Editorial: Results of the FAST-MAG Trial


You may have seen the above image circulating recently and/or you may have read this article by Rick Bukata, MD. FAST-MAG was a multicenter randomized, controlled clinical trial out of UCLA studying prehospital administration of magnesium sulfate to treat stroke. The results are in.

It didn’t work.

Not necessarily surprising. This paper states we’ve tested over 20 drugs in 270 preclinical trials with ~200 clinical trials being conducted with ~40 failed neuroprotectants.

The elephant in the room is why these drugs fail to translate from the bench to the bedside. Despite success in animal studies, trials in humans have yet to work. One of the pertinent questions that was previously raised to direct the future of neuroprotectant research was that of the therapeutic window, or the time frame in which the drug should be given.

Many animal studies have been conducted with the study drug being given immediately after the onset of injury and there is usually data showing the efficacy of a neuroprotectant decreases as the time from onset increases. This is well known, however one of the translational challenges is in the marketing of the investigational drug. Pharmaceutical companies balk at the limitation of placing a ‘2-hour’ time window of administration on a drug as it significantly decreases the marketability and in turn, the profitability. There is room for discussion on the role private drug companies should or should not play in clinical research. Drug companies are companies and companies exist to maximize shareholder profits. This creates a lot of pressure to find drugs which have wider administration windows than ‘immediately after a stroke’.

Enter magnesium sulfate. No drug company had a vested interest in it. There’s no patent. There’s no board of directors. There’s no shareholders. The design of FAST-MAG was to take this drug, which had no strings from the pharmaceutical industry attached, and test the 0-2 hour window. To answer the question which had been raised over and over again: Is the narrow time window the reason why neuroprotectants have failed to translate?

In the process a lot of data was generated and EMS agencies were thrust into the heart of clinical research. Also, a lot of money was spent: $16 million. Some feathers were ruffled in the wake hence the article by Dr. Bukata and ensuing discussion.

Open debate is always good. Science thrives on a clash of ideas and nothing should be free from rational critique. One of the goals we have with NeuroEMS is to reach out to study authors and deliver both commentary and critique from leading experts. In the wake of Dr. Bukata’s article I reached out to the principle investigators of the FAST-MAG trial for their reply. I’ve reproduced the responses received below:

Dr. Jeffrey Saver, Principal Investigator

Hi [redacted],

Thanks for contacting me. I was not previously aware of Dr. Bukata’s posting. I am cc’ing my co-Principal Investigator, Dr. Sidney Starkman, an Emergency Physician, and Sam Stratton, MD, and Marc Eckstein, MD, our EMS Medical Director Co-Principal Investigators, in case they wish to comment.

Here are some remarks I can offer:

“The Field Administration of Stroke Therapy – Magnesium (FAST-MAG) Phase 3 Trial was an innovative collaboration of prehospital, Emergency Department, and hospital systems. The FAST-MAG investigative group included 40 EMS Provider Agencies, 315 rescue ambulances, 2988 paramedics, and 60 receiving hospitals. Emergency Physicians were site PIs at each of the hospitals. The study was perhaps the largest ever undertaken by Emergency Medicine, with 715 Emergency Physician investigators, as well as 236 Neurologists, Neurosurgeon, and Hospitalist physician investigators.

The study had the specific aim of testing magnesium sulfate as a potential neuroprotective agent for stroke and the systems aim of demonstrating that prehospital start of treatment would permit delivery of therapy faster than prior ED-initiation studies, when there is the greatest potential to save threatened brain. The study succeeded in accomplishing both aims. The results on the specific aim were definitive, albeit disappointing – magnesium sulfate was not found to be a beneficial neuroprotective agent. The results on the systems aim were definitive and highly successful. Treatment initiation in the ambulance enabled start of infusion far faster than any prior stroke trial, a median of 45 minutes after stroke onset. Fully 74% of patients were treated in the first 60 minutes after onset, the “golden hour” in acute stroke when there is the greatest amount of brain still viable and the greatest opportunity for benefit.

As a result, the FAST-MAG collaboration has opened up a new treatment window in acute stroke, and the methods developed in the trial are already being mobilized to test many promising therapies in the pipeline, including NA-1, remote ischemic perconditioning, and hyperacute antihypertensive therapy.“

I hope this is the sort of comment you were seeking. Please let me know if I can provide further information that would be helpful.

