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ALISON SMOCK, MD DEPARTMENT OF NEUROLOGY MEDICAL UNIVERSITY OF SOUTH CAROLINA ischemic stroke.

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Presentation on theme: "ALISON SMOCK, MD DEPARTMENT OF NEUROLOGY MEDICAL UNIVERSITY OF SOUTH CAROLINA ischemic stroke."— Presentation transcript:

1 ALISON SMOCK, MD DEPARTMENT OF NEUROLOGY MEDICAL UNIVERSITY OF SOUTH CAROLINA ischemic stroke

2 definitions Transient ischemic attack  A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction  Tissue-based definition rather than time-based definition Stroke  Infarction of the central nervous system  May be symptomatic or silent  May not be evident by MRI Stroke. 2009;40:

3 epidemiology Transient Ischemic Attack  Estimated prevalence of self-reported physician-diagnosis TIA is approximately 2.3% (translates to ~5 million people)  Incidence of TIA increases with age and varies by sex and race/ethnicity  Men, blacks, and Mexican Americans have higher rates of TIA their their female and non-Hispanic white counterparts  Approximately 15% of all strokes are heralded by a TIA  10-15% of patients have a stroke within 3 months, with half occurring within 48 hours Circulation. 2013;127:e6-e245 Stroke. 2009;40:

4 epidemiology TIA  ABCD2 score  Clinical score to determine the risk for stroke within the first 2 days following a TIA AgeBPClinical FeaturesDurationDiabetes 1 point≥ 60SBP ≥ 140 OR DBP ≥ 90 Speech disturbance without unilateral weakness minYes 2 points-- Unilateral weakness with or without speech impairment ≥60 min-- Lancet. 2007;369:

5 epidemiology ABCD2 score2-day stroke riskComment %Hospital observation may be unnecessary without another indication (ie new onset Afib) %Hospital observation justified in most situations %Hospital observation worthwhile Lancet. 207;369:

6 epidemiology Stroke prevalence  Estimated 6.8 million Americans ≥20 years of age have had a stroke ( data)  Overall stroke prevalence during this period is an estimated 2.8%  Older adults, blacks, people with lower levels of education, and people living in the southeastern United States had higher stroke prevalence Circulation. 2013;127:e6-e245

7 epidemiology Stroke incidence  Each year, ~795,000 people experience a new or recurrent stroke (610,000 are first attacks, 185,000 are recurrent)  Of all strokes, 87% are ischemic, 10% are ICH, 3% are SAH  Each year, ~55,000 more women than men have a stroke  Women have a higher lifetime risk of stroke than men  Women have a lower age-adjusted stroke incidence than men  White women yo have lower stroke risk than white men, but women >85 yo have elevated risk compared to white men  Analysis of data from FHS and GCNKSS suggests that stroke incidence is declining over time Circulation. 2013;127:e6-e245

8 epidemiology Stroke mortality  In 2009, stroke accounted for 1 of every 19 deaths in the US  When considered separately from other CVDs, stroke ranks No. 4 among all causes of death  From 1999 to 2009, the annual stroke death rate decreased 36.9% and the actual number of stroke deaths declined 22.9% Circulation. 2013;127:e6-e245

9 epidemiology Circulation. 2013;127:e6-e245

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11 Circulation. 2013;127:e6-e245

12 so why does it matter? Disability  Stroke is the leading cause of serious long-term disability in the United States  In the NHLBI’s FHS, among ischemic stroke survivors who were ≥65yo, the following disabilities were observed at 6 months after stroke:  50% had some hemiparesis  30% were unable to walk without some assistance  46% had cognitive deficits  35% had depressive symptoms  19% had aphasia  26% were dependent in ADLs  26% were institutionalized in a nursing home Circulation. 2013;127:e6-e245

13 etiology

14 etiology of ischemic stroke TOAST criteria  Thrombosis or embolism due to atherosclerosis of a large artery  Embolism of cardiac origin  Occlusion of a small blood vessel  Other determined causes  Dissection  Aneurysm  Vasculitis  Undetermined cause (cryptogenic or incomplete investigation)

