Tales From The Cortex
Tales From the Cortex is a story-driven neurology podcast that takes you inside the mysteries of the human brain.
Each episode begins with a patient, a symptom, and a clinical mystery. Follow the story as it unfolds and become the patient's neurologist: What questions would you ask? Where would you localize the problem? Which tests would you order? And what would you do next?
Hosted by neurologists Dr. Andrew Micieli and Dr. Michelle Jaeggi, Tales From the Cortex explores how neurologists think, make decisions, and navigate uncertainty—one case at a time.
No medical degree required. Just curiosity.
Every symptom is a clue. Every brain has a story.
Tales From The Cortex
Episode 1: Last Seen Normal
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It’s 7:16 in the morning. Laura is having breakfast with her family when suddenly, she can’t speak.
Within minutes, an ordinary morning becomes a medical emergency.
In the first episode of Tales From the Cortex, follow Laura from the moment her symptoms begin through the rapid decisions that follow. Step into the neurologist’s chair as the clock starts ticking: What’s happening inside her brain? What would you do next? And how do you make critical decisions when every minute matters?
Along the way, we’ll explore how neurologists approach an acute neurological emergency, to reach the correct diagnosis, administer fast treatment, and the relentless search for why it happened.
Every symptom is a clue. Every brain has a story.
Welcome to Tales from the Cortex, Stories from Inside the Brain, a story-driven neurology podcast that takes you inside the mysteries of the human brain. I'm Neurologist Dr. Andrew Marcelli, and this is episode 1, Last Scene Normal. August 7, 2026, 7 16 AM Olivia, you're gonna miss the bus. Laura stood at the kitchen counter spreading peanut butter across a piece of toast. Nothing about that morning felt important. The expresso machine gave a quiet hiss behind her, the news on the TV was playing in the living room, and her husband Michael sat at the kitchen table scrolling through emails while their fifteen year old daughter searched frantically for something upstairs. Mom, have you seen my blue sweater? Laura rolled her eyes. It's in the she stopped. Michael continued looking at his phone. Laura tried again. It's the uh she knew where it was, the laundry room. She could see it in her mind. She had folded it the night before, but the word wouldn't come out. The room blue Michael looked up. What? Laura stared at him. She tried again. Olivia's blue there Michael put down his phone. Laura she looked annoyed. What? Except what came out wasn't what? It was a collection of sounds. Michael stared at her. Laura looked at him as if he was the one behaving strangely. Then he noticed her face. The right corner of her mouth was hanging slightly lower than the left. Laura smile. She tried. The right side barely moved. Michael had seen this before. But not in real life, on a poster. The acronym FAST, F standing for face, A for arm, S for speech, T for time. Laura raise both your arms. Laura stared at him. Raise your arms. She did, but she could not lift her right arm as well as the left. Michael frantically reached for his phone and called nine one. Seven eighteen AM nine one, what's your emergency? My wife is having a stroke. Laura heard the word from across the kitchen. Stroke. Seven twenty five AM The paramedics arrived seven minutes later. By then Olivia was downstairs. She stood against the wall in her school uniform, backpack still over her shoulder. Is mom gonna be okay? Michael didn't answer. One paramedic knelt beside Laura. Can you tell me your name? Laura. Better than before. What month is it? She paused. She knew the answer. J nothing. The right side of her face was still weak. Can you hold your arms out? Her right arm slowly drifted downward. The paramedic looked at his partner. Stroke screened positive. He checked her glucose, it was normal at 4.7, and then checked her vitals. Blood pressure was 175 over 100, heart rate 74 and regular. Rhythm strip was normal sinus. The paramedics asked, When was she last completely normal? Michael looked at the clock. We were talking at breakfast, maybe 7.15. The paramedic wrote it down. Last known well 715 AM. Does she have any past medical history? No, she's healthy and she only takes vitamins. Laura was placed on the stretcher. Olivia started crying. Laura reached towards her. I'm she couldn't finish. Michael put his arm around their daughter. She's going to be okay. He had no idea whether that was true. 741 AM. The ambulance radioed ahead. Fifty year old female, acute onset aphasia, right facial weakness, right arm drift, and right grip strength weakness. Lamb score four. Last known well, seven fifteen AM. At the Regional Stroke Center, the triage nurse sends out a fan page that goes to the emergency department, stroke team, and radiology. Cold stroke. The clock has started. 