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2020 Scientific Abstracts (Thurs. Oct 15)

Abstract 1 - 0900-0915

Category: Clinical

Presenter: Dr Robert Hammond, Western University

Abstract: Congenital CMV Infection Presenting With Massive Intracerebral Hemorrhage

Barbra deVrijer 1, Diana Crowley 2, Delaney Cosma 2, Giulio Muscedere 3 and Robert Hammond 2, 4
1 Department of Obstetrics and Gynaecology
2 Department of Pathology and Laboratory Medicine
3 Department of Medical Imaging
4 Department of Clinical Neurological Sciences Schulich School of Medicine & Dentistry, Western University, London Health Sciences Centre and St Joseph's Health Care, London, Ontario, Canada

Cytomegalovirus (CMV) is among the most common of intrauterine infections against which we have no effective preventative or therapeutic options. The developing nervous system is a frequent target of CMV and while most injuries are subclinical, severe insults leading to microcephaly and migration defects are well known. A 20-week gestational age fetus was found to have several abnormalities on prenatal ultrasound, the most prominent of which was a large echogenic focus in one cerebral hemisphere. Congenital CMV infection was identified by amniocentesis and maternal serology. The pregnancy was ended by early induction of labour for a 368g stillborn infant. Postmortem examination revealed massive intracerebral hemorrhage as the correlate for the sonographic finding. The microscopic examination of the brain was also striking for extensive polymicrogyria, a high burden of CMV and abundant angiocentric CMV pathology. Catastrophic intracerebral hemorrhage has not been previously reported in association with congenital CMV infection. The present case expands the range of potential injuries the developing brain is subject to in the setting of CMV infection and raises the possibility of a direct vascular injury.

At the end of the session, participants will be able to:

  • Consider intracerebral hemorrhage in the range of potential outcomes in congenital CMV infection
  • Describe how polymicrogyria may result from an insult during proliferation and migration
  • Discuss possible mechanisms of injury to the developing brain by CMV

Target Audience: Pathologists, Residents

CanMEDS: Medical Expert (the integrating role), Communicator, Health Advocate, Scholar

Speaker Profile:

Dr Robert Hammond is a Neuropathologist at London Health Sciences Centre and a Professor of Pathology and Clinical Neurological Sciences at Western University in the Schulich School of Medicine and Dentistry.


Abstract 2 - 0915-0930

Category: Clinical

Presenter: Dr. Alice Graham, McMaster University

Abstract: Brain Toxoplasmosis Comorbid With Autoimmune Disease: Complicated Immune Response And Case Demonstration

Alice Graham 1, Crystal Fong 2, Asghar Naqvi 1, Jian-Qiang Lu 1,3
1 Department of Pathology and Molecular Medicine;
2 Department of Diagnostic Imaging;
3 Neuropathology Section, McMaster University, Hamilton, ON, Canada

Toxoplasmosis is an opportunistic infection caused by Toxoplasma gondii (TG), commonly involving the brain. Symptomatic clinical disease of TG infection is much more commonly associated with immunodeficiency; clinicopathological manifestations of brain toxoplasmosis are linked to individual immune responses including brain infiltration of T-cells that are thought to fight against toxoplasmosis. In patients with autoimmune diseases, immune status is typically characterized by T-cell infiltration, and complicated mainly by immunosuppressant and/or immunomodulatory treatment. In this study, we demonstrate clinical and radiological features correlated with pathological features of brain toxoplasmosis at different disease stages in a patient with coexisting autoimmune diseases, including systemic lupus erythematosus and autoimmune hepatitis. The infiltration of CD8+ T-cells in toxoplasma immunostaining-positive acute lesions was greater than that in toxoplasma immunostaining-negative chronic lesions. We also review previously reported cases of brain toxoplasmosis with comorbid autoimmune diseases. Our present case and literature review suggest that brain toxoplasmosis in patients with autoimmune diseases may be asymptomatic unless disease complications occur; it may present as an incidental finding at postmortem examination of rapidly developed lesions. T-cell infiltration in patients with autoimmune diseases and coexisting toxoplasmosis may be at least partially reduced; ultimately, the roles of T-cell infiltration in brain toxoplasmosis deserve further investigation.

At the end of the session, participants will be able to:

  • Discuss complicated immune response to toxoplasmosis in patients with autoimmune diseases.
  • Describe clinical, radiological, and pathological features of brain toxoplasmosis in patients with autoimmune diseases

Target Audience: Pathologists, Residents

CanMEDS: Medical Expert (the integrating role), Communicator, Collaborator, Health Advocate, Scholar

Speaker Profile: N/A


Abstract 3 - 0930-0945

Category: Clinical

Presenter: Bradley Chaharyn, University of British Columbia

Abstract: Small Vessel Vasculitis In Biopsies Of Anti-mog Encephalitis.

