Stroke in 2021

Clinical presentation, review of stroke pathophysiology, and the evidence-based updates on prehospital care from the American Stroke Association®

Educational Objectives

• Examine the history and evolution of stroke diagnosis and treatment.

• Discuss the pathophysiology behind stroke and compare with other medical conditions that mimic it.

• Examine the latest evidence-based guideline updates from the American Stroke Association 2019 update as it applies to the prehospital setting.

• Describe clinical features associated with stroke affecting either the left or right hemisphere.

• Consider prehospital assessment and communication techniques to optimize care of the post-stroke patient. • Explore modifiable factors to reduce the risk of stroke.

Introduction to Stroke

A cerebral vascular accident (CVA, or stroke) is the leading cause of serious, permanent disability in the United States.

In the US, someone is diagnosed with a stroke every 40 seconds, and sadly, a person dies from one every 4 minutes.1 EMS can decrease disability and death by recognizing stroke signs and symptoms, notifying the hospital with early activation, and providing appropriate treatment and care.

Page | 1

Table of Contents

Educational Objectives ...... 1 Introduction to Stroke ...... 1 Stroke: Just another modern-day disease? ...... 3 Jumping to the 17th century...... 3 19th century...... 4 20th century...... 4 21st century ...... 4 The impact of stroke in the United States ...... 5 Pathophysiology of stroke ...... 6 Ischemic stroke ...... 6 Hemorrhagic stroke ...... 7 The great imitators ...... 9 A few of the stroke mimics ...... 9 Updated EMS guidelines for the acute stroke victim ...... 12 Living a changed life after stroke ...... 17 Reviewing brain anatomy...... 17 Examples of hemisphere-affected stroke survivors ...... 19 Avoiding another stroke ...... 21 References ...... 23 Image credits ...... 24

Page | 2

Stroke: Just another modern-day disease?

troke is often thought as a modern-day disease caused by S obesity, genetic disposition, and stress, but it really has a long history dating before Cheetos™ and desk jobs. Stepping back thousands of years, strokes not only existed but were even recognized as a serious impairment of the vascular system by ancient healers.

During the neo-Sumerian period (2112 to 2004 BCE) in the Mesopotamia area of modern-day Iran, various healers documented the assessment, diagnosis, and their treatment recommendations for suspected stroke on clay tablets.2 They even differentiated stroke from temporary facial paralysis (Bell’s Palsy) based on signs, symptoms, and the patient’s time to recovery.2

During that time period, an āšipu was described as a practitioner who followed a philosophy of healing by warding away evil spirits that caused illness and death. They were the opposing profession to other ancient practitioners who embraced objective evidence and treatment, like today’s physicians. But even the more spiritual āšipu Tablet K.2418 contains 26 lines of Akkadian script recognized the signs of stroke and its prognosis. He knew that right- about the medical treatment of stroke. From the sided paralysis with aphasia carries a gloomier outcome compared to library of Ashurbanipal II at Kouyunjik in modern- left-sided paralysis in the stroke patient. day Mosul Governorate, Iraq. Neo-Assyrian period, 7th century BCE. Image: Karim 2018. The āšipu’s recognition of paralysis caused by a mild stroke or transient ischemic attack (TIA) was discovered in a translation of one mof their early writings:2

“If he has a stroke and either his left side or his right side is affected and his shoulder is not released, but he can straighten out his fingers and he can lift his hand and stretch it out and he is not of food or drink-affliction by a ghost of the steppe. Recovery in three days.”

The ancient healers also predicted whether the patient was likely to die from stroke after evaluation of the patient’s consciousness, areas affected by paralysis, and responsiveness to stimuli.2

Jumping to the 17th century: The cause and pathophysiology of stroke was not well defined until just a few hundred years ago. Swiss physician Johan Jakob Wepfer (1620–1695) was one of the first physicians specializing in vascular anatomy to observe that the paralysis associated with stroke was caused by cerebral hemorrhage.

Page | 3

19th century: Later in the early 19th century, Scottish physician John Abercrombie reported a link between arterial occlusive disease and areas of cerebral softening from infarctions (dead brain tissue).2,3 The pathophysiology behind strokes was now gaining more interest both for the hemorrhagic and ischemic forms.

20th century: During the 1960s, transient ischemic attacks (TIAs) were defined as sudden, focal neurological deficits caused by a vascular problem that lasted less than 24 hours. However, there was no basis for the 24-hour cutoff --- it appeared to be just an arbitrarily-assigned endpoint.3 In other words, just pulled out of the air.

