Cause Of Subarachnoid Hemorrhage Research Articles

Molecular basis for the development of intracranial aneurysm

Saccular intracranial aneurysm (sIA) is the leading cause of subarachnoid hemorrhage, one of the most catastrophic forms of stroke. Given a high mortality rate and severe disability after subarachnoid hemorrhage, it is mandatory to develop a novel therapeutic modality that prevents sIA progression and rupture. The multifactorial nature of this disease hampers our comprehensive understanding of the pathophysiology of sIA. Recent advances in genetics, gene-expression profiling and molecular biological techniques have provided us with a wide variety of evidence supporting the notion that sIA is closely associated with inflammation, pathological vascular remodeling and apoptosis. Molecular mechanisms of sIA rupture remain to be elucidated and should be continuously discussed as a future issue. This would help in selecting patients with sIA that is prone to rupture, and in preventing sIA from rupture less invasively.

脳動脈解離 出血性椎骨脳底動脈領域の動脈解離の自然歴―保存的治療症例の長期経過観察による解析―

Vertebrobasilar artery dissection began to attract attention as a cause of subarachnoid hemorrhage (SAH) in the late 1970s. Although reports on this disease have gradually increased, the natural history of vertebrobasilar artery dissection remains obscure, and long-term follow-up of patients without surgical treatment is necessary to determine appropriate treatment. We describe the long-term clinical course of ruptured vertebrobasilar artery dissection treated non-surgically. Fourteen subjects with ruptured vertebrobasilar artery dissection were treated conservatively in 7 neurosurgical departments. We reviewed their clinical outcomes, image findings and the chronological changes at the dissection site from their charts. The modified Rankin Scale was Grade 0 in 13 of 14 cases, and Grade 2 in 1 case. The configuration of dissection did not change during the follow-up period in 12 of 14 cases, but occlusion and restoration were recognized in a single case each. Good prognosis was common in the patients with ruptured vertebrobasilar artery dissection who were treated non-surgically. It is essential to accumulate more data on the clinical course and changes in image findings of long-term survival cases to establish a definite strategy for ruptured vertebrobasilar artery dissection.

L’exposition aux radiations ionisantes dans la neurochirurgie rachidienne en 2009

Subarachnoid haemorrhage (SAH), secondary to spinal hemangioblastoma (HBL), is extremely rare, with only a few case reports to date. We report the experience of our reference centre for spinal tumours and Von Hippel–Lindau (VHL) disease in patients with spinal HBL presenting with SAH. We further performed a systematic review of the literature.We report two cases. A systematic search was performed using the PubMed, Embase and Cochrane databases, with no limit for publication date. Inclusion criteria were: patients with HBL presenting with SAH, with or without VHL. The systematic review retrieved only 10 studies, including 16 patients.In our centre, the first case concerned radicular HBL at D12 level, presenting with spinal and brain SAH. The patient underwent uneventful microsurgical en bloc resection. Postoperative course was normal. The second case concerned HBL with SAH at the cervico-medullary junction, with rapidly fatal course. The systematic review revealed female predominance, at a median age of 40 years, with HBL predominantly located at cervical level, common preoperative symptoms being headache and signs of meningeal irritation.In conclusion, spinal HBL is an extremely rare cause of SAH. The systematic review found putative risk factors: female gender, age 40–50 years, cervical location, and median size 2 cm. Diagnosis can be difficult when presentation mimics intracerebral SAH. We advocate early surgical removal. The risk of rapidly fatal course, in case of major haemorrhage, needs to be borne in mind.

Hémorragie méningée focale et angiopathie amyloïde cérébrale : une association non fortuite

Introduction Cerebral amyloid angiopathy is a degenerative angiopathy due to amyloid deposits in the walls of the meningeal and cortical vessels. It is considered as a major cause of cerebral hemorrhage to the elderly. It was recently demonstrated that the association of focal meningeal bleedings and cerebral hemorrhage is very suggestive of cerebral amyloid angiopathy. In contrast, the links between subarachnoid hemorrhage and amyloid angiopathy are less well-known. Cases reports We report nine cases of cerebral amyloid angiopathy. The clinical presentation was variable, but all had at least one inaugural meningeal bleeding. As cortico-meningeal biopsies were not performed the Boston criteria were used to establish the diagnosis. Conclusion Cerebral amyloid angiopathy is an underestimated cause of subarachnoid hemorrhage. Our observations show that this diagnosis should be evoked when focal meningeal bleeding occurs without head trauma or when focal subarachnoid hemorrhage is followed by a subcortical hematoma in an elderly subject.

