Recurrent Transient Ischemic Attacks Revealing Cerebral Amyloid Angiopathy: A Comprehensive Case

This case report investigates the manifestation of cerebral amyloid angiopathy (CAA) through recurrent Transient Ischemic Attacks (TIAs) in an 82-year-old patient. Despite initial diagnostic complexities, cerebral angiography-MRI revealed features indicative of CAA. Symptomatic treatment resulted in improvement, but the patient later developed a fatal hematoma. The discussion navigates the intricate therapeutic landscape of repetitive TIAs in the elderly with cardiovascular risk factors, emphasizing the pivotal role of cerebral MRI and meticulous bleeding risk management. The conclusion stresses the importance of incorporating SWI sequences, specifically when suspecting a cardioembolic TIA, as a diagnostic measure to explore and exclude CAA in the differential diagnosis. This case report provides valuable insights into these challenges, highlighting the need to consider CAA in relevant cases.

Management of cerebral amyloid angiopathy and atrial fibrillation:We are still far from precision medicine

The use of anticoagulation therapy could prove to be controversial when trying to balance ischemic stroke and intracranial bleeding risks in patients with concurrent cerebral amyloid angiopathy(CAA)and atrial fibrillation(AF).In fact,CAA is an age-related cerebral vasculopathy that predisposes patients to intracerebral hemorrhage.Nevertheless,many AF patients require oral systemic dose-adjusted warfarin,direct oral anticoagulants(such as factor Xa inhibitors)or direct thrombin inhibitors to control often associated with cardioembolic stroke risk.The prevalence of both CAA and AF is expected to rise,due to the aging of the population.This clinical dilemma is becoming increasingly common.In patients with coexisting AF and CAA,the risks/benefits profile of anticoagulant therapy must be assessed for each patient individually due to the lack of a clear-cut consensus with regard to its risks in scientific literature.This review aims to provide an overview of the management of patients with concomitant AF and CAA and proposes the implementation of a risk-based decision-making algorithm.

Primary imaging features and recent application of PET tracers in cerebral amyloid angiopathy

Cerebral amyloid angiopathy(CAA)is a small vessel disease of the brain characterized by the progressive deposition of amyloid-β(Aβ)plaques in the walls of cerebral blood vessels.It presents with a subtle course and sudden onset,and currently,there are no specific therapeutic interventions available.Accurate diagnosis of CAA could enable targeted interventions in the early stages of the disease,potentially mitigating the disease’s effects.Herein,we review the primary imaging biomarkers used in the diagnosis of CAA,including their mechanisms,imaging characteristics,and significance.We also provide an interpretation of the latest version(v2.0)of the Boston criteria,which are commonly used in the clinical diagnosis of CAA.Additionally,this study introduces various positron emission tomography(PET)tracers for CAA and reviews their application values in the diagnosis of CAA.

Dysfunction of blood-brain barrier in cerebral amyloid angiopathy

Increasing evidence demonstrated that the blood-brain barrier(BBB)was involved in developing cerebral amyloid angiopathy(CAA).The BBB participates in the neurovascular coupling and regulates the transport of substances,which is closely related to neurodegenerative diseases.In CAA,the deposition of amyloid beta(Aβ)in arteries,capillaries,and arterioles of meninges and cerebral cortex results in the destruction of the BBB,chronic inflammatory response,chronic cerebral hypoperfusion,and dysfunction of the neurovascular unit,which eventually leads to neurodegeneration.At the same time,CAA is an age-related disease.Patients with CAA often have some risk factors for cerebrovascular diseases,such as hypertension and diabetes,which can further aggravate the damage to the BBB.Thus,it is of great significance to pay attention to the BBB in the pathogenesis and future intervention targets of CAA.Therefore,this manuscript reviewed the dysfunction of the BBB in CAA.

