Just after New Year’s Day in 2013, I was asked by a local news station about a story in the mainstream media involving a “blood clot in the brain.” At-the-time Secretary of State Hillary Clinton had fallen and hit her head, and this was followed soon afterwards by a diagnosis of a blood clot “in the vein between the brain and…skull,” according to this news article. I recognized over the following week while the story played out in the news that, while Clinton’s clot was not the same thing as one might think of an ischemic stroke, there was little understanding outside of the medical community of how her neurological issue differed from the large majority of blood clots in the brain. I even received several questions about it from patients, the most common one being – did Hillary Clinton have a stroke? And my answer was – not exactly.
Ischemic strokes, as we think of them, involve an obstruction in an artery that is preventing oxygen-rich blood from reaching its target destination within the brain. Arteries can be blocked by blood clots, plaque accumulation within the wall of the vessel, a torn lining in the wall of the artery (dissection), or even overgrowth of cells within the blood vessel wall (hyperplasia). Veins, on the other hand, drain blood away from the brain and back to the heart once the oxygen has been extracted from it. Veins of significant size in the brain are called venous sinuses, as they are structured more like collecting pools for the drainage of blood that is no longer rich in oxygen. A clot that occurs in one of these venous sinuses are known as a cerebral venous sinusthrombosis (CVST). It is much less common to develop an obstruction blocking blood flow in one of the brain’s veins than it is within an artery. According to the scientific statement published by the American Heart Association/American Stroke Association in 2011, only 0.5 to 1 percent of strokes result from a blood clot in a cerebral vein.
People might be familiar with the concept of a venous clot, such as in a leg if one sits in a car or on an airplane for a prolonged period of time. However, venous clots can occur anywhere in the body, including in the brain.
Various factors may lead to increased risk of clotting in one of the venous sinuses or in a cerebral vein. It is important to understand that in all of us, our blood is in a constant state of flux. Just as the American government is set up with checks and balances such that the branches can more-or-less keep each other in check, our blood has millions of molecules pushing it towards clotting, and millions breaking down clots. We need to clot so we do not hemorrhage. Yet, our blood needs to be able to flow to our organs, and if it can’t because of extensive clotting then heart attacks, strokes, and other catastrophes develop.
There are certain genetic mutations that can cause blood to clot more readily, such as the factor V Leiden mutation or the prothrombin mutation. There are people who lack certain proteins that assist with breaking down clots, and in the absence of these proteins clots are more likely to develop. Deficiencies of protein C and protein S are two of the more common examples of this. Autoimmune disorders can increase the risk for clotting in general, such as can be seen with lupus and antiphospholipid antibody syndrome. The use of certain types of birth control pills can cause elevated risk of CVST, as can pregnancy, because elevated estrogen levels have been associated with thrombosis. Cancers and systemic infections/sepsis can cause massive hemorrhaging or diffuse clotting. Significant concussions or skull fractures can also result in CVST.
The most common initial symptoms of CVST are headache, visual changes, and/or seizure. A headache that continues to escalate for days to weeks, especially in a patient taking birth control pills, who is pregnant, or who has a history of abnormal clotting should undergo MRI of the brain. Standard MRIs are sensitive enough to detect most CVST, but if there is any question an MR-venogram or a CT-venogram of the head should be performed. If CVST is identified, the treatment is an anticlotting medication. Warfarin is the most common medication used for this, although rivaroxaban (Xarelto), apixaban (Eliquis), and dabigatran (Pradaxa) have been used more recently as off-label agents. In pregnant patients, enoxaparin (Lovenox) is typically used because it is thought to be safe (pregnancy Category B). Warfarin is known to cause birth defects (pregnancy Category X), and the effects of the other oral agents on fetal development is unknown at this time. Warfarin can be used safely in breastfeeding mothers once the baby is delivered.
Venous sinuses within the brain drain blood and send it back to the heart. Image source: http://www.dartmouth.edu/~humananatomy/
In my experience, patients with CVST do very well clinically once started on an anticlotting therapy, especially if the clot is identified early. Secretary Clinton’s treating physician claimed in this news article that she had a clot in the transverse sinus. The nice thing about transverse sinuses is that there are two of them, and when one is blocked due to the presence of clot, blood is usually still able to drain from the brain. Her physician also noted that she had a deep venous thrombosis (DVT) in the 1990s, suggesting she might be at risk for clots. If people are at particular risk for clot formation, being dehydrated does not help (Clinton was reported to have influenza during that time), as the blood becomes more concentrated. While he described the condition as “potentially life-threatening,” in the dozens of transverse sinus thromboses I have treated, none of these patients have died, and the recovery is very favorable. Even patients with very large superior sagittal sinus thromboses do very well typically if recognized early and started on therapy.