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a common and frequently devastating condition, accounting for ≈5% of all strokes and affecting as many as 30 000 Americans each year.1,2 The American Heart Association (AHA) previously published “Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage.”3 Since then, considerable advances have been made in endovascular techniques, diagnostic methods, and surgical and perioperative management paradigms. Nevertheless, outcome for patients with SAH remains poor, with population-based mortality rates as high as 45% and significant morbidity among survivors.4–9 Several multicenter, prospective, randomized trials and prospective cohort analyses have influenced treatment protocols for SAH. However, rapid evolution of newer treatment modalities, as well as other practical and ethical considerations, has meant that rigorous clinical scientific assessment of the treatment protocols has not been feasible in several important areas. To address these issues, the Stroke Council of the AHA formed a writing group to reevaluate the recommendations for management of aneurysmal SAH. A consensus committee reviewed existing data in this field and prepared the recommendations in 1994.3 In an effort to update those recommendations, a systematic literature review was conducted based on a search of MEDLINE to identify all relevant randomized clinical trials published between June 30, 1994, and November 1, 2006 (search terms: subarachnoid hemorrhage , cerebral aneurysm , trial ; Table 1). Each identified article was reviewed by at least 2 members of the writing group. Selected articles had to meet one of the following criteria to be included: randomized trial or nonrandomized concurrent cohort study. Case series and nonrandomized historical cohort studies were reviewed if no studies with a higher level of evidence were available for a particular topic covered in the initial guidelines. These were chosen on the basis of sample size and the relevance of the particular studies to subjects that …

An unusual cause of subarachnoid haemorrhage in a patient with newly diagnosed neurofibromatosis: a case report

IntroductionIn this report we discuss an unusual cause of subarachnoid haemorrhage in association with neurofibromatosis.Case presentationA previously fit 55-year-old man developed sudden onset headache with loss of consciousness. He was comatose on admission with no focal neurological signs. Numerous neurofibromas and café-au-lait patches were noted, indicating neurofibromatosis type 1 which had not been previously diagnosed. Computer Tomography brain revealed a grade IV subarachnoid haemorrhage in association with numerous vascular lesions on cerebral angiography.ConclusionA rare cause of subarachnoid haemorrhages was identified and is discussed in detail.

Intracranial subarachnoid hemorrhage resulting from cervical spine dural arteriovenous fistulas: literature review and case presentation

Cervical dural arteriovenous fistulas (dAVFs) are a rare cause of intracranial subarachnoid hemorrhage (SAH) but should be considered when other sources are not found. Subarachnoid hemorrhage caused by dAVF is thought to occur as a result of venous hypertension in most cases. The clinical presentation, acute onset of severe headache, is similar to that in patients with other causes of SAH; however, severe neurological deficits (Hunt and Hess Grade IV and V SAH) have not been reported in SAH caused by cervical dAVFs. Patients with this type of SAH commonly report suboccipital headache, neck pain, and nausea, and thus these hemorrhages can be easily dismissed as perimesencephalic SAH. Vigilant evaluation with 4-vessel cerebral angiography, including selective catheterization of both proximal vertebral arteries, should be performed. The practice of unilateral vertebral artery injection with reflux into the contralateral vertebral and posterior inferior cerebellar arteries has the potential to overlook cervical dAVF. Magnetic resonance imaging may be useful to evaluate for other causes of SAH but is probably not sensitive for the identification of a cervical dAVF. Surgical treatment of this lesion has an excellent outcome.

