clinical case study ppt template

Newly Launched - AI Presentation Maker

Researched by Consultants from Top-Tier Management Companies

AI PPT Maker

Powerpoint Templates

Icon Bundle

Kpi Dashboard

Professional

Business Plans

Swot Analysis

Gantt Chart

Business Proposal

Marketing Plan

Project Management

Business Case

Business Model

Cyber Security

Business PPT

Digital Marketing

Digital Transformation

Human Resources

Product Management

Artificial Intelligence

Company Profile

Acknowledgement PPT

PPT Presentation

Reports Brochures

One Page Pitch

Interview PPT

All Categories

Top 7 Medical Case Presentation Templates with Samples and Examples

Sarojit Hazra

How does information expand beyond essential recollection? Facts alone can diminish in value over time. Context and implementation are crucial to form deep connections and roots. Here comes the role of case studies for clinical personnel in the medical field.

In the always-growing healthcare industry, medical case presentation is essential as it is a suggestion for new researchers. A medical case study is a report where a medical practitioner shares a patient's case. It comprises every detail related to patients. It is beneficial for describing a new medical condition, management options, or treatment for diseases.

Medical case presentations contribute significantly to the evolution of medical knowledge and research.

Case study analysis is essential for every business or industry, like the medical industry. It helps in managing the twists and turns of the industry. Want to take some ideas? Have a look at SlideTeam’s blog Case Analysis Templates .

Let us highlight some significant benefits of medical case presentation:

• Case study presentations are extremely good at depicting realistic clinical frameworks.
• It helps to enhance student participation alongside the joy of learning.
• These are ideal for sharing the latest information on the clinical landscape.
• It promotes critical thinking.
• It can also make better clinical outcomes.

If you are in the healthcare sector, another important tool is the medical dashboard. For a deeper insight, quickly take a look at Medical dashboard Templates .

Each of the slides is 100% editable and customizable. The 100% customizable nature of the templates allows you to edit your presentations. The content-ready slides give you the much-needed structure. Below, let’s explore a wide array of ready to use, content ready medical case presentation templates fit for your organization.

Template 1: Case Study on Blockchain Application in Healthcare: Medical Staff Credential Verification

Blockchain is becoming a potential solution to verify medical credentials. Though these are open to the public, they can be restricted through permissions. Are you finding it difficult to understand and implement? SlideTeam introduces this PPT Template that highlights how to operationalize medical staff verification process using blockchain technology. It explains that healthcare-based systems can also be used to verify the credentials of medical staff. Solutions-based blockchain to track the experiences of medical professionals. The PPT slides are designed with suitable icons, designs, graphs and other relevant material. Grab it quickly and draft your case study as per the client’s requirements.

Click to Download

Template 2: Cost Benefits IOT Digital Twins Implementation Use Cases in the Medical Domain

This PPT template is designed to focus on the use cases in the medical domain, including research and development, diagnosis, surgery, medical equipment, etc. The slide offers a brief description of the mentioned use cases to understand the scenario better. Use it as an essential tool and captivate your audience. Get it Now!

Template 3: Major Use Cases for Tracking Medical Assets Asset Tracking and Management IoT 

Want to simplify medical complexities? The asset tracking solution is here to accompany you. It enables the medical sector to locate patients, clinicians, and medications more accurately and quickly. IoT development has made this task much more accessible by guiding you through every significant aspect of a medical asset-tracking solution. Introducing our slide exhibiting use cases of medical tools that can be tracked with IoT technology . Medical assets, including medical tools, medical equipment tracking, medications , etc., are shown in the layout with their use cases and impacts. Each topic is depicted in separate tables with appropriate icons.

Template 4: AIoT Healthcare Applications in Medical Imaging

AIoT is making the medical sector smarter and wiser to improve data management and human-machine interaction. When AIoT is applied to healthcare, enables virtual monitoring and accurate diagnosis of patients to develop a personalized patient experience. Here, we introduce our premium PPT Templates showcasing applications of Artificial Intelligence of Things (AIoT) in radiology. You can provide detailed information about remote diagnosis , personalized treatment , and real-time monitoring. Adapt it now to increase your presentation threshold and educate your audience.

Template 5: Case Study of Leading Medical Devices Manufacturing Organization

An array of disruptive themes is shaping the medical device industry, and cloud computing is one of them. Soon, cloud computing will have a more significant impact on this industry. So, for your convenience, we are presenting our slide covering a case study of blue cloud with lending medical devices manufacturing organization. It covers significant topics like client objective, problem, our solution, and results chronologically. Consisting of three essential stages, this template is excellent for educating and enticing your audience.

Template 6: IoT Technology Use Case for Medical Treatment

IoT, or the Internet of Things, is gaining significance across industries, and the medical sector is no exception. It has taken medical treatment to a new level. This custom-built PowerPoint Template exhibits the use of IoT technology in domains of the healthcare industry. It provides a digital solution for patient treatment. The key elements are primary care, acute care, virtual hospital, etc., which are depicted along with descriptions, benefits, and additional comments. Each illustration is highlighted, colored and has a relevant icon for instantaneous identification. 

Template 7: IoT Medical Healthcare Technology Use Cases

The transformation of healthcare into digital healthcare has resulted in the rise of IoMT, or medical IoT . It refers to connected devices in medical healthcare and has become one of the fastest-growing industries in the IoT market. It would help if you dived deeper to manage, monitor, and preserve IoT devices in medical healthcare. This PPT presentation demonstrates uses of IoT Medical Healthcare Technology in monitoring patient health. Moreover, the slide includes remote patient monitoring, reduced waiting time, identifying chronic diseases, and drug management. Download this template design and present your case study with ultimate professionalism.

HEALTH CONSULTATION WILL BE QUICKER, SAFER AND SECURE

Case studies have a great history as an educational tool for clinicians. These are highly beneficial for nurturing deeper insights and learning. Access to such visually appealing and comprehensively presented Top 7 Medical Case Presentation Templates enables medical professionals to quickly present their patients' case studies. Be it tracking of medical assets, application of IoT in the clinical field, IoT medical healthcare technology uses, and so on, these templates serve as essential equipment in implementing all.

P.S. For perfection and success, you should dig into SlideTeam's fantastic blog, Medical Report Templates .

Related posts:

• How to Design the Perfect Service Launch Presentation [Custom Launch Deck Included]
• Quarterly Business Review Presentation: All the Essential Slides You Need in Your Deck
• [Updated 2023] How to Design The Perfect Product Launch Presentation [Best Templates Included]
• 99% of the Pitches Fail! Find Out What Makes Any Startup a Success

Liked this blog? Please recommend us

Top 10 Training Framework Templates with Examples and Samples

Top 5 Product Strategy Framework Templates with Samples and Examples

This form is protected by reCAPTCHA - the Google Privacy Policy and Terms of Service apply.

--> Digital revolution powerpoint presentation slides

--> Sales funnel results presentation layouts

--> 3d men joinning circular jigsaw puzzles ppt graphics icons

--> Business Strategic Planning Template For Organizations Powerpoint Presentation Slides

--> Future plan powerpoint template slide

--> Project Management Team Powerpoint Presentation Slides

--> Brand marketing powerpoint presentation slides

--> Launching a new service powerpoint presentation with slides go to market

--> Agenda powerpoint slide show

--> Four key metrics donut chart with percentage

--> Engineering and technology ppt inspiration example introduction continuous process improvement

--> Meet our team representing in circular format

A quick note about our cookies

We use cookies so we can give you the best website experience possible and to provide us with anonymous data so we can improve our marketing efforts. Read our cookie policy and privacy policy.

Login to your account

New here? Sign up in seconds!

Use social account

Or login with an email

Create an account

Already have an account? Login here

Or sign up with an email

We’re uploading new templates every week

We’d like to send you infrequent emails with brief updates to let you know of the latest free templates. Is that okay?

Reset your Password

Please enter the email you registered with and we will send you a link to reset your password!

Check your email!

We’ve just sent you a link to
 . Please follow instructions from our email.

• Most Popular Templates
• Corporate & Business Models
• Data (Tables, Graphs & Charts)
• Organization & Planning
• Text Slides
• Our Presentation Services

Get your own design team

Tailored packages for corporates & teams

Clinical Case Study Presentation Template

Number of slides: 10

A clinical case study is a report where medical practitioners share a patient’s case. Generally, clinical case studies are valuable tools for medical research as they provide detailed information on the development of a disease or illness in particular individuals. Use this PowerPoint template to document extraordinary patient cases and share your findings with the healthcare community. You can also use these slides to report the progress of your patient’s disease and work on the proper treatment alongside your team.

• About this template
• How to edit
• Custom Design Services

Free Template for presenting a Clinical Case Study in PowerPoint

Patient’s clinical profile.

Before starting, share the patient’s clinical profile. This slide is great to describe your patient’s clinical history, underlying conditions, and other relevant health information. You can include demographic data and specific facts related to your patient but remember to keep their anonymity.

Clinical Treatment Slide

This is one of the most important sections of your patient’s case study. You’ll find a creative slide to explain the medical treatment stage by stage. You can go deep into the medicines or drugs the patient used and their reaction in different stages of the treatment. This means you’ll be able to cover the evolution of your patient from the beginning and provide detailed insights. 

Medical Team Slide

As in any research, you should acknowledge the professionals that worked with you. So, here’s a slide to showcase the whole medical team involved in the case study. You can add photos and short descriptions of each team member. Make sure to ask for professional images and double-check the spelling of role titles and names.   

Roadmaps for Clinical Case Study Presentations

If you’re wondering how to present a patient case study in PowerPoint, the best way to do so is by taking full advantage of its visual elements. Here you’ll find creative roadmaps, diagrams, and icons

Medical PowerPoint Slides

The Clinical Case Study PowerPoint template has a clean and minimalistic style that makes your work stand out in high-level professional slides.

Medical icons in PowerPoint

You’ll find medical icons on every PowerPoint slide. Use them to organize your information and direct your audience’s attention exactly where you want it to be.

FIND OUT MORE ABOUT OUR CUSTOM DESIGN SERVICES

Todd Speranzo

VP of Marketing at Avella

"24Slides helps us get PowerPoints on-brand, and improve overall design in a timeframe that is often “overnight”. Leveraging the time zone change and their deep understanding of PowerPoint, our Marketing team has a partner in 24Slides that allows us to focus purely on slide content, leaving all of the design work to 24Slides."

Gretchen Ponts

Strata Research

"The key to the success with working with 24Slides has been the designers’ ability to revamp basic information on a slide into a dynamic yet clean and clear visual presentation coupled with the speed in which they do so. We do not work in an environment where time is on our side and the visual presentation is everything. In those regards, 24Slides has been invaluable."

"After training and testing, 24Slides quickly learnt how to implement our CVI, deliver at a high quality and provide a dedicated design team that always tries to accommodate our wishes in terms of design and deadlines."

What's included in Keynote Template?

I want this template customized class="mobile-none"for my needs!

69 beautifully designed slides 67 icons included PowerPoint and Keynote ready 16:9 full HD class="mobile-none"resolution

Check out other similar templates

Text Slides Sales Presentation Template

General Sales Slides Templates

Generic Text Slides Templates

General Agenda Presentation Template

Clinical Case

What do you think of this template.

Product details

Clinical case reports have been the earliest form of medical communication. A clinical case report or case study is a means of disseminating new knowledge gained from clinical practice. Medical practitioners often come across patient cases that are different or unusual such as a previously unknown condition, a complication of a known disease, an unusual side effect or adverse response to a mode of treatment, or a new approach to a common medical condition. Thus, a clinical case report is expected to discuss the signs, symptoms, diagnosis, and treatment of a disease.

Clinical case reports are the first-line evidence in medical literature as they present original observations and can be an excellent way for medical students and practitioners to get started with academic writing. Additionally, a published case report is definitely a contribution to medical science and a great addition to a CV.

Informed consent in an ethical requirement for most studies involving humans. It is important to take written consent from the patient before you start writing your case report as all journals will require you to provide patient consent at the time of manuscript submission. In case the patient is a minor, parental consent is required.  For adults who are unable to consent to investigation or treatment, consent of closest family members is required. In general, all case reports include the following components – an abstract, an introduction, a case, and a discussion. 

The abstract should summarize the case, the problem it addresses, and the message it conveys. Abstracts of case studies are usually very short, preferably not more than 150 words. The introduction gives a brief overview of the problem that the case addresses, citing relevant literature where necessary. The introduction generally ends with a single sentence describing the patient and the basic condition that he or she is suffering from.

Case studies are a vehicle for doctors around the world to share their experiences with handling challenging patient cases. These can be valuable sources of information and guidance for clinical practitioners when faced with puzzling or challenging conditions in patients they attend to.

This template will be useful for healthcare professionals and doctors when preparing a report on a new type of disease or a new symptom of a disease. You can structure and present your new patient data. Also, this template can be used for training with interns, which will be conducted by experienced hospital doctors.

Also, this template will be useful for specialists in research centers and pharmaceutical companies. You can use the slides in this template to prepare for a Doctorate Symposium or to speak to medical students.

Clinical Case Template is a stylish and professional template that contains four slides. All slides in the template can be easily customized to suit your corporate color requirements. Clinical Case Template will be useful for doctors and medical professionals, teachers of medical universities. This template’s slides will be a great addition to your professional presentation collection.

Related Products

Eisenhower Matrix Template

Blood Pressure Chart

Skeleton Template

Diffusion of Innovation Model

RACI Matrix Template

Business Pricing Tables

Kotter's Change Model

Lean Canvas Template

Change Management Plan

Brain Template

You dont have access, please change your membership plan., great you're all signed up..., verify your account.

PowerSlides.com will email you template files that you've chosen to dowload.

Please make sure you've provided a valid email address! Sometimes, our emails can end up in your Promotions/Spam folder.

Simply, verify your account by clicking on the link in your email.

• Presentations

Clinical Case Presentation Template

Present your patient’s history and the impact of medication using this presentation template..

Use high-resolution stock photos, icons, charts and graphs alongside the bullet-point form of text to summarize your patient’s case.

This presentation template offers you the opportunity to present clinical cases to peers and attendings. You can also use it to present patient history and course of treatment during your oral board certification exam.

• Change colors, fonts and more to fit your branding
• Access free, built-in design assets or upload your own
• Visualize data with customizable charts and widgets
• Add animation, interactivity, audio, video and links
• Download in PDF, PPTX, MP4 and HTML5 format
• Share online with a link or embed on your website

Ace clinical case presentation on your next exam with this impactful template, or take a look at our other presentation templates for a better fit.

Edit this template with our  Presentation Software

Template Specifications

9 Slides, 1366 x 768 pixels – 16:9 Aspect Ratio (HD Presentation Quality)

Customizable

This template can be fully customized. You can edit content, change image(s), apply custom colors, input your own fonts and logo, and more.

Download as a PDF to share with your recipient or generate a shareable link for online sharing.

Compatibility

Related tags.

• presentations
• presentation
• slide decks

Explore other presentation themes

Create your Presentation using thousands of gorgeous slides in 20+ content categories.

More like this

Nature Background Presentation

Educate your audience on environmental topics or organic products with this nature presentation template.

Comms Pitch Deck Presentation

Share your creative business ideas with investors using this Intercom-inspired pitch deck template.

Evolution of the Projector Presentation

Communicate to and engage with your audience the right way with this educational media presentation template.

HR SWOT Analysis Presentation

Explore small-business HR with this artistic SWOT Analysis presentation template.

Graphic Design - Webinar Presentation

Give your audience a crash course on graphic design using this colorful webinar presentation template.

Communication Skills - Keynote Presentation

Give a show-stopping presentation on the importance of workplace communication with this modern keynote presentation template.

Employee Handbook Interactive Presentation

Transform your employee handbook into a dazzling interactive presentation with this professional interactive presentation template.

Business Case Presentation

Showcase your company's latest case study with this beautiful presentation template.

Risk Analysis Presentation

Walk your audience through conducting a risk analysis with this finance presentation template.

Employee Engagement Presentation

Explain how to boost employee engagement in the workplace using this presentation template.

Business Development Presentation

Create an engaging presentation on your company’s history and showcase its portfolio.

Design Tool Presentation

Use this compelling sales presentation template to highlight your SaaS company and product.

Purple and Black Business Presentation

This all-around, creative business presentation template is a definite head-turner. Get started today.

50 Years After the Moon Landing - Presentation

Design an eye-catching space exploration presentation with this stunning presentation template.

Cybersecurity SWOT Analysis Presentation

Learn about the importance of cybersecurity with this stellar SWOT Analysis presentation template.

Entrepreneurship Webinar Presentation

Reveal the secrets of successful entrepreneurship using this vibrant keynote presentation template.

Free Presentation Templates by Visme

Marketing is all about communication, yes - but it's also about making the best possible impression on your target audience. What you're saying is important, but how you choose to say it is equally so. You can only make one first impression, so you'd better make it the best one that you can - and now, thanks to Visme's presentation templates, it's easier than ever to do precisely that.

Loaded with countless stunning, versatile and totally customizable presentation templates , Visme's presentation software makes it possible to design the engaging, creative collateral that you need without requiring years of design experience under your belt. Visme offers presentation templates for every conceivable industry that you're a part of, making sure that the tools are always available to guarantee that your audience will pay attention to your every word.

Our presentation templates are equal parts colorful, visual, vivid and attractive - but they're also easy to use and even easier to edit, as well. These presentation templates also come with a massive number of free stock images for you to use, guaranteeing that you'll always be able to broadcast your message in exactly the right way at exactly the right moment in your relationship with your audience.

Create Your Presentation

Medical Case Study PowerPoint Template

The Medical Case Study PowerPoint Template with astonishing backgrounds contains the healthcare industry layouts. This PowerPoint template is a unique design for professionals and learners in the healthcare industry, such as doctors, nurses, pharmaceuticals, and other professionals in hospitals and universities who need to present their findings. The PowerPoint presentation has amazing gradient backgrounds and top-quality graphics that allow you to fill in the details easily. The medical theme of the presentation is an incredible tool for healthcare professionals with designs to display various topics. Further, choose the necessary slides as a part of main presentations. The useful editing features assist users in applying changes in theme colors and organizing the template format. View the latest SlideModel PowerPoint medical template of shapes and clipart.

The Medical Case Study PowerPoint Template is a 10-slide presentation providing a variety of infographic layouts. These slides include several presentation icons, and clip art PowerPoint shapes relevant to the healthcare industry. For example, the icon of heart rate graph, human heart, stethoscope, first aid, operation symbols, and health insurance. Furthermore, the clipart includes a heart plus symbol for aid and an angle wings figure used by pharmaceutical companies and research labs. Therefore, the medical case study PowerPoint is an exclusive template for hospitals and the medical aid and equipment supplier companies. The template of medical case study presents the slides of agenda with four and six sections layout. Moreover, there is a detail introduction template follow by three sections of case study and brilliant heart rate graph timeline.

