PURPOSE:Subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm is a neurologic emergency with diagnostic and management challenges. While traditional imaging techniques such as CT angiography and digital subtraction angiography remain essential, they may be inconclusive at identifying the culprit aneurysm when multiple aneurysms are present. METHODS/RESULTS:We present a patient with SAH and four intracranial aneurysms identified on initial CT angiogram. MR vessel wall imaging (VW-MRI) played a pivotal role: it revealed focal wall enhancement in the basilar tip aneurysm, guiding successful targeted balloon assisted coiling. CONCLUSION:This case illustrates the value of VW-MRI in identifying ruptured aneurysms by assessing wall abnormality rather than just lumen morphology. VW-MRI employs high-resolution, black-blood MR techniques to visualize vessel wall pathology. Our findings support integrating VWI into acute management algorithms when conventional imaging is inconclusive, potentially improving diagnostic accuracy and outcomes in patients with complex aneurysmal SAH presentations.

Background: Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a rare and poorly understood inflammatory disorder of the central nervous system centered on the pons. It has a characteristic imaging appearance with enhancing and T2-hyperintense punctate and curvilinear lesions in the pons. The lesions lack restricted diffusion and have relatively little perilesional edema. Although patients typically present with gait ataxia and other sequelae of brainstem inflammation including diplopia, there is scant literature focusing on patients who present with primarily neuro-ophthalmic manifestations. Methods: Case series of 3 patients presenting with diplopia who had a final diagnosis of CLIPPERS. Results: Case descriptions of a 71-year-old man, 61-year-old woman, and 38-year-old man are reported. Diplopia was the chief presenting complaint, owing to internuclear ophthalmoplegia, sixth nerve palsy, or skew deviation. All patients had nystagmus and gait ataxia. Brain MRI displayed punctate or curvilinear enhancement of pontine/middle cerebellar peduncle lesions without restricted diffusion. All patients achieved rapid improvement after corticosteroid treatment. Conclusions: In 3 patients with CLIPPERS, the main presenting complaint was diplopia. The distinctive imaging signs led to a strong presumption of CLIPPERS, permitting a truncated evaluation and early corticosteroid treatment, which provided rapid reversal of clinical and imaging manifestations.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Background The diagnosis of leptomeningeal metastatic disease has major prognostic and therapeutic implications. We report 13 patients with a radiologically distinct kind of focal, enhancing leptomeningeal lesion on brain MRI that mimics leptomeningeal metastatic disease.Methods These patients were assessed at University Health Network (Toronto, Canada) between January 2001 and December 2023.Results Median age was 68 years (range, 55-78 years) and 10 patients were women. All patients had brain magnetic resonance imaging (MRI) including contrast-enhanced T2-weighted fluid attenuation inversion recovery (FLAIR) and T1-weighted spin echo sequences. MRI in all 13 patients showed a focal enhancing lesion located along the leptomeningeal surface of the brain. The MRI exams were reported as possible or likely leptomeningeal metastatic disease for the majority (9/13) of patients. Each lesion was curvilinear rather than sheet-like, and some lesions consisted of multiple connected/branching curvilinear structures with the appearance of abnormal vessels. The lesions were distinct from normal blood vessels. Some lesions had a visible connection with a nearby cortical vein. Follow-up contrast-enhanced brain MRI for 8/13 (62%) patients at a median of 3.9 years (IQR 2.4-6.6 years) showed all lesions were unchanged over time. Another 2/13 (15%) patients had clinical and CT brain follow-up after one year with no evidence of metastatic disease.Conclusions We describe a distinct kind of focal, enhancing leptomeningeal lesion on brain MRI that mimics metastatic disease. These lesions are likely a type of low-flow vascular anomaly. Their curvilinear/branching shape and intense enhancement particularly on T2-weighted FLAIR images distinguish these lesions from tumors.

Background and Purpose Perivascular spaces (PVS) are interstitial fluid-filled spaces surrounding blood vessels traversing the deep gray nuclei and white matter of the brain. These are commonly encountered on CT and MR imaging and are generally asymptomatic and of no clinical significance. However, occasional changes in the size of focal PVS, for example, when enlarging, may mimic pathologies including neoplasms and infections, hence potentially confounding radiological interpretation. Given these potential diagnostic issues, we sought to better characterize common clinical and imaging features of focal PVS demonstrating size fluctuations. Materials and Methods Upon institutional approval, we retrospectively identified 4 cases demonstrating PVS with size changes at our institution. To supplement our cases, we also performed a literature review, which identified an additional 14 cases. Their clinical and imaging data were analyzed to identify characteristic features. Results Of the 18 total cases (including the 4 institutional cases), 10 cases increased and 8 decreased in size. These focal PVS ranged from 0.4–4.5 cm in size. Whereas a decrease in size did not represent a diagnostic issue, focal increase in size of PVS led to concerning differential diagnoses in at least 30% of the radiology reports. These enlarging PVS were most found in the basal ganglia and temporal lobe, and in patients with previous brain radiation treatment. Conclusion Focal size change of PVS can occur, especially years after brain radiation treatment. Being cognizant of this benign finding is important to consider in the differential diagnosis to avoid undue patient anxiety or unnecessary medical intervention.

