Reversible cerebral vasoconstriction syndrome associated with brain parenchymal hemorrhage

We described a 7-year-old girl with reversible cerebral vasoconstriction syndrome associated with brain parenchymal hemorrhage. She initially presented with high fever and pancytopenia, leading to a diagnosis of most severe type aplastic anemia. We treated her with cyclosporine, methylprednisolone and anti-thymocyte globulin. Thereafter she recurrently complained of a very severe headache called as thunderclap, and finally exhibited loss of consciousness. Brain imaging revealed massive parenchymal hemorrhage between the left occipital and parietal lobes on computed tomography, and diffuse cerebral vasoconstriction on magnetic resonance angiography. The cerebral vasoconstriction resolved within two months, and thus we diagnosed her as having reversible cerebral vasoconstriction syndrome associated with brain parenchymal hemorrhage. This syndrome has been frequently reported in adult females, but rarely in children. However, even in children, a so called thunderclap headache may become a clue for the diagnosis of reversible cerebral vasoconstriction syndrome, especially in cases taking immunosuppressive agents. Immediate magnetic resonance angiography is essential to diagnose this syndrome, and a prompt application of calcium channel inhibitors should be considered to resolve constriction of the vessels and to prevent subsequent brain damage.     

Bilateral multiple border zone infarctions after massive bleeding: report of two cases]

We present two patients who developed bilateral border zone brain infarctions after massive bleeding. Patient 1 was a 46-year old woman who developed bilateral visual disturbance and left hand monoparesis after excessive menstruation with severe anemia. Diffusion-weighted MRI of brain showed multiple border zone infarcts bilaterally in cerebral and cerebellar hemispheres while brain MRA was normal. Patient 2 was a 67-year old man who developed disturbance of consciousness and right hemiplegia after upper gastrointestinal tract bleeding. Diffusion-weighted MRI of brain showed bilateral multiple border zone infarcts in cerebral hemispheres, although he had asymptomatic occlusion of the left internal carotid artery. The bilateral multiple border zone infarcts are one of the key findings suggesting the presence of anemic hypoxia as a result of global brain hypoperfusion caused by massive blood loss.     

Cranial magnetic resonance imaging findings in bacterial endocarditis: the neuroimaging spectrum of septic brain embolization demonstrated in twelve patients.

Infective endocarditis (IE) is an elusive systemic disorder that is often associated with neurologic complications. The contribution of brain magnetic resonance imaging (MRI) to the diagnosis of IE and the spectrum of such findings has been only sparsely described previously. The authors report cranial MRI findings in 12 patients with IE. Each of the patients had MRI evidence of cerebral embolization, with multiple brain lesions noted in most patients (n = 10). Cortical branch infarction was the most common lesion (n = 8), which usually involved the distal middle cerebral artery tree. The next most common finding (n = 7) was numerous small embolic lesions which typically lodged in the supratentorial gray-white junction, some of which were clinically silent and many of which enhanced (probable microabscesses). Brain hemorrhages were noted in four patients, most commonly subarachnoid hemorrhage (n = 3). Two patients developed multiple frank parenchymal macroabscesses/cerebritis lesions. A previously unreported finding in septic embolization, a stroke that became infected with abscess formation ("septic infarction"), was noted in two patients. MRI showed orbital cellulitis in two patients. Most patients studied with gadolinium showed enhancement of lesions (n = 5/8). The authors conclude that cranial MRI may be a valuable tool in the evaluation of patients with IE. The presence of characteristic cranial MRI lesions, especially of multiple types, may prompt early diagnosis and treatment.     

Cerebral infarction secondary to vasospasm after perimesencephalic subarachnoid hemorrhage

Perimesencephalic subarachnoid hemorrhage (pSAH) has been described as a distinct form of subarachnoid hemorrhage (SAH) associated with good outcomes. We report a 48-year-old female who developed cerebral infarction due to severe diffuse vasospasm following pSAH. The patient presented with non-aneurysmal pSAH and was discharged home on day 5. However, one week later she developed an acute onset of right hemiparesis. A brain MRI showed acute infarctions on diffusion weighted imaging and her cerebral angiogram showed diffuse vasospasm. The patient received intra-arterial diltiazem and hypervolemic-hypertensive-hemodilution therapy with resulting resolution of the vasospasm and hemiparesis. While not as common as in SAH, there is a potential for the occurrence of cerebral infarction due to vasospasm after pSAH.     

