United States

Background
Decreased levels of gangliosides have been observed in the brain tissue of patients with Parkinson’s (PD) and Huntington’s disease (HD), complex neurodegenerative disorders which currently have no established treatment. Further understanding of the neuroprotective and neurotrophic effects of gangliosides have driven investigation into their pathogenic and clinical role in PD, HD, and other neurodegenerative disorders. Several studies reported the reversal of neurochemical, neurohistological, and clinical signs of PD and HD in animal models after receiving GM1 injections. Additionally, motor symptom improvement was documented in clinical studies of PD patients who received a series of GM1 injections. Although GM1 has shown early clinical promise in PD/HD animal models and PD patients, a comprehensive mechanism for its role in the pathogenesis of these disorders has not yet been elucidated. C. Elegans, a hermaphrodite nematode with easily manipulated genetics, can prove to be a time saving and cost-effective animal model to explore further research on gangliosides and neurodegenerative disorders. 

Methods
C. Elegans N2 Bristol wild-type strain (control), WLZ3 strain transgenic for LRRK2:G2019S mutation (Parkinson’s disease model), and AM101 strain with 40 CAG repeats (Huntington’s disease model) from the Caenorhabditis Genetics Center in Minneapolis, MN. Worms were maintained on NGM plates seeded with E. coli OP50 at 20 °C. Age-synchronized L4 larvae were plated across three replicate plates per condition. GM1 or GM3 was applied to the bacterial lawn at 50uM or 100uM. Control plates received no gangliosides. On day 1 of adulthood, worms underwent 3 hours of heat stress at 35°C. After, worms were documented as alive or dead. This heat stress protocol was repeated until all worms were dead. The survival data was then analyzed using the OASIS 2 Kaplan-Meier log-rank test. 

Results
GM1 altered heat-stress survival in a strain- and dose-dependent manner. GM1 significantly enhanced survival under heat stress in the PD model (WLZ3) at both 50 µM and 100 µM, whereas effects in the HD model (AM101) were modest and limited to 50 µM. In WT worms (N2), GM1 at 50 µM unexpectedly decreased survival. GM3 (50 &amp; 100 µM) showed no significant changes in survival in any strain.

Conclusion
GM1 enhances survival under heat stress in the PD model, with strain- and dose-dependent effects also observed in HD and WT. GM3 shows no survival benefit under these conditions. Results are consistent with prior GM1 neuroprotective literature, particularly in PD, and point to non-linear dose–response and context dependence. Future work in C. elegans should leverage genetic tools, dose mapping, and timing studies to define when and why GM1 is protective. These results support the use of C. elegans as a rapid platform to dissect ganglioside biology in neurodegeneration


AMA Research Challenge 2025 

Effects of Gangliosides on Heat Stress Survival in Caenorhabditis Elegans Models of Huntington’s and Parkinson’s Diseases


Colleagues and Friends:

I am very happy to welcome you to the 14th annual Canadian Neuroscience Meeting, and to the first virtual edition of our meeting. I want to highlight the important work the CAN meeting chair, **Roger Thompson** and co-chair, **Alyson Fournier**, did to put together the great program we are offering this year. Moving to a virtual format required a complete re-design of the program, and both Roger and Alyson did a splendid job in providing us with an appealing and well adapted program for our first virtual event. I wish to thank them for this very important effort.

Highlights of this year’s scientific meeting include invited speakers **Michael Hausser, Franck Polleux, Gwyneth Card, Magdalena Götz**and Brain Prize winner **Huda Zoghbi**. Plenary and parallel symposia, proposed by our members complete our diverse [scientific program.](https://can-acn.org/meeting-2021/program-2021/)

The 2021 Advocacy session, chaired and organized by CAN advocacy committee chair **Karun Singh**, will feature a special lecture and question period with Member of Parliament and past Science Minister **Kirsty Duncan**. This will be followed by a short overview of CAN’s advocacy activities over the last year. We invite you to participate in this session for insight from Dr. Duncan on the workings of Parliament Hill, and to learn more about what CAN has been doing to promote neuroscience research in Canada.

We are also excited to host **Lisa Willis** in the Equity Diversity and Inclusion session, organized by EDI committee chair **Jibran Khokhar**.