Cerebrospinal Fluid Biomarkers in Dementia Patients with Cerebral Amyloid Angiopathy

Objective To study the changes of biomarkers in cerebrospinal fluid(CSF) in cerebral amyloid angiopathy(CAA) dementia and Alzheimer's disease.Methods Levels of amyloid protein β(Aβ42,Aβ40) and phosphorylated Tau-protein(P-tau) in CSF and ratio of Aβ42/Aβ40 were tested in 5 cases with CAA dementia and 20 cases with Alzheimer's disease collected at Peking Union Medical College Hospital from December 2001 to March 2011.Results The levels of Aβ42,Aβ40,and P-tau in CSF and ratio of Aβ42/Aβ40 were(660.4±265.2) ng/L,(7111.0±1033.4) ng/L,(71.8±51.5) ng/L,and 0.077±0.033,respectively in CAA dementia and(663.6±365.6) ng/L,(5115.0±2931.1) ng/L,(47.7±38.8) ng/L,and 0.192±0.140,respectively in Alzheimer's disease patients.There were no statistically significant differences between CAA dementia and Alzheimer's disease in terms of these CSF biomarkers(all P>0.05).Conclusion Measurements of CSF biomarkers may not be helpful in differential diagnosis of CAA and Alzheimer's disease.

Study of clinical features of amyloid angiopathy hemorrhage and hypertensive intracerebral hemorrhage

Objective: The purpose of this study was to differentiate between cerebral amyloid angiopathy (CAA) and hypertension (HTN) based on hemorrhage pattern interpretation. Methods: From June 1994 to Oct., 2000, 83 patients admitted to our service with acute intracerebral hemorrhage (ICH) were investigated retrospectively; 41 patients with his-tologically proven diagnosis of cerebral amyloid angiography and 42 patients with clear history of hypertension were investigated. Results: Patients with a CAA-related ICH were significantly older than patients with a HTN-related ICH (74.0 years vs 66.5 years, P<0.05). There was a significantly higher number of hematomas> ml in CAA (85.3%) when compared with HTN (59.5%). No basal ganglional hemorrhage was seen in CAA, but in 40.5% in HTN. In CAA-related ICH, su-barachnoid hemorrhage (SAH) was seen in 26 patients (63.4%) compared to only 11 patients (26.2%) in HTN-related ICH. Intraventricular hemorrhage was seen in 24.4% in CAA, and in 26.2% in HTN. Typical features of CAA-related ICH included lobar distribution affecting mainly the lobar superficial areas, lobulated appearance, rupture into the subarachnoid space, and secondary IVH from the lobar hemorrhage. More specifically, multiplicity of hemorrhage, bilaterality, and repeated episodes also strongly suggest the diagnosis of CAA. Multiple hemorrhages, defined as 2 or more separate he-matomas in multiple lobes, accounted for 17.1% in CAA-related ICH. Conclusion: There are certain features in CAA on CT and MRI and in clinical settings. To some extent, these features may contribute to distinguishing CAA from HTN related ICH.

Amyloid beta-peptide worsens cognitive impairment following cerebral ischemia-reperfusion injury

Amyloid 13-peptide, a major component of senile plaques in Alzheimer＇s disease, has been implicated in neuronal cell death and cognitive impairment. Recently, studies have shown that the pathogenesis of cerebral ischemia is closely linked with Alzheimer＇s disease. In this study, a rat model of global cerebral ischemia-reperfusion injury was established via occlusion of four arteries; meanwhile, fibrillar amyloid [3-peptide was injected into the rat lateral ventricle. The Morris water maze test and histological staining revealed that administration of amyloid 13-peptide could further aggravate impairments to learning and memory and neuronal cell death in the hippocampus of rats subjected to cerebral ischemia-reperfusion injury. Western blot showed that phosphorylation of tau protein and the activity of glycogen synthase kinase 313 were significantly stronger in cerebral ischemia-reperfusion injury rats subjected to amyloid [3-peptide administration than those undergo- ing cerebral ischemia-repetfusion or amyloid 13-peptide administration alone. Conversely, the activ- ity of protein phosphatase 2A was remarkably reduced in rats with cerebral ischemia-reperfusion injury following amyloid 13-peptide administration. These findings suggest that amyloid 13-peptide can potentiate tau phosphorylation induced by cerebral ischemia-reperfusion and thereby aggravate cognitive impairment.

