At the conclusion of this activity, participants will be able to: 1. Classify different etiologies of ischemic stroke

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Lambert Hopkins
5 years ago
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1 Alan Dobson MD

2 At the conclusion of this activity, participants will be able to: 1. Classify different etiologies of ischemic stroke 2. Identify different approaches for recanalization for ischemic stroke 3. Recognize signs and symptoms of ischemic stroke and common missed stroke syndrome and stroke mimics

3 I Have No Conflicts of Interest to Disclose

4 Term refers the sudden onset of symptoms from the Stroke of God s Hand Stroke is a sudden onset of neurological signs and symptoms from either focal cerebral ischemia or hemorrhage (older term apoplexy) By definition symptoms need to last for 24 hours. If symptoms are less and no damage to CNS found this is referred to as a Transient Ischemic Attack(TIA)

5 600,000 ischemic strokes and 100,000 hemorrhagic strokes per year in the US Leading cause of permanent disability in adults and 3 rd leading cause of death

7 Stroke distribution correlates with other vascular risk factors (DM, Obesity, Hypertension) in the Stroke Belt

Transient and sudden neurological dysfunction best explained by focal CNS ischemia without permanent damage lasting less then 24 hours Most TIAs are approx.

8 Transient and sudden neurological dysfunction best explained by focal CNS ischemia without permanent damage lasting less then 24 hours Most TIAs are approx minutes. Symptoms lasting more than a couple hours are likely due to a small stroke Risk for stroke can be calculated by using ABCD2-higest in first 90 days

10 Diagnosis of TIA is all in a detailed history of symptoms and signs Anterior circulation (Carotid) Ipsilateral Amaurosis Fugax Contralateral sensory or motor dysfunction Aphasia or hemianopsia(can also be posterior circulation) Posterior Circulation (Vertebral) Ipsilateral face contralateral body(crossed findings) Two or more of the following vertigo, diplopia, dysphagia, dysarthria, ataxia- Symptoms not acceptable as evidence of TIA Syncope, dizziness, confusion, or isolated - vertigo, diplopia, dysarthria, ataxia, or amnesia

11 Embolism 32% Lacunes 18.5% Hypertensive hemorrhage 15.5% Atherosclerotic thrombosis 12% Indeterminate 9.5% Other 8% Ruptured aneurysms and vascular malformation 4.5% Data from Boston City Hospital Autopsy study 1949 C.M. Fisher R.D. Adams

12 Cerebrovascular disorders mechanism/etiology

Usually present as sudden onset of symptoms Artery to artery emboli from atheromas or dissection, most commonly emboli can arise from the aorta and carotid for anterior circulation, or aorta,

13 Usually present as sudden onset of symptoms Artery to artery emboli from atheromas or dissection, most commonly emboli can arise from the aorta and carotid for anterior circulation, or aorta, subclavian or vertebral system for posterior circulation strokes Cardiogenic- (Atrial fibrillation, Valves, Endocarditis Mural Thrombus, Myxoma) Paradoxical emboli (from the venous system due to right to left shunting)-pfo Air and fat emboli from trauma or IVs

14 Atherosclerotic plaques causing atherothrombotic occlusion of large vessels Can have slower symptom onset and more waxing and waning then embolic events Most common locations are areas of turbulent flow such as: Origin of internal carotid artery-amenable to CEA Cavernous Carotid artery-not amenable to CEA Vertebral artery at the junction with basilar artery Proximal middle cerebral artery Posterior cerebral artery Anterior cerebral artery Microhyalinosis causing gradual thrombosis of small angiographic invisible penetrating arteries causes lacunar strokes Most common locations for lacunar strokes- Basil ganglia, Pons, Cerebellum, deep white matter of the hemispheres-are these the white matter changes seen in older hypertensive patients?

Mitochondrial disorders such as MELAS can cause cell death from cellular level energy failure Prolonged seizures can cause cell death from glutamate induced

15 Mitochondrial disorders such as MELAS can cause cell death from cellular level energy failure Prolonged seizures can cause cell death from glutamate induced excitotoxicity Anoxia, carbon monoxide poisoning, severe hypoglycemia and other metabolic problems Migraines usually with aura and can cause stroke-focal vasospasm?

