Multiple Microhemorrhages Research Articles

Amyloid related imaging abnormalities in the emergency setting.

Since the 2021 FDA approval of the first monoclonal antibody (MAB) therapy for Alzheimer's disease (AD), treatment has progressed from symptom management to targeting and reducing amyloid β plaque burden. While these therapies offer hope of altering the disease course, they come with risks, such as amyloid-related imaging abnormalities (ARIA), which include ARIA-E (edema and effusion) and ARIA-H (hemorrhage). This report details the case of a 64-year-old woman undergoing donanemab treatment who developed severe ARIA, characterized by extensive vasogenic edema and multiple microhemorrhages. The increasing use of MABs necessitates heightened awareness and expertise among emergency radiologists to identify findings of ARIA effectively, ensuring timely and appropriate care for patients undergoing these novel therapies.

NeuroMix with MRA: A Fast MR Protocol to Reduce Head and Neck CTA for Patients with Acute Neurologic Presentations.

Overuse of CT-based cerebrovascular imaging in the emergency department and inpatient settings, notably CTA of the head and neck for minor and nonfocal neurologic presentations, stresses imaging services and exposes patients to radiation and contrast. Furthermore, such CT-based imaging is often insufficient for definitive diagnosis, necessitating additional MR imaging. Recent advances in fast MRI may allow timely assessment and a reduced need for head and neck CTA in select populations. We identified inpatients or patients in the emergency department who underwent CTAHN (including noncontrast and postcontrast head CT, with or without CTP imaging) followed within 24 hours by a 3T MRI study that included a 2.5-minute unenhanced multicontrast sequence (NeuroMix) and a 5-minute intracranial time of flight MRA) during a 9-month period (April to December 2022). Cases were classified by 4 radiologists in consensus as to whether NeuroMix and NeuroMix + MRA detected equivalent findings, detected unique findings, or missed findings relative to CTAHN. One hundred seventy-four cases (mean age, 67 [SD, 16] years; 56% female) met the inclusion criteria. NeuroMix alone and NeuroMix + MRA protocols were determined to be equivalent or better compared with CTAHN in 71% and 95% of patients, respectively. NeuroMix always provided equivalent or better assessment of the brain parenchyma, with unique findings on NeuroMix and NeuroMix + MRA in 35% and 36% of cases, respectively, most commonly acute infarction or multiple microhemorrhages. In 8/174 cases (5%), CTAHN identified vascular abnormalities not seen on the NeuroMix + MRA protocol due to the wider coverage of the cervical arteries by CTAHN. A fast MR imaging protocol consisting of NeuroMix + MRA provided equivalent or better information compared with CTAHN in 95% of cases in our population of patients with an acute neurologic presentation. The findings provide a deeper understanding of the benefits and challenges of a fast unenhanced MR-first approach with NeuroMix + MRA, which could be used to design prospective trials in select patient groups, with the potential to reduce radiation dose, mitigate adverse contrast-related patient and environmental effects, and lessen the burden on radiologists and health care systems.

Risk factors in developing amyloid related imaging abnormalities (ARIA) and clinical implications.

Alzheimer's disease (AD) affects over 6 million people over the age of 65. The advent of new anti-amyloid monoclonal antibodies as treatment for early Alzheimer's disease these immunotherapeutics may slow disease progression but also pose significant risks. Amyloid related imaging abnormalities (ARIA) identified on MRI following administration of these new monoclonal antibodies can cause both brain edema (ARIA-E) and hemorrhage (ARIA-H). While most ARIA is asymptomatic, some patients can develop headache, confusion, nausea, dizziness, seizures and in rare cases death. By analyzing lecanemab, aducanumab, gantenerumab, donanemab, and bapineuzumab clinical trials; risk factors for developing ARIA can be identified to mitigate some of the ARIA risk. Risk factors for developing ARIA-E are a positive Apoε4 carrier status and prior multiple cerebral microhemorrhages. Risk factors for ARIA-H are age, antithrombotic use, and history of prior strokes. With lecanemab, ARIA-E and ARIA-H were seen at lower rates 12 and 17%, respectively, compared to aducanumab (ARIA-E 35% and ARIA-H 19%) in treated patients. ARIA risk factors have impacted inclusion and exclusion criteria, determining who can receive lecanemab. In some clinics, almost 90% of Alzheimer's patients are excluded from receiving these new anti-amyloid therapeutics. This review aims to discuss risk factors of ARIA and highlight important areas for further research. With more anti-amyloid monoclonal antibodies approved by the Food and Drug Administration, considering patient risk factors for developing ARIA is important to identify to minimize patient's risk while receiving these new therapies.

