Different Strokes for Different Folks

Barb Bancroft, RN, MSN, PNPCPP Associates, Inc.

www.barbbancroft.com

The usual first slide with statistics• 3rd leading cause of death in U.S.• 1st leading cause of disability in U.S.• 795,000 new cases per year• Broadly divided into ischemic (87%) and

hemorrhagic strokes (13%)• 46% of all ischemic strokes (320,000)are caused

by sudden occlusion of a large cerebral vessel• One large vessel ischemic stroke occurs every 90’• Worse prognosis vs. small-vessel ischemic stroke(Roger VL, et al. and Smith WS)

The second usual slide with more startling numbers…

• In the first minute of a stroke, your brain loses an estimated 1.9 million cells, resulting in the loss of 14 billion synapses and 7.5 miles of pathways—what you would lose in three weeks of normal aging. (January 2006 Stroke)

• But the loss continues every minute the stroke is left untreated. If a stroke runs its usual 10-hour course, it can kill 1.2 billion nerve cells—what a normal brain loses over the course of 36 years. (UCLA neurologist Jeffrey Saver) (Interview) 2007:34(2).

• TIME IS BRAIN!!

Is neurogenesis possible?

• Prior to 1998 the answer was NO—all you could do was KILL neurons—booze, trauma, strokes, stress

• Dr. Spickerman• Gerd Kemperman and Fred Gage discovered

neurogenesis• BUT only in 2 areas of the brain…• The hippocampus and the olfactory bulb• How can you stimulate neurogenesis?

Say YES to drugs…

• Antidepressants• Statin drugs• Lithium

Exercise

• One of the best ways to stimulate the growth of new neurons is to EXERCISE!

Meditation…and the monks…

• Find a nice quiet environment• Close your eyes• Deep breaths• Relax muscles• “oingy-boingy, oingy-boingy, oingy-boingy”

Does the brain have the capability of forming new synapses?

• Yes…• It’s called “plasticity”• Use it! Range of motion, start PT and OT within 24 to

48 hours if possible• Exercise—recruitment of pathways• Mirror neurons—monkey see, monkey do; LOOK in

the mirror, move the right arm and the paralyzed arm will also move

Brain boosters

• Challenge your powers of navigation—turn off the GPS and use a map; vary your routine—walking, driving home from work

• Math on the fly—add shopping purchases, calculate miles when driving

• Mind games—memorize phone numbers, CC#s, spell cities and states forward and backward

• Ballroom dancing—learning steps—spatial, planning movements, balance

Brain boosters

• New recipes—following steps, directions, planning• Tai chi—planning, sequence of movements• Assemble furniture—fix things at home• Musical instrument—fine motor, auditory,

processing, procedural thinking• Drawing, painting , sculpture class—visual memory,

creative imagination• Read the news actively every day—activates

attention centers; remembering scores of sports events

A review of neuroanatomy

• The lobes• The brainstem• The blood supply—anterior supply, posterior

supply

• REMEMBER THE WORD SYMMETRY

Orientation to the 3D brain--Lateral view—boxing glove

ANTERIOR • Lobes—frontal, parietal, temporal, occipital• Sulci• Gyri• Lateral fissure (Fissure of Sylvius)• Central sulcus—precentral and postcentral gyrusPOSTERIOR• Cerebellum• Brainstem

Sagittal (medial) section—location of brainstem

• Dura• Tentorium cerebelli• Infratentorial• Supratentorial

Meningeal layers

• Epidural (between bone and dura)—arteries from the external carotid branch across the top of the dura (epidural hematoma)

• Dura• Subdural space—bridging veins (subdural hematoma)• Arachnoid• Subarachnoid space—this is the space where all of the cerebral

arteries are located…anterior and posterior blood supplies meet at the base of the brain in the Circle of Willis (subarachnoid hemorrhage

• Pia• brain

Lateral and coronal view

Homunculus (motor and sensory)

Corticospinal tract

Inferior surface—brainstem view

NIH STROKE SCALE (NIHSS)• NIHSS score is a measure of stroke severity rated from 1 to

42 based on findings on physical exam when the patient is evaluated at baseline, 2 hours, 24 hours, 7-10 days and 3 months, and then time varies

• The higher the number, the greater the impairment• 1-7 = mild impairment• 8-15 = moderate impairment• Over 15 = severe impairment• NIHSS score greater than or equal to 12 has a 91%

predictive positive value of a central large-vessel stroke• EMERGENCY! Actions taken during first few hours have a

significant impact on the extent of future disability

THE FRONTAL LOBES…

• Prime real estate of the brain• Comprises one-third of the cerebral cortex• Pre-frontal lobe--this is your “Mother”• “No, negative, don’t, stop…” She is inhibitory…• Gamma-amino-butyric-acid (GABA)• Judgment, insight, forward planning, following steps,

directions, procedural thinking, socialization (you need bilateral frontal lobe disease to lose socialization)

Abstraction…

• Textbooks tell you to interpret proverbs…What does “a rolling stone gathers no moss” mean?

• HUH? Abstract (conceptual thinking vs. concrete thinking)

• How are a car, plane and boat alike?• Cow, horse, and pig?