Bradley M. Chaharyn1 and Christopher P. Dunham1
1Division of Neuropathology, University of British Columbia, Vancouver, BC.

We report the neuropathology of two pediatric brain biopsy cases associated with serum anti-myelin oligodendrocyte glycoprotein (MOG) positivity. Descriptions of anti-MOG associated neuropathology are limited, with initial reports describing various patterns of inflammatory demyelination. Our first patient presented with confusion, speech abnormalities and personality changes following a treated strep throat infection. Our second patient had a past medical history of neurofibromatosis type 1 (NF1) and presented with hypersomnolence and focal neurological deficits. MRI abnormalities included diffuse scattered T2 FLAIR hyperintensities +/- enhancement. CSF was positive for anti-MOG antibodies in both cases, while one case exhibited additional anti-NMDA-R antibodies. Brain biopsies revealed vasocentric mononuclear inflammation featuring a predominance of lymphocytes that included intramural forms, as well as diffuse microglial activation, but no evidence of microglial nodules or microorganisms. One case demonstrated mild perivascular demyelination. The prevailing pattern in both cases was suggestive of "small vessel childhood primary angiitis of the central nervous system" (SVcPACNS). Our results parallel recent reports of anti-MOG neuropathology describing small vessel vasculitis, contrary to initial and subsequent reports that describe "encephalitis". The foregoing suggests that the neuropathology associated with serum anti-MOG positivity may be broader than first appreciated. Moreover, this pattern of vasculitis might have implications for the natural history of this nascent disorder.

At the end of the session, participants will be able to:

  • Define anti-MOG encephalitis.
  • Recognize the pathologic spectrum of reported cases of anti-MOG encephalitis.
  • Contrast the pathologic features of pediatric and adult CNS vasculitis.
  • Describe the histologic overlap of vasculitis and encephalitis.

Target Audience: Pathologists, Residents

CanMEDS: Medical Expert (the integrating role), Scholar

Speaker Profile: Dr. Chaharyn is a PGY4 Neuropathology resident at the University of British Columbia in Vancouver, BC, Canada. He received his MD in 2017 from the University of Saskatchewan where he also completed his undergraduate studies in Anatomy and Cell Biology.


Abstract 4 - 0945-1000

Category: Clinical

Presenter: Murad Alturkustani, Division of Neuropathology, London Health Sciences Centre

Abstract: Spectrum Of White Matter Changes In Ischemic Lesions

Murad Alturkustani 1,2, Lee -Cyn Ang 1
1 London Health Sciences Centre, London, ON, Canada
2 King Abdulaziz University, Jeddah, Saudi Arabia

Morphological studies on cerebral ischemia concentrate mainly on the grey matter and white matter changes are regarded as secondary or overlapping injuries. Immunohistochemical (IHC) studies to highlight the combination of various cellular changes in ischemic white matter but have not well documented. We selected 11 archival cases of 3 different ischemic processes (i.e. large vessel occlusion, small vessel occlusion, and hypoperfusion) with survival period range 2-35 days from the ischemic event. The white matter was examined using HE-LFB histochemistry, APP, GFAP, and HLA-DR immunostains focussing on myelin, axonal, astrocytic and microglial changes respectively. The various white matter changes are probably reflective of the different mechanism, duration, severity and extent of ischemia. The APP-IHC shows patchy axonal expression, swelling, and finally complete axonal loss. HLADR-IHC highlights early microglial injuries (fragmentation of processes), complete cell loss, and subsequent replacement by cells of macrophage phenotype. Surrounding the ischemic areas are reactive microglia. Astrocytic changes range from fragmentation of processes (clasmatodendrosis) to different stages of cell loss. Astrocytic swelling tends to occur with cerebral edema. Large vessel occlusion results in complete tissue loss while in small vessel disease the damage is more selective. The injury is generally more subtle in hypoperfusion but can be pronounced focally. Our study has documented the spectrum of white matter injury in different scenarios of cerebral ischemia.