脑静脉窦血栓形成的影像学表现及脑实质病变预测

目的总结脑静脉窦血栓形成(CVST)患者的临床和MRI表现特征并探讨继发脑实质病变的预测因素。方法回顾57例CVST患者的临床及头颅MRI资料,分析患者MRI表现特征,并对临床及影像学指标进行对比分析。结果57例患者中男22例,女35例,年龄15~72岁(平均35岁)。临床症状头痛29例,癫痫发作11例,感觉变化8例,局灶性神经功能缺损9例;头颅MRI示静脉窦血栓形成部位上矢状窦9例,横窦2例,乙状窦1例,直窦1例,其中同时累及2个或2个以上静脉窦44例。静脉窦血栓伴发脑实质病变36例,其中出血性静脉梗死20例,非出血性静脉梗死12例,脑实质内出血4例。对伴和不伴脑实质病变2组患者的对比分析显示,伴脑实质病变组女性比例明显高于不伴脑实质病变组;伴脑实质病变组癫痫、感觉异常及局部神经功能缺损症状发生率均明显高于不伴脑实质病变组;伴脑实质病变组直窦血栓的发生率明显高于不伴脑实质病变组(P<0.05)。结论MRI可清楚显示CVST的直接及间接征象,通过分析CVST患者的临床和静脉窦血栓表现特征还可帮助预测严重的脑实质病变发生风险。     

“Unusual Pattern of Cerebral Microbleeds and Petechial Hemorrhages after Veno-Arterial Extracorporeal Membrane Oxygenation Support. A Report of 2 Cases”

Objectiveto report an unusual pattern of brain petechial hemorrhages in 2 patients after veno-arterial extracorporeal membrane oxygenation support (VA-ECMO)Case 1a 28-year-old man (Marfan disease) presented in the early post-operative period a multi-organ failure associated with a disseminated intravascular coagulation (DIC). He was placed on continuous veno-venous hemofiltration and VA-ECMO. He was weaned from ECMO 4 days later. He then developed bacterial pneumoniae leading to respiratory failure and requiring mechanical ventilation. MRI 30 days later showed widespread petechial hemorrhages in the subcortical and deep white matter (WM) (optic radiations, corpus callosum, predominantly in the splenium, internal and external capsules), caudate nuclei, basal ganglia, frontal and parietal cortex and in infratentorial structures. These hemorrhages were bilateral and almost symmetric and marked at the border zones of the carotid arteries territories.Case 2a 60-year-old man presented an out-of-hospital refractory hypothermic cardiac arrest. At arrival, cardiopulmonary resuscitation was continued; he presented bleeding at the puncture sites related to DIC and associated with multi-organ failure. VA-ECMO was implanted. After ECMO removal (day 7) he presented a severe spatial orientation deficit. MRI showed petechial hemorrhages in both hippocampi and microbleeds at the cerebral cortex and the juxta-cortical WM. Both patients had good functional outcome.ConclusionTwo unusual presentations of brain hemorrhages in patients who underwent VA-ECMO are reported. If their specific cause remains unclear, there seems to be a relationship in time between DIC and microhemorrhages in these cases, even if in case 1 brain hemorrhages seem to have a multifactorial cause.     

3.0T磁共振SWI在高血压脑内微出血中的应用及临床意义

目的探讨磁敏感加权成像(SWI)在高血压脑内微出血中的应用及临床意义。方法选53例高血压患者,应用3.0T MR行常规MRI和SWI序列成像检查并结合临床资料进行分析。结果32例高血压患者脑内有微出血灶,在SWI上呈点状、圆形、椭圆形低信号。总数达887个,直径为0.3mm～7.6mm。分布于皮层、皮层下和基底节区。其中17例伴发缺血性脑血管病,5例出血性腔隙性梗塞,7例伴发出血性脑血管病,3例无临床症状。结论SWI序列可敏感的显示高血压脑内微出血灶,对伴发缺血性和出血性脑血管病的诊断治疗有重要的指导价值。     

The clinical utility of dual-energy CT in post-thrombectomy care: Part 2, the predictive value of contrast density and volume for delayed hemorrhagic transformation