The stunning design of medical case study template helps clearly communicate the medical ideas and thoughts. The icons representing the sections elements of case study . This medical case study PowerPoint is an ideal template of academic purposes. The slides have text placeholders to add textual details for the analysis and engage the audience with relevant visual content. Hence, the PowerPoint medical presentation is a complete guide to demonstrate case study analysis and research reports. Alternative to this Medical Case presentation PPT you can download other medical presentation templates for professional PowerPoint presentations.

You must be logged in to download this file.

Favorite Add to Collection

Subscribe today and get immediate access to download our PowerPoint templates.

Related PowerPoint Templates

Arrows SWOT Analysis PowerPoint Template

5-Step Current State vs Future State PowerPoint Template

Science Project Presentation Template

Performance Analysis PowerPoint Template

• Collections
• Medical Case Study PowerPoint

Attractive Medical Case Study PPT And Google Slides Template

Medical Case Study Powerpoint Slide

Feature of this template.

• 100% customizable slides and easy to download.
• The slide contains 16:9 and 4:3 formats.
• Easy to change the colors of the slide quickly.
• Highly compatible with PowerPoint and Google Slides.
• Medical Case Study
• Clinical Case Study
• Clinical Case
• Medical Case
• Medical Case Studies
• Healthcare Case Study
• Google Slides

321+ Templates

26+ Templates

23+ Templates

Opportunity

24+ Templates

181+ Templates

169+ Templates

1103+ Templates

550+ Templates

183+ Templates

You May Also Like These PowerPoint Templates

Clinical Case 04-2019

How to download the Clinical Case 04-2019 template for Powerpoint

How to download the template clinical case 04-2019 in google slides, description.

Seafaring Tale Book

A Tale of Dinosaurs

Higher Education

• Clinical Case Template

The term clinical case is applied to information on the history of symptoms that a patient suffers during the course of a treatment. It is almost always applied in rare diseases or because the treatment options are complex or new. To provide information regarding this topic, you should consider using this disease care and prevention inspired case report template in your presentations.

This clinical case study template for PowerPoint and Google Slides stands out a lot for its eye-catching images and 100% editable tools. In its 36 slides you can find a background color scheme that is very pleasing to the human eye. In addition, you can make effective and quick presentations, very easily, just download this free ppt file and take it to Canva editing.

Free Clinical Case Template for PowerPoint and Google Slides

Main features

• 36 slides 100% editable
• 16:9 widescreen format suitable for all screens
• High quality royalty-free images
• Included resources: charts, graphs, timelines and diagrams
• More than 100 icons customizable in color and size
• Main font: Roboto Slab
• Predominant color: Turquoise

Download this template

To enjoy an optimal state of health, it is the most advisable for any living being, to contribute to their care we have these themes Google Slides and Health PowerPoint Templates on this website. Each of these represents a crucial issue for the care and welfare of living beings, the best thing is that all content is 100% editable.

We use cookies to improve the experience of everyone who browses our website. Cookies Policy

Accept Cookies

The Ultimate Patient Case Presentation Template for Med Students

• April 6, 2024
• / Reviewed by: Amy Rontal, MD

Knowing how to deliver a patient presentation is one of the most important skills to learn on your journey to becoming a physician. After all, when you’re on a medical team, you’ll need to convey all the critical information about a patient in an organized manner without any gaps in knowledge transfer.

One big caveat: opinions about the correct way to present a patient are highly personal and everyone is slightly different. Additionally, there’s a lot of variation in presentations across specialties, and even for ICU vs floor patients.

My goal with this blog is to give you the most complete version of a patient presentation, so you can tailor your presentations to the preferences of your attending and team. So, think of what follows as a model for presenting any general patient.

Here’s a breakdown of what goes into the typical patient presentation.

Looking for some help studying your shelf/Step 2 studying with clinical rotations? Try our combined   Step 2 & Shelf Exams Qbank  with 5,500 practice questions— free for 7 days!

7 Ingredients for a Patient Case Presentation Template

1. the one-liner.

The one-liner is a succinct sentence that primes your listeners to the patient.

A typical format is: “[Patient name] is a [age] year-old [gender] with past medical history of [X] presenting with [Y].

2. The Chief Complaint

This is a very brief statement of the patient’s complaint in their own words. A common pitfall is when medical students say that the patient had a chief complaint of some medical condition (like cholecystitis) and the attending asks if the patient really used that word!

An example might be, “Patient has chief complaint of difficulty breathing while walking.”

3. History of Present Illness (HPI)

The goal of the HPI is to illustrate the story of the patient’s complaint. I remember when I first began medical school, I had a lot of trouble determining what was relevant and ended up giving a lot of extra details. Don’t worry if you have the same issue. With time, you’ll learn which details are important. 

The OPQRST Framework

In the beginning of your clinical experience, a helpful framework to use is OPQRST:

Describe when the issue started, and if it occurs during certain environmental or personal exposures.

P rovocative

Report if there are any factors that make the pain better or worse. These can be broad, like noting their shortness of breath worsened when lying flat, or their symptoms resolved during rest. 

Relay how the patient describes their pain or associated symptoms. For example, does the patient have a burning versus a pressure sensation? Are they feeling weakness, stiffness, or pain?

R egion/Location

Indicate where the pain is located and if it radiates anywhere.

Talk about how bad the pain is for the patient. Typically, a 0-10 pain scale is useful to provide some objective measure.

Discuss how long the pain lasts and how often it occurs.

A Case Study

While the OPQRST framework is great when starting out, it can be limiting. Let’s take an example where the patient is not experiencing pain and comes in with altered mental status along with diffuse jaundice of the skin and a history of chronic liver disease. You will find that certain sections of OPQRST do not apply. In this event, the HPI is still a story, but with a different framework. Try to go in chronological order. Include relevant details like if there have been any changes in medications, diet, or bowel movements.

Pertinent Positive and Negative Symptoms

Regardless of the framework you use, the name of the game is pertinent positive and negative symptoms the patient is experiencing. I’d like to highlight the word “pertinent.” It’s less likely the patient’s chronic osteoarthritis and its management is related to their new onset shortness of breath, but it’s still important for knowing the patient’s complete medical picture. A better place to mention these details would be in the “Past Medical History” section, and reserve the HPI portion for more pertinent history. As you become exposed to more illness scripts, experience will teach you which parts of the history are most helpful to state. Also, as you spend more time on the wards, you will pick up on which questions are relevant and important to ask during the patient interview.   By painting a clear picture with pertinent positives and negatives during your presentation, the history will guide what may be higher or lower on the differential diagnosis. Some other important components to add are the patient’s additional past medical/surgical history, family history, social history, medications, allergies, and immunizations.

The HEADSSS Method

Particularly, the social history is an important time to describe the patient as a complete person and understand how their life story may affect their present condition. One way of organizing the social history is the HEADSSS method: – H ome living situation and relationships – E ducation and employment – A ctivities and hobbies – D rug use (alcohol, tobacco, cocaine, etc.) Note frequency of use, and if applicable, be sure to add which types of alcohol consumption (like beer versus hard liquor) and forms of drug use. – S exual history (partners, STI history, pregnancy plans) – S uicidality and depression – S piritual and religious history   Again, there’s a lot of variation in presenting social history, so just follow the lead of your team. For example, it’s not always necessary/relevant to obtain a sexual history, so use your judgment of the situation.

4. Review of Symptoms

Oftentimes, most elements of this section are embedded within the HPI. If there are any additional symptoms not mentioned in the HPI, it’s appropriate to state them here.

5. Objective

Vital signs.

Some attendings love to hear all five vital signs: temperature, blood pressure (mean arterial pressure if applicable), heart rate, respiratory rate, and oxygen saturation. Others are happy with “afebrile and vital signs stable.” Just find out their preference and stick to that. 

Physical Exam  

This is one of the most important parts of the patient presentation for any specialty. It paints a picture of how the patient looks and can guide acute management like in the case of a rigid abdomen. As discussed in the HPI section, typically you should report pertinent positives and negatives. When you’re starting out, your attending and team may prefer for you to report all findings as part of your learning. For example, pulmonary exam findings can be reported as: “Regular chest appearance. No abnormalities on palpation. Lungs resonant to percussion. Clear to auscultation bilaterally without crackles, rhonchi, or wheezing.” Typically, you want to report the physical exams in a head to toe format: General Appearance, Mental Status, Neurologic, Eyes/Ears/Nose/Mouth/Neck, Cardiovascular, Pulmonary, Breast, Abdominal, Genitourinary, Musculoskeletal, and Skin. Depending on the situation, additional exams can be incorporated as applicable.

Now comes reporting pertinent positive and negative labs. Several labs are often drawn upon admission. It’s easy to fall into the trap of reading off all the labs and losing everyone’s attention. Here are some pieces of advice: 

You normally can’t go wrong sticking to abnormal lab values. 

One qualification is that for a patient with concern for acute coronary syndrome, reporting a normal troponin is essential. Also, stating the normalization of previously abnormal lab values like liver enzymes is important.

Demonstrate trends in lab values.

A lab value is just a single point in time and does not paint the full picture. For example, a hemoglobin of 10g/dL in a patient at 15g/dL the previous day is a lot more concerning than a patient who has been stable at 10g/dL for a week.

Try to avoid editorializing in this section.

Save your analysis of the labs for the assessment section. Again, this can be a point of personal preference. In my experience, the team typically wants the raw objective data in this section. This is also a good place to state the ins and outs of your patient (if applicable). In some patients, these metrics are strictly recorded and are typically reported as total fluid in and out over the past day followed by the net fluid balance. For example, “1L in, 2L out, net -1L over the past 24 hours.”

6. Diagnostics/Imaging

Next, you’ll want to review any important diagnostic tests and imaging. For example, describe how the EKG and echo look in a patient presenting with chest pain or the abdominal CT scan in a patient with right lower quadrant abdominal pain. Try to provide your own interpretation to develop your skills and then include the final impression. Also, report if a diagnostic test is still pending.

7. Assessment/Plan

This is the fun part where you get to use your critical thinking (aka doctor) skills! For the scope of this blog, we’ll review a problem-based plan. It’s helpful to begin with a summary statement that incorporates the one-liner, presenting issue(s)/diagnosis(es), and patient stability. Then, go through all the problems relevant to the admission. You can impress your audience by casting a wide differential diagnosis and going through the elements of your patient presentation that support one diagnosis over another.  Following your assessment, try to suggest a management plan. In a patient with congestive heart failure exacerbation, initiating a diuresis regimen and measuring strict ins/outs are good starting points. You may even suggest a follow-up on their latest ejection fraction with an echo and check if they’re on guideline-directed medical therapy. Again, with more time on the clinical wards you’ll start to pick up on what management plan to suggest. One pointer is to talk about all relevant problems, not just the presenting issue. For example, a patient with diabetes may need to be put on a sliding scale insulin regimen or another patient may require physical/occupational therapy. Just try to stay organized and be comprehensive.

A Note About Patient Presentation Skills

When you’re doing your first patient presentations, it’s common to feel nervous. There may be a lot of “uhs” and “ums.”

Here’s the good news: you don’t have to be perfect! You just need to make a good faith attempt and keep on going with the presentation.

With time, your confidence will build. Practice your fluency in the mirror when you have a chance. No one was born knowing medicine and everyone has gone through the same stages of learning you are!

Practice your presentation a couple times before you present to the team if you have time. Pull a resident aside if they have the bandwidth to make sure you have all the information you need. 

One big piece of advice: NEVER LIE. If you don’t know a specific detail, it’s okay to say, “I’m not sure, but I can look that up.” Someone on your team can usually retrieve the information while you continue on with your presentation.

Example Patient Case Presentation Template

Here’s a blank patient case presentation template that may come in handy. You can adapt it to best fit your needs.   One-Liner:   Chief Complaint:   History of Present Illness:   Past Medical History: Past Surgical History: Family History: Social History: Medications: Allergies: Immunizations:   ROS:   Objective:   Vital Signs : Temp ___ BP ___ /___ HR ___ RR ___ O2 sat ___   Physical Exam:

General Appearance:

Mental Status:

Neurological:

Eyes, Ears, Nose, Mouth, and Neck:

Cardiovascular:

Genitourinary:

Musculoskeletal:

Most Recent Labs:

Previous Labs:

Diagnostics/Imaging:

Impression/Interpretation:

Assessment/Plan:

One-line summary:

#Problem 1:

Assessment:

#Problem 2:

Final Thoughts on Patient Presentations

I hope this post demystified the patient presentation for you. Be sure to stay organized in your delivery and be flexible with the specifications your team may provide.   Something I’d like to highlight is that you may need to tailor the presentation to the specialty you’re on. For example, on OB/GYN, it’s important to include a pregnancy history. Nonetheless, the aforementioned template should set you up for success from a broad overview perspective.   Stay tuned for my next post on how to give an ICU patient presentation. And if you’d like me to address any other topics in a blog, write to me at [email protected] ! Looking for more (free!) content to help you through clinical rotations? Check out these other posts from Blueprint tutors on the Med School blog:

• How I Balanced My Clinical Rotations with Shelf Exam Studying
• How (and Why) to Use a Qbank to Prepare for USMLE Step 2
• How to Study For Shelf Exams: A Tutor’s Guide

About the Author

Hailing from Phoenix, AZ, Neelesh is an enthusiastic, cheerful, and patient tutor. He is a fourth year medical student at the Keck School of Medicine of the University of Southern California and serves as president for the Class of 2024. He is applying to surgery programs for residency. He also graduated as valedictorian of his high school and the USC Viterbi School of Engineering, obtaining a B.S. in Biomedical Engineering in 2020. He discovered his penchant for teaching when he began tutoring his friends for the SAT and ACT in the summer of 2015 out of his living room. Outside of the academic sphere, Neelesh enjoys surfing at San Onofre Beach and hiking in the Santa Monica Mountains. Twitter: @NeeleshBagrodia LinkedIn: http://www.linkedin.com/in/neelesh-bagrodia

Related Posts

How to Study For Shelf Exams: A Tutor’s Guide

• May 6, 2024

The Ultimate ICU Patient Presentation Template for Med Students

• May 3, 2024

Quiz: Which “Scrubs” Character Are You in Your Clinical Rotations?

• March 26, 2024

Free PowerPoint Case Study Presentation Templates

By Joe Weller | January 23, 2024

• Share on Facebook
• Share on LinkedIn

Link copied

We’ve collected the top free PowerPoint case study presentation templates with or without sample text. Marketing and product managers, sales execs, and strategists can use them to arrange and present their success stories, strategies, and results.

On this page, you'll find six PowerPoint case study presentation templates, including a  marketing case study template , a  problem-solution-impact case study , and a  customer journey case study template , among others. Plus, discover the  key components of successful case study presentations , find out the  different types of case study presentations , and get  expert tips .

PowerPoint Single-Slide Case Study Presentation Template

Download the Sample Single-Slide Case Study Presentation Template for PowerPoint Download the Blank Single-Slide Case Study Presentation Template for PowerPoint

When to Use This Template:  Use this single-slide case study presentation template when you need to give a quick but effective overview of a case study. This template is perfect for presenting a case study when time is limited and you need to convey key points swiftly.

Notable Template Features: You can fit everything you need on one slide. Download the version with sample text to see how easy it is to complete the template. Unlike more detailed templates, it focuses on the main points, such as the problem, solution, approach, and results, all in a compact format. It's great for keeping your audience focused on the key aspects of your case study without overwhelming them with information.

PowerPoint Marketing Case Study Template

Download the Sample Marketing Case Study Template for PowerPoint

Download the Blank Marketing Case Study Template for PowerPoint

When to Use This Template: Choose this marketing case study template when you need to dive deep into your marketing strategies and results. It's perfect for marketing managers and content marketers who want to showcase the detailed process and successes of their campaigns. 

Notable Template Features: This template focuses on the detailed aspects of marketing strategies and outcomes. It includes specific sections to outline business needs, results, and strategic approaches.

PowerPoint Problem-Solution-Impact Case Study Template

Download the Sample Problem-Solution-Impact Case Study Template for PowerPoint

Download the Blank Problem-Solution-Impact Case Study Template for PowerPoint

When to Use This Template:  This problem-solution-impact case study template is useful for focusing on how a challenge was solved and the results. Project managers and strategy teams that want to clearly portray the effectiveness of their solutions can take advantage of this template. 

Notable Template Features: This template stands out with its clear structure that breaks down the case into problem, solution, and impact. Use the template — available with or without sample data — to help you tell a complete story, from the issue faced to the solution and its results, making it perfect for presentations that need to show a clear cause-and-effect relationship.

PowerPoint Comparative Study Template

Download the Sample Comparative Study Template for PowerPoint  

Download the Blank Comparative Study Template for PowerPoint  

When to Use This Template:  Choose this comparative study template — available with or without sample data — to illuminate how different products, strategies, or periods stack up against each other. It's great for product managers and research teams who want to do side-by-side comparisons. 

Notable Template Features: This template lets you put things next to each other to see their differences and similarities, with a focus on direct comparisons. Use the columns and split slides to make the content easy to understand and visually appealing, perfect for highlighting changes or different approaches.

PowerPoint Customer Journey Case Study Template

Download the Sample Customer Journey Case Study Template for PowerPoint

Download the Blank Customer Journey Case Study Template for PowerPoint

When to Use This Template: This template is useful for customer experience managers and UX designers who need to understand and improve how customers interact with what they offer. Use the customer journey case study template with sample data to see how to show every step of a customer's experience with your product or service. 

Notable Template Features:  This template focuses on the whole path a customer takes with a product or service. It follows them, from first learning about the offering to after they buy it.

PowerPoint Case Study Storyboard Template

Download the Sample Case Study Storyboard Template for PowerPoint   Download the Blank Case Study Storyboard Template for PowerPoint  

When to Use This Template:  Creative teams and ad agencies should use this case study storyboard template — with or without sample data — to tell a story using more images than text.

Notable Template Features: This template transforms a case study into a visual story. Effectively communicate the journey of a business case, from the challenges faced to the solutions implemented and the results achieved.

Key Components of Successful Case Study Presentations

The key components of successful case study presentations include clear goals, engaging introductions, detailed customer profiles, and well-explained solutions and results. Together they help you present how your strategies succeed in real-world scenarios. 

