United States

Background:
The posterior femoral cutaneous nerve (PFCN) is a purely sensory nerve arising from the sacral plexus that supplies sensation to the posterior thigh, gluteal fold, and upper medial thigh. Isolated PFCN mononeuropathies are rare, underrecognized, and present with neuropathic pain without motor deficits; very few cases are documented as of 2025. Posterior thigh pain is often misattributed to sciatic or pudendal nerve involvement or musculoskeletal strain, leading to misdiagnosis and ineffective treatment and the deep anatomical location further complicates identification. While peripheral nerve blocks are increasingly used in pain management, selective ultrasound-guided blockade of the PFCN is seldomly reported.

Case Presentation:
A 20-year-old collegiate track athlete presented with persistent right posterior thigh, hip, and gluteal pain following a hamstring strain during sprint training. Despite physical therapy and MRI ruling out musculoskeletal or sciatic nerve pathology, she reported sharp, stabbing pain with numbness radiating to the posterior thigh and gluteal fold. The pain impaired daily activities and prevented her from competing in her track meets. Examination revealed sensory changes along the PFCN distribution without motor weakness. Given the pure sensory distribution, an ultrasound-guided PFCN block was performed using 0.25% Bupivacaine with epinephrine and betamethasone. The patient experienced immediate, near-complete pain relief with no motor deficit, allowing ambulation and return to activity the same day. Within two weeks, she returned to full competition, reaching the state finals. At four-week follow-up, she remained over 90% symptom-free.

Discussion:
This case highlights the therapeutic potential of selectively targeting the PFCN in isolated posterior thigh neuropathic pain. While nerve blocks are well-established for mixed motor-sensory nerves such as the sciatic nerve, there is minimal literature on ultrasound-guided sensory-only blocks for the PFCN. Anatomically, the PFCN lies within the gluteal deep investing fascia (GDIF), medial to the inferior gluteal artery and superficial to the sciatic nerve, which lies deeper and lateral. Accurate identification of this fascial plane is critical. Hydrodissection separates the gluteus maximus from the fascia to safely visualize the PFCN. Advancing too deep risks spread into the sciatic compartment, potentially causing motor blockade. This precise approach enabled the patient to receive a purely sensory blockade without motor compromise to allow her to return to competition. This rare but effective intervention for isolated posterior thigh neuropathic pain emphasizes the need to include PFCN mononeuropathy in the differential for athletes with refractory thigh pain and highlights the role of targeted nerve blocks in restoring function while preserving motor integrity.

AMA Research Challenge 2025 

Cutting the pain, not the power: Posterior Femoral Cutaneous Nerve Block Restores Competitive Drive

Welcome to the largest national, multi-specialty research event **featuring research from 750 medical students, residents and fellows, and international medical graduates.**


#### Event Details
The 2022 American Medical Association Research Challenge includes a poster symposium hall and a semifinals hall with the top scored research. Log in at any time throughout the event to:
* **View posters and presentations** on a variety of topics and specialties
* **Score posters in the semifinals** to help decide the top five finalists (AMA member exclusive opportunity)
* **Connect with participants** and provide feedback to help advance their research

At the conclusion of this event, the AMA will announce the top five finalists who will advance to the AMA Research Challenge finals, present their research to an elite panel of judges and compete to win a $10,000 grand prize sponsored by Laurel Road.
<br>

#### Attend Live Forums
**Oct. 20, 6 — 7 p.m. Central**
<br>**How to plan a career in academic medicine** 
<br>Learn how to plan a career in academic medicine and get your questions answered. [Access Here](https://underline.io/events/363/lounge)
<br>
<br>**Speakers**
![](https://assets.underline.io/uploads/markdown_image/1/image/d5adb133dfc58eb0a6d469e9cedcd5d4.jpg)
Ricardo Correa, MD, EdD
![](https://assets.underline.io/uploads/markdown_image/1/image/5f9437ab87861538bf02b9ca7c0d926e.jpg)
Stuart M. Greenstein, MD
![](https://assets.underline.io/uploads/markdown_image/1/image/05b1b637c99286d558c371f8e8b185ce.jpg)
Stephanie Strohbeen, MD
<br>
<br>**Oct. 22, 11 a.m. — Noon Central**
<br>**How to get published**
<br>Learn tips to get your research published and get your questions answered. [Access Here](https://underline.io/events/363/lounge)
<br>
<br>**Speakers**
![](https://assets.underline.io/uploads/markdown_image/1/image/8ce6235e957d31cb5e6f9097cc6f6972.jpg)
Jessica Li, MD/PhD Candidate
![](https://assets.underline.io/uploads/markdown_image/1/image/9950ef2e0237f54cb3d8280334d42491.jpg)
Charles Lopresto, DO

