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Atraumatic Non-aneurysmal sulcal subarachnoid hemorrhage is very rare. Sulcal subarachnoid hemorrhage (sSAH) is characterized by isolated bleeding in one or a few adjacent sulci. Central sulcus hemorrhage is a rare imaging finding. There are many causes for sSAH. In older patients, sSAH is due to Cerebral Amyloid Angiopathy (CAA), while in younger patients, reversible cerebral vasoconstriction syndrome (RCVS) is the most frequent etiology. Imaging studies help in the evaluation of sSAH. We report a rare case of an isolated central sulcus hemorrhage on computed tomography. sSAH usually occur on the side with acute ischemic stroke, and it is unusual for sSAH to occur on the opposite side of the infarct territory, but in our case sSAH occurred on opposite side, but after a gap of 3 years.
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Transient focal neurological episodes, also called amyloid spells occur as recurrent, transient episodes of spreading paresthesia seen in 14% of cerebral amyloid angiopathy (CAA) patients. An 81-year-old gentleman with coronary artery disease and a left ventricular clot was on anticoagulant treatment. He presented with three episodes of tingling in the left fingers spreading to the left arm and left leg, each lasting for 10 min. Magnetic resonance imaging of the brain with susceptibility imaging showed convexity hemorrhage, and curvilinear blooming in sulcal spaces of the right cerebral convexity and left precuneus. Warfarin was stopped. He was treated with clobazam, aspirin, and atorvastatin. He improved, so was discharged after 2 days. Amyloid spells can be confused with transient ischemic attack (TIA) or its mimics and the treatment given for TIA can lead to intracranial hemorrhage in CAA patients. Radiological features aid in the diagnosis of CAA and antiplatelets need to be administered cautiously in patients with suspected TIA.
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Cerebral amyloid angiopathy (CAA) is a cerebral small vascular disease caused by pathological deposition of β-amyloid protein in cortical and pial arteries and capillaries. It is the main cause of non-traumatic cerebral lobular hemorrhage and has a high risk of recurrent hemorrhage. Studies have shown that specific imaging markers, such as cerebral microbleeds, cortical superficial siderosis, convexal subarachnoid hemorrhage, centrum semiovale-perivascular spaces and the overall burden of cerebral small vascular disease, may be more effective in predicting the risk of bleeding recurrence in patients with CAA. This article reviews the imaging markers used to predict the risk of recurrent bleeding in patients with CAA, in order to provide a new direction for the establishment of a risk assessment system for recurrent bleeding.
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Cerebral small vessel disease (CSVD) is a series of clinical, imaging, and pathological syndromes resulting from various etiologies affecting small arteries (microarteries, capillaries, microvenules, and small veins in the brain). The diagnosis of CSVD is based on imaging presentations, but the high cost and bleeding risk of cranial imaging methods make the diagnosis of rare CSVD more difficult. Retinal vessels are the only vasculature visible in vivo and share anatomical and embryological features with small brain vessels. Retinal vascular abnormalities have been shown to exist in rare CSVD such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), cerebral amyloid angiopathy (CAA) and moyamoya disease (MMD). Retinal vascular examination may provide new ideas for the study of rare CSVD.
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Cerebral amyloid angiopathy(CAA)is a small vascular disease caused by the deposition of amyloid protein in the vascular wall, mainly involving the cortical and leptomeningeal arterioles and capillaries.The main pathological and clinical manifestations are lobar hemorrhage, cerebral microbleeds, cortical superficial siderosis, subarachnoid hemorrhage, cortical infarction, white matter abnormalities, CAA-related autoimmune meningoencephalitis and dementia.Patients with CAA are prone to spontaneous cerebral hemorrhage.For CAA patients, the anticoagulant therapy for prevention of cardioembolism of artrial fibrillation or intravenous thrombolytic therapy for acute ischemic stroke may increase the chance of cerebral hemorrhage and lead to aggravation of the disease.Therefore, the risk of hemorrhage associated with CAA needs to be evaluated before antithrombotic therapy.CAA-related inflammation is a critical condition.Corticosteroids and immunosuppressive agents are effective treatments.Early diagnosis and treatment can significantly improve the prognosis.