The definition then continued where if the signs and symptoms of the TIA persisted beyond seven days, the patient was diagnosed with a stroke.3 Neurological events that lasted between 24 hours and the seven day stroke threshold were classified as a “reversible ischaemic neurological deficit” – a term that’s now obsolete.3 Image: Scottish physician John Abercrombie (October 10, 1780 – November 14, 1844) During this time, a TIA was also considered as a condition with little to no brain injury. Although a full recovery is expected after a TIA, it wasn’t until years later that physicians understood the actual damage experienced during the event. Some brain injury does occur during a TIA with the decreased blood perfusion and symptoms.4 However, the damage may not be extensive enough to produce obvious physical or cognitive disability post-recovery.

21st century: In 2009, the American Heart Association/American Stroke Association™ revised its definition of a TIA to recognize both the injury pattern associated with the condition and to de- emphasize the 24-hour time constraint. A TIA is now defined as, “a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction”.5

This definition suggests that a TIA occurs when the patient has signs and symptoms associated with a stroke that do resolve, but brain imaging finds nothing significant enough to support a stroke diagnosis. Conversely, if an infarction did develop in the patient’s brain and was found with imaging (CT scan or MRI), the patient would then be diagnosed with a stroke.

Page | 4

The impact of stroke in the United States

In short, a stroke refers to damage of the brain caused by a disruption of the cerebral blood supply. This can either be from a clot (thrombus or emboli) blocking an arterial vessel or hemorrhage. In the United States, a stroke is more than just permanent paralysis or weakness --- It’s the 5th leading cause of death.1

1 Stroke Facts

Approximately 795,000 people suffer a new or recurrent stroke annually --- Every 40 seconds, one American has a stroke.

In the United States, there is one death every 4 minutes from stroke.

Nearly 25% of strokes are recurrent ones, where the patient already has a history of stroke and it develops again.

87% of strokes are ischemic, which are usually caused by a clot.

Stroke is a leading cause of serious long-term disability.

Stroke reduces mobility in more than half of stroke survivors age 65 and over.

Risk of having a first stroke is nearly twice as high for blacks as for whites, and blacks have the highest rate of death due to stroke.

In 2009, 34% of people hospitalized for stroke were less than 65 years old.

Page | 5

Pathophysiology of stroke

A stroke occurs when there is a disruption of the cerebral blood supply to one or more areas of the brain. A vessel can be obstructed by a clot that prevents oxygenated blood from reaching areas distal to it. Or, a vessel can tear and bleed into the cranial cavity. Blood is a non-compressible liquid, so it pushes directly over areas of the brain and prevents circulation underneath it. Brain tissue dies when it does not receive a constant supply of oxygenated blood, whether by a roadblock (clot) or direct pressure (hemorrhage).

Ischemic stroke: The most common type of stroke is ischemic, where a thrombus or embolus blocks an arterial vessel and prevents blood from reaching distal brain tissue. More than four out of five strokes are ischemic.1

A thrombus is a clot that develops along a plaque-lined vessel wall. The thrombus formed from a plug of aggregated platelets and red blood cells bound with cross-linked fibrin protein. A thrombus is stationary and narrows an artery, reducing blood flow.

An embolus is anything that is flowing through the bloodstream and can eventually occlude a vessel. For example, a gas embolus forms when an IV line is not primed with fluid and air enters into the vein. Solid emboli include pieces of fat, bone marrow, or even pieces of sheared medical devices, such as an IV catheter tip.

Page | 6

If part of a vessel’s thrombus breaks away, this now becomes an embolus. When it occludes a vessel, it’s then called a thromboembolism.

Material: Description:

Thrombus A stationary clot that forms and stays on the vessel wall.

Embolus A free-flowing solid piece or air bubble that travels through a vessel.

A thrombus that breaks away from a vessel wall, becomes an embolus, and Thromboembolism then lodges and occludes a vessel.

Hemorrhagic stroke: Hemorrhagic strokes make up about 13 percent of stroke cases.6 They are usually caused by a ruptured or torn cranial vessel, usually at the site of a cerebral aneurysm. During a hemorrhagic stroke, blood accumulates and compresses the surrounding brain tissue, causing ischemia and eventually death of that tissue if not addressed appropriately.

The two most common types of hemorrhagic strokes are intracranial (within the brain, including intracerebral) hemorrhage or subarachnoid (below the bony skull) hemorrhage. Other brain hemorrhages include subdural hematomas and epidural hematomas, but these are usually traumatic in nature and not caused by a weakened cranial vessel within the brain.

An intracranial hemorrhage is further subdivided into two primary mechanisms: Bleeding within the brain tissue itself (intraparenchymal hemorrhage) or the ventricles (intraventricular hemorrhage). The brain's ventricular system is where cerebrospinal fluid (CSF) is produced and circulated to the subarachnoid space and spinal cord.

Subarachnoid hemorrhage (SAH) is not from a torn artery within the brain tissue but instead, occurs in the space between the arachnoid membrane and pia mater that follows over the brain’s surface. Page | 7

Cutaways of the Brain and Areas of Hemorrhage

Image: Layers of the scalp. A subarachnoid hemorrhage develops between the arachnoid membrane and the pia mater, which surrounds the brain and follows along the surface of the folds.