Frontal lobes…

• Voluntary speech center (left frontal operculum) • Dr. Pierre Paul Broca• Broca’s aphasia (aphasia--communication

disorder)*• Non-fluent aphasia—telegraphic, staccato speech• *~20% of strokes present with some type of

aphasia• Kids and strokes• Left-handed people and strokes

Frontal lobes…• Pre-central gyrus– the motor

cortex—upper motor neurons)• Voluntary movement center of

brain• Send message through the

Corticospinal tract through the internal capsule of cortex through the midbrain to brainstem where it crosses at the medulla (pyramids)

• Contralateral symptoms (opposite side, below where it crosses)

• FAT leg

Corticospinal Tract

Upper Motor Neurons/CS tract

• Contralateral hemiparesis• ~(70% of anterior strokes present with

hemiparesis)

NIH STROKE SCALE--#5 and #6 testing motor function of arms and legs

• Extend the arms (palms down) 90 degrees (if sitting) or 45 degrees (if supine) and the leg 30 degrees (always tested supine)

• Drift is scored if the arm falls before 10 seconds or the leg before 5 seconds)

• Each arm is tested, in turn, beginning with the non-paretic arm.

Scoring

• 0=no drift; 1=drifts before 10 seconds but does not hit bed; 2=some effort against gravity, cannot get to or maintain 90 (or 45) degrees; some effort against gravity; 3=no effort against gravity, limb falls; 4=no movement at all

• Do same with legs—hold the leg supine at 30 degrees, drift is scored if the leg falls before 5 seconds (scored as above)

Motor function

• The initial shock of the stroke—the patient may not be able to even hold the arm up

• Reflexes may be absent• But as the nervous system recovers and the

shock of the stroke is over…• Motor function may begin to recover, but will

recover without a normal “MOM” or inhibitory input

Upper Motor Neurons/CS tract• No MOM? • Hemiparalysis (spastic

paralysis)• Hyperreflexia• Babinski reflex present

or absent?* (don’t’ use terms positive or negative—confusing)

• “And that’s why we always stand to the side when we check reflexes…”

Josef Francois Felix Babinski• The Babinski reflex• Babinski, Josef Francois Felix,

(1857-1932), a Parisian of Polish origin, described the famous abnormality of the extensor plantar response seen in disorders involving the corticospinal tracts in a series of short articles beginning in 1896.

• English physicians used their “Rolls Royce” key

Upper vs. Lower Motor Neuron damage

Reflex Chart—normal vs. stroke

• Achilles, patellar, biceps, triceps (S1,2; L3,4; C5,6; C7,8)

• Normal--2+ to 3+• REMEMBER SYMMETRY is

the word of the day….

Reflex Chart—normal vs. stroke

• Areflexia may be present on the opposite side due to the “shock” of the stroke)—0

• As the brain recovers, and there’s no “mother” (inhibition), the reflexes are uncontrolled

• Hyperreflexia 4+ in the limbs involved (more later)

• TOES up

TEMPORAL LOBES…

• Wernicke’s area (superior temporal gyrus)—reception of speech

• Do you hear me? (Cranial nerve VIII, the acoustic nerve; primary sensory modality)

• Do you understand what I am telling you? Higher cortical function (hearing and coma)

• Interpretation of speech and sounds (superior temporal gyrus)

• Coins jingling in pocket• Auditory agnosia

Best language (#9 on stroke scale)

• In the NIHSS there is a picture attached as part of the evaluation; the patient is asked to describe what is happening in the picture, to name the items on the attached naming sheet, and to read from the attached list of sentences.

• Comprehension is judged from the responses as well as to all of the commands on stroke scale questions #1-#8.

Scoring #9

• 0 = no aphasia• 1 = mild to moderate aphasia—some obvious

loss of fluency or facility of comprehension• 2 = severe aphasia—all communication is

through fragmentary expression; listener carries the burden of communication

• 3 = mute, global aphasia—no usable speech or auditory comprehension; coma patients

TEMPORAL LOBES…• Recent memory (hippocampus)• Remember 3 items…• Red ball, clock, tennis shoe• Repeat them after me…immediate recall• Red ball, clock, tennis shoe• Continue with exam for 10 minutes and ask them to repeat

those 3 items• Only two areas of the brain are capable of neurogenesis—the

olfactory bulb and the hippocampus (CN I connected to the uncus connected to the hippocampus—smell and memory)

PARIETAL LOBES…• Postcentral gyrus (somatosensory cortex)• Right parietal lobe interprets left side of your

body and the left side of your world• Damage to the parietal lobes results in difficulty

recognizing body parts and acknowledging the opposite side of your world

• Contralateral hemisensory loss• Integration of tactile sensations—touch,

pressure, vibration, and proprioception (do you know where your body parts are? Did you have to look for them?)

