Tom Sorensen, a Charlotte-based sports columnist known for infusing wit into his writings on sports in the Carolinas, has returned to print after sustaining an intracerebral hemorrhage. He emerged back into print in The Charlotte Observer this week, opening up about his journey since tripping on a curb in September of this year.
His story is another example of why medical attention should be sought when something just does not seem right neurologically. It also may provide hope to those out there struggling to recover from a brain injury. Life can be good again.
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.
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.
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.
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:
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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