Jodi Gehring, MD, Author at The Stroke Blog

Author Archive

Mistakes young stroke patients make

by Jodi Gehring, MD on Dec 3, 2014 • 2 Comments

I will keep today’s post brief, but wanted to relay mistakes that young stroke patients frequently make in hopes that they will not perpetuate. Yesterday I saw a young stroke patient who decided to rest when symptoms began, so it is worth reiterating errors made and why these actions should be avoided.

Taking a nap/lying down when stroke symptoms begin. Remember, an ischemic stroke patient is only eligible for IV t-PA (the “clot busing” medicine) for 3-4.5 hours after a stroke begins, and with each passing minute that the brain does not receive blood flow, approximately two million cells will perish. When a stroke patient awakens from a nap, it is often too late to intervene. Call 911.
Driving himself/herself to the hospital. This is a terrible mistake for many reasons. A stroke patient is more likely to be involved in a motor vehicle collision if trying to drive while the brain is not receiving adequate blood flow/oxygen. Vision and cognition may be impaired. There could be delays in care with traffic on the road. Instead of being brought directly back to be evaluated by the emergency medicine physician, a patient may incorrectly be asked to wait in the triage area if not arriving by ambulance, which creates further delays. Do not drive to the hospital if you may be having a stroke.
Taking aspirin at home. Remember that 20% of all stroke are hemorrhagic, or “bleeding strokes.” Aspirin may worsen bleeding, and no one will know whether a stroke is ischemic (due to a blood clot blocking blood flow to the brain) or hemorrhagic until a head CT scan or MRI can be performed to visualize the brain.

I had the privilege of providing a basic overview about stroke on May 1, 2014 on a local news show in Charlotte, NC to start Stroke Awareness Month this year. If you are interested in viewing this, click here. Remember the FAST mnemonic for identifying stroke early so we can work to prevent disability from stroke.

Face – Is a facial droop present on one side?
Arm – If both arms are extended, and one drifts down due to weakness, this could be a stroke until proven otherwise
Speech – Is there slurred speech? Is there difficulty finding the words with which to communicate?
Time – Time is critical, as stated in the above points. Call 911.

Stroke in the Mainstream Media

Australian cricket star Phillip Hughes dies after traumatic injury to vertebral artery

by Jodi Gehring, MD on Nov 27, 2014 • No Comments

Phillip Hughes, Australian cricket star, died as a result of a vertebral artery dissection and hemorrhagic stroke after being hit in the neck. Photo source: Associated Press

Making headlines in the sporting world as Americans celebrated Thanksgiving today was news of the tragic death of Australian cricket player Phil Hughes. According to media reports, Hughes was reportedly struck near his left ear, and “as a result of that blow, his vertebral artery was compressed by the ball. That caused the artery to split and for bleeding to go up into the brain,” according to the article from CNN’s site. BBC reports that Hughes never regained consciousness after the injury, and that this incident is generating discussion around safety in the game.

This suggests that Hughes sustained a vertebral artery dissection, or a tear within at least one layer of the artery’s wall. In most people, there are two vertebral arteries – one on each side – traveling through small canals in the spine while carrying blood to the cerebellum, brainstem, and the posterior portions of the brain. The vertebral arteries join after they have entered the skull to form the basilar artery. A prior post on The Stroke Blog in October 2014 described this anatomy with illustration in the context of two cases of carotid artery dissection, which can be accessed here.

Sudden abrupt movements to the neck or direct trauma can result in tearing of the artery. Most vertebral artery dissections involve separation of the innermost layer in the artery, called the endothelium, from the vessel wall, but if severe enough trauma occurs, the splitting can result in rupture of the artery and hemorrhage.

I extend my sincere condolences to Mr. Hughes’s family, friends, team mates, and his fans in Australia who might read this. It is a reminder that life is precious, that tomorrow is not guaranteed to any of us, and that no one is immune from stroke.

Musings on Stroke

It’s Raining, It’s Pouring: Why the old man couldn’t get up in the morning

by Jodi Gehring, MD on Nov 23, 2014 • 3 Comments

Disclaimer: Read no further if you have a special fondness for nursery rhymes and do not wish to have one ruined for you permanently.

Today I awoke to a rainy morning in Charlotte, North Carolina, and it continued to rain throughout most of the day. This evening, the steady rain transitioned into a downpour. One of my children said: “It’s raining, it’s pouring…”

Most of us are familiar with the well known nursery rhyme:

          It’s raining, it’s pouring;
         The old man is snoring.
         He went to bed and bumped his head,
          and couldn’t get up in the morning.

I vividly recall this nursery rhyme carrying an entirely different meaning for me after I started my neurology residency. It was a rainy day in Seattle, and as this rhyme came to mind while I was driving, it suddenly struck me – the old man sustained either a subdural hemorrhage or an epidural hemorrhage. He experienced a period of lucidity after hitting his head (enough such that he was able to get to bed), but he did not get up the following morning. The story became grim.

Layers of the meninges (tissue coating the surface of the brain); ref: http://www.merckmanuals.com

The meninges, or the thin tissue coating the surface of the brain, have three basic layers: the dura (outermost layer, which is adjacent to the skull), the arachnoid, and then the pia (adjacent to the brain). When an aneurysm ruptures, typically it is into the subarachnoid space, meaning just beneath the arachnoid layer of the meningeal coating. Thus, a subarachnoid hemorrhage occurs when blood fills the space below the arachnoid layer.

This is a CT scan taken from a patient with an epidural hemorrhage, or bleeding from the middle meningeal artery into the space between the skull and the dura. Note the severe compression occurring on the brain.

An artery that travels between the dura and the skull, known as the middle meningeal artery, is vulnerable to tearing with direct trauma to the skull. Typically there is a brief loss of consciousness followed by quick recovery, and these patients often do not seek medical attention because the immediate drama is so short-lived. However, as blood pools from the middle meningeal artery between the dura and the skull, the pressure on the dura creates significant compression on the brain and can quickly become a fatal situation. This is what occurred as the cause of death in actress Natasha Richardson when she fell while skiing in Canada in 2009. She died at the age of 45.

This is a CT scan taken from a patient with a subdural hemorrhage (the crescent-shaped collection of white material along the inside of the skull is blood), bleeding from a torn vein in the space beneath the dura layer of the meninges. I suspect this was the cause of death in the old man from the familiar nursery rhyme, given that these hemorrhages are more common in the elderly.

Subdural hemorrhages are more common in the elderly patient population. Large numbers of veins fill the space between the dura layer and the arachnoid layer, and as the brain ages and decreases in size (yes, the brain shrinks with aging), more sheer stress occurs on these veins. A relatively small hit on the head, or even a cough or a sneeze, can result in the tearing of one of these veins, and the subdural space begins to fill slowly with blood. The key word here is slowly. This is not usually as rapid of a neurological demise for the patient as occurs in a patient with an epidural hemorrhage, because epidural hemorrhages involve an artery, which carries blood under high pressure, filling the space rapidly. Blood flowing from a vein flows more slowly because the pressure is lower. Picture water gushing from a water hose (epidural hemorrhage) versus dripping slowly from a faucet (subdural hemorrhage). The pattern of blood layering on a head CT scan can also distinguish between an epidural hemorrhage and a subdural hemorrhage as well, as the images reflect.

