clinical presentation of cerebrovascular disease

47
Clinical Clinical Presentation of Presentation of Cerebrovascular Cerebrovascular Disease Disease David Griesemer, MD David Griesemer, MD Department of Neurosciences Department of Neurosciences Medical University of South Medical University of South Carolina Carolina

Upload: jared56

Post on 08-Dec-2014

2.096 views

Category:

Documents


2 download

DESCRIPTION

 

TRANSCRIPT

Page 1: Clinical Presentation of Cerebrovascular Disease

Clinical Presentation Clinical Presentation of Cerebrovascular of Cerebrovascular DiseaseDisease

David Griesemer, MDDavid Griesemer, MDDepartment of NeurosciencesDepartment of Neurosciences

Medical University of South Medical University of South CarolinaCarolina

Page 2: Clinical Presentation of Cerebrovascular Disease

Presentation OutlinePresentation Outline

Stroke from the patient’s perspectiveStroke from the patient’s perspective Definition of transient ischemic Definition of transient ischemic

attacksattacks ““Classic” presentations of stroke Classic” presentations of stroke

typestypes Focus on lacunar strokesFocus on lacunar strokes Prevention pearlsPrevention pearls Diagnostic pitfallsDiagnostic pitfalls

Page 3: Clinical Presentation of Cerebrovascular Disease

The Patient The Patient PerspectivePerspective

Page 4: Clinical Presentation of Cerebrovascular Disease

Stroke StatisticsStroke Statistics

15% of adults > age 50 15% of adults > age 50 cannot name a cannot name a single symptomsingle symptom of stroke of stroke

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

58% of stroke patients 58% of stroke patients don’t present don’t present during the first 24 hoursduring the first 24 hours after onset after onset

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

Page 5: Clinical Presentation of Cerebrovascular Disease

Stroke KnowledgeStroke Knowledge

MYTHSMYTHS

– Can’t prevent strokeCan’t prevent stroke– Can’t treat strokeCan’t treat stroke– Stroke affects the heartStroke affects the heart– Stroke affects the Stroke affects the

elderlyelderly– Recovery happens for a Recovery happens for a

few months after strokefew months after stroke

FACTSFACTS

– Stroke is preventableStroke is preventable– Stroke is treatableStroke is treatable– Stroke is a brain attackStroke is a brain attack– Stroke affects anyoneStroke affects anyone– Stroke recovery occurs Stroke recovery occurs

throughout lifethroughout life

Page 6: Clinical Presentation of Cerebrovascular Disease

Stroke SymptomsStroke Symptoms

Sudden Sudden numbness or weaknessnumbness or weakness of face, arm of face, arm or leg, especially on one side of the bodyor leg, especially on one side of the body

Sudden Sudden confusionconfusion, trouble understanding or , trouble understanding or speakingspeaking

Sudden Sudden trouble seeingtrouble seeing in one or both eyes in one or both eyes

Sudden Sudden trouble walkingtrouble walking, dizziness, loss of , dizziness, loss of balance or coordinationbalance or coordination

Sudden Sudden severe headachesevere headache with no known with no known causecause

Page 7: Clinical Presentation of Cerebrovascular Disease

Other SymptomsOther Symptoms

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

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

Page 8: Clinical Presentation of Cerebrovascular Disease

The Three R’s for Brain The Three R’s for Brain AttackAttack

ReduceReduce risk risk

RecognizeRecognize symptoms symptoms

RespondRespond by calling 911 by calling 911

Page 9: Clinical Presentation of Cerebrovascular Disease

TIA: The First ClueTIA: The First Clue

Page 10: Clinical Presentation of Cerebrovascular Disease

Transient Ischemic Transient Ischemic AttackAttack ““Sudden, focal neurologic deficit Sudden, focal neurologic deficit

lasting less than 24 hourslasting less than 24 hours, confined to , confined to an area of the brain or eye perfused by an area of the brain or eye perfused by a specific artery.”a specific artery.”

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

Time criterion is Time criterion is arbitraryarbitrary..

Page 11: Clinical Presentation of Cerebrovascular Disease

Problems with TIA Problems with TIA DefinitionDefinition Most TIAs Most TIAs last seconds to 10 minuteslast seconds to 10 minutes, with , with

symptoms lasting greater than 1 hour in only symptoms lasting greater than 1 hour in only 25% of patients25% of patients

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

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

The “24-hour” rule leads to The “24-hour” rule leads to complacency and complacency and delaydelay..