Abstract: A 61-year-old woman with a history of untreated low-grade B-cell lymphoma presented with blurry vision, unsteadiness, and worsening pain on touching skin of the upper trunk was enrolled. Blurry vision was attributed to oscillopsia from downbeat nystagmus, which later evolved into macrosaccadic oscillations. MRI brain and spine showed mild, longitudinally extensive T2 hyperintensity in the central gray matter of the spinal cord extending from the medulla to T11 level. Serum paraneoplastic panel was negative; however, she had very high titers of anti-Ma2 antibodies in cerebrospinal fluid. The diagnosis of paraneoplastic neurological syndrome was made. Empiric treatment with high dose of intravenous steroids followed by intravenous immunoglobulin infusions did not improve her symptoms. An extensive search for an underlying tumor commenced and was initially unrevealing. However, two-month follow-up positron emission tomography scan showed increased uptake in a right pulmonary nodule, which when biopsied confirmed diagnosis of extranodal marginal zone lymphoma. The final diagnosis was anti-Ma2 antibody-mediated paraneoplastic cerebellar degeneration and myeloneuropathy secondary to lymphoma.

BACKGROUND: A venous pattern of infarction on neuroimaging is used as a clue to undiagnosed cerebral venous thrombosis (CVT); prevention of venous infarction is a goal of CVT management; and venous infarction is a factor used for clinical prognostication. Despite widespread use of the term venous infarct, the prevalence of true venous infarction is unclear. Our primary aim was to determine the prevalence of venous infarction in patients with CVT. We also measured the prevalence of diffusion abnormality without infarction, vasogenic edema, and intracranial hemorrhage. METHODS: Single-center, retrospective cohort study using a registry of 110 consecutive patients admitted to hospital with cerebral venous thrombosis between 2004 and 2014. Inclusion criteria were brain magnetic resonance imaging (MRI) and contrast-enhanced venography at presentation, and repeat brain MRI ≥1 month later. Exclusion criteria were dural arteriovenous fistula, arteriovenous malformation, cavernous sinus thrombosis, or previous neurosurgical procedure. Main outcome was proportion of patients with venous infarction (irreversible ischemic injury) diagnosed using diffusion-weighted MRI at presentation, confirmed using T2-weighted fluid-attenuated inversion recovery MRI ≥1 month later, and reported with 95% CI using the Wilson score interval method. We also report the prevalence of transient diffusion MRI abnormality without infarction, vasogenic edema, and intracranial hemorrhage. RESULTS: Seventy-three patients met the inclusion criteria, and after exclusions, the final study population was 59 patients with median age 41 years (interquartile range, 32–57). Venous infarction occurred in 12% (7/59 [95% CI, 6%–23%]) of patients, and final infarct volume was >1 mL in only 5.1% (3/59) of patients. An additional 8% (5/59 [95% CI, 4%–18%]) of patients had a transient diffusion MRI abnormality without infarction. Prevalence of cerebral vasogenic edema and intracranial hemorrhage were 66% (39/59 [95% CI, 53%–77%]) and 54% (32/59 [95% CI, 41%–66%]), respectively. CONCLUSIONS: In patients with CVT, venous infarction is uncommon and venous infarcts are typically very small. Vasogenic edema and hemorrhage are more common consequences of CVT.