A special highlight of our meeting will be the lectures by award-winning young neuroscientists. We are please to host the CAN 2020 Young Investigator Award winner **Mihaela Iordanova**, and CAN 2021 Young Investigator Award winners **Aaron Phillips** and **Tabrez Siddiqui**. Highlights will also include presentation by the top three winners of the CAN-CIHR-INMHA Brain Star Award winners, **Claire Gizowski, Nuria Daviu Abant** and **Lukas Tamayo-Orrego**.

Independently organized satellite symposia complement and complete this exciting program, check them out here: https://can-acn.org/meeting-2021/2021-satellite-symposia/

Some of the most engaging sessions are always the poster sessions featuring the work of our trainees, so make sure to log in to Gather Town during the poster sessions to chat with the presenters.
We hope you enjoy this program, and look forward to welcoming you, virtually.

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Please head to https://can-acn.org/meeting-2021/registration-2021/ to register. 

CAN-ACN 2021

14th Canadian Neuroscience Meeting from August 23rd-25th

Background
Decreased levels of gangliosides have been observed in the brain tissue of patients with Parkinson’s (PD) and Huntington’s disease (HD), complex neurodegenerative disorders which currently have no established treatment. Further understanding of the neuroprotective and neurotrophic effects of gangliosides have driven investigation into their pathogenic and clinical role in PD, HD, and other neurodegenerative disorders. Several studies reported the reversal of neurochemical, neurohistological, and clinical signs of PD and HD in animal models after receiving GM1 injections. Additionally, motor symptom improvement was documented in clinical studies of PD patients who received a series of GM1 injections. Although GM1 has shown early clinical promise in PD/HD animal models and PD patients, a comprehensive mechanism for its role in the pathogenesis of these disorders has not yet been elucidated. C. Elegans, a hermaphrodite nematode with easily manipulated genetics, can prove to be a time saving and cost-effective animal model to explore further research on gangliosides and neurodegenerative disorders. 

Methods
C. Elegans N2 Bristol wild-type strain (control), WLZ3 strain transgenic for LRRK2:G2019S mutation (Parkinson’s disease model), and AM101 strain with 40 CAG repeats (Huntington’s disease model) from the Caenorhabditis Genetics Center in Minneapolis, MN. Worms were maintained on NGM plates seeded with E. coli OP50 at 20 °C. Age-synchronized L4 larvae were plated across three replicate plates per condition. GM1 or GM3 was applied to the bacterial lawn at 50uM or 100uM. Control plates received no gangliosides. On day 1 of adulthood, worms underwent 3 hours of heat stress at 35°C. After, worms were documented as alive or dead. This heat stress protocol was repeated until all worms were dead. The survival data was then analyzed using the OASIS 2 Kaplan-Meier log-rank test. 

Results
GM1 altered heat-stress survival in a strain- and dose-dependent manner. GM1 significantly enhanced survival under heat stress in the PD model (WLZ3) at both 50 µM and 100 µM, whereas effects in the HD model (AM101) were modest and limited to 50 µM. In WT worms (N2), GM1 at 50 µM unexpectedly decreased survival. GM3 (50 & 100 µM) showed no significant changes in survival in any strain.

Conclusion
GM1 enhances survival under heat stress in the PD model, with strain- and dose-dependent effects also observed in HD and WT. GM3 shows no survival benefit under these conditions. Results are consistent with prior GM1 neuroprotective literature, particularly in PD, and point to non-linear dose–response and context dependence. Future work in C. elegans should leverage genetic tools, dose mapping, and timing studies to define when and why GM1 is protective. These results support the use of C. elegans as a rapid platform to dissect ganglioside biology in neurodegeneration


poster

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Background: The rising prevalence of metabolic syndrome (MetS) is linked to modern lifestyle factors, including disruptions to circadian rhythms. These endogenous 24-hour cycles regulate key physiological processes, and their disruption through factors like irregular sleep patterns or late meal timing is increasingly common. MetS is characterized by chronic inflammation, often exacerbated by gut-derived inflammation from a compromised intestinal barrier. We hypothesized that the link between circadian disruption and MetS is mediated by alterations in the gut microbiome and subsequent gut barrier dysfunction. This study investigates this proposed mechanistic pathway in an at-risk obese population.