Inhibiting p38 mitogen-activated protein kinase attenuates cerebral ischemic injury in Swedish mutant amyloid precursor protein transgenic mice

Cerebral ischemia was induced using photothrombosis 1 hour after intraperitoneal injection of the p38 mitogen-activated protein kinase （MAPK） inhibitor $B239063 into Swedish mutant amyloid precursor protein （APP/SWE） transgenic and non-transgenic mice. The number of surviving neurons in the penumbra was quantified using Nissl staining, and the activity of p38 MAPKs was measured by western blotting. The number of surviving neurons in the penumbra was significantly reduced in APP/SWE transgenic mice compared with non-transgenic controls 7 days after cerebral ischemia, but the activity of p38 MAPKs was significantly elevated compared with the non-ischemic hemisphere in the APP/SWE transgenic mice. SB239063 prevented these changes. The APP/SWE mutation exacerbated ischemic brain injury, and this could be alleviated by inhibiting p38 MAPK activity.

Cerebral amyloid angiopathy vs Alzheimer’s dementia:Diagnostic conundrum

BACKGROUND Diagnosis of a dementia subtype can be complex and often requires comprehensive cognitive assessment and dedicated neuroimaging.Clinicians are prone to cognitive biases when reviewing such images.We present a case of cognitive impairment and demonstrate that initial imaging may have resulted in misleading the diagnosis due to such cognitive biases.CASE SUMMARY A 76-year-old man with no cognitive impairment presented with acute onset word finding difficulty with unremarkable blood tests and neurological examination.Magnetic resonance imaging(MRI)demonstrated multiple foci of periventricular and subcortical microhaemorrhage,consistent with cerebral amyloid angiopathy(CAA).Cognitive assessment of this patient demonstrated marked impairment mainly in verbal fluency and memory.However,processing speed and executive function are most affected in CAA,whereas episodic memory is relatively preserved,unlike in other causes of cognitive impairment,such as Alzheimer’s dementia(AD).This raised the question of an underlying diagnosis of dementia.Repeat MRI with dedicated coronal views demonstrated mesial temporal lobe atrophy which is consistent with AD.CONCLUSION MRI brain can occasionally result in diagnostic overshadowing,and the application of artificial intelligence to medical imaging may overcome such cognitive biases.

Houshiheisan compound prescription protects neurovascular units after cerebral ischemia

Houshiheisan is composed of wind-dispelling （chrysanthemun fower, divaricate saposhnikovia root, Manchurian wild ginger, cassia twig, Szechwan lovage rhizome, and platycodon root） and deficiency-nourishing （ginseng, Chinese angelica, large-head atractylodes rhizome, Indian bread, and zingiber） drugs. In this study, we assumed these drugs have protective effects against cerebral ischemia, on neurovascular units. Houshiheisan was intragastrically administered in a rat model of focal cerebral ischemia. Hematoxylin-eosin staining, transmission electron microscopy, immu- nofluorescence staining, and western blot assays showed that Houshiheisan reduced pathological injury to the ischemic penumbra, protected neurovascular units, visibly up-regtflated neuronal nuclear antigen expression, and down-regulated amyloid precursor protein and amyloid-[3 42 expression. Wind-dispelling and deficiency-nourishing drugs maintained NeuN expression to varying degrees, but did not affect amyloid precursor protein or amyloid-~ 42 expression in the ischemic penumbra. Our results suggest that the compound prescription Houshiheisan effectively suppresses abnormal amyloid precursor protein accumulation, reduces amyloid substance depo- sition, maintains stabilization of the internal environment of neurovascular units, and minimizes injury to neurovascular units in the ischemic penumbra.