Mason, Ryan MD, PhD; Jeeva-Patel, Trishal MD; Mandell, Daniel MD, PhD; Shannon, Patrick MD; Margolin, Edward A. MDEditor(s): Avery, Robert DO; Golnik, Karl C. MD; Froment, Caroline MD, PhD; Wang, An-Guor MD Author Information

HomeStrokeVol. 53, No. 7Detecting Silent Acute Microinfarcts in Cerebral Small Vessel Disease Using Submillimeter Diffusion-Weighted Magnetic Resonance Imaging: Preliminary Results Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBDetecting Silent Acute Microinfarcts in Cerebral Small Vessel Disease Using Submillimeter Diffusion-Weighted Magnetic Resonance Imaging: Preliminary Results Karen Misquitta, Marietou Daou, John Conklin, Congyu Liao, Kawin Setsompop, Julien Poublanc, Zahra Shirzadi, Bradley J. MacIntosh, George Tomlinson, Melanie Cohn, Richard I. Aviv, Frank L. Silver and Daniel M. Mandell Karen MisquittaKaren Misquitta https://orcid.org/0000-0002-5006-3005 University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. , Marietou DaouMarietou Daou University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. , John ConklinJohn Conklin https://orcid.org/0000-0001-9921-2086 Massachusetts General Hospital, Boston (J.C.). , Congyu LiaoCongyu Liao https://orcid.org/0000-0003-2270-276X Stanford University, Stanford, CA (C.L., K.S.). , Kawin SetsompopKawin Setsompop Stanford University, Stanford, CA (C.L., K.S.). , Julien PoublancJulien Poublanc https://orcid.org/0000-0001-8377-9846 University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. , Zahra ShirzadiZahra Shirzadi https://orcid.org/0000-0001-6854-9356 Department of Medical Biophysics (Z.S., B.J.M.), University of Toronto, Canada. , Bradley J. MacIntoshBradley J. MacIntosh https://orcid.org/0000-0001-7300-2355 Department of Medical Biophysics (Z.S., B.J.M.), University of Toronto, Canada. , George TomlinsonGeorge Tomlinson https://orcid.org/0000-0002-9328-6399 University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. , Melanie CohnMelanie Cohn https://orcid.org/0000-0003-2921-7505 University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. , Richard I. AvivRichard I. Aviv https://orcid.org/0000-0003-0259-970X University of Ottawa, Canada (R.I.A.). , Frank L. SilverFrank L. Silver https://orcid.org/0000-0002-7569-8429 University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. and Daniel M. MandellDaniel M. Mandell Correspondence to: Daniel M. Mandell, MD, PhD, Toronto Western Hospital, 399 Bathurst Street, Toronto, Canada, M5T2S8. Email E-mail Address: [email protected] University Health Network (K.M., M.D., J.P., G.T., M.C., F.S., D.M.M.), University of Toronto, Canada. Originally published13 Jun 2022https://doi.org/10.1161/STROKEAHA.122.039723Stroke. 2022;53:e251–e252Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 13, 2022: Ahead of Print Vascular dementia is most often caused by cerebral small vessel disease (SVD). There are few SVD clinical trials and no established therapies. Barriers include difficulty identifying which patients to include in trials, and slow deterioration of cognition necessitating long trials. Future trials will require neuroimaging biomarkers for patient selection and outcome assessment.White matter hyperintensity on T2-weighted magnetic resonance imaging is a biomarker of prior injury from SVD. But white matter hyperintensity is often stable over years1 suggesting it may be a poor marker of active disease.Clinically silent, acute microinfarcts detected using diffusion-weighted magnetic resonance imaging (DWI) are another potential biomarker of SVD.2 Silent acute microinfarcts are a marker of active disease, but they are infrequently detected in vivo. Infrequent detection could reflect limited sensitivity of DWI rather than true rarity of these acute events. We conducted a prospective study to determine if DWI with substantially improved spatial resolution detects more silent acute microinfarcts than conventional DWI in patients with SVD.MethodsProspective observational study with institutional review board approval. Participants provided written informed consent. The data that support the findings of this study are available from the corresponding author upon reasonable request. Inclusion criteria: age >55 years; moderate/severe SVD (Fazekas scale ≥grade 2).3 Exclusion criteria: cardio-embolic risk factor; cervical/intracranial arterial stenosis ≥50%; cortical infarct. Neurologists recruited 5 participants. Each week for 10 consecutive weeks, participants had clinical assessment (National Institutes of Health Questionnaire for Verifying Stroke-Free Status), 3-Tesla magnetic resonance imaging brain using a 10-minute whole-brain g-SLIDER-SMS DWI4 with isotropic 860 µm voxel dimensions and conventional DWI. Primary outcome was proportion of acute microinfarcts detected on submillimeter DWI that were also visible on conventional DWI. Secondary outcome was proportion of submillimeter versus conventional DWI exams showing evidence of active SVD (defined as presence of acute or subacute microinfarcts; details in Supplemental Material).ResultsFive participants (3 women, 2 men) with median age 76 years (range, 58–78). Table S1 provides additional details. Weekly