16 Sinus Thrombosis (Thrombosis of cerebral venous outflow PRES(Posterior Reversible encephalopathy Syndrome) Cerebral Vasoconstriction

17 Occlusion of the dural venous sinus (superior sagittal, internal cerebral veins, transverse/sigmoid) accounts for approx.. 1% of all strokes and commonly missed and treatable Can present with headaches, papilledema, 6 th nerve palsy, increased ICP or focal neurological deficits Can produce venous infarctions or intracranial hemorrhages from venous congestion frequently bilateral Can occasionally be seen on CT by looking for increased density of the sinuses. Best found on MRI or dedicated MRV Treatment is with anticoagulation or rarely intrasinus intervention (TPA, mechanical clot extraction) More common after dehydration, hypercoagable disorders and in the peripartum period

19 Syndrome of loss of normal autoregulatory control of cerebral blood flow. Believed to affect the posterior circulation preferentially Classic history is rapid change in BP causing confusion and vision problems(cortical blindness) Can also occur with pregnancy as well as in patients treated with VEGF inhibitors MRI can show edema and in severe cases irreversible infarction (restricted diffusion) Treatment is controlling blood pressure and symptoms usually resolve within two weeks but could persist if infarction occurs

20 34 y/o female with amnesia and blindness with preeclampsia and methamphetamine use 56 y/o male treated with Avastin for CLL with confusion and vision problems

21 Best described in patient with aneurysmal Subarachnoid hemorrhage Patients develops spasms of cerebral vasculature causing focal ischemia In aneurysmal subarachnoid patients treated with hypervolemia, hypernatremia and hypertension as well as Calcium channel Nimodipine or catheter intervention Can also occur in the peripartium period, migraine patients, and patients exposed to vasoactive compounds (SSRI, SNRI, nicotine, triptans, etc.) Cerebral vasospasm usually resolves within two months

22 MRI shows Left Posterior inferior Cerebellar Artery Stroke(PICA) Marked narrowing of vertebral arteries and basilar arteries

23 Todds paralysis after focal seizure (transient cerebral dysfunction after seizure) Migraine can cause a variety of focal neurological deficits (vision, parasthesia, hemiplegia, confusion, aphasia) Conversion reaction *Cervical spine problems (may be unilateral early on but should spare cranial nerves) Metabolic derangements (glucose, hepatic, uremia, hypercapnia, periodic paralysis) Worsening of old stroke symptoms with infection Peripheral vertigo Masses such as tumors or intracranial abscess

24 Named after Robert Todd Irish Neurologist in 1849 Is due to persistent focal cerebral dysfunction (hemiparesis, hemanopsia, aphasia etc.)usually more common after a focal motor seizures. History of LOC and rhythmic movements can be helpful in detecting Todd's Paralysis Usually resolves within 36 hours

25 Patient can have focal neurological deficits before, after or without onset of headaches Most common deficits are scotomas, confusion or parsthesia that begin in hands or lips and progress in somatotopic fashion. However any neurological deficits can be a result of migraine History of recurrent stereotyped episodes with negative MRIs should raise suspicion for Migraines Neurological deficits believed to be due to spreading cortical depression and careful history might reveal symptoms spread in somotopic fashion

26 Usually hereditary disorder characterized by recurrent episodes of transient hemiplegia Caused by a variety of genetic channelopathies of sodium channel genes that can also have progressive neurological symptoms (episodic ataxia, Spinocerbellar ataxia type 6, etc.) Best characterized gene are CACNA1A, ATP1A2, SCN1A which genetic testing is available Sometimes responds to verapamil or acetazolamide

27 Can be due to structural lesions (disk, abscess, tumor), vascular disease (Stroke, AVMs, Dural AV fistula) or inflammation (transverse myelitis, infections) Key physical exam finding are sensory and myotomal level with sparing of cranial nerves. Can be asymmetric symptoms. Depending on chronicity might have upper motor nerve finding of hyperreflexia and Babinski

29 Salvaging viable brain tissue with therapies such as thrormobolysis and revascularization in acute period (IV TPA and intra-arterial therapy) Avoidance of post stroke complications (Cerebral Edema, DVT, Aspiration Pneumonia) Evaluation for rehabilitation Secondary Stroke prevention Addressing stroke risk factors

Every minute 2 million neurons die in a MCA stroke TPA Treatment within the first 90 minutes of onset increased the odds of an excellent outcome by 2.