### Sponsor
AMA would like to thank Laurel Road for sponsoring a $10,000 grand prize for the winner of the AMA Research Challenge. Laurel Road is not involved in the judging or scoring process to select the winner. The winner will be announced on Dec. 7 during the AMA Research Challenge finals. Payment of the grand prize will be directly from Laurel Road. See the AMA Research Challenge Official Rules for terms and conditions.

![](https://assets.underline.io/uploads/markdown_image/1/image/611e331d4a0eba0920f240cfc04b4d77.png)

<br>

**There is no registration fee for this event! **

Register to explore research in a variety of topics. AMA members get exclusive access to score posters in the semifinals.

**Please use the link below to register for free if you have not already done so:**

https://www.ama-assn.org/about/events/ama-research-challenge

Registration Is Required

AMA Research Challenge 2022

Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


poster

Congratulations to all the researchers who have qualified for the AMA Research Challenge virtual poster symposium and semifinals!

Welcome to the **largest national, multi-specialty research event** featuring research from nearly 1,000 medical students, residents, fellows, and international medical graduates across six topic areas - basic science, clinical and translational research, clinical vignettes, health systems science, medical education, and public health and health policy.

#### Access the Event
Use the buttons below or navigation menu to access the event. 

[![](https://assets.underline.io/markdown_image/1/image/d4076f2146939317a29eb9f69c53ad41.png)](https://underline.io/events/506/sessions?searchGroup=all)
[![](https://assets.underline.io/markdown_image/1/image/6bcee0b523a4874c4292ca0415d88dde.png)](https://underline.io/events/506/posters?searchGroup=all)

#### Event Details
The 2025 AMA Research Challenge includes the following symposium halls:
* **Semifinals hall:** Features research from 54 medical students, residents and international medical graduates that received top scores during first round scoring. 
* **Poster symposium hall:** Features research from nearly 1,000 medical students, residents and international medical graduates categorized by topics and subtopics.

**Here’s how to participate:**
* **View posters and presentations** on a variety of topics and specialties
* **Score posters in the semifinals** to help decide the top five finalists (AMA member exclusive opportunity)
* **Connect with presenters** and provide feedback to help advance their research
* **New this year: Watch live poster presentations** by topic area and engage directly with researchers

At the conclusion of this event, the AMA announced the top five finalists who advanced to the AMA Research Challenge final round, presented their research to an elite panel of judges, and competed to win a $10,000 grand prize presented by Laurel Road.

**Addison Shenk, a fourth-year medical student from Edward Via Virginia College of Osteopathic Medicine, was the winner of the 2025 AMA Research Challenge and was awarded the grand prize of $10,000, presented by Laurel Road.**

#### A message from Dr. Bobby Mukkamala, AMA President
<div style="position: relative; width: 100%; padding-bottom: 56.25%; height: 0; overflow: hidden;">
  <iframe 
    src="https://underline.io/embed/136894-ama-video?t=0"
    title="AMA Welcome Video"
    allowfullscreen
    style="position: absolute; top: 0; left: 0; width: 100%; height: 100%; border: 0;">
  </iframe>
</div>


#### Recognized Institutions
In 2025, 1,400 abstracts were submitted across six topic areas representing 174 medical schools and more than 150 residency and health care institutions. [See if your institution is represented this year!](https://drive.google.com/file/d/1eFrTqCmCeobx9pr5drJK2hllvsIpFNOY/view?usp=drive_link)

#### Grand Prize Sponsor
AMA would like to thank Laurel Road, a brand of KeyBank, for sponsoring a $10,000 grand prize for the winner of the AMA Research Challenge. Laurel Road and KeyBank are not involved in winner selection process. The winner will be announced during the AMA Research Challenge final round. Payment of the grand prize will be directly from Laurel Road/KeyBank. See the [AMA Research Challenge Official Rules for terms and conditions](https://www.ama-assn.org/system/files/research-challenge-official-rules.pdf).