 Dr. Sam Stratton, EMS Medical Director & Co-Principal Investigator

Hello [redacted],

As one of the Co-principle investigators in the FAST-MAG Trial I appreciate the opinion of Dr. Bukata, but not his lack of support for true scientific exploration of the clinical actions taken in Emergency Medicine and specifically the subpecialty of Emergency Medical Services (EMS).

The FAST-MAG trial is the model for the future scientific development of clinical practice in EMS. It appeared with early research and theory that magnesium sulfate may be beneficial as a neuro-protective agent if administered early in stroke, preferably as soon as stroke was suspected. Logically, administration in the pre-hospital setting was preferred.

Rather than adopt magnesium into the clinical practice of EMS based on early research and theory, the FAST-MAG Trial was designed to scientifically explore the intervention and was supported by NIH with no pharmaceutical company support or ability by universities to develop a new patent. FAST-MAG was the purest of science that has rarely been matched by “science-like” studies in almost all other area of medicine. The Trial accomplished exactly what it should have – showed that adding a treatment that looked promising, had advocates, and made people feel like they were doing something to improve outcome was in fact not of the benefit expected. Without the FAST-MAG trial, the EMS community would not have the scientific evidence to address whether magnesium administration in the EMS setting for acute stroke was appropriate.

Those who fail to understand the significance of the scientific method in making evidence-based decisions also fail to understand that EMS and secondarily Emergency Medicine have progressed from following the loudest opinion to that of developing by way of true science as is illustrated by the FAST-MAG trial. FAST-MAG has raised the bar for future development of EMS and has been a study that all EMS and emergency medicine providers should be proud as being representative of the profession. For the future, FAST-MAG will serve as the ultimate example for scientific exploration in medicine.

I also reached out to Dr. Bukata and spoke with him by phone. He stood by his article as published in EPMonthly and his sentiment that the ED was the proper place to conduct the trial and not EMS.

In closing, I (Stephen) would like to offer a gentle reminder that the data should speak for itself. Boring statistics and cold, hard facts should rule the day over flashy graphics and catchy phrases. I take a bit of an issue with the image above and it was created with the intent to be retweeted, shared, and spread all throughout the world. It does not offer a rational critique of trial but rather an emotional appeal. There’s enough spin and drama in the world. Let’s conduct our scientific critiques through words not graphics which bear resemblance to the political propaganda clogging our daily news feeds. Perhaps this sounds puritanical but I think it leads to more informed discussion and less bias.

In the interest of disclosure I presently work on NIH/NINDS funded clinical research.


12 Lead ECG and Stroke, pt. 1 (Overview)


15-30% of strokes are cardioembolic and 60-90% of stroke patients present with ECG abnormalities. (Source)

So let me ask you some questions. Is it important to obtain a 12 lead ECG during a suspected acute stroke in the prehospital setting? Why? Why not? Does it really matter either way? Before we discuss the answer…

Here’s the abnormalities you’re likely to encounter in acute stroke:

1. Long QTc & Ischemic ST changes. Found in 76% of hemorrhagic strokes & 90% in ischemic strokes. (Source)

2. Afib. Detected in up to 25% of new ischemic strokes. (Source)

Here’s what you’re unlikely to encounter in acute stroke:

1. STEMI. Outside of a few case studies (and good anecdote) there’s little in the literature of concomitant STEMI & stroke however each disease tends to follow one another within days or months. 2-6% of stroke patients die of cardiac causes in the first 90 days after stroke. (Source)

2. Changes indicative of acute PE. Again the literature was scarce.

Now let’s look at some literature:

1. Electrocardiographic Changes in Patient’s with Acute Stroke: A Systemic Review. (Khechinashvili, et al):

“In patients with ischemic stroke and intracerebral hemorrhage, these ECG abnormalities (and QT prolongation) most often represent preexisting coronary artery disease. The specificity of ECG changes to diagnose acute myocardial infarction is low in the acute phase of stroke.”

The authors note that the ST & QTc changes most likely were due to arteriosclerosis and it was extremely difficult to look at an acute stroke patient’s ECG and correctly say that the patient was not having an MI. In other words the physicians were unable to distinguish that the patient was not suffering an MI from that patient suffering an MI.

2. Electrocardiographic Changes and Prognosis in Ischemic Stroke. (Buzluolcay, et. al.) [n=87]

“The six-month mortality rate in the patients with ECG changes was 38.9% whereas it was 15.2% in those with normal ECG”.

The authors note that observing an abnormal ECG in an acute stroke patient more than doubled their mortality rate at 6 months (likely due to the severity of the underlying cardiovascular disease).