A NOVEL IKBKG MUTATION IDENTIFIED IN A PATIENT WITH RECURRENT SKIN LESION

<h3>Introduction</h3> Pathogenic variants in the inhibitory kB kinase g gene (<i>IKBKG</i>), which encodes nuclear factor kB essential modulator (NEMO), have a wide variety of presentations. Patients with NEMO deficiency have varying degrees of ectodermal dysplasia (ED), anhidrosis, and immune deficiency. Herein, we describe the initial presentation of a patient with a novel pathogenic variant in <i>IKBKG</i>. <h3>Case Description</h3> A 6-month-old male with two prior episodes of cellulitis was admitted for fever and right lower extremity swelling. Blood cultures grew <i>Enterobacter cloacae</i> and remained positive despite appropriate antimicrobial coverage. Brain MRI was obtained and demonstrated multiple microhemorrhages concerning for septic emboli. Right extremity biopsy was not consistent with cellulitis. Immunology evaluation (Table 1) was significant for hypogammaglobinemia, abnormal proliferation assays, and diminished NK cell cytotoxicity. Over time, findings of ED became evident including lymphedema, anhidrosis, and delayed tooth eruption with conical incisors. Whole exome sequencing (WES) was obtained but failed to identify an underlying cause. Since findings were concerning for NEMO deficiency, <i>IKBKG</i> sequencing was obtained, which identified a previously unreported duplication in exon 7 c.815_817dup (p.E272dup) in both the patient and his mother. <h3>Discussion</h3> Patients who present with ED and immunodeficiency should raise high clinical suspicion for NEMO deficiency syndrome. This patient also demonstrates how WES may not detect all significant variants. The <i>IKBKG</i> pseudogene<i>, IKBKGP1</i>, limits the accuracy of WES. While findings in NEMO deficiency syndrome can vary, few immune deficiencies are associated with ED, and disease phenotype must remain a consideration in selecting and interpreting genetic testing.

Complete neurological recovery from fat embolism syndrome in sickle cell disease after sequential red cell exchange transfusion and therapeutic plasma exchange

Fat embolism syndrome in sickle cell disease is associated with great mortality, while more than half of survivors suffer severe neurological sequelae. Release of fat droplets leads to obstruction of the microcirculation as well as generation of proinflammatory cytokines that can cause direct tissue injury. Red cell exchange transfusion can be life-saving but the addition of therapeutic plasma exchange may further improve outcomes by removing such inflammatory mediators. Here, we describe the case of a 27-year-old male patient with sickle cell anaemia presenting with typical features of fat embolism syndrome including neurological involvement with greatly reduced level of consciousness. MRI of his brain showed multiple widespread microhemorrhages giving the characteristic "star field" pattern but also a cytotoxic lesion of the corpus callosum, known to be the result of direct neurotoxicity by proinflammatory cytokines. The patient underwent emergency red cell exchange transfusion leading only to modest clinical improvement but fully regained consciousness after three cycles of therapeutic plasma exchange. This case highlights the deleterious effect of the hyperinflammatory state characteristic of many sickle cell complications and supports further exploring the potential benefit from plasma exchange as an adjunct to red cell exchange in order to remove proinflammatory cytokines during acute complications of sickle cell disease.