747 AM The ambulance doors open. Laura expected an emergency department waiting room, but she never saw one. The nurse was waiting for her and helped rush her to the emergency resuscitation room. An emergency physician and stroke neurologist were waiting for her, along with others in the room. She could only focus on her husband. She heard a voice. Hi Laura, I'm the stroke neurologist. He walked alongside the stretcher. He seemed to be surveying the room. He knew that each minute that passed two million of Laura's brain neurons would die. He had to act quickly, but not rush. The EMS gave their report to the stroke team while the neurologist was examining her in parallel. The nurses were drawing blood to send for CBC, electrolytes, creatinine, coagulation profile, random blood glucose level. The neurologist seemed to want key information from the EMS crew. When was she last seen normal? What are her neurological symptoms? What is her relevant past medical history and medications? Is she on any blood thinners? What is her baseline functional status and occupation? What were her vitals, cardiac rhythm strip, glucose en route? The neurologist turned to Laura. Can you tell me what happened? Laura tried. Breakfast talk couldn't she stopped. That's okay. He turned to Michael. Tell me exactly what you saw. Michael described everything, the sudden difficulty speaking, the right facial droop, and the right arm weakness. The neurologist continued examining her. She had obvious right facial weakness, it involved the lower part of the right face sparing the frontalis and obicularis oculi, suggestive of an upper motor neuron pattern of weakness, consistent with a stroke. She had a right arm pronator drift downward to the bed. He seemed to be quickly doing math in his head and blurted out NIHSS at least eight. The diagnosis seemed clear to him, and her symptoms were clearly disabling for a 50-year-old mother. He had enough information, and the next step was rushing her to the CT scanner. Most likely she was having a stroke that localized to the left MCA territory. Although most likely this was ischemic rather than a hemorrhage or bleeding into the brain, a CT head was needed to confirm that prior to starting treatment. Some clinical clues that suggest an intracranial hemorrhage rather than an ischemic stroke are if there's any progressive neurological deterioration, decreased level of alertness at presentation, thunderclap headache, head trauma, if they're on blood thinners or have a known bleeding diathesis. These clinical clues are suggestive but not specific. 7 fifty two AM Laura disappeared into the scanner. The first images appeared on the screen. The neurologist scrolled through them in the CT control room. No hemorrhage. There were no signs of early ischemic change. Aspects ten, which meant there was no obvious damage yet. This made sense as not enough time had passed for severe damage to have occurred. There was a clinical imaging mismatch, aka lots of brain to save. He could see a left hyperdense M1 on the CT scan. Michael stood outside the room. More images quickly appeared, this time the CT angiogram. The neurologist knew what he would see. A blood vessel on the left side of Laura's brain abruptly ended, a distal left M1 occlusion, localizing to her stroke deficits. He looked proximally at the aortic arch and extracranial circulation, and there was no clear cause on the CTA, as the rest of the arteries were open, no dissection, atherol, or other vascular abnormality. A clot. Downstream from that clot were the parts of Laura's brain responsible for language and movement on the right side of her body. He told the technician to skip the CT perfusion scan, aka a fancy color map of blood flow. A CT and CT angiogram was enough. The CT perfusion was not needed as it would not change her management and only delay treatment. We had to quickly start treatment to restore blood flow to those important brain areas, otherwise she would be severely disabled or worse. eight oh one AM As the structure is being quickly pushed back to the resuscitation room, the neurologist is speaking to Laura and her husband. Laura, you're having a stroke. She stared at him. There's a blood clot blocking one of the major arteries supplying the left side of your brain. Michael squeezed her hand. The neurologist carried on. If we act quickly, we can potentially save important brain tissue. The goal here is to restore blood flow to the brain areas that