I now carry the curse and the blessing of pondering traumatic intracranial hemorrhages every time I hear this nursery rhyme performed on a children’s CD or when I see it printed in an anthology. Perhaps I have passed this on to you as well and the rhyme will carry a different meaning going forward. The story of the old man offers an important lesson in neurological vigilance, though.

When a young person hits his or hear head after falling while skiing or in any other traumatic fashion, anytime there is even the briefest loss of consciousness, a head CT scan is strongly indicated, even if it does disturb vacation plans. When an elderly person hits his head just before going to bed, maybe it is not a terrible idea to wake him up several hours later and ask a few questions, just to be on the safe side. It’s also important to remember that after an elderly person hits his head, even if he does get up in the morning, when he still has a headache a week or two later, that head CT scan can be life-saving if it detects a subdural hemorrhage.

Stroke and Pain

Rules for Treating Migraine in Stroke Patients

by Jodi Gehring, MD on Nov 15, 2014 • 5 Comments

Treating migraines as a physician is one thing, but once a patient has had a stroke, the ground rules for managing pain in this population change dramatically. One of the challenges a neurologist faces is that many of the tools in the medication arsenal to use against migraines suddenly become contraindicated, or not able to be used, because the risks posed by the medication outweigh the benefits that can be gained from taking them. Here are nine of my personal rules for treating migraines in patients who have survived stroke:

Rule #1 – Avoid triptans. Triptans became game changers in the management of migraine when sumatriptan (Imitrex) became available in 1991. Many patients who experienced migraines prior to the sumatriptan era have recounted to me the misery they faced routinely in not having an effective tool to abort migraines without extreme sedation as a side effect of the medications that they were taking. Over time, other triptans were developed – rizatriptan (Maxalt), frovatriptan (Frova), eletriptan (Relpax), and then the injectable triptans, such as injectable sumatriptan. While triptans do not benefit all migraine patients (are migraines ever truly alike between different individuals, or is migraine the final common manifestation of many varying pathways?), millions of people have found relief with this class of medication and have been able to lead more productive lives. Instead of depending on a very sedating medication and spending the rest of the day sleeping, medication can be taken at work, and the headache, if it responds well, might vanish within an hour or two while the day marches on. The problem is – most stroke patients should not use triptans! Triptans can result in constriction of arteries within the brain and, depending on the mechanism of the patient’s stroke, could potentially further raise the risk for a repeat stroke. At times we have to get extremely creative in the management of migraine symptoms when triptans are a no go.
Rule #2 – Stroke patients with pain must sleep at night! Have you ever wondered why people feel tired at night and awake during the day (largely)? Our brains are wired for us to sleep at night. When light vanishes from the environment, a hormone called melantonin is produced by the pineal gland in the brain, which helps to regulate the circadian rhythms involved in our sleep cycles. When light returns, melatonin production decreases. Adequate, restful sleep is a critical part of pain management in all patients, but in particular in the stroke population. If a patient is not sleeping and has refractory migraines, my first goal is to get the sleep issue under better control. It makes no sense to load a patient on medications for pain if helping him/her to sleep better will produce 70% of the improvement desired. Following brain injury, stroke patients can have difficulty regulating circadian rhythms and may need assistance. Caffeine elimination, avoiding excessive fluid intake before bed, a regular bedtime routine, going to sleep at a time that will allow for 7-8 hours of sleep during dark hours (not 1AM until 9AM if light will enter the environment once again at 6AM) – all of these are important considerations. Working night shifts makes treating pain nearly impossible in the stroke population, and I often encourage those who work overnight to inquire about switching to a shift that takes place during daylight hours. If these changes do not work to yield a full night of restful sleep reliably, sleep medication aids may be utilized. They all have the potential for side effects, so sleep aid medication should be individualized based on each patient’s history and symptoms. If a stroke patient cannot sleep because of extreme anxiety, for example, then a benzodiazepine (medication that can be used for sleep and for anxiety) might be chosen. If a stroke patient does not sleep well and has refractory pain, the pain will never be controlled until the sleep issue is addressed.
Rule #3 – Be aggressive about treating anxiety. Anxiety is common following a stroke, especially in the younger stroke population. Younger patients are not expecting a stroke to become a part of their lives, and this event can prove very distressing. If the underlying cause of the stroke is not identified, the anxiety over wondering if another stroke will occur can be disabling. Additionally, after a brain injury, surges of stress hormones (cortisol, epinephrine, norepinephrine) may occur, which can result in panic attacks in patients with no prior psychiatric history. I am usually fairly aggressive about managing anxiety early so that it does not escalate. If the anxiety is severe enough, then I will ask for assistance from psychiatry in managing the patient. I have encountered resistance from patients who feel they will be labeled in a negative way by seeking care from a psychiatrist, but this is a stigma that needs to end. Anxiety is a serious problem with many consequences for the patient and his/her family if left untreated. Counseling may also be recommended in some cases. Patients with chronic pain and anxiety following stroke stand a better chance of improving pain when anxiety is under control.
Rule #4 – Maintain a lower threshold for starting daily preventative medication. Many migraine patients who are easily able to abort migraines with the use of a triptan do not end up requiring a daily medication intended to decrease the frequency and severity of migraines, known as preventative therapy. However, when many of the effective medications intended to stop migraines are unable to be utilized, the strategy may switch to using daily medication to reduce the number of migraine attacks, or to lessen the severity of the migraines that do occur. Anti-seizure medications, such as topiramate (Topamax), can be helpful, as can some antidepressants. A patient with pain and anxiety may benefit from an antidepressant, depending on the patient’s history and other symptoms. If multiple oral medications are tried and are ineffective, greater occipital nerve blocks and/or trigger point injections may also be useful, but are frequently painful as they involve multiple injections of local anesthetic in the scalp, neck, and trapezius to alleviate pain. Botulinum toxin (Botox, Dysport) has been very effective for some patients with refractory migraine, but does not work for everyone. This also involves multiple injections, and usually has to be repeated every three months for efficacy.
Rule #5 – Lifestyle changes should be emphasized. Exercise, biofeedback, yoga, tai chi – I have seen all of these hugely impact pain management. There are also pain rehabilitation programs involving daily physical therapy and sessions with rehabilitation psychologists available that can be effective.
Rule #6 – Treat obstructive sleep apnea! Obstructive sleep apnea has been associated with an increased risk for stroke, myocardial infarction (heart attack), high blood pressure, and not only that, but patients with untreated sleep apnea often experience frequent headaches. If a patient is waking up with headaches in the morning and the bed partner (spouse, significant other, etc.) claims that he/she snores, then a polysomnogram (sleep study) is worth the time and effort. I have lost count of the number of patients who have relayed to me that once they started treating their sleep apnea, usually with CPAP (continuous positive airway pressure, or air that blows through a mask at night to keep the airway open and improve oxygen intake while sleeping), their morning headaches improved and they had more energy during the day.
Rule #7 – Set realistic goals. Managing pain after stroke is extremely daunting in some cases for neurologists. We have tools that we can use, but the chance of turning refractory pain into a pain-free existence is a rare occurrence. I discuss goals with patients, and will often ask: “Will you be happy if you can get 50% relief from what you are currently experiencing?” Most patients will say yes, anything is better than what is happening right now.
Rule #8 – Be patient. The physician treating pain as well as the patient must both remain – well, patient, for lack of a better word. If something does not work, try something else. If that does not work, try something else. Medication is not the be all and end all for every patient, and other patients require multiple medications to achieve a level of functionality. The goal is not to give up, though, and to remain hopeful. When the patient loses hope, the physician must not. Pain management is a collaboration, and there must be dedication on both side to achieving a desirable outcome.
Rule #9 – Believe the stroke patient who claims to be in pain. Pain is a subjective experience, and it differs from person to person. My sympathy for the vascular dissection and thalamic stroke patient populations is great because the pain can be so unrelenting. However, because many of these patients look so normal externally, they are not believed when they describe the severity of their pain. My pain during routine dental visits and procedures is unreal at times, and I have stopped trying to explain to others how much suffering I endure in that situation because no one around me really believes it. Perhaps I am just not tough enough. Perhaps my “pain threshold” is low. Whatever. The pain, as I experience it, is real and it is awful. However, my dentist is a kind, empathetic person who believes me, and a little empathy goes a long way. I have to believe that patients who experience pain on a daily basis that nears or exceeds the severity of the pain I endure in the dental office might feel a little more hopeful if the physician who is supposed to be treating them believes that their pain is real.