ObjectivesDual-energy CT allows differentiation between blood and iodinated contrast. This study aims to determine the predictive value of contrast density and volume on post-thrombectomy dual-energy CT for delayed hemorrhagic transformation and its impact on 90-day outcomes.Materials and MethodsA retrospective analysis was performed on patients who underwent thrombectomy for anterior circulation large-vessel occlusion at a comprehensive stroke center from 2018-2021. Per institutional protocol, all patients underwent dual-energy CT immediately post-thrombectomy and MRI or CT 24 hours afterward. The presence of hemorrhage and contrast staining was evaluated by dual-energy CT. Delayed hemorrhagic transformation was determined by 24-hour imaging and classified into petechial hemorrhage or parenchymal hematoma using ECASS III criteria. Univariable and multivariable analyses were performed to determine predictors and outcomes of delayed hemorrhagic transformation.ResultsOf 97 patients with contrast staining and without hemorrhage on dual-energy CT, 30 and 18 patients developed delayed petechial hemorrhage and delayed parenchymal hematoma, respectively. On multivariable analysis, delayed petechial hemorrhage was predicted by anticoagulant use (OR,3.53;p=0.021;95%CI,1.19-10.48) and maximum contrast density (OR,1.21;p=0.004;95%CI,1.06-1.37;per 10 HU increase), while delayed parenchymal hematoma was predicted by contrast volume (OR,1.37;p=0.023;95%CI,1.04-1.82;per 10 mL increase) and low-density lipoprotein (OR,0.97;p=0.043;95%CI,0.94-1.00;per 1 mg/dL increase). After adjusting for potential confounders, delayed parenchymal hematoma was associated with worse functional outcomes (OR,0.07;p=0.013;95%CI,0.01-0.58) and mortality (OR,7.83;p=0.008;95%CI,1.66-37.07), while delayed petechial hemorrhage was associated with neither.ConclusionContrast volume predicted delayed parenchymal hematoma, which was associated with worse functional outcomes and mortality. Contrast volume can serve as a useful predictor of delayed parenchymal hematoma following thrombectomy and may have implications for patient management.     

Delayed Shrinkage of the Brain After Ischemic Stroke: Preliminary Observations With Voxel-Guided Morphometry

BACKGROUND AND PURPOSE: The most important effect of cerebral ischemia is brain infarction. In this magnetic resonance imaging (MRI) study, the authors aimed at assessing postischemic brain atrophy. METHODS: Ten patients suffering from their first acute cerebral ischemia in the territory of the middle cerebral artery were studied retrospectively. Three-dimensional MRI volume scans were recorded in the acute and chronic stage after infarction and analyzed voxel by voxel intraindividually with the newly developed voxel-guided morphometry. RESULTS: Shrinkage of brain tissue was detected in all patients, not only in the perilesional cortical structures but also in contralateral homolog cortex areas and subcortically in the striatum and thalamus. This secondary shrinkage was not related to the size of the infarcts or to the clinical outcome of patients. CONCLUSIONS: Our study suggests that delayed brain atrophy after acute ischemic stroke involved areas anatomically connected with the ischemic brain lesion but nevertheless was accompanied by a simultaneous improvement of the neurological deficit.     

Venous infarction associated with carotid-cavernous fistula]

We report an 88-year-old woman who developed a hemorrhagic venous infarction in the left cerebral hemisphere and brainstem, in association with left carotid-cavernous fistula (CCF). Without aura the patient noticed diplopia due to left abducens palsy, and exophthal mos and congestion of the left eye. Brain CT revealed extrusion of the left eye, and dilatation of left superior orbital vein and cerebral cortical veins. She received diagnosis of CCF. Brain CT also revealed a small mass in the left ethmoidal sinus, which was not attached to the CCF. Biopsy of the mass was done under local anesthesia. On the following she had high fever. Her consciousness level deteriorated and she developed right hemiparesis FLAIR images of MRI showed, extensive high signal lesions in the left frontal and temporal cortices, basal ganglia, thalamus, midbrain and pons. These findings were consisted with venous infarction, possibly associated with peri-operative infection and hypovolemia. Intracranial hemorrhage occur in 3% of cases with CCF, but venous infarction was much rarer. The patients with CCF, who show dilatation of cortical veins in CT or MRI, have a higher risk of cerebral hemorrhage or infarction, and should be carefully observed.     

脑小血管病磁共振影像研究概况

脑小血管病（cerebral small vessel disease,cSVD）是血管性痴呆最常见的病因,且约占 卒中病因的1/5。目前对cSVD的认识主要是通过磁共振成像（magnetic resonance imaging,MRI）进 行,cSVD在MRI上的表现包括腔隙性梗死（lacunar infarction,LI）与腔隙灶、白质高信号（white matter hyperintensities,WMH）、血管周围间隙扩张（dilated Virchow-Robin space,dVRS）、脑微出血（cerebral microbleeds,CMBs）及脑萎缩。本文综述上述cSVD磁共振影像学表现定义、分级及推荐序列等的研究 概况。     

脑微出血与卒中

脑微出血作为一种具有出血倾向的脑小血管病变,随着影像学技术的发展,其检出率越来越高.目前,大量研究表明,脑微出血与缺血性卒中、脑出血和溶栓或抗栓治疗后症状性脑出血关系密切.本文旨在探讨脑微出血与上述疾病的相关性,将有利于脑微出血患者卒中防治策略的制定.     

