scholarly journals Arachnoid cell involvement in the mechanism of coagulation-initiated inflammation in the subarachnoid space after subarachnoid hemorrhage

2010 ◽  
Vol 11 (7) ◽  
pp. 516-523 ◽  
Author(s):  
Zhao-liang Xin ◽  
Xiao-kang Wu ◽  
Jian-rong Xu ◽  
Xi Li
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Arachnoid Cell

scholarly journals Role of perivascular and meningeal macrophages in outcome following experimental subarachnoid hemorrhage

2021 ◽  
pp. 0271678X2098029
Author(s):  
Hoyee Wan ◽  
Shakira Brathwaite ◽  
Jinglu Ai ◽  
Kullervo Hynynen ◽  
R Loch Macdonald
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Perivascular Spaces ◽  
Perivascular Cells ◽  
Perivascular Inflammation ◽  
Perivascular Macrophages ◽  
Pre Treatment ◽  
Preferential Uptake

The distribution and clearance of erythrocytes after subarachnoid hemorrhage (SAH) is poorly understood. We aimed to characterize the distribution of erythrocytes after SAH and the cells involved in their clearance. To visualize erythrocyte distribution, we injected fluorescently-labelled erythrocytes into the prechiasmatic cistern of mice. 10 minutes after injection, we found labelled erythrocytes in the subarachnoid space and ventricular system, and also in the perivascular spaces surrounding large penetrating arterioles. 2 and 5 days after SAH, fluorescence was confined within leptomeningeal and perivascular cells. We identified the perivascular cells as perivascular macrophages based on their morphology, location, Iba-1 immunoreactivity and preferential uptake of FITC-dextran. We subsequently depleted meningeal and perivascular macrophages 2 days before or 3 hours after SAH with clodronate liposomes. At day 5 after SAH, we found increased blood deposition in mice treated prior to SAH, but not those treated after. Treatment post-SAH improved neurological scoring, reduced neuronal cell death and perivascular inflammation, whereas pre-treatment only reduced perivascular inflammation. Our data indicate that after SAH, erythrocytes are distributed throughout the subarachnoid space extending into the perivascular spaces of parenchymal arterioles. Furthermore, meningeal and perivascular macrophages are involved in erythrocyte uptake and play an important role in outcome after SAH.

Local Delivery of Ibuprofen via Controlled-release Polymers Prevents Angiographic Vasospasm in a Monkey Model of Subarachnoid Hemorrhage

2005 ◽  
Vol 57 (suppl_1) ◽  
pp. 184-190 ◽  
Author(s):  
Gustavo Pradilla ◽  
Quoc-Anh Thai ◽  
Federico G. Legnani ◽  
Richard E. Clatterbuck ◽  
Philippe Gailloud ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Subarachnoid Hemorrhage ◽  
Controlled Release ◽  
Adhesion Molecule ◽  
Subarachnoid Space ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Cynomolgus Monkeys ◽  
Monkey Model ◽  
Angiographic Vasospasm

Abstract OBJECTIVE: Adhesion and migration of leukocytes into the periadventitial space play a role in the pathophysiology of vasospasm after subarachnoid hemorrhage (SAH). Intercellular adhesion molecule-1 is a determinant cell adhesion molecule involved in this process. Ibuprofen has been shown to inhibit intercellular adhesion molecule-1 upregulation and prevent vasospasm in animal models of SAH. In this study, we report the toxicity and efficacy of locally delivered ibuprofen incorporated into controlled-release polymers to prevent vasospasm in a monkey model of SAH. METHODS: Ibuprofen was incorporated into ethylene-vinyl acetate (EVAc) polymers at 45% loading (wt:wt). For the toxicity study, cynomolgus monkeys (n = 5) underwent surgical implantation of either blank/EVAc polymers (n = 3) or 45% ibuprofen/EVAc polymers (n = 2) in the subarachnoid space, were followed up for 13 weeks, and were killed for histopathological analysis. For the efficacy study, cynomolgus monkeys (n = 14) underwent cerebral angiography 7 days before and 7 days after surgery and SAH and were randomized to receive either a 45% ibuprofen/EVAc polymer (n = 7; mean dose of ibuprofen, 6 mg/kg) or blank EVAc polymers (n = 7) in the subarachnoid space. Angiographic vasospasm was determined by digital image analysis. Student's t test was used for analysis. RESULTS: Animals implanted with ibuprofen polymers showed no signs of local or systemic toxicity. Animals treated with ibuprofen polymers had 91 ± 9% lumen patency of the middle cerebral artery, compared with 53 ± 11% of animals treated with blank/EVAc polymers (P < 0.001). CONCLUSION: Ibuprofen polymers are safe and prevent angiographic vasospasm after SAH in the monkey model. These findings support the role of cell adhesion molecules and inflammation in the pathophysiology of vasospasm.