Stroke in the Mainstream Media / Stroke Patient Tales

Can chiropractic manipulation cause stroke?

by Jodi Gehring, MD on Nov 9, 2014 • 8 Comments

Since this story hit the news media last week, several blog readers have inquired into whether neck manipulation can result in stroke.

To summarize (and what I know is what the media is reporting – this is my disclaimer), Jeremy Youngblood, a 30 year old man in Oklahoma, died from complications of a cerebellar stroke following a visit to his chiropractor. While the media has not directly stated that Youngblood sustained a vertebral artery dissection, or a tear in the lining of the artery, this has been implied. The vertebral arteries (there are typically two – one on each side, traveling within openings through the vertebrae of the neck) supply blood to the brainstem and the cerebellum, which controls balance and coordination. Spinal fluid produced in the brain drains through a canal, called a ventricle, near the cerebellum. If a vertebral artery dissection occurs, inflammation occurs at that site in the blood vessel wall, and platelets begin to collect in that area. These platelet-rich clots then can break loose and travel to the brainstem and/or cerebellum, blocking blood flow to those sites, and resulting in ischemic stroke.

The danger in cerebellar stroke is that if swelling occurs in the area of damage and tissue expands, spinal fluid may not be able to leave the brain if the ventricle is closed off. The brain will still continue to produce spinal fluid, though, raising the pressure within the brain as a life-threatening condition called hydrocephalus occurs.

So – is there an increased risk of vertebral artery dissection following chiropractic neck manipulation? Many vascular neurologists would say they suspect the answer is probably, while acknowledging that many thousands of patients undergo this procedure without complications. In my own practice, I see two or three patients each year with a vertebral artery dissection that occurred somewhere in the midst of neck manipulation. However, often these patients sought help from their chiropractors in the first place for neck pain or headaches, so it is not possible to ascertain whether the dissection was already present. When patients state that within seconds of the manipulation stroke symptoms begin (sudden vertigo, nausea, vomiting, weakness on one side of the body, numbness on one side of the body, an inability to swallow – I have heard all of these as symptoms that have begun immediately following manipulation in patients later confirmed to have vertebral artery dissections with brainstem or cerebellar strokes on MRI), does that mean that the manipulation caused the dissection? Or was the dissection small, and worsened by the manipulation.

Recently, the American Stroke Association issued a scientific statement about this controversial issue. In this statement, the claim is made that evidence is lacking to definitively associate the two, but that review of many population studies by the statement’s authors indicate an association between neck manipulation and vertebral artery dissection in young patients. The recommendation is that patients undergoing this treatment be informed of the potential, even if the risk is small.

Approximately half of vascular dissections are spontaneous – meaning, there is no explanation identified for how the lining of the artery, called the endothelium, was injured. In those where a source of trauma is identified, not infrequently the trauma is relatively minor. Some of the more interesting vertebral artery dissection stories I have heard are: head turning while swimming freestyle and feeling a “rip,” sneezing forcefully and experiencing sudden pain in the neck, lifting weights during a routine workout. There is the classic “beauty parlor dissection,” acquired when leaning back and extending the neck against the sink or dryer. One question is – how is it that a person can undergo the same activity 999 times without incident, and on that thousandth time be so unfortunate? What is it about circumstance and timing that makes the difference between a routine day at the gym (or at the chiropractor’s office), and the potential for stroke? While we know there are conditions that can place someone at additional risk for vascular injuries, such as Ehlers-Danlos syndrome or fibromuscular dysplasia, for the majority of vertebral dissection patients, there is no good explanation.

Stroke and Pain

Examining the Migraine-Stroke Relationship

by Jodi Gehring, MD on Nov 7, 2014 • 7 Comments

If a random sample of our population was challenged with describing a typical stroke survivor, what words would be used to construct such an image? I have actually asked this question of those around me in non-medical environments, curious as to what most people consider to be typical. “Paralyzed” is a common perception. “Slurred speech,” “unable to talk,” “can’t walk,” and “can’t move” are others. What I don’t often hear, though, is “refractory pain.” Strokes have been described as clinically silent, with the general perception being that a heart attack is painful, but a brain attack is not.

The reality is – every patient is different, and every stroke is different. Strokes can be painless, or they can be excrutiating, unrelenting, and painful beyond anything imaginable.

Over the coming months, I intend to write a series of posts addressing the issue of chronic pain following stroke – headaches, neck pain, scalp and facial pain, pain affecting arms and legs, thalamic pain syndrome. Pain can be quite prominent aftermath of stroke, especially in the younger stroke population. Often, these patients may have recovered well enough from a physical standpoint to receive numerous comments along the lines of: “You don’t look like you’ve had a stroke.” The response they may desire to give in return is: “You may think that, but I feel like I’ve had a stroke.”

To start the discussion, it is important to understand the relationship that exists between migraine and stroke.

So what is a migraine? This is another question I have posed to random individuals in non-medical settings, and I often ask patients who are experiencing headaches in the clinic what their idea of a migraine is. Often, the explanation involves the notion that a migraine is severe – a headache so intense that the person suffering with it must go to bed in a dark room devoid of sound and light.

Then, I tell them the truth about migraines: “A migraine is not a headache.”

The follow up to this is: “Migraine is an overly excited state in the brain, and a headache is very commonly associated with migraine, but a person can experience frequent migraines and never have a headache.”

Isn’t that interesting? A migraine that does not involve a headache is a strange concept to many. Some people have aura, an associated neurological symptom due to this “overly excited state,” such as seeing flashing lights, zigzag lines, or a smudge in the vision that grows into a large crescent of to engulf all visual fields, a phenomenon known as a scotoma.

Some migraine sufferers experience sensory aura, which involves numbness and/or tingling over the face, arm, and/or leg.

