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Different Strokes for Different Folks

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Presentation on theme: "Different Strokes for Different Folks"— Presentation transcript:

1 Different Strokes for Different Folks
Barb Bancroft, RN, MSN, PNP CPP Associates, Inc.

2 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)

3 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!!

4 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?

5 Say YES to drugs… Antidepressants Statin drugs Lithium

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

7 Meditation…and the monks…
Find a nice quiet environment Close your eyes Deep breaths Relax muscles “oingy-boingy, oingy-boingy, oingy-boingy”

8 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

9 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

10 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

11 A review of neuroanatomy
The lobes The brainstem The blood supply—anterior supply, posterior supply REMEMBER THE WORD SYMMETRY

12 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 gyrus POSTERIOR Cerebellum Brainstem

13 Sagittal (medial) section—location of brainstem
Dura Tentorium cerebelli Infratentorial Supratentorial

14 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

15 Lateral and coronal view

16 Homunculus (motor and sensory)

17 Corticospinal tract

18 Inferior surface—brainstem view

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

20 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)

21 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?

22 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

23 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

24 Corticospinal Tract

25 Upper Motor Neurons/CS tract
Contralateral hemiparesis ~(70% of anterior strokes present with hemiparesis)

26 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.

27 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)

28 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

29 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…”

30 Josef Francois Felix Babinski
The Babinski reflex Babinski, Josef Francois Felix, ( ), 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


32 Upper vs. Lower Motor Neuron damage

33 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….

34 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

35 Corticobulbar tract BULB means brainstem
FACE upper motor neurons synapse in brainstem (bulb) on the SAME side Ipsalateral So a stroke patient can have IPSALATERAL lower facial weakness and CONTRALATERAL hemiparalysis

36 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

37 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.

38 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

39 TEMPORAL LOBES… Recent memory (hippocampus) Remember 3 items…
Red ball, clock, tennis shoe Repeat them after me…immediate recall 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)

40 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?)

41 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


43 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

44 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 Quarters have 119 grooves on its circumference; dimes 118 

45 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)

46 Homonymous hemianopia

47 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)

48 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)

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

50 The BRAINSTEM…(the “bulb”)
The optic disk (also known as the optic papilla) Papilledema (swelling of the optic disk due to increased intracranial pressure)

51 The BRAINSTEM… CN III, IV, VI—follow my finger (extraocular movements)
CNIII also elevates the eyelid (levator palpebre) diplopia

52 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

53 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

54 Facial Nerve--VII Muscle of facial expression—smile, frown, surprise, close eyes Checking for symmetry Show me your teeth “BBBBB”

55 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

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

57 The BRAINSTEM… CN XII (Hypoglossal)—tongue movement and strength
“LaLaLaLa” Stick tongue out Push tongue against cheek

58 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)

59 Anterior blood supply


61 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)

62 Face, arm, and leg—internal capsule, subcortical hemorrhage
Lenticulostriate artery rupture and hemorrhage

63 Contralateral hemiparesis of extremities
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

64 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)

65 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

66 Posterior circulation—vertebro-basilar (brainstem)

67 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

68 Motor dysfunction of ipsilateral face and or extremities
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

69 Posterior circulation—vertebro-basilar (brainstem)

70 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

71 Part 2 Types of stroke Risk factors for stroke

72 Principle stroke types
Thrombotic stroke Embolic stroke Lacunar stroke (the first 3 are ischemic strokes) Hemorrhagic stroke

73 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

74 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”

75 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

76 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

77 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 paresis Associated with hypertension resulting from vasoconstriction/occlusion of the small perforating arterioles

78 Lacunar strokes (20%) May be gradual 30% with preceding TIAs
0 with altered mental status Small, deep infarction Pure motor, or pure sensory stroke

79 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)

80 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

81 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%)

82 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

83 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

84 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

85 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

86 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”

87 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 and 0.76 at 85 and older

88 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

89 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

90 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

91 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)

92 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)

93 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

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

95 Treatment of TIAs Long-term management addresses the patient’s risk factors Lower BP with “prils” gradually Statins for atherosclerosis Antiplatelet drugs

96 Hypertension– a modifiable risk factor
Ideal BP = 120/80 Acceptable BP with treatment is 130/80 140/90 is TOO HIGH

97 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.

98 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

99 Hypertension Decreasing diastolic blood pressure by 5-6 mmHg or decreasing systolic blood pressure by 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?

100 Treatment of high blood pressure
Weight loss (excess weight is also a risk factor for stroke)

101 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

102 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?

103 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)

104 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

105 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”

106 “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…

107 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

108 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

109 Smoking…a modifiable risk factor
Even passive smoke elevates the risk

110 How can you stop smoking?
Cold turkey? Nicotine replacement patches or gum Bupropion (Zyban) Varenicline (Chantix) Psychotherapy

111 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)

112 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) 24 hours for alcoholic beverages starting at age 20 and every 5 years subsequentlylk

113 Say “YES” to drugs to lower LDL cholesterol
The ‘statin sisters’ Simvastatin (Zocor) Atorvastatin (Lipitor) Fluvastatin (Lescol) Rosuvastatin (Crestor) Pravastatin (Pravachol) Pitavastatin (Livalo)

114 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

115 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

116 “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

117 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…

118 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

119 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

120 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

121 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)

122 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 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

123 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

124 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

125 Atrial fibrillation (AF)
Greater than 10% over 80; median age 75; AF reduces CO by % 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

126 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

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

128 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!!!

129 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.

130 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

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

132 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”

133 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

134 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

135 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

136 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

137 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 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

138 General Management Supplemental O2– saturated O2 less than 93%; or hypotensive Temperature—avoid hyperthermia, use oral or rectal acetaminophen, cooling blankets PRN

139 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

140 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

141 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

142 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

143 General Management Start rehabilitation assessment within 24 to 48 hours OT PT Speech therapy Interdisciplinary approach decreases death and improves outcomes

144 Nursing care Frequent neuro assessment of course!
Bleeding risk assessment Skin Bowel Bladder Lungs Musculoskeletal Psychological assessment

145 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


147 Thanks. Barb Bancroft, RN, MSN, PNP

148 Selected Bibliography
STROKE 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.

149 Selected Bibliography
Johnston SC, et al. National Stroke Association Guidelines for the management of transient ischemic attacks. Ann Neurol. 2006; 60(3): 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): Kang JH, Ho JD, Chen YH, Lin HC. Increased risk of stroke after a herpes zoster attack. A population-based follow-up study. Stroke October 8, 2009.

150 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)

151 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):

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