Methods: This secondary analysis used data from a trial of 87 obese adults. MetS was scored using NCEP-ATP III criteria. Circadian phenotypes were assessed using the Munich Chronotype Questionnaire (central) and a Food Timing Screener (peripheral). Intestinal permeability was measured via urinary excretion of sugar probes. Using a multi-omics approach, we developed a continuous Metabolic-Inflammatory (MI) score to capture underlying dysregulation. A moderated sequential mediation analysis tested the hypothesis that the gut microbiome and barrier function mediate the relationship between circadian disruption and the MI score.

Results: After adjustments, a late chronotype was associated with a 4.20-fold increased odds of having MetS (95% CI: 1.33–13.27, p=0.014). A graded association was observed where a greater degree of combined circadian disruption (late chronotype and late eating) was associated with a progressively higher prevalence of MetS. Late eating (after 8 PM) was linked to significantly increased small bowel and colonic permeability, evidenced by higher urinary mannitol (p=0.037) and sucralose (p=0.013). A 19-feature multi-omic signature strongly predicted MetS status (R²=0.71), forming a continuous MI score. This MI score increased with greater circadian disruption and was strongly correlated with markers of gut permeability (24h mannitol, R²=0.65). Crucially, mediation analysis demonstrated that the effect of circadian disruption on the MI score was significantly mediated by gut barrier dysfunction. A final sequential model confirmed this mechanism, identifying a pathway where circadian disruption alters specific gut microbes, which in turn impacts gut permeability, ultimately driving metabolic and inflammatory dysregulation.

Conclusion: Circadian disruption is strongly associated with metabolic dysregulation in obese individuals. Our findings provide evidence for a novel mechanistic pathway where misaligned circadian behaviors influence the gut microbiome, leading to increased intestinal permeability and subsequent systemic inflammation. This highlights the circadian-microbiome-gut axis as a key mediator and a potential therapeutic target for mitigating the adverse metabolic consequences of circadian disruption.



Assessing the Contribution of Circadian Misalignment and Gut Dysfunction to Metabolic Syndrome

Background 

The modified frailty index (mFI-5) is a National Surgical Quality Improvement Program (NSQIP)-derived 5-factor index that has been validated as a reliable measure of frailty. mFI-5 has demonstrated utility in predicting postoperative complications and mortality following various otolaryngologic procedures, including skull base surgery, laryngectomies, composite resections, and transoral robotic surgery. Cochlear implantation (CI) has become an increasingly common intervention for restoring auditory function, particularly as the aging population grows and the prevalence of hearing loss rises significantly with age. However, the predictive role of frailty in postoperative complications of CI remain unclear. Thus, we evaluated whether the mFI-5 is predictive of complications following CI surgery. 

Methods 

We used a multicenter national database within the TriNetX US Collaborative Network. Patients aged 18 or older who underwent CI between June 2005 and June 2025 were included (N=33,556). Patients were categorized based on their mFI-5 scores (0 to 5, with higher scores indicating increased frailty). mFI-5 criteria included: heart failure, chronic obstructive pulmonary disease, hypertension, diabetes mellitus, and non-independent functional status. Comparative analyses were conducted between patients with mFI-5 scores >0 vs. those with mFI-5 = 0. Cohorts were propensity score-matched by age, gender, race, and ethnicity. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated 6 months post-CI for mortality, major complications (prolonged intubation, sepsis, thrombophlebitis, pulmonary embolism, cerebrovascular accident, surgical site infection, acute kidney injury, pneumonia), minor complications (blood transfusion, urinary tract infection), and otologic complications (facial nerve injury, vertigo, fall, labyrinthitis, tympanic membrane perforation, otitis, device displacement/revision/removal). 

Results 

Among 33,556 patients who underwent CI, 11,585 were identified as non-frail (mFI-5 = 0, 34.5%), 4,666 were identified as pre-frail (mFI-5 = 1, 13.9%), 2,445 were identified as frail (mFI-5 =2, 7.3%), and 1,116 were identified as severely frail (mFI-5 ≥ 3, 3.3%)after matching. Compared to non-frail, pre-frail patients had significantly increased risk of mortality (OR = 2.00, 95% CI: 1.08-3.70), major complications (OR 2.27, 95% CI: 1.64-3.23), minor complications (OR 2.38, 95% CI: 1.39-4.17). Similarly, frail patients had increased risk of mortality and major and minor complications compared to non-frail patients. There were no significant differences in otologic complications among non-frail, pre-frail, and frail patients. When comparing non-frail patients and severely-frail patients, severely-frail patients had significantly increased risk of mortality and major, minor, and otologic complications (OR 2.86, 95% CI: 1.67-5.00). 