3. The Effect of Acute Stroke on Cardiac Functions as Observed in an Intensive Stroke Care Unit. (Lavy, et. al.) [n=43]

“Both disturbances in rhythm and conduction and “ischemic” ST-T alterations were detected and the frequency of the former exceeded that of the latter. The ECG alterations were transient in 32 patients and permanent in four. New electrocardiographical abnormalities in patients without evidence of heart disease prior to the stroke were associated with poorer prognosis.”

The authors noted a high incidence of transient abnormalities vs. permanent ones. (remember paroxysmal Afib was one of the potential causes of cryptogenic stroke we covered in Tales from the Cryptogenic, pt. 1)

4. Prolonged QTc as a Predictor of Mortality in Acute Ischemic Stroke. (Stead, et. al.)

“Patients with a prolonged QTc interval were more likely to die within 90 days compared with patients without a prolonged interval…The estimated survival at 90 days was 70.5% and 87.1%, respectively…The identified threshold cutoffs for increased risk of death at 90 days were 440 milliseconds for women and 438 milliseconds for men.”

5. The Electrocardiogram in Stroke: Relationship to Pathophysiological Type and Comparison with Prior Data. (Goldstein) [n=150]

“Of the 150 patients with stroke, 138 (92%) showed ECG abnormalities. The most common abnormalities were also changes from prior tracings: QT prolongation (68 patients, 45%), ischemic changes (59, 35%), U waves (42, 28%), tachycardia (42, 28%), and arrhythmias (41, 27%). Patients with cerebral embolus had a significantly increased frequency of atrial fibrillation (9 patients, 47%); and with subarachnoid hemorrhage an increased frequency of QT prolongation (20, 71%) and sinus arrhythmia (5, 18%)…Stroke patients had an increased frequency of pathologic Q waves (30 patients, 20%) and left ventricle hypertrophy (39, 26%), but these were not new findings at the time of the stroke.”

An old paper from 1979 but a good read nonetheless.

6. Electrocardiographic Abnormalities in Acute Cerebral Events in Patients with/without Cardiovascular Disease. (Mansoureh, et. al) [n=361]

“The most common ECG abnormalities associated with stroke were T-wave abnormalities, prolonged QTc interval and arrhythmias, which were respectively found in 39.9%, 32.4%, and 27.1% of the stroke patients and 28.9%, 30.7%, and 16.2 of the patients with no primary cardiac disease. We observed that other ECG changes comprising pathologic Q- wave, ST-segment depression, ST-segment elevation, and prominent U wave may also occur in selected or non-selected stroke patients; thereby simulate an acute myocardial injury.”

Similar to #5 but published in 2013 and conducted in a different population furthering the validity of the changes as they correlate to stroke.

This should lay a foundation for us to further explore the relationship of the ECG to acute stroke. Back to answer the question from earlier regarding prehospital 12 leads….well…presently there’s simply not a hard and fast answer. A case can be made either way but the real goal is as always: recognition and activation of a stroke alert and rapid transport to an appropriate facility without delay. If you can snag a 12 lead without compromising this dictum then why not? If it slows you down, or if a protocol is broadly applied to standard 911 transport paramedics of unequal skill and efficiency then we are doing a disservice when one can be obtained in the ED. Prehospital 12 leads in acute stroke needn’t become distracting novelties.

Thus far there is consensus on in-hospital 12 leads but a lack of scientific consensus on prehospital 12 leads. Let the discussion ensue…

P.S., as a historical aside…the first paper ever published on the link between cardiac changes and stroke was in 1947.

Reading List – ‘Incognito’ by David Eagleman


“Three pounds of the most complex materials we’ve discovered in the universe…is built of cells called neurons and glia-hundreds of billion of them…[that] are connected to one another in a network of such staggering complexity that it bankrupts human language and necessitates a new kinds of mathematics. A typical neuron makes about 10,000 connections to neighboring neurons, which means that there are more connections in a few cubic centimeters of brain tissue than there are stars in the Milky Way galaxy.” -David Eagleman, Ph.D., Baylor University

In neurology, even the experts feel they can only see the tip of the iceberg so for someone with a new interest in the field the subject is certain to be overwhelming. Therefore starting with ‘Incognito’, we’re creating a recommended reading list. Look for selections geared towards all reading levels and join the NeuroEMS book club by commenting on and discussing each selection.