clinical screening for stroke symptoms was negative for all participants throughout the 10 weeks.Submillimeter DWI showed clinically silent, microinfarcts in one participant over the 10-week period: 16 acute microinfarcts and 4 subacute microinfarcts. These were located in the white matter (18/20) or basal ganglia (2/20). Conventional DWI detected 18% (3/16 [95% CI, 6.6%–43.0%) of the acute microinfarcts on submillimeter DWI (Figure). No microinfarcts were detected only on conventional DWI. Table S2 provides additional details. The participant with acute microinfarcts had evidence of SVD activity on 20% (2/10) of conventional DWI exams versus 100% (10/10) of submillimeter DWI exams.Download figureDownload PowerPointFigure. Conventional versus submillimeter isotropic diffusion magnetic resonance imaging (MRI) for detection of silent acute microinfarcts in a patient with cerebral small vessel disease. T2-weighted fluid-attenuated inversion recovery (FLAIR; A) shows patchy hyperintensity consistent with chronic white matter injury from small vessel disease. Conventional diffusion-weighted MRI (DWI; B) shows an acute microinfarct in the left frontal white matter (arrowhead). Submillimeter DWI shows the same acute microinfarct (arrowhead) and also a smaller acute microinfarct in the right parietal white matter (arrow; inset apparent diffusion coefficient map). Images more inferiorly (D–F) show another acute microinfarct on submillimeter DWI (arrow, F) with no corresponding abnormality on conventional DWI (circle, E).DiscussionWe have shown superior detection of clinically silent, acute microinfarcts in patients with SVD using a novel DWI technique with submillimeter, isotropic spatial resolution. A single submillimeter DWI scan might identify a subgroup of patients with SVD who have more active disease. A neuroimaging biomarker of cerebral SVD activity could identify those patients with the most active SVD for inclusion in clinical trials and enable rapid assessment of treatment response. Validation of a biomarker will require a larger sample size and a long-term study with rigorous exclusion of proximal embolic sources and neurocognitive outcome assessment.Article InformationSources of FundingThis work was supported by Heart and Stroke Foundation of Canada grant (G-19-0026550).Supplemental MaterialsMethodsTables S1–S2Disclosures None.FootnotesSupplemental Material is available at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.122.039723.For Sources of Funding and Disclosures, see page e252.Correspondence to: Daniel M. Mandell, MD, PhD, Toronto Western Hospital, 399 Bathurst Street, Toronto, Canada, M5T2S8. Email danny.mandell@uhn.caReferences1. Gouw AA, van der Flier WM, Fazekas F, van Straaten EC, Pantoni L, Poggesi A, Inzitari D, Erkinjuntti T, Wahlund LO, Waldemar G, et al; LADIS Study Group. Progression of white matter hyperintensities and incidence of new lacunes over a 3-year period: the leukoaraiosis and disability study.Stroke. 2008; 39:1414–1420. doi: 10.1161/STROKEAHA.107.498535LinkGoogle Scholar2. Conklin J, Silver FL, Mikulis DJ, Mandell DM. Are acute infarcts the cause of leukoaraiosis?: Brain mapping for 16 consecutive weeks.Ann Neurol. 2014; 76:899–904. doi: 10.1002/ana.24285CrossrefMedlineGoogle Scholar3. Fazekas F, Chawluk JB, Alavi A, Hurtig HSI, Zimmerman RA. MR signal abnormalities at 1.5 T in Alzheimer's dementia and normal aging.AJR Am J Roentgenol. 1987; 149:351–356. doi: 10.2214/ajr.149.2.351CrossrefMedlineGoogle Scholar4. Setsompop K, Fan Q, Stockmann J, Bilgic B, Huang S, Cauley SF, Nummenmaa A, Wang F, Rathi Y, Witzel T, Wald LL. High-resolution in vivo diffusion imaging of the human brain with generalized slice dithered enhanced resolution: Simultaneous multislice (gSlider-SMS).Magn Reson Med. 2018; 79:141–151. doi: 10.1002/mrm.26653CrossrefGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails July 2022Vol 53, Issue 7 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.122.039723PMID: 35695007 Originally publishedJune 13, 2022 Keywordsrisk factorneuroimagingbraincognitionwhite matterPDF download Advertisement

HomeStrokeVol. 53, No. 8Subdural Hematoma-Induced Cortical Perforator Thrombosis Causing Ischemic Strokes Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessCase ReportPDF/EPUBSubdural Hematoma-Induced Cortical Perforator Thrombosis Causing Ischemic Strokes Arjun Balachandar, Federico Carpani, Martin Del Campo and Daniel Mandell Arjun BalachandarArjun Balachandar Correspondence to: Arjun Balachandar, MD, Department of Neurology, University of Toronto, St Michael's Hospital, 30 Bond St, Toronto, ON M5B 1W8, Canada. Email E-mail Address: [email protected] https://orcid.org/0000-0002-7658-4749 Division of Neurology, Department of Medicine (A.B., F.C., M.D.C.), University of Toronto, ON, Canada. Division of Neuroradiology (A.B., F.C., M.D.C.), University of Toronto, ON, Canada. , Federico CarpaniFederico Carpani https://orcid.org/0000-0003-4696-5994 Division of Neurology, Department of Medicine (A.B., F.C., M.D.C.), University of Toronto, ON, Canada. Division of Neuroradiology (A.B., F.C., M.D.C.), University of Toronto, ON, Canada. , Martin Del CampoMartin Del Campo Division of Neurology, Department of Medicine (A.B., F.C., M.D.C.), University of Toronto, ON, Canada. Division of Neuroradiology (A.B., F.C., M.D.C.), University of Toronto, ON, Canada. and Daniel MandellDaniel Mandell https://orcid.org/0000-0001-8007-4947 Department of Medical Imaging (D.M.), University of Toronto, ON, Canada. Originally published26 May 2022https://doi.org/10.1161/STROKEAHA.122.039482Stroke. 