Cerebrovascular DiseaseA clinical approach ROBERT CONI, DO

Objectives

The participant should be able to:

Learn to take an appropriate stroke history and use that data to define the stroke syndrome.

Apply examination findings to stroke localization.

Be able to choose an appropriate imaging procedure to confirm a diagnostic impression.

Develop and apply an approach to the categorization of cerebrovascular diseases and then be able to apply an appropriate evaluation schema.

Understand the ecology of cerebrovascular diseases and be able to apply that knowledge in initial dx and then to secondary stroke prophylaxis.

What we will cover

The stroke syndrome, a definition

Diagnosis of stroke

Confirmation of a diagnosis

Evaluation of stroke patients

Treatment options

The stroke syndrome

Stroke

Syndrome is defined by a rapid onset of a focal neurological deficit which lasts greater than 24 hours.

TIA

Syndrome defined by a rapid onset of a focal neurological deficit which lasts less then 24 hours and resolves completely.

No imaging abnormality

Amaurosis fugax

Other definitions:

Stroke in evolution (or progressive stroke): a worsening of the focal neurological deficit over time.

Completed stroke: The deficit does not worsen over time and becomes fixed.

Presumptive Dx of Stroke

HISTORY

ECOLOGY

EXAMINATION AND LOCALIZATION

History taking in stroke

Purpose: Determining the mechanism of the stroke

Determining the location of the stroke

Factors helpful at defining mechanism: Activity at onset of symptoms

Temporal course of deficit progression

Accompanying symptoms

Anterior vs posterior circulations

Cortical vs subcortical

Cardiovascular

Prior cerebrovascular symptoms

Examination of heart and vascular system and eyes

Factors in localizing the stroke: Neurological examination

Evaluate signs and symptoms

Evaluate imaging procedures and vascular procedures

Ecology of stroke

Risk factor analysis

Demographics

Ecology of stroke

Non-modifiable risk factors Age

Gender

Ethnicity

Fam Hx

Prior stroke

Modifiable risk factors Hypertension

Cholesterol

Diabetes

Tobacco use

Inactivity

Excessive ETOH use

OSA

Stress

Birth control

Examination and LocalizationQuick review of stroke syndromes

Common Carotid / ICA

Variable presentation; borderzone or watershed infarct

MCA

Contralateral weakness/sensory loss and hemianopia; dominant vs or nondom hemisphere signs; eye deviation

ACA

Weakness (and/or sensory loss) of contralateral foot > leg >> arm

PCA

Contralateral vision loss and possibly cortical blindness; dominant hemisphere language

Vertebral Artery

PICA / Wallenberg syndrome

Basilar Artery

Weakness x 4; CB ataxia; diplopia; dizziness; nystagmus; blindness; coma

Clinical application – Case study one

JV was a 69 yo man, RH, brought to the ED with sudden left sided weakness which developed while shopping at Kroger. He states his left leg gave out on him and he fell. Also he felt he would pass out. He could not get himself off the floor and EMS was called. This occurred about 25 to 30 mins before presentation. He relates a past hx of DM and HTN.Database: Blood glucose was 109; BP 155/85Neurologic examination: Follows commands and gives a clear hx; Lt face droop and VF loss without language or speech loss; Left hemiataxic paresis; Lt sensory absence all modalities and left sided neglect.What else do you want to know?

CT – Negative, NIHSS – 10, No thinners, PT: 10.5 (INR_1.1), PTT: 32.8, Plts: 187Where is this lesion?What is the appropriate treatment at the time of presentation?

NIHSS

A 15-item neurologic examination stroke scale used to evaluate the effect of acute cerebral infarction on:

the level of consciousness and awareness

language

neglect

visual-field loss

extraocular movements and gaze

motor strength

ataxia

dysarthria

sensory loss

A trained observer rates the patent’s ability to answer questions and perform activities. Ratings for each item are scored with 3 to 5 grades with 0 as normal, and there is an allowance for untestable items. The single patient assessment requires less than 10 minutes to complete. 

The evaluation of stroke severity depends upon the ability of the observer to accurately and consistently assess the patient.

Case one

The patient went on receive IV rt-PA.

He had a CTA which showed an occlusion of a posterior MCA branch.

Clinical application – case two

KC was a 57 yo RH man working as a custodian cleaning a school when he suddenly collapsed. He had trouble getting up and was noted to have Rt hemiparesis with “confusion”. He was transported to our hospital where he was noted to have nonsensical speech with paraphasic errors and Rt hemiparesis. His EKG showed a sinus rhythm. His BP was 200/115 in the left arm and 185/85 on the right.

Where is the lesion?

What is the likely mechanism?

What would you do?

His CT showed a dense Lt MCA sign. What now?