Aphasic aura is an interesting migraine feature that is less common than visual aura or sensory aura, and very much can mimic a stroke at presentation. This involves the inability to speak clearly or potentially impaired understanding of language.

Migraine aura typically (but not always) resolves within an hour without medication, even if the associated headache lasts for hours or days. Other associated migraine symptoms include vertigo, tinnitus (ringing in the ears), nausea, confusion, and even fainting.

Migraine has long been established as a risk factor for stroke, particularly in young patients. The Collaborative Group for the Study of Stroke in Women published in 1975 that patients with migraine carried double the risk of stroke as patients without migraines. More recent data confirmed this risk. A French study found that there was no increased risk of stroke in elderly patients with migraines, while multiple studies have demonstrated an increased risk of stroke in the young migraine sufferer. Having migraine with aura carries an even higher relative risk of stroke than what is seen in patients with migraine who do not experience aura.

Consider this as well (I never miss an opportunity to preach about the dangers of cigarette smoking) – patients with migraine may carry twice the risk of stroke as patients without migraine, but patients with migraine who smoke cigarettes are ten times more likely to experience a stroke. Patients with migraine who smoke cigarettes and who use estrogen-containing birth control pills in one study were 34 times more likely to experience a stroke. I would encourage any migraine sufferer reading this who also uses birth control pills and who smokes to consider laying down the cigarettes and spending that money in other ways.

Why does having migraines increase one’s risk for stroke? Many theories exist, but the jury is still out on exactly why. It may be because the innermost lining of the arteries, called the endothelium, may differ from that which exists in the non-migraine population. It could have something to do with platelets (fragmented blood cells that assist in halting bleeding) functioning differently in migraineurs. Migraineurs are more susceptible to vasoconstriction, or spasming/squeezing in the arteries of the brain. The term for a stroke that occurs in the midst of a migraine episode is migrainous infarction.

Migraines can pose challenges to health care providers attempting to treat them in the young stroke population. Therapy for migraine is best broken down into two arms – abortive therapy, which is used as needed when migraines occur in order to gain relief, and preventative therapy, which is taken daily whether a migraine exists or not in an effort to decrease the frequency and severity of migraine episodes. Please check back for the upcoming post, covering the ground rules of treating migraine in the stroke patient.

Ethics in Stroke Care

What does “do not resuscitate” really mean?

by Jodi Gehring, MD on Oct 30, 2014 • No Comments

My husband, as well as dozens of others around us several Saturdays ago, witnessed an event drastically different when performed live and in close proximity from how it is portrayed on television – cardiopulmonary resuscitation (CPR). We were enjoying dinner at a restaurant when fire trucks and police cars rapidly approached the parking lot, and when we went outside, we found first responders in the midst of full court press CPR. A vehicle had struck a pedestrian as he attempted to cross the street, resulting in cardiac arrest from the trauma. Cars backed up past the first responders as citizens gazed from behind windows, clearly stunned at what they were seeing.

This is a graphic from the Australian Resuscitation Council, keeping things simple. If a person is unresponsive, not breathing, and has no pulse, rather than the rescuer agonizing over the correct ratio of chest compressions to breaths and becoming paralyzed with fear, he or she should just go for the chest compressions until help arrives. Remember – when a person is without a pulse and is not breathing, that person is effectively not alive, and CPR is the last hope to restore life. Do not be afraid of messing up and default to inaction as a result.

I remember very well the first time I performed CPR on a patient. Two specific factors that I had not previously anticipated surprised me greatly. First, after only two minutes, I was sweating profusely. The muscles in my shoulders, back, arms, and neck intensely ached, as if I had been running for hours. It is exhausting to perform CPR, and every two minutes we switched off between providers, taking turns on chest compressions in order to bring fresh energy to the situation. The second surprise came when I felt a rib snap under the force of one of my compressions. Think fingernails on a chalkboard times fifty. While that may seem disturbing, medical students and residents are taught to put things into proper perspective – to understand that by the time CPR is necessary, the person is effectively not alive. This is the last hope at restoring life, so fear of injuring the patient should be cast aside in favor of saving the person’s life.

On television, when a patient’s heart stops, everyone speaks in succession in a scripted format, while an indefatigable physician applies gentle chest compressions. Actors and actresses may display tousled hair, but sweating would disturb much-needed makeup, given the lighting. A study published in the New England Journal of Medicine in 1996 found that on three medically-themed television shows popular at that time (ER, Chicago Hope, and Rescue 911), the short term survival rate with CPR following cardiac arrest was an impressive 77% (the most optimistic short term survival rate in the medical literature is around 40%). The patients on television receiving CPR were typically much younger than actual patients with cardiac arrests, and more than the majority of the time, the patients sustained cardiac arrests due to trauma (again, not reflective of reality – primary cardiac causes, such as myocardial infarction or a fatal arrhythmia, are the most common reasons for cardiac arrest).

It is understandable why some patients would not find CPR a particularly desirable option, and in our system of healthcare, they can now indicate the preference for rescuers not to provide CPR when the time arrives. Very elderly patients with multiple medical ailments who experience cardiac arrest while hospitalized have a very low chance of surviving the hospitalization after CPR is performed. Terminally ill patients may express the wish to pass away peacefully. At times, patients state that they just don’t want CPR, and despite not having a defined reason for it, we respect the principle of autonomy in decision-making.

Health care providers routinely ask patients for their preferred code status when admitting them to the hospital. Typically, either a person chooses to be “full code” status, which means “do anything and everything possible to save me if my heart stops beating,” or a person opts to be “do not resuscitate” status, or DNR, which is intended to mean “if my heart stops pumping, do not perform CPR on me.” When I talk to stroke patients and their families about code status, I always emphasize that, in my opinion, DNR means I will still treat their urinary tract infections with antibiotics, and if they require intensive care and nursing, then I will place them in the neurological intensive care unit. DNR means everything except CPR. “Do not intubate,” or DNI, means not to place a patient on a mechanical ventilator to breathe for him or her. Many patients who request the DNR status will also request to be DNI, but not always.

Data demonstrates that this interpretation of the DNR status may not hold true in many hospitals, though. One study evaluated over 8,000 patients with hemorrhagic stroke (intracerebral hemorrhage, or ICH) at 234 different hospitals. It was found that hospitals with the highest rates of giving patients the DNR code status within the first 24 hours of ICH saw a higher risk of patient deaths. Does this mean these hospitals just had sicker patients who were more likely to die? Even after adjusting for age, medical illnesses, and other factors (comparing only sick patients to equally sick patients, leaving a situation where the only factor differing between the patients groups was whether or not patients were of the “full code” status or DNR status), carrying the DNR code status independently increased the chance of death. Hospitals with higher rates of using the DNR code status also saw a lower likelihood of using ventilators, performing brain surgery as a life-saving measure, or performing invasive imaging to identify aneurysms. If DNR only means withholding CPR in the event that the heart stops beating, then why are non-CPR aspects of medical care withheld from patients with hemorrhagic stroke?

Another study found that of patients who underwent elective surgical procedures, again with similar characteristics (age, same types of procedure being performed), patients with the DNR code status were twice as likely to die within 30 days of the surgery compared to those with the “full code” status.