Image: Cutaway of the brain showing different types of hemorrhages. Intraparenchymal and intraventricular hemorrhages are intracranial in nature, while a subarachnoid hemorrhage occurs near the brain surface and can bleed into the sulci (the brain fold’s valleys). These all represent hemorrhagic strokes. Epidural and subdural hematomas are usually associated with a traumatic head injury. Page | 8

About 80% of patients with subarachnoid hemorrhage caused by a ruptured aneurysm report a sudden onset of what they describe as the worst headache of their life.7 A previous sentinel headache two to eight weeks before aneurysmal rupture is a critical historical finding present in up to 40% of these patients.7

Usually, the patient with a subarachnoid hemorrhage reports a severe headache, vomiting, photophobia, seizures, neck stiffness, and/or presents with decreased level of consciousness. Because the bleeding occurs outside of the brain itself, persons with SAH may NOT always have focal neurologic signs such as arm weakness/drift or facial droop as you would normally expect for a person with a stroke.7

The great imitators

Several conditions mimic a stroke, but making a field diagnosis of stoke versus Bell’s Palsy versus electrolyte derangement should be avoided. The diagnosis of stroke still falls on imaging the head (non- contrast CT, MRI, CTA, etc.), serial assessment, labs, and other tests in the emergency center.

These mimics may be activated as a stroke by EMS and that’s okay. It’s safer to activate when sitting on the fence versus missing a stroke altogether. In several studies, nearly one-third of the patients presenting to the emergency center were later found to have a stroke mimic after the diagnostic tests were completed.8,9 However, this also means that over two-thirds of the patients presenting with stroke-like signs and symptoms were really experiencing a stroke. Since time to intervention is so important with stroke, err on the side of caution and activate if the patient meets stroke criteria.

A few of the stroke mimics

Seizures. Seizures can be a stroke mimic. In some cases, a stroke causes the seizure. After a patient experiences a seizure, they may have focal deficits such as weakness, difficulty with forming words, and confusion. Todd's paralysis is one of the most common presentations in the postictal that has signs and symptoms of a stroke.10

Todd's paralysis is a neurological condition where a seizure is followed by a brief period of temporary paralysis. The paralysis may be partial or complete but usually occurs on just one side of the body; it can include speech and visual affect as well. The paralysis can last from just half an hour up to 36 hours after Page | 9 the seizure, averaging about 15 hours. Once it resolves, the paralysis and other deficits are gone. This is a true neurological condition that usually affects those with epilepsy.

Migraine headaches. A migraine headache may precede a stroke in some cases or instead, simply feel painful enough to suggest a hemorrhagic stroke. Not all migraine suffers have the pre-headache aura, nausea, and sensitivity to light/sound --- they may have only one of these symptoms and even these can be associated with an actual stroke. While the debate is still out on what really causes a migraine headache at the tissue level, a recent hypothesis is that it involves a disorder of brain sensory processing (overwhelmed by input) and may also be influenced by genetics and the patient’s environment.11

Hypoglycemia or hyperglycemia. Focal neurological deficits such as facial droop, unilateral weakness, and confusion may be found in patients with hypoglycemia, which is why obtaining a blood glucose measurement regardless of diabetes history is found in nearly every EMS protocol. Stroke-like signs can be seen in up to 2% of patients with hypoglycemia.10 These signs and symptoms may be caused by cerebral vasospasms that lead to poor blood flow within certain areas of the brain.10,12

A person with severe hyperglycemia can develop a seizure, report blurred vision, have speech deficits, weakness, and other signs and symptoms.

Sepsis. Sepsis is a systemic infection that can be fatal if not treated appropriately. During severe sepsis, the patient may or may not have a fever but will be found with a decreased level of consciousness. History, event information from family, a good physical assessment, and vital signs are going to help determine if sepsis may be the cause of the signs you’re seeing with this patient.

Hypoxemia. Altered mental status, weakness, loss of balance/gait abnormalities, nausea, and other signs and symptoms are common with decreased oxygenation. It doesn’t have to be from an obvious illness. For example, carbon monoxide released from poorly- running gas heaters or car exhaust in a closed area will bind to the blood’s hemoglobin sites normally used by oxygen. On pulse oximetry, the wavelengths look the same whether its looking at hemoglobin saturated by carbon monoxide or oxygen, so a hypoxic person in this environment will show a

great SpO2. But, the nausea, headache, altered mental status, weakness, and other signs suggest the brain and body are not getting enough oxygen to function.

Page | 10

Tumors. A tumor growing within the brain may eventually occupy enough space to compress cerebral vessels. The onset of symptoms is usually slower compared to a stroke (over weeks), but this progressive onset of symptoms can also occur with a subdural hematoma from a head injury.