Conclusion 

The mFI-5 may serve as a useful tool in preoperative counseling to help inform patients about potential outcomes following CI.

The Modified Frailty Index-5 Predicts Postoperative Complications Following Cochlear Implantation: A Propensity Score-Matched Cohort Study

Background:
Musculoskeletal infections are challenging to diagnose and treat in the elderly. Comorbidities make older patients more susceptible to infection with atypical pathogens. Here, we report a rare case of necrotizing fasciitis, septic bursitis, and osteomyelitis due to co-infection with Mycobacterium avium-intracellulare (MAI) and coagulase-negative Staphylococcus (CoNS). A broader diagnostic approach is warranted in patients with specific characteristics or risk factors for atypical infection or lack of response to standard treatment. 

Case Presentation:
We describe a 90-year-old male who presented to the emergency department with a threeday history of progressive swelling, erythema, and pain localized to the left elbow, associated with restricted joint movement. His medical history was significant for diabetes mellitus, hypertension, interstitial lung disease, heart failure, and chronic kidney disease. Clinical examination, laboratory and imaging findings revealed the presence of osteomyelitis, olecranon bursitis, and forearm fasciitis. Following surgical debridement of necrotic tissue, cultures revealed growth of CoNS after 48 hours. Postoperatively, the patient was treated with intravenous antibiotics. However, after brief improvement, the patient developed fever and altered mentation necessitating transfer to the ICU. No clear cause for the clinical deterioration was found until postoperative day # 10 when tissue cultures from the debridement yielded the growth of MAI. No evidence of disseminated MAI was found. After the antibiotic regimen was modified to include azithromycin and ethambutol, the patient showed significant clinical improvement and was discharged. 

Discussion:
This case highlights the diagnostic challenges associated with atypical infections in elderly patients. Early diagnosis and treatment are imperative but the slow growth of atypical pathogens like MAI can lead to delayed diagnoses. In our case, although a timely diagnosis of necrotizing fasciitis led to debridement of necrotic tissue, antibiotic therapy was initially directed towards typical bacterial pathogens. However, the cultured pathogens – CoNS and MAI – were unusual. CoNS is a known, albeit uncommon, cause of necrotizing fasciitis, but MAI has never been reported as a causative agent. MAI typically affects the lungs or lymphatic system, making its presence in skin and soft tissue infections an unusual and important finding, especially in the absence of disseminated disease. Delayed diagnosis underscores the need for early use of AFB staining and broader microbiological workups when treating persistent or atypical infections. Timely surgical intervention combined with tailored antimicrobial therapy resulted in clinical improvement in this patient thereby reinforcing the significance of maintaining a high index of suspicion for atypical organisms in elderly patients.

Unlikely Culprits: Necrotizing Fasciitis Caused By Mycobacterium-Avium Intracellulare and Coagulase-Negative Staphylococci in a Geriatric Patient


From Benign to Critical: Acute Idiopathic Pericarditis Complicated by Delayed Cardiac Tamponade 

Background 

Pericarditis is a common diagnosis comprising around five percent of patients presenting with non-ischemic chest pain and 0.1-0.2 % of hospitalizations. It is usually idiopathic and often presents as a mild disease resolving on its own or with 
minimum treatment. 

Pericarditis is frequently accompanied by small pericardial effusions. A less common life-threatening event that can be associated with it is cardiac tamponade (CT). In the case of acute idiopathic pericarditis, CT is only seen in around 1.2 % of 
cases. 

CT is a medical emergency and its prompt diagnosis and treatment is crucial to avoid fatal complications including death. In this report we present a case of acute idiopathic pericarditis with associated CT. 

Case Presentation 

A 43 year-old male was evaluated in the emergency department for chest pain. On admission, a normal chest x-ray, EKG reflecting acute pericarditis, elevated D-dimer and CRP, normal troponin, normal ESR, and echocardiogram showing a small pericardial effusion were noted. He was started on Colchicine and Ibuprofen, monitored overnight, then discharged the following day on Colchicine for three months. 