In ‘Incognito’, Dr. Eaglemen, a prominent neuroscientist, describes his understanding of the inner workings of the brain and highlights interesting clinical case studies. He covers the oft-talked about case of Phineas Gage, a railroad worker whose construction accident and resultant personality change formed the basis for questioning the origin of emotion in the brain. He also discusses the case of Supreme Court Justice William Douglas and why Douglas denied disability after suffering a paralyzing stroke and enlightens us on why some patients being treated for Parkinson’s become compulsive gamblers. You can find a link to Dr. Eagleman’s website here.

Review courtesy of Michael Herbert.

Tales from the Cryptogenic, pt. 1


Depending on what statistic you’re looking at anywhere from 30-40% of strokes result from an unknown cause.

That’s right. A full work-up of these patients reveals no cardioembolic causes, no large-artery occlusive disease, and typically an absence of risk factors. It’s a diagnosis of exclusion and it’s called cryptogenic.

So what actually causes these strokes to occur? Why does a clot form and occlude a vessel if there are no known reasons for it to do so?

There’s a couple of theories (presently more like a collection of correlations):

1. Patent Foramen Ovale. PFO has been been shown to have an increased incidence in patients who suffer cryptogenic strokes. PFO is present in 17-35% of the general population but is witnessed in up to 45% of cryptogenic stroke patients. (Source)

2. Pathogenic/Immune Response. There’s a growing body of epidemiological studies indicating a correlation between receiving an annual flu vaccine and a pretty significant decrease in stroke & heart attacks. (Source

3. Subclinical Atrial Fibrillation. In one study (n=51; be wary of the small sample size) where patients wore a type of implantable arrhythmia detector A-fib was detecting in 25% of the subjects. The mean detection date was at Day 48 representing a very infrequent onset. Paroxysmal A-fib like is would be incredibly difficult to detect as it is so transient. (Source)

4. Undetected Genetic and/or Environmental Causes and/or Some Other Unknown. Research into environmental causes of neurological pathology is a pretty hot area of research and when it comes to genetics (and epigenetics) we are barely scratching the surface.

We’ll break down the research into #’s 1, 2, 3, & 4 in future posts!

Blood Flow Through the Brain, pt. 2 (The Ride to the Top)

Let’s get a little more familiar (and look at a cool image) with the path blood takes as it leaves the heart and travels up to the brain. If you don’t recall what we covered in Blood Flow Through the Brain Part 1, take a moment to review.


Remember the above picture? Now let’s take a look at what it really looks like, courtesy of an MRI scanner:


Pretty cool, huh? It’s a bit confusing but hang in there and let’s really nail those anatomic structures and take a look at what it looks like in real life. Starting at the bottom…see the horseshoe looking structure about parallel with the ‘A’? That’s the aorta as it arches out of the heart on towards the rest of the body. With the heart being the blob at the bottom, blood moves up starting from the left side and arching up towards the right and then down towards the abdominal organs.

Coming up from the aorta are two lateral curving projections outward. These are the subclavian arteries running beneath the clavicles and out to the arms. Now look at the two tangles, one on the right & one on the left, of vessels shooting straight up. You’re looking at the carotid & vertebral arteries.

Now keep looking directly upwards horizontal with the heart. See those two that are coming together and meet almost in the center of the head at the midline? That’s where the vertebral arteries come together to create the basilar artery, also called the vertebrobasilar system. Directly to the right and left, those large corkscrew-looking vessels, are the carotid arteries.

Pop quiz: Which vessels comprise the posterior circulation? Carotids or Vertebrobasilar?

A: Vertebrobasilar. The carotids give rise to the anterior circulation.

As such remember as you are looking at the images that the carotids are actually in front while the vertebral and basilar are in the back. View the MRI as if you were looking face to face with the patient. Follow those carotids up and the basilar up, almost to the top of the image, and draw a horizontal line in your mind. Right about the area where all those vessels cross that line is where the Circle of Willis lies. It’s hard to visualize from this view but we’ll cover it in-depth soon.

90 yom “Possible Stroke” (from ems12lead blog)

So let’s take a look at a case which Tom Bouthillet from the EMS 12 Lead blog posted and assess it from a neuro perspective. Let’s start by reviewing his post.

Let’s approach the case in a linear fashion (I’ve bolded certain elements of interest): This gentlemen was perfectly normal until he walked outside, lost his balance and fell, was helped back inside, and experienced loss of consciousness and seizure-like activity. He is fully alert & oriented at the time of assessment.