Dizziness, vertigo, and gait abnormalities. Sudden-onset dizziness and vertigo are a common stroke mimic. While dizziness or vertigo by itself may be a stroke mimic, a sober person reporting trouble with maintaining his or her balance now suggests an actual stroke that may be affecting vessels in the superior cerebellar artery distribution.10 This vessel injury is usually found in those patients who are older, have a history of hypertension, and have at least two stroke risk factors.10

Spinal cord injury or infection. Spinal cord lesions from trauma or central nervous system (CNS) infection can cause unilateral weakness and other signs of stroke. For example, meningitis is usually associated with a severe headache, neck stiffness, vomiting, and confusion and can be confused with a hemorrhagic stroke if afebrile. In one study, 18% of elderly patients with altered mental status diagnosed with meningitis (via lumbar puncture) did not have a fever.13

“Labs are off”. Sodium, potassium, calcium, and other ions interact with the membrane and alterations in their concentration can cause stroke-like symptoms in certain cases. Medications, illness, toxins, renal problems, and other factors can cause a person’s ion balance to be off and affect everything from mental status to skeletal muscle use.

Bell’s Palsy. Bell’s Palsy (idiopathic facial palsy) is a classic example of a well-known stroke mimic where the patient's facial nerve (cranial nerve VII) becomes temporarily paralyzed. Cranial nerve VII becomes inflamed and swells where it exits the skull at the stylomastoid foramen, a narrow canal near the ear. The nerve cells distal to it do not receive transmission, resulting in facial paralysis on that side. This swelling may be caused by latent viral infection, trauma, stress, or other factors.

Cranial nerve VII controls the muscles on one side of the face, including eye blinking, closing, and facial expressions such as smiling. In most cases, there’s no permanent effect from this paralysis and it usually resolves after several months.

Page | 11

Updated EMS guidelines for the acute stroke victim

The American Stroke Association (ASA) updated their guidelines for early management of stroke patients in 2019.14 A few of the updated, reworded, or new guidelines that pertain to EMS are listed in the table below. Details about specific guidelines and how they impact EMS care follow the table.

ID American Stroke Association Guideline 14 COR: Class of (Has no bearing on Recommendation importance of the (verbatim - as printed) ASA guideline) by the ASA

EMS personnel should provide prehospital notification to the receiving A hospital that a suspected stroke patient is enroute so that the Strong (I) appropriate hospital resources may be mobilized before patient arrival.

Patients with a positive stroke screen or who are strongly suspected to B have a stroke should be transported rapidly to the closest healthcare Strong (I) facilities that are able to administer IV alteplase.

When several IV alteplase–capable hospital options exist within a New defined geographic region, the benefit of bypassing the closest to bring C the patient to one that offers a higher level of stroke care, including Should be mechanical thrombectomy, is uncertain. considered (IIb)

Effective prehospital procedures to identify patients who are ineligible for IV thrombolysis and have a strong probability of large vessel New D occlusion (LVO) stroke should be developed to facilitate rapid transport Should be of patients potentially eligible for thrombectomy to the closest considered (IIb) healthcare facilities that are able to perform mechanical thrombectomy.

All patients with suspected acute stroke should receive emergency brain E imaging evaluation on first arrival to a hospital before initiating any Strong (I) specific therapy to treat AIS. (AIS = acute ischemic stroke)

Systems should be established so that brain imaging studies can be New F performed as quickly as possible in patients who may be candidates for IV fibrinolysis or mechanical thrombectomy or both. Strong (I)

Supplemental oxygen should be provided to maintain oxygen saturation Strong (I) G greater than 94%.

Hypoglycemia (blood glucose less than 60 mg/dL) should be treated in Strong (I) H patients with AIS.

Page | 12

Early prehospital notification. Time is brain. A stroke kills some cells regardless of what A we do in the prehospital setting, but our primary purpose is to minimize cellular death surrounding the infarcted area. This region of reversible injury is called a penumbra, and it surrounds the core of dead brain tissue. The sooner the penumbra sees oxygenated blood, the less permanent brain injury that should occur.

From the ASA guidelines: In the AHA “Get With The Guidelines” (GWTG) registry, EMS personnel provided prearrival notification to the destination ED for 67% of transported stroke patients. EMS prenotification was associated with increased likelihood of alteplase treatment within 3 hours (82.8% versus 79.2%), shorter door-to-imaging times (26 minutes versus 31 minutes), shorter DTN times (78 minutes versus 80 minutes), and shorter symptom onset-to-needle times (141 minutes versus 145 minutes).

Appropriate destination. The American Stroke Association places a strong B recommendation on expedient transport of the suspected stroke patient to a hospital that can administer IV alteplase. Alteplase (Activase®) is an intravenous (IV) “clot buster” (anti- thrombolytic) used for stroke, pulmonary embolism, myocardial infarction, and even clogged catheters.