Case two

CTA

Lt ICA Occlusion with Lt M2 posterior branch obstruction and a significant penumbra

The patient received rt-PA and then was sent to MUSC for endovascular intervention

Confirming the Diagnosis

DIFFERENTIAL DIAGNOSIS OF STROKE IMAGING PROCEDURES IN STROKE

Differential diagnosis

Step one is ascertaining if the s/s meet the “stroke syndrome” definition

Next one must differentiate ischemic from hemorrhagic strokes

Finally one must identify the stroke subtype:

Large artery vs small artery

Embolic vs thrombotic

Consider other vascular events:

Arteritis

Cortical venous occlusions

Dissections

Stroke mimics – misdiagnosis has been estimated at about 13%

Stroke mimics

Most common misdiagnosis occurs from unwitnessed or unrecognized seizure with postictal state and/or postictal Todd’s paralysis.

Tumors

Multiple sclerosis

Encephalitis

Vertigo

Hepatic encephalopathy

Radial nerve palsy / Bell’s palsy

Hypoglycemia

Migraine

Metabolic encephalopathy

Functional hemiparesis

Imaging in stroke

Imaging is used to:

Exclude hemorrhage

Determine the vascular insult and identify the stroke subtype

Assess the degree of brain injury

Advanced techniques can be used to determine the volume of injury and of salvageable brain tissue

Initial technique is the CT scan

Imaging in stroke

The early CT scan: Usually does not clearly show stroke within first 24 hours

However, in an analysis of several studies some radiologic signs can be seen early, after 6 hours:

Hypoattenuation in a portion of the MCA distribution

Obscuration of the lentiform nucleus

Cortical sulcal effacement

Hyperdense MCA sign (or other large vessel)

Focal parenchymal hypoattenuation

Loss of the insular ribbon or sylvian fissue

Loss of gray-white differentiation in basal ganglia

Imaging in stroke

CTA – better resolution than MRA

Can obtain perfusion imaging to identify penumbra but there is no clear utility to this technique currently

MRI:

In stroke we include DWI and a sequence for detecting extravasated blood

MRA can overestimate stenosis

Can obtain perfusion / diffusion scans for mismatch to identify penumbra but again no clear advantage as yet identified.

Evaluation of the Patient

VASCULAR DISEASE RISK FACTOR ASSESSMENT

Stroke workup

Labs: PT/PTT; anticardiolipin ab and thrombosis w/u if elevated PTT or young patient

Homocysteine

HgbA1c

Fasting lipid panel

CBC and Platelet count

C-RP and ESR

Chemistries

Consider blood cultures in cardioembolic stroke

MRI: as stated previously, can aid differentiation of TIA from stroke. Review the DWI studies. When MRI is not possible, repeat CT for changes at 24 to 48 hrs

Stroke workup

Carotid artery study: to exclude symptomatic stenosis Duplex ultrasound

CTA or MRA

Seeking degree of stenosis

In patients with severe, symptomatic carotid stenosis, CEA achieves a lower rate of stroke or death than carotid stenting.

Severe stenosis is 70%

In patients with asymptomatic stenosis, medical therapy achieves low death/stroke rates

Cardiac studies: to exclude cardioembolic source ECG

Trans thoracic ECHO

Trans esophageal ECHO

Telemetry and event or holter monitors

Other orders and discharge considerations

Therapy assessments: PT/OT/SLP

If the patient fails the nursing swallow assessment, make pt NPO

Document considerations for rehabilitation

Case management consultation

Consults: Neurology; consider Cardiology and PM&R

Secondary prophylaxis

Antiplatelet agents vs anticoagulants

Statin

Control hypertension

DVT prophylaxis – antithrombotic boots / low dose anticoagulation

Diabetes control; diabetic teaching

Stroke teaching – emphasizing low Na and fat diet, regular exercise

Smoking cessation

Immunizations – influenza and pnemonia

Treatment of the patient

ACUTE THERAPIES

SECONDARY STROKE PROPHYLAXIS

Acute therapies

“Time is brain”

rt-PA

given IV

Given IA

Interventional endovascular approaches

When the patient is out of the t-PA window but within a 6(-8) hr window post stroke

In these cases, perfusion images via CTA or diffusion-perfusion via MRI can give objective evidence of viable penumbra before embarking

In cases of larger vessel occlusions and dense radiographic vessel signs on CT

Secondary stroke prevention

What is at risk?

Often patients are not meeting benchmarks for secondary stroke prevention

There is a 30% risk of stroke recurrence over the first 5 years

800,000 stroke a year of which, 25% or about 185,000 are recurrent events.

20% occur within 30 days and lead to readmissions with increased morbidity and mortality

What percentage of patients who have had a stroke receive all of the appropriate recurrent stroke preventative measures?

1) 10 %

2) 30 %

3) 50 %

4) 70 %

5) 90 %

Secondary stroke prevention

With intensive risk factor and antithrombotic recurrent stroke preventative management, what relative risk reduction for subsequent major vascular events may be achieved?

1) 40 - 50%

2) 51 - 60%

3) 61 - 70%

4) 71 - 80%

5) 81 - 90%

What are these factors?