The following components are fundamental to crafting a compelling and effective marketing case study presentation:   

• Clear Objective:  Define the goal of your case study, ensuring it addresses specific questions or goals. 
• Engaging Introduction:  Start with an overview of the company, product, or service, as well as the context to provide necessary background information. 
• Customer Profile:  Detail your target customer demographics and their needs to help the audience understand who the marketing efforts are aimed at and their relevance. 
• The Challenge:  Clearly articulate the primary problem or issue to overcome to establish the context for the solution and strategy, highlighting the need for action. 
• Solution and Strategy:  Describe the specific strategies and creative approaches used to address the challenge. These details should demonstrate your approach to problem-solving and the thought process behind your decisions. 
• Implementation:  Explain how the solution was put into action to show the practical application. This description should bring your strategy to life, allowing the audience to see how you executed plans. 
• Results and Impact:  Present measurable outcomes and impacts of the strategy to validate and show its effectiveness in real-world scenarios. 
• Visual Elements:  Use charts, images, and infographics to make complex information more accessible and engaging, aiding audience understanding. 
• Testimonials and Quotes:  Include customer feedback or expert opinions to add credibility and a real-world perspective, reinforcing your strategy’s success. 
• Lessons Learned and Conclusions:  Summarize key takeaways and insights gained to show what the audience can learn from the case study. 
• Call to Action (CTA):  End with an action you want the audience to take to encourage engagement and further interaction.

Different Types of Case Study Presentations

The types of case study presentations include those that compare products, showcase customer journeys, or tell a story visually, among others. Each is tailored to different storytelling methods and presentation goals.

The following list outlines various types of case study presentations:   

• Problem-Solution-Impact Case Study:  This type focuses on a clear narrative structure, outlining the problem, solution implemented, and final impact. It's straightforward and effective for linear stories. 
• Comparative Case Study:  Ideal for showcasing before-and-after scenarios or comparisons between different strategies or time periods. This option often uses parallel columns or split slides for comparison. 
• Customer Journey Case Study:  Centered on the customer's experience, this option maps out their journey from recognizing a need to using the product or service, and the benefits they gained. It's a narrative-driven and customer-focused case study format. 
• Data-Driven Case Study:  Emphasizing quantitative results and data, this format is full of charts, graphs, and statistics. This option is perfect for cases where numerical evidence is the main selling point. 
• Storyboard Case Study:  Use this type to lay out the case study in a storytelling format. This option often relies on more visuals and less text. Think of it as a visual story, engaging and easy to follow. 
• Interactive Case Study:  Designed with clickable elements for an interactive presentation, this type allows the presenter to dive into different sections based on audience interest, making it flexible and engaging.
• Testimonial-Focused Case Study:  This format is best for highlighting customer testimonials and reviews. It leverages the power of word of mouth and is highly effective in building trust.

Expert Tips for Case Study Presentations

Expert tips for case study presentations include knowing your audience, telling a clear story, and focusing on the problem and solution. They can also benefit from using visuals and highlighting results.

“Case studies are one of the most powerful tools in an organization’s marketing arsenal,” says Gayle Kalvert, Founder and CEO of  Creo Collective, Inc. , a full-service marketing agency. “Done correctly, case studies provide prospective buyers with proof that your product or service solves their business problem and shortens the sales cycle.”   

“Presentations are probably the most powerful marketing asset, whether for a webinar, a first meeting deck, an investor pitch, or an internal alignment/planning tool,” says marketing expert  Cari Jaquet . “Remember, the goal of a case study presentation is not just to inform, but also to persuade and engage your audience.” 

Use these tips to make your presentation engaging and effective so that it resonates with your audience:   

• Know Your Audience:  Tailor the presentation to the interests and knowledge level of your audience. Understanding what resonates with them helps make your case study more relevant and engaging. “Presentations can also be a forcing function to define your audience, tighten up your mission and message, and create a crisp call to action,” explains Jaquet.
• Tell a Story:  Structure your case study like a story, with a clear beginning (the problem), middle (the solution), and end (the results). A narrative approach keeps the audience engaged. 
• Focus on the Problem and Solution:  Clearly articulate the problem you addressed and how your solution was unique or effective. This section is the core of a case study and should be given ample attention. 
• Use Data Wisely:  Incorporate relevant data to support your points, but avoid overwhelming the audience with numbers. Use charts and graphs for visual representation of data to make it more digestible. 
• Highlight Key Results:  Emphasize the impact of your solution with clear and quantifiable results. This could include increased revenue, cost savings, improved customer satisfaction, and similar benefits.
• Incorporate Visuals:  Use high-quality visuals to break up text and explain complex concepts. Consider using photos, infographics, diagrams, or short videos.  “I put together the graphics that tell the story visually. Speakers often just need a big image or charts and graphs to help guide their talk track. Of course, if the audience expects details (for example, a board deck), the graphic helps reinforce the narrative,” shares Jaquet.
• Include Testimonials:  Adding quotes or testimonials from clients or stakeholders adds credibility and a real-world perspective to your presentation. 
• Practice Storytelling:  A well-delivered presentation is as important as its content. Practice your delivery to ensure you are clear, concise, and engaging. At this point, it also makes sense to solicit feedback from stakeholders. Jaquet concurs: “Once my outline and graphics are in place, I typically circulate the presentation draft for review. The feedback step usually surfaces nuances in the story or key points that need to show up on the slides. There is no point in building out tons of slides without alignment from the speaker or subject matter experts.”
• End with a Strong Conclusion:  Summarize the key takeaways and leave your audience with a final thought or call to action. 
• Seek Feedback:  After your presentation, request feedback to understand what worked well and what could be improved for future presentations. 

“Don't underestimate the power of a great presentation. And don't wait until the last minute or try to invent the wheel on your own,” advises Jaquet. “Many times, getting the next meeting, winning the deal, or getting the project kicked off well, requires your audience to understand and believe your story.”

Streamline and Collect All the Elements Needed for a Case Study with Smartsheet

Empower your people to go above and beyond with a flexible platform designed to match the needs of your team — and adapt as those needs change. 

The Smartsheet platform makes it easy to plan, capture, manage, and report on work from anywhere, helping your team be more effective and get more done. Report on key metrics and get real-time visibility into work as it happens with roll-up reports, dashboards, and automated workflows built to keep your team connected and informed. 

When teams have clarity into the work getting done, there’s no telling how much more they can accomplish in the same amount of time.  Try Smartsheet for free, today.

Discover why over 90% of Fortune 100 companies trust Smartsheet to get work done.

Free Clinical Case Google Slides Themes And Powerpoint Templates

Create moving, zooming presentations that grab attention and keep it.

Appear right alongside your content while presenting to your audience.

Make stunning interactive charts, reports, maps, infographics, and more.

You're about to create your best presentation ever

Clinical Case Study Powerpoint Template

Clinical Case Study

Transcript: CT 9/23/17: 21.81 (High, normal is 4-11, indication of infection) 10/6: Atelectasis of right and left upper lobes were present at the beginning of patients stay 10/16: Patient was prescribed Metaneb Q6 with albuterol -Metaneb is a chest expansion therapy used to expand the lungs, break up secretions, prevent atelectasis and pneumonia. -Albuterol is a bronchodilator used to relax and open up the airway. Pt was also prescribe Pulmicort BID -Pulmicort is a steroid used to improve lung function and is used as a preventative for asthma. Pt was also given an IS to use at bedside when he was able to cooperate ABGs 11/13/17: HGB: 10.2 (Low) HCT: 32.0 (Low) Vent Settings Patient was admitted on 9/23/17 Intubated 9/23/17 and put on vent Trached 9/24/17 Taken off Vent 10/6/17 Put on 28% trach collar Weaned to 21% by 10/17/17 Trach capped 10/17/17 Patient was discharged 11/13/17 11/13/17: 3.52 (low) Atelectasis Hemopneumothorax Rib Fractures Jaw fracture Acquired brain injury Admitting Data, CC RBC: Patient was placed on vent 9/24/17 Patient was trached in trauma ICU Vent was removed on 10/6/17 Patient was placed on 28% trach collar Patient was placed on capping trial on 10/16/17 Patient was capped on 10/17/17 Radiology / X-Ray 9/24/17: -Patient was intubated in the ER on 9/23/17 , Size 7 ET tube, Depth: 25cm -Vent settings: FiO2: 100% Vent Mode: Assist / Control Tidal Volume: 500ml Rate: 20 PEEP: 7.5 9/28/17: Vent mode: Volume support / pressure support Tidal Volume: 610ml Rate: 29 Peak inspiratory pressure: 34.0 Mean airway pressure: 16.0 , (high, normal for patients with normal compliance is 5-10cmH2O.) Treatments and Outcomes Continued 10/9/17: Chest CT without contrast Pleural effusion, atelectasis in right lung base / upper lobe, left compressive lung atelectasis, normal heart size, no enlarged mediastinum, hillier or axillary, increased size of left pleural effusion Clinical Case Study OU Medical Center Fall Semester 1 Issues With Labs or X-Rays 9/23/17: 299,000 (Normal, normal is 150,000 to 400,000) 10/24/17: 11.98 (High) 10/24/17: HGB: 10.2 (Low) HCT: 33.7 (Low) 10/9/17: pH: 7.39(normal) CO2: 44(normal) CO3: 27(normal) Sat: 98% Within Normal Limits. Working / Admitting Diagnosis Lab Data Patient was intubated with size 7 ET tube 24 cm deep and was placed on a vent upon arriving to the hospital Patient was not given any long term care plans related to respiratory care. Patient brought IS home and was instructed to use as needed if patient was not ambulated for long periods of time. Pertinent Treatment or Outcomes Respiratory Treatments Vent Settings 9/23/17: HGB: 13.7(Normal, 13-18) HCT: 41.0 (normal, 39.0-52.0) 9/30/17: pH: 7.25(low) CO2: 56(high) CO3: 24(normal) Sat: 94% Uncompensated Respiratory Acidosis Patient was admitted with ear lac, left upper arm lac, contusion to the left jaw / neck, jaw fracture, acute hemopneumothorax with compression atelectasis, air in the left chest / lung, lower contusion below hemopneumothorax, fractured ribs 1-11, acquired brain injury result from skull fracture. 10/3/17: Vent Mode: CMV FiO2: 100% PEEP: 5 Flow by: 60 Pressure Support: 0 PIP: 26 Volume: 500 Rate: 16 MVC/Roll over 9/23/17: 4.41 (low, normal male RBC is 4.5-5.9) Lab Data 9/23/17: Radiology notes included that left-sided hemopneumothorax was still present, bilateral air opacities noted, slightly increased on the left, findings suggest a volume overload. Cardiac and Mediastinal findings are overall similar, soft tissues unchanged, multiple rib fractures noted. 10/20/17: Lung volumes are noted as slightly smaller, more prominent bronchovascular crowding at the right lung base suggestive of atelectasis given the smaller lung volumes. Opacity in the left lung region has not changed. No discrete pneumothorax or large pleural effusion is present. Left lower rib fractures are noted. Cardiac and mediastinal appear unchanged. Impression: Smaller lung volumes with probable worsening of right basilar atelectasis. Admitting Data, CC WBC: Treatment for hemopneumothorax: -1 chest tube , connected to suction , -Location: Left upper lateral chest Drainage: Bloody During admission, patient was unresponsive and unconscious. After being transferred from the ER to ICU, the patient was intubated. Patient history was not able to be obtained due to the patient being unconscious and intubated. Patient History Medical, Family, Social, Occupational Length of stay, Prognosis, Etc. 11/13/17: 5.65 (Normal) 9/24/17: pH: 7.26(low) CO2: 34(low) CO3: 15(low) Sat: 97% Partially Compensated Metabolic Acidosis LB 33 year old Male 5'8 265lbs (obese) Issues With Labs or X-Rays 10/24/17: 3.56 (low) Admitting Vital Signs 9/23/17: HR: 146 RR: 55 BP: 205/155 O2 saturation: 99 Temp: 37.9 C Patients neurological function and status were questionable and altered throughout his stay. Altered respiratory condition was also noted. Platelets Treatments and Outcomes 10/24/17: 468,000 (High, normal is 150,000 to 400,000) CT Hemoglobin / Hematocrit: Patient

Transcript: Proprioceptive/Balance Athlete complained of left shoulder pain Denied head or neck pain Also denied neurological symptoms Lacked concussive symptoms Able to skate off ice/ change before evaluation Off ice the athlete complained of "collar bone" pain and pain on top of the shoulder Pain control IFC Game ready (cryo-compression) Ibuprofen Ice bags Injury Mechanism of Injury Patient: Male, Hockey athlete MOI: Fell shoulder first into boards/Ice Initial Treatment Grade 1 AC Sprain Goals: control pain/inflammation, also increase AROM and strength Point tender over AC ligament and distal clavicle Minor soreness over Coracoid process Shoulder flex/abd pain free to 90 Pain with IR Clinical Case Study Brayden Starr Athletic Training clinical skills-I High plank -Dyna disc -Physio ball Strength Isometrics -flex/ext -abd/add -IR/ER -5 sets @ 10sec -Push as hard a possible w/o eliciting pain Dumb bell -IR, ER, side-lying abduction, prone row w/ external rotation, standing shoulder flexion) 3x15 w/3lb Wall circles 3 sets @ 30 sec Palpation Tests IR/flex/abd 4/5 strength test Horizontal add 3/5 Piano key (-) AC traction test (+) *pain only Equiptment Abnormal carrying angle on left side Held left arm to torso Left shoulder slightly elevated ROM exercises Signs and SYmptoms Athlete iced after assessment, and again that afternoon Use of NSAID's permitted S&S continued 10/22: Skated, pain free stick handling 10/23: wrist shots pain free, slap shots at 50% pain free 10/24: non-contact practice, slap shots at 100% pain free 10/25:"Felt good" 10/26: took part in Hardest shot challenge, no pain, felt good. 10/27: contact practice, took/gave hits no problem, pain free Codman's Pendulum 3 sets of 10 repetitions PROM -increase PROM - Traction Assisted pulley -abd/flex -PROM Wall walks -AAROM Return to Play -AC pad -New pads

Transcript: Evidence-based practice guidelines for instructing individuals with neurogenic memory impairments: What have we learned in the past 20 years? Clinical Case Study Level Ia-ANCDS systematic review "Now I'm not missing everything on my calendar" "There's a new me!" Takeaway . . . Efficacy for metacognitive strategy instruction in middle-age adults with TBI Functional goals Self-monitor performance Level IIa K and the ICF Ehlhardt, L. A., Sohlberg, M. M., Kennedy, M., Coelho, C., Ylvisaker, M., Turkstra, L., & Yorkston, K. (2008). Evidence- based practice guidelines for instructing individuals with neurogenic memory impairments: What have we learned in the past 20 years? Neuropsychological Rehabilitation; an International Journal, 18(3), 300-342. doi:10.1080/09602010701733190 Kennedy, M. T., Coelho, C., Turkstra, L., Ylvisaker, M., Moore Sohlberg, M., Yorkston, K., Chiou, H. H., Kan, P. (2008). Intervention for executive functions after traumatic brain injury: A systematic review, meta- analysis and clinical recommendations. Neuropsychological Rehabilitation; an International Journal, 18(3), 257-299. doi:10.1080/09602010701748644 Kim, Y., Yoo, W., Ko, M., Park, C., Kim, S. T., & Na, D. L. (2009). Plasticity of the attentional network after brain injury and cognitive rehabilitation. Neurorehabilitation and Neural Repair, 23(5), 468-477. doi:http://dx.doi.org.weblib.lib.umt.edu:8080/10.1177/1545968308328728 Sohlberg, M. M., Avery, J., Kennedy, M., Ylvisaker, M., Coelho, C., Turkstra, L., & Yorkston, K. (2003). Practice guidelines for direct attention training. Journal of Medical Speech-Language Pathology, 11(3), xix-xxxix. Sohlberg, M. M & Mateer, C. A. (2010). Attention Process Training: A direct attention training program for persons with acquired brain injury. Youngsville, NC: Lash & Associates Publishing/Training Inc. Dani Perry CSD 675 Spring 2016 Attention Training + Strategy Instruction Computer-based Continuous self-reflection Target Population: acquired brain injury External Evidence Intervention for executive functions after traumatic brain injury: A systematic review, meta-analysis, and clinical recommendations Metacognitive Strategy Instruction Plasticity of the attentional network after brain injury and cognitive rehabilitation PMH: Epileptic seizures and pyogenic brain abscesses Impairment: Moderate cognitive-linguistic disorder -Moderate executive attention -Moderate prospective memory Activity Limitations: Trouble completing household/vocational duties, managing finances, staying focused w/o distractions Participation restrictions: Grocery shopping independently, engaging in conversations w/o becoming "lost," must walk everywhere-cannot drive Breaking complex tasks into steps Game face! Blocking internal/external distractions (Kennedy et al., 2008) Data Collection Results Takeaway . . . Plasticity of the neural networks Redistribution of attentional network resources Effortfull processing increases cognitive flexibility and generalization Aware of need for compensatory strategies Subjective evidence for redistribution of executive attention network (Kim et al., 2009) Level Ia Snapshot . . . Attention Process Training, 3rd Edition P: 42-year-old female with moderate cognitive-linguistic disorder secondary to amygdalohippocampectomy I: Attention Process Training with instruction in cognitive compensatory strategies C: Traditional cognitive rehabilitation therapy O: Increased cognitive functioning for IADLs Clinical Question References Implications Attention Process Training Test Level of Difficulty Accuracy Focus (Ehlhardt et al., 2008) Takeaway . . . Systematic Instruction Errorless learning + vanishing cues Intense/dispersed practice Effective for multiple populations

Transcript: Diminished and Clear Bilaterally No cough PT: 12.7 IN: 1.17 PTT and DIC were not recorded Patient Overview Current Resp Orders Owns a resturant Lives in rural Indiana From Eastern Kentucky Blood cultures Negative Urine cultures Negative Chest X-ray Inspection Albuterol 2.5mg/3mL Budesonide 0.5mg Q12 Breo Ellipta 100/25 1 QD Decrease in ADL Reduced mobility In and out of hospital for 6 months Wounds Artificial urinary sphincter removed 2 weeks prior to admission Possible UTI upon admission Glassgow score 15 Cap Refill of < 3 secs No clubbing No cyanosis No edema CAD COPD Vascular stent Patient's Current Assessment WBC: 7.7 k/cmm RBC: 3.34 mil/cmm Hb: 10 GM/dL HCT: 33.0% Platelets: 223 k/cmm Age: 77 Height 180.3 cm Weight: 72.3 kg Smoking Hx: Yes 1.5-2 ppd not quit Chief Complaint: AMS Cardiovascular Gastrointestinal Genitourioary Musculoskeletal Pyschological Behavioral Learning Respiratory Other Pertinent Data Dyspnea Percussion Medications HR: 61 Resp Pattern: Normal/Nonlabored BP: 134/65 Temp: 36.9 Celcius Kidney Function Albuterol 2.5mg/3mL QID Budesonide 0.5mg Q12 Breo Ellipta 100/25 QD Guafenesin 600mg BID Fluconazole Q24 Amiodarone Metoprolol Family History Occupational History Keep on current medications Draw ABG Start lung expansion Suggest a PFT Follow up with pulmonologist after d/c Smoking cessation classes Pt has COPD Barrel chest Active pace maker Areas of Importance Vitals Hollow sounding Areas of Concern Auscultation Patient Information Coagulation SOB while supine position WOB is nonlabored Clinical Case Study Ivy Tech Community College By: Caitlyn King BUN: 14 mg/dL CrL 0.92mg/dL I/O: 720/0 today, 1078/1085 yesterday Weight: today 72.3 kg, yesterday 73.5 kg Falling asleep Oriented while awake very pale frail skinny barrel chest shallow breathing skin discoloration History CBC Bibasilar opacities Hemithorax Emphysemitus change likely Costerfrenic anges visible Chest staples visible Very short lungs Heart shadow not very defined Mediasteinum visible and normal Plan of Care Test Results No family history was noted. UTI Admitting diagnosis Hx of COPD Dyspnea Glassgow score CXR Lack of Cough Smoking Hx Past medical history Medical hardware Current Meds Cultures Other Past Medical History