What does this mean? In my opinion, it means that patients and the providers who care for them need to align their expectations. If a patient expects that a DNR status means withholding CPR but otherwise receiving aggressive medical care, and those providing the care think of DNR as meaning not giving every other effort to save a person’s life, then there is a problem. DNR does not mean withholding aggressive medical care. The term for that is “comfort care,” when goals shift from sustaining life and fighting for recovery to comfort becoming the most important goal for the patient over anything else. DNR is not synonymous with “comfort care,” but it appears that it may be morphing into a cousin to it without many patients recognizing this when opting for the DNR status. I am hopeful that, sooner rather than later, there will be a national dialogue about this topic, with patients leading the discussion.

Diagnosing Stroke / Stroke Patient Tales / Young Stroke Survivors

A Normal Head CT Scan Does Not “Rule Out” Ischemic Stroke – Part II

by Jodi Gehring, MD on Oct 22, 2014 • 4 Comments

As a follow up to last week’s post about head CT scans failing to demonstrate evidence of ischemic stroke in certain situations (early stroke, strokes of small sizes, strokes in the brainstem or cerebellum), I wanted to share several cases illustrating the truth behind the assertion.

The head CT image on the right was obtained from a young woman who was 31 years old at the time of her stroke. She presented to an outside emergency department at a small hospital with numbness and jerking movements of her left arm. Her blood pressure was high, and she was discharged home with a diagnosis of hypertension. Her head CT scan was normal at that time. Shortly after arriving home, she developed prominent left-sided weakness, returned to the ER, and then was diagnosed with an early ischemic stroke. The patient’s right cerebral hemisphere (which is on the left side on our view – the patient is facing us on this CT image, so what we see as the left side is actually the patient’s right side) appears darker than in the left hemisphere. This is because edema (swelling) and ischemic injury have occurred in the brain. Several years later, she has reduced use of her left hand and struggles with anxiety. She and her husband have been a source of great inspiration to me as I have had the privilege of observing them persevere through her challenges.

The MRI to the left belongs to a woman who presented to an ER with isolated leg weakness, and a stroke was “ruled out” with a normal head CT scan. She returned home, and later returned when her symptom worsened. Her brain MRI demonstrates acute cerebral ischemia (injury emerging from lack of blood flow) in the territory of the right anterior cerebral artery (the white arrow tip indicates the location of the stroke). See my previous post, A Tale of Two Carotid Artery Dissections, and the Miracle of the Circle of Willis, for a tutorial on the major arteries bringing blood to the brain.

For all of the frustration that I hear from patients about strokes that have been missed on CT scans, though, I feel that it is necessary to celebrate when a not-so-obvious stroke is diagnosed early enough for what it actually is, and the patient is able to receive the appropriate therapy for the best shot at a positive outcome. It does actually happen, and I tell the following story to offer hope. Sometimes things run as they should on the front lines of medicine, and it is quite refreshing when things go right!

A woman suddenly became very dizzy and had difficulty speaking clearly. The alignment of her eyes became skewed, and she was unable to focus on a single target. Following this, she became confused and disoriented, and was unable to move her right side. Her symptoms were fluctuating, and those around her could not figure out in that moment exactly what was occurring. She was brought to a local hospital, and the ER physician, concerned for possible stroke, called the on call neurologist. The patient had the head CT scan to the right, which was interpreted as normal by the radiologist (and which I agree is unremarkable). The patient received IV t-PA immediately after the CT scan was able to exclude this as a hemorrhagic stroke, on the assumption that the patient was in the midst of an early ischemic stroke.

On the following morning, the patient’s right-sided weakness had completed resolved, her speech was clear, and her thinking and reasoning had returned to normal. The only symptom that remained were some visual abnormalities. At this point, that has improved as well.

Her brain MRI (on the left) that was performed the following day revealed that she had, indeed, sustained an ischemic stroke. Fortunately, she was able to receive IV t-PA early enough to minimize the damage. Thank goodness the emergency medicine physician did not “rule out” stroke with her normal head CT scan. On the following night, the same emergency medicine physician was working and called about a different neurological patient. During the discussion, feedback was provided to him about how the previous night’s patient had improved, and how the MRI did confirm the presence of ischemic stroke. His response was: “It always feels good to know that you’ve made the right decision.” Yes, it certainly does.

Diagnosing Stroke / Young Stroke Survivors

A Normal Head CT Scan Does Not “Rule Out” Ischemic Stroke – Part I

by Jodi Gehring, MD on Oct 15, 2014 • 7 Comments

“Head CT ruled out stroke.”

It happens multiple times each week. A patient arrives for a consultation, bringing outside medical records from the emergency department where his or her initial evaluation took place. Inevitably I will find the above statement, or some slight variation of it, stated in the notes, as if serving as a justification for why it was okay to send the patient home. Often the patient wonders why he developed partial visual loss for 30 minutes, or why the left side of her body was tingling for hours even prior to the decision to seek medical attention. After all, the symptoms seemed real at the time, but how to explain what happened since the head CT ruled out a stroke?

From my own experience caring for young stroke patients, I hear the same themes reiterated:

“Everyone tells me that I don’t look like I’ve had a stroke, but I have never felt like the same person since my stroke.”
“I have so much difficulty focusing and concentrating since my stroke, and I’m worried about my short term memory.”
“I was told that I shouldn’t still be experiencing pain now that my vertebral artery dissection has healed, but my headaches are still awful.”

I could list at least 20 bulleted themes commonly heard when talking with young stroke patients, but perhaps the most common one that I hear is: “The first time I went to the ER, I was sent home.”

There are, of course, significant concerns about a young stroke patient seeking medical attention in the ER with stroke-like symptoms, and then being discharged home. The most critical reason to identify early ischemic stroke symptoms in a patient of any age is to take advantage of the only FDA-approved medication in the treatment of acute ischemic stroke – IV t-PA. As mentioned in a previous post, t-PA is a “clot-busting” medication. When a clot blocks blood from flowing in an artery, the administration of t-PA can dissolve the clot, relieving the obstruction and allowing blood to start flowing again. In acute stroke, every minute that passes equates to the death of approximately 1.5 to 2 million neurons (cells in the brain or spinal cord).

With each passing minute that blood is not flowing to part of the brain, the likelihood of a good functional recovery decreases. In addition to the decreasing benefit of t-PA with the passage of time during those first hours of an ischemic stroke, the risk of cerebral hemorrhage from giving t-PA increases. As tissue in the brain sustains injury from this lack of blood flow, the tissue becomes “leaky” and starts swelling, and giving a clot-busting medication like t-PA to a patient with brain tissue that has already died raises the risk that the drug could cause a brain hemorrhage.