Neonatal Seizures, Intracerebral Hematoma, and Subarachnoid Hemorrhage in Full-Term Infants

PEDIATRICS ◽  
1979 ◽  
Vol 63 (5) ◽  
pp. 812-815
Author(s):  
Edward R. Chaplin ◽  
Gary W. Goldstein ◽  
David Norman
Keyword(s):  
Metabolic Disease ◽  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Term Infant ◽  
Full Term ◽  
Spinal Fluid ◽  
Intracerebral Hematoma ◽  
Neonatal Seizures ◽  
Presumptive Diagnosis ◽  
Term Infants

During the first days of life intracranial hemorrhage is a frequent cause of convulsions in the full-term infant.1,2 If spinal fluid is bloody and there is no evidence of asphyxia, infection, or acute metabolic disease, then a presumptive diagnosis of primary subarachnoid hemorrhage is often made.1-3 These infants appear remarkably well in the interictal period, and their outcome is usually good.1,2 Since pathologic confirmation is not available, it has been assumed that bleeding occurs directly into the subarachnoid space and not as an extension of a subdural, intraventricular, or intracerebellar hemorrhage.1,3-5 During a 13-month period at our institution, only four full-term infants had seizures and bloody spinal fluid.

scholarly journals The False Falx and Tentorium Sign: Case Report of Subdural Haematoma and Sickle Cells Disease

2014 ◽  
Vol 21 (3) ◽  
pp. 331-335
Author(s):  
Hernando Raphael Alvis-Miranda ◽  
Carlos Fernando Lozano-Tangua ◽  
Gabriel Alcala-Cerra ◽  
Andres M. Rubiano ◽  
Luis Rafael Moscote-Salazar
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Subdural Haematoma ◽  
Contrast Material ◽  
Ct Scans ◽  
Cell Disease ◽  
Intravenous Contrast ◽  
Sickle Cells ◽  
High Doses ◽  
Basal Cisterns

Abstract The increased density in the basal cisterns and the subarachnoid space on CT scans is a well-known characteristic of subarachnoid hemorrhage. Have been described diverse conditions that can emulate subarachnoid hemorrhage, such as purulent leptomeningitis, intrathecal contrast material and leak of high doses of intravenous contrast material to the subarachnoid space. We present the case of a male patient who presented a subdural hematoma in the setting of non-diagnosed sickle cell disease. To this patient was performed a panangiography which discard any aneurismal hemorrhage origin

scholarly journals A Case of Spontaneous Spinal Subdural Hematoma Complicated by Cranial Subarachnoid Hemorrhage and Spinal Adhesive Arachnoiditis

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Taihei Go ◽  
Toshiyuki Tsutsui ◽  
Yasuaki Iida ◽  
Katsunori Fukutake ◽  
Ryoichi Fukano ◽  
...  
Keyword(s):  
Back Pain ◽  
Subarachnoid Hemorrhage ◽  
Subdural Hematoma ◽  
Subarachnoid Space ◽  
Clinical Symptoms ◽  
Neurological Manifestation ◽  
Subdural Space ◽  
Spinal Subdural Hematoma ◽  
Magnetic Resonance Imaging Mri ◽  
To Come

A 76-year-old woman with a spinal subdural hematoma (SDH) was presented with severe back pain without headache. Magnetic resonance imaging (MRI) performed 4 days after onset showed SDH extending from Th2 to L3. She was diagnosed with spontaneous SDH without neurological manifestation, and conservative treatment was selected. Transient disturbance of orientation appeared 7 days after onset. Small subarachnoid hemorrhage (SAH) was detected on head CT, and strict antihypertensive therapy was started. Symptoms changed for the better. Back pain disappeared 4 weeks after onset. On follow-up MRI at 6 months after onset, the SDH had been resolved spontaneously. Although adhesive arachnoiditis was observed at Th4-6, the recurrence of clinical symptoms was not observed at one year and a half after onset. Spinal subdural space is almost avascular; a hematoma in a subdural space is considered to come from a subarachnoid space when it is a lot. A hemorrhage in subarachnoid space was flushed by cerebral spinal fluid; hematoma or arachnoiditis was not formed in general. In our case, hemorrhage was a lot and expansion of SDH was large enough to cause cranial SAH and arachnoiditis. But longitudinally expanded SDH did not show neurological manifestation and resolved spontaneously in our case.

