Clinical Presentation ofClinical Presentation of
David Griesemer, MDDavid Griesemer, MD
Department of NeurosciencesDepartment of Neurosciences
Medical University of South CarolinaMedical University of South Carolina
Presentation OutlinePresentation Outline
Stroke from the patient’s perspectiveStroke from the patient’s perspective
Definition of transient ischemic attacksDefinition of transient ischemic attacks
““Classic” presentations of stroke typesClassic” presentations of stroke types
Focus on lacunar strokesFocus on lacunar strokes
Prevention pearlsPrevention pearls
Diagnostic pitfallsDiagnostic pitfalls
Stroke StatisticsStroke Statistics
15% of adults > age 5015% of adults > age 50 cannot name acannot name a
single symptomsingle symptom of strokeof stroke
13 hours after onset of symptoms is the13 hours after onset of symptoms is the
median time to presentationmedian time to presentation
58% of stroke patients58% of stroke patients don’t present duringdon’t present during
the first 24 hoursthe first 24 hours after onsetafter onset
52% of stroke patients in the ED are52% of stroke patients in the ED are
unaware that they are experiencing a strokeunaware that they are experiencing a stroke
Stroke KnowledgeStroke Knowledge
– Can’t prevent strokeCan’t prevent stroke
– Can’t treat strokeCan’t treat stroke
– Stroke affects the heartStroke affects the heart
– Stroke affects the elderlyStroke affects the elderly
– Recovery happens for aRecovery happens for a
few months after strokefew months after stroke
– 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 occursStroke recovery occurs
throughout lifethroughout life
Stroke SymptomsStroke Symptoms
SuddenSudden numbness or weaknessnumbness or weakness of face, arm orof face, arm or
leg, especially on one side of the bodyleg, especially on one side of the body
SuddenSudden confusionconfusion, trouble understanding or, trouble understanding or
SuddenSudden trouble seeingtrouble seeing in one or both eyesin one or both eyes
SuddenSudden trouble walkingtrouble walking, dizziness, loss of balance, dizziness, loss of balance
or coordinationor coordination
SuddenSudden severe headachesevere headache with no known causewith no known cause
Other SymptomsOther Symptoms
SuddenSudden nausea, fever and vomitingnausea, fever and vomiting,,
distinguished from a viral illness by rapid onsetdistinguished from a viral illness by rapid onset
(minutes or hours vs. days)(minutes or hours vs. days)
Brief loss of consciousnessBrief loss of consciousness or period ofor period of
decreased consciousness (fainting,decreased consciousness (fainting,
confusion, convulsions or coma)confusion, convulsions or coma)
The Three R’s for BrainThe Three R’s for Brain
RespondRespond by calling 911by calling 911
Transient IschemicTransient Ischemic
““Sudden, focal neurologic deficitSudden, focal neurologic deficit lasting lesslasting less
than 24 hoursthan 24 hours, confined to an area of the, confined to an area of the
brain or eye perfused by a specific artery.”brain or eye perfused by a specific artery.”
Based onBased on assumptionassumption that TIAs do notthat TIAs do not
cause infarction or other permanent braincause infarction or other permanent brain
Time criterion isTime criterion is arbitraryarbitrary..
Problems with TIA DefinitionProblems with TIA Definition
Most TIAsMost TIAs last seconds to 10 minuteslast seconds to 10 minutes, with, with
symptoms lasting greater than 1 hour in only 25% ofsymptoms lasting greater than 1 hour in only 25% of
Less than 15% of patients with symptoms lasting >Less than 15% of patients with symptoms lasting >
1 hour resolve within 24 hours1 hour resolve within 24 hours
Following TIAs,Following TIAs, evidence of infarctionevidence of infarction is found inis found in
20% by CT imaging and almost 50% with MRI20% by CT imaging and almost 50% with MRI
The “24-hour” rule leads toThe “24-hour” rule leads to complacency and delaycomplacency and delay..
Tissue Definition of TIATissue Definition of TIA
““A TIA is a brief episode of neurologicA TIA is a brief episode of neurologic
dysfunction caused by focal brain or retinaldysfunction caused by focal brain or retinal
ischemia, with clinical symptoms typicallyischemia, with clinical symptoms typically
lasting less than one hourlasting less than one hour, and without, and without
evidence of acute infarction.”evidence of acute infarction.”