15 traditional other Hypertension Hyperlipidemia Diabetes mellitus Smoking Coronary artery disease Heart failure Cardiac arrhythmias Chronic kidney disease Physical inactivity Drug use History of prior stroke Family history Underlying rheumatologic disease Hypercoagulable states CNS infection Sepsis Sleep apnea risk factors Circulation. 2013;127:e6-e245

16 etiology and presenting symptoms Large vessel strokes (ICA, MCA, ACA, PCA)  Cardio-embolic  Atherosclerosis  Artery-artery embolism  Dissections  Aneurysms Small vessel strokes  Uncontrolled hypertension  Uncontrolled diabetes  Uncontrolled hyperlipidemia  Smoking  Sympathomimetics

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18 Carotids

19 Internal Carotids and MCAs

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21 Circle of Willis

22 large vessel stroke syndromes – cortical MCA – dominant hemisphere  Contralateral hemiparesis (face/arm > leg)  Contralateral hemisensory changes  Head and eye deviation toward stroke  Contralateral hemianopia  Language difficulty  Alexia  Agraphia  Acalculia  Apraxia

23 large vessel stroke syndromes – cortical MCA – non-dominant hemisphere  Contralateral hemiparesis (face/arm > leg)  Contralateral hemisensory changes  Neglect/extinction  Anosognosia  Loss of prosody of speech  Flat affect ACA  Crural paresis > arm paresis  Frontal signs (eg, abulia)

24 large vessel stroke syndromes – cortical Posterior Circulation ECVA/ICVA Dizziness/Vertigo Cranial nerve lesions Cerebellar symptoms  PCA Homonymous hemianopia Hemisensory changes (lateral thalamus) Left PCA – alexia without agraphia, Gerstmann (acalculia, agraphia, finger agnosia, R/L disorientation) Right PCA – prosopagnosia, visual neglect Bilateral – cortical blindness (Anton’s syndrome)

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26 large vessel stroke syndromes – cortical Basilar artery  Typically presents as ischemia in the pons  Asymmetric but bilateral motor and reflex abnormalities  Bulbar involvement  Respiratory involvement  “Tip of the Basilar”  Decreased LOC  Oculomotor/pupillary abnormalities

27 small vessel stroke syndromes – subcortical Pure motor  Corona radiata, posterior limb of the internal capsule, pons, medulla Pure sensory  Thalamus Sensorimotor  Thalamus, basal ganglia Ataxic hemiparesis  Corona radiata, anterior limb of the internal capsule Dysarthria-clumsy hand syndrome  Upper pons, junction between CR and IC

28 acute stroke

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30 FDA approved options (r)tPA (recombinant) tissue plasminogen activator – Gold Standard  Approved for use within 3 hours of onset of neurologic deficits in a defined population of patients Aspirin 325mg  Approved for use in patients who do not receive tPA who do not have any contraindications (drug allergy) and 24 hours after receiving tPA if there is no hemorrhage on 24h post-tPA CT/MRI scan

31 tPA mechanism of action

32 tPA – evidence based medicine National Institute of Neurological Disorders and Stroke (NINDS) tPA Trial  NEJM.1995;333: European Cooperative Acute Stroke Study (ECASS) I  JAMA 1995;274(13): ECASS II  Lancet. 1998;352(9136): ECASS III  NEJM. 2008;359:

33 tPA What do you need to give IV tPA  Last known normal  Focal neurologic deficits by physical examination  Non-contrasted head CT  Finger stick blood glucose

34 thrombectomy Indications  Large vessel strokes (even after receiving IV tPA)  Outside of the window for IV tPA  Imaging suggestive of penumbra Contraindications  Matched deficit on CTP

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37 stroke = brain attack Why should you call a BAT  Sudden development of focal neurologic findings Why you should NOT call a BAT  Altered mental status (without focal neurologic findings)  To get a faster head CT Who gets paged – it is an emergency after all…  Neurology residents on call  All vascular neurology attendings  All NSICU attendings  All neuroradiology attendings  On call radiology residents  All neurointerventional radiologists  NIR techs and nurses  CT techs  NSICU, 9E and 9W charge nurses