Association of Clinical, Biological, and Brain Magnetic Resonance Imaging Findings With Electroencephalographic Findings for Patients With COVID-19

There is evidence of central nervous system impairments associated with coronavirus disease 2019 (COVID-19) infection, including encephalopathy. Multimodal monitoring of patients with COVID-19 may delineate the specific features of COVID-19-related encephalopathy and guide clinical management. To investigate clinical, biological, and brain magnetic resonance imaging (MRI) findings in association with electroencephalographic (EEG) features for patients with COVID-19, and to better refine the features of COVID-19-related encephalopathy. This retrospective cohort study conducted in Pitié-Salpêtrière Hospital, Paris, France, enrolled 78 hospitalized adults who received a diagnosis of severe acute respiratory syndrome coronavirus 2 (SARS-Cov2) and underwent EEG between March 30 and June 11, 2020. Detection of SARS-CoV-2 from a nasopharyngeal specimen using a reverse transcription-polymerase chain reaction assay or, in the case of associated pneumonia, on a computed tomography scan of the chest. Data on the clinical and paraclinical features of the 78 patients with COVID-19 were retrieved from electronic patient records. Of 644 patients who were hospitalized for COVID-19, 78 (57 men [73%]; mean [SD] age, 61 [12] years) underwent EEG. The main indications for EEG were delirium, seizure-like events, and delayed awakening in the intensive care unit after stopping treatment with sedatives. Sixty-nine patients showed pathologic EEG findings, including metabolic-toxic encephalopathy features, frontal abnormalities, periodic discharges, and epileptic activities. Of 57 patients who underwent brain MRI, 41 showed abnormalities, including perfusion abnormalities, acute ischemic lesions, multiple microhemorrhages, and white matter-enhancing lesions. Fifty-five patients showed biological abnormalities, including dysnatremia, kidney failure, and liver dysfunction, the same day as the EEG. The results of cerebrospinal fluid analysis were negative for SARS-Cov-2 for all tested patients. Nine patients who had no identifiable cause of brain injury outside COVID-19 were further isolated; their brain injury was defined as COVID-19-related encephalopathy. They represented 1% (9 of 644) of patients with COVID-19 requiring hospitalization. Six of these 9 patients had movement disorders, 7 had frontal syndrome, 4 had brainstem impairment, 4 had periodic EEG discharges, and 3 had MRI white matter-enhancing lesions. The results from this cohort of patients hospitalized with COVID-19 suggest there are clinical, EEG, and MRI patterns that could delineate specific COVID-19-related encephalopathy and guide treatment strategy.

Cerebral amyloid angiopathy, comorbid atrial fibrillation

Cerebral amyloid angiopathy (CAA) is caused by the deposition of β-amyloid in small vessels in the cerebral cortex and leptomeninges. Nowadays, CAA is recognized more often due to the development of neuroimaging technologies. The frequency of CAA increases in old age that explains its frequent association with cardiovascular diseases. Combination of CAA with atrial fibrillation (AF) causes particular difficulties in managing of the patients, since antithrombotic drugs prescribed to patients with AF mostly contraindicated in CAA because of increased risk of intracerebral hemorrhages. The article presents a case report of the patient with AF who was admitted to the stroke center with acute ischemic stroke. According to MRI, the focus of acute ischemia was small and localized in the cerebellum. This stroke was regarded as having an undetermined etiology according TOAST classification. Small-vessel occlusion subtype was not diagnosed because the TOAST criteria do not attribute an ischemic focus in the cerebellum to a lacunar stroke, while cardioembolic subtype was rejected due to a small (less than 1.5 cm in diameter) size of the focus. Probable CAA in the patient was diagnosed on the basis of the following MRI data: multiple cortical-subcortical micro-hemorrhages (T2*GRE); a single cortical focus with features of the hemorrhage at the stage of intracellular methemoglobin deposition (T1- weighted MR images); bilateral enlargement of perivascular spaces in semioval centers (FLAIR); a negative fronto-occipital gradient (T2-weighted MR images). A diagnosis of CAA was made in accordance with the 2010 Boston criteria and 2019 recommendations of the International CAA Association. The article discusses the hemorrhagic and non-hemorrhagic MRI features of CAA. Frequency of occurrence of cortical microinfarcts in CAA is discussed as well as their differences from small cardioembolic infarcts in AF. Algorithms for antithrombotic therapy for secondary prevention of ischemic stroke in patients with CAA and AF are considered.