Page 12: Clinical Presentation of Cerebrovascular Disease

Tissue Definition of TIATissue Definition of TIA

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

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

Page 13: Clinical Presentation of Cerebrovascular Disease

AdvantagesAdvantages

Acknowledges that transient neurologic Acknowledges that transient neurologic symptoms symptoms may cause permanent brain may cause permanent brain injuryinjury

Supports Supports rapid interventionrapid intervention to diagnose to diagnose and treat acute brain ischemiaand treat acute brain ischemia

More accurately reflects the presence or More accurately reflects the presence or absence of brain infarctionabsence of brain infarction

Avoids assigning an arbitrary time Avoids assigning an arbitrary time criterion to define TIAcriterion to define TIA

Page 14: Clinical Presentation of Cerebrovascular Disease

TIATIA - Differential - Differential DiagnosisDiagnosis

Anxiety (panic Anxiety (panic attack)attack)

HyperventilationHyperventilation Neuropathy (focal)Neuropathy (focal) Neuropathy Neuropathy

(ischemic)(ischemic) VertigoVertigo DisequilibriumDisequilibrium

MigraineMigraine Orthostatic Orthostatic

hypotensionhypotension SyncopeSyncope Arrhythmias Arrhythmias

(ischemia)(ischemia) SeizuresSeizures Conversion disorderConversion disorder

Page 15: Clinical Presentation of Cerebrovascular Disease

TIA v. DizzinessTIA v. Dizziness

Isolated symptom Isolated symptom unlikely to be unlikely to be ischemicischemic (true also for blurred (true also for blurred vision or diplopia)vision or diplopia)

Evidence of brainstem dysfunctionEvidence of brainstem dysfunction– Ataxia or nystagmusAtaxia or nystagmus– Cranial nerve abnormalityCranial nerve abnormality– ContralateralContralateral corticospinal tract corticospinal tract

abnormalityabnormality

Page 16: Clinical Presentation of Cerebrovascular Disease

TIA v. MigraineTIA v. Migraine

Onset in middle ageOnset in middle age Aura without headacheAura without headache Dysfunction in periaqueductal gray region Dysfunction in periaqueductal gray region

of brainstem, not vascularof brainstem, not vascular

Progressive visual scintillation affecting Progressive visual scintillation affecting both eyesboth eyes

Stereotypic episodesStereotypic episodes or or positive family positive family historyhistory, especially with familial hemiplegic , especially with familial hemiplegic migrainemigraine

Page 17: Clinical Presentation of Cerebrovascular Disease

Stroke: The Initial Stroke: The Initial SymptomsSymptoms

Page 18: Clinical Presentation of Cerebrovascular Disease

Clinical Presentations of Clinical Presentations of StrokeStroke

Focal ischemia Focal ischemia (85%)(85%)– EmbolismEmbolism– ThrombosisThrombosis

Hemorrhage Hemorrhage (15%)(15%)– EpiduralEpidural– SubduralSubdural– IntraparenchymalIntraparenchymal

Page 19: Clinical Presentation of Cerebrovascular Disease

Cerebral IschemiaCerebral Ischemia

EmbolismEmbolism

Abrupt onsetAbrupt onset Small vascular areaSmall vascular area Focal deficitFocal deficit

– Pure aphasiaPure aphasia– Pure hemianopiaPure hemianopia

Acute CT normalAcute CT normal High recurrence riskHigh recurrence risk

ThrombosisThrombosis Preceded by TIAsPreceded by TIAs Abrupt onsetAbrupt onset Large vascular areaLarge vascular area More complex More complex

symptomssymptoms

Acute CT normalAcute CT normal

Page 20: Clinical Presentation of Cerebrovascular Disease

Cerebral HemorrhageCerebral Hemorrhage

Epidural hemorrhageEpidural hemorrhage Smooth onsetSmooth onset Arterial originArterial origin Mass effect causes Mass effect causes

coma over hourscoma over hours Similar (but slower Similar (but slower

in evolution) to in evolution) to hemorrhage in hemorrhage in basal gangliabasal ganglia

Subdural hemorrhageSubdural hemorrhage Smooth onsetSmooth onset Venous originVenous origin May be recurrentMay be recurrent Fluctuating, falsely Fluctuating, falsely

localizing signslocalizing signs

Page 21: Clinical Presentation of Cerebrovascular Disease

Remember Lacunar Remember Lacunar StrokesStrokes

Page 22: Clinical Presentation of Cerebrovascular Disease

Lacunar StrokesLacunar Strokes

15 – 20% of ischemic strokes15 – 20% of ischemic strokes– Small penetrating branchesSmall penetrating branches of circle of of circle of

Willis, MCA, or vertebrobasilar arteryWillis, MCA, or vertebrobasilar artery– Atherothrombotic or lipohyalinotic Atherothrombotic or lipohyalinotic

occlusionocclusion Infarct of Infarct of deepdeep brain structures brain structures

– Basal ganglia, cerebral white matter, Basal ganglia, cerebral white matter, thalamus, pons, and cerebellumthalamus, pons, and cerebellum