Effects of chronic cerebral hypoperfusion of beta- and gamma-secretase on learning and memory in rats

BACKGROUND： Chronic cerebral hypoxia and ischemia have been shown to be related to occurrence of sporadic Alzheimer＇s disease, and β- and y-secretase play an important role in the generation of β-amyloid protein. Early clinical symptoms in Alzheimer＇s disease patients include learning and memory deficits. OBJECTIVE： To measure learning and memory, as well as β- and β-secretase activities in the hippocampus of a cerebral ischemia/hypoxia rat model with chronic cerebral hypoperfusion. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Pathology, Capital Medical University from March to December, 2008. MATERIALS： β- and y-secretase activity kits were purchased from R ＆ D Systems, USA. METHODS： Male Sprague Dawiey rats, aged 23 weeks, were randomly assigned to model （n = 56） and sham-surgery （n = 46） groups. Cerebral hypoperfusion rat models were established by bilateral common carotid occlusion. MAIN OUTCOME MEASURES： Morris water maze was used to test changes in escape latency and path length, and β- and y-secretase activities were measured on days 10, 30, 90, and 180 following surgery. RESULTS： Progressive cognitive impairment resulted from 30 days of chronic cerebral hypoperfusion, which lasted for 180 days after cerebral hypoperfusion. β-secretase activity was increased at 10 days after hypoperfusion, which continued until 180 days, with a 14.25% increase compared to the sham-surgery group; y-secretase activity was increased by 10.5%. CONCLUSION： Chronic cerebral hypoperfusion results in impaired spatial memory and upregulated β- and y-secretase activities, which could play an important role in β-amyloid production.

The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease

Neurovascular dysfunction,as an integral part of Alzheimer's disease,may have an important influence on the onset and progression of chronic neurodegenerative processes.The bloodbrain barrier(BBB)pathway is one of the main pathways that mediates the clearance of amyloidbeta(Aβ)in the brain parenchyma.A large number of studies have shown that receptors and ATPbinding cassette transporte rs expressed on endothelial cells play an important role in Aβtransport across the BBB,but the specific mechanism is not clear.In this review,we summarize the possible mechanisms of Aβproduction and clearance,and in particular the relationship between Aβand brain capillary endothelial cells.Aβis produced by abnormal cleavage of the amyloid precursor protein via amyloidogenic processing under pathological conditions.Dys regulation of Aβclearance is considered to be the main reason for the massive accumulation of Aβin the brain parenchyma.Several pathways mediating Aβclearance from the brain into the periphery have been identified,including the BBB pathway,the blood-cerebros pinal fluid barrier and arachnoid granule pathway,and the lymphoidrelated pathway.Brain ca pilla ry endothelial cells are the key components of Aβclearance mediated by BBB.Receptors(such as LRP1,RAGE,and FcRn)and ATP-binding cassette transporters(such as P-gp,ABCA1,and ABCC1)expressed on endothelial cells play a critical role in Aβtranscytosis across the BBB.The toxic effects of Aβcan induce dysregulation of receptor and transpo rter expression on endothelial cells.Excessive Aβexerts potent detrimental cerebrovascular effects by promoting oxidative stress,inducing chronic inflammation,and impairing endothelial structure and functions.All of these are main causes for the reduction in Aβclearance across the BBB and the accumulation of Aβin the brain parenchyma.Therefo re,studies on the intera ctions between Aβand brain capillary endothelial cells,including their receptors and transporters,studies on inhibition of the toxic effects of Aβon endothelial cells,and studies on promoting the ability of endothelial cells to mediate Aβclearance may provide new therapeutic strategies for Aβclearance in Alzheimer's disease.