2022;53:e381–e382Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: May 26, 2022: Ahead of Print Key PointSubdural hematomas may cause ischemic strokes through direct mechanical compression of pial vessels, leading to perforator vessel thrombosis and small infarcts.A 71-year-old woman with traumatic left cerebral convexity subdural hematoma presented with right face, arm, and leg weakness. After evacuation, brain magnetic resonance imaging showed a small acute infarct in the left frontal white matter (Figure [A]). Head/neck computed tomography-angiogram and echocardiogram were normal. The small infarct was in the distribution of cortical perforating arteries, and susceptibility-weighted magnetic resonance imaging showed thrombosis of a long-perforating vessel. We hypothesize that direct mechanical compression of pial vessels or an irritative phenomenon led to thrombosis of this perforator, which is a distinct phenomenon from other subdural hematoma-related strokes.1,2 The infarct was likely subclinical, and weakness resolved post-evacuation.Download figureDownload PowerPointFigure. Neuroimaging of subdural hematoma and infarct. Computed tomography brain showed large left cerebral convexity acute subdural hematoma (A). Diffusion-weighted magnetic resonance imaging (B) showed tiny left frontal white matter acute-subacute infarct (arrow). Coronal susceptibility-weighted image (SWI; C) showed linear region (arrows) extending from superior to infarct (circle) toward the cortex consistent with thrombosed perforator. Axial SWI (D) showed thrombosed vessel cross-section.See the Supplemental Material for the CARE checklist.Article InformationAcknowledgmentsDr Balachandar drafted the manuscript for intellectual content. Dr Carpani helped to draft the manuscript for intellectual content. Dr Del Campo designed and conceptualized the study; revised the manuscript for intellectual content. D. Mandell designed and conceptualized the study; revised the manuscript for intellectual content.Sources of FundingNone.Disclosures None.FootnotesSupplemental Material is available at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.122.039482.For Sources of Funding and Disclosures, see page e382.Correspondence to: Arjun Balachandar, MD, Department of Neurology, University of Toronto, St Michael's Hospital, 30 Bond St, Toronto, ON M5B 1W8, Canada. Email arjun.balachandar@mail.utoronto.caReferences1. Yamada SM, Tomita Y, Takaya Y. Lacunar infarction caused by chronic subdural hematoma.Neurol Med Chir (Tokyo). 2020; 60:397–401. doi: 10.2176/nmc.oa.2019-0183CrossrefGoogle Scholar2. Alkhachroum AM, Fernandez-Baca Vaca G, Sundararajan S, DeGeorgia M. Post-subdural hematoma transient ischemic attacks: hypoperfusion mechanism supported by quantitative electroencephalography and transcranial doppler sonography.Stroke. 2017; 48:e87–e90. doi: 10.1161/STROKEAHA.117.016388LinkGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails August 2022Vol 53, Issue 8 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.122.039482PMID: 35616022 Originally publishedMay 26, 2022 Keywordshematomathrombosisbrain ischemiaischemic strokemagnetic resonance imagingPDF download Advertisement SubjectsImagingIschemic Stroke

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BACKGROUND:Various neurological sequalae have been described following COVID-19 vaccination. Here we describe the first case of untreated post COVID-19 vaccine encephalitis with spontaneous resolution of contrast enhancing hyperintensities on MRI concomitant with clinical improvement. CASE PRESENTATION:A 59-year-old woman presented with a two-day history of unsteady gait, incoordination, visual symptoms, and lethargy. She had received AZD1222 (AstraZeneca) and mRNA-1273 (Moderna) COVID-19 vaccines at 3 months and 12 days, respectively, before presentation. Brain MRI showed no abnormality on the non-enhanced sequences, but numerous enhancing lesions in the cerebral cortex, deep grey matter, brainstem, and cerebellum. Treatment was expectant, the patient improved clinically over 10 days, and repeat MRI showed near complete resolution of the imaging abnormality. CONCLUSIONS:We describe neurological deterioration 12 days after a second dose of COVID-19 vaccine. There was no evidence of edema or demyelinating lesions in the brain on MRI, but there was extensive contrast-enhancement indicating loss of blood-brain barrier (BBB) integrity. This provides a potential in vivo, clinical-imaging correlate of the post-mortem evidence that SARS-CoV-2 spike protein may induce loss of BBB permeability. While this adds to the list of rare adverse neurological reactions to COVID-19 vaccination, the benefits of receiving the vaccine far outweigh these risks.