When making a determination about whether a patient has had a stroke if an artery is blocked, we require that some degree of damage has occurred in the brain before calling it a stroke. If there is no damage and the patient has no lingering symptoms in this scenario, then the diagnosis of a TIA, or transient ischemic attack, is made. In the case of CVST, if diagnosed and treated early and lacking any evidence of damage to the brain, it probably should not be labeled as a stroke either. While it may be convenient to throw all CVST cases in the “stroke” bucket, many of these patients will not sustain permanent brain injury, and will go on to lead productive lives without lingering evidence that such an event ever occurred. So did Secretary Clinton have a stroke? I stand by my answer of – not exactly.
Would I expect something like this in Secretary Clinton’s medical history to prevent her from carrying out the duties of the presidency if she is elected in November? No more than migraines would have stood in Michele Bachmann’s way in 2012, or than atrial fibrillation would have prevented Bill Bradley from performing presidential tasks. By the time adults reach their 50s or 60s, it is almost an inevitability that a health condition of some sort will be present. If we want candidates for president in near-perfect health, we could change our laws and elect a very young person as our commander-in-chief, but then we lose the presence of life experience.
The traditional teaching about the role of the cerebellum has typically been that it coordinates movements and “fine tunes” them. It provides balance when walking, and stability of a hand when reaching for a glass of water. When the cerebellum sustains an injury or is malfunctioning, then the result may be gait disturbance, falls, dizziness, or tremor.
The cerebellum is featured in red in this image. Image credit: http://www.brainhealthandpuzzles.com
The ideas above are what I learned in high school biology, in anatomy, and in physiology. Even throughout my neurology residency training, I largely thought of the cerebellum as a structure that provided balance and fine tuned movement.
It has interested me during my time in clinical practice to witness the fallout from cerebellar stroke, particularly in the younger stroke population, because it is often far beyond balance and movement. Yes, the symptoms mentioned above are often present in some form when the cerebellar stroke occurs, perhaps along with a headache and/or nausea. However, the patients who struggle with recovery for months or years following a cerebellar stroke often complain of symptoms that do not fit with the traditional concepts of what the cerebellum is supposed to be doing.
Some of the complaints I have heard from numerous cerebellar stroke patients are as follows:
– Many struggle with the same cognitive symptoms that patients with strokes injuring the frontal or parietal lobes experience, such as difficulty with focus and multitasking, and because of this, they complain of difficulty with short term memory retention.
– Other cognitive symptoms may exist as well, such as feeling overstimulated, or having difficulty following a conversation in a group of people.
– Difficulty with language fluency (aphasia) has afflicted cerebellar stroke patients in my own experience, and their frustration after being denied disability benefits is palpable.
– Some cerebellar stroke patients express that they are unable to dream any longer, or that when they close their eyes to picture a scene – being at the beach on a breezy day, or running through a field of grass and flowers – they are unable to mentally visualize such a thing.
– Sometimes their significant others claim these patients have demonstrated changes in their moods or personalities, and that their relationships seem different since their strokes.
MR images of Jonathan Keleher’s brain (A and B). The black diamond-shaped void in images A and B reveals Mr. Keleher’s missing cerebellum. The images on the right demonstrate the presence of a cerebellum in the space in a normally developed brain. Photo credit: Massachusetts General Hospital, courtesy of Jeremy Schmahmann for use on NPR.org
Last month, as I was driving home from work one evening, I heard this segment on National Public Radio’s All Things Considered, and I thought – yes! I have to share this on The Stroke Blog with readers! This piece summarizes the complexities of the cerebellum so well for the public, and I hope those of you who read this will take a few minutes to listen to the segment if cerebellar injury is of interest.