This graph appeared in the paper that outlined the results of a stroke clinical trial known as the ECASS 3 study. ECASS 3 was a trial that demonstrated that some patients benefitted in terms of functional recovery from receiving t-PA out to four and a half hours after the start of their stroke symptoms. Prior to this trial, the “window” for giving t-PA to an ischemic stroke patient was three hours after stroke symptoms began. The FDA in the United States has not approved t-PA for use beyond three hours into an ischemic stroke, although in other parts of the world t-PA has been approved for up to 4.5 hours based on this data. I include the graph from that paper to demonstrate that minutes do count. The higher the solid line is on the graph, the better the likelihood of a good functional outcome without significant disability after a stroke. As time passes on the x-axis (numbers on the x-axis represent the number of minutes that have passed since a stroke began), one can see the line trending down, indicating smaller chances of seeing a good outcome. Once the line crosses at 1.0, this is the time point at which is becomes more dangerous to give t-PA because the risk of bleeding is no longer outweighed by the benefit. At this point, for the majority of patients, brain tissue has died, and there is no more benefit to be gained.

When the assumption is made that a patient with stroke-like symptoms is not having a stroke, a CT scan of the head is usually obtained to confirm this assumption. This is flawed reasoning though. The sensitivity of a CT scan without contrast within the first 12-24 hours of an ischemic stroke is around 65%. This means that 35% of patients presenting 12-24 hours after a stroke has started will have essentially normal head CT scans. Now, consider patients who are within the time window for consideration for t-PA. The sensitivity of a head CT scan during the first three to four and a half hours of a stroke is even lower.

A head CT scan is a very good tool for diagnosing bleeding that occurs in the brain, and this is the reason why patients presenting with stroke symptoms are supposed to have a CT scan – to look for blood. The purpose of a CT scan should not be to diagnose an ischemic stroke. The likelihood of detecting hemorrhage in the brain is around 90-95% with a CT scan. Since 20% of strokes are of the hemorrhagic type, but it is impossible to determine based on a patient’s symptoms alone whether a stroke is ischemic (due to a blood clot blocking blood flow) or hemorrhagic, a CT scan clarifies the stroke type.

When I am seeing an acute stroke patient in the ER, I expect to see one of three things on the head CT: 1) evidence of bleeding (hemorrhagic stroke), 2) evidence of ischemic stroke (which means swelling and cell death has already occurred), or 3) a normal head CT scan. It is the patient with the normal head CT scan who should receive t-PA, because this is the patient who is very early into an ischemic stroke. An early stroke can be a treatable stroke, but if a patient is sent home on the assumption that a normal CT scan “ruled out” a stroke, then the only evidence-supported medical therapy for treatment has been denied to that person.

Stroke Patient Tales / Young Stroke Survivors

A Tale of Two Carotid Artery Dissections, and the Miracle of the Circle of Willis

by Jodi Gehring, MD on Oct 8, 2014 • 11 Comments

Nature is kind to some, and not so merciful to others. Much of what happens to us on a daily basis stems from chance, and almost every evening I try to reflect at least briefly on my good fortune to have experienced another day with my family, friends, and patients, knowing that it can all change so abruptly.

In order to understand the wonder and tragedy that lies within the following anecdote, it is necessary to understand some of the basic vascular anatomy of the brain – the plumbing that enables blood to circulate, that sustains the function and viability of the organ that makes us who we are.

Image credit: http://www.deviantart.net

There are typically four arteries that bring blood to the brain – an internal carotid artery on each side (A) and a vertebral artery on each side (B); the vertebral arteries join together to form the basilar artery (C), which supplies blood to the brainstem and the back of the brain. The major arteries that extend from the internal carotid arteries in the brain are the middle cerebral arteries (D), and again, there is one on each side. The middle cerebral arteries supply blood to approximately 2/3 of the cerebral hemispheres. Smaller arteries supplying the inner midline surfaces of the brain also arise from the internal carotid arteries, called the anterior cerebral arteries (E). In the majority of people, there is a bridge connecting the right and left anterior cerebral arteries, called the anterior communicating artery (commonly called the AComm, F). With the AComm comes a connection between blood flow going to the right and left sides of the brain. I have seen patients arrive with completely blocked carotid arteries and absolutely no symptoms, and when evaluating cerebral blood flow with ultrasound or with angiographic imaging, it is clear that the side of the brain with the carotid artery occlusion is borrowing blood from the other side, using what is called collateral flow. There is also the potential for sharing blood between the front of the brain and the back, via posterior communicating arteries (PComms, G, potentially one on each side). A complete circle in patients with both an AComm and PComms in addition to the other normal arteries in the brain is known as the Circle of Willis. About 30% of people possess a complete Circle of Willis.

During a weekend when I was on call, a previously healthy man in his 40s transferred from an outside hospital for management of an extensive right hemispheric ischemic stroke. He was critically ill upon arrival with an extremely concerning neurological exam. His angiographic imaging (imaging of his arteries) revealed that he had a right internal carotid artery dissection (essentially, tearing of the inner lining of the artery) with thrombus (clot) obstructing flow. His right hemisphere was ischemic, and he was unable to generate alternative ways of obtaining blood flow to this region in his brain. He lacked a complete Circle of Willis – no AComm and no PComms.

I find that certain days exist in which neurological themes declare themselves. On some days, I will see four patients consecutively who all have atrial fibrillation, an irregular heart rhythm that can result in ischemic strokes. On other days, I may receive three referrals for stroke that occurred during pregnancy or in the postpartum period. On that particular weekend, though, the theme was clearly carotid artery dissections. As I was leaving this man’s room in the neurological intensive care unit, the ER paged me, requesting guidance on a woman who had arrived with drooping of an eyelid (ptosis), and her pupil on the same side was more constricted than in the eye on the other side. This sounded like a classic Horner syndrome. Horner syndrome can occur with an injury to the internal carotid artery, which can result in both of the findings mentioned as well as abnormal sweating on the affected side of the face. I recommended that the patient have a brain MRI along with an MR-angiogram of the head and neck to exclude the possibility of a carotid artery dissection, a potential cause of Horner syndrome. I received a page soon after this that her imaging was, indeed, consistent with a significant carotid artery dissection. Fortunately, there was no stroke present. Aside from the eyelid droop and abnormally sized pupil, she was completely neurologically normal. Her MR-angiogram of the brain revealed that she possessed something valuable that the first patient lacked – she had an AComm.

The blue arrow delineates flow in this patient’s normal left internal carotid artery. The green arrow demonstrates the absence of blood flow in the right internal carotid artery. The red arrow identifies the AComm, connecting the left (normal) circulation in the brain to the right side, and enabling the patient to avoid a stroke.

When I evaluated the patient in the ER, she told me that she became concerned about the abnormal appearance of her pupil, and had decided to seek medical attention for this in the ER rather than waiting until Monday to talk to her primary care provider. She was started on antiplatelet therapy for stroke prevention, and did not sustain a stroke. Nearly one year later, her Horner syndrome has improved (although not completely resolved) and she is doing well.

I am convinced that carotid artery dissections are underdiagnosed. Frequently, these patients present to the ER or to their primary care providers with headaches that seem like migraines at first glance. Perhaps a head CT scan is performed, which is not an effective study for excluding ischemic stroke (especially very early stroke). A brain MRI is a more sensitive tool for identifying early ischemic stroke, but if a carotid artery dissection is present, this will only be seen on a brain MRI if the dissection is located close to the brain and is large. If the dissection is small, or located farther down in the neck, a brain MRI will miss it. If a patient seeks medical attention for a severe headache unlike any other previously experienced, a migraine that differs from the patient’s description of his/her typical migraines if the person is already a migraine sufferer, or if the patient has any associated neurological symptoms involving the face, eyes, speech, or extremities, a brain MRI along with some sort of imaging of the arteries in the head and neck should be performed.