PARIETAL LOBES..testing

• Double simultaneous stimuli—kids vs. adults• Touch two areas at the same time..• The neglect syndrome in adults (non-

dominant parietal lobe)• Kids will always neglect their body and will

recognize touch on the face

Stroke scale #11

• Extinction and inattention (formerly Neglect)• See scale• 0 = no abnormality• 1 = visual, tactile, auditory, spatial or personal

inattention or extinction to bilateral simultaneous stimulation in one of the sensory modalities

• 2 = profound hemi-inattention or extinction to more than one modality; does not recognize own hand or orients to only one side of space

PARIETAL LOBES..testing• Ability to localize stimuli• Sharp vs. dull• Tests for proprioception—what’s proprioception?• Graphesthesia/agraphesthesia• Stereognosis/astereognosis• Anosognosia (unawareness of illness, denial of

hemiplegia)—nondominant hemisphere• Apraxia—example: a dressing apraxia

ideomotor apraxia constructional apraxia

OCCIPITAL LOBES…

• Do you see this object?• If they can see it, CN2 (the optic nerve)• What is it? The occipital cortex (interpretation—

higher cortical function)• Visual integration—problems manifest as cortical

blindness (visual agnosia)• Optic radiations via temporal and parietal lobes--

homonymous hemianopia• Visual field testing (#3 on the NIH STROKE SCALE)

Homonymous hemianopia

Loss of vision—optic tract and optic radiations

• Right parietal lobe sees the Left LOWER visual field in both eyes

• Right temporal lobe sees the left UPPER visual field in both eyes

• Stroke in parietal and temporal optic radiations = homonymous (same) hemianopsia (half loss of vision)

Brainstem (bulb)—midbrain, pons, medulla, and cerebellum (sits on top of brainstem)

• Cranial nerve assessment Midbrain—optic—II; oculomotor—III• Pons—Ascending Reticular Activating System; pupils

(pontine pupils)—(coma) CN V, VI, VII, VIII • Medulla—CV/respiratory center CN IX, X, XI, XII• Cerebellum—coordination, synergy, equilibrium

(dysmetria, dysarthria, dyssynergia)

The light reflex tests two cranial nerves—CNII and CNIII—sensory via II, and motor via III

• PERRLA (pupils equal, round, reactive to light and accommodation)

• Located just beneath the tentorium• As the uncus herniates over the tentorium it

puts pressure on the CNIII (severe cerebral edema, or a large intracranial bleed)

• Dilated pupil on the side of the herniation

The BRAINSTEM…(the “bulb”)

• The optic disk (also known as the optic papilla)• Papilledema (swelling of the optic disk due to

increased intracranial pressure)

The BRAINSTEM…

• CN III, IV, VI—follow my finger (extraocular movements)

• CNIII also elevates the eyelid (levator palpebre)

• diplopia

NIH STROKE SCALE--#2—best gaze

• Only horizontal eye movements will be tested• CN III and VI• If the patient has a conjugate deviation that

can be overcome by voluntary or reflexive activity (oculocephalic testing or Doll’s eye maneuver) the score will be 1

• Patient’s with forced deviation, or total gaze paresis not overcome by the oculocephalic maneuver will score a 2

The BRAINSTEM…

• CN V supplies sensation to the face—do you feel this? this? this? Check all 3 roots…

• CN V supplies motor to the masseter and temporalis—clench your teeth

• V (Trigeminal) and VII (Facial) work together

• Corneal reflex—touch cornea with a cotton wisp and the patient blinks

Facial Nerve--VII

• Muscle of facial expression—smile, frown, surprise, close eyes• Checking for symmetry• Show me your teeth• “BBBBB”

NIH STROKE SCALE -- #4• Facial palsy: ask, or use pantomime to encourage the

patient to show teeth or raise eyebrows and close eyes. Score symmetry of grimace in response to noxious stimuli in the poorly responsive or non-comprehending patient

• 0 = normal• 1 = minor paralysis )flattened nasolabial fold,

asymmetry on smiling• 2 = partial paralysis (total or near total paralysis on

lower face)• 3 = complete paralysis of one or both sides—upper

and lower

The BRAINSTEM…

• VIII (acoustic)—(dizziness)• IX (Glossopharyngeal) and X (Vagus)• Swallowing (dysphagia)• The gag reflex• The uvula

The BRAINSTEM…

• CN XII (Hypoglossal)—tongue movement and strength

• “LaLaLaLa”• Stick tongue out• Push tongue against cheek

Cerebral circulation—anterior circulation

• Aorta, common carotids (CCA), internal carotids (ICA), ophthalmic arteries, middle cerebral arteries (MCA), and anterior cerebral arteries (ACA)

• Middle cerebral arteries (MCA and the lateral aspects of the frontal, temporal lobes and parietal lobes—exits at the lateral fissure

• The lenticulostriate arteries branch off the MCA (fragile and tend to rupture with hypertension) and extend into the brain parenchyma

• Anterior cerebral arteries go straight up the middle between both lobes—connected by the anterior communicating artery of the Circle of Willis (subarachnoid space)

Anterior blood supply

The anterior circulation

• Supplies the frontal lobes, parietal lobes, most of the temporal lobes, the basal ganglia, and the internal capsule

• Major signs of a vascular event affecting the anterior circulation include hemiparesis and aphasia (dominant hemisphere)

• Face and arm more than leg? Cortical distribution• Face = arm = leg—internal capsule (subcortical)

Face, arm, and leg—internal capsule, subcortical hemorrhage

• Lenticulostriate artery rupture and hemorrhage

Anterior ischemic symptoms and signs (cerebral hemispheres—frontal- temporal- parietal)

• Contralateral hemiparesis of extremities• Sensory deficits of contralateral extremities• Loss of vision in ipsilateral eye (if the

ophthalmic artery is involved)• Homonymous hemianopia• Aphasia—Broca’s, Wernicke’s, global