Alteplase binds to fibrin, which is a key component in a blood clot. Through a series of steps, alteplase enables the enzyme plasmin to break down fibrin and dissolve the clot. Computerized tomography (CT) needs to be available to image the patient’s head and confirm the stroke is not caused by an intracranial bleed first. Giving alteplase to a person with a bleed will adversely affect the normal clotting process. When used in the right patient (ischemic stroke with no sign of intracranial bleed) and within a specific treatment window (within 4.5 hours of last known well when there were no stroke symptoms), alteplase can provide rapid, safe reperfusion of brain tissue and return of function.

Why doesn’t every hospital offer alteplase? Alteplase is expensive and may be difficult for smaller hospitals to keep in stock. In 2014, the base cost of an expected dose of alteplase (100 mg vial) was over $6100. This is what the hospital paid to buy the medication and reflects an 111% increase in their cost from just 10 years prior. However, reimbursement by insurance carriers (Centers for Medicare and Medicaid Services [CMS]) only increased by 8% during this time, leaving the hospital with a 102% difference to cover on their own.15

Page | 13

To add insult to injury, CMS’ patient care reimbursement for this treatment also dropped from $8306 to $5911 per case.15 Besides the cost of the drug, some smaller hospitals may not have CT available or if they have a machine, it could be offline for repair. This is another reason why early notification is needed in case EMS needs to be diverted.

Time to needle is important. This guideline suggests that it may be better to transport the C patient to the closest hospital with IV alteplase capabilities versus a comprehensive stroke center offering higher level interventions, such as mechanical thrombectomy (physical clot removal for large vessel occlusions).

While the American Stroke Association gives this guideline a weak “should be considered” strength of recommendation based on evidence, it does suggest that starting alteplase in eligible patients sooner is more important than spending more time in an ambulance heading to a higher level of care. This includes patients with a suspected large vessel occlusion (LVO) who would benefit from mechanical thrombectomy. These patients usually start with IV alteplase therapy first if they meet criteria anyway.

While distance isn’t an issue in Lubbock with the two major hospitals only a mile apart from each other, this does impact other EMS services that have a local hospital with alteplase capabilities. In their case, transporting the patient to the local hospital to start therapy could be better than bypassing for a primary stroke center in a larger city.

Door to Needle Time

Shortening the time from stroke onset to start of IV alteplase (“needle”) first starts with community education on recognizing the signs of stroke and calling 9-1-1.

When EMS arrives, their role is to assess the patient quickly for stroke, minimize scene time, and perform necessary diagnostics to support that field impression. Blood glucose measurement, ECG, blood draw, and early hospital notification expedites the patient’s care at the hospital.

The current standard is emergency center door-to- needle time of 60 minutes or less for at least 75% of ischemic stroke patients and in less than 45 minutes for 50% or more of ischemic stroke patients. Getting as much done in the ambulance as possible helps meet this goal and ultimately, the patient.

Page | 14

The VAN, LAMS, FAST-ED, CSTAT, MEND, ROSIER and other large vessel occlusion (LVO) stroke D scales are still new assessment tools for EMS. There is no 100% accurate LVO scale that is quick and easy to use in the prehospital setting, so the American Stroke Association has not designated a preference of one over another, even in this guideline update. As described by the ASA below, none of the current LVO scales have both a high sensitivity AND high specificity. The one we currently use (VAN Scale) has a very high sensitivity at detecting those with an LVO, but it has a lower specificity (ruling out those who don’t, or your “false positives”). Sensitivity: The test’s ability to determine if the person From the ASA guidelines: At least 6 stroke severity scales does have an LVO. The higher targeted at recognition of LVO in the prehospital setting to the sensitivity, the greater the facilitate transfer to endovascular centers have been published. odds that the test will result as The 2018 AHA systematic review on the accuracy of prediction positive for those with an LVO. instruments for diagnosing LVO in patients with suspected stroke concluded that “No scale predicted LVO with both high sensitivity Specificity: The test’s ability and high specificity.” Specifically, the probability of LVO with a to correctly identify those who positive LVO prediction test was thought to be only 50% to 60%, do not have an LVO. A high whereas >10% of those with a negative test may have an LVO. specificity means that a Thus, more effective tools are needed to identify suspected negative test is more accurate stroke patients with a strong probability of LVO. at suggesting the person does not have an LVO. This helps In EMS though, it may be better to have an LVO scale that reduce “false positives” where includes more “false positives”, where the scale suggests there’s a test indicates the person has an occlusion of a large vessel where later it’s found to not be the an LVO, but really does not. case. This reduces the rate of “false negatives”, where we miss patients who really have an LVO but the scale says they don’t. Missing an LVO stroke is far more disastrous than being too cautious and over-triaging patients.

All patients with suspected acute stroke should receive E emergency brain imaging upon hospital arrival before starting alteplase therapy. This is a safety measure to make sure that the patient does not have an intracranial bleed instead of a clot. A non-contrast CT scan or MRI can show “head bleeds” clearly, with the CT imaging being the fastest way to do so and the most popular option.