[![](https://assets.underline.io/uploads/markdown_image/1/image/611e331d4a0eba0920f240cfc04b4d77.png)](https://www.laurelroad.com/)

#### Code of Conduct
<html>
AMA has a code of conduct for its meetings – we ask all attendees to adhere to this code to participate in this year’s meeting. Please read and <a href="https://www.ama-assn.org/about/code-conduct" target="_blank">learn more here</a> about your conduct requirements.
<br><br>
	</html>
	

#### Semifinals Judges

You need to log in with the email address you registered with. Access credentials have been sent to your email. 

Please be sure to check your spam and other email folders if you do not see an email confirmation right away.

Need help? Contact us at <support@underline.io>.

Please log in to explore this event.

If you have used the AMA Research Challenge platform previously, please click the ‘Log-in’ button below. If you do not remember your password, please click “forgot password” and follow prompts to reset your password. After resetting your password, please refresh your webpage to access the platform. 

Register to explore research in a variety of topics. AMA members get exclusive access to score posters in the semifinals. 

**Please use [this link here](https://www.ama-assn.org/member-benefits/events/ama-research-challenge) to register for free. **

Join the AMA Research Challenge poster symposium and semifinals to explore top research posters and score posters in the semifinals (an AMA member exclusive opportunity).

Background
Delivery of messenger RNA (mRNA) offers potential to ameliorate numerous pathologies by translation of therapeutic proteins. Nevertheless, clinical translation of mRNA technologies has been limited due to a lack of delivery efficiency. Here we describe the development of a novel mRNA delivery system that overcomes barriers faced by existing systems.

Methods
We demonstrate that co-encapsulating gold nanoparticles (AuNPs) and mRNA within non-ionic surfactant vehicles (AuNSVs, termed “Aurniosoves”) improves tumor accumulation and vector uptake into cancer cells. This delivery system was validated through in vitro and in vivo studies with ovarian and hepatocellular carcinoma models utilizing reporter GFP-coding mRNA and therapeutic p53-coding mRNA. The mechanism of action was elucidated through fluorescence-based cellular uptake assays with relevant protein-AuNP interactions identified via pulldown assays.

Results
AuNSVs show improved tumor accumulation, protein expression, and therapeutic efficacy in delivery of p53 mRNA to p53-null cancer cells in comparison to NSV analogs (without AuNPs). Mechanistically, these effects are the result of a nanoengineered “iterative delivery” process in which AuNSVs enter the cell initially through clathrin-mediated endocytosis (CME) and release AuNPs into the cytoplasm. AuNPs subsequently adsorb and inactivate cellular trafficking regulators PP2A and Rab7, producing two primary effects: 1) rapid entry of additional AuNSVs through preferential activation of caveolin-mediated endocytosis (CvME), and 2) endosomal escape through inhibited endo-lysosomal fusion. These two mechanisms combine to drastically increase the delivery efficacy of therapeutic mRNA.

Conclusion
We have made two major advances: 1) nanoengineer a gold nanoparticle (AuNP)-mRNA hybrid therapeutic with translatable characteristics, and 2) improve the therapeutic efficacy of exogenous mRNA in cancer cells using an iterative delivery mechanism. We propose that this class of Aurniosoves and its associated mechanism of action may be exploited as next generation mRNA delivery systems for basic and translational biomedical applications.


Enhancing mRNA Therapy Through Iterative Delivery

Background:
Primary and metastatic brain tumors are clinically refractory to immunotherapies that demonstrate efficacy in peripheral cancer settings. While many immunotherapies aim to enhance effector CD8+ T cell action in established brain tumors, immunopreventative techniques leveraging memory CD8+ T cells remain understudied. Numerically enriched and functionally potent tissue-resident memory (TRM) CD8+ T cells can be generated in the brain following peripheral infection and vaccination. Unlike circulating memory T cells (TCIRCM) that continuously recirculate, TRM embed within the brain, providing local and immediate surveillance against antigenic threats. Our lab has previously shown that the generation of brain TRM can potently protect mice against otherwise lethal intracranial infections. However, the ability of tumor-specific brain TRM to protect against intracranial malignancy remains unknown. 

Methods:
Here, we first developed models where tumor-specific or bystander memory CD8+ T cells were generated in mice via attenuated peripheral infection. We were then able to deplete all tumor-specific TCIRCM using an antibody depletion strategy to isolate the protective action of brain TRM alone. Mice were then challenged with model melanoma or glioblastoma cell lines via orthotopic intracranial injections. To increase the translational value of this work, we later designed and synthesized an mRNA-lipid nanoparticle (LNP) vaccine encoding tumor epitopes or control viral epitopes to determine the immunogenicity and protective action of this emerging immunization strategy. Cellular outcomes were assessed by flow cytometry, tumor burden was surveyed via bioluminescent imaging, and survival outcomes were monitored across time. 