Cerebral circulation—posterior circulation—vertebrobasilar system

• Subclavian arteries to the vertebral arteries to the basilar artery to the posterior cerebral arteries (with a few other tributaries to the cerebellum and pons)

Posterior circulation

• Supplies the brainstem, thalamus, cerebellum, occipital lobe and a portion of the medial and inferior temporal lobes

• The anterior circulation and posterior circulation meet at the base of the brain—the Circle of Willis; aneurysms are most common at the Circle of Willis (more later)

• Don’t forget that all of these LARGE, major arteries are running through the subarachnoid space—with a rupture, subarachnoid hemorrhage

Posterior circulation—vertebro-basilar (brainstem)

Signs suggesting posterior circulation localization

• The D’s…diplopia, dysphagia, dysarthria, dizziness—(dizziness has to be found with one of the other Ds)—signify a posterior circulation problem

Posterior ischemic symptoms and signs (brainstem and occipital lobes and cerebellum)

• Motor dysfunction of ipsilateral face and or extremities

• Ataxia, vertigo• The D’s—diplopia, dysphagia, dysarthrias,

disequilibrium/dizziness• These TIAs are more likely than those with

anterior symptomatology to lead to ischemic stroke

Posterior circulation—vertebro-basilar (brainstem)

One last reminder:

• Large vessel artery strokes are most common• Large vessels mean any greater than 2 mm in

diameter and include the internal carotid, middle cerebral artery, anterior cerebral artery, vertebral artery, and basilar arteries

Part 2

• Types of stroke• Risk factors for stroke

Principle stroke types

• Thrombotic stroke• Embolic stroke• Lacunar stroke(the first 3 are ischemic strokes)• Hemorrhagic stroke

What is the clinical profile of a thrombotic stroke?

• The rupture of an atherosclerotic plaque in one of the large cerebral arteries leads to sudden clot or thrombus formation

• The presentation can be gradual, stuttering, or in a stepwise progression

• Carotid distribution usually

Thrombotic strokes (40%)• Older population with history high cholesterol and

atherosclerosis• May have hypertension• Onset may be gradual• 50% of the time there is a preceding TIA• 5% with mental status changes• MRI/CT shows ischemic infarction• May hear a carotid bruit• Stroke during sleep, wake up with a

“stroke in progress”…when was the patient last observed as normal? “last known normal”

What is the clinical profile of an embolic stroke?

• Sudden onset, often during usual daily activity• Deficit is generally maximal at onset, often with

improvement shortly afterward as the embolus breaks up and portions travel farther out into more distal branches of the affected artery—MCA territory

• The heart is usually the source and atrial fibrillation is a big offender, as are mechanical valves, or endocarditis

• Onset may be associated with palpitations, initiation of a cardiac arrhythmia, or following the Valsalva maneuver, heavy lifting or voiding

Embolic strokes (30%)

• Sudden onset, older population• 10% with preceding TIAs• 1% with altered mental status• MRI/CT shows superficial/cortical infarction• Underlying heart disease, atrial fib, peripheral

emboli, strokes in different vascular territories

What is the clinical profile of a lacunar stroke?

• 4 classic lacunar stroke syndromes; 1st two are most common

1) pure motor hemiparesis—FAT & leg equally affected 2) pure hemisensory stroke 3) clumsy hand-dysarthria, in which there is significant disuse

of the affected arm out of proportion to the amount of weakness evident

4) ataxia with paresisAssociated with hypertension resulting from

vasoconstriction/occlusion of the small perforating arterioles

Lacunar strokes (20%)

• May be gradual• 30% with preceding TIAs• 0 with altered mental status• Small, deep infarction• Pure motor, or pure sensory stroke

What is the clinical profile of a hemorrhagic stroke?

• Sudden onset, along with a prominent decrease in consciousness early in the course; fluctuation of mental status is a common feature. Hypertension often occurs with bradycardia (Cushing reflex) along with other signs of increased ICP

• Ruptured cerebral aneurysms w/ subarachnoid hemorrhage (Circle of Willis), ruptured AV malformation, ruptured penetrating arteries (such as the lenticulostriate arteries w/ HBP)

Hemorrhagic strokes (10%)

• Sudden onset, “worst headache EVER”• 30-60% may have less severe HA if aneurysm leaks• 5% with preceding TIAs• 25% with altered mental status• MRI• CT with hyperdense area (white area)• Nausea, vomiting, coma, stiff neck, photophobia

Aneurysm location• Anterior Communicating artery

—30-35%• Internal carotid/posterior

communicating artery—29 – 35%

• Middle cerebral artery—20%• Basilar apex – 5%• Vertebrobasilar junction (2%)• Superior cerebellar artery (3%)• Posterior inferior cerebellar

artery (3%)

Incidence of aneurysms

• Aneurysmal SAH = 6-8% of strokes• Women greater than men• 50% rupture• 50% mortality rate with rupture• 15% increase with a first degree relative with

one

AVM—another cause of SAH

• Arteriovenous malformation• 2-17% hemorrhagic strokes• 8.6% of SAH• 64% diagnosed before age 64• 29% mortality• S and S—spontaneous intracranial hemorrhage