At the end of the session, participants will be able to:

  • Describe the cellular and immunohistochemical changes in the ischemic white matter

Target Audience: Pathologists, Residents, Medical Students

CanMEDS: Medical Expert (the integrating role), Health Advocate, Scholar

Speaker Profile: Neuropathologist in King Abdulaziz University, Jeddah, Saudi Arabia


Abstract 5 – 1000-1015

Category: Clinical

Presenter: Dr David Munoz

Abstract: Relevance of tissue eosinophilia in subdural hematomata

Benjamin Davidson1, Michael Cusimano1, David G. Munoz2
1 Division of Neurosurgery, Department of Surgery, St. Michael's Hospital, University of Toronto, Ontario, Canada.
2Division of Pathology, Department of Laboratory Medicine, St. Michael's Hospital, University of Toronto, Ontario, Canada

Chronic subdural hematomata (CSDH) are treated by evacuation. Recurrence occurs in 3-20% of cases, but the factors determining its occurrence have not been determined. Having observed that eosinophil cell infiltrates are often present in the outer membrane of CSDH, our aim was to determine whether such infiltrates are associated with risk of recurrence. Histological sections of the resections from 72 patients with primary CSDH (Mean age 73.4) and 16 with recurrent CSDH (Mean age 72.1) stained with H&E were graded by blinded observers for eosinophilic cell infiltrates using a semiquantitative 0 to 3 scale. The risk of recurrence requiring reoperation (RrR) in primary CSDH was 11.1%, and 12.5% in recurrent CSDH (meaning third surgery was required). A dense (grades 2 or 3) eosinophilic infiltrate was present in 22.2% of primary CSDH; the RrR was 0% in these cases, as compared with 14.8% in cases with sparse (grades 0-1) eosinophilic infiltrate. Among recurrent CSDH cases, 12.5% (2/15) showed a dense eosinophilic infiltrate; the RrR was also 0%, contrasting with 14.3% in those with sparse eosinophilic infiltrate. We conclude that eosinophils either play a role or are a marker of a process leading to stabilizing CSDH, making them less prone to rebleeding. Abstract not previously published

At the end of the session, participants will be able to:

  • Describe the risk of recurrence following surgical evacuation of chronic subdural hematomata
  • Recognize the variable presence of eosinophils in chronic subdural hematomata
  • Cite the presence of eosinophils is predictive of absence of recurrence

Target Audience: Pathologists, Residents

CanMEDS: Medical Expert (the integrating role), Communicator, Health Advocate, Scholar

Speaker Profile:


Abstract 6 – 1115-1130

Category: Basic Science

Presenter: Professor Gabor Kovacs, University Health Network

Abstract: Subpial Thorn-shaped Astrocytes Are Prevalent In Guam ALS/PDC

GG Kovacs 1, JL Robinson 2, DP Perl 3, VMY Lee 2, JQ Trojanowski 2
1 Laboratory Medicine Program, University Health Network, Toronto, Ontario, Canada
2 Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia, Pennsylvania, USA;
3 Uniformed Services University of the Health Sciences, Bethesda, MD, USA

Guam amyotrophic lateral sclerosis/parkinsonism-dementia complex is a progressive neurodegenerative disorder characterized by neuronal and glial tau pathologies. With the aim to evaluate aging-related tau astrogliopathy (ARTAG) we examined the collection at the University of Pennsylvania, consisting of blocks of the frontal parietal, temporal, and occipital cortices. Formalin fixed, paraffin-embedded tissue blocks were evaluated using anti-tau antibodies PHF-1 and AT8. In addition to neuronal and oligodendroglial tau pathology, granular/fuzzy astrocytes in the gray matter and thorn-shaped astrocytes (TSAs) in subpial location were also observed. Twenty-one out of 33 cases (63%) showed subpial TSAs diffusely along the cortical surface in one or more cortical regions. Accumulation of TSAs in the depth of the sulci were seen in 41% in the temporal, 7% in the frontal and 14% in parietal cortex. This was not associated with perivascular neuronal tau pathology in the depth of the sulci. Accumulation of TSAs in the depth of cortical sulci in this cohort is approximately 20 times more frequent than reported in a European aging cohort. The presence of subpial TSAs in the depth of cortical sulci in CTE and Guam PDC, and less frequently in aging brains, might suggest common mechanisms.

At the end of the session, participants will be able to:

  • Describe the spectrum of neuropathology in Guam ALS/PDC
  • Describe the frequency of tau positive cortical subpial thorn-shaped astrocytes

Target Audience: Pathologists

CanMEDS: Medical Expert (the integrating role)

Speaker Profile:

Dr. Kovacs is Professor in the Department of Laboratory Medicine and Pathobiology at the University of Toronto, a Consultant Neuropathologist at the Laboratory Medicine Program (LMP) at the University Health Network (UHN) and a Principal Investigator at the Tanz Centre for Research in Neurodegenerative Disease.
Dr. Kovacs completed his medical training at the Semmelweis University (Budapest, Hungary) where he specialized in Neurology (1998) and Neuropathology (2003) and obtained a PhD in Neuroscience (2002). From 2004 to 2007, Dr. Kovacs was the Head of the Department of Neuropathology at the National Institute of Psychiatry and Neurology in Budapest, Hungary. From 2007 to 2019, he was an Associate Professor at the Institute of Neurology at the Medical University of Vienna, Austria. He was the leader of the Hungarian (2004-2019) and Austrian (2011-2019) Reference Center for Human Prion Diseases. Dr. Kovacs has also trained at Indiana University (2007) and University of Pennsylvania (2016 and 2017) as a visiting professor/scholar.
His major research interest is the neuropathology of neurodegenerative diseases. He has published more than 290 peer-reviewed papers and edited two books on Neuropathology. Dr. Kovacs's aim is to use his expertise in the neuropathology of neurodegenerative diseases to probe the molecular mechanisms underlying neurodegenerative proteinopathies using state-of the-art methodologies and to facilitate collaborative research.

Conflict of Interest:

  • Receives direct financial payments including receipt of honoraria from Biogen; Consultancy
  • Patents on a drug, product or device: Roboscreen GmbH; Shared patent for 5G4 antibody

Abstract 7 - 1130-1145

Category: Clinical

Presenter: Professor Gabor Kovacs, University Health Network

Abstract: Complex Protein Astrogliopathy In An Octogenarian

GG. Kovacs 1, S. Klotz 2, P. Fischer 3, M. Hinterberger 3, G. Ricken 2, S.Hönigschnabl 3, E. Gelpi 2
1 University Health Network, Toronto, Ontario, Canada.
2 University of Vienna, Vienna, Austria;
3 Danube Hospital Vienna, Vienna, Austria;

Combination of multiple neurodegenerative proteinopathies is frequent in the elderly. We report the case of an octogenarian who attempted suicide and deceased after hospital admission. Anatomical mapping was performed in several cortical and subcortical brain regions using antibodies against phospho-tau, 4R tau, 3R tau, phospho-TDP-43, ubiquitin, -synuclein, A and p62. Unexpectedly, histopathologic examination showed prominent subpial, subependymal, grey and white matter, and perivascular aging-related tau astrogliopathy (ARTAG) widespreadly affecting cortical and subcortical brain regions. This pathology was associated with intermediate Alzheimer's disease neuropathologic change, cerebral amyloid angiopathy, Lewy-body-type and astroglial synuclein proteinopathy and a multiple system TDP-43 proteinopathy involving also the astroglia. This unusual case of extensive and widespread ARTAG with a complex multiproteinopathy may represent an independent disease entity in the elderly with tau astrogliopathy as the leading force.

At the end of the session, participants will be able to:

  • Recognize astroglial protein deposits in neurodegeneration

Target Audience: Pathologists

CanMEDS: Medical Expert (the integrating role)

Speaker Profile: IBID

Conflict of Interest: IBID


Abstract 8 – 1145-1200

Category: Clinical

Presenter: Dr. Shervin Pejhan, Western University

Abstract: Somatotroph Adenoma With Dual Transcription Factor Expression

Shervin Pejhan1, Stan VanUum2, Neil Duggal3, Brian Rotenberg4, Michael Mayich5, Robert Hammond1,3 and Qi Zhang1,3
1 Department of Pathology
2 Department of Medicine (Division of Endocrinology)
3 Department of Clinical Neurological Sciences
4 Department of Otolaryngology
5 Department of Medical Imaging Schulich School of Medicine & Dentistry, Western University, London, Canada

A 20 year old male presented with evidence of gigantism/acromegaly. Endocrinological investigations identified elevated growth hormone levels and a failed glucose tolerance test. Imaging revealed a macroadenoma expanding the sella with encroachment on the optic chiasm and cavernous sinuses. Trans-sphenoidal resection was undertaken and a gross total removal was achieved. Histopathological features were typical of a densely granulated somatotroph adenoma with abundant growth hormone expression, scattered prolactin expression and sparse examples of fibrous bodies. Unexpectedly, the adenoma not only expressed PIT-1 but also SF-1 transcription factors. This finding suggests that the adenoma may have been pluripotent. The prognostic significance of this finding is uncertain although the patient is stable from an endocrinological and imaging perspective approximately one year post-op. A pituitary adenoma of this nature has not been previously reported. The recent literature on atypical transcription factor expression patterns and revisions to the classification of pituitary adenomas will be reviewed.

At the end of the session, participants will be able to:

  • Appreciate the rarity of dual transcription factor expression in pituitary adenomas
  • Rationalize the use of transcription factor characterization in the revised WHO classification of pituitary adenomas

Target Audience: Pathologists, Residents, Medical Students, Medical Laboratory technologists, Graduate students

CanMEDS: Medical Expert (the integrating role), Communicator, Collaborator, Scholar, Professional

Speaker Profile: I am a first year Neuropathology resident at Western University.