Transcript: - Factors that are critically important in the development of venous thrombosis: (1) venous stasis (2) activation of blood coagulation (3) vein damage. These three componants are known as the Virchow triad (Cunha, 2014). - Sepsis is usually caused by a progression of an infection. In the case of this patient his sepsis was a result of a common femoral puncture in his right groin area. - The puncture became infected and the infection caused cellulitis in the patient’s right leg. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. - If the infection that caused cellulitis is not taken care of it can enter the blood stream causing sepsis. If the sepsis progresses it can lead to septic shock, which will cause a life threatening, drop in blood pressure and potentially kill the patient (Herchline, 2014). Medications - DVT - Sepsis - UTI, not specified - Cellulitis of the right leg - Seizures (chronic) - Acute encephalopathy - Hypotension, unspecified Signs and Symptoms Comparison Negative Thank You! - Continuous pulse Ox Surgical History Outcomes/potential Problems Positive Dyspnea Hypothermia, hyperthermia Weakness Fatigue Heat/pain/swelling/unusual drainage at site of infection entry Tachypnea Hypotension Potential Problems For Tomorrow Initials: CG Encephalopathy in Sepsis - piperacillin/tazobactam (Zosyn)--> to treat cellulitus/septecimia (The patients pain was not assessable at 0730 and 1510 due to Altered Levels of consciousness) Allergies: No known - enoxaparin (Lovenox) --> for treatment of Deep Vein Thrombosis Patients was diagnosed with encephalopathy Patient displayed signs of dyspnea Lowest Blood pressure was 90/56mmhg Tachypnea, patients respiratory rate reached 22 breaths/min which is above the normal range of 12-20 breaths/minute. Patient also displayed an altered level of consciousness. Patient frequently disoriented Patient displayed signs of weakness in extremities Patient displayed shallow respirations Clinical Case Study - aspirin (Ascuprin)--> prevention of myocardial infarction DVT Pathophysiology (Dates for either procedure were not indicated in chart) Recent Findings ➢ The presentation in bladder cancer may resemble urinary tract infection (UTI), or the 2 conditions may coexist (Steinberg, 2014). ➢ The patient’s acute encephalopathy could be caused by hypercapnia r/t COPD (Claudett, 2014). ➢ Sepsis could be the cause of the patient’s encephalopathy (Davis, 2014). ➢ A-fib could have been the cause of the patient’s stroke (Rosenthal, 2014). ➢ Sepsis could be the cause of the patients hypotension. If sepsis progresses it could leap to septic shock (Mayo Clinic, 2011). ➢ Sepsis could be the progression of the bacteria that caused the patient’s Cellulitis (Herchline, 2014). ➢ The patient’s cellulitis was caused by a common femoral puncture in the right groin area. - Stroke - Atrial-fibrillation - Bladder cancer - COPD - multivitamin (Theragran)--> vitamin supplement References - Aspiration/dysphagia diet - Oxygen therapy 2L via nasal cannula - PIV (26 gauge) left antecubitol Typical Signs and Symptoms - Vitals q2hr Encephalopathy is commonly caused by liver problems. An uncommon side effect of sepsis is encephalopathy. Severe or advanced sepsis can cause Myasthenia crisis, which can eventually lead to encephalopathy. (Karnatovskaia, 2012, pp. 144-153). - Decreased vein wall contractility and vein valve dysfunction--> blood pools --> venous stasis promotes clotting --> DVT Vitals and Labs By: Kelsey "Black Cloud" Trujillo Vitals: - Deficient fluid volume r/t shift intravascular volume to interstitial space. Gender: Male - atorvastin (Lipitor) --> decreases cholesterol and prevents myocardial infarction - hydrocodone-acetaminophen--> for pain treatment Age: 80 No further increase in temperature Absence of chills and diaphoresis Pulse and respiratory rate within normal range for client WBC and differential counts returning to normal Negative blood culture results. Basic Info - Ineffective breathing breathing pattern r/t septic shock - Ineffective tissue profusion r/t progression to septic shock as evidence by decreased cardiac output. - Deficient fluid volume r/t shift intravascular volume to interstitial space. Causations and Risk Factors Past Medical History - acetaminophen (Tylenol)--> to treat mild pain Precautions: Seizure, high fall risk, aspiration, and skin integrity 4/22 at 0938 ➢ Low white blood cells can be the result of sepsis ➢ The decrease in the RBCs could be a sign of bleeding/anemia but it can also be from the patience bladder cancer. It could also be the result of sepsis the infection that entered the blood stream could be causing hemolysis ➢ The low hemoglobin could be caused by the patient’s cancer or sepsis, which causes hemolysis. ➢ The low Na could be a sign of dehydration. In dehydration, the body loses fluid and electrolytes. ➢ The decreased Ca could be a sign the patient has low albumin levels in the blood. Albumin is an

Transcript: Progressive mobility levels - bed rest/lateral rotation to sitting up at edge of bed Moderate decline in mental status - acute neurologic deterioration Aspirin 325 mg tab PO daily & 81 mg chewable tab PO once daily Func. class: nonopioid analgesic, nonsteroidal anti-inflammatory, antipyretic, antiplatelet Action: blocks pain impulses by blocking COX-1 in CNS, reduces inflammation by inhibition of prostaglandin synthesis, decreases platelet aggregation Side effects: seizures, coma, intracranial hemorrhage, GI bleeding, thrombocytopenia, agranulocytosis, leukopenia, neutropenia, hemolytic anemia, bronchospasm, anaphylaxis, largyngeal edema, angioedema Pt rationale: prevent MI and stroke due to recent hx of stroke For short term goals cont. Heparin 5000 units/mL SQ q8 hrs Func. class: anticoagulant, antithrombotic Action: prevents conversion of fibrinogen to fibrin and prothrombin to thrombin by enhancing inhibitory effects of antithrombin III Side effects: hematuria, hemorrhage, thrombocytopenia, anemia, anaphylaxis Pt rationale: to prevent DVT, PE, MI, stroke Right MCA clot Dysphagia Decreased left upper & lower extremity function Impaired balance/gait Confusion/disorientation Limited mobility Risk for impaired skin integrity Activity/exercise intolerance Muscle weakness Self care deficit Frailty Impaired communication Risk for interrupted family processes Progression since admission Pantoprazole 40 mg IV injection daily reconstituted with 10 mL NS Func. class: proton pump inhibitor Action: suppresses gastric secretion by inhibiting hydrogen/potassium ATPase enzyme system in gastric parietal cell; characterized as gastric acid pump inhibitor because it blocks the ifnal step of acid production Side effects: pancreatitis, rhabdomyolysis, myaglia, pneumonia, Stevens-Johnson syndrome, toxic epidermal nerolysis, anaphylaxis, angioedema Pt rationale: prevent duodenal/gastric/NSAID ulcer due to stress on body from recent stroke, reminaing in lying position for extended period of time, and inactivity Nursing Interventions Transferred from Charlotte Hungerford CT showed MCA infarct - pt sent to HH No TPA or thrombolytic therapies used upon admission Course of tx, anticipated length of stay, and discharge plans undetermined EKG, chest x-ray, CT scan performed Adult Assessment Guide Cont. 1. Client will engage in neuromotor physical activity every day to improve physical function 2. Client will be able to identify her own physical limitations 1. Client/family members will alter the environment to minimize the incidence of falls Adult Assessment Guide Cont. Adult Assessment Guide Cont. Adult Assessment Guide Cont. Long Term Goal Evaluation For Short Term Goals ECG Risk for falls r/t acute ischemic right MCA stroke a/e/b decreased ROM/strength in left upper & lower extremities, impaired gait/balance, sensory impairment, neurologic deterioration Short Term Goals' Evaluation Adult Assessment Guide Cont. Nursing Interventions I will continue to assist the client in progressing to increasing levels of activity tolerance. Following 1 month, I will determine if the patient is able to perform self care without risk. If the patient is unable to perform her own ADLs, then I will encourage her to keep working toward her goal, and reevaluate her techniques to determine if she should alter her pathway and try new methods Social Hx 1. Client will describe methods to avoid injury 2. Client will remain free of falls that result in injury Chest x-ray Lung apices trace bibasilar pleural effusions w/ mild compressive atelectasis 1. First, I will consult with the provider and physical therapy for a safety evaluation before initiating a mobility plan. 2. Then, I will provide the client with resources such as exercise classes, educational and recreational programs, and volunteer opportunities that can enhance socialization and appropriate activity. 3. Next, I will establish a slow pace of care 4. Then, I will instruct the patient to stop the activity immediately and notify the health care provider if she is experiencing new/worsened intensity/increased frequency of discomfort 5. I will also evaluate for medications and diet changes that would afford the patient strength to improve her motor skills Nursing Dx Levothyroxine 100 mcg tab PO daily Func. class: thryoid hormone Action: increases metabolic rate; controls protein synthesis; increase cardiac output, renal blood flow, O2 consumption, body tempearture, blood volume, growth, development at cellular level via action on thyroid hormone receptors Side effects: insomnia, tremors, tachycardia, angina, palpitations, dysrhythmias, thyroid storm, cardiac arrest Pt rationale: hypothyroidism Long Term Goal Evaluation Medications Typical diet: NPO Chewing/swallowing issues: aspiration risk due to left sided weakness resulting from stroke; unable to swallow Mouth: lips, tongue, gums, palate slightly dry & swollen; generalized redness; teeth clean, no debris; saliva thin/watery/plentiful Skin

Transcript: Conclusion :This patient has a decreased Hg/Hct and RBC due to the bleeding ulcer, with blood being excreted in her stool. Potassium is likely low due to vomiting/fluid loss. Chloride is slightly elevated. This can sometimes be due to excessive vomiting or diarrhea. It is still important to monitor, as hyperchloremia can affect O2 transport to the cells. (5) Two Hours Later.... As evidenced by our conversation, symptoms of her untreated mental illness of bipolar disorder were present. She was accusatory of staff, not showing evidence of understanding why requesting pain medication so frequently was bad. She had impulsive episodes of threatening to leave, and yelling at others. Two hours later, she was smiling and stated "I was the only one who cared about her". This is definitely a barrier to learning, as she was not receptive to staff at most times. Other barriers to learning may be that the patient has possible undiagnosed dementia. In collaboration with doctors and other nurses, we all agree that the patient exhibits some signs of dementia. This includes not being able to recall the previous days events, and that she does not recall being previously taught about her disease, or that she has been hospitalized in the past for ulcers. Assessment FIndings Pt C.D. is a 72 yo female who presents to the ED with severe abdominal pain and excessive vomiting. After complete work up by physicians, it is confirmed that she has a micro-perforation in the duodenum and a presumed pre-pyloric ulcer. Pt was placed on NPO status, and a Protonix drip. Doctors informed the staff that education to the patient was provided in the ED. It is now hospitalization day 4. Zosyn 3.375 G /50ml IV Piggyback Dilaudid 1-2 mg IVP PRN Q2 hours Lorazepam 1mg IVP PRN Q12 hours Protonix: 80 mg/100ml IV drip, infuse over 8 hours. Potassium Chloride 10meq/100ml Q1hr X2. C.D. became upset at my response, shaking her head and laughing. She stated that I "did not care about her", and she was going to leave this hospital. When trying to redirect C.D., I informed her I was concerned about her. I asked "Do you know why you have the ulcer?" She replied "No". I then educated her about the large doses of pain medications (NSAIDS, Vicoden) she uses at home, and how that is likely the cause of her ulcer. I discussed how using a lot of pain medications, whether at home or in the hopsital, was not healthy . C.D. again stated I was being accusatory, stood up, and asked to leave. I told her that she legally had the option to leave AMA, but that it is not advised. When her husband told her to sit down and listen to the nurse and doctors, C.D yelled at him, saying "You don't make the decisions in this relationship; Be quiet". (7) -Pt received an upper GI endoscopy to confirm her diagnosis. -H-Pylori testing was also done. (Result came back negative). This test is done to detect the presence of the bacteria H-Pylori, in the GI tract. H-pylori is a gram negative bacteria, found in those with patients who have ulcers. H-pylori lives in about 50% of people, who remain asymptomatic and never develop an ulcer (mechanism uknown)(3) Pt also received an upper GI series X ray with a barium swallow to confirm diagnosis. Patient's Lab Values Vital Signs: HR: 86 BP: 154/85 T: 37.7 (99.86) RR-18 02- 94% 1L02 Extensive Smoking History NSAID abuse for chronic pain -Suggest OT do a mini mental examination to test for orientation and dementia. -Collaborate with social work on suggesting the client possibly be discharged with services for regulation of medications. -If appropriate, refer patient to psychiatry to assess needs for medications and extent of mental illness. -Educate patient on risk factors for disease, and necessary lifestyle changes to prevent an ulcer from reoccurring (smoking cessation, decreased NSAID use, decreased caffeine consumption) (8) -Give information to patient in concise and short form to prevent further confusion and agitation. - Involve C.D.'s husband in teaching and care, for support at home. Nursing Implications for C.D. Psychological: Patient is diagnosed with Bipolar Disorder, although patient is not receiving any psychiatric medications while here in the hospital. Patient denies taking any psychiatric medications, but she is known to be a poor historian. NURSING 612 CLINICAL CASE STUDY The Increased Sodium is also likely d/t excessive vomiting. This patient's BUN is low, which normally is not of concern, since so many factors contribute to a person's BUN. Antibiotics, Liver Damage, and Female sex all contribute to a low BUN. (6) Patient Assessment Patient Assessment.... Peptic Ulcer Disease Barriers To Learning Most common cause is infection from H pylori bacteria. The bacterium causes these ulcers by damaging the mucous coating that protects the stomach and duodenum. Damage to the mucous coating allows stomach acid to get through to the sensitive lining beneath. (1) Other causes are increased acid and pepsin(digestive enzyme found in gastric

Transcript: Rationale 26 y/o Female Findings during Examinations Reasonalbe Short Term Plan Findings Cont. Reason for coming in the ER SOB Patient history History of asthma Tylenol Mucinex Protonix General appearance Inspection CXR Initial Treatment Clinical Case Study Antibiotics Organ evaluation. Rocephin Azithromycin Treatment Patient Backgroud DuoNeb Pulmicort Ventolin Other Medications Respiratory Medication Current Treatment

Explore our templates for more presentation inspiration

Sales KickOff - Rocket

Description: The sky’s the limit. Boost your new sales initiative into orbit with an engaging and compelling SKO presentation. This template features a effective sales kickoff theme that makes it easy to be engaging. Like all Prezi SKO templates, it’s fully customizable with your own information.

Customer Stories - Office

Description: Storytelling is at the heart of great service. Use this stunning, customizable business presentation template to highlight employees who do exceptional work or position your customers as the heroes of your business.

Quarterly Business Review - Downtown

Description: Add some color to your quarterly business review with this vibrant business presentation template. The bold visuals in this business template will make your next QBR a memorable one.

Marketing Proposal Template for Powerful Presentations | Prezi

Description: Catch the eye and engage the imagination with this cool-looking Prezi proposal template. The bold, bright design and highly dynamic theme all but guarantee success for your next sales or marketing proposal. All Prezi presentation templates are easily customized.

Now you can make any subject more engaging and memorable

• The Science
• Conversational Presenting
• For Business
• For Education
• Testimonials
• Presentation Gallery
• Video Gallery
• Design Gallery
• Our Customers
• Company Information
• Prezi Support
• Prezi Classic Support
• Hire an Expert
• Data Visualization
• Infographics

July 25, 2024

July 22, 2024

July 18, 2024

• Latest posts

© 2024 Prezi Inc. Terms

• Search Menu
• Sign in through your institution
• Advance articles
• Editor's Choice
• Author Guidelines
• Submission Site
• Why publish with this journal?
• Open Access
• Self-Archive Policy
• About Brain Communications
• Editorial Board
• Advertising & Corporate Services
• Observers Programme
• Reviewer Academy
• Journals on Oxford Academic
• Books on Oxford Academic

Article Contents

Introduction, materials and methods, supplementary material, acknowledgements, competing interests, data availability.