(50%), seizure (30%), headache (11-14%), evolving neurologic symptoms

Subarachnoid hemorrhage—Hunt-Hess grading scale

• Grade 1—alert, mild headache, stiff neck• Grade 2—alert, vision problems, moderate to

severe headache, stiff neck• Grade 3—lethargy or confusion, weakness or

partial paralysis on one side of body• Grade 4—stupor, moderate to severe

paralysis on one side of body• Grade 5—comatose

Survival rates based on SAH severity

• Grade 1 – 70% survival• Grade 2 – 60% survival• Grade 3 – 50% survival• Grade 4 – 20% survival• Grade 5 – 10% survival• Overall mortality rate for SAH is 50% at 1 year;

25% of survivors have persistent neuro deficits

KNOW your risk factors--Some you can’t modify…some you can…

• The number one risk factor you can’t modify is AGE…the older you are, the higher the risk…

• 2/3 of all strokes occur over the age of 65• Blood vessels “age”

Some risk factors you can’t modify…

• Gender—in any given year more women than men will suffer a stroke, and women account for more than 60% of all stroke deaths in the US

• Men’s stroke incidence rates are greater than women’s at younger ages but not at older ages. The male/female incidence ratio is 1.25 at ages 55-64; 1.50 for ages 65-74; 1.07 at 75-84 and 0.76 at 85 and older

Some you can’t modify…

• Family History influences your risk for cardiovascular disease of any nature—parent, grandparent, sister, brother

• Especially if they had a stroke before the age of 65

Risk Factors you can’t modify…

• Ethnicity--American Indian, people of African or South Asian descent are more likely to have hypertension and diabetes and therefore an increased risk of stroke

Risk factors you can’t modify

• Previous TIA or stroke• Currently a TIA lasts no longer than 24 hours;

however, this definition is currently being revised to focus on manifestations that last for no more than one hour

• The majority of TIAs last 10 to 60 minutes

TIAs (transient ischemic attacks) or “mini-strokes”

• 15 to 19% of ischemic strokes are preceded by a TIA• 4 to 5% will experience a progression to stroke

within 48 hours• “Front-loaded”—half of the strokes that occur within

90 days happen within the first 48 hours after a TIA(Rothwell PM and Warlow CP. Timing of TIAs preceding stroke:

Time window for prevention is very short. Neurology 2005 Mar 8;64:817-20)

Most common symptoms

• Temporary loss of vision (amaurosis fugax—a transient monocular blindness) (“Feels like a curtain was pulled down over my eye…”)

• Aphasia• Hemiparesis• Paresthesias (unilateral)

Treatment of TIAs

• Early intervention after thorough evaluation by PCP or neurologist

• Antiplatelet and anticoagulant therapy has been found to reduce risk for early TIA recurrence or ischemic stroke by 80%

• Initial treatment with antiplatelet therapy—aspirin 50 to 325 mg/d

Treatment of TIAs• 2nd line—ASA + dipyramidole (Aggrenox);

substantial benefit in using this combo to reduce BP and prevent secondary progression to stroke

• 3rd line—clopidogrel (Plavix) in patients who cannot tolerate ASA

• Warfarin for patients with AF (INR target 2-3, 2.5), valvular heart disease (INR 2.5-3.5), crescendo TIAs

• Carotid endarterectomy for patients with greater than 70% stenosis or high-dose ASA and clopidogrel (Plavix)

Treatment of TIAs

• Long-term management addresses the patient’s risk factors

• Lower BP with “prils” gradually• Statins for atherosclerosis• Antiplatelet drugs

Hypertension– a modifiable risk factor

• Ideal BP = 120/80• Acceptable BP with treatment is 130/80• 140/90 is TOO HIGH

Hypertension

• Hypertension is the most important risk factor for ischemic and hemorrhagic stroke. The incidence of stroke increases directly in relation to the degree of elevation of systolic and diastolic blood pressure. More important, there has been conclusive evidence for more than 30 years that control of hypertension prevents strokes. Meta-analyses of randomized controlled trials confirm an approximate 30 to 40% reduction in stroke risk with lowering of blood pressure.

Hypertension in the elderly• Depending on co-morbidities it maybe kept slightly

higher in the elderly to avoid hypotension, falls, and a broken hip

• But not TOO high—66% of all strokes are due to hypertension

• Keeping the blood pressure BELOW 140/90 prevents strokes, acute coronary syndromes, chronic heart failure, dementia, and renal failure

• Is your patient hypertensive? Check HbA1c—type 2 diabetes is 2.5x more likely to develop in patients with hypertension

Hypertension

• Decreasing diastolic blood pressure by 5-6 mmHg or decreasing systolic blood pressure by 10-12 mmHg over 2-3 years decreases the risk of stroke by 38%

• So, what can we do to reduce blood pressure and thus, reduce stroke risk?

Treatment of high blood pressure

• Weight loss• (excess weight is also a risk factor for stroke)

The DASH diet to lower BP

• Dietary Approaches to Stopping Hypertension• Increase potassium-containing foods • 4,700 mg of potassium per day• People who are potassium deficient are 1.5 to 2.5

times more likely to have a stroke

DASH diet—K+ containing foods (mg)

• Oranges (260 mg)• Raisins (1/2 cup) (543 mg)• Halibut (654 mg)• Potato (926 mg)• Canteloupe (1 cup)(547)• Banana (451mg)• Milk (1 cup) (290 mg)

• Before adding K+ containing foods— Are they on ACE inhibitors? Spironolactone? Both?