Importance A carotid web (CW) is a shelf-like lesion along the posterior wall of the internal carotid artery bulb and an underrecognized cause of young stroke. Several studies suggest that patients with symptomatic CW have a high risk of recurrent stroke, but high-quality data are lacking. Objective To assess the 2-year risk of recurrent stroke in patients with a symptomatic CW. Design, Setting, and Participants A comparative cohort study used data from the MR CLEAN trial (from 2010-2014) and MR CLEAN Registry (from 2014-2017). Data were analyzed in September 2020. The MR CLEAN trial and MR CLEAN Registry were nationwide prospective multicenter studies on endovascular treatment (EVT) of large vessel occlusion (LVO) stroke in the Netherlands. Baseline data were from 3439 consecutive adult patients with anterior circulation LVO stroke and available computed tomography (CT)-angiography of the carotid bulb. Two neuroradiologists reevaluated CT-angiography images for presence or absence of CW and identified 30 patients with CW ipsilateral to the index stroke. For these 30 eligible CW participants, detailed follow-up data regarding stroke recurrence within 2 years were acquired. These 30 patients with CW ipsilateral to the index stroke were compared with 168 patients without CW who participated in the MR CLEAN extended follow-up trial and who were randomized to the EVT arm. Main Outcomes and Measures The primary outcome was recurrent stroke occurring within 2 years after the index stroke. Cox proportional hazards regression models were used to compare recurrent stroke rates within 2 years for patients with and without CW, adjusted for age and sex. The research question was formulated prior to data collection. Results Of 3439 patients with baseline CT-angiography assessed, the median age was 72 years (interquartile range, 61-80 years) and 1813 (53%) were men. Patients with CW were younger (median age, 57 [interquartile range, 46-66] years vs 66 [interquartile range, 56-77] years; P = .02 and more often women (22 of 30 [73%] vs 67 of 168 [40%]; P = .001) than patients without CW. Twenty-eight of 30 patients (93%) received medical management after the index stroke (23 with antiplatelet therapy and 5 with anticoagulant therapy). During 2 years of follow-up, 5 of 30 patients (17%) with CW had a recurrent stroke compared with 5 of 168 patients (3%) without CW (adjusted hazard ratio, 4.9; 95% CI, 1.4-18.1). Conclusions and Relevance In this study, 1 of 6 patients with a symptomatic CW had a recurrent stroke within 2 years, suggesting that medical management alone may not provide sufficient protection for patients with CW.

Cerebrovascular reactivity (CVR) is defined as the change in cerebral blood flow induced by a change in a vasoactive stimulus. CVR using BOLD MRI in combination with changes in end-tidal CO2 is a very useful method for assessing vascular performance. In recent years, this technique has benefited from an advanced gas delivery method where end-tidal CO2 can be targeted, measured very precisely, and validated against arterial blood gas sampling (Ito et al., 2008). This has enabled more precise comparison of an individual patient against a normative atlas of healthy subjects. However, expected control ranges for CVR metrics have not been reported in the literature. In this work, we calculate and report the range of control values for the magnitude (mCVR), the steady state amplitude (ssCVR), and the speed (TAU) of the BOLD response to a standard step stimulus, as well as the time delay (TD) as observed in a cohort of 45 healthy controls. These CVR metrics maps were corrected for partial volume averaging for brain tissue types using a linear regression method to enable more accurate quantitation of CVR metrics. In brief, this method uses adjacent voxel CVR metrics in combination with their tissue composition to write the corresponding set of linear equations for estimating CVR metrics of gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF). After partial volume correction, mCVR and ssCVR increase as expected in gray matter, respectively, by 25 and 19%, and decrease as expected in white matter by 33 and 13%. In contrast, TAU and TD decrease in gray matter by 33 and 13%. TAU increase in white matter by 24%, but TD surprisingly decreased by 9%. This correction enables more accurate voxel-wise tissue composition providing greater precision when reporting gray and white matter CVR values.