Six days later, he presented with worsening chest pain, shortness of breath, hypotension, and heart palpitations. Echocardiogram showed diastolic compression of the right ventricle with a circumferential pericardial effusion confirming the 
diagnosis of CT. He underwent an emergent pericardial window and left thoracotomy. Fluid analysis confirmed exudative effusion. Cultures did not grow any organisms. 

After recovering, he was discharged with a one month supply of Prednisone and Colchicine. 

Discussion 

Patients with acute pericarditis present with a myriad of symptoms that distinguish it from other cardiovascular diseases. The most common abnormality reported on echocardiograms are small pericardial effusions. Hemodynamically significant 
pericardial effusions, especially those causing tamponade are rare. 

Other findings include leukocytosis, elevated ESR and C-reactive proteins. The combined presence of effusion and elevated C-reactive protein has been associated with an increased risk of recurrence and complications. 

Our patient initially presented with both of these signs; however, he was discharged without further workup. 

Patients with evidence of large and symptomatic effusions and those causing tamponade should undergo pericardiocentesis, pericardial window or placement of chest tube to avoid cardiovascular collapse. High risk features including fever, evidence of cardiac tamponade, failure to clinically improve after receiving at least 7 days of therapy with colchicine and NSAID, trauma, among others should prompt a hospital admission and possible emergent intervention. On the second admission, these features were recognized and treated. 



From Benign to Critical: Acute Idiopathic Pericarditis Complicated by Delayed Cardiac Tamponade

Background
Pustular psoriasis (PP) is a rare cutaneous disorder of autoimmune origin. Little information is available about the possible triggers, causes, treatment and pathophysiology. A hypothesized etiology includes mutations in the genes coding for IL36RN, CARD12 and AP1S3. PP is thought of as a broader category for three dermatoses: generalized pustular psoriasis (GPP), palmoplantar psoriasis, and acrodermatitis continua of Hallopeau. GPP is a systemic disease consisting of yellowish pustules on an erythematous base appearing on
the skin. The pustules can present to localized regions of the body, or can be widespread showing a predominant neutrophilic infiltrate pattern.
Since GPP is an uncommon disease, it is important to raise its awareness among clinicians to help aid in the diagnosis and care strategies.

Case Presentation
A 59 year-old male with a past medical history of untreated GPP was evaluated for an eczematous purulent lesion. The patient had associated trauma from a beach umbrella wire just prior to his initial symptoms. On admission, multiple scattered pink plaques with overlying thick brown crust and scaling on his bilateral thighs, knees, forearms, and abdomen were observed. Nuclear medicine bone scan showed cellulitis above the left forearm with no evidence of osteomyelitis. CT of left arm showed diffuse subcutaneous soft tissue swelling, dorsal subcutaneous emphysema and skin thickening. The infected tissue was debrided with lateral and medial fasciotomies performed on the forearm. Empiric antibiotic treatment was started. Wound cultures grew pseudomonas aeruginosa. The rash was treated daily with chlorhexidine wash and mupirocin ointment. After improvement he was discharged on oral ciprofloxacin.

Discussion
This case describes a patient experiencing the generalized variant of PP (GPP), which is considered to be the most severe type of psoriasis. It presents with a sudden onset of rapidly expanding aseptic pustules as seen in our patient.
Overall, the extent of each flare varies, with some patients experiencing the characteristic GPP rash and others requiring hospitalization.
Triggering factors include infections, pregnancy, medications, vaccines, electrolytes imbalances, stress and corticosteroid treatment withdrawal. In our patient, possible triggers may have been from poor hygiene, working in the sun, and
exposure to pathogens from the pool and beach sand from a penetrating wound.
There are no specific treatment guidelines for GPP; however, there is a focus on early identification and removal of specific triggers. Topical steroids, phototherapy, and vitamin D derivatives have also been recommended. For acute flares, cyclosporin, acitretin and biologics have also been reported as effective management.