Brain magnetic resonance imaging in adult survivors of extracorporeal membrane oxygenation.

Despite the common occurrence of neurologic complications in patients with extracorporeal membrane oxygenation (ECMO), data on magnetic resonance imaging (MRI) findings in adult ECMO are limited. We aimed to describe the MRI findings of patients after ECMO cannulation. Records of patients who underwent ECMO from September 2017 to June 2019 were reviewed. MRI studies were performed using multiplanar sequences consisting of T1-, T2-weighted, fluid attenuated inversion recovery (FLAIR), diffusion-weighted imaging (DWI), and susceptibility weighted images (SWI). Of the 78 adult patients who underwent ECMO, 26 (33%) survived. Of 26, eight patients (31%) had MRI studies, with a median age of 47 years (interquartile range [IQR]: 25-57). The median ECMO support time was 8 days (IQR: 4-25) and the median time from decannulation to MRI was 12 days (IQR: 1-34). Five (63%) of eight patients had ischemic infarcts; 4 (50%) had cerebral microhemorrhage; 2 (25%) had intracranial hemorrhage; and 1 (13%) had thoracic cord ischemic infarct. There were no patients with normal MRI. All patients underwent transcranial Doppler (TCD). Four of 8 (50%) showed presence of microemboli with TCD; 3 of 4 (75%) had ischemic infarcts; and 1 of 4 (25%) had presence of multiple cerebral microhemorrhages on MRI. All ischemic infarcts had diffuse pattern of punctate to small lesions for ECMO survivors. The location of cerebral microhemorrhages included lobar (n = 4, 100%), deep (n = 2, 50%), and both (n = 2, 50%). Of the MRI studies, cerebrovascular related lesions were the most frequent, with punctate ischemic infarct being the most common type that may be associated with TCD microemboli. The results of the study suggest that subclinical cerebral lesions are commonly found in patients with ECMO support. Further research is needed to understand long-term effect of these cerebral lesions.

Retrospective Observational Study of Brain MRI Findings in Patients with Acute SARS-CoV-2 Infection and Neurologic Manifestations.

BackgroundThis study provides a detailed imaging assessment in a large series of COVID-19 patients with neurological manifestations.PurposeTo review the MRI findings associated with acute neurological manifestations in COVID-19 patients.MethodsThis was a cross-sectional study conducted between March 23 and May 7, 2020 at the Pitié-Salpêtrière University Hospital, a reference center for COVID-19 in the Paris area. Inclusion criteria were: adult patients diagnosed with SARS-CoV-2 infection, presenting with acute neurological manifestations and referred for a brain MRI examination. Patients were excluded if they had a previous history of neurological disease. The characteristics and the frequency of different MRI features were investigated. The findings were analyzed separately in patients in intensive care units (ICU) and other departments (non-ICU).ResultsDuring the inclusion period, 1176 consecutive patients were hospitalized for suspected COVID-19. Out of 308 patients with acute neurological symptoms, 73 patients met the inclusion criteria (23.7%) and were included: 35 ICU patients (47.9%) and 38 non-ICU patients (52.1%). The mean age was 58.5 ± 15.6 years, with a male predominance (65.8% vs. 34.2%). Forty-three patients presented pathological MRI findings 2-4 weeks after symptom onset (58.9%), including 17 with acute ischemic infarct (23.3%), 1 with a deep venous thrombosis (1.4%), 8 with multiple microhemorrhages (11.3%), 22 with perfusion abnormalities (47.7%), 3 with restricted diffusion foci within the corpus callosum consistent with cytotoxic lesions of the corpus callosum (CLOCC, 4.1%). Multifocal white matter enhancing lesions were seen in 4 ICU patients (5%). Basal ganglia abnormalities were seen in 4 other patients (5%). The cerebrospinal fluid (CSF) analysis was negative for SARS-CoV-2 in all tested patients (n=39).ConclusionIn addition to cerebrovascular lesions, perfusion abnormalities, CLOCC and ICU-related complications, we identified two patterns including white matter enhancing lesions and basal ganglia abnormalities that could be related to SARS-CoV-2 infection.