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Cerebral amyloid angiopathy (CAA) is a common age-related small vessel disease characterized by amyloid-β (Aβ) deposition in the wall of small arterioles and capillaries of the leptomeninges and cerebral cortex. Several molecular imaging technologies such as amyloid-β positron-emission tomography (PET) and 18F-fluorodeoxyglucose-PET have been successfully applied in the patients with CAA. Amyloid-PET may indicate the distribution and burden of Aβ deposition by the tracer′s specific binding to the pathological markers, providing qualitative and quantitative information for the diagnosis of CAA. However, amyloid-β PET is inadequate to differentiate CAA from other Aβ-related diseases like Alzheimer′s disease. Other novel techniques of molecular imaging including tau-PET, single photon emission computed tomography and other highly selective PET radioligands have been investigated widely at present. This article mainly reviewed the advances in molecular imaging of CAA.
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Cerebral small vessel disease (CSVD) is an important cause of ischemic stroke and vascular dementia, which brings heavy burden to families and society. The prevention and treatment of CSVD has always been a research hotspot, but its pathogenesis is still not completely clear. This article reviews the pathogenesis of CSVD, including chronic cerebral hypoperfusion, blood-brain barrier dysfunction, vascular endothelial dysfunction, interstitial fluid reflux disorder, inflammatory response, and genetic factors, in order to provide more sufficient theoretical basis for early intervention and treatment of CSVD.
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Optical coherence tomography-based angiography (OCTA) is a novel non-invasive technique for quantitatively evaluating retinal microvascular perfusion. Due to the similar embryonic origin, anatomical characteristics, and physiological characteristics of the retina and cerebral small vessels, changes in retinal microvasculature may provide a new perspective for studying the mechanisms of cerebral small vessel diseases. This article summarizes the application of OCTA in cerebrovascular diseases, aiming to evaluate whether OCTA can become an effective tool for early prediction of the occurrence of cerebrovascular disease and monitoring disease changes.
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Cerebral amyloid angiopathy (CAA) is a common cerebral small vessel disease, mainly caused by β-amyloid deposition on the small vessels less than 200 μm in diameter in cortex and leptomeninges. CAA is a major cause of spontaneous intracerebral hemorrhage in the elderly, especially lobar location. Early symptoms are insidious, and as the disease progress, they manifest as cerebral hemorrhage, cognitive decline, transient focal neurological episodes, cerebral infarction, epilepsy, headache, etc. MRI revealed that CAA is a disease in which bleeding and ischemia coexist, and even inflammation and immune responses are involved. MRI findings of CAA include cerebral hemorrhage, cerebral microbleeds, convexity subarachnoid hemorrhage and cortical superficial siderosis, cortical microinfarcts, CAA-associated inflammation, white matter hyperintensities, enlarged perivascular spaces, cerebral atrophy and lacune, etc. The same patient often has several of the above manifestations, and each manifestation has different specificity for the diagnosis of CAA. The rapid development of MRI technology has led to the improvement of the diagnostic level of CAA, and it is of great clinical significance to understand these imaging findings. This article reviews the MRI findings of sporadic CAA.
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Cerebral amyloid angiopathy presents with lobar intracerebral hemorrhage, dementia or tran sient neurological events. It occurs due to P-amyloid deposits in the media and adventitia of small arteries, leptomeningeal capillaries and the cerebral cortex. Its prevalence increases with age, and its association with cognitive impairment is well established. We present the case of an 80-year-old previously independent woman with no disabilities or cognitive impairment, and a history of well-controlled systemic arterial hypertension who consulted due to a de novo seizure and focal neurological deficits. On imaging follow up, two bilateral parietal-occipital macrohemorrhages were found, which occurred at two different times during the development of the clinical condition. These findings were attributed to cerebral amyloid angiopathy, and the patient ultimately died during this hospitalization. In this case presentation, we discuss the diagnostic criteria for considering the presence of cerebral amyloid angiopathy, its prognosis, and the reason it led to death. (Acta Med Colomb 2022; 47. DOI:https://doi.org/10.36104/amc.2022.2567).