If alteplase is given to someone with active bleeding (head or any other organ), it can inhibit the clotting components needed to repair injured vessels.

Page | 15

In the update, a new recommendation was put into writing that should already be in place: F “Systems should be established so that brain imaging studies can be performed as quickly as possible in patients who may be candidates for IV fibrinolysis or mechanical thrombectomy or both”. Not all hospitals were understanding the importance of early, rapid imaging for stroke care, and this guideline made this need clear. The ASA supported this guideline with the following:

From the ASA guidelines: The benefit of IV alteplase is time dependent, with earlier treatment within the therapeutic window leading to bigger proportional benefits. A brain imaging study to exclude ICH is recommended as part of the initial evaluation of patients who are potentially eligible for these therapies.

And…

Reducing the time interval from ED presentation to initial brain imaging can help to reduce the time to treatment initiation. Studies have shown that median or mean door-to-imaging times of ≤20 minutes can be achieved in a variety of different hospital settings.

While this is not something we can directly affect in EMS, we can be aware of the expectations in emergency center care, notify the hospital early while on scene, and advocate optimal care for our suspected stroke patients.

A strong recommendation made by the ASA is: “Supplemental oxygen should be provided to G maintain oxygen saturation greater than 94%”. The guidelines add that there appears to be no functional benefit from oxygen administration to those whose pulse oximetry is greater than 94%. But, the study cited by the ASA involving over 8000 patients did not document significant harm. Considering the short duration of time EMS has with the patient and not knowing if the stroke is from an ischemic or hemorrhagic cause, oxygen therapy should be administered early as indicated in protocol.

One of the more common stroke mimics is hypoglycemia. This is not a new ASA guideline, but H one worth repeating.

A blood glucose measurement is expected with anyone presenting with acute altered mental status, weakness, or other symptoms that could also suggest a stroke. This measurement needs to be obtained regardless of the patient’s diabetic history; Diabetes doesn’t always start in childhood. There could be other causes for hypoglycemia as well, including certain medications, alcohol consumption, and onset of liver or kidney disease.

Page | 16

Living a changed life after stroke

The impact of a stroke extends beyond hospitalization. At home, the patient and family need to learn new ways to communicate, improve mobility, and improve home safety; this doesn’t happen overnight. Depending on where the infarct was located, the patient may be able to communicate well but have mobility issues. Or conversely, he can walk and navigate his surroundings well, but can’t put words to his thoughts. A stroke involves much more than just a weak arm; it usually has effect on language, memory, comprehension, and/or spatial orientation, all tied to the physical location and extent of the brain injury.

The brain will work towards learning ways to accomplish everyday tasks and in some cases, could be very successful at recovering a lot of functionality lost from stroke. This could take years though, if ever.

Reviewing brain anatomy. The brain is divided into two separate parts: The left hemisphere and the right hemisphere. The dividing valley is called the longitudinal fissure. At the bottom of this fissure is a core of tough neural tissue referred to as the corpus callosum. The corpus callosum is the communication link between the two hemispheres. If severed (intentionally or by genetic design), the left brain literally doesn’t know what the right brain is doing, and vice versa.

Different views of the brain to illustrate the location of the corpus callosum and longitudinal fissure. Image modified from Blausen (2014)

Page | 17

Knowing which hemisphere was affected by a stroke helps EMS both in the care of the acute stroke patient and when they respond to him or her again weeks or years later. There are ways to assess and effectively communicate with the stroke patient to minimize their apprehension, anxiety, and improves their level of trust in you. In the end, this makes for a far easier response to manage with a lot less stress on both the patient and the EMS crew.

In general, the left hemisphere is associated with expressive language (talking), understanding what others are saying (receptive language), and memory formation. Injury to this side of the brain can also affect the right visual field and the right side of the body (right arm/right leg weakness or paralysis).

The right hemisphere is usually associated with emotion, cognition/thinking, spatial-perceptual ability (sense of body position or even sensing that the body part belongs to them), left visual field, and left side of the body. This is usually a more difficult stroke to detect since the patient is still communicating with you, but may be showing poor judgement, a short attention span, and short-term memory loss. Now consider someone who is not experiencing a stroke but instead has hypoglycemia, abused alcohol, recent recreational drug use, is in pain, or even has a history of dementia --- similar signs in most cases.

These left brain/right brain associations are not set in stone since everyone is an individual and stroke damage is individualized as well, but for the most part, this represents the majority.

Page | 18

Examples of hemisphere-affected stroke survivors

A couple of scenarios are described below that represent stroke survivors at home --- one with a left hemisphere injury and the other with a stroke that injured the right hemisphere of his brain. Both examples represent patients who experienced a larger stroke area. However, you may find one or more of these same signs in stroke patients with a smaller infarct area.

