Nontraumatic Subarachnoid Hemorrhage

2021 ◽  
pp. 479-484
Author(s):  
Tia Chakraborty ◽  
Jennifer E. Fugate
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Early Recognition ◽  
Circle Of Willis ◽  
Thunderclap Headache ◽  
Recurrent Bleeding ◽  
Preventative Measures ◽  
Neurologic Deficits

Subarachnoid hemorrhage (SAH) is defined as blood in the subarachnoid space. Nontraumatic SAH is most commonly caused by rupture of an aneurysm located at the circle of Willis. Patients often present with acute thunderclap headache but also may lose consciousness or have focal neurologic deficits. Detection of an aneurysm, if present, and its treatment are needed urgently to prevent recurrent bleeding. Patients with nontraumatic SAH are prone to numerous complications that require preventative measures, early recognition, and treatment.

Aneurysmal Subarachnoid Hemorrhage

2019 ◽  
pp. 577-584
Author(s):  
Giuseppe Lanzino ◽  
Biagia La Pira
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Aneurysm ◽  
Subarachnoid Space ◽  
Early Recognition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Circle Of Willis ◽  
Neurologic Deficits ◽  
Considerable Morbidity ◽  
Basal Cisterns

The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space. The term spontaneous is used to distinguish causes other than traumatic. The characteristic SAH pattern of most aneurysmal causes is SAH blood around the basal cisterns or around the circle of Willis. This chapter focuses on aneurysmal SAH (aSAH) related to rupture of an intracranial aneurysm. A medical and neurosurgical emergency, aSAH is associated with a 1-month mortality as high as 40%, and survivors have considerable morbidity and persisting neurologic deficits. Early recognition and management of aSAH are critical to optimizing outcomes.

Terson sign:

2020 ◽  
Vol 2 (1) ◽  
pp. 38-43
Author(s):  
Luiz Severo Bem Junior ◽  
Gustavo De Souza Andrade ◽  
Joao Ribeiro Memória Júnior ◽  
Hildo Rocha Cirne de Azevedo Filho
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Early Recognition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Case Reports ◽  
Clinical Status ◽  
Vitreous Hemorrhage ◽  
Anterior Communicating Artery ◽  
Inclusion Criteria ◽  
Relationship Of ◽  
The Relationship

Terson's sign (TS) is classically defined as vitreous hemorrhage associated with subarachnoid hemorrhage of aneurysmal origin, being an important predictor of severity, indicating greater morbidity and mortality when compared to patients without the sign. The objective of this study is to review the relationship of Terson syndrome/Terson sign with the prognosis of aneurysmal subarachnoid hemorrhage. A search for original articles, research and case reports was performed on the PubMed, Scielo, Cochrane and ScienceDirect platform, with the following descriptors: Terson sign and subarachnoid hemorrhage. Retrospective, prospective articles and case reports published in the last 5 years and which were in accordance with the established objective and inclusion criteria were selected. Ten (10) articles were selected, in which the available results show an unfavorable prognostic relationship of TS and subarachnoid hemorrhage, because these patients had a worse clinical status assessed on the Glasgow scales ≤ 8, Hunt & Hess > III, Fisher > 3, in addition to intracranial hypertension and location of the aneurysm in the anterior communicating artery complex. The early recognition of this condition described by Albert Terson in 1900 brought an important contribution to neurosurgery, being recognized until nowadays.

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.

Thunderclap Headache

2016 ◽  
Author(s):  
Ji Y. Chong ◽  
Michael P. Lerario
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Presentation ◽  
Clinical Symptoms ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Thunderclap Headache ◽  
Reversible Cerebral Vasoconstriction Syndrome ◽  
Cerebral Vasoconstriction ◽  
Vasoactive Medication ◽  
Angiographic Findings

Reversible cerebral vasoconstriction syndrome can cause thunderclap headache, subarachnoid hemorrhage, and stroke. The clinical presentation can be similar to aneurysmal subarachnoid hemorrhage and therefore requires rapid angiography. Angiographic findings of vasculopathy and resolution of clinical symptoms and imaging abnormalities support this diagnosis. This syndrome is most often incited following pregnancy or the ingestion of a vasoactive medication.

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