La angiopatía amiloide cerebral se presenta con hemorragia intracerebral lobular, demencia o eventos neurológicos transitorios. Ocurre como resultado del depósito de (3-amiloide en la media y la adventicia de las arterias pequeñas, los capilares de las leptomeninges y la corteza cerebral. Su prevalencia aumenta con la edad y su asociación con deterioro cognitivo está bien establecido. Se presenta el caso de una mujer de 80 años, previamente independiente, sin discapacidad ni deterioro cognitivo, con antecedente de hipertensión arterial sistémica bien controlada, quien consultó por episodio convulsivo de novo y focalización neurológica. Durante el seguimiento imagenológico se documentó presencia de dos macrohemorragias parietooccipitales bilaterales, acontecidas en dos momentos diferentes durante la evolución del cuadro clínico, hallazgos que fueron atribuidos a la presencia de angiopatía amiloide cerebral, finalmente la paciente falleció durante dicha hospitaliza ción. En esta presentación de caso se discuten los criterios diagnósticos para considerar la presencia de angiopatía amiloide cerebral, el pronóstico y la razón que llevó a la muerte. (Acta Med Colomb 2022; 47. DOI:https://doi.org/10.36104/amc.2022.2567).
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Cerebral amyloid angiopathy-related inflammation is an inflammatory reaction process caused by beta-amyloid protein deposited in the cortical and leptomeningeal vessels, which is a rare type of cerebral amyloid angiopathy. Most of the patients are middle-aged and elderly, and manifest as progressive cognitive impairment, headache, seizures, and focal neurological deficits. Brain magnetic resonance imaging shows asymmetric T 2/fluid attenuated inversion recovery hyperintensity in cortical and subcortical white matter, in addition to multiple cerebral microbleeds. The disease often needs to be differentiated from primary angiitis of the central nervous system, glioma, and varicella-zoster virus encephalitis. Although the disease is rare, prompt treatment with glucocorticoids and immune suppressants can reduce death and disability and significantly improve outcome. Therefore, it is necessary to improve the ability of early diagnosis and treatment of this disease.
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Amyloid angiopathy (AA) is a selective deposition of amyloid in the walls of the brain vessels. It is a form of sporadic and localized amyloidosis, constituted by the Aβ4 protein, the same of Alzheimer's disease senile plaques. The most consistent clinical effect of AA is spontaneous brain hemorrhage (BH). It is the second most common cause of BH after arterial hypertension (HT). Other clinical manifestations are cognitive impairment and transient focal neurological episodes. AA BH is characteristically localized in the cerebral cortex and subcortical white matter (lobar hemorrhage), consistent with the preferential deposit of amyloid in the walls of leptomeningeal and intracortical small cerebral vessels. Other types of AA hemorrhagic complications are microbleeds (MB), cerebral convexity subarachnoid hemorrhage (cSAH) and superficial hemosiderosis (cSS). The diagnosis of AA BH is based on the Boston criteria. Using these criteria, several non-hemorrhagic biomarkers of AA have been identified that can be useful in its diagnosis. The principal AA BH risk factor is age, followed by cSS, MB, Apolipoprotein E gen ε2 and ε4 alleles, HT and the use of antithrombotics. This condition has a high recurrence rate that shares the same risk factors. There is no specific treatment for AA BH. It has a better prognosis than HT BH during the acute period, but worse on the long term, due to its high recurrence rate and cognitive impairment.
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Humanos , Hemorragia Subaracnoidea , Angiopatía Amiloide Cerebral/complicaciones , Encéfalo/diagnóstico por imagen , Imagen por Resonancia Magnética , Hemorragia Cerebral , Hemorragias IntracranealesRESUMEN
Based on a comprehensive literature review with long-term experiences of clinical practice and researches, the authors propose the following concepts of the diagnosis, treatment and research of acute cerebral small vessel disease: (1) Cerebral small vessel disease could be grouped into acute and non-acute categories. Acute cerebral small vessel disease indicates an acute stroke due to small vessel disease, including ischemic (ie. acute lacunar stroke) and hemorrhagic (hypertensive arteriopathy- and cerebral amyloid angiopathy-related intracerebral hemorrhage) stroke. (2) Acute ischemic cerebral small vessel disease, defined traditionally by the infarction size (lacunar stroke), is regarded as the syndrome caused by a variety of mechanisms recently, although mainly characterized by lipohyalinosis in the small arterioles. The understanding of pathological mechanisms has experienced a history from autopsy observation, to inference based on risk factors, and then to direct observation of arteriole morphology using high-resolution magnetic resonance angiography. The advancement in imaging technology has brought new opportunities for studies on pathological mechanisms of cerebral small vessel disease. (3) Acute cerebral small vessel disease is manifested as acute stroke, which could be with or without the non-acute symptoms or imaging markers. (4) Individualized treatment based on the pathogenesis is the future direction for practice and research of cerebral small vessel disease. Reducing the incidence, recurrence and major outcomes (death, disability and dementia) is the main target of prevention and treatment.