A Costly Flare: Unmanaged Pustular Psoriasis Leading to a Severe Soft Tissue Infection

Abstract Title 

Guillain-Barré Syndrome Following Anti-CD19 CAR-T Therapy in a Patient with Relapsed DLBCL 

Background 

Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS) is a well-recognized complication of chimeric antigen receptor T-cell (CAR-T) therapy related to cytokine-mediated blood-brain barrier disruption presenting as encephalopathy. In contrast, Guillain-Barré syndrome (GBS), an acute, immune-mediated peripheral demyelinating process is characterized by symmetric ascending weakness and hyporeflexia, and is rarely reported following CAR-T therapy. ICANS is managed with corticosteroids, while GBS requires intravenous immunoglobulins (IVIG) or plasmapheresis. Concurrent presentations pose diagnostic and therapeutic challenges. 



Case Presentation 

A 64-year-old male with relapsed diffuse large B-cell lymphoma received CAR T-cell therapy. On day 10, he experienced sudden lower extremity weakness and collapsed while walking. Exam revealed proximal upper extremity and hip flexor weakness (4/5) with intact reflexes and sensation. By day 12, he was encephalopathic (Immune Effector Cell-Associated Encephalopathy score [ICE] 8/10), hypotensive (BP 77/62 mmHg), hypoxic (SpO₂ 83%), and febrile. He received IV dexamethasone 10mg and tocilizumab for grade 2 CRS. Brain MRI was normal. By day 15, his mentation worsened (ICE 2/10), with intermittent apnea, diminished gag reflex, and impaired secretion clearance, prompting intubation. High-dose methylprednisolone (250 mg IV q6h) and anakinra were initiated for ICANS management. On day 18, he was minimally responsive (ICE 0–1/10). He also developed progressive symmetric weakness, flaccid tone, diminished reflexes and positive Babinski sign. Imaging remained unchanged. An electroencephalogram showed no seizures. Cerebrospinal fluid analysis revealed protein 110 mg/dL, WBC 7, negative for infection, malignancy, and autoimmune encephalopathy. Electrodiagnostic studies demonstrated reduced CMAP and SNAP amplitude. The evolving weakness, preserved sensation, albuminocytologic dissociation, and electrophysiologic findings supported a diagnosis of GBS. Due to lack of response to ICANS therapy, IVIG (0.4 g/kg/day for 5 days) was initiated on day 29 along with seven sessions of plasmapheresis. He remained encephalopathic, although with gradual neurological recovery – eye tracking, tongue movement, and light motor responses. He was discharged to a long-term acute care and was eventually weaned off ventilator support. 

Discussion: 

This case highlights the rare presentation of GBS following CAR T-cell therapy which is a distinct entity from the more commonly occurring ICANS. The patient’s early proximal weakness was atypical for ICANS and suggested peripheral involvement. Though ICANS co-occurred and progressed, concurrent GBS manifested as progressive flaccid paralysis with reduced CMAP/SNAP amplitudes and albuminocytologic dissociation. Early distinction between ICANS and GBS is crucial, as treatments differ significantly. Overlapping features delayed diagnosis and increased morbidity. Further research is needed to understand mechanisms and improve diagnostic strategies for atypical neurotoxicity following CAR-T.

Guillain-Barré Syndrome Following Anti-CD19 CAR-T Therapy in a Patient with Relapsed DLBCL

Background
A massive brain abscess caused by otogenic Klebsiella pneumoniae is a neurological emergency in the United States and worldwide. We present a rare case of an otogenic massive brain abscess caused by Klebsiella pneumoniae to guide clinicians in establishing a prompt diagnosis and preventing significant morbidity and mortality.
Case Presentation
A 23-year-old male with a past medical history of uncontrolled type 1 diabetes and a recent presentation for otitis media was brought to the emergency department unresponsive. On initial examination, he was non-verbal, showed abnormal posturing to painful stimuli, and had a purulent, pinkish discharge from his left ear. He was found to be in Diabetic ketoacidosis. CT Head without contrast revealed a 5.8 cm x 4.9 cm left temporoparietal lobe abscess with significant edema, a 1.4 cm midline shift and extensive left-sided mastoiditis. Blood culture revealed Rhodotorula mucilaginosa and Aureobasidium. An emergent craniotomy evacuated 120 mL of purulent material, which grew otogenic Klebsiella pneumonia. Due to rapid pathogen identification, patient's condition stabilized with drainage of abscess, antibiotics, and comprehensive management.
Discussion
Otogenic Klebsiella pneumoniae is rarely considered as a cause of brain abscesses. A report from the Centers for Disease Control and Prevention identified only one case of Klebsiella pneumoniae as a cause of pediatric brain abscess between January 2016 and August 2022. Due to its rarity, the CDC's Active Bacterial Core surveillance system, which tracks invasive bacterial diseases, does not currently include Klebsiella pneumoniae. However, a massive brain abscess can be caused by otogenic Klebsiella pneumoniae in patients with diabetic ketoacidosis or any immunocompromised states, leading to high morbidity and mortality. 
Conclusion
This case report underscores the importance of including Klebsiella pneumoniae in the differential diagnosis of otogenic brain abscess, especially in the setting of DKA or other immunocompromised states. Early neuroimaging, prompt surgical intervention, and targeted antimicrobial therapy are critical for improving outcomes in these life-threatening infections. Clinicians should maintain a high index of suspicion for atypical pathogens to reduce diagnostic delays and prevent severe neurological sequelae.