are dying. We have two treatments we can offer, and together we'll give the best chance at recovery. He took a deep breath. The first is a clotbusty medication called tenectoplase or TNK. This is the standard of care and I recommend it for your disabling symptoms. We have strong data to support it can improve your symptoms, especially given we are very early from when this started. Neurologists call this the golden window. The neurologist knew that TNK increases the probability of improvement compared to placebo, a number needed to treat of 10 for excellent neurological outcome if given between 0 to 3 hours. Time is clot. TNK resolves clot best when given very early. She had no contraindications. The neurologist spoke again. There is a small risk of serious bleeding in the head. That risk is about 3% for you, and a smaller risk of bleeding elsewhere in the body. But the benefits here in your case greatly outweigh the risk, and I recommend we treat as soon as possible. The faster we start treatment, the better. The 3% risk reflected the recent literature, specifically the ACT trial, a large landmark trial completed in Canada, a trial the neurologist was very proud to be a part of. A less common but important complication from thrombolysis is swelling of the lips or tongue known as angioedema. This can occur in about 1% of treated patients. This risk is higher if the patient is on an ACE inhibitor or if they have a right MCA stroke involving the insular apicular region. Laura and Michael agreed to proceed. As the nurse was drawing up the medication, the neurologist immediately started discussing the second treatment, endovascular therapy. It involved mechanically taking out the clot and is one of the most effective treatments in all of medicine. If used quickly, it can also have a mortality benefit. This was demonstrated in the Canadian-led escape trial. The interventional radiologist would maneuver through the arteries with a small wire to access the blockage and then take it out. Laura and Michael eagerly agreed to proceed with both treatments. The neurointerventional radiologist had already looked at the images and agreed with the neurologist to quickly proceed. Laura had already received TNK with a fast door to needle time of 16 minutes and was being rushed to the angial suite. Things were moving quickly. A catheter was introduced into the femoral artery. Under X-ray guidance, it traveled upward toward the neck and into the crowded artery and toward the arteries of the brain. Contrast appeared on the screen. And once again the blood flow stopped. There was the clot. The team advanced their equipment. Michael sat in the waiting room staring at his phone. At 8 53 the neurointerventional radiologist came out and explained that the entire clot was removed. He even showed Michael a photo of the small thing that had the potential to cause so much damage. The treatment went as well as could be. Laura opened her eyes. Michael was sitting beside her. She looked at him. He waited. Hi. One word. Do you know where you are? Laura looked around. Hospital. Did you know why? She paused. Stroke. He squeezed her hand. Then she looked towards the door. Where she stopped. Michael waited. The she became frustrated. The kids Olivia's with my mom, they're okay. Laura closed her eyes. The language was back mostly but not completely. The next morning. She was admitted to the intensive care unit and had an unremarkable night without issues or complications from the treatment, aside from the nurse waking her up every hour to check on her. The neurologist came by to round and examined her. He hardly recognized her. Her NIHSS score was two, one for mild language difficulty and one for mild facial weakness. A significant change from pretreatment. She was so much better, and he was very happy with her progress. A repeat CT head was completed that day which showed a very small stroke and no bleeding. A relatively small area of the left hemisphere had been injured. The treatments were a success. The rest of the brain had been salvaged with their timely and effective treatment. T and K had been administered quickly and endovascular thrombectomy had achieved complete reperfusion quickly. The entire visible clot had been removed and the blood was flowing again. She was started on aspirin 81 milligrams daily. Laura could walk. She could use her right hand, she understood conversations, but occasionally a word disappeared. She would know exactly what she wanted to say, but needed several seconds to find it. A mild, residual, expressive aphasia. The stroke had left a fingerprint, but compared to what might have happened, her recovery was remarkable. She was working with the therapists, speech