DASH diet

• Limit sodium intake to 2.4 g per day (slightly more than one teaspoon)

• Say no to processed foods• Say no to Lean Cuisine• Say no to other processed foods (bacon, bologna, ham)

DASH diet—calcium containing foods…

• Increase calcium-containing foods (low-fat dairy products)

• Got low-fat milk? • Low–fat yogurt?• 320 mg of calcium per 8 ounces of skim milk

Say YES to drugs to reduce blood pressure…

• Thiazide diuretics• ACE inhibitors— “the prils”—• ARBs—the “sartans”• Calcium channel blockers– “the dipines”• Beta blockers— “olols, alols, ilols”

“Prils”—The ACE inhibitors (Brazilian pit viper)

• Captopril (Capoten)• Enalapril (Vasotec)• Lisinopril (Prinivil, Zestril)• Perindopril (Aceon)• Moxepril (Univasc)• Benazepril (Lotensin)• Quinapril (Accupril)• Trandolapril (Mavik)• Ramipril (Altace)• Etc…

The “prils” against stroke…

• Perindopril (Aceon) Protection Against Recurrent Stroke Study (PROGRESS)—decreased stroke by 28%

• Ramipril (Altace) in the HOPE (Heart Outcomes Prevention Evaluation) showed ramipril decreased the risk of stroke even if the patients were not hypertensive

Risk factors that can be modified…smoking

• Accelerates atherosclerosis• Accelerates aging• Vasoconstricts cerebral vessels• Current smokers who smoke 20 or more per

day have a 2 to 4x greater stroke risk

Smoking…a modifiable risk factor

• Even passive smoke elevates the risk

How can you stop smoking?

• Cold turkey?• Nicotine replacement patches or gum• Bupropion (Zyban)• Varenicline (Chantix) • Psychotherapy

READ my LIPIDS…Hypercholesterolemia

• Fat plaques in all of the major arteries including the precerebral arteries--aorta and the carotids and the vertebral arteries (supplying the posterior portion of the brain and brainstem)

Read my lipids… cholesterol numbers

• The good cholesterol—HDL (greater than 40 mg/dl for guys; greater than 50 mg/dlwould be ideal)

• The bad cholesterol—(LDL less than 100 mg/dl if you have diabetes or heart disease or a risk 70 mg/dl would be ideal

• Triglycerides (less than 150 mg/dl; new AHA guidelines say less than 100 mg/dl)

Say “YES” to drugs to lower LDL cholesterol

• The ‘statin sisters’ • Simvastatin (Zocor)• Atorvastatin (Lipitor)• Fluvastatin (Lescol)• Rosuvastatin (Crestor)• Pravastatin (Pravachol)• Pitavastatin (Livalo)

Statins

• The statins should also be prescribed for all patients who have had an ischemic stroke/TIA to goal of LDL-C less than 2.0 mmol/L

• Aggressive reduction results in a 20% to 30% relative risk reduction in recurrent vascular events for patients with a history of stroke without coronary artery disease

What do the statins do?• Reduce total cholesterol and LDL levels• Decrease fatty plaque formation, shrink plaques that

are already present in major arteries, stabilize plaques, and prevent plaque rupture in the aorta and carotid arteries

• Increase the bioavailability of nitric oxide (vasodilator)

• The statins also lower BP!

• anti-inflammatory effects prevent plaque rupture

“Sugar” diabetes• Risk of stroke is 2.5-4x greater in diabetics• Diabetes is a proatherosclerotic disease• Increased triglycerides and low HDLs• High triglycerides cause the LDLs to be small and dense• Small and dense LDLs are deposited easily into the walls of

the arteries• Diabetics also have hypertension• Treat the hypertension, treat the elevated lipids, and treat

the hyperglycemia

Excessive alcohol consumption

• Limit # of drinks to less than 9 per week for women and less than 14 per week for men

• 12 ounces of beer of 5% alcohol• 5 ounces of wine of 12% alcohol• 1.5 ounces of 40% alcohol • This is a YES…

Physical inactivity

• Physical inactivity increases the risk of heart disease or stroke by two-fold

• 30 minutes most days of the week, working your way to 60 minutes most days of the week

Oral contraceptives and strokes

• There are about 4.4 ischemic strokes for every 100,000 women of childbearing age. Birth control pills increase the risk 1.9 times, to 8.5 strokes per 100,000 women, according to a well-performed "meta-analysis" cited in the article. This is still a small risk; there's one additional stroke for every 25,000 women who take birth control pills

Oral contraceptives and strokes

• For women who take birth control pills AND also smoke, have hypertension, or have a history of migraines, the stroke risk is significantly higher.