Massive Brain Abscess Caused by Otogenic Klebsiella pneumoniae in a Young Adult with Diabetic Ketoacidosis

Background:
Tumefactive multiple sclerosis (TMS) is a rare and diagnostically challenging variant of multiple sclerosis characterized by large demyelinating brain lesions that mimic neoplasm, abscess, or ischemic stroke. Representing less than 3 per 1,000 MS cases, TMS often presents with focal neurological deficits and mass-like imaging findings that can delay diagnosis and treatment.
Case Presentation:
A 24-year-old woman with anemia presented with two weeks of left facial droop, bilateral hand paresthesias, blurry vision, and mild dysphagia. Without prior neurological history, her initial non-contrast head CT revealed subcortical hypodensities in the right frontal and left temporal lobes, prompting a stroke workup. Her recent prolonged travel and echocardiogram-confirmed patent foramen ovale raised suspicion for paradoxical embolic stroke. However, MRA/MRV, hypercoagulable labs, and extensive malignancy screening including CT chest/abdomen/pelvis were all unremarkable.
MRI brain demonstrated T2 hyperintense, incomplete ring-enhancing lesions with vasogenic edema, concerning for tumefactive demyelination versus neoplasm. MR spectroscopy was nonspecific. Lumbar puncture showed 10 isolated CSF oligoclonal bands (OCBs), confirming a diagnosis of multiple sclerosis. Remarkably, the patient’s facial droop resolved spontaneously without corticosteroid treatment, and she was discharged neurologically intact with outpatient neurology follow-up.
Discussion:
This case highlights the profound diagnostic complexity of TMS, a condition that challenges even experienced clinicians due to its ability to mimic stroke, malignancy, or abscess, both clinically and radiographically. The patient’s initial imaging findings were highly suggestive of ischemic stroke and as in many TMS cases, the early workup prioritized life-threatening differentials, delaying the eventual diagnosis.
Pathophysiologically, tumefactive demyelination involves mass-like inflammatory demyelination with associated edema, blood-brain barrier disruption, and axonal injury, leading to imaging findings that overlap significantly with high-grade gliomas and abscesses. The hallmark incomplete/open-ring enhancement on MRI, alongside vasogenic edema and CSF oligoclonal bands, is critical to distinguishing TMS. However, OCBs are detected in 30-80% of tumefactive demyelination cases, and this variability frequently prompts unnecessary biopsies amid diagnostic uncertainty.
This case is particularly notable because the patient’s neurological deficits resolved spontaneously without corticosteroid therapy, which is highly atypical in MS where deficits typically worsen or persist without treatment. This unusual self-limited course underscores the heterogeneity of TMS presentations and the diagnostic confusion it creates.
While TMS is not a newly recognized condition, its broad clinical and radiographic variability continues to challenge timely diagnosis. Case reports such as this are essential, not for novelty, but to build a clearer and more complete picture of this rare MS subtype and improve diagnostic accuracy across disciplines.

The Great Neurologic Imposter: Tumefactive Multiple Sclerosis Mimicking Stroke, Neoplasm And Everything In Between

Background
Synovial sarcoma is a rare malignant mesenchymal tumor typically arising in the
extremities of young adults. Primary pulmonary synovial sarcoma is exceedingly rare, and recurrence within the female reproductive tract has not been previously described in the literature.