The piece features Jonathan Keleher, a 33 year old man who was born without a cerebellum. In the segment, it is explained that Mr. Keleher struggles with emotional complexity, language, and other cognitive tasks beyond imbalance and impaired motor skills. However, because he received intensive physical and speech therapy at a young age while lacking a diagnosis, he was able to demonstrate the wonder of neuronal plasticity – the ability to utilize other parts of the brain to accomplish tasks normally dependent on the cerebellum. He walks independently, and he works in an office environment. He lives independently.
We like to believe that each function is neatly packaged within a certain compartment of the brain. Patients often ask: “If my stroke was here [pointing to a specific part of the brain], then what problems should I expect to have?” While some structures in the brain correlate more or less with certain functions, it really is not that simple, as evidenced by the complexity of the cerebellum, and by what a young man who lacks one has been able to accomplish in its absence. The brain is a large community of cells, an interdependent network that makes us who we are, and which enables us to survive from one second to the next.
Update on November 14, 2017:
When I published the above blog post on cerebellar stroke in 2015, I never dreamed that it would become the most frequently visited page on The Stroke Blog day after day. The comments readers have posted in response to it, and the emails I have received from patients and their loved ones, have underscored the need for more resources about cerebellar stroke. I have heard you, and am working currently to create such a resource beyond a blog post. Stay tuned.
I have also received many emails from patients who have been diagnosed as having vertebral artery dissections believed to have caused their cerebellar strokes. Until recently, there was no largely comprehensive resource for patients struggling through the aftermath of vertebral dissection, but a few months ago, my speech language pathologist colleague, Amanda Anderson, and I published a book for vertebral and carotid artery dissection survivors (click here for more information) and their families in hopes that it would provide badly-needed answers to lingering questions. If you are a vertebral artery dissection survivor, I sincerely hope you find the book useful, and that it at least somewhat helps to validate your “new normal.”
Cerebellar stroke can be more difficult to accurately diagnose because the symptoms frequently don’t scream “Stroke!” the way that weakness on one side of the body or a facial droop may. I have seen cerebellar stroke patients in the acute setting diagnosed with migraine, benign forms of vertigo, intoxication, and substance abuse. When diagnosed early, situations leading to cerebellar stroke can be successfully treated with better outcomes for patients. Awareness of cerebellar stroke in both the community and amongst medical providers is critical for earlier diagnosis and more optimal management.
A reporter for WABC in New York City, Lisa Colagrossi, died over the weekend after an aneurysm in her brain ruptured. Colagrossi, 49, apparently experienced the very sudden onset of symptoms, and was maintained on life support in the neurological intensive care unit at New York-Presbyterian Weill Cornell Medical Center. Unfortunately, despite the care provided, she did not survive.
Layers of the meninges covering the surface of the brain. It is in the subarachnoid space that the major arteries of the brain are positioned, and a ruptured aneurysm results in bleeding along the surface of the brain. Ref: http://www.merckmanuals.com
What happens when an aneurysm ruptures? Where does the bleeding take place within the brain?
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.
Because the subarachnoid space covers the surfaces of the brain (not just the superficial surface adjacent to the skull, but the deeper surfaces positioned further from the skull as well), bleeding into this space tends to produce a characteristic pattern on a head CT scan that differs from bleeding that is confined the portions of the brain adjacent to the skull (click here for descriptions of other patterns of bleeding from a prior blog post). A head CT scan is a very useful tool in quickly evaluating a patient complaining of symptoms concerning for subarachnoid hemorrhage. The image to the right is a more severe example of this.
What are symptoms that are concerning for subarachnoid hemorrhage? Typically, I use the word “sudden” in describing what occurs. A sudden headache that goes from non-existent to “the worst headache of my life” within seconds, also known as a thunderclap headache, should be urgently evaluated as a subarachnoid hemorrhage (911 call, head CT scan, urgent work up) until it is proven to be otherwise. Sudden loss of consciousness can be consistent with this presentation. Sudden weakness or numbness on one side of the body, as might be seen in any type of stroke, can also reflect a subarachnoid hemorrhage in process. If a head CT scan is normal but the symptoms or history are still concerning for potential ruptured or “leaking” aneurysm, then a lumbar puncture is performed to evaluate for the presence of blood products (blood that is breaking down) in the patient’s spinal fluid. If concern persists, then a catheter cerebral angiogram, a test in which a catheter is threaded through the arteries, typically from the femoral artery in the groin, to image the arteries of the brain closely, may be performed.