卒中合并脑微出血的影像学研究

目的 探讨ICH和脑梗死患者合并脑微出血（cerebral microbleeds，CMBs）数量分级及部位分布差异。 方法 连续选取2017年8月-2018年12月在北京市大兴区人民医院神经内科病房住院且资料完整的 卒中患者，分为ICH和脑梗死两组。收集患者发病2周内头颅MRI磁敏感加权成像影像，统计ICH与脑梗 死患者中CMBs数量分级及部位分布特点。 结果 共入组患者234例，其中ICH组79例，脑梗死组155例。ICH组合并CMBs 65例（82.3%），其中 CMBs＞5个的患者41例（51.9%）；脑梗死组合并CMBs 73例（47.1%），其中CMBs＞5个的患者21例 （13.6%），两组差异有统计学意义（P＜0.001）。ICH组中，CMBs同时累及脑叶和深部脑组织的患者40例 （50.6%）；脑梗死组中，CMBs同时累及脑叶和深部脑组织的患者25例（16.1%），两组差异有统计学意 义（P＜0.001）。 结论 CMBs病灶＞5个多见于ICH患者；CMBs同时累及脑叶及深部脑组织多见于ICH患者。     

Contralateral Cerebral Infarction after Stent Placement in Carotid Artery: An Unexpected Complication

Stenting is a useful alternative treatment modality in carotid artery stenosis patients who are too high-risk to undergo carotid endarterectomy (CEA). We report a case of contralateral cerebral infarction after stenting for extracranial carotid stenosis. A 78-year-old woman was admitted to the hospital with left-sided weakness. Based on magnetic resonance imaging (MRI) of the brain and conventional angiography, she was diagnosed with an acute watershed infarct of the right hemisphere secondary to severe carotid stenosis. Stenting was performed for treatment of the right carotid artery stenosis after a one-week cerebral angiogram was completed. Thirty minutes after stent placement, the patient exhibited a generalized seizure. Four hours later, brain MRI revealed left hemispheric cerebral infarction. Complex aorta-like arch elongation, tortuosity, calcification, and acute angulation at the origin of the supra-aortic arteries may increase the risk of procedural complications. In our case, we suggest that difficult carotid artery catheterization, with aggressive maneuvering during stenting, likely injured the tortuous, atherosclerotic aortic arch, and led to infarction of the contralateral cerebral hemisphere by thromboemboli formed on the wall of the atherosclerotic aorta.     

Protein aggregation after focal brain ischemia and reperfusion.

Two hours of transient focal brain ischemia causes acute neuronal death in the striatal core region and a somewhat more delayed type of neuronal death in neocortex. The objective of the current study was to investigate protein aggregation and neuronal death after focal brain ischemia in rats. Brain ischemia was induced by 2 hours of middle cerebral artery occlusion. Protein aggregation was analyzed by electron microscopy, laser-scanning confocal microscopy, and Western blotting. Two hours of focal brain ischemia induced protein aggregation in ischemic neocortical neurons at 1 hour of reperfusion, and protein aggregation persisted until neuronal death at 24 hours of reperfusion. Protein aggregates were found in the neuronal soma, dendrites, and axons, and they were associated with intracellular membranous structures during the postischemic phase. High-resolution confocal microscopy showed that clumped protein aggregates surrounding nuclei and along dendrites were formed after brain ischemia. On Western blots, ubiquitinated proteins (ubi-proteins) were dramatically increased in neocortical tissues in the postischemic phase. The ubi-proteins were Triton-insoluble, indicating that they might be irreversibly aggregated. The formation of ubi-protein aggregates after ischemia correlated well with the observed decrease in free ubiquitin and neuronal death. The authors concluded that proteins are severely damaged and aggregated in neurons after focal ischemia. The authors propose that protein damage or aggregation may contribute to ischemic neuronal death.     