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Objective:To investigate the clinical, cerebrospinal fluid (CSF) and neuroimaging characteristics and their associations with prognosis in cerebral amyloid angiopathy(CAA)-related inflammation (CAA-ri).Methods:Seventeen patients with CAA-ri, 59 patients with CAA-related intracerebral hemorrhage (ICH) and 15 patients with CAA-related cognitive decline were recruited from Huashan Hospital, Fudan University from November 2015 to May 2020 and the First Affiliated Hospital of University of Science and Technology of China from January 2018 to May 2020. Vascular risk factors and imaging features of cerebral small vessel disease were compared among three groups. Clinical manifestations, CSF results, lesion features on magnetic resonance imaging, treatment options and follow-up data were collected in patients with CAA-ri. The good prognosis was defined by clinical and radiographic improvement with no disease recurrence. The associations between clinical characteristics and the immunosuppressive therapy or the good prognosis were analyzed by binary Logistic regression models.Results:Patients with CAA-ri showed earlier disease onset [(61.5±11.7) years vs (70.9±8.6) years, t=9.428, P=0.001] and more lobar cerebral microbleeds [69.0 (43.5, 134.3) vs 10.0 (5.0, 59.0), H=3.363, P=0.002] compared to patients with CAA-ICH, and higher prevalence of male (14/17 vs 6/15, χ2=6.099, P=0.014) and lower white matter hyperintensity Fazekas score [4.0 (2.0, 6.0) vs 6.0 (5.0, 6.0), H=2.461, P=0.042] compared to patients with CAA-related cognitive decline. In patients with CAA-ri, the immunosuppressive therapy was positively correlated with CSF protein>600 mg/L (odds ratio 16.50, 95% confidence interval 1.09-250.18, P=0.043), and during a follow-up of (3.0±1.9) years, the good prognosis was positively correlated with CSF protein<1 000 mg/L plus immunosuppressive therapy (odds ratio 20.00, 95% confidence interval 1.39-287.60, P=0.028). Conclusions:CAA-ri is a special subtype of CAA with earlier disease onset and higher prevalence of hemorrhagic imaging makers compared to CAA-ICH and CAA-related cognitive decline. CAA-ri patients with normal or slightly elevated CSF protein receiving immunosuppressive therapy are more likely to have good prognosis.
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RESUMO As alterações neurológicas associadas à COVID-19 têm sido frequentemente descritas, principalmente nos casos de maior severidade, e estão relacionadas a causas multifatoriais, como a disfunção endotelial, a liberação de mediadores inflamatórios (cytokine storm), a disfunção endotelial e a hipoxemia. Relatamos o caso de uma paciente do sexo feminino, 88 anos, com quadro de hemorragia cerebral associada à angiopatia amiloide, no contexto de infecção por SARS-CoV-2.
ABSTRACT The neurological changes associated with COVID-19 have been frequently described, especially in cases of greater severity, and are related to multifactorial causes, such as endothelial dysfunction, inflammatory mediator release (cytokine storm), endothelial dysfunction and hypoxemia. We report the case of a female patient, 88 years old, with cerebral hemorrhage associated with amyloid angiopathy in the context of SARS-CoV-2 infection.
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Humanos , Femenino , Anciano de 80 o más Años , Hemorragia Cerebral/diagnóstico por imagen , Angiopatía Amiloide Cerebral/diagnóstico por imagen , COVID-19/complicaciones , Hemorragia Cerebral/virología , Angiopatía Amiloide Cerebral/virología , COVID-19/diagnósticoRESUMEN
ABSTRACT Background: Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by progressive deposition of β-amyloid peptides in the walls of small and medium-sized cortical and leptomeningeal vessels. Until today, the prevalence of CAA is unknown in our region. Objective: This study aims to analyze the prevalence of this entity in a specific elderly population in a tertiary hospital in Northeastern Brazil. Methods: A cross-sectional, retrospective study with the enrollment of patients aged 65 or older followed in the neurological outpatient service of the Universidade Federal do Piauí, Brazil, who underwent brain magnetic resonance imaging (MRI) from July 2016 to June 2018. Results: One hundred and seventy-four patients were enrolled, of whom 100 were women (57.4%) and 74, men (42.6%), aged from 65 to 91 years old (median age 73.27). Nine patients were excluded from the study due to unavailability of MRI sequences needed for an appropriate analysis. Out of the 165 remaining patients, 12 (7.2%) had established the diagnosis of CAA, according to the modified Boston criteria. Conclusion: The prevalence of CAA in our study was like those of medical literature, with a progressive age-related increase.