We describe a case of subacute bacterial endocarditis and mycotic brain aneurysm caused by Rothia dentocariosa due to untreated dental caries. R. dentocariosa is a rare cause of endocarditis that has a high incidence of aneurysmal and haemorrhagic complications. All patients with intracranial aneurysms who have signs of systemic infection should be considered to have mycotic aneurysms until proven otherwise. Dental habits should be included in regular medical assessment and dental care should be considered for patients presenting with infectious symptoms.

A 72-year-old woman noticed progressive ptosis and binocular diplopia for the past 3 months. She had a known history of stage-4 breast cancer diagnosed 3 years ago with metastases to the spine, pleura, and mediastinal lymph nodes for which she has been undergoing chemotherapy with nanoparticle albumin-bound paclitaxel. She also had a remote history of pituitary macroadenoma diagnosed 23 years ago and treated with transsphenoidal excision, followed by radiation therapy (RT) (3-field technique with 50 Gy in 25 fractions). On examination, she had complete right upper lid ptosis, 2 mm of anisocoria (right pupil larger than left), and complete limitation of adduction, supraduction, and inferoduction of the right eye in keeping with the diagnosis of complete right pupil-involving cranial nerve 3 (CN3) palsy (CN3P). Intorsion of the right eye was intact, and there were no signs of aberrant regeneration. MRI and time-of-flight MRA of the brain performed 2 weeks ago elsewhere was reported as normal with exception of unchanged pituitary gland enlargement, stable compared with imaging performed 3 years ago. When imaging was re-examined, striking bilateral enhancement of the cisternal portion of both CN3 was seen that was not present on the last available postcontrast MRI images from 3 years ago. Repeat MRI of brain and orbits with gadolinium and steady-state imaging 2 weeks later again showed marked smooth enhancement and mild thickening of cisternal segments of both oculomotor nerves but showed no other areas of leptomeningeal or intraparenchymal enhancement (Fig. 1A–C). Two large volume lumbar punctures (LPs) 1 month apart showed normal cerebrospinal fluid (CSF) composition (both with no white blood cells and normal protein and glucose), and cytological analysis was negative for malignancy on both occasions. Patient continued to do well systemically, although CN3P remained unchanged. MRI repeated 6 months later demonstrated unchanged thickening and enhancement of cisternal portion of both oculomotor nerves and unchanged pituitary gland enlargement with no evidence of leptomeningeal enhancement elsewhere (Fig. 1D, E).FIG. 1.: T2 axial SPACE sequence (A) shows the location of the oculomotor nerves (arrows). T1 axial spin echo sequences before (B) and after (C) intravenous contrast injection show diffuse smooth enhancement of the cisternal segments of the oculomotor nerves (arrows). T1 coronal sequence after intravenous contrast injection (D) shows persisting enhancement of cisternal segments of both oculomotor nerves (arrows) and T2 axial FLAIR sequence (E) shows hyperintensity of cisternal segments of both oculomotor nerves (arrows).Initially, carcinomatous meningitis was believed to be the cause of clinical 3NP and bilateral enhancement of cisternal portions of CN3s on neuro-imaging; thus high-volume LPs were performed looking for presence of malignant cells in the CSF. Although CSF cytology has poor sensitivity for detecting central nervous system (CNS) spread of solid malignancies, it does increase with subsequent LPs. Third LP was planned but patient declined further investigations. The working diagnosis was CNS spread of cancer causing seeding of CN3s. However, the patient continued to be stable clinically and had no new neurological symptoms. When MRI remained unchanged 6 months later, we concluded that the diagnosis must be postradiation cranial neuropathy (PRCN) because prognosis in patients with carcinomatous meningitis is uniformly poor, whereas our patient continued to be well with no changes on neuro-imaging. Diplopia and cranial neuropathy in patients with a history of cancer should always raise suspicion of metastases or tumor recurrence. Neuromyotonia is another rare entity that may present with episodic diplopia in patients who have undergone cranial radiotherapy. Although aneurysmal compression should be ruled out first in cases of 3NP, balanced steady-state gradient echo MRI sequences should be performed in all patients with a history of cancer presenting with cranial nerve palsy (1). Enhancement of the oculomotor