30 Every minute 2 million neurons die in a MCA stroke TPA Treatment within the first 90 minutes of onset increased the odds of an excellent outcome by 2.6-fold In the 91- to 180-minute window by 1.6-fold In the 181- to 270-minute window by 1.3 fold Every 10 minutes in which therapy is delayed, one fewer of each hundred treated patients benefits.

32 Approved based on NINDS trial in 1995 Of 100 patients treated within the first 3 hours, 32 had a better outcome as a result and 3 had a worse outcome compared to placebo Number needed to treat for minimal or no disability at follow up compared to placebo was 8 ECASS hour window had about ½ benefit with a similar number needed to harm

5 hours, patients who receive TPA sooner generally have lower bleeding risk and greater chances of recovery

33 IV TPA has been FDA approved since 1996 for up to 3 hours after last time patient seen well ECASS III showed benefit in select patient up to 4.5 hours While it can be given up to 4.5 hours, patients who receive TPA sooner generally have lower bleeding risk and greater chances of recovery Intra-arterial therapy is available at UNM 24/7 and generally can be used up to 6-24 hours in patients with large vessel occlusion (Internal Carotid, Basilar artery, Middle Cerebral Artery)

34 Oral anticoagulant use Major surgery or serious trauma in previous 14 days Administration of heparin within 48 hrs and an elevated PTT at Presentation or upper limits of normal Pregnancy Age less then 18? Stroke or intracranial surgery in last 3 months

35 IV TPA has poor recanalization rates for large vessel disease Multiple randomized trial have shown clear benefit compared to IV TPA alone Mechanical embolectomy in general double the chance of independent living (modified Rankin less then 3 compared to IV TPA Is now considered standard of care for large vessel strokes NIH scale greater then 8 can help predict patients with large vessel occlusion

37 Improved rates of recanualization compared to older devices Allows immediate restoration of blood flow to ischemic tissue

38 Solitaire Trevo

39 M R CLEAN First large trial in 2016 which showed clear benefit of mechanical revascularization over TPA for symptoms less then 6 hours DAWN trial-preliminary data shows benefit up to 24 hours out in select patient with large Bessel occlusion After 20 years finally catching up to the cardiology data for catheter therapy

40 Aspiration Pneumonia is common after stroke due to a variety of issues Decreased Level of Consciousness Weakness of oral and pharyngeal musculature Weak cough All stroke patients need to have dysphagia screen performed before POs given and have the swallowing function monitored. If any doubt have patient made NPO until seen by speech therapy

41 Why even get an MRI I know my patient has a Stroke MRI can help clarify if symptoms are from a stroke or one of the mimics Localization to know which vascular territory (the 60% carotid stenosis is asymptomatic if stroke is in the occipital lobe unless patient has a fetal PCA) Size and location of infract can help determine etiology- lacunar stroke from microvascular disease or bilateral embolic stroke from aorta or heart Size and location can help determine prognosis and other associated symptoms: memory problems from hippocampal damage or executive problems from frontal or parietal lobe

42 CT most commonly and easily available tool. However, it is associated with radiation exposure. In addition early strokes, small strokes and posterior fossa strokes can be missed MRI(without contrast) is best study as it can show almost all ischemic strokes (small brain stem strokes can still be missed). MRI also visualizing intracranial vessels by viewing the normal flow voids Acute Strokes less then 14 days usually show as areas of restricted diffusion on Diffusion weighted Imaging sequence (DWI) and ADC map

44 Can help detect patient with internal carotid narrowing >50% that might benefit from carotid endarterectomy Can be useful in finding dissection which is usually treated with anticoagulation Aortic dissection and hematomas can present with stroke as first symptoms Rare disorders like fibromuscular dysplasia and moyamoya, cerebral vasospasm might be detected by vascular imaging