• balance the risks and benefits for each individual patient

• The higher the estrogen content of the pill, the greater the risk (“old OCs vs. new OCs”)

• two possible mechanisms are the increased risks of blood clots and hypertension associated with oral contraceptives

Stroke, causes in young adults Cardiac factors (ASD, MVP, patent foramen ovale);

Inflammatory factors (SLE, polyarteritis nodosa); Infections (endocarditis, neurosyphilis); Drugs (cocaine, heroin, meth, decongestants);

Arterial dissection;Hematologic factors (DIC, TTP, homocysteinemia, lupus anticoagulant);migraine WITH aura; postpartum angiopathy ;

Others: premature atherosclerosis, fibromuscular dysplasia, sickle cell disease

(Ferri; 2010, 8th edition)

New study—ischemic stroke in young adults

• Ages 16-54; 15% atherothrombosis; 8% small vessel disease; 8% cardioembolism usually associated with atrial fibrillation; 14% other definitive causes including cervical or cerebral artery dissection

• 19% potential but not definite causes—patent foramen ovale

• Ages 16-44 less likely to have a definitive cause• Larrue V et al. Etiologic investigation of ischemic stroke in

young adults. Neurology 2011 June 7; 76:1983

Carotid stenosis and the risk of ischemic stroke…

• Up to half of all ischemic strokes are associated with carotid stenosis

• Stenting vs. ASA 325mg and Clopidogrel/Plavix 75mg x 90 days followed by ASA monotherapy? Followed by ASA monotherapy

• Chimowitz MI, et al. N Engl J Med 2011 Sept 15; 365:993

A few more notes on carotid artery disease

• Patients with carotid territory TIA or minor stroke and high-grade ipsalateral carotid artery stenosis are at very high risk of early stroke recurrence. The absolute benefit from carotid endarterectomy is highly time-dependent.

• Carotid artery imaging (ultrasound) should be performed within 24 hours of the event

Atrial fibrillation (AF)

• Greater than 10% over 80; median age 75; AF reduces CO by 10-15 %

• Fibrillation potentiates clot formation and results in 2-5 fold greater risk for embolic stroke

• % of stroke attributable to atrial fibrillation is < 2% under age 60; 20% over age 80

Atrial fibrillation--anticoagulation

• Warfarin—gold-standard, long-term anticoagulation with warfarin reduces risk of stroke by 66%; Vitamin K antidote; $80/month

• INR – 2-3; mitral valve disease or mechanical prosthetic valves—INR 2.5 to 3.5

• Dabigatran (Pradax in Canada; Pradaxa in US)—direct thrombin inhibitor—no monitoring; prevents 5 more strokes per 1000 patients per year; BID/$240/month

• Rivaroxaban (Xarelto)—first oral factor Xa inhibitor; QD; no better than warfarin; cost same as dabigatran

Stay tuned…

• Apixaban (Eliquis)—to be approved this year; more effective than both of the above with less bleeding

Ischemic/embolic strokes

If the ischemia continues long enough, brain infarction occurs. In the case of large-vessel ischemic stroke, an initial core area of infarct is often surrounding by a watershed area of ischemic tissue known as the penumbra. If circulation is restored within the first few hours of the ischemia, some or all of the penumbra may be salvaged

TIME IS BRAIN!!!

Ischemic/embolic strokes

• As stroke volume increases, risk increases that opening a blocked vessel may result in catastrophic intracerebral hemorrhage rather than reperfusion, because necrotic, infarcted vessels cannot contain blood.

• This phenomenon, known as hemorrhagic conversion, imparts severe time limitations on the treatment of large vessel stroke.

Treatment of Ischemic/embolic strokes

• Prehospital care—ABGs, O2, IV lines, serum glucose

• Notify ER of possible stroke patient to mobilize the stroke team

• ER—continuing assessment with NIH STROKE SCALE; prep for fibrinolytic therapy

NIH STROKE SCALE (NIHSS)• Higher NIHSS score with large vessel strokes• NIHSS score is a measure of stroke severity rated from

1 to 42 based on findings on physical exam• The higher the number, the greater the impairment• 1-7 = mild impairment• 8-15 = moderate impairment• Over 15 = severe impairment• NIHSS score greater than or equal to 12 has a 91%

predictive positive value of a central large-vessel stroke

• EMERGENCY! Actions taken during first few hours have a significant impact on the extent of future disability

Recommended stroke evaluation time

• Door to MD – 10 minutes• Access to neuro expert – 15 minutes• Door to CT scan completion – 25 minutes• Door to CT scan interpretation – 45’• Door to treatment – 60 minutes• Admission to monitored bed – 3 hours• “Time is brain”

General Management--LAB

• Glucose—hypoglycemia is the most common electrolyte abnormality that produces stroke-like symptoms

• a) treat with D50• b) hyperglycemia at the time of the acute

stroke increases the infarct size and is associated with poor clinical outcomes; Treat with insulin

General Management--LAB

• Electrolytes• CBC—Hemoglobin, Hematocrit, platelet count• PT and aPTT—many patients with acute stroke

are on anticoagulants, such as heparin or warfarin; Rx decisions such as thrombolytic use, require data on coagulation status; an increase in INR may preclude patients from thrombolytics

General Management--LAB

• Cardiac enzymes/troponin—patients with stroke may also experience an acute coronary syndrome

• ABGs—avoid if thrombolytics are considered• Other tests tailored to individual patients—

ANA, homocysteine, coagulation factors such as protein S, C, antithrombin III, Factor V Leiden, anticardiolipin antibodies

Imaging studies

• CT—noncontrast CT scans are very sensitive in detecting intracerebral bleeds and subarachnoid hemorrhages, as well as subdural hematomas