Atypical causes of nontraumatic intracranial subarachnoid hemorrhage

Background To analyze the management and outcome of patients presenting with atypical causes of intracranial subarachnoid hemorrhage (SAH). Methods We performed a review of our last 820 nontraumatic-SAH patients and analyzed the management and outcome of patients where the SAH origin was not a ruptured aneurysm. The Glasgow Outcome Scale (GOS) was used to assess outcome 3 months after event. Results Thirty-two patients had atypical causes of SAH. In 15 patients with Hunt and Hess (H&H) scores from 1 to 3 without focal neurological deficit (FND), 8 perimesencephalic nonaneurysmatic SAH, 4 blood coagulation disorders, 1 sinus thrombosis, 1 vasculitis, and 1 unknown-origin-SAH (UOS) were diagnosed. Fourteen (93%) of these 15 patients were conservatively treated. In 17 patients with H&H scores from 3 to 5 and FND, 8 tumors, 1 cavernoma, 1 sinus thrombosis, 1 arteriovenous malformation, 1 blood coagulation disorders, 2 UOS, and 3 dural fistulas were diagnosed. Fifteen (88%) of these 17 patients were interventionally treated. The neurological condition 3 months later was good (GOS 4 and 5) in 12 of the 15 cases (80%) admitted with low-H&H scores, as well as in 13 of the 17 cases (76%) admitted with high-H&H scores. Three patients died and four developed a severe disability. Conclusions Patients presenting with atypical causes of SAH and high-H&H scores at admission are likely to harbor an intracranial organic process producing the bleeding. Despite this poor initial condition, their 3-month outcome can be similar to those of patients with low-H&H scores if the origin of the bleeding is properly treated.

Spinal cord arteriovenous malformation in a toddler presenting with altered mental status and fever

Central nervous system arteriovenous malformations (AVMs) are a rare cause of subarachnoid hemorrhage and neurologic deficits. About 90% of these lesions are supratentorial, with a smaller percentage occurring in the posterior fossa and an even smaller number found throughout the spine. Although spinal AVMs are uncommon, these disorders represent a treatable cause of significant morbidity in a young age group. We report a case of a T11-T12 spinal AVM in a 14-month-old girl presenting with low-grade fever and lethargy who was found to have subarachnoid hemorrhage on evaluation and describe a reasonable stepwise approach to these patients in the emergency department utilizing computed tomography, lumbar puncture, magnetic resonance imaging, and angiography.

Manejo general en Cuidados Intensivos del paciente con hemorragia subaracnoidea espontánea

Aneurysmal subarachnoid hemorrhage (SAH) is a neurologic emergency and often a neurologic catastrophe. Nontraumatic subarachnoid hemorrhage is characterized by the extravasation of blood into the spaces covering the central nervous system. The leading cause of SAH is rupture of an intracranial aneurysm, which accounts for about 80-85% of cases. Mortality and morbidity can be reduced if SAH is treated urgently. Sudden, explosive headache is a cardinal but nonspecific feature in the diagnosis of SAH; computered tomography (CT) scanning is mandatory in all the patients with symp toms that are suggestive of SAH. Catheter angiography for detecting aneurysms is gradually being replaced by CT angiography. Diagnosing SAH can be challenging and treatment is complex, sophisticated and multidisciplinary. Reble eding is the most imminent danger, which must be prevented by endovascular occlusion with detachable coils (coiling) or by surgical clipping of the aneurysm; the risk of delayed cerebral ischemia is reduced with nimodipine and avoiding hypovolemia; hydrocephalus can be treated by ventricular drainage. Intensive care plays a more important role in the management of SAH than in any other neurological disorder. Excellence in neurologic diagnosis, in operative neurosurgery or neuroradiologic procedures must be accompanied by excellence in Intensive Care. This review emphasizes treatment in the Intensive Care Unit, surgical and endovascular therapeutic options and the current state of treatment of major complications such as rebleeding, cerebral vasospasm and acute hydrocephalus.