45 Usually dramatic presentations-not the stroke patients try to sleep off High NIH Stroke scale (greater then 10) If not recognized and treated 80% of patients can not live independently Left MCA -Global aphasia, Right sided hemiplegia Right MCA-Neglect, gaze deviation left hemiplegia Basilar-Cranial nerve findings, ataxia, obtundation

46 Right hemiplegia Global Aphasia Right hemianopia Left gaze Preference Right hemianopia No response to pain on right

47 No Aphasia but some dysarthria Left hemiplegia Profound Right gaze preference Profound Neglect (frequently will deny any problems) I m OK despite severe neurological deficits No response to pain on left

49 DENSE MCA SIGN COMPLETED INFARCT

50 One basilar artery formed by confluence of the two vertebral arteries Common symptoms include Bilateral weakness and sensory loss Crossed finding (Cranial nerve on one side, weakness or sensory loss on contralateral side) Diplopia and vision loss (hemianopia, cortical blindness) Ataxia Severe dysarthria but not aphasia Lethargy with progression to coma and posturing Symptoms can progress over days and if left untreated is 99% fatal

53 Sudden onset of hemiplegia is rarely missed by many stroke cause no focal weakness Wallenberg or lateral medullary infarct-sudden onset of dysphagia Wernicke aphasia-sudden onset of receptive aphasia with fluent speech Cerebellar hemispheric strokes-sudden onset of vertigo nausea and vomiting

54 Adolf Wallenberg German neurologist described in early 20 th century this common brain stem stroke syndrome No weakness but has the following: Ipsilateral facial numbness(cn V) Ipsilateral ataxia, nystagmus and vertigo (cerebellar tracts and vestibular nuclei) Ipsilateral paralyzed palate (CN X ) Contralateral decreased pain and temperature but intact light touch vibration (spinothalamic track) Hiccups (medullary hiccup center), Horner's (descending symphatic fibers) Frequently missed as thought to be GI, however, sudden onset as well as Horner's, facial numbness and loss of pain and temperature key findings Dysphagia can be debilitating and almost half require G tube

55 Infarction of lateral medulla in distribution of Posterior Inferior Cerebellar Artery (PICA) Frequently associated with vertebral artery disease

56 Usually present with sudden onset of vertigo, intractable nausea and ataxia Ataxia might be subtle but can usually be picked up by gait exam, dysmetria with finger to nose and finger chase. Would have low threshold for MRI in patient with sudden vertigo, nausea and intractable vomiting

57 Wernicke aphasia, fluent aphasia, receptive aphasia-usually parietal temporal lobe region mostly embolic in nature No weakness but has impaired comprehension and fluent but frequently paraphasic speech(semantic errors, neologisms Carefully examination might show a hemi or quandratopsia Frequently misdiagnosed as confused or psychotic Key features are that the symptoms occurred suddenly and patient can follow non verbal commands (pantomime) with good attention

58 A problem of language not of cognition In isolation is a frequently missed stroke symptom Often patients are labeled confused or psychiatric diagnosis considered Need to determine if difficulty with speech is from dysarthria, confusion or a true language problem

60 Also know as Wernicke, Sensory, fluent or posterior aphasia Presents with fluent speech but nonsensical. Occasional stock phrases can be clear (yes, no thank you, profanity) Does not follow verbal commands but can follow nonverbal communications (gestures) Need to check visual fields as can be associated with hemianopia or quandratopsia given proximity to optic radiations

62 Also know as Broca, Motor, anterior or nonfluent aphasia Presents with decreased spontaneous speech and intact comprehension May be able to repeat (transcortical motor aphasia) typically patients are not able to write May be associated with facial droop or tongue deviation given proximity to motor strip Slow stuttering speech is almost never due to ischemic stroke

factor Untreated sleep apnea should also be treated Antiplatelet

64 Hypertension is the largest modifiable stroke risk factor Hyperlipidemia should be treated Diabetes is major stroke risk factor Untreated sleep apnea should also be treated Antiplatelet should be given to decrease risk for ischemic stroke and treat comorbid cardiac conditions