• < Previous

Clinical criteria for a limbic-predominant amnestic neurodegenerative syndrome

• Article contents
• Figures & tables
• Supplementary Data

Nick Corriveau-Lecavalier, Hugo Botha, Jonathan Graff-Radford, Aaron R Switzer, Scott A Przybelski, Heather J Wiste, Melissa E Murray, Robert Ross Reichard, Dennis W Dickson, Aivi T Nguyen, Vijay K Ramanan, Stuart J McCarter, Bradley F Boeve, Mary M Machulda, Julie A Fields, Nikki H Stricker, Peter T Nelson, Michel J Grothe, David S Knopman, Val J Lowe, Ronald C Petersen, Clifford R Jack, David T Jones, Clinical criteria for a limbic-predominant amnestic neurodegenerative syndrome, Brain Communications , Volume 6, Issue 4, 2024, fcae183, https://doi.org/10.1093/braincomms/fcae183

• Permissions Icon Permissions

Predominant limbic degeneration has been associated with various underlying aetiologies and an older age, predominant impairment of episodic memory and slow clinical progression. However, the neurological syndrome associated with predominant limbic degeneration is not defined. This endeavour is critical to distinguish such a syndrome from those originating from neocortical degeneration, which may differ in underlying aetiology, disease course and therapeutic needs. We propose a set of clinical criteria for a limbic-predominant amnestic neurodegenerative syndrome that is highly associated with limbic-predominant age-related TDP-43 encephalopathy but also other pathologic entities. The criteria incorporate core, standard and advanced features, including older age at evaluation, mild clinical syndrome, disproportionate hippocampal atrophy, impaired semantic memory, limbic hypometabolism, absence of neocortical degeneration and low likelihood of neocortical tau, with degrees of certainty (highest, high, moderate and low). We operationalized this set of criteria using clinical, imaging and biomarker data to validate its associations with clinical and pathologic outcomes. We screened autopsied patients from Mayo Clinic and Alzheimer’s Disease Neuroimaging Initiative cohorts and applied the criteria to those with an antemortem predominant amnestic syndrome (Mayo, n = 165; Alzheimer’s Disease Neuroimaging Initiative, n = 53) and who had Alzheimer’s disease neuropathological change, limbic-predominant age-related TDP-43 encephalopathy or both pathologies at autopsy. These neuropathology-defined groups accounted for 35, 37 and 4% of cases in the Mayo cohort, respectively, and 30, 22 and 9% of cases in the Alzheimer’s Disease Neuroimaging Initiative cohort, respectively. The criteria effectively categorized these cases, with Alzheimer’s disease having the lowest likelihoods, limbic-predominant age-related TDP-43 encephalopathy patients having the highest likelihoods and patients with both pathologies having intermediate likelihoods. A logistic regression using the criteria features as predictors of TDP-43 achieved a balanced accuracy of 74.6% in the Mayo cohort, and out-of-sample predictions in an external cohort achieved a balanced accuracy of 73.3%. Patients with high likelihoods had a milder and slower clinical course and more severe temporo-limbic degeneration compared to those with low likelihoods. Stratifying patients with both Alzheimer’s disease neuropathological change and limbic-predominant age-related TDP-43 encephalopathy from the Mayo cohort according to their likelihoods revealed that those with higher likelihoods had more temporo-limbic degeneration and a slower rate of decline and those with lower likelihoods had more lateral temporo-parietal degeneration and a faster rate of decline. The implementation of criteria for a limbic-predominant amnestic neurodegenerative syndrome has implications to disambiguate the different aetiologies of progressive amnestic presentations in older age and guide diagnosis, prognosis, treatment and clinical trials.

Selective and predominant degeneration of the limbic system has been associated with an older age, predominant and circumscribed episodic memory impairment and slow clinical course. 1-5 Various underlying aetiologies are known to cause degeneration of the limbic system, the most frequent being limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC), which first involves the amygdala, followed by the hippocampus, and then the middle frontal gyrus, 1 , 6-9 and is found in ∼40% of autopsied brains beyond age 85 years. 10 , 11 Other rare neuropathologic findings have been associated with neurodegeneration of the limbic system, including argyrophilic grain disease, vascular disease and rare forms of limbic Alzheimer’s disease. 12-18 By contrast, amnestic syndromes originating from neocortical degeneration are in vast majority caused by Alzheimer’s disease neuropathological changes (ADNCs) and often present with non-memory features, a more rapid clinical course and a relatively younger age than patients with predominant limbic degeneration. 2-4 , 19 However, the recognition of different aetiologies driving predominant amnestic syndromes in clinical practice has been hampered by the significant overlap in clinical features associated with predominant limbic versus neocortical degeneration. This endeavour is further complicated by the fact that the most common cause of limbic degeneration, namely, LATE-NC, is frequently comorbid with other neuropathologies including amyloid plaques and tau tangles, i.e. ADNC, with which LATE-NC partially shares pathogenic mechanisms. 9 , 15 , 20-22 This calls for much-needed clinical criteria to identify predominant amnestic syndromes caused by a predominant degeneration of the limbic system and to distinguish such syndromes from those with a predominant neocortical presentation, which may differ in terms of underlying aetiology, disease course and therapeutic needs. The current work aims to define and establish clinical criteria for the neurological syndrome associated with the selective degeneration of the limbic system, which we term limbic-predominant amnestic neurodegenerative syndrome (LANS). It is important to mention at the outset of this investigation that while LANS is associated with various underlying aetiologies, we primarily focus on LATE-NC in the context of this study to provide construct validity to the LANS criteria given the much higher frequency of LATE-NC in old age, its frequent comorbidity with ADNC 1 , 11 , 12 , 23 and the far more extensive research that has been done on LATE-NC compared to other pathologies associated with limbic degeneration.

Several efforts based on retrospective clinicopathological studies have aimed to characterize the clinical profile of individuals who had predominant limbic degeneration and LATE-NC at autopsy and to disambiguate this profile from those who had ADNC without LATE-NC. The most common finding across studies is that episodic memory impairment dominates the clinical profile of individuals with LATE-NC, while cognitive functions functionally associated with neocortical areas (e.g. visuospatial processing) are relatively preserved. Studies that evaluated the longitudinal trajectory of cognitive impairment in LATE-NC consistently found a milder and slower decline of episodic memory and global function relative to ADNC and a steeper rate of decline in patients with evidence for both diseases, i.e. ADNC/LATE-NC. Evidence of semantic memory impairment in LATE-NC is measured through object naming, verbal fluency and knowledge of famous faces and events. 2 , 19 , 24 For instance, a recent study from our group showed that an important feature of object naming failure in individuals with LATE-NC is loss of semantic memory, while word retrieval difficulties are more specific in patients with ADNC. 25 However, these studies either did not assess semantic memory impairment in the context of a predominant amnestic syndrome, directly compared patients with LATE-NC versus ADNC or accounted for global severity of impairment, thus rendering the operationalization of semantic memory impairment in amnestic syndromes caused by limbic degeneration challenging. Overall, evidence supports a clinical profile characterized by a relatively isolated amnestic syndrome with an indolent progression in patients with LATE-NC relative to ADNC, in addition to semantic memory impairment, although less documented.

In vivo neuroimaging markers of autopsy-confirmed LATE-NC have been described. The hippocampus is a known locus of LATE-NC pathology. For example, MRI studies have repeatedly found smaller hippocampal volume and faster rates of hippocampal atrophy associated with LATE-NC when accounting for the extent of ADNC. 21 , 26-28 Hippocampal sclerosis (severe cell loss and gliosis in the hippocampal formation, often with accentuated atrophy) is a frequent finding at autopsy associated with LATE-NC. 21 , 23 , 29 In fact, studies have described patients with a dense amnestic syndrome who were either tau-negative on PET imaging or had TDP-43–related hippocampal sclerosis with minimal ADNC at autopsy. 30 , 31 This strongly supports the hypothesis that LATE-NC is an independent driver of hippocampal atrophy that is sufficient to cause a progressive amnestic syndrome.

Fluorodeoxyglucose (FDG)-PET has also been proven useful for delineating patterns of involvement associated with LATE-NC and has the potential to objectively index impaired limbic function in the setting of preserved neocortical function. Botha et al . 28 first developed the inferior-to-medial temporal (IMT) ratio as a marker of TDP-43–related hippocampal sclerosis in tau-negative amnestic dementia, where such patients exhibit prominent medial temporal lobe hypometabolism relative to the lateral temporal lobe, while the opposite pattern is typically associated with ADNC. Buciuc et al . 22 subsequently showed that this marker is specific and sensitive to advanced LATE-NC regardless of hippocampal sclerosis status. A recent study by Grothe et al . 31 showed that autopsy-confirmed cases of LATE-NC exhibit prominent temporo-limbic hypometabolism compared to those with ADNC and that independent patients with a clinical diagnosis of Alzheimer’s disease dementia showing this ‘LATE-NC–like’ pattern had an older age at evaluation, a memory-dominant cognitive impairment profile, a slower clinical course and lower Alzheimer’s disease biomarkers levels. These findings position temporo-limbic–predominant hypometabolism, in addition to disproportionate hippocampal atrophy on MRI, as a promising candidate for the in vivo identification of individuals with predominant limbic degeneration highly associated with underlying LATE-NC and for distinguishing such patients from those with neocortical degeneration and ADNC as the primary driver of their symptoms.

Despite the significant advances in identifying in vivo features indicative of limbic degeneration, especially in the context of LATE-NC, clinically applicable criteria of a predominant amnestic syndrome driven by a pattern of limbic-predominant degeneration do not currently exist. The in vivo identification of patients with a high likelihood of limbic degeneration as the primary driver of their symptoms has relevance for symptom management and prognosis and prediction of underlying aetiology, which are thought to differ from other amnestic syndromes associated with predominant neocortical degeneration. The detection of causes for predominant amnestic symptoms is also highly relevant in this era of emerging disease-modifying therapies to prevent patients from being inadvertently treated with inappropriate therapies, 32 , 33 given that several non–Alzheimer’s disease aetiologies are associated with limbic degeneration.

We propose a set of clinical criteria for LANS. LANS is defined as a degenerative neurologic syndrome in that it refers to a set of clinical signs and symptoms associated with a requisite functional neuroanatomic localization, i.e. the limbic system. While the definition of LANS is agnostic to molecular pathology, this syndrome is highly associated with LATE-NC but also other less common neuropathologic entities as mentioned earlier. In the absence of one-to-one mapping with a single underlying pathology and lack of clinically applicable in vivo biomarker of TDP-43, LANS can be framed as a clinico-radiological, or neurologic, entity rather than clinicopathologic. 34 , 35 While the current investigation focuses on LANS associations with LATE-NC, data on other neuropathologies are provided in Supplementary material . The LANS criteria include core, standard and advanced criteria that can be measured in vivo along with levels of certainty that clinical symptoms are caused by the predominant degeneration of the limbic system (described in Box 1 ). We operationalized this set of criteria based on clinical, imaging and biomarker features that can be obtained in current clinical practice for evaluating neurologic symptoms. It is important to specify that the LANS criteria and associated likelihoods are meant to guide decision-making in clinical practice. The quantitative operationalization of the LANS criteria described in the context of this specific study is meant to provide construct validity to the criteria by retrospectively applying it to a cohort of autopsied patients from the Mayo Clinic and Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohorts. This operationalization thus serves a validation purpose in the context of current and future studies and is not meant to be concretely applied in clinical practice. For example, we recommend that current clinical standards for interpreting brain imaging be used rather than quantitative metrics that are not routinely available (see Box 1 ).

Clinical criteria

‘Core clinical features’

Must present with a slow, amnestic, predominant neurodegenerative syndrome (insidious onset with gradual progression over 2 or more years) without another condition that better accounts for the clinical deficits.

‘Standard supportive features’

Older age at evaluation (generally ≥75 years old)

Mild clinical syndrome with largely preserved neocortical-predominant functions

Hippocampal atrophy out of proportion to syndrome severity

Impaired semantic memory in the setting of a mild syndrome

‘Advanced supportive features’

Limbic hypometabolism and absence of neocortical degenerative pattern on FDG-PET imaging

Low likelihood of significant neocortical tau pathology

‘Degree of certainty’

Low likelihood: meets core features and ≤2 standard features

Moderate likelihood: meets core features and ≥3 standard features or meets core features and ≥2 standard and 1 advanced features

High likelihood: meets core features, ≥3 standard features and 1 advanced feature or meets core features, ≥2 standard features and 2 advanced features

Highest likelihood: meets all core, standard and advanced features

Participants

Two clinicopathological cohorts were used for this study. The primary cohort came from the Mayo Clinic Study of Aging and Alzheimer’s Disease Research Center research programmes from Mayo Clinic, Rochester (now referred to as ‘Mayo cohort’). The second cohort came from the ADNI cohort. We screened all autopsied patients from these two cohorts (Mayo cohort, n = 922; ADNI cohort, n = 93) and included those with an antemortem history of a predominant and progressive amnestic syndrome. This was defined by a clinical diagnosis of amnestic Alzheimer’s-type dementia or single- or multi-domain amnestic mild cognitive impairment at baseline according to widely accepted criteria. 36-38 Specifically, an amnestic syndrome was defined as an impaired ability to learn and remember new information (e.g. repetitive questions, misplacing personal items, forgetting events/appointments), and these deficits had to be considered to reflect a decline from a premorbid level of functioning. The diagnostic process primarily relied on medical history obtained from the patient and a reliable informant and neurological examination including cognitive screening. Additional diagnostic assessments, including imaging and/or neuropsychological assessments, were often conducted as part of clinical care or co-enrollment in research programmes. While these assessments supported clinical diagnoses, they did not determine it. We additionally excluded patients with insufficient pathology data, i.e. missing information about amyloid plaques, tau and Lewy bodies and LATE-NC. The primary analyses only considered patients with a pathological diagnosis of ADNC, LATE-NC or comorbid ADNC/LATE-NC. This resulted in a final sample of 165 patients from the Mayo cohort and 53 patients from the ADNI cohort. The workflow of patient inclusion is found in Supplementary Fig. 1 . Analyses considering all primary neuropathological diagnoses associated with a progressive and predominant amnestic syndrome were conducted separately and are in Supplementary material (referenced in-text where appropriate). Data from 112 age- and sex-matched cognitively unimpaired (CU) controls from the Mayo Clinic Study of Aging were collected for imaging comparison purposes (MRI, FDG-PET) in the Mayo cohort. CUs had to be amyloid- and tau-negative based on PET imaging and have MRI and FDG-PET imaging available for inclusion in the study.

Patients and/or their legal representative provided written consent for their data to be used for research purposes. This study met HIPAA guidelines and was approved by the Mayo Clinic Institutional Review Board.

Neuropathological assessment

Assessments for the Mayo and ADNI cohorts were performed by experienced neuropathologists in accordance with current diagnostic protocols 39 and are described in Supplementary material . ADNC was diagnosed according to the ABC ranking score 40 which includes the Thal staging of amyloid plaques, Braak staging of neurofibrillary tangles 41 and the density measurement of neuritic plaques. 39 A stage of Braak IV or less in the absence of significant amyloidosis (<2 Thal stage) was classified as primary age-related tauopathy (PART). 42 In the Mayo cohort, TDP-43 type A was defined as TDP-43 immunoreactive neuronal cytoplasmic inclusions, dystrophic neurites and neuronal intranuclear inclusions in vulnerable cortical and subcortical areas. TDP-43 type B had predominantly neuronal cytoplasmic inclusions. 43 Similar procedures were applied in ADNI (see https://adni.loni.usc.edu/methods/neuropath-methods/ ). TDP-43 staging was classified as FTLD-TDP-43–related or not (i.e. LATE-NC) based on its spatial distribution. LATE-NC staging was done in 40/90 of patients with confirmed TDP-43 from the Mayo cohort and all patients from the ADNI cohort. Lewy body disease (LBD) was staged according to published criteria, 44 and significant burden was considered when pathology was documented in limbic and/or neocortical areas. Corticobasal degeneration was diagnosed by the presence of cortical and subcortical neuronal and glial lesions (i.e. astrocytic plaques) and thread-like processes in grey and white matter. 45 Progressive supranuclear palsy staging was performed according to published criteria. 46 Corticobasal degeneration and progressive supranuclear palsy were categorized as ‘FTLD-tau’. A diagnosis of argyrophilic grain disease was made if there were silver and tau-positive spindle-shaped lesions, coiled bodies and balloon neurons in trans-entorhinal and entorhinal cortex, amygdala or cingulate gyrus. 16 The presence of other pathologies including hippocampal sclerosis and vascular disease (cerebral amyloid angiopathy, infarcts and lacunes, microbleeds, haemorrhages, arteriolosclerosis) was also assessed.

Imaging acquisition and processing

Acquisition protocols for MRI and PET images are in Supplementary material . Regional MRI and FDG-PET data were generated for both the Mayo and ADNI cohorts using in-house processing pipelines from Mayo Clinic using Statistical Parameter Mapping 12 (SPM12). PET images were co-registered to their corresponding MRI image. All images were normalized into the Mayo Clinic Adult Lifespan Template and smoothed with a 6-mm full-width at half-maximum smoothing kernel. FDG-PET images were normalized to the pons to yield regional standard uptake value ratios (SUVRs). The FDG-PET IMT ratio was derived by dividing SUVR values from the inferior temporal lobe by the size-weighted sum of SUVR values from the amygdala and hippocampus, 31 , 47 where higher values are indicative of LATE (thresholding procedures are described in the ‘Statistical analyses’ section).

Hippocampal volume calculation is described in separate publications. 48 , 49 Briefly, it was corrected for intracranial volume by calculating the residuals from a linear regression based on a sex-specific formula. This is similar to the approach from Jack et al ., 49 except for the use of SPM12 instead of FreeSurfer and a different CU sample as described in Stricker et al . 45 This measure was combined across hemispheres.

Different methods were used to determine abnormality thresholds for global FDG-PET, amyloid-PET and tau-PET SUVR meta-regions of interest (meta-ROIs) across the Mayo and ADNI cohorts due to differences in processing pipelines, radiotracers for amyloid-PET and cohorts studied. This was done only for global measures, whereas regional data were generated using the same pipeline as described above. Briefly, global FDG-PET (normalized to the pons), amyloid-PET and tau-PET (normalized to the cerebellar crus) were derived from established meta-ROIs. 50-52 Images from the Mayo cohort processed with the pipeline described above were used, and abnormality thresholds set at ≤1.47 (FDG-PET), ≥1.48 (amyloid-PET; PiB) and ≥1.29 (tau-PET; flortaucipir) according to published methods. 50 , 52 Images from the ADNI cohort processed in Berkeley (CA, USA) using published methods 53 were used. Abnormality thresholds were set at ≤1.21 (FDG-PET), ≥1.11 (amyloid-PET; florbetapir), ≥1.0818 (amyloid-PET; florbetaben) and ≥1.29 (tau-PET; flortaucipir) according to published methods. 51 , 53 , 54 Amyloid-PET values from both cohorts were transformed into centiloids for descriptive purposes.

Fluid biomarkers

CSF samples from both the Mayo and ADNI cohorts were analysed using published protocols. 55 , 56 Briefly, samples were analysed using Elecsys β-Amyloid (1-42) CSF, Total-Tau CSF and Phospho-Tau (181P) CSF electrochemiluminescence immunoassays (Roche Diagnostics). Quality control procedures and technical limits were handled as previously described. 55 Thresholds were set at ≤1026 pg/ml for Aβ42, ≥22 pg/ml for P-tau and ≥0.023 for the Aβ42/P-tau ratio. 55 , 57 , 58

Procedures for the analysis and quality control of plasma assays for the Mayo cohort are described in a separate publication. 59 Briefly, plasma phosphorylated-Tau 181 (pTau181) was measured with the Simoa® pTau-181 Advantage V2 kit following instructions from the manufacturer and ran on a Quanterix HD-X Analyzer (Quanterix, Lexington, MA, USA). The pTau181 threshold was set at <2.56 pg/ml according to previous research assessing the relationship between pTau181 and ADNC. 59 Plasma assays in ADNI were collected and processed according to published methods 60 , 61 and were measured using an in-house assay as previously described. 62 Plasma pTau181 was measured with Simoa HD-X instruments (Quanterix, Billerica, MA, USA) as described elsewhere. 63 The pTau181 threshold was set at <17.7 pg/ml according to previous research assessing the relationship between pTau181 and Alzheimer’s disease biomarkers. 63 Of note, differences in pTau181 thresholds across the Mayo and ADNI cohorts are due to differences in scaling, threshold determination methods and assays (as noted above).