– From 3 mm to 2 cmFrom 3 mm to 2 cm

Page 23: Clinical Presentation of Cerebrovascular Disease

Presentation of Lacunar Presentation of Lacunar StrokeStroke

Risk factors Risk factors – DiabetesDiabetes– HypertensionHypertension– PolycythemiaPolycythemia

Variable course progressing over daysVariable course progressing over days– Fluctuating; progressing in steps; or Fluctuating; progressing in steps; or

remittingremitting– Preceded by TIAs in 25%Preceded by TIAs in 25%– Without headache or vomitingWithout headache or vomiting

Page 24: Clinical Presentation of Cerebrovascular Disease

Lacunar Stroke Lacunar Stroke SyndromesSyndromes Well-defined syndromesWell-defined syndromes

– Pure motor hemiparesisPure motor hemiparesis (with dysarthria) (with dysarthria)– Pure sensory strokePure sensory stroke (loss or (loss or

paresthesias)paresthesias)– Dysarthria-clumsy handDysarthria-clumsy hand (with (with

contralateral face and tongue weakness)contralateral face and tongue weakness)– Ataxia-hemiparesisAtaxia-hemiparesis (contralateral face (contralateral face

and leg weakness)and leg weakness)– Isolated motor-sensory strokeIsolated motor-sensory stroke

Page 25: Clinical Presentation of Cerebrovascular Disease

Lacunar Stroke Lacunar Stroke OutcomeOutcome ManagementManagement

– Long-term Long-term blood pressure controlblood pressure control– Empiric Empiric anti-platelet therapyanti-platelet therapy– Omega-3 oilOmega-3 oil 1 gm TID to improve 1 gm TID to improve

viscosityviscosity

PrognosisPrognosis– Good recovery of functionGood recovery of function– Other lacunes developOther lacunes develop

Page 26: Clinical Presentation of Cerebrovascular Disease

Prevention PearlsPrevention Pearls

Page 27: Clinical Presentation of Cerebrovascular Disease

Reducing Reducing PrimaryPrimary Risk Risk - 1- 1 Obstructive sleep apneaObstructive sleep apnea Homocysteine Homocysteine folate, B6, B12 folate, B6, B12 Hypertension – morning BP surgeHypertension – morning BP surge Smoking Smoking 50% risk reduction in 1 50% risk reduction in 1

yryr Hyperlipidemia Hyperlipidemia statins statins Migraine Migraine triptans triptans Drugs – cocaine, ephedra, PPADrugs – cocaine, ephedra, PPA

Page 28: Clinical Presentation of Cerebrovascular Disease

Reducing Reducing PrimaryPrimary Risk Risk - 2- 2 Asymptomatic carotid stenosisAsymptomatic carotid stenosis

– Endarterectomy for > 60% stenosisEndarterectomy for > 60% stenosis– Risk reduction for 3% to 1% per yearRisk reduction for 3% to 1% per year– Benefit related to surgical riskBenefit related to surgical risk

Nonvalvular atrial fibrillationNonvalvular atrial fibrillation– Aspirin for patients < 65 years, Aspirin for patients < 65 years,

healthyhealthy– Warfarin for patients > 65 years or Warfarin for patients > 65 years or

having other stroke risk factorshaving other stroke risk factors

Page 29: Clinical Presentation of Cerebrovascular Disease

Reducing Reducing SecondarySecondary RiskRisk

Reducing risk of Reducing risk of recurrencerecurrence TIA with ipsilateral carotid stenosis TIA with ipsilateral carotid stenosis

endarterectomy for > 70% stenosisendarterectomy for > 70% stenosis

Cardiogenic embolism Cardiogenic embolism warfarin warfarin

Lacunar infarcts Lacunar infarcts aspirin, aspirin, dipyridamoledipyridamole

Cryptogenic infarcts (40% embolic) Cryptogenic infarcts (40% embolic) anticoagulation? anticoagulation?

Page 30: Clinical Presentation of Cerebrovascular Disease

Reducing Risk in Reducing Risk in ChildrenChildren Sickle cell diseaseSickle cell disease

– Screen with transcranial doppler q 6 moScreen with transcranial doppler q 6 mo– Transfusion therapy for 2 abnormal Transfusion therapy for 2 abnormal

studiesstudies Congenital heart diseaseCongenital heart disease Arterial dissections (trauma)Arterial dissections (trauma) Prothrombotic disordersProthrombotic disorders Mitochondria disorders (MELAS)Mitochondria disorders (MELAS)

Page 31: Clinical Presentation of Cerebrovascular Disease

Medical EvidenceMedical Evidence

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

Page 32: Clinical Presentation of Cerebrovascular Disease

Decreasing Salt IntakeDecreasing Salt Intake

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

Reduction in stroke risk parallels Reduction in stroke risk parallels reduction in salt intake.reduction in salt intake.