I reflect back on the ironic juxtaposition of these two patients presenting on the same morning, and marvel at what a difference the presence of a tiny artery in the brain can make. In this case, it was the difference between returning to a good, normal life without stroke, and tragically in the first patient’s case, an untimely death. He passed away within the week, despite the intensive medical care that he received.

I have often wondered if I have a complete Circle of Willis. Do I have an AComm? I don’t know. I do not have an answer, and perhaps I will never seek one, because what is up there is working for now, and I cannot change what I have. Certain cards are dealt to us long before we ever take our first breaths in the world, and as much as we like to feel empowered to create our own destinies, we do not have a say in whether our Circles are complete or not. Stroke brings the realization of a loss of control, and with this comes fear and anxiety. Stroke is more than just a diagnosis with symptoms. But when I see a patient with a carotid artery dissection and an Acomm providing flow, I see perseverance, and it gives me pause.

Stroke in the Mainstream Media / Stroke Patient Tales / Young Stroke Survivors

Deconstructing the “Mini-Stroke”

by Jodi Gehring, MD on Oct 5, 2014 • 23 Comments

On Sunday, November 3, 2013, the Houston Texans played an NFL home game against the Indianapolis Colts, which began relatively uneventfully. However, it became clear that the game would not proceed in a typical manner as millions of viewers observed live footage of Texans head coach Gary Kubiak, 52, collapse on the field while exiting to the locker room at halftime.

The following headlines filled the national media during the week after Kubiak’s event:

TIA “mini-stroke” may increase risk for serious stroke – CBS News, November 6, 2013

Texans’ Kubiak Had Mini-Stroke, out Indefinitely – Associated Press, November 5, 2013

Kubiak Released From Hospital After Suffering Mini-Stroke – 740AM KTRH Houston, November 5, 2013

Gary Kubiak Had Mini-Stroke: Houston Texans Coach Released From Hospital, Out Indefinitely – The Huffington Post, November 5, 2013

I am a vascular neurologist, a neurologist who has completed additional fellowship training in order to specialize in the treatment and prevention of stroke. Since completing my stroke fellowship in 2010, I have had the great privilege of caring for many patients just like Gary Kubiak, adults on the relatively young side who never expect such an event to disrupt their lives. The unfortunate reality is that stroke can happen at any age and can affect anyone.

A concern I felt with the headlines above is the reference to Kubiak’s event as a mini-stroke. This is a term that has become very popular in our American culture, and I hear it all of the time from my patients and their family members. “It was just a slight mini-stroke.” “Aunt Mildred had a mini-stroke while eating dinner.” “He had a touch of the mini-stroke.”

A stroke is a stroke. Period. A stroke results in an injury to the brain. There are two basic types of strokes – ischemic and hemorrhagic. An ischemic stroke occurs when blood cannot reach part of the brain for a prolonged period of time and permanent damage to brain tissue takes place. A hemorrhagic stroke occurs when a blood vessel ruptures and bleeding occurs within the brain. Roughly 80% of strokes are of the ischemic type.

A transient ischemic attack, or TIA, occurs when blood flow is disrupted to the brain and symptoms concerning for stroke occur, but then blood flow is either restored or the brain compensates for the absence of blood flow by seeking and acquiring blood from other sources and no damage to the brain occurs.

During a stroke, brain damage occurs. During a TIA, damage does not occur.

What about a TIA during which damage does occur? What is that called? The answer is – a stroke.

To describe a TIA as a “mini-stroke” misses the difference between the two terms. A TIA is not a stroke because damage is avoided. A stroke is not a TIA because brain damage has occurred. I like to refer to a TIA as an almost-stroke as opposed to a mini-stroke. Throughout the lifetime of this blog, I will continuously refer to TIAs as almost-strokes.

Sometimes patients may refer to a stroke with relatively mild deficits as a “mini-stroke” to distinguish it from a stroke that leaves someone externally and obviously disabled. This is also inaccurate. I have seen patients without a single physical visible deficit from a stroke who are significantly disabled from the cognitive impairment that frequently occurs following a brain injury. I have cared for a patient for the past two years whose only symptom from her “mini-stroke” (the term she used at her first appointment with me) was a left-sided neglect syndrome. This occurs when the brain fails to recognize that the left side of the body exists, even though the left arm and leg may move appropriately and strength on the left side can be left fully intact. She was a successfully employed person prior to her stroke in her 50s, and she has not been able to work since her stroke. She does not factor in columns on the left half of the screen when working with spreadsheets because her brain fails to recognize the left half of her conceptual world. She neglects to brush the left side of her hair and has tooth decay in the left side of her mouth because she does not brush her teeth on that side. She cannot drive because she visually neglects cars that appear in the left half of her world, even though her vision on the left side is intact. Is this really a mini-stroke?

In the initial evaluation of a stroke patient, this graphic is presented in order to calculate a score known as the National Institutes of Health Stroke Scale Score (NIHSS Score). The examiner asks the patient to describe what is seen in the picture as a test of language fluency. However, patients with profound left visual neglect will describe the woman washing dishes at the sink, but will fail to recognize the children in the left half of the scene.

Perhaps the other reason why I prefer to avoid the modifier “mini” in front of a word as significant as “stroke” is because patients tend to downplay the importance of the event. I love caring for patients after TIAs, because the damage has not yet occurred, and we can intervene to prevent a stroke! If a patient has a TIA and refers to it as “mini,” then I find there is less motivation for the person to quit smoking, comply with therapy, eat healthily, or exercise regularly. After all, it was only a mini-stroke.

The other piece to these headlines is the relatively young age of the Texas coach. I definitely see patients at 52 with accelerated atherosclerosis (plaque buildup in the blood vessels, or “hardening of the arteries”), high blood pressure, diabetes, elevated cholesterol levels – some of the more typical stroke risk factors seen in older adults. However, it brings to light that a person is never too young to have a stroke, and more awareness hopefully will result in a call to 911 when stroke symptoms develop as opposed to taking a nap in an effort to sleep it off. Young people frequently do not believe their symptoms might represent a stroke, and choose to rest in hopes that the episode will resolve spontaneously. When they awaken, often there are no interventional options available, and therapy shifts from acute treatment of the current stroke to rehabilitating more long lasting deficits and focusing on how to prevent the next stroke.

During my stroke fellowship at the University of Washington/Harborview Medical Center in Seattle, I experienced my first encounter with stroke in the truly young patient. Samantha (not her actual name) was 16 years old when she developed weakness on the right side of her body and was diagnosed with an ischemic stroke based on her Magnetic Resonance Imaging (MRI) of her brain. Her physician recommended that she start taking aspirin daily, a medicine that assists in “preventing platelets from sticking to plaque in the blood vessel wall and from sticking to one another.” I put this phrase in quotes because I use it often when explaining why healthcare providers use aspirin for the prevention of strokes and heart attacks. While Samantha took her aspirin compliantly, she had a second stroke. Clopidogrel (trade name: Plavix) was added to her daily medication regimen. Take what I said aspirin does, and for most people, the effect is essentially more robust with clopidogrel.

