral Vascular Injury in Traumatic Brain Injury

Cerebral Vascular Injury in Traumatic Brain Injury

Trauma-Specific Brain Abnormalities in Suspected Mild Traumatic Brain Injury Patients Identified in the First 48 Hours after Injury: A Blinded Magnetic Resonance Imaging Comparative Study Including Suspected Acute Minor Stroke Patients

Ablation of matrix metalloproteinase-9 gene decreases cerebrovascular permeability and fibrinogen deposition post traumatic brain injury in mice

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