Clinical Presentation of Cerebrovascular DiseaseDavid Griesemer, MDDepartment of NeurosciencesMedical University of South Carolina

Presentation OutlineStroke from the patients perspectiveDefinition of transient ischemic attacksClassic presentations of stroke typesFocus on lacunar strokesPrevention pearlsDiagnostic pitfalls

The Patient Perspective

Stroke Statistics15% of adults > age 50 cannot name a single symptom of stroke

13 hours after onset of symptoms is the median time to presentation

58% of stroke patients dont present during the first 24 hours after onset

52% of stroke patients in the ED are unaware that they are experiencing a stroke

Stroke KnowledgeMYTHS

Cant prevent strokeCant treat strokeStroke affects the heartStroke affects the elderlyRecovery happens for a few months after stroke

FACTS

Stroke is preventableStroke is treatableStroke is a brain attackStroke affects anyoneStroke recovery occurs throughout life

Stroke SymptomsSudden numbness or weakness of face, arm or leg, especially on one side of the body

Sudden confusion, trouble understanding or speaking

Sudden trouble seeing in one or both eyes

Sudden trouble walking, dizziness, loss of balance or coordination

Sudden severe headache with no known cause

Other SymptomsSudden nausea, fever and vomiting, distinguished from a viral illness by rapid onset (minutes or hours vs. days)

Brief loss of consciousness or period of decreased consciousness (fainting, confusion, convulsions or coma)

The Three Rs for Brain AttackReduce risk

Recognize symptoms

Respond by calling 911

TIA: The First Clue

Transient Ischemic AttackSudden, focal neurologic deficit lasting less than 24 hours, confined to an area of the brain or eye perfused by a specific artery.

Based on assumption that TIAs do not cause infarction or other permanent brain injury.

Time criterion is arbitrary.

Problems with TIA DefinitionMost TIAs last seconds to 10 minutes, with symptoms lasting greater than 1 hour in only 25% of patients

Less than 15% of patients with symptoms lasting > 1 hour resolve within 24 hours

Following TIAs, evidence of infarction is found in 20% by CT imaging and almost 50% with MRI

The 24-hour rule leads to complacency and delay.

Tissue Definition of TIAA TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.

Parallel to distinction between angina and myocardial infarction (i.e. depends on the absence of tissue injury rather than the resolution of symptoms)

AdvantagesAcknowledges that transient neurologic symptoms may cause permanent brain injury

Supports rapid intervention to diagnose and treat acute brain ischemia

More accurately reflects the presence or absence of brain infarction

Avoids assigning an arbitrary time criterion to define TIA

TIA - Differential DiagnosisAnxiety (panic attack)HyperventilationNeuropathy (focal)Neuropathy (ischemic)VertigoDisequilibriumMigraineOrthostatic hypotensionSyncopeArrhythmias (ischemia)SeizuresConversion disorder

TIA v. DizzinessIsolated symptom unlikely to be ischemic (true also for blurred vision or diplopia)

Evidence of brainstem dysfunctionAtaxia or nystagmusCranial nerve abnormalityContralateral corticospinal tract abnormality

TIA v. MigraineOnset in middle ageAura without headacheDysfunction in periaqueductal gray region of brainstem, not vascular

Progressive visual scintillation affecting both eyesStereotypic episodes or positive family history, especially with familial hemiplegic migraine

Stroke: The Initial Symptoms

Clinical Presentations of StrokeFocal ischemia (85%)EmbolismThrombosis

Hemorrhage (15%)EpiduralSubduralIntraparenchymal

Cerebral IschemiaEmbolism

Abrupt onsetSmall vascular areaFocal deficitPure aphasiaPure hemianopiaAcute CT normalHigh recurrence riskThrombosisPreceded by TIAsAbrupt onsetLarge vascular areaMore complex symptoms

Acute CT normal

Cerebral HemorrhageEpidural hemorrhageSmooth onsetArterial originMass effect causes coma over hoursSimilar (but slower in evolution) to hemorrhage in basal gangliaSubdural hemorrhageSmooth onsetVenous originMay be recurrentFluctuating, falsely localizing signs

Remember Lacunar Strokes

Lacunar Strokes15 20% of ischemic strokesSmall penetrating branches of circle of Willis, MCA, or vertebrobasilar artery Atherothrombotic or lipohyalinotic occlusionInfarct of deep brain structuresBasal ganglia, cerebral white matter, thalamus, pons, and cerebellumFrom 3 mm to 2 cm

Presentation of Lacunar StrokeRisk factors DiabetesHypertensionPolycythemia

Variable course progressing over daysFluctuating; progressing in steps; or remittingPreceded by TIAs in 25%Without headache or vomiting

Lacunar Stroke SyndromesWell-defined syndromesPure motor hemiparesis (with dysarthria)Pure sensory stroke (loss or paresthesias)Dysarthria-clumsy hand (with contralateral face and tongue weakness)Ataxia-hemiparesis (contralateral face and leg weakness)Isolated motor-sensory stroke