Biological warfare had essentially been declared on Samantha’s platelets. She was also started on a statin, a class of medications to lower cholesterol and to protect blood vessels from accumulating plaque, or to protect against “hardening of the arteries.” Surely she was not going to have another stroke. But she did.

This is when I had the privilege of meeting Samantha. My stroke fellowship had just begun, and in my first weeks I encountered this young girl and her frightened mother. I did not know where to start, and I remembered words from mentors throughout medical school and my neurology residency training: Ninety percent of the relevant information for solving a medical mystery is in the history, or what the patient tells us. The rest of it – lab tests, radiology studies, you name it – confirms or denies a healthcare provider’s assessment of what the patient has described. Essentially, if the patient is describing symptoms of a stroke – weakness on one side of the body, drooping of the face, slurred speech – then my tests are to confirm or deny my suspicion. This is why taking the time to listen to patients is critical in providing care.

When Samantha recounted the stories of each stroke, there seemed to be a strong headache element. Headaches can occur with strokes, but many strokes are painless, and it seemed important that she would remember headaches while experiencing stroke symptoms. Not infrequently patients with strokes do not immediately recall a headache, because they are so alarmed by the weakness, numbness, or slurred speech that they forget to tell their physicians about the headache.

Samantha began her tale of her first stroke with details about a headache. My fellowship mentor and I decided that her strokes probably did not stem from platelets, blood clots, or plaque accumulation in her blood vessels. She was 16 years old, so how much plaque could she possibly have accumulated at that point in her young life? We determined that her strokes may have resulted from blood vessels constricting, or spasm/squeezing, as part of a newly described syndrome called Reversible Cerebrovascular Vasoconstriction Syndrome. In order to formally make the diagnosis a patient should undergo imaging of the blood vessels during an episode to demonstrate narrowing and constricting, and then repeat this imaging later to show that the constriction was reversible. We did not have this opportunity with Samantha as the episode was completed by the time we evaluated her, but we did decide to empirically start her on verapamil, a medication that can assist blood vessels with relaxation. The thought is that it can help to prevent constriction of the arteries.

Magnetic Resonance Imaging (MRI) of the brain of a young stroke patient with Reversible Cerebrovascular Vasoconstriction Syndrome. The bright areas are regions where blood flow has been recently disrupted as a result of arteries constricting.

Samantha did not have another stroke. We stopped her statin for cholesterol control, and we stopped her clopidogrel as antiplatelet therapy. Off of these two medications, she did not start having strokes again. I continued seeing her in the stroke clinic throughout my fellowship year, and she did very well in her recovery. I recently reconnected with her, and since that time she has had a healthy baby without stroke complicating her pregnancy.

The valuable lesson I learned from Samantha is that the young stroke patient is an entity of its own. Because many strokes in the general population stem from plaque accumulation and platelets adhering to it, stroke patients end up on medications that prevent platelets from functioning and on statins to prevent plaque buildup. In many cases, this is a correct, evidence-based course of action. But a 16 year old is not a typical stroke patient, and the origin of her stroke was not going to be typical either.

When a young celebrity has a stroke, it makes the national news, and there is dialogue for a few days about how surprising it is that someone so young could have a stroke: Bret Michaels, 47 at the time of his stroke; Frankie Muniz, 26 at the time of his “mini-stroke” (TIA). While gone from recent memory, Curly Howard of The Three Stooges fame died from complications of a stroke at the age of 48. Jean-Dominique Bauby, the editor of the French magazine Elle, sustained a severe stroke at the age of 43, resulting in locked-in syndrome, a phenomenon I will examine in a future blog post. Bauby “dictated” his memoir, The Diving Bell and the Butterfly, by blinking his left eye when his associate, Claude Mendibil, would speak the desired character after verbally scanning through the alphabet, starting with letters most frequently used in the French language for more optimal efficiency.

In my own practice, it seems like every week I evaluate someone who had sustained a stroke under the age of 50. The cumulative sum of patients in this population increases with each passing month, and in 2011, after practicing for one year following my stroke fellowship, I noticed that most of the young stroke patients seemed to experience similar issues that created significant stress in their lives. To start, young stroke patients spoke of feeling alone in their struggles because the people they knew with strokes were older, and thus they found it difficult to relate to the experiences of other stroke patients. These patients found their strokes to be financially stressful, as they typically were working full time prior to their events, and had not yet invested enough for retirement. One of the challenging questions frequently was whether to try to return to work for badly needed income despite deficits in functioning, or whether to apply for disability, knowing the amount would be substantially less than these patients were used to earning. Some of these patients had just become parents within the past several years, and others found that their relationships with their spouses had changed after stroke. One complaint I hear recurrently is the frustration young stroke patients feel when they are told: “You don’t look like you’ve had a stroke.” They feel an expectation to perform at their pre-stroke levels and to return to normalcy, but many feel forever changed in some way. It became clear that these patients needed a support group, and we launched the Young Stroke Survivor Support Group in May (Stroke Awareness Month) 2012 at our neurology clinic in Charlotte, North Carolina.

There is interest in stroke and how it can affect younger people, but there are few resources for this patient group. The Stroke Blog will tell the tales, with the blessings of the patients, of some of the young individuals affected by stroke who have entrusted me with their care. When a stroke appears in the mainstream media, I will attempt to break it down in an understandable way for readers here. While I probably will not be able to answer all of the questions that are sent my way, I will select questions that yield the opportunity for education and dialogue with the hope that greater understanding of stroke will come for my readers and will write about suggested topics. I will be unable to offer specific medical advice through the blog, though, and also kindly ask that if someone is experiencing concerning symptoms (weakness, numbness, visual loss, headaches, trouble speaking, etc.) that 911 be called as opposed to submitting a blog comment!

It is worth noting that approximately 25-30% of strokes, even after an extensive diagnostic workup, remain “cryptogenic” – that is, a flowery medical term for “we don’t know why this happened.” In these cases, I remain true to the principle that what the patient tells the physician is ninety percent of the answer. Then, I make the best decision I feel I can make, knowing that some things remain unknown, and regardless of what we may desire, tomorrow is not guaranteed to any of us. Young stroke patients have taught me more than I can possibly recount about humility, despair that transitions to optimism and hope, enduring love between partners, strength, determination, and how to keep going.

I sincerely hope that you will find The Stroke Blog useful, and I look forward to the journey.

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Mistakes young stroke patients make

Australian cricket star Phillip Hughes dies after traumatic injury to vertebral artery

It’s Raining, It’s Pouring: Why the old man couldn’t get up in the morning

Rules for Treating Migraine in Stroke Patients

Can chiropractic manipulation cause stroke?

Examining the Migraine-Stroke Relationship

What does “do not resuscitate” really mean?

A Normal Head CT Scan Does Not “Rule Out” Ischemic Stroke – Part II

A Normal Head CT Scan Does Not “Rule Out” Ischemic Stroke – Part I

A Tale of Two Carotid Artery Dissections, and the Miracle of the Circle of Willis

Deconstructing the “Mini-Stroke”

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