38 stroke = brain attack What information is helpful to us?  Last known normal  Symptoms that prompted the BAT  Reason for admission  Current medications  Current labs – including finger stick  Recent vitals  DNR/DNI status

39 MUSC policy for calling a BAT Altered mental status  MET is called first, then the MET resident can determine if a BAT is warranted  “If an in-patient is experiencing a change in mental status or confusion the Medical Emergency Team (MET) should be paged to the bedside to assess the patient – not the Brain Attack Team!”  “Once the Medical Emergency Team (MET) has assessed the patient and determines that a BAT should be called, at that time the BAT will respond.”

40 VA policy for calling a BAT Regular hours (730a-530p weekdays)  There is always a neurology resident in house, simply page them After hours  If there is an inpatient that has stroke-like symptoms, the upper level medicine resident is expected to evaluate the patient (ie NIHSS), speak with the neurology resident on call if there is concern for acute stroke and the neurology resident will help direct care while going over to the VA

41 standard inpatient work up Neuroimaging  24 hour post tPA scan  MRI if indicated  Vessel imaging  CTA vs MRA vs carotid dopplers Labs  A1c, lipids, UA, UDS  When are TFTs indicated  When is B12/folate/RPR indicated TTE  Agitated saline? PT/OT/SLP consults

42 primary prevention

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44 non-modifiable risk factors Age  Risk of ischemic stroke and ICH doubles for each successive decade after age 55 Gender  More prevalent in men than in women Low Birth Weight Race/Ethnicity Genetics  A meta-analysis of cohort studies showed that a positive family history of stroke increases risk of stroke by approximately 30% [OR 1.3; 95% CI, 1.2 to 1.5, P < ]  Cardioembolic stroke is the least heritable type of stroke compared with other ischemic stroke subtypes

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46 modifiable risk factors Hypertension Cigarette smoking Diabetes Dyslipidemia Atrial fibrillation Other cardiac conditions Asymptomatic carotid stenosis Sickle cell disease Postmenopausal hormone therapy Oral contraceptives Diet and nutrition Physical inactivity Obesity and body fat distribution

47 secondary prevention

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49 modifiable risk factors Hypertension  <120/80 Diabetes  A1c <7% Lipids  LDL-c <70mg/dL  Treatment with niacin or gemfibrozil in patients with low HDL-c Cigarette smoking  Advisement to quit  Avoid environmental/passive smoking  Cessation Physical activity

50 interventional approaches to patients with large artery atherosclerosis Symptomatic extracranial carotid disease  CEA recommended if:  Patients with recent TIA or ischemic stroke within the past 6 months and ipsilateral severe (70-99%) stenosis  Patients with recent TIA or ischemic stroke and ipsilateral moderate (50-69%) stenosis, depending on patient-specific risk factors (age, sex, comorbidities)  Indicated for patients with TIA or stroke, surgery within 2 weeks is reasonable rather than delaying surgery  CAS indicated if:  Alternative to CEA for symptomatic patients at average or low risk of complications associated with endovascular intervention with ICA stenosis >70%

51 interventional approaches to patients with large artery atherosclerosis Extracranial vertebrobasilar disease  Optimal medical therapy  Endovascular and surgical treatment of patients with EVS may be considered if refractory to medical therapy

52 interventional approaches to patients with large artery atherosclerosis Intracranial atherosclerosis  Stroke or TIA due to 50-99% stenosis of a major intracranial artery, aspirin preferred over warfarin  90 days ASA 325mg and Plavix 75mg, then ASA monotherapy thereafter  No indication for dual antiplatelet therapy beyond 90 days  ASA = Plavix = Aggrenox … except for side effect profile and cost  Aggressive medical management  BP <140/90 mmHg  Total cholesterol <200 mg/dL  Angioplasty and/or stent placement is not warranted and considered investigational

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