Time course of vasospasm in man

1978 ◽  
Vol 48 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Bryce Weir ◽  
Michael Grace ◽  
John Hansen ◽  
Charles Rothberg
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Time Course ◽  
Content Type ◽  
Base Of Skull ◽  
Fine Print

✓ Measurements were made at eight predetermined positions on 627 sets of angiograms from 293 patients with aneurysms. A ratio between the sum of the vessel diameters in the subarachnoid space to the sum in the base of skull and neck was calculated and plotted against time. Vasospasm has its onset in man about Day 3 after subarachnoid hemorrhage, is maximal at Days 6 to 8, and is gone by Day 12. There is a tendency for patients in poor clinical grades to have more vasospasm. The patients with most vasospasm have a significantly higher mortality than those with the least.

scholarly journals Blocking Hepatoma-Derived Growth Factor Attenuates Vasospasm and Neuron Cell Apoptosis in Rats Subjected to Subarachnoid Hemorrhage

2021 ◽  
Author(s):  
Chia-Li Chung ◽  
Chieh-Hsin Wu ◽  
Yu-Hua Huang ◽  
Shu-Chuan Wu ◽  
Chee-Yin Chai ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Growth Factor ◽  
Western Blot ◽  
Blot Analysis ◽  
Subarachnoid Space ◽  
Cell Apoptosis ◽  
Neurological Outcome ◽  
Post Treatment ◽  
Inflammatory Factors ◽  
Protein Levels

Abstract Subarachnoid hemorrhage (SAH) is an important subcategory of stroke due to its unacceptably high mortality rate as well as the severe complications it causes, such as cerebral vasospasm, neurological deficits, and cardiopulmonary abnormality. Hepatoma-derived growth factor (HDGF) is a growth factor related to normal development and is involved in liver development and regeneration. This study explored the relationship between SAH and HDGF. Sixty rats were divided into five groups (n = 12/group): (A) control group; (B) rHDGF ab only group [normal animals treated with 50 µM recombinant HDGF antibodies (rHDGF ab)]; (C) SAH group; (D) SAH + pre-rHDGF ab group (SAH animals pre-treated with 50 µM rHDGF ab into the subarachnoid space within 24 h before SAH); and (E) SAH + post-rHDGF ab group (SAH animals post-treated with 50 µM rHDGF ab into the subarachnoid space within 24 h after SAH). At 48 h after SAH, serum and cerebrospinal fluid (CSF) samples were collected to measure the levels of pro-inflammatory factors by ELISA, and rat cortex tissues were used to measure protein levels by western blot analysis. Immunofluorescence staining for Iba-1, GFAP, TUNEL, and NeuN was detected proliferation of microglia and astrocyte and apoptosis of neuron cells. Neurological outcome was assessed by ambulation and placing/stepping reflex responses. Morphology assay showed that pre-treatment and post-treatment with rHDGF ab attenuated vasospasm after SAH. SAH up-regulated the levels of TNF-α, IL-1β, and IL-6 in both the CSF and serum samples, and both pre- and post-treatment with rHDGF ab inhibited the up-regulation of these pro-inflammatory factors, except for the serum IL-6 levels. Western blot analysis demonstrated that SAH up-regulated pro-BDNF and NFκB protein levels, and both pre- and post-treatment with rHDGF ab significantly reduced the up-regulation. The result from immunofluorescence staining showed that SAH induced proliferation of microglia and astrocyte and apoptosis of neuron cells. Both pre- and post-treatment with rHDGF ab significantly attenuated proliferation of microglia and astrocyte and inhibited apoptosis of neuron cells. Furthermore, treatment with rHDGF ab significantly improved neurological outcome. Blocking HDGF attenuates neuron cell apoptosis and vasospasm through inhibiting inflammation in brain tissue at early phase after SAH.

scholarly journals Antivasospastic and antiinflammatory effects of caspase inhibitor in experimental subarachnoid hemorrhage

2007 ◽  
Vol 107 (1) ◽  
pp. 128-135 ◽  
Author(s):  
Keiichi Iseda ◽  
Shigeki Ono ◽  
Keisuke Onoda ◽  
Motoyoshi Satoh ◽  
Hiroaki Manabe ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Separate Experiment ◽  
Caspase Inhibitor ◽  
Caspase 1 ◽  
Delayed Cerebral Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Antiinflammatory Effects ◽  
Arterial Endothelial Cells