A head CT scan from a patient with a ruptured left middle cerebral artery aneurysm. Blood appears white on this form of imaging. Blood is layering along the various inner surfaces of the brain.
What causes aneurysms to form in the arteries of the brain? There are certain situations where genetics play a role, but the majority of ruptured aneurysms and subarachnoid hemorrhages occur in families without a history of similar occurrences. Modifiable risk factors, or activities that place people at risk that can be changed through behavioral changes, include cigarette smoking and chronic alcohol use. Hypertension has also been shown to increase the risk of aneurysm development. Smoking seems to be the universal risk factor, doesn’t it? But yes, cigarette smoking has been demonstrated as increasing the risk for aneurysm formation in the brain in numerous studies at this point.
What should be done if an aneurysm that has not ruptured is found? One of the challenges in evaluating patients with cerebral aneurysms is knowing when to pursue treatment of an aneurysm in the brain, and when to monitor the aneurysm. A common scenario is that of the patient experiencing headaches that turn out to be part of a migraine syndrome, but the headaches lead to imaging of the arteries of the brain. Then, a small aneurysm is identified. Now what? Evaluating this patient population involves weighing benefit against risk. If an aneurysm is quietly present, not causing problems, and the risk of rupture is extremely low, then the risk of a procedure to “fix” the aneurysm is not justified. If an aneurysm is at higher risk of rupture and hemorrhage, then the risk of intervening is outweighed by the benefit in securing the aneurysm and preventing a catastrophic hemorrhage. There are many factors to consider when making a decision about whether to intervene on an aneurysm. The location (the artery affected by the aneurysm) is important, as is size, the patient’s age, and the patient’s medical history.
Unfortunately, Ms. Colagrossi’s passing is another example of how anyone can be affected by stroke, and that a person is never too young to face this diagnosis. If her family and friends come across this at some point, I offer them my sincerest condolences on their loss.
In honor of the holiday season, I wanted to share this article, profiling the Miracle Minstrels, a choral group in the Sacramento area comprised largely of stroke survivors with aphasia.
In the majority of people, language function is largely housed in the left hemisphere of the brain. A stroke or brain injury involving injury to these centers or pathways on the left side can result in language impairment. This is known as aphasia. Sometimes symptoms may be consistent with motor aphasia, also known as Broca’s aphasia, in which expressed language impairment exists while potentially sparing interpreted language (understanding what others are saying or retaining the ability to read written language). Sensory aphasia, also known as Wernicke’s aphasia, occurs when interpreted language is impaired, although the person may still speak fluently. However, the speech may not make sense to others. More commonly, there is at least some component of both aphasia types present, even if one aphasia type is more noticeable than the other.
The Miracle Minstrels, a singing group comprised mostly of stroke survivors with aphasia, performs at a holiday luncheon. Photo by Brian Baer, featured in The Sacramento Bee
A speech therapist in California, Renee Garner, and a stroke survivor, Barbara LaPlaca, started a choral group of aphasic brain injury survivors as a way to provide social engagement and to continue rehabilitation beyond speech therapy sessions. The brain’s musicality section, where musical familiarity, recognition, and production is generated, is housed in the right side of the brain. These creative individuals utilize music as a way of bypassing language impairment to allow patients to share their voices.
Among the countless ways the brain has amazed me during my time as a neurologist is witnessing the musicality that may be present in patients who are otherwise unable to speak. During my residency training, a hospitalized woman who remained completely silent for a week after a large left-brain stroke suddenly sprung to verbal life as a small group of us entered her room one morning, singing “Happy Birthday to You.” Overwhelmed by the familiarity of this tune (Do any of us actually remember the first time we heard this song?), she joined us for the fourth and final line. We then continued to sing the song a second time, not wanting the experience to cease, and she was able to vocalize some of the words as long as they were part of a song.
There is a memorable scene in Corrie ten Boom’s memoir, The Hiding Place, in which her mother, left severely aphasic after a stroke, suddenly starts to sing her favorite hymn when it is played at a wedding. Corrie sees this event as miraculous. Regardless of an individual’s religious beliefs, it is difficult not to experience awe and to marvel at the organization and processing capabilities within the human brain. It is fascinating.
My figurative hat is off to the Miracle Minstrels, for stepping outside of a comfort zone to perform in front of audiences after brain injuries have left them struggling with language, as well as to the founders for their clever idea and motivation to start such a group.
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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