COVID-19-associated Diffuse Leukoencephalopathy and Microhemorrhages.

Diffuse leukoencephalopathy and juxtacortical and/or callosal microhemorrhages were brain imaging features in critically ill patients with coronavirus disease 2019.Coronavirus disease 2019 (COVID-19) has been reported in association with a variety of brain imaging findings such as ischemic infarct, hemorrhage, and acute hemorrhagic necrotizing encephalopathy. Herein, the authors report brain imaging features in 11 critically ill patients with COVID-19 with persistently diminished mental status who underwent MRI between April 5 and April 25, 2020. These imaging features include (a) confluent T2 hyperintensity and mild restricted diffusion in bilateral supratentorial deep and subcortical white matter (in 10 of 11 patients) and (b) multiple punctate microhemorrhages in juxtacortical and callosal white matter (in seven of 11 patients). The authors also discuss potential pathogeneses.© RSNA, 2020Online supplemental material is available for this article.

A rare cause of first seizure

A 52 year old man with no history of seizures presented following multiple generalized tonic-clonic seizures at home. He had a recent history of anorexia, weight loss and incoordination. Clinical examination revealed reduced level of consciousness, left-sided weakness and neglect. T2-weighted MRI (Fig. 1) and MRI SWAN (Fig. 2) are provided.Fig. 2MRI SWAN demonstrates widespread punctate hypodense foci.View Large Image Figure ViewerDownload Hi-res image Download (PPT) A.Glioblastoma multiformeB.Acute Haemorrhagic EncephalomyelitisC.Intravascular lymphomaD.Primary CNS lymphomaE.Progressive multifocal leukoencephalopathy Answer: Intravascular lymphoma The MRI scan (Fig. 1) demonstrates T2 hyperintensity in right frontal lobe with central irregular enhancement and other foci of hyperintensity. MRI SWAN (Fig. 2) demonstrates multiple punctate hypointense foci consistent with microhemorrhages. Brain biopsy confirmed CD10+ Intravascular Lymphoma (IVL). IVL is a rare form of Non-Hodgkin lymphoma characterized by lymphocyte proliferation within blood vessels [[1]Ponzoni M. Ferreri A.J. Campo E. et al.Definition, diagnosis, and management of intravascular large B-cell lymphoma: proposals and perspectives from an international consensus meeting.J Clin Oncol. 2007; 25: 3168Crossref PubMed Scopus (345) Google Scholar]. Radiologic findings are largely nonspecific and brain biopsy is required for diagnosis. Although hemorrhagic infarcts are well described in the pathological literature, the potential for microhemorrhages on SWAN or T2 sequences has been rarely described [[2]Alexandrescu S. Orengo J.P. Toossi S. et al.CNS intravascular large cell lymphoma in a patient with autoimmune hemolytic anemia.Neuropathology. 2015; 35: 170-174Google Scholar]. This case well illustrates this finding, and adds to the differential diagnosis for multiple regional microhemorrhages. The patient in this case responded well to treatment with chemotherapy.