Amyloid β and free heme：bloody new insights into the pathogenesis of Alzheimer＇s disease

The cerebral formation of Amyloid β（Aβ） is a critical pathological feature of Alzheimer＇s disease（AD）.An accumulation of this peptide as senile plaques（SP） was already reported by Alois Alzheimer,the discoverer of the disease.Yet the exact contribution of Aβ to AD development remains elusive.Moreover,while extensive cerebral Aβ formation leads to fibril formation in many species,AD-like symptoms apparently depend on the highly conserved N-terminal residues R5,Y10 and H13.The amino acids were also shown to lead to the formation of Aβ-heme complexes,which exhibit peroxidase activity in the presence of H_2O_2.Taking together these observations we propose that the formation and enzymatic activity of the named complexes may represent an essential aspect of AD pathology.Furthermore,Aβ is also known to lead to cerebral micro-vessel destruction（CAA） as well as to hemolytic events.Thus we suggest that the Aβ-derived cerebral accumulation of blood-derived free heme represents a likely precondition for the subsequent formation of Aβ-heme complexes.

未知病变类型脑血管中β-amyloid、α-actin、collagen Ⅳ的含量

目的研究未知病变类型脑血管病变的结构特征。方法通过刚果红染色、免疫组织化学染色、计算机图像分析技术对未知病变类型脑血管病变的β-amyloid、α-actin、collagenⅣ的含量进行研究。结果未知病变类型脑血管壁α-actin、collagenⅣ呈少量阳性染色,与正常脑血管存在显著差异(P<0.05);β-amyloid染色呈阴性,与正常脑血管无差异(P>0.05)。病变血管壁中上述三种蛋白的表达特点与脑血管淀粉样变(cerebralamyloidangiopathy,CAA)及小动脉硬化玻璃样变不同。结论未知病变类型脑血管病变具有不同于CAA的病变特征。

Mutant amyloid precursor protein and presenilin-1 genes effect on ischemia vulnerability via calcium homeostasis disturbance

BACKGROUND： Previous studies have demonstrated that mutant amyloid precursor protein （APP） or presenilin-1 （PS1） genes increase susceptibility to ischemic brain damage induced by middle cerebral artery occlusion. Possible mechanisms include over-production of beta-amyloid peptide （Aβ）. OBJECTIVE： Because Aβ is over-produced in the APP/PS1 double-transgenic mouse, the present study focused on mechanisms of increased ischemic damage due to mutant APP and PS1 genes by measuring oxidative stress, mitochondrial function, and calcium homeostasis. DESIGN, TIME AND SETTING： The non-randomized, controlled, in vivo and in vitro experiments were performed at the Medical Research Center, Second Clinical College, Jinan University between May and October 2008. MATERIALS： Male APP transgenic mice carrying the mutant 695swe gene and female PS1 transgenic mice carrying the mutant Leu235Pro gene were donated from the University of Hong Kong. SHSY5Y human neureblastoma cells were purchased from ATCC （Manassas, VA, USA）, and Aβ1-42 was obtained from Sigma-Aldrich （St. Louis, MO, USA）. METHODS： APP transgenic mice were mated with PS1 transgenic mice to produce APP/PS1 double-transgenic mice and wildtype littermates mice. The photothrombotic stroke model was induced in six APP/PS1 double-transgenic and 6 wildtype littermates mice. SHSY5Y human neuroblastoma cells were cultured in vitro, and were divided into 4 groups： Aβ group, cells were exposed to 5 pmol/L Aβ for 24 hours; oxygen-glucose deprivation （OGD） group, cells were exposed to OGD for 1 hour after treatment with sterile, ultra-pure water for 24 hours; OGD＋Aβ group, cells were exposed to OGD and Aβfor 1 hour after treatment with 5 pmol/L Aβ for 24 hours; sham control group： cells were exposed to sterile, ultra-pure water for 25 hours. OGD was achieved by exposing the cells to glucose-free DMEM and placing the cells in an anaerobic chamber flushed with 5% CO2 and 95% N2 （v/v） at 37 ℃ for 1 hour. MAIN OUTCOME MEASURES： TTC staining was used to measure infarct volume 7 days after photothrombotic stroke. Cell viability was evaluated using the MTT kit. Opening of the mitochondrial permeability transition pore, intracellular concentration of superoxide anion, and calcium after OGD were detected with fluorescence intensity of calcein-AM, hydroethidine, and fluo-3/AM. RESULTS： At 7 days after stroke, total infarct volume and cortical infarct volume were significantly greater in the APP/PS1 transgenic mice compared with the wildtype littermates mice （P 〈 0.01）. Aβ, OGD, and Aβ ＋ OGD significantly decreased cell viability and increased fluorescence intensity of hydroethidine and fluo-3/AM （P 〈 0.01）. Compared with the Aβ or OGD group, Aβ ＋ OGD significantly decreased cell viability （P 〈 0.01） and significantly increased fluorescence intensity of calcein-AM, hydroethidine, and fluo-3/AM （P 〈 0.01 or P 〈 0.05）. CONCLUSION： The APP/PS1 double-transgenic mice were more vulnerable to ischemia. The possible mechanisms included enhanced opening of the mitochondrial permeability transition pore, overproduction of superoxide anion due to pore opening, and disturbed calcium homeostasis induced by excess superoxide anion.