Results:
Here, we demonstrate that tumor-specific, but not bystander, brain TRM durably protected mice against intracranial malignancy even in the absence of TCIRCM. These brain TRM persisted in tumor surviving mice long-term and offered protection against a secondary challenge. Mechanistically, we show that TRM activation reduces brain tumor-associated neuroinflammation and peripheral immunosuppression to enhance survival outcomes. We also demonstrate that mRNA-LNP vaccines generate protective brain TRM upon intramuscular immunization. These vaccine-induced brain TRM abrogated adverse outcomes associated with brain malignancy and neurovirulent disease in an antigen-defined manner. 


Conclusion:
Altogether, this work points to the utility of brain TRM in tumor immunoprevention and supports the development of anti-cancer mRNA vaccines as a non-invasive approach to bolster brain immunity. Ongoing work will determine the therapeutic utility of mRNA vaccine technology against established tumors and will investigate whether protective anti-tumor TRM can be generated at distant organ sites (i.e. brain) after administration. 


Brain-resident memory CD8+ T cells provide durable protection against intracranial malignancy

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


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


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

Abstract Title
Delayed Flap Reconstruction of Bilateral Stage IV Pressure Ulcers in a Pediatric Spinal Cord Injury Patient
Background
Pressure ulcers (PUs) are common and severe complications in patients with spinal cord injury (SCI), particularly among those who are non-ambulatory. Pediatric SCI patients present unique reconstructive challenges, as preserving core muscle function is essential for long-term posture, respiratory support, and mobility. While musculocutaneous flaps are the gold standard for treating advanced PUs, they may result in functional compromise. The use of delayed fasciocutaneous flaps offers a muscle-sparing alternative by enhancing vascularity and increasing flap reliability. This report describes the use of a delayed flap in a pediatric patient with bilateral stage IV PUs following SCI.
Case Presentation
A seven-year-old girl developed paraplegia after sustaining multiple gunshot wounds, resulting in a complete T3 SCI. Over the following year, she developed chronic bilateral stage IV PUs over the anterolateral hips. Despite aggressive wound care, debridement, and prior surgical attempts at an outside hospital, the ulcers failed to heal. Imaging revealed extensive soft tissue loss, anterior compartment necrosis, and osteomyelitis of the right femur. A delayed superficial inferior epigastric artery (SIEA) fasciocutaneous flap was selected for the right hip to preserve muscle function and avoid anterior thigh donor site morbidity. The flap was delayed with a distal skin bridge for four days prior to inset. The left hip was reconstructed using a rectus femoris muscle flap with subsequent skin grafting. Postoperatively, the delayed flap maintained strong Doppler signals and demonstrated healthy granulation and successful graft take. Complications on the left included delayed healing and drainage, requiring further intervention.
Discussion
This case illustrates the utility of delayed flap techniques in complex pediatric PU reconstruction. By enhancing vascularity through the delay phenomenon, the SIEA flap achieved robust perfusion despite the patient’s compromised circulation and prior tissue damage. The muscle-sparing approach preserved essential core function in a growing child with SCI. Traditional muscle flaps were avoided to prevent long-term deficits in posture and mobility. This flap strategy was particularly beneficial given the patient’s anatomical limitations, previous flap exhaustion, and high risk of perfusion compromise with hip flexion. While complications occurred on the contralateral side, the delayed flap healed well, supporting its use as a viable alternative to muscle sacrifice in pediatric SCI patients.


Delayed Flap Reconstruction of Bilateral Stage IV Pressure Ulcers in a Pediatric Spinal Cord Injury Patient

Posterior circulation strokes can present with a range of subtle or fluctuating symptoms, often delaying diagnosis and complicating treatment decisions. We present the case of a 59-year-old woman with a prior history of transient ischemic attack (TIA), ischemic stroke, and antiphospholipid syndrome who was brought to the emergency department with acute dysarthria, vertigo, tinnitus, and vomiting. Imaging was initially unrevealing, but brain MRI confirmed acute infarcts in the superior vermis and right cerebellar hemisphere. Further workup revealed a patent foramen ovale (PFO) and May-Thurner syndrome (MTS), which were suspected contributors to a paradoxical embolic stroke. She underwent successful PFO closure and stent placement for left iliac vein compression. This case highlights the diagnostic challenge of posterior strokes and underscores the importance of considering underlying embolic and structural contributors in cryptogenic stroke presentations.