• Not sensitive for early ischemia (less than 6 hours); some findings can suggest early changes;

• May also p/u tumors, meningeal bleeds, aneurysms abscess, AV malformation, hydrocephalus

General management• Blood pressure management—elevated BPs in patients

with ischemic stroke typically are not treated until they reach 220/120 mg

• ECG—Acute coronary syndrome, atrial fibrillation• ECHO in a young patient may pick up a patent foramen

ovale• IV—avoid D5W; use isotonic saline @ 50 mL/h unless

otherwise indicated• NPO until swallowing is assessed (usually brainstem

strokes); 55% of new-onset stroke patients have dysphagia; high risk of aspiration, pneumonia, dehydration, poor nutrition

General Management

• Supplemental O2– saturated O2 less than 93%; or hypotensive

• Temperature—avoid hyperthermia, use oral or rectal acetaminophen, cooling blankets PRN

Ischemic strokes• Fibrinolytic therapy—IV rtPA (alteplase) for

appropriate patients within 4.5 hours from symptom onset in carefully selected patients

• Converts plasminogen to plasmin; plasmin breaks down fibrin and dissolves clots

• 0.9 mg/kg via combined IV bolus and 60 minute infusion

• Strict exclusion criteria due to increased risk of bleeding

• When did the symptoms start? REMEMBER, TIME IS BRAIN

Underused!

• Recanalization rates for IV rtPA alone are 6% - 31% for the MCA and 13% to 30% for the ICA

• An estimated 28.7% of ischemic stroke patients would qualify for use, only 1 – 3% receive it

• Major reason? A delay in presentation!!• 2nd reason? Lack of designated stroke centers• 3rd reason? Lack of 24-hour CT availability

Intra-arterial rt-PA (prourokinase)

• Delivered directly to MCA via catheter within 6 hours of symptom onset

• Much smaller dose than IV rt-PA (2-4 mg) directly to site of occlusion, within 6 hours of symptom onset

• ONLY GIVE AT STROKE CENTER with a highly skilled neurointerventional physician

Mechanical thrombectomy: MERCI retriever and the Penumbra device

• Used for large-vessel stroke• May be used up to 8 hours after symptom

onset• When used alone? 57.3% recanalization• When used with IA rtPA the recanalization

rate is 69.5% • Penumbra device—breaks up clot with

continuous aspiration with 81.6% revascularization

General Management

• Start rehabilitation assessment within 24 to 48 hours

• OT• PT• Speech therapy• Interdisciplinary approach decreases death

and improves outcomes

Nursing care

• Frequent neuro assessment of course!• Bleeding risk assessment• Skin• Bowel• Bladder• Lungs• Musculoskeletal • Psychological assessment

Stroke and depression• Left cerebral cortex with damage to frontal

pole=depression (especially seen with stroke patients; high risk within 1st 2 years after stroke)

• Subcortical infarcts in thalamus and caudate predispose to depression also

• SSRIs for patients with severe, persistent tearfulness• Sertraline (Zoloft) and escitalopram (Cipralex) are

excellent choices• Improves compliance with physical therapy• Recent evidence that SSRIs may improve motor

recovery

REMEMBER!!!

• TIME IS BRAIN!!!

Thanks.

• Barb Bancroft, RN, MSN, PNP

• bbancr9271@aol.com• www.barbbancroft.com

Selected Bibliography• 1-888-4STROKE American Stroke Association• Canadian Best Practice Recommendations for Stroke

Care: 2006• Gommans J, Barber PA, Fink J. Preventing strokes:

the assessment and management of people with transient ischemic attack N Z Med J. 2009;122(1293):3556.

• Halsey MP. TIA Update. Clinician Reviews. 2009;19(10):18-22.

Selected Bibliography• Johnston SC, et al. National Stroke Association

Guidelines for the management of transient ischemic attacks. Ann Neurol. 2006; 60(3):301-13.

• Josephson SA, Sidney S. Pham TN, et al. Higher ABCD2 score predicts patients most likely to have true transient ischemic attack. Stroke. 2008;39(11):3096-3098.

• Kang JH, Ho JD, Chen YH, Lin HC. Increased risk of stroke after a herpes zoster attack. A population-based follow-up study. Stroke 2009. October 8, 2009.

Selected Bibliography• Klein-Ritter D. An evidence-based review of the

AMA/AHA guideline for the primary prevention of ischemic stroke. Geriatrics. 2009; 64(9):16-20.

• Lloyd-Jones D, Adams R, Carnethon M, et al. Heart disease and stroke statistics—2009 update. A Report from the AHA Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009;119(3):321-e181.

• Roger VL, et al. Heart disease and stroke statistics—2011 update: a report from the AHA. Circulation. 2011;123(4)

Bibliography• Smith WS, et al. Significance of large vessel

intracranial occlusion causing acute ischemic stroke and TIA. Stroke. 2009;40(12)

• Weinberger J. Antiplatelet agents for stroke prevention following a transient ischemic attack. South Med J. 2008:101(1):70-78.

• Wu CM, McLaughlin K, Lorenzetti DL, et al. Early risk of stroke after transient ischemic attack: a systematic review and meta-analysis. Arch Intern Med. 2007;167(22):2417-2422.