language pathology, occupational therapy, and physiotherapy in hospital. The nurses on the stroke unit were keeping a close eye on her, monitoring her vitals and neurological examination. There was still one problem. The neurologist had to figure out why this had happened. Laura was 50 years old. She didn't smoke, she didn't have diabetes, her cholesterol wasn't particularly remarkable, her neck arteries didn't contain significant athosclerotic disease, there was no arterial dissection or web, no atrial fibrillation had appeared on monitoring. The neurologist took a detailed history. There was no preceding infection, history of DVT or PE, recent chiropractic manipulation, she was not on hormone replacement therapy, no family history of stroke at a young age or recent travel, a detailed review of systems was negative. The Bubbles A stroke in the young workup was sent. As a first-tier workup, a echo with bubble, 48-hour holter, MRI brain, leg dopplers, blood work for antiphospholipid antibodies, C reactive protein, ANA, and homocysteine was sent, with reflexive investigations depending on those results. Two days later, Laura was lying in bed when a cardiac sonographer arrived. We're going to do an ultrasound of your heart, an echocardiogram. Partway through the test, the sonographer placed an IV and explained that they were going to inject agitated saline, essentially tiny micro bubbles into a vein. Laura watched the ultrasound screen. The bubbles entered the right side of the heart. Normally they shouldn't cross directly to the left side, but they did. A large number of them. The cardiologist reviewed the images. Laura had a large patent foramen ovali, a PFO. The neurologist returned later that afternoon. You found something, Michael asked. Yes. He drew a simple heart on a piece of paper. Before we're born, there's a normal opening between the upper chambers of the heart. After birth, it usually seals. He drew a small line between the chambers. In roughly a quarter of adults, it doesn't completely close. That's called a patent for Amen Ovalley. Laura frowned. So I've had a hole in my heart for fifty years? In a sense, but there's important context. PFOs are common. Most people who have one will never know about it and never have a problem from it. Then how could it cause a stroke? The neurologist drew another arrow. Normally, a cloth that forms in the vein travels toward the lungs, where the circulation acts as a filter, but a PFO can potentially provide a shortcut from the right side of the heart to the left. He moved his pen across the opening. A clot could cross through the PFO, enter the arterial circulation, travel towards the brain, and block an artery. Michael looked at him. So that's what happened? It's a possibility. Her PFO has high risk features, and assuming the rest of the stroke workup is normal, this is the most likely culprit. We will need to wait for all the blood work to come back, but now that we found this, I'm going to arrange for further blood work. The neurologist ordered Protein C and Protein S, prothrombin, antithhrombin, factor V liden, and Jack II. Laura underwent the appropriate investigations for a young patient with an otherwise unexplained embolic stroke. No alternative cause emerged. A paradoxical embolism through the PFO was the most likely explanation. This was a probable PFO-related stroke. The case was reviewed in the context of Laura's age, imaging pattern, vascular risk factors, and the absence of another convincing stroke mechanism. This is reflected in the rope score. Laura was discharged from hospital on appropriate antithrombotics with an urgent referral place to interventional cardiology for PFO closure and close follow-up with the stroke neurologist. She was planning to complete outpatient rehab for her residual minor deficits. Because of TNK and EVT, she was only in hospital for five days. This is not uncommon in the days of endovascular therapy. Six weeks later. Laura was awake for the procedure. Once again, a catheter traveled through her vascular system. But this time nobody was racing against dying brain cells. A closure device was positioned across the PFO. The pathway between the two atria was sealed. The procedure was over. Three months later. The kitchen looked exactly the same. Same coffee machine, same table, same argument about whose turn it was to empty the dishwasher. Mom, Olivia shouted from upstairs, where's my black sweater? Laura smiled. In the laundry room. The words came out easily. Michael looked up from his coffee. Laura caught him watching her. What? Nothing. You're doing that thing again. What thing? Watching me talk. He smiled. Sorry. Laura shook her head. The neurologist told her that