Case Presentation
A 53-year-old woman with a history of primary pulmonary synovial sarcoma presented with abnormal uterine bleeding. Pelvic ultrasound demonstrated a vascular endometrial mass protruding through the external cervical os. Histopathologic analysis following dilation and curettage identified a spindle cell neoplasm consistent with synovial sarcoma, confirmed by molecular studies and reviewed at both Brigham and Women’s Hospital and Cleveland
Clinic. There was no radiographic evidence of disease elsewhere. The patient has
undergone dilation and curettage, and further surgical management including
hysterectomy is under consideration.

Histopathologic Comparison:
The patient's original pulmonary tumor measured 7.1 cm, was poorly differentiated, and showed strong immunohistochemical positivity for SS18::SSX and SSX C terminal antibodies. Cytogenetic testing confirmed a chromosomal translocation (BS-22 E06488). It was negative for Cam5.2, MYF-4, NKX2.2, LCA, STAT6, and BCOR. The gynecologic recurrence demonstrated strong nuclear SS18::SSX positivity, as well as CD99, ER, PR, WT1, vimentin, and β-catenin. Focal positivity was also seen for desmin, CD10, and p53. Notably, PAX8, p16, pancytokeratin, and SMA were negative. The molecular and histologic profiles mirrored the original pulmonary tumor, confirming recurrence. 

Discussion
This case represents a unique gynecologic recurrence of a previously pulmonary
synovial sarcoma, a presentation not previously documented. The unusual metastatic pattern raises important considerations about the natural history and surveillance strategies of rare sarcomas in women. The endometrial location, protrusion through the cervical os, and lack of disease elsewhere suggest hematogenous spread, challenging assumptions about recurrence sites and routes. Although rare, this case emphasizes the role of tissue confirmation in patients with abnormal uterine bleeding and oncologic history—even when imaging findings suggest a benign etiology. This report underscores the importance of maintaining a broad differential diagnosis in patients with prior rare malignancies and highlights the need for individualized surveillance strategies. Awareness of atypical recurrence patterns may facilitate earlier diagnosis and improve outcomes in similar future cases. The findings further support cross-disciplinary collaboration in complex oncologic presentations, particularly when involving rare tumor biology and metastatic behavior.


Rare Gynecologic Recurrence of Pulmonary Synovial Sarcoma: A Case Report and Literature Review

Abstract Title: More Than Skin Deep: Mental Health and Skin Disease Among People Experiencing Homelessness

Background: People experiencing homelessness (PEH) face a wide range of health disparities, with skin conditions among the most visible and commonly reported concerns. Chronic or untreated dermatologic conditions (eczema, psoriasis, acne, infections, scarring, etc.) can be painful, stigmatizing, and challenging to manage without stable housing, hygiene access, or continuity of medical care. Emerging research highlights the strong link between dermatologic disease and mental health conditions such as depression, anxiety, and social withdrawal. Yet, these psychosocial impacts are often underrecognized among PEH, who face additional barriers to care. At Haven for Hope, a student-run dermatology clinic, we serve PEH with skin conditions. This project aimed to assess the perceived mental health effects of skin disease among PEH to inform integrated care approaches.

Methods: An anonymous paper survey was distributed to Haven for Hope Skin Clinic patients, with a Spanish and English version available. The survey included questions on embarrassment, stigma, and social avoidance, along with validated mental health screening items from the PHQ-2 assessing anhedonia and anxiety symptoms. Patients were also asked whether they desired mental health support. Data collection is ongoing. This study was deemed IRB-exempt.

Results: 22 patients have responded thus far. Nearly one-third (29.4%) reported feeling “a lot” of embarrassment about their skin condition, and 55% reported anxiety related to their skin at least several days in the past two weeks. Over half (52.9%) reported decreased interest or pleasure in activities, a core PHQ-2 symptom, at least several days during the same period. While 35.3% reported avoiding others because of their skin, most (70.6%) did not perceive external stigma.

Conclusion: 
Preliminary findings show a significant psychosocial burden of skin disease among PEH, with high rates of anxiety and anhedonia. These results emphasize the need for brief mental health screening in dermatology clinics serving PEH. Continued data collection will guide integration of mental health assessments into dermatologic care, supporting a more holistic approach for PEH.

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