On exam he presents pale & diaphoretic, tachycardic, with diastolic hypotension & a widened pulse pressure. A quick Cincinnati screen is negative (However a negative Cincinnati doesn’t mean the patient is 100% not suffering a stroke). Past pointing is observed. [This commonly refers to motor activity which overshoots a particular target. For example if I was trying to pick up a coffee cup and unintentionally reached 12 inches to the right of it.] His EKG is sinus in origin and negative for atrial fibrillation (pertinent negative for a neuro exam, since A-fib leads to clots).

Our patient takes a beta blocker, an Alzheimer’s medication, and cholesterol medication. His past history includes mild cognitive impairment (precursor to Alzheimer’s), hypertension and high cholesterol (stroke risk factors). Lets assume everything else is normal with the patient except for what has been mentioned. (One thing not given is the blood glucose level. Definitely remember to check this but for the purpose of the case we will assume it is within normal limits)

Starting with our chief complaint of a possible stroke, we can hold-off for now on activating a stroke alert since our patient is presently without deficit. Let’s ask ourselves if the patient’s symptoms have a neurologic origin, a cardiovascular origin, or a combination of the two?

1. One of the first things we want to know is did the patient quickly stand-up and walk outside right before the fall occurred or had he been up moving around for a while? Sudden changes in body position, especially in the elderly, easily lead to syncope or near-syncope as it takes the body time to adjust and keep a steady flow of blood going up to the brain.

2. Let’s look at the pulse pressure which is 62 mmHg. Typical pulse pressure (the difference between the systolic and the diastolic) is 30-40 mmHg. A wide (or high) pulse is a great, great indicator for cardiovascular risk and tells us that vascular compliance is low, meaning the heart is having to work extra hard when it contracts to get blood flowing. This is indicative of narrowed arteries, fitting in with the history of hyperlipidemia & hypertension. We also see a low diastolic of 53 (normally this would be >60). This was measured while the patient was sitting. Perhaps the patient is dehydrated, has been recently ill, or for other reasons has a slightly lower than usual circulating blood volume (or in geriatric patients, simply doesn’t command the reserve of blood a younger patient would). The systolic pressure is high because the heart must beat hard & crank up the pressure in order to force the blood through potentially narrowed vasculature. Blood pressure measures pressure, not volume, although the two are distinctly related. This low diastolic ties in with #1. If we have a resting DBP of 53, what happens to it when the patient suddenly stands and begins moving? We could surmise it would temporarily drop until the body compensates which may have caused dizziness.

3. Loss of balance & past pointing. This may be explained by the mild cognitive impairment. Remember, MCI & Alzheimer’s destroy neurons which can effect motor function. We should quickly ask about the progression of the patient’s disease and if balance issues and motor coordination have been observed previously. These could also simply be associated with the normal aging process. There could be a number of neurological causes for these symptoms and acute onset of neurologic deficit is always concerning. Knowing whether this is the first time these have been observed or not is crucial and should be asked. We could consider vertigo or some type of vestibular (system in the inner ear creating the sense of balance) disorder. We also can keep TIA (transient ischemic attack) on the list. There may have been a temporary clot which only briefly disrupted blood flow but this really doesn’t fit the clinical picture and would be atypical.

4. Here’s the tricky part. Upon sitting down, the patient’s eyes rolled back into his head and he began shaking all over. It’s difficult to tell much from a written case study versus actually assessing a patient. Could he have suffered a seizure? It’s a possibility. Seizures can result from a hypotension severe enough to cause near-syncope. If we think about it, our patient potentially stood up (causing a shift in the blood/cardiovascular system), exerted himself by walking outside (causing a shift in the blood/cardiovascular system), fell down (causing a shift in the blood/cardiovascular system), stood up, (causing a shift in the blood/cardiovascular system), and sat down on the toilet (causing a shift in the blood/cardiovascular system). This may have been enough disruption in the blood supply to the neurons to cause a brief seizure.  It’s a possible explanation and fits the clinical picture. Just like #3, we want to ask if this is the first time this has ever occurred. And remember, we assumed the blood glucose level was normal because it wasn’t given but think how things would change if we had a low BGL on top of all the other issues our patient has. All the more reason to have irritated neurons and a potential seizure.

1+2+3+4 leans us toward a cardiovascular origin of the patient’s complaint. However, we can’t discount the role the neurologic system plays in contributing to the patient’s condition, nor can we say for certain there isn’t an underlying neurologic condition behind it all. It’s highly unlikely, but this could be the first manifestation of an invasive, quick-moving, brain tumor.