nerve always indicates underlying pathology but does not always correlate with a clinically apparent CN3P (2). The differential diagnosis for enhancing CN3 consists of inflammatory entities (demyelinating if involving the fascicle of the nerve and radiation-induced and ophthalmoplegic migraine if involving cisternal portion), infiltrative or neoplastic lesions (primary CN3 schwannoma, lymphoma, leukemia, or infiltration by perineural spread or carcinomatous meningitis presenting with irregular thickening along with enhancement) as well as infectious etiologies (1–3). One case series reviewed 13 patients with enhancement of cisternal portion of 3CN on MRI; in 6, enhancement was bilateral and of these 4 had unilateral CN3P clinically, like the patient in our case, with remaining 2 not showing any abnormalities of ocular motility. The main causes of enhancement were hematological malignancies (5/13), infections (2/13), and nonspecific inflammatory entities (6/13) (2). None of these patients had PRCN. As radiation is commonly used for treatment of skull base and nasopharyngeal tumors, there is a lot of literature on PRCN involving lower (IX–XII) cranial nerves, reporting its incidence of ∼5% with 5–7 years being an average time from RT to onset of cranial neuropathy (4). Literature on PRCN involving oculomotor (third, fourth, and sixth) cranial nerves is scanty, however, because of the anatomical proximity of sella to cisternal and cavernous portions of oculomotor nerves; RT for treatment of sellar tumors can produce PRCN involving these nerves. In one recent retrospective case series of 6 patients who have undergone transsphenoidal resection followed by RT for pituitary adenoma, one patient had third, 4 had sixth, and one had both sixth and fourth cranial nerve palsies (5). The time between RT and onset of cranial neuropathy was anywhere between 4 and 96 months, the longest interval between RT and onset of cranial neuropathy to our knowledge to date (5). Although it is well established that the risk for PRCN is related to a radiation dose (with 20–68 Gy range being the total dose previously described), peculiarly, interval between RT and onset of PRCN is inversely related to a dosage with patients receiving a lower dosage having later onset of cranial neuropathy thus emphasizing the need for a long-term follow-up of these patients (5,6). It is also possible that patients receiving chemotherapy might be at an increased risk of developing PRCN. PRCN less commonly affects oculomotor nerves compared with the more sensitive anterior visual pathway (optic nerves and chiasm) (3,7). This is likely because oculomotor cranial nerves are myelin free and their function depends on the integrity of more radioresistant Schwann cells compared with the radiosensitive oligodendrocytes that myelinate the optic nerves and chiasm (5). Although exact mechanism for PRCN is unknown, histologically fibrosis and Wallerian degeneration are seen in cranial nerves after RT (4,5). Progressive soft tissue fibrosis of the areas adjacent to the nerve causing delayed injury to the vasa nervosum has also been implicated (4). It is not clear why in PRCN there is often bilateral enhancement of cranial nerves yet clinically only one nerve is involved, this could be related to the threshold of accumulated damage to the axons before the function of the nerve is impaired where the impairment is enough to produce a nerve palsy on one side and spare the function on the other. In summary, we present a unique case with the longest reported interval between administration of RT and onset of PRCN that reminds us that PRCN should always be on the differential diagnosis of all patients with new onset of cranial neuropathy and history of RT. It also emphasizes importance of obtaining high-resolution balanced steady-state gradient echo MRI sequences in all patients who do not fit a typical profile for microvascular cranial nerve palsy and do not demonstrate improvement in ocular motility 2–3 months after onset of symptoms. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: E. Margolin, D. Mandell, T. Jeeva-Patel, T. Le; b. Acquisition of data: E. Margolin, D. Mandell, and T. Jeeva-Patel; c. Analysis and interpretation of data: E. Margolin, D. Mandell, T. Jeeva-Patel, and T. Le. Category 2: a. Drafting the manuscript: E. Margolin, D. Mandell, T. Jeeva-Patel, and T. Le; b. Revising it for intellectual content: E. Margolin, D. Mandell, T. Jeeva-Patel, and T. Le. Category 3: a. Final approval of the completed manuscript: E. Margolin, D. Mandell, T. Jeeva-Patel, and T. Le.

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