Diet and BG control; exercise; ASA; statin tx; BP control

Risk factor control

Hypertension

Hypertension is the single most important modifiable risk factor for both hemorrhagic and ischemic strokes

Affects 1/3 of adults in the USA: 140/90 or greater

Another 30% have “prehypertension”: Systolic between 120-139 and 80-89 diastolic

Every 10 mm Hg reduction in BP gives a 33% risk reduction in primary prevention

In secondary prevention there is a 25% relative risk reduction with or without preexisting HTN

Elevated BP in the postacute phase is associated with recurrent stroke; the goal s/be 120-140/80-90

With DM or renal disease goal s/be < 130/80

In all cases, seek a 10 mm hg reduction in systolic pressure and 5 mm hg in diastolic

Risk factor modification

Dyslipidemia

25% of adults have elevated cholesterol

LDL is most associated with risk of CV disease, not HDL or triglyceride levels

LDL lowering is the primary goal of therapy

For each 39 mg/dl reduction in LDL, a 21% relative risk reduction in stroke risk was obtained.

Goal level has been < 100 mg/dl but recent changes for secondary stroke prevention made the goal less than 70 mg/dl

Studies have shown the most efficacy with atorvastatin and rosuvastatin

For low HDL levels, tx with Niacin may be considered despite lack of efficacy in cardiovascular risk

Risk factor modification

Diabetes Mellitus Defined as HgbA1c > 6.5%; affects 19 million in US but 90 million have prediabetes

Trials of aggressive tx for secondary prevention have not shown efficacy when targets are HgbA1c < 6.5

Targets thus are set at <7.0 using diet, exercise, and medications AND BP goals (less than 130/80) as well as statin LDL goals (less than 70)

During acute stroke, hyperglycemia > 140mg/dl during the first 24 hours post stroke is a poor prognostic indicator

We recommend treatment in acute stroke to keep glucose at a level < 180 mg/dl

Obstructive Sleep Apnea Associated with several physiologic changes: BP, cardiac hypertrophy, a fib

While data on RRR with CPAP are lacking, evaluation post stroke for OSA and treatment when found are recommended

Risk factor modification

Smoking Cessation

Relative risk of stroke in smokers was 2.3 in men and 3.1 in women in the Framingham study. Also there is a dose response relationship

Consider secondhand smoke a risk

After 5 years of not smoking risks return to nonsmoker levels

Physician counseling has some benefit (7.5% quit rate)but support groups and group counseling do better (20% quit rates)

Spontaneous quit rates are 3-5%

Consider nicotine replacement and bupropion or varenicline or even combinations which do best

Risk factor modification

Diet Fat

Cochrane Meta-analysis showed: Reduced dietary fat yielded a 14% reduction in CV events and the major contribution was reduced saturated fat

Sodium

Studies show a decrease below 1800 mg/day are associated with:

2 mm Hg systolic and 1 mm Hg diastolic bp drop in non hypertensive pts

5 mm Hg systolic and 2.7 mm Hg diastolic bp drop in hypertensive pts

Thus the AHA recommends less than 1500 mg/day of dietary Sodium

Other possibilities: High fiber, low dairy and animal protein and the Mediterranean diet

Physical activity AHA recommends 30 min of moderate activity 5 days a week or 25 mins of

vigorous activity 3 days a week

Risk factor modification

Antithrombotic therapy

ASA should be initiated in all patients within 48 hours and if no reperfusion therapy is administered, it should start in the ED

In cases of reperfusion tx, it is initiated after 24 hours and only after a negative CT

Early tx leads to a 1% absolute recurrent stroke risk reduction in the next 2 weeks

Under study in the early post acute phase is a combination of ASA and clopidogrel, shown in China to add benefit

It has been well established that anticoagulation with heparin does not improve outcome in unselected patients

Risk factor modification

Atrial fibrillation 5% annual risk of stroke in general but other risks stratified better under CHADS2 scores

Despite score, a history of stroke or TIA is typically enough to justify anticoagulation

Higher risk of death, stroke recurrence and severity of stroke with institutionalization in strokes associated with atrial fibrillation

A fib is likely to be underdiagnosed in cryptic stroke

Warfarin with INR at 2.0 to 3.0 effectively reduces risk 68%; corresponding to an absolute risk reduction in the annual stroke rate to 1.5%

ASA in contrast only reduces risk 21%

For patients unsuitable for anticoagulation, adding clopidogrel to ASA increases stroke risk reduction but at a cost of added risk of major bleeding

Can use the HASBLED score to determine risk

Newer agents approved: Direct Thrombin inhibitors or Factor 10a antagonists

Risk factor modification

Non Vit K antagonist drugs

Less risk of cerebral hemorrhage

Digatraban and rivaroxiban have a higher incidence of GI bleeding than warfarin

Disadvantages:

Liver and kidney disease limit use

No specific antidote

Lack of a reliable test for compliance

Expense

Increased stroke risk if stopped

What about anticoagulation in acute stroke?

Risk of hemorrhagic transformation can be influenced by

size of the infarct

Blood pressure

Evidence of bleeding on special MRI sequences, SWAN

Thank you for your attention