65 Up to 20% of patient without a clear cause of stroke(cryptogenic) are believed to have occult afib Detection of atrial fibrillation in a patient with stroke markedly change management Paroxysmal atrial fibrillation can be difficult to detect and average length of cardiac monitoring for detection of atrial fibrillation is 4 months

$Permissive hypertension up to 220/120 is allowed for the first several days to allow perfusion of viable tissue at risk for infraction (ie, Penumbra of the stroke) In patient with large vessel$

66 The largest modifiable stroke risk factor All patient with ischemic stroke should be treated for uncontrolled hypertension ACE inhibitors and ARB with diuretics are usually first line therapy Permissive hypertension up to 220/120 is allowed for the first several days to allow perfusion of viable tissue at risk for infraction (ie, Penumbra of the stroke) In patient with large vessel occlusion (carotid, vertebral) might benefit from longer period of HTN

respond to osmotic agents (mannitol and 3% saline)-would avoid hypotonic fluids(d5 1/2NS) Large middle cerebral artery infarcts in young

67 Cytotoxic edema from cell death can cause significant mass effect and damage normal brain tissue by herniation and secondary ischemia in large ischemic strokes Usually peaks at 3-5 days after an ischemic stroke Cytotoxic edema does not respond to corticosteroids but may respond to osmotic agents (mannitol and 3% saline)-would avoid hypotonic fluids(d5 1/2NS) Large middle cerebral artery infarcts in young patient or posterior fossa strokes (cerebellum) might warrant prophylactic hemi-craniectomy to prevent further damage and life threating herniation

69 DVT Seizures Pneumonia Spasticity-usually develops several months after damage to corticospinal tract Can be treated with baclofen, tizandine, splinting, ROM and Botox. Thalamic pain syndrome-painful parasthesia that develop after damage to thalamus-treated with neuropathic pain meds (TCA, gabapentin, etc.)

70 Discharged on Antithrombotic VTE Prophylaxis Stroke Education Discharged on lipid lowering Medication if LDL greater then 100 Ischemic Stroke-Assessed for Rehabilitation Patients with afib discharged on anticoagulant Patient who present within 2 hours evaluated for Thrombolysis Door to needle time less than 60 minutes Dysphagia screen done before any POs given (including ASA) NIH stroke scale done in first 24 hours

71 USES Standardized scoring system for patients with ischemic stroke Good interrater reliability All patient will have NIH stroke scale on admission and during hospitalization Allows objective determination of severity of stroke Points given for weakness, aphasia, ataxia, neglect, cognition, vision, sensory changes etc MORE POINTS LARGER DEFICITS 0= no stroke 1-4= minor stroke 5-15= moderate stroke 15-20= moderate/severe stroke 21-42= severe stroke Training available from American Heart Association

72 Patients with aneurysmal subarachnoid hemorrhage (patients do better when treated at aneurysm center) Patients with significant intraventricular hemorrhage Patients needing intra-arterial therapy Patients that might need decompressive craniectomy -patients with large posterior fossa stroke (cerebellum) or large MCA strokes in younger patients

73 Evaulate patient and obtain time last seen well (not when the symptoms where discovered) Order labs(cbc, Chem, PT, PTT, CBG, and non contrast head CT, page rad tech) Contact neurology via dedicated stroke pager Review TPA contraindication and CT + labs Consider CTA head and neck for large strokes

74 All patients with acute ischemic stroke should be evaluated for TPA if presents within 4.5 hours Patients with clinical suspicion for large vessel occlusion should be evaluated for IA therapy Patients should be screened for causes of stroke, receive education and secondary prevention (Hypertension, Hyperlipidemia, DM, Afib etc) Appropriate rehab and follow up needed

Stroke School for Internists Part 1

Stroke School for Internists Part 1 November 4, 2017 Dr. Albert Jin Dr. Gurpreet Jaswal Disclosures I receive a stipend for my role as Medical Director of the Stroke Network of SEO I have no commercial