Anticoagulación tras una hemorragia cerebral

Atrial fibrillation causes 50% of cardioembolic strokes and 20% of all strokes. Strokes produced by atrial fibrillation are larger, more disabling and more often fatal. Antivitamin K antagonists are able to prevent 64% of strokes, but increase the risk of intracranial haemorrhage. Direct oral anticoagulants have a 50% lower risk of producing intracranial haemorrhage than vitamin K antagonists. The number of patients receiving anticoagulation has increased markedly in the last decade and, consequently, so has the risk of anticoagulant-associated intracranial haemorrhage. Although the associated morbidity and mortality are very high, the need to resume anticoagulation must be considered among survivors at risk of stroke. Currently available data are drawn from observational studies. Based on these studies, the clinical practice guidelines have established general recommendations with low levels of evidence, which include avoiding anticoagulation in lobar intracranial haemorrhages and individualisation of anticoagulation in deep intracranial haemorrhages. Until new scientific evidence is available on the most effective preventive strategy, decisions should be individualised in each patient depending on certain factors such as age, the localisation and cause of the intracranial haemorrhage, the anticoagulant that produced the cerebral bleed, prior embolisms, and the presence or absence of multiple cerebral microhemorrhages. The treatments of choice are direct oral anticoagulants or percutaneous closure of the left atrial appendage.

Teaching NeuroImages: Distinct brain microhemorrhage pattern in critical illness associated with respiratory failure.

A 51-year-old man with dementia presented with altered mental status and unremarkable initial brain CT and MRI. Hospitalization was complicated by aspiration pneumonia, hypoxia, and acute respiratory distress syndrome requiring intubation. He improved with antibiotics, but 1 week later developed seizures. MRI revealed new multiple microhemorrhages involving the subcortical white matter, internal capsules, and corpus callosum, sparing the deep white matter and deep gray nuclei (figure). This distinctive pattern is seen in critically ill patients with respiratory failure1 and resembles high altitude exposure.2 It is important to distinguish this from other causes of microhemorrhages including hypertension, diffuse axonal injury, and amyloid angiopathy.

024 STARFRUIT - THE FORBIDDEN FRUIT FOR RENAL FAILURE PATIENT. REMINDER FROM A FATAL CASE OF NEUROTOXICITY

Category: Other Presenter: Dr KWEK FOONG CHEW Keywords: Starfruit toxicity, neurotoxicity, Hemodialysis, CVVHDF, charcoal hemoperfusion, status epilepticus, seizure Starfruit (SF), also known as Carambola, is common in South East Asia, usually consumed raw or taken as a juice. It is known to cause neurotoxicity due to neurotoxin called Caramboxin. This toxin has a glutamatergic ionotropic molecular action, with potent excitatory, convulsant, and neurodegenerative properties. Here we described a case of fatal starfruit intoxication in an end stage renal failure (ESRF) patient. A 67 years old lady with ESRF whom recently commenced on regular haemodialysis (HD). She presented with hiccups, insomnia, lethargy and episodes of blank stares one day after ingesting two SF. She became unconscious and developed generalized tonic-clonic seizures which progressed to status epilepticus. She was put on mechanical ventilation and required multiple anti-epileptics and propofol infusion. She was treated with HD initially and then was put on continuous veno-venous hemodiafiltration (CVVHDF) and charcoal heamoperfusion treatment. However, she did not obtain any significant neurological recovery. Electroencephalography (EEG) showed an encephalopathic picture. Magnetic resonance imaging (MRI) showed bilateral gyriform hyperintense signal changes and multiple microhemorrhages changes. Eventually she succumbed to nosocomial infection. High index of suspicion and active enquiry regarding SF ingestion is required for ESRF patients presenting with hiccups and seizure. Early diagnosis and treatment is important as immediate haemodialysis is potentially beneficial in starfruit neurotoxicity. Poor conscious level and seizures development in SF neurotoxicity are poor prognosis factors. Patients with renal failure should be advised to avoid starfruit ingestion.