Left hemisphere injury. Your patient is sitting in a chair and you notice a small bowl of applesauce sitting on a table to his left side. His wife was helping him eat before 9-1-1 was called for his complaint of left shoulder pain.

You introduce yourself by name and he nods his head repeatedly; you’re not sure if he’s acknowledging you or just “going through the motions”. He watches you closely and moves his left hand carefully to his lap. He doesn’t seem to understand many of the questions you ask and only follows a few simple commands. When he does answer, you can see that he’s forming words with some effort, his speech is a bit slurred, but he is otherwise pleasant to converse with. However, he’s already forgotten why you’re here and can’t even recall your name. But he does smile at you.

Your partner moves his applesauce away to his right side, and the patient appears immediately concerned that his lunch has disappeared. His wife steps in and gently places her hand on his left cheek and using quiet, slow words encourages him to look to the right --- he then sees that a bowl of applesauce is sitting there for him.

Right hemisphere injury. Your patient is sitting in a chair and rambles about the injustices of the world, and when he sees you and your partner approach, he becomes irritated but won’t explain why. He appears to understand everything you tell him, but he feels you are “out to get him” and tells you that he will “call the President of the United States” himself to have you removed from his home.

He starts to stand up and immediately stumbles into the table with his left side. He doesn’t seem to care about the skin tear that just ripped into his left arm and instead, grumbles about the table not moving out of his away. Your partner calmly asks him to sit down but he snaps, “I am sitting!”.

His wife quietly adds that he sometimes gets impatient and steps over to his right side to talk with him. She’s able to calm him down and tells him he did hurt his left arm, but he continues to deny the injury and says that he’s fine.

Page | 19

COMPARING LEFT AND RIGHT-SIDES STROKES (IN GENERAL)

Damage to the LEFT Hemisphere Damage to the RIGHT Hemisphere

Paralysis or weakness to right side of body Paralysis or weakness to left side of body

Right visual field deficit. Left visual field deficit

Language: Expressive, receptive, or global aphasia Impulsive behavior and poor judgment

Slow, cautious behavior Easily distracted; Time is distorted

Difficulties with memory Spatial-perceptual deficits

Chewing or swallowing problems Lack of deficit awareness – “everything’s fine”

Visual field deficit: The individual may not be able to see on that side of his body unless he makes a conscious effort to look in that direction. If the patient has this deficit, try to keep items within the “good side” so he can see what you’re doing. If not possible, keep him updated to what you’re doing on the affected side.

Language: For some individuals who suffered a left hemisphere stroke, they may have trouble speaking (expressive aphasia), understanding what others are telling him (receptive aphasia), or global aphasia (both). It can also affect their ability to write and understand what’s written. If your patient has any of these deficits, communication is obviously going to be difficult. Don’t raise your voice, get louder, or become impatient; Keep communication simple but don’t degrade the patient’s level of intelligence. Enlist the help of family while still keeping the patient actively informed and involved in his care.

Spatial-perceptual deficits: This is more commonly found with right hemisphere brain injury. The individual has a difficult time understanding exactly where the boundaries are surrounding his body. For example, he doesn’t instinctively know where the end of his hand is in relation to himself. It’s a lot like not understanding there’s a boundary of skin and air, particularly on the side weakened by the stroke. Oftentimes, they can’t comprehend that the arm or leg affected by the stroke still belongs to them and is attached. These individuals tend to be less cautious on that side of the body and will cause unintentional harm to themselves by running into objects on that side.

Page | 20

Spatial awareness deficits can also be applied towards objects. The person may not be able to accurately determine where a coffee cup is in relation to the space around him, so objects are frequently knocked over or dropped. Tripping over a rug, misjudging the height of stairs, and even missing the edge of a chair when sitting down are frequent problems associated with this deficit.

Time distortion. Particularly with right hemisphere injury, the person may not comprehend how fast or slowly time is moving. For example, he may have just finished lunch and half an hour later, feels it’s nearly time for supper even though he’s not hungry. This deficit can complicate other conditions associated with right hemisphere brain injury, leaving the individual impatient and frustrated when things are not going as expected per his sense of time.

Depression. Depression is real and common for those who suffered a stroke and affects about one- third of stroke patients in the US.16 Stroke survivors have lost functionality or cognitive ability that may take years to regain, if ever at all. They are not the same person they were before the stroke and are aware of that fact. Self-control is lost; they are now dependent on others for rehabilitation and activities of daily living. Then there’s the financial impact of stroke treatment and post-stroke care that affects the entire family.

Avoiding another stroke

Once a person has a stroke or a TIA, they remain at risk for another one. While genetic tendencies towards a stroke can’t be changed, behavior modification combined with pharmaceutical interventions can help reduce the risk for another stroke. Some of the most important treatable risk factors for stroke include:

• Control high blood pressure (hypertension). Hypertension is a known contributor towards hemorrhagic stroke and plays a role in ischemic stroke as well.