Regional differences in the rate of energy impairment after threshold level ischemia for induction of cerebral infarction in gerbils

The development of infarction and/or selective neuronal death in the brain after transient cerebral ischemia depends on the severity of the ischemic episode. After transient cerebral ischemia of the threshold level for the induction of infarction, both changes evolve slowly in various postischemic regions. We examined the relationship of disturbances of energy metabolism to infarction and selective neuronal death in various regions of the postischemic brain subjected to two 10-min occlusions of the unilateral common carotid artery. Our results indicated that in various cerebral regions that developed infarction, the tissue ATP content, in parallel with the succinic dehydrogenase activity, fell to their lowest levels at different times over a 4-day period after circulation had been restored (earliest to latest: dorsolateral thalamus > dorsolateral caudate > chiasmal level cortex > hippocampal CA3 sector > hippocampal CA1 sector). In the cortex at the infundibular level, disseminated selective neuronal death developed over a 7-day period following restoration of circulation; it was accompanied by only a slight alteration in energy metabolism. The present results indicate that regional differences existed in the rate of energy impairment and evolving infarction in the postischemic gerbil brain. Energy impairment, in association with mitochondrial enzymatic dysfunction, seems to be indispensable for the delayed manifestation of cerebral infarction but not for disseminated selective neuronal death. Received: 1 December 1999 / Revised, accepted: 6 March 2000     

Hemispatial visual defect in Alzheimer's disease

We describe a 56-year-old woman with Alzheimer's disease with left hemispatial neglect and left homonymous hemianopsia with macular sparing considered a manifestation of Alzheimer's disease resulting from severe degenerative change in the right primary visual cortex. Hemispatial neglect normally results from brain damage to the right cerebral hemisphere. Homonymous hemianopsia is commonly the result of localized brain disease, especially cerebral infarction or hemorrhage. To our knowledge, a patient with Alzheimer's disease showing hemispatial neglect and homonymous hemianopsia with macular sparing has not previously been reported.     

Early ischemic lesion demonstrated by ictal diffusion-weighted MRI during prior TIA in a patient with cerebral infarction]

We reported a patient with transient ischemic attack (TIA), subsequently evolving to a cerebral infarction, in whom ictal diffusion-weighted magnetic resonance imaging (MRI) detected early ischemic lesion in the left hemisphere. The patient was a 30-year-old right-handed male medical doctor, who had an in-hospital episode of TIA with obtundation and right hemiparesis, which lasted for 150 minutes. Ictal diffusion-weighted MRI obtained 110 minutes after symptom onset demonstrated an area of high signal intensity in the left striatum and corona radiata, whereas T 2-weighted and FLAIR images were entirely normal. Ictal magnetic resonance angiography (MRA) showed occlusive lesions in the M 2 branches of the left middle cerebral artery. The second MRA obtained 90 minutes after resolution of the symptoms showed nearly complete recanalization of the left middle cerebral artery, suggesting that the TIA was embolic mechanism. However the patient rapidly developed similar neurological symptoms again 58.5 hours after the TIA episode, evolving finally to a completed stroke. A brain CT obtained 1 hour after the second episode demonstrated diffuse hypodense lesions in the left basal ganglia and corona radiata, and in the left temporal lobe. MRIs 3 and 7 days later displayed completed infarcts, of which distribution was consistent with that of the hypodense lesions on the earlier CT. The left middle cerebral artery remained patent on the follow-up MRAs. The patient fairly recovered and returned to his premorbid position as medical doctor with a mild residual right hand clumsiness. In this patient, ictal and post-ictal MRAs documented an occlusion and a reopening of the middle cerebral artery. The embolic mechanism remains unknown despite detailed cardiac, vascular, and hematological examinations. In addition to recurrent embolism, we would like to point out that the reperfusion injury, secondary delayed neuronal death, and other factors may be involved in the second exacerbation evolving to the completed stroke.     

A case of duret hemorrhage demonstrated by computed tomography]

Brainstem hemorrhage in descending transtentorial herniation is well known as Duret hemorrhage. However, CT or MRI rarely reveals Duret hemorrhage. The authors report a case of brainstem hemorrhage after craniotomy of spontaneous acute subdural hematoma. A 47-year-old man suffered sudden onset of severe headache and progressive consciousness disturbance. Initial CT scan demonstrated a right acute subdural hematoma and a marked shift of the midline structures to the left. Emergency craniotomy was performed but he remained comatose. CT scan after 8 days showed multiple petechial hemorrhages in the brainstem. We reported a rare case of Duret hemorrhage diagnosed by CT scan. Duret hemorrhage is almost fatal.