Diagnostic Challenge of Diffusion Tensor Imaging in a Patient With Hemiplegia After Traumatic Brain Injury.

A 51-year-old man showed hemiplegia on his right side after a traumatic brain injury (TBI). On initial brain computed tomography (CT) scan, an acute subdural hemorrhage in the right cerebral convexity and severe degrees of midline shifting and subfalcine herniation to the left side were evident. On follow-up brain magnetic resonance imaging (MRI), there were multiple microhemorrhages in the left parietal and occipital subcortical regions. To explain the occurrence of right hemiplegia after brain damage which dominantly on the right side of brain, we used diffusion tensor imaging (DTI) to reconstruct the corticospinal tract (CST), which showed nearly complete injury on the left CST. We also performed motor-evoked potentials, and stimulation of left motor cortex evoked no response on both sides of upper extremity. We report a case of patient with hemiplegia after TBI and elucidation of the case by DTI rather than CT and MRI.

Deferoxamine inhibits microglial activation, attenuates blood-brain barrier disruption, rescues dendritic damage, and improves spatial memory in a mouse model of microhemorrhages.

Cerebral microbleeds are strongly linked to cognitive dysfunction in the elderly. Iron accumulation plays an important role in the pathogenesis of intracranial hemorrhage. Deferoxamine (DFX), a metal chelator, removes iron overload and protects against brain damage in intracranial hemorrhage. In this study, the protective effects of DFX against microhemorrhage were examined in mice. C57BL6 and Thy-1 green fluorescent protein transgenic mice were subjected to perforating artery microhemorrhages on the right posterior parietal cortex using two-photon laser irradiation. DFX (100mg/kg) was administered 6h after microhemorrhage induction, followed by every 12h for three consecutive days. The water maze task was conducted 7days after induction of microhemorrhages, followed by measurement of blood-brain barrier permeability, iron deposition, microglial activation, and dendritic damage. Laser-induced multiple microbleeds in the right parietal cortex clearly led to spatial memory disruption, iron deposits, microglial activation, and dendritic damage, which were significantly attenuated by DFX, supporting the targeting of iron overload as a therapeutic option and the significant potential of DFX in microhemorrhage treatment. Irons accumulation after intracranial hemorrhage induced a serious secondary damage to the brain. We proposed that irons accumulation after parietal microhemorrhages impaired spatial cognition. After parietal multiple microhemorrhages, increased irons and ferritin contents induced blood-brain barrier disruption, microglial activation, and further induced dendrites loss, eventually impaired the water maze, deferoxamine treatment protected from these damages.

Pseudotumoral presentation of cerebral amyloid angiopathy-related inflammation.

To identify the clinical and radiologic features that should raise suspicion for the pseudotumoral presentation of cerebral amyloid angiopathy-related inflammation (CAA-I). We retrospectively reviewed the characteristics of 5 newly diagnosed and 23 previously reported patients in whom the CAA-I imaging findings were initially interpreted as CNS neoplasms. Most cases (85%) occurred in patients >60 years old. The clinical characteristics at presentation included subacute cognitive decline (50%), confusion (32%), focal deficits (32%), seizures (25%), and headaches (21%). Brain MRI demonstrated infiltrative white matter lesions that exhibited a loco-regional mass effect without parenchymal enhancement (93%). In general, these findings were interpreted as low-grade glioma or lymphoma. Eighteen patients (64%) underwent a biopsy, which was nondiagnostic in 4 patients (14%), and 6 patients (21%) underwent a surgical resection. The primary reason for the misinterpretation of the imaging findings was the absence of T2*-weighted gradient recalled echo (T2*-GRE) sequences on initial imaging (89%). When subsequently performed (39%), the T2*-GRE sequences demonstrated multiple characteristic cortical and subcortical microhemorrhages in all cases. Perfusion MRI and magnetic resonance spectroscopy (MRS), which were performed on a subset of patients, indicated markedly reduced relative cerebral blood flow and a normal metabolic ratio. The identification of one or several nonenhancing space-occupying lesions, especially in elderly patients presenting with cognitive impairment, should raise suspicion for the pseudotumoral presentation of CAA-I and lead to T2*-GRE sequences. Perfusion MRI and MRS appear to be useful techniques for the differential diagnosis of this entity.