Operationalization of the LANS criteria

The operationalization of the LANS criteria involves in vivo clinical, imaging and biomarker data. These operationalized criteria are not meant to be concretely applied to clinical practice; rather, their purpose is to provide construct validity to our proposed LANS criteria. In particular, the assessment of imaging criteria should be based on visual read in clinical practice as generally done in clinical neurology and radiology rather than quantitative methods as described below. These operationalized criteria are as follows:

Older age at evaluation (standard feature): age of ≥75 and older. Age at first visit was used. While we used 75 years old as threshold to operationalize this criterion in the context of this study, this is not a rigid cut-off for its application in clinical practice. Rather, older age increases the likelihood that the amnestic syndrome is caused by the degeneration of the limbic system.

Mild clinical syndrome (standard feature): diagnosis of mild cognitive impairment or mild amnestic dementia [i.e. score ≤4 on the Clinical Dementia Rating Sum of Boxes (CDR-SB)]. 64 The score at the first visit was used.

Hippocampal atrophy out of proportion to syndrome severity (standard feature): hippocampal volume smaller than expected according to the CDR-SB score (see procedure in ‘Statistical analyses’). The hippocampal volume at the last MRI was used.

Mildly impaired semantic memory (standard feature): given the less well-established literature in the context of LATE-NC, this feature is not operationalized in this iteration of the LANS criteria and is not included in the calculation of likelihoods in the context of the current study. However, its use is encouraged in clinical practice using expert clinical judgement.

Limbic hypometabolism (advanced feature): above-threshold value on the FDG-PET IMT ratio (see procedure in ‘Statistical analyses’). IMT ratio at the last FDG-PET was used.

Absence of neocortical degenerative disease pattern (advanced feature): above-threshold value on an established FDG-PET Alzheimer’s disease meta-ROI, which is indicative of an absence of the ADNC pattern. The score at the last FDG-PET was used. We used a meta-ROI in the context of this study, but this applies to any imaging biomarker indicative of neocortical degeneration, regardless of underlying aetiology.

Low likelihood of significant neocortical tau pathology (advanced feature): multiple scenarios are possible and are prioritized as follows: (i) negative amyloid-PET SUVR as it can serve as a surrogate marker of absence of neocortical tau 64 ; (ii) positive amyloid-PET SUVR and negative tau-PET SUVR; (iii) negative CSF biomarkers for Alzheimer’s disease pathology if PET imaging is not available; and (iv) negative plasma biomarkers for Alzheimer’s disease pathology if PET imaging and CSF are not available.

To add context to the assessment of neocortical tau, the rationale of this criterion is to reduce the likelihood that the clinical syndrome is primarily driven by neocortical pathology as seen in the multi-domain forms of Alzheimer’s disease. 65 , 66 The specification of ‘neocortical’ tau as opposed to tau in general is to account for the limbic variant of Alzheimer’s disease wherein associated clinical and pathologic findings localize to the limbic system, 67 , 68 thus qualifying for LANS. Another point that deserves mention is that while we used a tau-PET SUVR that is highly associated with neocortical tau in this study, 50 , 53 visual assessment as recommended by the FDA guidelines is recommended in clinical practice, which includes the posterior lateral temporal lobe as the only temporal region to count towards neocortical tau positivity (see https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212123s000lbl.pdf ). In regard to plasma biomarkers, current assays are mostly sensitive to amyloid pathology, and current thresholds are not useful in determining limbic versus neocortical tau. 69 The same applies to the CSF P-tau/Aβ ratio. Fluid biomarkers, in their current state of development, should only be used to rule out amyloidosis. If positive, these LANS criteria are not met, and further workup is recommended to investigate the presence of neocortical versus limbic distribution of tau.

Statistical analyses

Statistical analyses were performed using R version 4.2.3. One-way ANOVAs and χ 2 tests were used to assess between-group differences on demographic, clinical and biomarker data, and post hoc analyses were performed when the omnibus test was significant.

We compared FDG-PET and MRI findings between ADNC, ADNC/LATE-NC and LATE-NC patients and CUs from the Mayo cohort in a pairwise fashion using SPM12, resulting in t-maps. We applied a false discovery rate correction to control for multiple comparisons at the peak level. Cluster-level correction does not apply since we used unthresholded maps.

The procedure to assess disproportionate hippocampal atrophy according to clinical severity consisted of fitting a mixed linear model with CDR-SB as a predictor of hippocampal volume accounting for intra-individual change in the ADNI cohort. This was done including all patients with an amnestic syndrome with available CDR-SB and hippocampal volume, regardless of underlying pathology ( n = 85, 435 time points). We then calculated the scaled residuals between predicted and true values. We used a receiver operating characteristic (ROC) curve analysis on Z -scored residuals to determine the optimal threshold for discriminating patients with LATE-NC (LATE and ADNC/LATE-NC) from those without LATE-NC (ADNC, ADNC/LBD, LBD, PART) based on the last MRI scan obtained. We applied this threshold in the ADNI cohort and in the Mayo cohort after predicting the residuals using the model defined in ADNI. We used a similar ROC curve analysis in the ADNI cohort to determine the FDG-PET IMT threshold that best discriminates individuals with LATE-NC (LATE and ADNC/LATE-NC) from those without LATE-NC (ADNC, ADNC/LBD, LBD, PART) based on the last FDG-PET scan obtained ( n = 63). We then applied this threshold in the ADNI and Mayo cohorts.

Counts for standard and advanced LANS features and likelihoods derived from the operationalized criteria were measured for each patient with LATE-NC, ADNC/LATE-NC and ADNC. χ 2 analyses followed by post hoc tests were conducted to assess the distribution of pathological diagnoses within likelihoods and the distribution of likelihoods within pathological diagnoses. This was done while combining highest and high likelihoods within a single category. We then fit a mixed linear model with an interaction between time from baseline (in years) and likelihood group (highest, high, moderate, low) as predictor and CDR-SB as outcome measure accounting for intra-individual change to assess differences in clinical progression across likelihoods. We then assessed FDG-PET differences between likelihood categories (highest/high, moderate, low) and CUs in pairwise fashion as described above.

We fit a logistic regression model in the Mayo cohort to perform a binary classification of patients with LATE-NC (i.e. LATE-NC and ADNC/LATE-NC) versus ADNC using LANS features as input. Only the tau score was considered as a categorical variable (positive, negative), whereas other variables (age at examination, CDR-SB score, hippocampal volume, IMT ratio, FDG-PET meta-ROI) were considered as continuous. We then performed out-of-sample predictions in the ADNI cohort using the model fitted in the Mayo cohort.

We performed an exploratory analysis specifically in patients with ADNC/LATE-NC from Mayo Clinic on the premise that some of these patients may have LATE-NC as a primary pathology and ADNC as a secondary pathology, and vice versa. We stratified ADNC/LATE-NC patients into highest/high, moderate and low LANS likelihoods. We fit a mixed linear model with an interaction between time from baseline (in years) and group (ADNC, ADNC/LATE-NC highest/high, ADNC/LATE-NC moderate, ADNC/LATE-NC low, LATE-NC) as predictor and CDR-SB as outcome measure accounting for intra-individual change to assess differences in clinical progression across groups. We then assessed FDG-PET differences between ADNC/LATE-NC likelihood groups and CUs in a pairwise fashion as described above.

Sample characteristics

Demographic, clinical and biomarker data at baseline for patients with ADNC, LATE-NC and ADNC/LATE-NC from the Mayo and ADNI cohorts are displayed in Table 1 . The data for all pathological diagnoses are displayed in Supplementary Table 1 . LATE-NC and ADNC/LATE-NC patients were older than ADNC patients at presentation and death in the Mayo cohort only. In both cohorts, there were more APOE4 carriers in ADNC and ADNC/LATE-NC groups compared to LATE-NC, and ADNC and ADNC/LATE-NC groups had higher amyloid-PET centiloid values compared to LATE-NC. ADNC/LATE-NC patients had, on average, higher baseline CDR-SB scores than LATE-NC patients in the ADNI cohort only. There were no other differences.

Demographic, clinical and biomarker data of the Mayo and ADNI cohorts

CDR-SB, Clinical Dementia Rating Scale Sum of Boxes; ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-related TDP-43 encephalopathy neuropathological changes; MCI, mild cognitive impairment; SUVR, standard uptake value ratio.

a One observation only. Values are expressed as counts or median and interquartile ranges.

The distribution of pathological diagnoses underlying a progressive and predominant neurodegenerative amnestic syndrome in the Mayo and ADNI cohorts is displayed in Fig. 1 . ADNC, ADNC/LATE-NC and LATE-NC accounted for 35, 37 and 4% of cases in the Mayo cohort, respectively, and 30, 22 and 9% of cases in the ADNI cohort, respectively. Vascular pathologies (cerebral amyloid angiopathy, infarcts/lacunes, microbleeds, haemorrhages, arteriolosclerosis) were not considered in primary pathological diagnoses unless they were the only significant pathological feature (i.e. vascular dementia). The presence and severity of vascular pathologies across pathological diagnoses are listed in Supplementary Table 2 .

Primary neuropathological diagnoses associated with a predominant and progressive neurodegenerative amnestic syndrome in the Mayo and ADNI cohorts. ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-associated TDP-43 encephalopathy neuropathological changes; LBD, Lewy body disease; AGD, argyrophilic grain disease; FTLD, fronto-temporal lobar degeneration; PART, primary age-related tauopathy; VaD, vascular disease.

FDG-PET and MRI findings

FDG-PET and MRI contrasts comparing patients groups to CUs showed patterns of degeneration in lateral temporal and hippocampal areas in ADNC/LATE-NC patients and in lateral temporo-parietal and precuneus areas in ADNC. FDG-PET findings are displayed in Fig. 2 , and MRI findings are displayed in Supplementary Fig. 2 . Only one contrast between patient groups survived correction for multiple comparisons for both MRI and FDG-PET modalities. This contrast revealed that ADNC/LATE-NC had significantly more temporo-limbic degeneration involving the hippocampal, insular, temporo-polar, middle frontal and orbitofrontal areas compared to ADNC patients. Comparisons involving LATE-NC patients failed to reveal significant differences at the group level, likely owing to the small sample size.

FDG-PET findings between ADNC, ADNC/LATE-NC, LATE-NC and CU controls. The ‘less than’ sign reflects less metabolism in a given group relative to the other and vice versa. Contrasts were generated using SPM12 using pairwise t -comparisons between groups at the voxel level and involved 53 ADNC cases, 33 ADNC/LATE-NC cases, 4 LATE-NC cases and 112 CUs. ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-associated TDP-43 encephalopathy neuropathological changes; CU, cognitively unimpaired; FDR, false discovery rate; N.S., non-significant; FDG-PET, fluorodeoxyglucose-PET.

LANS likelihood differences

Table 2 indicates the distribution of ADNC, LATE-NC and ADNC/LATE-NC patients across stand-alone LANS features and LANS likelihoods for the Mayo and ADNI cohorts. These data for all pathological diagnoses are displayed in Supplementary Table 3 . The assessment of differences in the distribution of LANS likelihood only applied to patients for whom all LANS features were available. Given the small numbers in each group, especially LATE-NC, we emphasize the qualitative assessment of frequencies of pathological diagnoses across LANS likelihoods, although inferential statistics have also been performed.

LANS features and likelihoods across pathological diagnoses for the Mayo and ADNI cohorts

LANS, limbic-predominant amnestic neurodegenerative syndrome; ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-related TDP-43 encephalopathy neuropathological changes.

In the Mayo cohort, all LATE-NC (4/4) patients had a highest/high likelihood. Thirty-one of forty-nine (63%), 17/49 (35%) and 1/49 (2%) of ADNC patients had low, moderate and highest/high likelihoods, respectively. Twelve of thirty-three (36%), 8/33 (24%) and 13/33 (39%) of ADNC/LATE-NC patients had low, moderate and highest/high likelihoods, respectively. Assessments of the distribution of pathological diagnoses within likelihood categories revealed that there were proportionally more ADNC/LATE-NC than ADNC patients within the highest/high likelihood category ( P = 0.007). There were more ADNC and ADNC/LATE-NC patients than LATE-NC patients within the moderate likelihood category ( P < 0.001 and P = 0.02, respectively). There were more ADNC and ADNC/LATE-NC patients than LATE-NC patients ( P = 0.004) and more ADNC patients than ADNC/LATE-NC patients ( P < 0.001) within the low likelihood category. Assessment of the distribution of likelihood categories within pathological diagnoses revealed that there were more ADNC patients with low and moderate likelihoods compared to highest/high likelihoods ( P < 0.001 and P = 0.002, respectively). There were no other differences.

In the ADNI cohort, 4/6 (67%) and 2/6 (33%) of LATE-NC cases had highest/high and low likelihoods, respectively. Eleven of eighteen (61%) and 7/18 (39%) of ADNC cases had low and moderate likelihoods, respectively. Eight of twelve (67%), 3/12 (25%) and 1/12 (8%) of ADNC/LATE-NC patients had low, moderate and highest/high likelihoods, respectively. Assessments of the distribution of pathological diagnoses within likelihood categories only revealed a trend towards more ADNC patients than LATE-NC patients within the moderate likelihood category ( P = 0.09). Assessment of the distribution of likelihood categories within pathological diagnoses revealed that there were more ADNC patients with a low likelihood compared to highest/high likelihoods ( P = 0.04). There were no other differences.

Assessment of longitudinal trajectories of CDR-SB according to LANS likelihood and FDG-PET findings comparing LANS likelihoods to CUs are displayed in Fig. 3 . Results from mixed linear modelling between longitudinal CDR-SB and LANS likelihoods are in Supplementary Table 4 . This analysis showed that all groups had equivalent CDR-SB scores at baseline. LANS likelihoods differed in their CDR-SB trajectory over time in that patients with a high likelihood had a slower increase of CDR-SB score than those with a low likelihood. There were trends towards significance for a slower increase of CDR-SB scores in patients with a high likelihood compared to those with moderate and low likelihoods.

FDG-PET and longitudinal CDR-SB findings across LANS likelihoods. ( A ) FDG-PET findings comparing LANS likelihoods to CUs. Contrasts were generated using SPM12 using pairwise t -comparisons between groups at the voxel level and involved 42 cases with a low likelihood, 25 cases with a moderate likelihood, 15 cases with a highest/high likelihood and 112 CUs. ( B ) Longitudinal CDR-SB trajectories at the individual and group level are displayed on the right. CU, cognitively unimpaired; FDR, false discovery rate; CDR-SB, Clinical Dementia Rating Scale Sum of Boxes.

FDG-PET findings showed that patients with highest/high likelihoods had patterns of degeneration mostly involving the temporo-limbic system and inferior frontal areas with little involvement of neocortical areas compared to CUs. In contrast, those with a low likelihood had more pronounced neocortical degeneration mostly involving lateral temporo-parietal areas with little involvement of the medial temporal lobe. The moderate likelihood showed a mixture of these patterns, with involvement of both medial temporo-limbic and neocortical areas.

Binary classification of LATE-NC

A logistic model classifying patients with (LATE-NC, ADNC/LATE-NC) or without LATE-NC (ADNC) based on operationalized LANS criteria (age at examination, CDR-SB score, hippocampal volume, IMT ratio, FDG-PET meta-ROI, tau positivity) achieved a balanced accuracy of 74.6% in the Mayo cohort. The sensitivity and specificity of the model were 78.6 and 70.6%, respectively. There were 12/15 (80%) true positives (i.e. correctly classified with LATE-NC) and 11/16 (68.75%) true negatives (i.e. correctly classified without LATE-NC). Out-of-sample predictions in the ADNI cohort using the model fitted in the Mayo cohort achieved a balanced accuracy of 73.3% in the ADNI cohort. The sensitivity and specificity of the model were 60.9 and 85.7%, respectively. There were 9/15 (60%) true positives (i.e. correctly classified with LATE-NC) and 14/15 (93.33%) true negatives (i.e. correctly classified without LATE-NC). A qualitative assessment of age and CDR-SB scores in misclassified cases showed that false positive (predicted to have LATE-NC whereas they did not) were older and less impaired than ADNC cases (i.e. true negatives) and that false negatives (predicted not to have LATE-NC whereas they did) were younger and more impaired than ADNC/LATE-NC and LATE-NC cases (i.e. true positives). While these comparisons were not statistically significant, this suggests that these cases may have mixed clinical features and are not representative of the archetypical profiles of ADNC or LATE-NC, respectively.

ADNC/LATE-NC heterogeneity

We conducted an exploratory analysis on the clinical heterogeneity of ADNC/LATE-NC patients on the premise that some have LATE-NC as a primary pathology and ADNC as a co-pathology and vice versa. We stratified ADNC/LATE-NC patients based on their LANS likelihood into highest/high ( n = 13), moderate ( n = 8) and low ( n = 12) likelihoods. This was only done in the Mayo cohort given the relatively low heterogeneity of LANS likelihoods in ADNC/LATE-NC patients from the ADNI cohort. Results from these analyses are visually depicted in Fig. 4 .

FDG-PET and longitudinal CDR-SB findings in ADNC/LATE-NC according to LANS likelihoods relative to other groups. ( A ) FDG-PET findings comparing ADNC/LATE-NC to CUs. Contrasts were generated using SPM12 using pairwise t -comparisons between groups at the voxel level and involved 12 ADNC/LATE-NC cases with a low likelihood, 8 ADNC/LATE-NC cases with a moderate likelihood, 13 ADNC/LATE-NC cases with a high/highest likelihood and 112 CUs. ( B ) Longitudinal CDR-SB trajectories at the individual and group level are displayed on the right. ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-associated TDP-43 encephalopathy pathological changes; CU, cognitively unimpaired; FDR, false discovery rate; CDR-SB, Clinical Dementia Rating Scale Sum of Boxes.

Results from the mixed linear model assessing the longitudinal trajectory of CDR-SB scores according to time since baseline across groups (ADNC, ADNC/LATE-NC highest/high, ADNC/LATE-NC moderate, ADNC/LATE-NC low, LATE-NC) are in Supplementary Table 5 . This analysis showed that all groups had statistically equivalent CDR-SB scores at baseline. Groups differed in their CDR-SB trajectory over time in that ADNC/LATE-NC patients with a low likelihood had a steeper increase in CDR-SB scores compared to all other groups.