Gene Expression during the Development of Experimentally Induced Cerebral Aneurysms

Cerebral aneurysms are a major cause of subarachnoid hemorrhage, but the mechanism of their development remains unclear. In this study, we investigated candidate genes whose expression is significantly changed during the development of experimentally induced cerebral aneurysms using adaptor-tagged competitive polymerase chain reaction (ATAC-PCR). Twenty-four rats received sham operation (control) or the operation for the induction of experimental cerebral aneurysms. Rats were sacrificed at time 0, 2 weeks, 1 month and 3 months after the operation (n = 6 for each group). RNAs from right anterior cerebral artery/olfactory artery (ACA/OA) bifurcations were assessed via a 191-gene data matrix expression profile by ATAC-PCR. We identified 15 genes whose expression is significantly altered during cerebral aneurysm formation, including major heparan sulfate proteoglycan, cathepsin B, hevin and β₄-integrin. We also confirmed protein expression of β₄-integrin in rat cerebral aneurysms by quantitative real-time PCR and immunohistochemistry. The ATAC-PCR revealed temporal changes in gene expression during the development of experimental cerebral aneurysms. The genes that were significantly changed in this study would be the candidates for future studies concerning the development of cerebral aneurysms.

Dissecting aneurysms of the vertebrobasilar system. A comprehensive review on natural history and treatment options

Vertebral artery dissection has been recognized as an uncommon cause of ischemic stroke. However, it is less well known as a cause of subarachnoid hemorrhage. Even if dissecting aneurysms of the vertebral artery are rare, their importance arise from their high morbidity and mortality with rebleeding occurring more often than in cases of saccular aneurysms. Dissecting aneurysms of the vertebrobasilar system are a complex entity which requires a rapid and effective treatment to prevent rerupture. The sole stenting technique stands as a promising approach, allowing to occlude the aneurysm while preserving the vessel patency and reconstructing the diseased segment.

Cerebral venous sinus thrombosis as a rare cause of thunderclap headache and nonaneurysmal subarachnoid haemorrhage

Sirs: In a clinical setting, isolated thunderclap headache is commonly assumed to be benign in origin once subarachnoid haemorrhage (SAH) has been excluded [1]. However, cerebral venous sinus thrombosis (CVST) is an infrequent, alternative cause of sudden-onset headache and is not conclusively excluded by normal conventional CT and LP. CVST is also a recognised rare cause of SAH. Here, we report a case of CVST presenting with thunderclap headache and complicated by delayed SAH. A previously well 53-year-old woman presented with spontaneous, sudden-onset occipital headache as her sole symptom. Neurological examination including fundoscopy was normal, with no evidence of meningism. Acute head CT and subsequent LP performed 16 hours after onset were unremarkable (opening pressure 19 cm, CSF acellular with no bilirubin detectable on spectrophotometry). The headache resolved completely within 24 hours and the patient was discharged with a diagnosis of primary thunderclap headache. The following day, she represented with sudden-onset headache at rest accompanied by mild neck stiffness. Her symptoms resolved before a further suddenonset headache occurred two days later. Examination remained normal throughout. Repeat, unenhanced head CT demonstrated a small, high left frontal SAH along the cranial convexity without involvement of the basal cisterns (Fig. 1a). CT angiography detected no arterial aneurysm, but its venous phase showed changes suggestive of superior sagittal sinus thrombosis, which was confirmed on MR venography (Fig. 1b). Screening for secondary causes of thrombosis was negative. She was initially treated with intravenous unfractionated heparin to allow rapid reversal in case of rebleeding, before being warfarinised under cover from low molecular weight heparin. She remained well at follow-up six months later. Repeat MR angiography showed resolution of the superior sagittal sinus thrombosis, with no other vascular or brain parenchymal abnormalities. Thunderclap headache is an unusual presentation of CVST, perhaps seen in fewer than 20 % of cases [2]. Rarely, there may be no concomitant findings to suggest the presence of a CVST, such as focal neurological signs, seizures or features of raised intracranial pressure. Most patients with CVST have a raised opening pressure and abnormal CSF constituents, but absence of these features does not conclusively rule out the diagnosis. In a previous series of 38 cases, nine patients had both opening pressure and CSF constituents measured, and in one of them all parameters were normal [3]. SAH is a very rare complication of cerebral venous thrombosis, with only 30 cases reported to date. It has been suggested that venous intraparenchymal haemorrhages may rupture into the subarachnoid space, thus causing sudden-onset headache in CVST [2, 4]. However, we hypothesise that our patient’s first headache was caused by the CVST, as there was no evidence of SAH on initial brain CT and bilirubin was not detectable in the CSF. The second or third episode of headache may have been caused by SAH. LETTER TO THE EDITORS

An Unusual Cause of Subarachnoid Hemorrhage

A 47-year-old man presented to our hospital with collapse secondary to a subarachnoid hemorrhage. A careful history taking revealed symptoms of anaphylaxis before his collapse. This case illustrates an unusual cause of subarachnoid hemorrhage.