A quick clinical tip: If you have the time and while you have your stethoscope out, take a listen to the patient’s carotid arteries. Abnormal (swooshing) sounds are called bruitsand indicated a narrowing of the artery. The patient is already at high risk for stenosis and if there is significant carotid stenosis then this contributes much towards the theory that adequate blood isn’t able to reach the brain.

Blood Flow Through the Brain, pt. 1 (Overview)

We all remember blood flow through the heart being pounded into our heads in school. Knowing the blood flow through the brain is every bit as important and proficiency in the basics of cerebral vasculature can quickly improve your assessment of stroke patients. There is a concept in stroke diagnosis known as localization. This refers to connecting the pattern of a patient’s symptoms back to the location where the clot might be lodged. An experienced physician can often determine the area of the brain involved in the stroke and the vessel which is occluded based off of a physical assessment.

For EMS, knowing the anatomy & common presentation patterns (or syndromes) can help a medic further his/her understanding of stroke pathophysiology & severity.

Let’s look at a couple of pictures to help visualize the anatomy. Don’t get too caught up in all the vessels…there are only a couple we will be discussing for now: the Carotid Arteries, the Basilar Artery, the Vertebral Arteries, the Circle of Willis, and the Right & Left Middle Cerebral Arteries.



Take a moment and make sure you can identify exactly where the above-mentioned vasculature is located. Don’t worry about any of the others yet.

The picture on the top is a view as if you were standing face to face with someone while the view on the bottom is what you would see if you were standing directly on top of the heart tilting your head back and looking up towards the brain.

Let’s take a closer look at the mentioned structures starting with the carotids. Somewhere about the level of the thyroid cartilage the carotid arteries bifurcate into the interior and exterior carotids. The exterior go on to provide circulation to the face while the interior continue upwards to the brain. The internal carotids form the anterior circulation of the brain. The vast majority of strokes occur in the anterior vasculature.

The vertebral arteries arise from the subclavian arteries (underneath the clavicles) and continue up along the spinal cord merging together to become the basilar artery. These vessels account for the posterior circulation of the brain.

The carotids and the vertebrobasilar connect together and form an amazing structure called the Circle of Willis. This is a large circular structure sitting beneath the brain which creates the blood supply of the brain and feeds arteries which branch out from it. One of the unique facets of the Circle of Willis’ design is that if the vertebrobasilar arteries cease functioning there is still some supply of blood being circulated around from the carotids (and vice versa). This helps to ensure continued blood flow.

There are two main vessels which arise from the Circle of Willis: the right & left Middle Cerebral Arteries. The MCA supplies the vast majority of the brain’s blood supply and by virtue accounts for a significant number of strokes. The Right MCA branches off and feeds the right side of the brain whereas the Left MCA branches off and feeds the left side.

To circle back around to the concept of localization let’s consider the case of a 90 year old female presenting with complete left-side hemiparesis, left-side facial paralysis, left-side vision loss, left-side neglect, and significant dysarthria. Where is the stroke likely to be occurring?

Remember that motor function is controlled by the opposite side of the brain. If our patient presents with left-sided deficit then we can start looking to the right side of the brain. Now let’s use what we just learned about vasculature to narrow down the likely location.

We have the complete loss of function to the left side which indicates that this is a severe stroke and indicative of a complete loss of the blood supply since absolutely nothing is presently working. [Consider as the blood supply begins to slow, full function turns to numbness, which turns to weakness, which worsens until full paralysis is achieved when blood flow ceases. The symptoms on numbness, weakness, and paralysis can help us understand the severity of the stroke and the amount of the vessel which has become blocked.]

Since we know the Circle of Willis helps to provide some continued blood flow, it is unlikely that the occlusion is occurring at this level or lower. We can think about ruling out the Circle of Willis, the vertebrobasilar arteries, and the carotids. This leaves us with the Middle Cerebral Arteries. Since our patient is symptomatic on the left side, and motor control is opposite, we are looking at the Right MCA as the culprit. In fact, this patient’s presentation is classic Right MCA Syndrome. Flip the symptoms to the other side and we would be thinking about Left MCA Syndrome.

Of course, stroke pathophysiology and localization is complex and requires years of dedicated training to master but hopefully this gives you a greater understanding of the cerebral vasculature and how strokes present. There are a multitude of syndromes and varying degrees of severity but the Right & Left MCA syndromes are the classic patterns which we teach EMS providers to look for. Remember that complete acute loss of function compared to the varying degrees of acute weakness can reveal how much of the blood supply has been cut off.

Now on to Part 2 (The Ride to the Top)