Effects of long-term estrogen replacement therapy on beta-amyloid precursor protein and mRNA expression in ovariectomized rat hippocampus

BACKGROUND： In vitro cultures of neural stem cells have shown that estrogen can regulate beta-amyloid precursor protein （β-APP） metabolism and reduce amyloid-beta production. OBJECTIVE： To investigate the effects of long-term oral administration of compound nylestriol or low-dose 17beta-estradiol on β-APP and mRNA expression in the hippocampus of ovariectomized （OVX） rats. DESIGN, TIME AND SETTING： This randomized and controlled experiment was performed at the Animal Laboratory and Laboratory of Endocrine and Metabolic Disease, Xiangya Second Hospital of Central South University between April 2003 and May 2004. MATERIALS： According to body mass, 50 six-month-old female Sprague-Dawley rats were randomly divided into five groups （n = 10 per group）： normal control, sham operation, OVX model, 17beta-estradiol （Sigma, USA）, and compound nylestriol tablet （Laboratory of Endocrine and Metabolic Disease, Xiangya Second Hospital of Central South University） groups. METHODS： Rats in OVX plus 17beta-estradiol and OVX plus compound nylestriol tablet groups underwent ovariectomy. On the second day after surgery, rats were intragastrically given 17beta-estradiol （100 μg/kg）, once per day or compound nylestriol tablet （0.5 mg/kg） and levonorgestrel （0.15 mg/kg） every 2 days. MAIN OUTCOME MEASURES： β-APP expression in the hippocampus of OVX rats was determined using immunohistochemistry （SABC method） and β-APP mRNA expression was analyzed by in situ hybridization. The results were quantitatively analyzed using cell counting and average optical density. RESULTS： The number and optical density of β-APP-positive neurons in every subregion of the hippocampus of OVX rats was dramatically increased compared with normal and sham operation groups following 35 weeks of administration （P 〈 0.05）. Levels of β-APP were decreased following oral administration of compound nylestriol or 17beta-estradiol. In situ hybridization showed that long-term estrogen deficiency and oral administration of compound nylestriol or 17beta-estradiol did not alter the number of β-APP mRNA-positive neurons. CONCLUSION： The results show that long-term estrogen deficiency results in an increase of expression of β-APP though no changes in the expression of β-APP mRNA are detected. Replacement of estrogen with low-dose 17 beta-estradiol or compound nylestriol tablet inhibits the expression of β-APP in the hippocampus to the same extent.