光学的センサーによる脳動脈瘤塞栓用coilの挿入力測定装置の開発

Recently, cerebral endovascular treatments using catheters have been rapidly developing. Such treatments typically include coil embolization for preventing a cerebral aneurysm rupture, which is a cause of subarachnoid hemorrhage. In embolization, inserting coils with an excessive force may cause a rupture of the aneurysm,resulting in severe complications, Removal of the tip of the catheter from the aneurysm may result in insufficient embolus formation. We will report the development of a device which measures the insertion force of the coils using an optical system, present a device overview and the results of its basic experiments.

Dissecting aneurysm of the radiculomedullary artery originating from extracranial vertebral artery dissection in a patient with rheumatoid cervical spine disease: an unusual cause of subarachnoid hemorrhage

✓The authors report the case of a 65-year-old woman with atlantoaxial subluxation caused by rheumatoid arthritis. The patient had been hospitalized because of an infection after a total-knee replacement, when she suddenly lost consciousness and became apneic after an episode of intractable neck pain. Cranial computed tomography scanning demonstrated subarachnoid hemorrhage (SAH), and angiography revealed a dissecting aneurysm of the radiculomedullary artery that had originated from an extracranial vertebral artery dissection at the level of the atlantoaxial joint. Although coil embolization for the parent artery, including the dissecting aneurysm, was performed successfully, the patient died of worsening infection. The authors believe that the SAH occurred because of a ruptured dissecting aneurysm in the intradural portion of the radiculomedullary artery.

Dissecting aneurysm of the radiculomedullary artery originating from extracranial vertebral artery dissection in a patient with rheumatoid cervical spine disease: an unusual cause of subarachnoid hemorrhage

The authors report the case of a 65-year-old woman with atlantoaxial subluxation caused by rheumatoid arthritis. The patient had been hospitalized because of an infection after a total-knee replacement, when she suddenly lost consciousness and became apneic after an episode of intractable neck pain. Cranial computed tomography scanning demonstrated subarachnoid hemorrhage (SAH), and angiography revealed a dissecting aneurysm of the radiculomedullary artery that had originated from an extracranial vertebral artery dissection at the level of the atlantoaxial joint. Although coil embolization for the parent artery, including the dissecting aneurysm, was performed successfully, the patient died of worsening infection. The authors believe that the SAH occurred because of a ruptured dissecting aneurysm in the intradural portion of the radiculomedullary artery.

Postcesarean Subarachnoid Hemorrhage as the Initial Presentation of Cerebral Venous Thrombosis

The risk of stroke is increased in the peripartum period because of the hypercoagulable state that accompanies pregnancy [1]. The reported incidence of pregnancyrelated stroke varies from 19.2 to 46.2 per 100,000 pregnancies [2,3], with cerebral venous thrombosis (CVT) accounting for a reported 22%. CVT is also more common in parturient women, with 73% of CVT cases occurring postpartum [4]. It is also strongly associated with cesarean delivery. CVT results from thrombus in one of the outflow tracts of the brain and causes venous hypertension. The clinical manifestations include headache (the most common, occurring in 70% to 90%), nausea, changes in mental status, seizures, and focal neurologic deficits [5]. Diagnosis of CVT may be very challenging, because the symptoms are common and nonspecific. Acute subarachnoid hemorrhage (SAH) has been reported as an initial sign of CVT [6], which further complicates the diagnosis, since other causes of SAH must also be considered. We report a case of postcesarean section CVT with SAH. A previously healthy 38-year-old woman, gravida 3, para 1, abortion 1, was admitted at 38 weeks’ gestation with ruptured membranes and uterine contractions. She had a previous elective cesarean section. She was a non-smoker and denied a history of hypertension. She had regular prenatal care at our obstetric clinic, with no evidence of any complications. A cesarean section was performed under spinal anesthesia, with 12 mg of 0.5% heavy bupivacaine administered uneventfully using a 27-gauge spinal needle and with only one attempt. A live 3,250 g baby girl was delivered without difficulty and the placenta removed completely. Total blood loss was about 300 mL. In the recovery room, the patient complained of severe headache with neck stiffness approximately 20 minutes after surgery had completed. An electrocardiogram showed bradycardia with heart rate of 42 beats/minute. A brain computed tomography scan showed SAH with blood accumulation within the cerebral cortical sulci (Figure). The ventricular system showed negative findings. Thus, cerebral angiography was immediately performed to find the source of SAH. Cerebral angiographic study for SAH was performed using a right femoral arterial approach, with catheterization of the bilateral internal and external carotid arteries. No evidence of aneurysm or vascular malformation was noted. A prominent transcerebral vein with absence of cortical vein was noted at the right parietal lobe. The study suggested the possibility of CVT. Heparin was not given