Page 33: Clinical Presentation of Cerebrovascular Disease

Using StatinsUsing Statins

Pooled results after 5 yearsPooled results after 5 years Pravastatin or Simvastatin 40 Pravastatin or Simvastatin 40

mg/daymg/day Changes in cholesterol levelsChanges in cholesterol levels

– Total cholesterol Total cholesterol decreaseddecreased 20% 20%– LDL cholesterol LDL cholesterol decreased decreased 28%28%– HDL cholesterol HDL cholesterol increased increased 5%5%– Triglycerides Triglycerides decreased decreased 13%13%

Page 34: Clinical Presentation of Cerebrovascular Disease

Using StatinsUsing Statins

Reducing LDL cholesterol by 1 Reducing LDL cholesterol by 1 mmol/Lmmol/L– 22% stroke 22% stroke reductionreduction in patients with in patients with

known vascular diseaseknown vascular disease

– 6% stroke reduction in patients without 6% stroke reduction in patients without known vascular diseaseknown vascular disease

– 28% reduction in thromboembolic stroke28% reduction in thromboembolic stroke

Page 35: Clinical Presentation of Cerebrovascular Disease

Diagnostic PitfallsDiagnostic Pitfalls

Page 36: Clinical Presentation of Cerebrovascular Disease

Practical GuidancePractical Guidance

Goldszmidt and Caplan, Goldszmidt and Caplan, Stroke Stroke EssentialsEssentials, Physicians’ Press, 2003, Physicians’ Press, 2003

www.physicianspress.comwww.physicianspress.com

Page 37: Clinical Presentation of Cerebrovascular Disease

Pitfall #1Pitfall #1

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

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

Page 38: Clinical Presentation of Cerebrovascular Disease

Pitfall #2Pitfall #2

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

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

Page 39: Clinical Presentation of Cerebrovascular Disease

Pitfall #3Pitfall #3

Overlooking a mimic of TIA or stroke.Overlooking a mimic of TIA or stroke.

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

Common confoundersCommon confounders– SeizuresSeizures– Systemic infectionSystemic infection– Brain tumorBrain tumor– Toxic-metabolic encephalopathyToxic-metabolic encephalopathy

Page 40: Clinical Presentation of Cerebrovascular Disease

Pitfall #4Pitfall #4

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

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

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

Page 41: Clinical Presentation of Cerebrovascular Disease

Pitfall #5Pitfall #5

Failing to investigate Failing to investigate intracranialintracranial as as well as well as extracranialextracranial circulations. circulations.

Emboli or thrombi can come from anywhere in Emboli or thrombi can come from anywhere in the carotid or vertebrobasilar. Carotid duplex the carotid or vertebrobasilar. Carotid duplex imaging does imaging does notnot investigate the intracranial investigate the intracranial circulation.circulation.

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

Page 42: Clinical Presentation of Cerebrovascular Disease

Pitfall #6Pitfall #6

Failing to distinguish severe carotid Failing to distinguish severe carotid stenosis from total occlusion.stenosis from total occlusion.

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

Page 43: Clinical Presentation of Cerebrovascular Disease

Pitfall #7Pitfall #7

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

CT has 90% sensitivity for subarachnoid blood CT has 90% sensitivity for subarachnoid blood on day of onset, but sensitivity decreases over on day of onset, but sensitivity decreases over time. Also, small hemorrhages can be missed.time. Also, small hemorrhages can be missed.

For patients with suspected SAH who have a For patients with suspected SAH who have a negative CT, lumbar puncture is needed.negative CT, lumbar puncture is needed.

Page 44: Clinical Presentation of Cerebrovascular Disease

Pitfall #8Pitfall #8

Considering only embolism in stroke Considering only embolism in stroke patients with atrial fibrillation.patients with atrial fibrillation.

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

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

Page 45: Clinical Presentation of Cerebrovascular Disease

Pitfall #9Pitfall #9

Overtreating hypertension in acute Overtreating hypertension in acute stroke.stroke.

Because Because autoregulation is lostautoregulation is lost in ischemic in ischemic brain, aggressive lowering of BP may cause brain, aggressive lowering of BP may cause infarct extension. infarct extension.

Treat BP > 200/120Treat BP > 200/120 in absence of thrombolytics in absence of thrombolytics or > 180/115 with thrombolyticsor > 180/115 with thrombolytics

Page 46: Clinical Presentation of Cerebrovascular Disease

Pitfall #10Pitfall #10

Failing to adequate evaluate the Failing to adequate evaluate the heart.heart.

Silent myocardial infarction and arrhythmias Silent myocardial infarction and arrhythmias are common complications of stroke. are common complications of stroke.

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

Page 47: Clinical Presentation of Cerebrovascular Disease