RESUMO Introdução: A angiopatia amiloide cerebral (AAC) é uma desordem vascular causada pela deposição progressiva de peptídeos β-amiloides nas paredes de pequenos e médios vasos corticais e leptomeníngeos. Até a presente data, a epidemiologia da AAC é desconhecida em nossa região. Objetivos: Avaliar a prevalência da AAC em uma população específica de pacientes idosos de um hospital terciário no nordeste brasileiro. Métodos: Estudo transversal, retrospectivo, com seleção de pacientes com idade igual ou superior a 65 anos, acompanhados no serviço de Neurologia do Hospital Universitário da Universidade Federal do Piauí, Brasil, e que foram submetidos a exame de ressonância nuclear magnética entre julho de 2016 e junho de 2018. Resultados: Foram recrutados 174 pacientes, dos quais 100 eram mulheres (57,4%) e 74 homens (42,6%), com idades entre 65 e 91 anos (média de 73,27). Nove pacientes foram excluídos devido à indisponibilidade de sequências de ressonância magnética necessárias para uma análise apropriada. Dos 165 pacientes restantes, 12 (7,2%) foram diagnosticados com AAC de acordo com os critérios de Boston modificados. Conclusão: A prevalência da AAC em nosso estudo foi semelhante ao resultado encontrado na literatura médica, com um aumento progressivo relacionado à idade.
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Humanos , Masculino , Femenino , Anciano , Anciano de 80 o más Años , Angiopatía Amiloide Cerebral , Brasil , Boston , Estudios Transversales , Estudios Retrospectivos , Péptidos beta-Amiloides/metabolismo , Péptidos beta-Amiloides/químicaRESUMEN
Objective To analyze the clinical manifestation,imaging data and genetics mutation variants of late onset familial Alzheimer's disease concomitant with a novel mutation of presenilin 1.Methods The clinical manifestations and auxiliary examination recordings of the pedigree were analyzed.DNA was extracted from peripheral blood samples of the proband and her sons.Mutational analysis was performed by the next-generation sequencing technology and the mutation event was confirmed by Sanger sequencing technology.Results Two patients of the family presenting as Alzheimer's dementia were late onset.MRI of the proband showed extensive cerebral microbleeds.The gene detection showed p.S289P mutation in the exon 8 of presenilin 1 of the proband.Conclusion Mutation of p.S289P in the presenilin 1 gene may contribute to late onset Alzheimer's disease accompanied by amyloid angiopathy.
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Objective To analyze the relationship of cerebral microbleeds (CMBs)of different regions,especially mixed-CMBs,with cerebral amyloid angiopathy (CAA)detected using 18F-AV45 positron emission tomography(PET).Methods A total of 52 consecutive patients (68.17 ± 9.89 years old)with memory decline and CMBs found in susceptibility-weighted images(SWI)according to the inclusive and exclusive criteria were recruited.Patients were divided into three groups based on different regions of CMBs,the strictly lobar CMBs (SL-CMBs) group,the deep-CMBs (D-CMBs) group and the mixed-CMBs (M-CMBs)group.Patients in the three groups underwent 18F-AV45 PET detection and then were analyzed based on the results of 18F-AV45 PET.Results The positive rates of cerebral amyloid angiopathy in the SL-CMBs,M-CMBs and D-CMBs groups were 68.4 % (13/19),82.4 % (14/17) and 25.0 % (4/16),respectively,with statistical significance (P =0.002).There were significant differences in positive rates of cerebral amyloid angiopathy between the D-CMBs group and the M-CMBs group and between the D-CMBs group and the SL-CMBs group(P =0.001 and 0.010,respectively),while there was no difference between the M-CMBs and SL-CMBs groups in positive rates of cerebral amyloid angiopathy(P =0.335).Using the D-CMBs group as the reference group,multivariate logistic regression analysis showed that the odds ratios of positive CCA detected by PET in SL-CMBs and M-CMBs were 30.585(95%CI:2.492-375.360)and 8.107(95%CI:1.072-61.295),respectively.Conclusions Compared with D-CMBs,M-CMBs and SL-CMBs are more likely to be related to cerebral amyloid angiopathy.The presence of M-CMBs also indicates that patients have a high probability of CAA.