Endothelial injury and inflammatory response induced by hemodynamic changes preceding intracranial aneurysm formation: experimental study in rats

Intracranial aneurysms are the leading cause of subarachnoid hemorrhage, which is associated with high morbidity and mortality rates. Despite advances in the microsurgical and endovascular treatment of intracranial aneurysms, little is known about the mechanisms by which they originate, grow, and rupture. To clarify the series of early events leading to formation of intracranial aneurysms, the authors compared aneurysmal morphological changes on vascular corrosion casts with parallel pathological changes in the cerebral arteries of rats. The authors induced cerebral aneurysms by renal hypertension and right common carotid artery ligation in 40 male Sprague-Dawley rats; 10 intact rats served as the controls. The anterior cerebral artery-olfactory artery bifurcation was assessed morphologically by using vascular corrosion casts of Batson plastic reagent and immunohistochemically by using antibodies against endothelial nitric oxide synthase, alpha-smooth muscle actin, macrophages, and matrix metalloproteinase-9. Surgically treated rats manifested different degrees of aneurysmal changes. Based on these staged changes, the authors propose that the formation of intracranial aneurysms starts with endothelial injury at the apical intimal pad (Stage I); this leads to the formation of an inflammatory zone (Stage II), followed by a partial tear or defect in the inflammatory zone. Expansion of this defect forms the nidus of the intracranial aneurysm (Stage III). This is the first study to demonstrate the in vivo mechanisms of intracranial aneurysm formation. The inflammatory response that follows endothelial injury is the basic step in the pathogenesis of these lesions. In this study the investigators have expanded the understanding of the origin of intracranial aneurysms and have contributed to the further development of measures to prevent and treat aneurysms.

INTRACRANIAL SUBARACHNOID HEMORRHAGE FOLLOWING LUMBAR MYELOGRAPHY IN TWO DOGS

Intracranial subarachnoid hemorrhage is a rare but serious complication of lumbar puncture in humans. Possible sequelae include increased intracranial pressure, cerebral vasospasm, or mass effect, which can result in dysfunction or brain herniation. We describe two dogs that developed intracranial subarachnoid hemorrhage following lumbar myelography. In both dogs, myelography was performed by lumbar injection of iohexol (Omnipaque). Both the dogs underwent uneventful ventral decompressive surgery for disk herniation; however, the dogs failed to recover consciousness or spontaneous respiration following anesthesia. Neurologic assessment in both dogs postoperatively suggested loss of brain stem function, and the dogs were euthanized. There was diffuse subarachnoid hemorrhage and leptomeningeal hemorrhage throughout the entire length of the spinal cord, brain stem, and ventrum of brain. No evidence of infectious or inflammatory etiology was identified. The diagnosis for cause of brain death was acute subarachnoid hemorrhage. Our findings suggest that fatal subarachnoid hemorrhage is a potential complication of lumbar myelography in dogs. The cause of subarachnoid hemorrhage is not known, but may be due to traumatic lumbar tap or idiosyncratic response to contrast medium. Subsequent brain death may be a result of mass effect and increased intracranial pressure, cerebral vasospasm, or interaction between subarachnoid hemorrhage and contrast medium.