Neuropathology of Natural Cytauxzoon felis Infection in Domestic Cats.

Cytauxzoonosis is a tick-borne disease of felids caused by the protozoan Cytauxzoon felis. This article characterizes the neuropathologic changes in 8 cases of natural C. felis infection in domestic cats with typical clinical signs and pathologic changes in multiple organs. Histologic changes in the brain included intravascular schizont-laden macrophages in leptomeningeal and parenchymal arterioles and venules. Small capillaries throughout the gray and white matter and choroid plexus also appeared occluded. Affected vessels were often surrounded by small to moderate numbers of lymphocytes and plasma cells and multiple areas of hemorrhage. Vasculitis and fibrin thrombi were occasionally present. Parenchymal changes consisted of variable degrees of vacuolation of the gray and white matter, with microgliosis, astrocytosis, astrogliosis, and multiple microhemorrhages. Multiple well-demarcated areas of necrosis observed in 4 cases were characterized by marked vacuolation of the gray or white matter, with necrotic neurons containing shrunken hypereosinophilic cytoplasm and pyknotic nuclei, nuclear debris, swollen axons, and scattered foamy macrophages. The changes in the brains of affected cats were attributed to vascular occlusion and secondary ischemia caused by the protozoal infection.

Microhemorrhages in the corpus callosum after treatment with extracorporeal membrane oxygenation

Cerebral microhemorrhages (MH) are diminutive focal bleedings which can be detected best by MRI using susceptibility-weighted imaging sequences (SWI). They can be found in a variety of neurologic diseases. The pattern of distribution can lead to the underlying pathomechanism [1]. Survivors of high-altitude cerebral edema (HACE) showed multiple MH, predominantly in the splenium of the corpus callosum. Mountaineers with a lack of acclimatization to high altitudes tend to suffer from HACE. Hypoxemia in great heights is discussed to be the main trigger of HACE [2]. Acute respiratory distress syndrome (ADRS) is characterized by oxygenation failure in mechanically ventilated patients. The severity is classified by the ratio of arterial oxygen tension to fraction of inspired oxygen [3]. In some patients suffering from severe ARDS, refractory to conventional therapy, venovenous extracorporeal membrane oxygenation therapy is the therapeutic option to ensure oxygenation.

SWAN MRI revealing multiple microhemorrhages secondary to septic emboli from mucormycosis

The Neuro Image by Scully et al.1 attempted to show that the new T2* susceptibility-weighted angiography (SWAN) MRI is more sensitive to show microbleeds not visualized on T2*-GRE. SWAN MRI may not be a familiar term to all neurologists. ESI techniques have recently gained popularity for being more sensitive in showing paramagnetic tissues compared with the standard T2*-GRE. This was initially commercialized as susceptibility-weighted imaging (SWI) by Siemens (Malvern, PA) MRI. SWI uses additional phase information to increase the sensitivity.2 We previously reported evidence for higher sensitivity of SWI over GRE.3 Since then, it is gradually replacing T2*-GRE in clinical imaging, especially in settings where Siemens MRI is used. Due to licensing and patent issues, different MRI vendors are often forced to slightly modify a sequence technique to avoid infringement. To provide an equivalent ESI technique, General Electric (Milwaukee, WI) modified the T2*-GRE by multiecho acquisition and postprocessing reconstruction as weighted average in its MRI and called it SWAN. Similarly, Philips (Andover, MA) MRI uses a different postprocessing technique called phase difference enhanced imaging (PADRE) to combine the phase information. The different ESI are probably superior to T2*-GRE. It would be interesting to compare ESI techniques from different vendors, comparing apples to apples.