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PURPOSE: Cerebral small vessel disease (SVD) is known to be associated with ischemic stroke, intracerebral hemorrhage (ICH), and cognitive impairment. In this retrospective observational study, we explored SVD markers on MRI relevant to spontaneous ICH. MATERIALS AND METHODS: The ICH group consisted of 150 consecutive patients with a first primary parenchymal ICH, and the control group consisted of 271 age- and sex-matched individuals who underwent brain MRI in a health care center. We compared cerebral microbleeds (CMBs), white matter hyperintensities (WMHs), enlarged perivascular space (EPVS), and lacunae in the ICH and control groups. RESULTS: A total of 1278 CMB lesions were identified in 121 of the 150 patients in the ICH group (80.6%), while 77 CMB lesions were found in 32 of the 271 individuals in the control group (11.8%). WMH and EPVS were more severe and lacunae were more frequent in the ICH patients than in the control group. When receiver operating characteristic (ROC) curves were plotted, number of CMBs most significantly predicted ICH. All imaging markers were significantly associated with ICH in every age group. The location of CMBs coincided with the location of ICH, and ICH volume correlated with CMB count. CONCLUSION: All MRI markers for SVD were worse in ICH patients than in healthy controls, and these markers were prominent even in young ICH patients. Lacunae, WMH, EPVS, and CMB should be considered as factors related with spontaneous ICH.
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Humanos , Encéfalo , Angiopatía Amiloide Cerebral , Hemorragia Cerebral , Enfermedades de los Pequeños Vasos Cerebrales , Trastornos del Conocimiento , Atención a la Salud , Hipertensión , Hemorragias Intracraneales , Imagen por Resonancia Magnética , Estudio Observacional , Estudios Retrospectivos , Curva ROC , Accidente Cerebrovascular , Sustancia BlancaRESUMEN
La hemorragia subaracnoidea (HSA) no traumática es un subtipo de ictus hemorrágico que representa aproximadamente el 5% de todos los accidentes vasculares encefálicos (AVE). El 85% de los casos de HSA espontánea (no traumática) son secundarios a un aneurisma intracraneano roto, el 10% a hemorragia perimesencefálica no aneurismática y el otro 5% a otras causas. Entre estas se incluyen malformaciones arterio-venosas, fístulas durales, vasculits, trombosis de vena cortical, síndrome de vasoconstricción reversible, angiopatía amiloidea y síndrome de encefalopatía posterior reversible. La aproximación inicial a una HSA no traumática requiere un estudio angiográfico no invasivo con tomografía computada para la toma de decisiones terapéuticas. Si no se detecta un aneurisma sacular intradural que explique el sangrado, las conductas a seguir dependerán del patrón de distribución de la sangre. En esta revisión sugerimos una aproximación basada en 1) revisar el estudio inicial tomando en cuenta los puntos ciegos para la detección de aneurismas, 2) analizar el patrón de distribución de la sangre y 3) analizar los hallazgos en imágenes de acuerdo a las posibles causas según patrón.
Non-traumatic subarachnoid hemorrhage represents approximately 5% of strokes. From these, 85% of nontraumatic subarachnoid hemorrhage are secondary to a ruptured aneurysm, 10% to nonaneurysmal perimesencephalic hemorrhage and the other 5% to other causes. These include but are not limited to arteriovenous malformations, dural fistulae, vasculitis, cortical vein thrombosis, reversible cerebral vasoconstriction syndrome, amyloid angiopathy and posterior reversible encephalopathy syndrome. Initial workup of nontraumatic subarachnoid hemorrhage requires a non-enhanced CT and CT angiography for decision making and management. If there is no aneurysm as a source of hemorrhage, subsequent imaging studies will depend on blood distribution pattern. In this review we suggest an approach: 1) review blind spots for aneurysm detection in the initial CT angiography, 2) analyze blood distribution pattern and 3) evaluate imaging findings and possible causes according to each pattern.