• Stop smoking. Smoking greatly increases the risk of plaque buildup in vessels, hypertension, and increases the clotting potential in blood.

• Exercise regularly and maintain weight. Obesity and inactivity are associated with hypertension, diabetes, and heart disease. Being overweight greatly increases the risk of ischemic stroke.

• Lower cholesterol levels. High cholesterol can lead to a buildup of fatty substances (atherosclerosis) in blood vessels, reducing the vessel diameter and ultimately, the volume of blood and oxygen delivered to the brain.

Page | 21

• Stay on prescribed medications if diagnosed with hypertension, high cholesterol, or abnormal cardiac rhythms such as atrial fibrillation. Daily low-dose aspirin may also be prescribed by the patient’s physician to reduce the risk of clot formation.

• Manage diabetes. Inflammation from poorly-controlled diabetes can cause destructive changes in blood vessels throughout the body, including the brain.

Be sure to complete the CE course and contact a member of the training staff with any questions.

Page | 22

References

1 Stroke Facts. Centers for Disease Control and Prevention. Reviewed September 8, 2020. Available at: https://www.cdc.gov/stroke/facts.htm. Accessed on November 29, 2020.

2 Karim SK, Amin OSM. Stroke in Ancient Mesopotamia. Med Arch. 2018 Dec;72(6):449-452. doi: 10.5455/medarh.2018.72.449-452.

3 Coupland AP, Thapar A, Qureshi MI, et al. The definition of stroke. J R Soc Med. 2017 Jan;110(1):9-12. doi: 10.1177/0141076816680121.

4 Albers GW, Caplan LR, Easton JD, TIA Working Group. Transient ischemic attack--proposal for a new definition. N Engl J Med. 2002 Nov 21;347(21):1713-6. doi: 10.1056/NEJMsb020987.

5 Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. Stroke 2009; 40:2276–2293.

6 Hemorrhagic Stroke (Bleeds). American Stroke Association. Available at: https://www.stroke.org/en/about-stroke/types-of-stroke/hemorrhagic-strokes-bleeds. Accessed on December 19, 2020.

7 Yew KS, Cheng EM. Diagnosis of acute stroke. Am Fam Physician. 2015 Apr 15;91(8):528-36.

8 Merino JG, Luby M, Benson RT, et al. Predictors of acute stroke mimics in 8187 patients referred to a stroke service. J Stroke Cerebrovasc Dis. 2013 Nov;22(8):e397-403. doi: 10.1016/j.jstrokecerebrovasdis.2013.04.018.

9 Hand PJ, Kwan J, Lindley RI, et al. Distinguishing between stroke and mimic at the bedside: The brain attack study. Stroke. 2006 Mar; 37(3):769–75.

10 Ray S, Chakravarty K, Kathuria H, et al. Errors in the Diagnosis of Stroke-Tales of Common Stroke Mimics and Strokes in Hiding. Ann Indian Acad Neurol. 2019 Oct-Dec;22(4):477-481. doi: 10.4103/aian.AIAN_80_19.

11 Goadsby PJ, Holland PR, Martins-Oliveira M, et al. Pathophysiology of Migraine: A Disorder of Sensory Processing. Physiol Rev. 2017 Apr;97(2):553-622. doi: 10.1152/physrev.00034.2015.

12 Kukaj V, Jashari F, Boshnjaku D, et al. Hypoglycemia-induced hemiparesis in a diabetic woman after childbirth. Case Rep Neurol Med. 2015;2015:210613. doi: 10.1155/2015/210613. Epub 2015 Apr 23. PMID: 25984373; PMCID: PMC4423000.

13 Shah K, Richard K, Edlow JA. Utility of lumbar puncture in the afebrile vs. febrile elderly patient with altered mental status: a pilot study. J Emerg Med. 2007 Jan;32(1):15-8. doi: 10.1016/j.jemermed.2006.05.032.

Page | 23

14 Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec;50(12):e344-e418. doi: 10.1161/STR.0000000000000211.

15 Kleindorfer D, Broderick J, Demaerschalk B, et al. Cost of Alteplase Has More Than Doubled Over the Past Decade. Stroke. 2017 Jul;48(7):2000-2002. doi: 10.1161/STROKEAHA.116.015822. Epub 2017 May 23. PMID: 28536176.

16 Robinson RG, Jorge RE. Post-Stroke Depression: A Review. Am J Psychiatry. 2016 Mar 1;173(3):221-31. doi: 10.1176/appi.ajp.2015.15030363.

Image credits

Alam D. Rehabilitation of long-standing facial nerve paralysis with percutaneous suture-based slings. Arch Facial Plast Surg. 2007 May-Jun;9(3):205-9. doi: 10.1001/archfaci.9.3.205. PMID: 17515497.

Blausen.com staff. "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.

Page | 24