most people meeting her would never know she'd had a stroke. He was right. She was back at work. She was driving again after medical clearance from her neurologist. She was exercising. But occasionally, especially when she was tired, a word would hide from her. She'd pause, wait, and then find it. A small reminder of a Tuesday morning when an artery in her brain suddenly closed. And that's where Laura's story ends. But before we finish, think about everything that had to happen correctly. Michael recognized the signs of stroke. He didn't drive her to the hospital, he called 911. Paramedics moved quickly and accurately recognized a possible stroke and notified the hospital. The stroke team established the timeline, clinched the diagnosis, interpreted the imaging, and provided timely treatment. The interventional neuroradiologist completely removed the entire clot very quickly, restoring blood flow. The stroke neurologist diligently searched for the stroke etiology and it was found and definitively treated. A team effort. But there was one moment in this entire story that I want you to remember. Not the TNK orthrombectomy, not the CT scanner, not the PFO closure. Go back to the kitchen. 7 16 AM in the morning. Laura couldn't speak, her face drooped, her arm became weak, and Michael recognized that something was wrong. Everything that happened afterward depended on that moment. Because we have extraordinary treatments for stroke, we can dissolve clots, navigate catheters into the arteries of the brain, reverse stroke symptoms, but none of those treatments can help someone sitting at home waiting for their symptoms to improve or going to bed hoping in the morning things would be better. Remember, face, arm, speech, time. If stroke symptoms appear suddenly, call 911. Because sometimes the most important person in a stroke team isn't the physician, it's the person sitting across the breakfast table. I'm neurologist Dr. Andrew Michelli, and this is Tales from the Cortex, stories from inside the brain. Subscribe to stay up to date with our new episodes. Hope you enjoyed episode one. Keep listening for more bonus content. For neurologists in training, and for physicians who don't routinely manage acute stroke, examining a patient with a suspected stroke can be challenging. There's a lot happening at once. While you're examining the patient, someone is registering them. Another person is drawing blood, the history is being gathered, imaging is being ordered, and the clock is running. A high-stakes situation. So let's discuss some practical tips on how to examine a patient during a cold stroke as a pragmatic neurologist, focused on speed, accuracy, and gathering information that actually changes management. Because in a stroke, every minute matters. The faster an eligible patient is treated, the better their chance of a functionally independent outcome. And remember, this is not a full neurological examination you might perform in a clinic or on the ward. A NIH stroke scale is the standardized exam that is completed during a stroke assessment. It's a 15-item scale with a total score ranging from 0 to 42. A higher score indicates more severe deficits, and correlates with stroke size and can predict long-term outcomes after a stroke. Parts of the neurological examination that are not included in the NIH stroke scale are cognitive assessment, visual acuity, pupils, vertical eye movements, and nystagmus, cranial nerves 8 through 12, muscle tone, formal power testing, distal limb weakness, reflexes, sensation to vibration, proprioception, cortical sensation, Romberg, and gait assessment. Although these parts can be incorporated into your exam on a case-by-case basis. After all the action of the cold stroke has settled, a more detailed neurological examination can be completed. Ideally, the full NIH stroke scale is completed before the patient goes to the CT scanner, but practically this is not always feasible, as the highest priority is getting the patient to the scanner as soon as possible. Let's imagine you're standing beside me in the emergency department. Before I even touch the patient, I'm already examining them. Are they awake? Are they looking at me? Are their eyes deviated to one side? Are they moving both sides of their body? Can they understand what people are saying? Can they speak? Are they neglecting part of the room? The first five seconds can tell you an enormous amount of detail. Then I introduce myself. Hi Laura, I'm the neurologist. Can you tell me your name? Her answer isn't just conversation. I'm listening to her language. Does she understand the question? Can she find the words? Are the words appropriate? Is her speech fluent? And importantly, is this