Abstract 9 – 1200-1215

Recipient of the 2020 Morris Finlayson Award (Ms. Delaney Cosma)

Category: Basic Science

Presenter: Ms Delaney Cosma, Western University, Schulich School of Medicine & Dentistry

Abstract: Cortical Dysplasia: Teaching Pathology To A Machine

Delaney Cosma1, Ali Khan2 and Robert Hammond1,3
1 Department of Pathology
2 Department of Medical Biophysics
3 Department of Clinical Neurological Sciences Schulich School of Medicine & Dentistry, Western University, London, Canada

Many patients with epilepsy do not achieve adequate pharmacologic control of their seizures and must consider surgical options. Many such patients undergo temporal lobectomy and experience a marked reduction in the frequency and severity of their seizures. However, many are less fortunate. One suspected factor for the latter group is the limited ability of clinical imaging to delineate subtle epileptogenic abnormalities, leading to subtotal resection of lesional tissue. A long range goal in this field is to increase the sensitivity and specificity of detecting such abnormalities by "training" MRI with pathology, feature analysis and machine learning. A key component of this is the ability to segment histopathology to facilitate its mapping to co-registered MRI. A foundational step in this process is to determine whether or not algorithms are capable of detecting the architectural abnormalities in cortical dysplasia on the basis of these segmentations. In brief, reliable semi-automated segmentations were developed to extract a number of features including neuron size, clustering, eccentricity, field-fraction and polarity. Feature analyses using t-Distributed Stochastic Neighbor Embedding (t-SNE) plots demonstrate a non-random association between selected features and diagnostic categories. These results indicate that automated algorithms are capable of distinguishing dysplastic from normal cortex on the basis of semi-automated segmentations.

At the end of the session, participants will be able to:

  • Describe the value of segmentation in image analysis
  • Define the role of feature analysis such as t-SNE in high dimensionality histopathology data

Target Audience:Pathologists, Residents, Medical Students, Medical Laboratory technologists, Graduate students

CanMEDS: Medical Expert (the integrating role), Communicator, Scholar

Speaker Profile: I am a medical student at the Schulich School of Medicine & Dentistry entering my third year (clerkship).


Abstract 10 - 1215-1230

Category: Clinical

Presenter: Werner Paulus, University Hospital Muenster, Muenster.

Abstract: Publishing A High-quality, Non-commercial Neuropathology Journal Without A Publisher: The First Nine Months

Marta Margeta1, Peter Gould2, Lili-Naz Hazrati3, Veronica Hirsch-Reinshagen4 and Werner Paulus5
1 University of California, San Francisco.
2 Hopital de l'Enfant-Jesus/Universite Laval, Quebec.
3 Hospital for Sick Children, Toronto.
4 University of British Columbia, Vancouver.
5 University Hospital Muenster, Muenster.

Scholarly communication faces increasing economical and ethical challenges, including pricing policies and overbearing behavior of commercial publishing houses. Based on the hypothesis that a diamond open access neuropathology journal of a high scientific and technical quality can be run entirely by neuropathologists, we launched Free Neuropathology (FNP; freeneuropathology.org) in January 2020. Classical publisher activities, such as copyediting, layout, website maintenance, and journal promotion, are undertaken by neuropathologists and neuroscientists using free open access software. The journal is free for both readers and authors, and papers are published under a Creative Commons BY SA licence, where copyright remains with the authors. Based on 26 articles published by August 2020, it takes FNP 11.1 days from submission to first, and 19.9 days to final, decision. High-quality copyediting, layout, and online publishing in the final format is accomplished in only 8 days. Absence of a commercial publisher enables prioritization of democratic and scientifically-driven decisions on editorial structure, website design, journal promotion, paper formatting, special article series, and number of accepted papers. This new model of journal publishing, which returns the control of scholarly communication to scientists, will be of interest to neuropathologists and wider scientific community alike.

At the end of the session, participants will be able to:

  • Summarize the current state and driving forces behind commercial and non-commercial scientific publishing in neuropathology
  • Describe the advantages and challenges of a non-commercial publishing platform for neuropathology.

Target Audience: Pathologists, Residents, Medical Students, Neuroscientists

CanMEDS: Communicator, Collaborator, Professional, Scholar

Speaker Profile: N/A

Declaration of Conflict of Interest

  • Investments or relationships that could be seen by a reasonable, well- informed participant as having the potential to influence the content of the educational activity; Free Neuropathology - Unpaid editor