Lacunar Stroke OutcomeManagementLong-term blood pressure controlEmpiric anti-platelet therapyOmega-3 oil 1 gm TID to improve viscosity

PrognosisGood recovery of functionOther lacunes develop

Prevention Pearls

Reducing Primary Risk - 1Obstructive sleep apneaHomocysteine folate, B6, B12Hypertension morning BP surgeSmoking 50% risk reduction in 1 yrHyperlipidemia statinsMigraine triptansDrugs cocaine, ephedra, PPA

Reducing Primary Risk - 2Asymptomatic carotid stenosisEndarterectomy for > 60% stenosisRisk reduction for 3% to 1% per yearBenefit related to surgical riskNonvalvular atrial fibrillationAspirin for patients < 65 years, healthyWarfarin for patients > 65 years or having other stroke risk factors

Reducing Secondary RiskReducing risk of recurrenceTIA with ipsilateral carotid stenosis endarterectomy for > 70% stenosis

Cardiogenic embolism warfarin

Lacunar infarcts aspirin, dipyridamole

Cryptogenic infarcts (40% embolic) anticoagulation?

Reducing Risk in ChildrenSickle cell diseaseScreen with transcranial doppler q 6 moTransfusion therapy for 2 abnormal studiesCongenital heart diseaseArterial dissections (trauma)Prothrombotic disordersMitochondria disorders (MELAS)

Medical Evidence

www.jr2.ox.ac.uk/bandolier/knowledge.html

Decreasing Salt IntakeReducing salt intake by 3 g per day lowers blood pressure; the effect is doubled with a 6 gm/day reduction and tripled with a 9 gm/d reduction.

Reduction in stroke risk parallels reduction in salt intake.

Using StatinsPooled results after 5 yearsPravastatin or Simvastatin 40 mg/dayChanges in cholesterol levelsTotal cholesterol decreased 20%LDL cholesterol decreased 28%HDL cholesterol increased 5%Triglycerides decreased 13%

Using StatinsReducing LDL cholesterol by 1 mmol/L22% stroke reduction in patients with known vascular disease

6% stroke reduction in patients without known vascular disease

28% reduction in thromboembolic stroke

Diagnostic Pitfalls

Practical Guidance

Goldszmidt and Caplan, Stroke Essentials, Physicians Press, 2003

www.physicianspress.com

Pitfall #1Basing treatment on brain imaging alone without a vascular work-up.

A left frontal stroke caused by tight carotid stenosis requires revascularization, but the same stroke caused by atrial fibrillation requires warfarin.

Pitfall #2Basing work-up and treatment on the temporal course of stroke.

Intervention should focus on the vascular lesion. In fact, the same vascular lesion could cause TIA, evolving stroke, or completed stroke.

Pitfall #3Overlooking a mimic of TIA or stroke.

19% of patients diagnosed with stroke in ED have an imitator of stroke

Common confoundersSeizuresSystemic infectionBrain tumorToxic-metabolic encephalopathy

Pitfall #4Mistaking the time of symptom onset for patients who wake up with stroke.

Strokes are painless and do not wake people up. Because of risk of late thrombolysis, onset time should be assumed to be when they were last awake.

Diffusion-weighted MRI may be helpful in determining benefit/risk of thrombolytic therapy.

Pitfall #5Failing to investigate intracranial as well as extracranial circulations.

Emboli or thrombi can come from anywhere in the carotid or vertebrobasilar. Carotid duplex imaging does not investigate the intracranial circulation.

Transcranial doppler or MRA can non-invasively detect intracranial lesions,l more common in African-American and Asian patients.

Pitfall #6Failing to distinguish severe carotid stenosis from total occlusion.

Severe stenosis may require urgent surgery; total occlusion usually requires medical therapy. Neither carotid duplex imaging nor MRA can fully distinguish between the two. Conventional angiography is the test of choice.

Pitfall #7Failing to check spinal fluid in patients with suspected subarachnoid hemorrhage.

CT has 90% sensitivity for subarachnoid blood on day of onset, but sensitivity decreases over time. Also, small hemorrhages can be missed.For patients with suspected SAH who have a negative CT, lumbar puncture is needed.

Pitfall #8Considering only embolism in stroke patients with atrial fibrillation.

More than 25% of ischemic strokes in patients with AF have causes other than cardiogenic embolism (e.g. aortic arch atheroma and intrinsic vascular disease).

Other interventions, such as carotid revascularization, may be required.

Pitfall #9Overtreating hypertension in acute stroke.

Because autoregulation is lost in ischemic brain, aggressive lowering of BP may cause infarct extension. Treat BP > 200/120 in absence of thrombolytics or > 180/115 with thrombolytics

Pitfall #10Failing to adequate evaluate the heart.

Silent myocardial infarction and arrhythmias are common complications of stroke.

MI occurs in 20% of patients with acute stroke. It is a common cause of death at 1 4 weeks.