Posterior Circulation Stroke in a Patient with May-Thurner Syndrome and Patent Foramen Ovale

Background

According to the AMA, the new Pass/Fail STEP 1 “reduc[es] the burden of exam preparation for medical students and creat[es] a more holistic residency-application selection process.” However, following the USMLE Step 1 transition to pass/fail in 2022, students began reporting pressure to accumulate research experience as a way of standing out among other applicants. This project seeks to evaluate the impact of research participation on medical student well-being
as well as student perceptions of the value and utility of their research.

Methods
Our team distributed a survey to medical students that included Likert-Scale questions on research participation, student well-being, perceived value of research, and if they feel pressure to participate in research. Response options included: Strongly Disagree, Disagree, Neither Agree nor Disagree, Agree, Strongly Agree, Not Applicable (do not plan to do research). Inclusion criteria included currently enrolled medical students. We received 122 responses to our survey. Of these respondents, 26 were M-1 year, 63 were M-2 year, 14 were M-3 year, and 22
were M-4 year. The remaining 8 students marked “other” or left that choice blank. Although not every student answered every question, we included all data that we received.


Results
Our data showed that 60% (strongly agree or agree) of students say that research participation has a negative impact on their well-being, with 87% stating that the main reason they are doing research is to help their residency application. With regard to the potential of their research to decrease healthcare costs, 27% answered affirmatively (strongly agree or agree). However, 51% of students believe (strongly agree or agree) that their research can help improve outcomes. In
addition, 38% believe (strongly agree or agree) that it can change treatment guidelines. When asked if students would still participate in research if it had no impact on their ERAS application, 32% said that they would still do research, while 56% answered they would not participate in research, 11% students were unsure if they would still participate.


Conclusion
Results showed that students feel pressure to participate in research, which is adversely affecting the majority of students’ well-being. Further many students are not finding value or utility in the research they do. Our data shows that students are mainly driven to participate in research to strengthen their ERAS application and improve their chance of a successful residency match.

Evaluating the Value and Purpose of Medical Student Research

An Assessment of Service Awareness for the Unhoused Population in San Diego County

Mapping Support: An Assessment of Service Awareness for the Unhoused Population in San Diego County

Background: Eyeglasses may influence children’s self-image and social perceptions, and as animated films are widely consumed by children and caregivers, the way spectacle-wearing characters are portrayed may shape attitudes toward spectacle use. This study aimed to determine common character traits associated with spectacle-wearing characters in animated films across major studios. 

Methods: A comprehensive review of 167 animated films from seven major studios was conducted. Characters who wore corrective eyewear and had at least one line of dialogue were included. Traits were evaluated by five independent reviewers, and statistical comparisons were performed using Fisher’s exact and two-sample proportion tests. 

Results: Among the 167 films, only 39% featured at least one character wearing glasses, totaling 121 characters from 66 films. Glasses-wearing characters were significantly more likely to be supporting (91%) than main characters (9%). Among children with glasses, the most frequent traits were socially awkward (52%) and weak (36%), both significantly more common than in Ó 2025 American Medical Association. All rights reserved. other age groups (p = 0.001 and p = 0.006). In contrast, children with glasses were least likely to be portrayed as mature (8%) or authoritative (8%; p < 0.001 and p = 0.002). Elderly spectacle-wearing characters were significantly more likely to be portrayed as mature (59% vs. 31%; p = 0.026), with a trend toward authority (50% vs. 30%; p = 0.087). Intelligence was a common trait across all age groups (~41%) but did not differ significantly by age (p > 0.8). 

Conclusion: Younger characters with glasses are commonly portrayed as socially awkward and weak, while older spectacle wearers are depicted as mature and authoritative. The relative scarcity and marginalization of glasses-wearing characters in animated films may limit positive identification for children who wear glasses. These age-dependent portrayals may reinforce stereotypes about spectacle wearers and influence how children perceive themselves and others who wear glasses.

Premium content

Downloads

Next from AMA Research Challenge 2025

Enhancing mRNA Therapy Through Iterative Delivery

Similar lecture

Feasibility of Nerve Blocks in Patients Undergoing Embolization Therapy for Vascular Malformations