肠道菌群影响脑淀粉样血管病中淀粉样蛋白沉积的潜在机制探讨

脑淀粉样血管病(CAA)是一种以淀粉样蛋白β(Aβ)进行性沉积于皮质、皮质下及软脑膜小动脉为主要病理特点的脑小血管病,在老龄化人群中多见,常以反复脑叶出血、认知障碍为特征性临床表现。近年来,肠道菌群多样性及其相关产物已被报道可通过神经炎症、破坏血-脑屏障等多种途径参与中枢神经系统疾病的致病过程。而肠道菌群在CAA中的潜在机制目前并不明晰。已有研究表明,肠道菌群紊乱可通过诱发颅内Aβ产生和聚集、血-脑屏障渗漏、Aβ转运受体失衡引起血管壁改变,并伴随神经炎症机制,可能一定程度推动了CAA的发生和发展。作者对肠道菌群影响CAA中淀粉样蛋白沉积的可能机制进行综述,以期为CAA潜在临床治疗靶点的探索提供理论参考。

首诊于精神科的脑淀粉样血管病1例

目的 探讨脑淀粉样血管病的临床症状及影像学表现。方法 回顾性分析1例首诊于精神科的脑淀粉样血管病的临床资料。结果 患者女性,56岁,临床主要表现为情感平淡、言语减少、记忆力减退。患者脑脊液蛋白0.51g/L,氯118.9mmol/L,潘氏试验弱阳性,脑电图α波不规则,慢波较多,磁敏感加权成像显示颅内弥漫性微出血,蒙特利尔认知评估11分,韦氏智力测试55分。给予甲强龙500 mg/d和罂粟碱90 mg/d治疗,出院2个月后复查,症状部分改善。结论 磁敏感加权成像对诊断脑淀粉样血管病具有较高的临床应用价值。

以凸面蛛网膜下腔出血为影像特征的脑淀粉样血管病临床特点分析

目的:探讨以急性凸面蛛网膜下腔出血(convexity subarachnoid hemorrhage,cSAH为影像特征的脑淀粉样血管病(cerebral amyloid angiopathy,CAA)的临床和影像学特点,及与患者脑出血再发的风险相关性。方法:回顾性分析2013年6月至2020年12月,北京安贞医院就诊的以cSAH为特征合改良Boston诊断标准的18例很可能的CAA患者,分析其流行病学资料、临床特点、头颅CT/头颅磁共振成像(magnetic resonance imaging,MRI)等信息。结果:18例患者男女比例为1:1.25,发病年龄59~91岁,平均(75±9)岁,最常见的临床症状为短暂性局灶性神经系统症状发作(transient focal neurological episodes,TFNE,12/18),头颅影像学表现为局限型(14/18)和弥漫型c SAH(4/18)。随访15个月,平均(15±5)个月,8例患者出现反复TFNE发作,4例再发c SAH,4例脑出血。结论:以cSAH为特征的CAA多见于老年人,TFNE为最常见的临床表现,头颅CT/MRI是最重要的诊断方法,应尽量避免抗栓治疗。

脑淀粉样血管病相关炎症的临床特点分析

目的分析脑淀粉样血管病相关炎症(CAA-I)的临床特点。方法回顾性分析8例CAA-I患者的临床资料,综合相关文献分析其临床特点。结果8例患者中,6例表现为不同程度的认知功能障碍,5例合并头痛,3例合并无力、失语、视力下降等局灶性神经功能缺损症状,2例伴发癫痫。8例患者头颅T_(2)W和Flair相表现为多发的白质高信号,SWI均表现为皮质-皮质下多发微出血。4例基因检测表现型为APOE4。7例患者经激素治疗后症状和影像学改变均明显改善,1例逐渐进展,1例治疗13个月后复发。结论CAA-I为临床罕见的可治性疾病,对免疫抑制治疗敏感,可动态观察影像学改变评估治疗效果。