FDG-PET findings showed that ADNC/LATE-NC patients with highest/high likelihoods had patterns of degeneration mostly involving the temporo-limbic system with little involvement of neocortical areas aside from the inferior frontal areas compared to CUs. In contrast, ADNC/LATE-NC patients with a low likelihood had more pronounced neocortical degeneration mostly involving lateral temporo-parietal areas with lesser involvement of the medial temporal lobe. ADNC/LATE-NC patients with a moderate likelihood showed an intermediate pattern, with involvement of both medial temporo-limbic and neocortical areas.

We developed a set of clinical criteria to identify individuals with a predominant and progressive amnestic syndrome driven by degeneration of the temporo-limbic system. We termed this clinical entity LANS to emphasize that it does not necessarily have a strict mapping to LATE-NC even though they share limbic predominance. This neurologic condition is characterized by progressive limbic degeneration and associated clinical signs and symptoms requiring comprehensive evaluation including history, physical, neuropsychological assessment, imaging and fluid biomarkers. Various combinations of neuropathologies like LATE-NC, ADNC, LBD, argyrophilic grain disease and PART have been observed in the setting of this neurologic syndrome. We operationalized and validated the LANS criteria by tying limbic degeneration to an older age at evaluation, mild clinical syndrome, disproportionate hippocampal atrophy according to clinical severity, limbic hypometabolism, absence of neocortical degenerative disease pattern and low likelihood of neocortical tau. The LANS criteria effectively categorized LATE-NC, ADNC/LATE-NC and ADNC patients from two clinicopathological cohorts (Mayo and ADNI). Most patients with highest or high LANS likelihoods had post-mortem evidence of LATE-NC, most patients with moderate or low LANS likelihoods had evidence of ADNC, and those with evidence of ADNC/LATE-NC patients had a wider distribution of LANS likelihoods. Assessing clinical and imaging features across LANS likelihood regardless of underlying pathology showed that patients with higher likelihoods had a slower clinical course and patterns of temporo-limbic degeneration with minimal involvement of neocortical areas, while those with lower likelihoods showed the opposite pattern. Stratifying ADNC/LATE-NC patients according to their LANS likelihoods revealed a high degree of heterogeneity, where those with higher likelihoods had a slower clinical course and those with lower likelihood had the worse clinical prognosis compared to all other groups. The implementation of LANS criteria has critical implications for clinical and therapeutic endeavours as well as for a deeper understanding of the aetiologic landscape of predominant and progressive amnestic syndromes.

Patients with LATE-NC had a mild level of cognitive impairment at presentation with relatively slow progression of impairment over time, which further consolidates findings from separate studies findings a memory-dominant profile characterized by an indolent clinical course in LATE-NC. 1 , 3 , 6 , 70 Interestingly, patients with ADNC/LATE-NC with a high LANS likelihoods showed a relatively similar profile in terms of clinical progression, which aligns with our hypothesis that these patients have LATE-NC as the primary driver of their clinical symptoms with ADNC as a secondary pathology. This is further supported by the finding of a more rapid clinical decline in ADNC/LATE-NC patients with a low LANS likelihood, which are hypothesized to have ADNC as the primary driver of their clinical symptoms and may thus have combined limbic and neocortical functional neurodegeneration. These findings bring nuance to the prevailing view that patients with evidence for both pathologies systematically have worse clinical outcomes than ADNC alone. 6 , 70 They also allow for the prediction of the primary symptom-driving pathology in vivo in the context of comorbidity.

FDG-PET and MRI imaging results are also indicative of a selective degeneration of the limbic system including strong involvement of the hippocampus associated with LATE-NC, above and beyond the contribution of ADNC. In fact, ADNC was significantly associated with degeneration of the lateral temporal lobe and posterior neocortical areas rather than the limbic system. This aligns well with previous studies assessing imaging features of LATE-NC and/or ADNC. 24 , 25 , 28-31

The proposed LANS criteria have several clinical implications. The primary implication of these criteria is to accurately diagnose patients for whom the cause of progressive and predominant amnestic symptoms is linked to the degeneration of the limbic system with a high likelihood of LATE-NC as a symptom-driving pathology. It is noteworthy that the diagnosis of LANS is based on likelihoods, and not on definitive categories as seen with other classifications. This means that the unavailability of some features does not preclude rendering LANS diagnosis. Rather, it prevents from reaching higher LANS likelihoods and prompts further workup to ascertain that symptoms are caused by predominant limbic degeneration. This underlines the critical role of imaging and biomarkers to increase the diagnostic confidence of LANS. Figure 5 demonstrates a prospective example of clinical case of LANS, where a moderate likelihood was assigned based upon the assessment of core and standard features. The assessment of advanced features (negative amyloid-PET, predominant limbic hypometabolism on FDG-PET) increased confidence that limbic degeneration was the culprit of symptoms, thus allowing for the highest LANS likelihood.

Case example of a prospective use of the LANS criteria in clinical settings. This patient was seen at Mayo Clinic, Rochester, to determine eligibility for an anti-amyloid monoclonal antibody therapy, and the LANS criteria were internally defined at the time of evaluation. The criteria were operationalized using clinical judgement of available data including visual reads of neuroimaging as is the current standard in clinical practice. This patient was a female over the age of 75 with a history of memory problems for several years. She lived alone, managed her instrumental activities of daily living independently and was still working part-time. Neuropsychological testing revealed moderate to severe impairment on measures of delayed recall and fragility of salient semantic knowledge (i.e. she could not recall details about the events occurring on 11 September 2001; she named another building than the World Trade Center and did not know how many buildings were hit). Performance was also mildly low on a task of object naming. The remainder of the assessment (i.e. global cognition, executive functions, visuospatial processing and language) was within or above expectations from a normative standpoint. The profile was consistent with single-domain amnestic mild cognitive impairment. MRI revealed disproportionate bilateral hippocampal atrophy, and she was assigned a moderate likelihood LANS diagnosis. Subsequently, a brain FDG-PET revealed prominent temporo-limbic and milder inferior frontal hypometabolism in the absence of a neocortical degenerative pattern by visual read. Amyloid-PET was read as negative. She thus met all core, standard and advanced criteria for LANS, corresponding to the highest likelihood. She did not meet criteria for an anti-amyloid monoclonal antibody therapy and was counselled about diagnosis, prognosis and most likely underlying aetiology.

The accurate diagnosis of LANS has the potential to improve prognostication and counselling of patients about the nature of their symptoms. Current evidence indicates that the symptomatology primarily involves episodic memory for recent events, while neocortical functions (e.g. executive functioning and visuospatial reasoning) are expected to remain relatively preserved throughout the disease course. 1 , 2 , 19 An accurate diagnosis is also relevant for prognostication, as LANS has a likelihood of being associated with LATE-NC, which is associated with a relatively slow and milder clinical course compared to canonical Alzheimer’s disease–type dementia per our results and other studies. 1 , 3 , 6 , 70 This is again exemplified in Fig. 5 , where a highest LANS likelihood allowed to have precise diagnosis, counsel prognosis, guide treatment options and provide answers about the mostly likely underlying aetiology in this patient allowing for engagement with research and other health information on this topic. Without a LANS construct, we are left only saying that a patient does not qualify for anti-amyloid treatment and that they do not have Alzheimer’s disease. Having a positive diagnosis serves additional utility beyond that and facilitates comprehensive medical care.

To put this work in contexts, recent work on terminology would characterize LANS as a subtype of amnestic MCI or amnestic dementia. 34 , 35 The addition of preservation of neocortical functions, older age at symptom onset, mild clinical severity and semantic memory impairment would make these amnestic syndromes more likely to be LANS and the additional imaging would localize the syndromes to the limbic system. These refinements would add greater specificity to the diagnosis for clinicians. LANS in the context of normal amyloid levels can also be examined through the lens of suspected non–Alzheimer disease pathophysiology, which refers to amyloid-negative, neurodegeneration-positive individuals. 71 However, suspected non–Alzheimer disease pathophysiology encompasses a broader spectrum of conditions than LANS, as it is a biomarker-based definition regardless of clinical status.

The LANS criteria have critical therapeutic implications. This is especially true in this era of emerging anti-amyloid monoclonal antibody therapies. 32 , 33 , 72 , 73 As these therapies make their way into clinical practice, the LANS criteria can be of relevance for identifying patients with a high likelihood of LATE-NC as the primary cause of their symptoms and guide clinical decision-making and counselling regarding potential therapeutic avenues. It is important to mention that positive Alzheimer’s disease biomarkers do not rule out a diagnosis of LANS, as a progressive and predominant amnestic syndrome caused by LATE-NC or other pathologies can be observed in concomitance with incidental amyloidosis or ADNC. 30 , 31 The use of the LANS likelihoods can help determine whether the amnestic syndrome is most likely driven by a primary non–Alzheimer disease pathophysiology with secondary ADNC or vice versa, as demonstrated by our analysis deciphering the heterogeneity of patients with ADNC/LATE-NC. It is important to mention that we do not make treatment recommendations based on this work, but the LANS criteria allow to study such a question. Future studies will be important to determine how patients with positive Alzheimer’s disease biomarkers respond to disease-modifying therapies according to their LANS likelihood. Finally, the LANS criteria are a major advancement in the overarching goal of tying an in vivo neurologic syndrome to underlying LATE-NC. The other critical component needed to achieve this is the development of in vivo diagnostic biomarkers of TDP-43 specific for LATE-NC. PET, CSF and biofluid biomarkers of TDP-43 are hopefully on the horizon. 1 , 74 , 75 This would allow for defining the clinical entity of LATE as a high-likelihood LANS syndrome with biomarker evidence of LATE-NC. Defining such a clinicopathological entity will be important for the design of clinical trials aimed at LATE-NC in terms of defining eligibility criteria and outcomes measures.

It is important to reiterate that while LANS is highly associated with LATE-NC, it can be associated with other pathologic entities that selectively target the limbic system. Supplemental analyses provide some evidence that pathologies associated with a predominant amnestic syndrome other than LATE-NC may, in rare instances, have a high LANS likelihood (e.g. LBD, argyrophilic grain disease, advanced PART). One example that can be a potential source of clinical conundrums is the limbic variant Alzheimer’s disease, where tau predominantly localizes to the limbic system and therefore qualifies for LANS. In this scenario, the advanced LANS criteria in combination with visual assessment of tau-PET can help in determining which pathology has the highest likelihood of driving clinical symptoms.

Notably, there were slightly lower LANS likelihoods in ADNC/LATE-NC patients in the ADNI cohort relative to the Mayo cohort. This is likely due to discrepancy in recruitment and sampling strategies. The Mayo cohort draws from clinical practice in a tertiary behavioural neurology clinic (Alzheimer’s Disease Research Center) and randomly selected individuals living in Olmsted County, MN, USA (Mayo Clinic Study of Aging). 76 It is thus designed to reflect a combination of the clinicopathologic variability encountered in Alzheimer’s disease–oriented clinical context and with more representative settings. On the other hand, ADNI was designed as a research cohort aimed at the clinical and biological characterization of individuals on the clinicopathologic spectrum of Alzheimer’s disease. 77 , 78 It is not meant to reflect the heterogeneity encountered in clinical practice. These fundamental differences may explain the relatively younger age of LATE-NC patients and the lower frequency of ADNC/LATE-NC with a high LANS likelihood. We believe the performance of the LANS criteria in the Mayo cohort is a more accurate reflection of how the LANS criteria are expected to perform in clinical settings. It is also important to mention that we undertook several steps to avoid overfitting the LANS criteria validation in the Mayo cohort. This includes the use of externally validated thresholds for most imaging and tau biomarkers (e.g. CSF, ptau181, molecular PET imaging) and deriving optimal thresholds for hippocampal atrophy and the IMT ratio in the ADNI cohort rather than Mayo.

There are some limitations to this work. An evident caveat is the low number of patients with LATE-NC without ADNC. The lack of statistical differences between these patients and other groups in terms of clinical and imaging features could be attributable to the small sample size rather than a genuine absence of differences. However, most patients with LATE-NC had highest and high LANS likelihoods, suggesting that our proposed criteria effectively identify these individuals. Although the proposed LANS criteria include impaired semantic memory, we did not incorporate this feature in the operationalized criteria given the less robust and variably defined evidence of such impairment. Efforts are underway to better characterize the nature and extent of semantic memory impairment in patients with LATE-NC and develop cognitive tests sensitive to such impairment. This should not, however, prevent clinicians from considering this feature in their clinical decision-making when LANS is in the differential, as highlighted in the case example in Fig. 5 . The classification model based on the features of the LANS criteria had modest accuracy in distinguishing LATE-NC from ADNC at autopsy, which may be due to a range of factors including increased pathological burden in late-stage disease and partially overlapping clinical and radiological features between the two pathological entities. Prospective studies are required to further assess the value of the LANS criteria in predicting underlying pathologies predominantly driving limbic versus neocortical degeneration. This study is retrospective in nature. The implementation of the LANS criteria in clinical settings and prospective studies are needed to further validate and refine this set of criteria. Finally, while we report vascular burden across both cohorts, this information was not utilized in assigning pathological diagnoses unless seen in isolation. Future work with sample allowing for such stratification is required to assess how vascular damage influences the clinical trajectory and pathophysiology of LANS.

In conclusion, we developed and validated a set of criteria for LANS designed to be used in clinical practice to identify individuals with a predominant amnestic syndrome driven by the degeneration of the temporo-limbic system with a high likelihood of underlying LATE-NC. This has important clinical implications including differential diagnosis with other common causes of episodic memory impairment such as neocortical degeneration driven by ADNC, counselling patients about the nature and course of their symptoms, providing appropriate treatments, referral to research programmes and the development of therapeutic efforts aimed at LATE-NC. Several steps lay ahead to improve the definition of LANS including the conduction of prospective studies and the development of clinical tools that are sensitive and specific to its cognitive features. Finally, the development of in vivo diagnostic markers of TDP-43 pathology is needed to embed LANS into a clinicopathological entity driven by LATE-NC, i.e. LATE.

Supplementary material is available at Brain Communications online.

We wish to thank our patients and their caregivers for their dedicated participation in our research programme. We would also wish to express our gratitude to all healthcare providers and research professionals who were involved in this study and patient care.

This work was funded in part by National Institutes of Health (NIH) grants P30 AG062677, P50 AG016574 and U01 AG006786 (R.C.P.) and R37 AG011378 and R01 AG041851 (C.R.J.), and by the Robert Wood Johnson Foundation, the Elsie and Marvin Dekelboum Family Foundation, the Liston Family Foundation, the Edson Family, the Gerald A. and Henrietta Rauenhorst (GHR) Foundation and the Foundation Dr. Corinne Schuler (Geneva, Switzerland).

V.J.L. consults for Bayer Schering Pharma, Piramal Life Sciences, Life Molecular Imaging, Eisai Inc., Avid Radiopharmaceuticals and Merck Research and receives research support from GE Healthcare, Siemens Molecular Imaging, Avid Radiopharmaceuticals and the NIH (NIA, NCI). D.S.K. serves on a Data Safety Monitoring Board for the DIAN study and for a tau therapeutic for Biogen but receives no personal compensation; is an investigator in clinical trials sponsored by Biogen, Lilly Pharmaceuticals and the University of Southern California; has served as a consultant for Roche, Samus Therapeutics, Third Rock and Alzeca Biosciences but receives no personal compensation; and receives funding from the NIH. B.F.B. receives honorarium for SAB activities for the Tau Consortium, is an investigator in clinical trials sponsored by Alector, Biogen, Cognition Therapeutics, EIP Pharma and Transposon and receives funding from the NIH. C.R.J. has no commercial conflicts and receives research support from the NIH, the GHR Foundation and the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic. R.C.P. consults for Roche, Inc.; Merck, Inc.; Biogen, Inc.; Genentech, Inc.; Eisai, Inc.; and Nestle, Inc. but does not receive significant fees due to NIH limitations from the U24 AG057437 Co-PI role.

Data from the Mayo Clinic Study of Aging and the Mayo Clinic Alzheimer’s Disease Research Center are available upon request ( https://www.mayo.edu/research/centers-programs/alzheimers-disease-research-center/data-requests ). ADNI data can be downloaded at https://adni.loni.usc.edu/ . The Mayo Clinic Adult Lifespan Template can be found at https://www.nitrc.org/projects/mcalt/ . The R code for the statistical analyses can be found on https://github.com/nickcorriveaul/R_scripts_manuscripts .

Nelson   PT , Dickson   DW , Trojanowski   JQ , et al.    Limbic-predominant age-related TDP-43 encephalopathy (LATE): Consensus working group report . Brain   2019 ; 142 ( 6 ): 1503 – 1527 .

Google Scholar

Gauthreaux   KM , Teylan   MA , Katsumata   Y , et al.    Limbic-predominant age-related TDP-43 encephalopathy: Medical and pathologic factors associated with comorbid hippocampal sclerosis . Neurology   2022 ; 98 ( 14 ): e1422 – e1433 .

Duong   MT , Wolk   DA . Limbic-predominant age-related TDP-43 encephalopathy: LATE-breaking updates in clinicopathologic features and biomarkers . Curr Neurol Neurosci Rep . 2022 ; 22 ( 11 ): 689 – 698 .

Dickson   DW , Davies   P , Bevona   C , et al.    Hippocampal sclerosis: A common pathological feature of dementia in very old (≥80 years of age) humans . Acta Neuropathol . 1994 ; 88 ( 3 ): 212 – 221 .

Young   AL , Vogel   JW , Robinson   JL , et al.    Data-driven neuropathological staging and subtyping of TDP-43 proteinopathies . Brain   2023 ; 146 ( 7 ): 2975 – 2988 .

Josephs   KA , Murray   ME , Whitwell   JL , et al.    Updated TDP-43 in Alzheimer’s disease staging scheme . Acta Neuropathol . 2016 ; 131 : 571 – 585 .

Coyle-Gilchrist   ITS , Dick   KM , Patterson   K , et al.    Prevalence, characteristics, and survival of frontotemporal lobar degeneration syndromes . Neurology   2016 ; 86 ( 18 ): 1736 – 1743 .

Nelson   PT , Brayne   C , Flanagan   ME , et al.    Frequency of LATE neuropathologic change across the spectrum of Alzheimer’s disease neuropathology: Combined data from 13 community-based or population-based autopsy cohorts . Acta Neuropathol . 2022 ; 144 ( 1 ): 27 – 44 .

Robinson   JL , Lee   EB , Xie   SX , et al.    Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated . Brain   2018 ; 141 ( 7 ): 2181 – 2193 .

Wennberg   AM , Tosakulwong   N , Lesnick   TG , et al.    Association of apolipoprotein E ε4 with transactive response DNA-binding protein 43 . JAMA Neurol . 2018 ; 75 ( 11 ): 1347 – 1354 .

Yang   HS , Yu   L , White   CC , et al.    Evaluation of TDP-43 proteinopathy and hippocampal sclerosis in relation to APOE ε4 haplotype status: A community-based cohort study . Lancet Neurol . 2018 ; 17 ( 9 ): 773 – 781 .