aphasia, a problem with language, or is it dysarthia, where the language is intact but the muscles producing speech aren't working properly? Cortical signs early in the examination, such as aphasia, neglect, gaze deviation, can be a tip-off to the presence of a large vessel occlusion, which has implications for activating the endovascular team. Here are a few tips when performing the NIH stroke scale under time pressure. Weakness, language, and gauge deviation are likely the highest yield elements of the examination when assessing the likelihood of stroke and localization. This information can be gathered in under one minute. See if this patient can speak fluently, name objects, understand a command, if they can repeat a sentence. Ask them to smile and raise both arms in the air for 10 seconds. Then, after that, ask them to lift one leg at a time for five seconds. As you become more experienced, you can tailor the exam to presenting symptomatology by starting with elements that are most relevant to the patient's presenting complaint. For example, if the patient presents with visual impairment and sensory loss, that would localize to the posterior cerebral artery territory. You would miss this localization by focusing only on motor or language assessment. Of course, it can be challenging at times. An 85-year-old presenting as a cold stroke with isolated speech difficulty can have multiple potential causes or etiologies at play. Delirious patients will have fluctuations in attention or consciousness, but should not be making paraphasic errors, whereas a stroke patient with isolated aphasia are usually attentive and trying to respond but making paraphasic errors. I challenge you to think carefully about the patient presenting with isolated speech difficulty with a normal CT, CT angiogram, and good quality CT perfusion. Are they having a stroke? Trunchal and gait ataxia, a posterior circulation sign, is not assessed in the NIH stroke scale, so a strategic posterior circulation stroke could potentially be missed if you're not checking balance and gait. Don't forget to check if the patient can sit, stand, or walk normally if this is suspected. Pay close attention to the vitals. If the patient is febrile, that changes things. Blood pressure is usually elevated in an acute stroke, whether it's ischemic or hemorrhagic, because of autoregulation of cerebral perfusion pressure, so it's often not helpful unless you suspect a mimic and the patient is normal tensive. Then it can support your pretest probability. In the cold stroke handbook, I elaborate on how to make sense of unusual signs on exam. How about right or wrong way eyes? Right way eyes occur in lesions affecting the frontal eye fields. The frontal eye fields normally aid in contralateral eye movements. However, when there is an injury from a stroke, for example, then the eyes look toward the side of the lesion, i.e., away from the hemiparietic side. Wrong way eyes look toward the side of the weakness and away from the side of the lesion. Some causes of this can include seizure activity in the cortex, which causes activation rather than damage of the frontal eye fields. Thalamic henrhage can disrupt the corticospinoid pathways of the internal capsule, leading to contralateral weakness and also cause wrong way eyes. These thalamic lesions are typically large though, and usually are accompanied by a deep coma. Lesions in the pontine basis and tegmetum disrupt the corticospinal fibers, leading to contralateral hemiplegia with the involvement of the sixth nerve nucleus or PPRF, causing ipsilateral horizontal gaze palsy. If the patient is diaphragic, confused, or have pale skin, this may suggest hypoglycemia or other metabolic abnormality or presyncopy. How about the pupils? If they're dilated, this suggests a sympathomimetic syndrome from hemphetamines, cocaine, pseudophedrin, cholinergic antagonist drugs, or others. If the pupils are constricted, this suggests opioid or narcotic overdose. Pontine tegmental injury typically results in pinpoint pupils. The most common cause is a pontine hemorrhage. Lesions in the lateral medullary tegmentum or Wallenberg syndrome may cause an ipsilateral horner syndrome. If the patient has a sensory level without cranial nerve deficits, this localizes to the spinal cord. Lastly, the history and exam help with localization. Frame a pretest probability for stroke and is supported by the appropriate neuroimaging you complete in the emergency department. If you suspect a few possible localizations, focus closely in those areas on your neuroimaging. Then discuss with the patient your findings and decide on the best course of treatment through shared decision making. Until next time.