Object Inflammation in the subarachnoid space and apoptosis of arterial endothelial cells have been implicated in the development of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). The authors investigated mechanisms of possible antivasospastic effects of N-benzyl-oxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK), a caspase inhibitor that can inhibit both inflammatory and apoptotic systems, in animal models of SAH. Methods Rabbits were assigned to three groups of eight animals each and were subjected to SAH by injection of blood into the cisterna magna. The experiments were performed in the following groups: SAH only, SAH + vehicle, and SAH + Z-VAD-FMK. The Z-VAD-FMK (1 mg) or vehicle (5% dimethyl sulfoxide) was intrathecally administered before SAH induction. Diameters of the basilar artery (BA) were measured on angiograms obtained before and 2 days after SAH. The BA diameter on Day 2 was expressed as a percentage of that before SAH. Interleukin (IL)–1β in the cerebrospinal fluid (CSF) was examined using Western blotting, and brains were immunohistochemically examined for caspase-1 and IL-1β. In a separate experiment, 20 rats were subjected to SAH and their brains were immunohisto-chemically assessed for caspase-1, IL-1β, and macrophages. Results In rabbits, Z-VAD-FMK significantly attenuated cerebral vasospasm (the BA diameter on Day 2 in SAH-only, SAH + vehicle, and SAH + Z-VAD-FMK groups was 66.6 ± 3.2%, 66.3 ± 3.7%, and 82.6 ± 4.9% of baseline, respectively), and suppressed IL-1β release into the CSF and also suppressed immunoreactivities of caspase-1 and IL-1β in macrophages infiltrating into the subarachnoid space. Immunoreactivities for caspase-1 and IL-1β were observed in immunohistochemically proven infiltrating macrophages in rats. Conclusions These results indicate that caspase activation may be involved in the development of SAH-induced vasospasm through inflammatory reaction.

Prevention of cerebral vasospasm by a humanized anti-CD11/CD18 monoclonal antibody administered after experimental subarachnoid hemorrhage in nonhuman primates

2003 ◽  
Vol 99 (2) ◽  
pp. 376-382 ◽  
Author(s):  
Richard E. Clatterbuck ◽  
Philippe Gailloud ◽  
Lynn Ogata ◽  
Abeyu Gebremariam ◽  
Gregory N. Dietsch ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Nonhuman Primates ◽  
Leukocyte Migration ◽  
Content Type ◽  
Areal Fraction ◽  
Chronic Vasospasm ◽  
Fine Print

Object. Leukocyte—endothelial cell interactions occurring in the first hours after subarachnoid hemorrhage (SAH) initiate changes in the endothelium and vessel wall that lead to an influx of leukocytes and the development of chronic vasospasm days later. Upregulation of intercellular adhesion molecule—1 (ICAM-1), also called CD54, appears to be a crucial step in this process. There is increasing experimental evidence that blocking the interaction between ICAM-1, which is expressed on endothelium, and integrins such as lymphocyte function—associated antigen—1 (CD11a/CD18) and macrophage antigen—1 (complement receptor 3, CD11b/CD18), which are expressed on the surface of leukocytes, prevents not only inflammation of vessel walls but also chronic vasospasm. The authors extend their previous work with monoclonal antibody (mAb) blockade of leukocyte migration to a nonhuman primate model of chronic, posthemorrhagic cerebral vasospasm. Methods. Before surgery was performed, six young adult male cynomolgus monkeys underwent baseline selective biplane common carotid and vertebrobasilar artery cerebral angiography via a transfemoral route. On Day 0, a right frontosphenotemporal craniectomy was performed with arachnoid microdissection and placement of 2 to 3 ml of clotted autologous blood in the ipsilateral basal cisterns. The animals were given daily intravenous infusions of 2 mg/kg of either a humanized anti-CD11/CD18 or a placebo mAb beginning 30 to 60 minutes postoperatively. The monkeys were killed on Day 7 after a repeated selective cerebral angiogram was obtained. The area of contrast-containing vessels observed in each hemisphere on anteroposterior angiographic views was calculated for the angiograms obtained on Day 7 and expressed as a percentage of the area on baseline angiograms (percent control areal fraction). Review of flow cytometry and enzyme immunoassay data confirmed the presence of the anti-CD11/CD18 antibody in the serum and bound to leukocytes in the peripheral blood of treated animals. Comparisons of the groups revealed 53 ± 4.8% control vascular areal fraction in the placebo group (two animals) and 95.8 ± 9.4% in the anti-CD11/CD18—treated group (three animals), a statistically significant difference (p = 0.043, t-test). Conclusions. These results show that blockade of leukocyte migration into the subarachnoid space by an anti-CD11/CD18 mAb is effective in preventing experimental cerebral vasospasm in nonhuman primates, despite the unaltered presence of hemoglobin in the subarachnoid space. These experimental data support the hypothesis that inflammation plays a role in cerebral vasospasm after SAH.

scholarly journals The kinetics of lymphocyte subsets and macrophages in subarachnoid space after subarachnoid hemorrhage in rats.

Stroke ◽  
1993 ◽  
Vol 24 (12) ◽  
pp. 1993-2000 ◽  
Author(s):  
T Kubota ◽  
Y Handa ◽  
A Tsuchida ◽  
M Kaneko ◽  
H Kobayashi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Lymphocyte Subsets ◽  
Kinetics Of
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