Josephs   KA , Whitwell   JL , Weigand   SD , et al.    TDP-43 is a key player in the clinical features associated with Alzheimer’s disease . Acta Neuropathol . 2014 ; 127 : 811 – 824 .

Murray   ME , Graff-Radford   NR , Ross   OA , Petersen   RC , Duara   R , Dickson   DW . Neuropathologically defined subtypes of Alzheimer’s disease with distinct clinical characteristics: A retrospective study . Lancet Neurol . 2011 Sep ; 10 ( 9 ): 785 – 796 .

Ding   ZT , Wang   Y , Jiang   YP , et al.    Argyrophilic grain disease: Frequency and neuropathology in centenarians . Acta Neuropathol . 2006 ; 111 ( 4 ): 320 – 328 .

Robinson   JL , Xie   SX , Baer   DR , et al.    Pathological combinations in neurodegenerative disease are heterogeneous and disease-associated . Brain . 2023 Jun 1 ; 146 ( 6 ): 2557 – 2569 .

Gauthreaux   K , Mock   C , Teylan   MA , et al.    Symptomatic profile and cognitive performance in autopsy-confirmed limbic-predominant age-related TDP-43 encephalopathy with comorbid Alzheimer disease . J Neuropathol Exp Neurol . 2022 ; 81 ( 12 ): 975 – 987 .

Kapasi   A , Yu   L , Boyle   PA , Barnes   LL , Bennett   DA , Schneider   JA . Limbic-predominant age-related TDP-43 encephalopathy, ADNC pathology, and cognitive decline in aging . Neurology   2020 ; 95 ( 14 ): e1951 – e1962 .

Brenowitz   WD , Monsell   SE , Schmitt   FA , Kukull   WA , Nelson   PT . Hippocampal sclerosis of aging is a key Alzheimer’s disease mimic: Clinical-pathologic correlations and comparisons with both Alzheimer’s disease and non-tauopathic frontotemporal lobar degeneration . J Alzheimers Dis . 2014 ; 39 ( 3 ): 691 – 702 .

Lopez   OL , Kofler   J , Chang   Y , et al.    Hippocampal sclerosis, TDP-43, and the duration of the symptoms of dementia of AD patients . Ann Clin Transl Neurol . 2020 ; 7 ( 9 ): 1546 – 1556 .

Katsumata   Y , Abner   EL , Karanth   S , et al.    Distinct clinicopathologic clusters of persons with TDP-43 proteinopathy . Acta Neuropathol . 2020 ; 140 : 659 – 674 .

Karanth   S , Nelson   PT , Katsumata   Y , et al.    Prevalence and clinical phenotype of quadruple misfolded proteins in older adults . JAMA Neurol . 2020 ; 77 ( 10 ): 1299 – 1307 .

Buciuc   M , Tosakulwong   N , Machulda   MM , et al.    TAR DNA-binding protein 43 is associated with rate of memory, functional and global cognitive decline in the decade prior to death . J Alzheimers Dis . 2021 ; 80 ( 2 ): 683 – 693 .

Wilson   RS , Yu   L , Trojanowski   JQ , et al.    TDP-43 pathology, cognitive decline, and dementia in old age . JAMA Neurol . 2013 ; 70 ( 11 ): 1418 – 1424 .

Josephs   KA , Martin   PR , Weigand   SD , et al.    Protein contributions to brain atrophy acceleration in Alzheimer’s disease and primary age-related tauopathy . Brain J Neurol . 2020 ; 143 ( 11 ): 3463 – 3476 .

Buciuc   M , Wennberg   AM , Weigand   SD , et al.    Effect modifiers of TDP-43-associated hippocampal atrophy rates in patients with Alzheimer’s disease neuropathological changes . J Alzheimers Dis . 2020 ; 73 ( 4 ): 1511 – 1523 .

Bejanin   A , Murray   ME , Martin   P , et al.    Antemortem volume loss mirrors TDP-43 staging in older adults with non-frontotemporal lobar degeneration . Brain   2019 ; 142 ( 11 ): 3621 – 3635 .

Amador-Ortiz   C , Lin   W , Ahmed   Z , et al.    TDP-43 immunoreactivity in hippocampal sclerosis and Alzheimer’s disease . Ann Neurol . 2007 ; 61 ( 5 ): 435 – 445 .

Botha   H , Mantyh   WG , Murray   ME , et al.    FDG-PET in tau-negative amnestic dementia resembles that of autopsy-proven hippocampal sclerosis . Brain   2018 ; 141 ( 4 ): 1201 – 1217 .

Botha   H , Mantyh   WG , Graff-Radford   J , et al.    Tau-negative amnestic dementia masquerading as Alzheimer disease dementia . Neurology   2018 ; 90 ( 11 ): e940 – e946 .

Buciuc   M , Botha   H , Murray   ME , et al.    Utility of FDG-PET in diagnosis of Alzheimer-related TDP-43 proteinopathy . Neurology   2020 ; 95 ( 1 ): e23 – e34 .

Grothe   MJ , Moscoso   A , Silva-Rodríguez   J , et al.    Differential diagnosis of amnestic dementia patients based on an FDG-PET signature of autopsy-confirmed LATE-NC . Alzheimers Dement . 2023 ; 19 ( 4 ): 1234 – 1244 .

McKhann   GM , Knopman   DS , Chertkow   H , et al.    The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease . Alzheimers Dement . 2011 ; 7 ( 3 ): 263 – 269 .

Albert   MS , DeKosky   ST , Dickson   D , et al.    The diagnosis of mild cognitive impairment due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease . Alzheimers Dement . 2011 ; 7 ( 3 ): 270 – 279 .

Petersen   RC , Weintraub   S , Sabbagh   M , et al.    A new framework for dementia nomenclature . JAMA Neurol . 2023 ; 80 ( 12 ): 1364 – 1370 .

Petersen   RC , Doody   R , Kurz   A , et al.    Current concepts in mild cognitive impairment . Arch Neurol . 2001 ; 58 ( 12 ): 1985 – 1992 .

Mirra   SS , Heyman   A , McKeel   D , et al.    The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD): Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease . Neurology   1991 ; 41 ( 4 ): 479 – 486 .

Hyman   BT , Phelps   CH , Beach   TG , et al.    National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease . Alzheimers Dement . 2012 ; 8 ( 1 ): 1 – 13 .

Braak   H , Alafuzoff   I , Arzberger   T , Kretzschmar   H , Del Tredici   K . Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry . Acta Neuropathol . 2006 ; 112 ( 4 ): 389 – 404 .

Crary   JF , Trojanowski   JQ , Schneider   JA , et al.    Primary age-related tauopathy (PART): A common pathology associated with human aging . Acta Neuropathol . 2014 ; 128 ( 6 ): 755 – 766 .

Mackenzie   IRA , Neumann   M , Baborie   A , et al.    A harmonized classification system for FTLD-TDP pathology . Acta Neuropathol . 2011 ; 122 ( 1 ): 111 – 113 .

Montine   TJ , Phelps   CH , Beach   TG , et al.    National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: A practical approach . Acta Neuropathol . 2012 ; 123 ( 1 ): 1 – 11 .

Dickson   DW , Bergeron   C , Chin   SS , et al.    Office of Rare Diseases neuropathologic criteria for corticobasal degeneration . J Neuropathol Exp Neurol . 2002 ; 61 ( 11 ): 935 – 946 .

Briggs   M , Allinson   KSJ , Malpetti   M , Spillantini   MG , Rowe   JB , Kaalund   SS . Validation of the new pathology staging system for progressive supranuclear palsy . Acta Neuropathol . 2021 ; 141 : 787 – 789 .

Jellinger   KA . Dementia with grains (argyrophilic grain disease) . Brain Pathol . 1998 ; 8 ( 2 ): 377 – 386 .

Stricker   NH , Stricker   JL , Karstens   AJ , et al.    A novel computer adaptive word list memory test optimized for remote assessment: Psychometric properties and associations with neurodegenerative biomarkers in older women without dementia . Alzheimers Dement (Amst) . 2022 ; 14 ( 1 ): e12299 .

Jack   CR  Jr , Wiste   HJ , Weigand   SD , et al.    Different definitions of neurodegeneration produce similar amyloid/neurodegeneration biomarker group findings . Brain . 2015 ; 138 ( Pt 12 ): 3747 – 3759 .

Ramanan   VK , Armstrong   MJ , Choudhury   P , et al.    Antiamyloid monoclonal antibody therapy for Alzheimer disease: Emerging issues in neurology . Neurology   2023 ; 101 ( 19 ): 842 – 852 .

Jack   CR  Jr , Wiste   HJ , Weigand   SD , et al.    Defining imaging biomarker cut points for brain aging and Alzheimer’s disease . Alzheimers Dement . 2017 ; 13 ( 3 ): 205 – 216 .

Landau   SM , Harvey   D , Madison   CM , et al.    Comparing predictors of conversion and decline in mild cognitive impairment . Neurology   2010 ; 75 ( 3 ): 230 – 238 .

Schwarz   CG , Gunter   JL , Wiste   HJ , et al.    A large-scale comparison of cortical thickness and volume methods for measuring Alzheimer’s disease severity . NeuroImage Clin . 2016 ; 11 : 802 – 812 .

Lowe   VJ , Lundt   ES , Albertson   SM , et al.    Tau-positron emission tomography correlates with neuropathology findings . Alzheimers Dement . 2020 ; 16 ( 3 ): 561 – 571 .

Landau   SM , Mintun   MA , Joshi   AD , et al.    Amyloid deposition, hypometabolism, and longitudinal cognitive decline . Ann Neurol . 2012 ; 72 ( 4 ): 578 – 586 .

Royse   SK , Minhas   DS , Lopresti   BJ , et al.    Validation of amyloid PET positivity thresholds in centiloids: A multisite PET study approach . Alzheimers Res Ther . 2021 ; 13 ( 1 ): 99 .

Van Harten   AC , Wiste   HJ , Weigand   SD , et al.    CSF biomarkers in Olmsted County: Evidence of 2 subclasses and associations with demographics . Neurology   2020 ; 95 ( 3 ): e256 – e267 .

Bittner   T , Zetterberg   H , Teunissen   CE , et al.    Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1–42) in human cerebrospinal fluid . Alzheimers Dement . 2016 ; 12 ( 5 ): 517 – 526 .

Blennow   K , Shaw   LM , Stomrud   E , et al.    Predicting clinical decline and conversion to Alzheimer’s disease or dementia using novel Elecsys Aβ (1–42), pTau and tTau CSF immunoassays . Sci Rep . 2019 ; 9 ( 1 ): 19024 .

Hansson   O , Seibyl   J , Stomrud   E , et al.    CSF biomarkers of Alzheimer’s disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in BioFINDER and ADNI cohorts . Alzheimers Dement . 2018 ; 14 ( 11 ): 1470 – 1481 .

Bermudez   C , Graff-Radford   J , Syrjanen   JA , et al.    Plasma biomarkers for prediction of Alzheimer’s disease neuropathologic change . Acta Neuropathol . 2023 ; 146 ( 1 ): 13 – 29 .

Mattsson   N , Cullen   NC , Andreasson   U , Zetterberg   H , Blennow   K . Association between longitudinal plasma neurofilament light and neurodegeneration in patients with Alzheimer disease . JAMA Neurol . 2019 ; 76 ( 7 ): 791 – 799 .

Mattsson   N , Andreasson   U , Zetterberg   H , Blennow   K ; Alzheimer’s Disease Neuroimaging Initiative . Association of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease . JAMA Neurol . 2017 ; 74 ( 5 ): 557 – 566 .

Karikari   TK , Pascoal   TA , Ashton   NJ , et al.    Blood phosphorylated tau 181 as a biomarker for Alzheimer’s disease: A diagnostic performance and prediction modelling study using data from four prospective cohorts . Lancet Neurol . 2020 ; 19 ( 5 ): 422 – 433 .

Karikari   TK , Benedet   AL , Ashton   NJ , et al.    Diagnostic performance and prediction of clinical progression of plasma phospho-tau181 in the Alzheimer’s Disease Neuroimaging Initiative . Mol Psychiatry . 2021 ; 26 ( 2 ): 429 – 442 .

O’Bryant   SE , Lacritz   LH , Hall   J , et al.    Validation of the new interpretive guidelines for the clinical dementia rating scale sum of boxes score in the national Alzheimer’s coordinating center database . Arch Neurol . 2010 ; 67 ( 6 ): 746 – 749 .

Jack   CR , Wiste   HJ , Botha   H , et al.    The bivariate distribution of amyloid-β and tau: Relationship with established neurocognitive clinical syndromes . Brain   2019 ; 142 ( 10 ): 3230 – 3242 .

Jones   DT , Graff-Radford   J , Lowe   VJ , et al.    Tau, amyloid, and cascading network failure across the Alzheimer’s disease spectrum . Cortex   2017 Dec ; 97 : 143 – 159 .

Sintini   I , Martin   PR , Graff-Radford   J , et al.    Longitudinal tau-PET uptake and atrophy in atypical Alzheimer’s disease . NeuroImage Clin . 2019 ; 23 : 101823 .

Tondo   G , Carli   G , Santangelo   R , et al.    Biomarker-based stability in limbic-predominant amnestic mild cognitive impairment . Eur J Neurol . 2021 ; 28 ( 4 ): 1123 – 1133 .

Caminiti   SP , De Francesco   S , Tondo   G , et al.    FDG-PET markers of heterogeneity and different risk of progression in amnestic MCI . Alzheimers Dement . 2023 ; 20 ( 1 ): 159 – 172 .

Jack   CR , Wiste   HJ , Algeciras-Schimnich   A , et al.    Predicting amyloid PET and tau PET stages with plasma biomarkers . Brain   2023 ; 146 ( 5 ): 2029 – 2044 .

Jack   CR  Jr , Knopman   DS , Chételat   G , et al.    Suspected non-Alzheimer disease pathophysiology—Concept and controversy . Nat Rev Neurol . 2016 ; 12 ( 2 ): 117 – 124 .

Knopman   DS , Hershey   L . Implications of the approval of lecanemab for Alzheimer disease patient care: Incremental step or paradigm shift . Neurology   2023 ; 101 ( 14 ): 610 – 620 .

Van Dyck   CH , Swanson   CJ , Aisen   P , et al.    Lecanemab in early Alzheimer’s disease . N Engl J Med . 2023 ; 388 ( 1 ): 9 – 21 .

Sims   JR , Zimmer   JA , Evans   CD , et al.    Donanemab in early symptomatic Alzheimer disease: The TRAILBLAZER-ALZ 2 randomized clinical trial . JAMA . 2023 ; 330 ( 6 ): 512 – 527 .

Feneberg   E , Gray   E , Ansorge   O , Talbot   K , Turner   MR . Towards a TDP-43-based biomarker for ALS and FTLD . Mol Neurobiol . 2018 ; 55 ( 10 ): 7789 – 7801 .

Kapaki   E , Boufidou   F , Bourbouli   M , et al.    Cerebrospinal fluid biomarker profile in TDP-43-related genetic frontotemporal dementia . J Pers Med . 2022 ; 12 ( 10 ): 1747 .

Roberts   RO , Geda   YE , Knopman   DS , et al.    The Mayo Clinic Study of Aging: design and sampling, participation, baseline measures and sample characteristics . Neuroepidemiology   2008 ; 30 ( 1 ): 58 – 69 .

Petersen   RC , Aisen   PS , Beckett   LA , et al.    Alzheimer’s disease neuroimaging initiative (ADNI): Clinical characterization . Neurology   2010 ; 74 ( 3 ): 201 – 209 .

Supplementary data

Email alerts

Citing articles via.

• Guarantors of Brain
• Advertising and Corporate Services
• Journals Career Network

Affiliations

• Online ISSN 2632-1297
• Copyright © 2024 Guarantors of Brain
• About Oxford Academic
• Publish journals with us
• University press partners
• What we publish
• New features  
• Open access
• Institutional account management
• Rights and permissions
• Get help with access
• Accessibility
• Advertising
• Media enquiries
• Oxford University Press
• Oxford Languages
• University of Oxford

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide

• Copyright © 2024 Oxford University Press
• Cookie settings
• Cookie policy
• Privacy policy
• Legal notice

This Feature Is Available To Subscribers Only

Sign In or Create an Account

This PDF is available to Subscribers Only

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

Got any suggestions?

We want to hear from you! Send us a message and help improve Slidesgo

Top searches

Trending searches

38 templates

53 templates

first day of school

68 templates

free template

97 templates

food business

188 templates

meet the teacher

31 templates

Clinical Case 04-2023

It seems that you like this template, clinical case 04-2023 presentation, premium google slides theme, powerpoint template, and canva presentation template.

When trying to prevent diseases, information is key, and if it’s reliable, all the better. With this new free medical template, you can show the results of a clinical case, including the symptoms, the patient monitoring, the treatment and all the important data. Its design will help you grab your audience’s attention for sure!

To begin with, the illustrations that we’ve included in the slides are so cool nobody will be able to take their eyes off the screen. These, along with the assortment of icons, demonstrate how good looking the flat style is. The next thing we should mention is color. The main protagonist in the slides design is blue, which is a color usually related to medical contexts. It’s not a surprise, since it conveys serenity and confidence; that’s exactly what you want to show in front of your audience, right? To make your titles readable and clear, a sans-serif font has been used. In fact, we’ve also chosen a sans-serif typeface for body text, but they are different enough and go well together. Don’t hesitate to make use of the graphs and infographics to explain in detail all the data gathered from your research. If you’re using Google Slides, then Flaticon’s extension will come in handy, as you’ll be able to access the largest database of free icons. Now that the prescription is complete, customize the presentation template and share your findings!

Features of this template

• 100% editable and easy to modify
• 26 different slides to impress your audience
• Available in five colors: blue, lilac, yellow, pink, and green
• Contains easy-to-edit graphics and maps
• Includes 1000+ icons and Flaticon's extension for customizing your slides
• Designed to be used in Google Slides, Canva, and Microsoft PowerPoint
• 16:9 widescreen format suitable for all types of screens
• Includes information about fonts, colors, and credits of the free resources used

What are the benefits of having a Premium account?

What Premium plans do you have?

What can I do to have unlimited downloads?

Combines with:

This template can be combined with this other one to create the perfect presentation:

Don’t want to attribute Slidesgo?

Gain access to over 29200 templates & presentations with premium from 1.67€/month.

Are you already Premium? Log in

Available colors

Original Color

Register for free and start downloading now

Related posts on our blog.

How to Add, Duplicate, Move, Delete or Hide Slides in Google Slides

How to Change Layouts in PowerPoint

How to Change the Slide Size in Google Slides

Related presentations.

Premium template

Unlock this template and gain unlimited access