Parallel to distinction between angina andParallel to distinction between angina and
myocardial infarction (i.e. depends on themyocardial infarction (i.e. depends on the
absence of tissue injury rather than theabsence of tissue injury rather than the
resolution of symptoms)resolution of symptoms)
Acknowledges that transient neurologicAcknowledges that transient neurologic
symptomssymptoms may cause permanent brain injurymay cause permanent brain injury
SupportsSupports rapid interventionrapid intervention to diagnose andto diagnose and
treat acute brain ischemiatreat acute brain ischemia
More accurately reflects the presence orMore accurately reflects the presence or
absence of brain infarctionabsence of brain infarction
Avoids assigning an arbitrary time criterion toAvoids assigning an arbitrary time criterion to
define TIAdefine TIA
TIA v. DizzinessTIA v. Dizziness
Isolated symptomIsolated symptom unlikely to be ischemicunlikely to be ischemic
(true also for blurred vision or diplopia)(true also for blurred vision or diplopia)
Evidence of brainstem dysfunctionEvidence of brainstem dysfunction
– Ataxia or nystagmusAtaxia or nystagmus
– Cranial nerve abnormalityCranial nerve abnormality
– ContralateralContralateral corticospinal tract abnormalitycorticospinal tract abnormality
TIA v. MigraineTIA v. Migraine
Onset in middle ageOnset in middle age
Aura without headacheAura without headache
Dysfunction in periaqueductal gray region ofDysfunction in periaqueductal gray region of
brainstem, not vascularbrainstem, not vascular
Progressive visual scintillation affectingProgressive visual scintillation affecting bothboth
Stereotypic episodesStereotypic episodes oror positive family historypositive family history,,
especially with familial hemiplegic migraineespecially with familial hemiplegic migraine
Stroke: The InitialStroke: The Initial
Lacunar StrokesLacunar Strokes
15 – 20% of ischemic strokes15 – 20% of ischemic strokes
– Small penetrating branchesSmall penetrating branches of circle ofof circle of
Willis, MCA, or vertebrobasilar arteryWillis, MCA, or vertebrobasilar artery
– Atherothrombotic or lipohyalinoticAtherothrombotic or lipohyalinotic
Infarct ofInfarct of deepdeep brain structuresbrain 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
Presentation of LacunarPresentation of Lacunar
Risk factorsRisk factors
Variable course progressing over daysVariable course progressing over days
– Fluctuating; progressing in steps; or remittingFluctuating; progressing in steps; or remitting
– Preceded by TIAs in 25%Preceded by TIAs in 25%
– Without headache or vomitingWithout headache or vomiting
Lacunar StrokeLacunar Stroke
Well-defined syndromesWell-defined syndromes
– Pure motor hemiparesisPure motor hemiparesis (with dysarthria)(with dysarthria)
– Pure sensory strokePure sensory stroke (loss or paresthesias)(loss or paresthesias)
– Dysarthria-clumsy handDysarthria-clumsy hand (with contralateral(with contralateral
face and tongue weakness)face and tongue weakness)
– Ataxia-hemiparesisAtaxia-hemiparesis (contralateral face and(contralateral face and
leg weakness)leg weakness)
– Isolated motor-sensory strokeIsolated motor-sensory stroke
Lacunar Stroke OutcomeLacunar Stroke Outcome
– Long-termLong-term blood pressure controlblood pressure control
– EmpiricEmpiric anti-platelet therapyanti-platelet therapy
– Omega-3 oilOmega-3 oil 1 gm TID to improve viscosity1 gm TID to improve viscosity
– Good recovery of functionGood recovery of function
– Other lacunes developOther lacunes develop
ReducingReducing PrimaryPrimary Risk -Risk -
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, healthyAspirin for patients < 65 years, healthy
– Warfarin for patients > 65 years or havingWarfarin for patients > 65 years or having
other stroke risk factorsother stroke risk factors
Reducing risk ofReducing risk of recurrencerecurrence
TIA with ipsilateral carotid stenosisTIA with ipsilateral carotid stenosis
endarterectomy for > 70% stenosisendarterectomy for > 70% stenosis
Cardiogenic embolismCardiogenic embolism warfarinwarfarin
Lacunar infarctsLacunar infarcts aspirin, dipyridamoleaspirin, dipyridamole
Cryptogenic infarcts (40% embolic)Cryptogenic infarcts (40% embolic)
Medical EvidenceMedical Evidence
Decreasing Salt IntakeDecreasing Salt Intake
Reducing salt intake by 3 g per dayReducing salt intake by 3 g per day
lowers blood pressurelowers blood pressure; the effect is; the effect is
doubled with a 6 gm/day reduction anddoubled with a 6 gm/day reduction and
tripled with a 9 gm/d reduction.tripled with a 9 gm/d reduction.
Reduction in stroke risk parallelsReduction in stroke risk parallels
reduction in salt intake.reduction in salt intake.
Using StatinsUsing Statins
Pooled results after 5 yearsPooled results after 5 years
Pravastatin or Simvastatin 40 mg/dayPravastatin or Simvastatin 40 mg/day
Changes in cholesterol levelsChanges in cholesterol levels
– Total cholesterolTotal cholesterol decreaseddecreased 20%20%
– LDL cholesterolLDL cholesterol decreaseddecreased 28%28%
– HDL cholesterolHDL cholesterol increasedincreased 5%5%
– TriglyceridesTriglycerides decreaseddecreased 13%13%
Using StatinsUsing Statins
Reducing LDL cholesterol by 1 mmol/LReducing LDL cholesterol by 1 mmol/L
– 22% stroke22% stroke reductionreduction in patients within patients with
known vascular diseaseknown vascular disease
– 6% stroke reduction in patients without6% stroke reduction in patients without
known vascular diseaseknown vascular disease
– 28% reduction in thromboembolic stroke28% reduction in thromboembolic stroke
Practical GuidancePractical Guidance
Goldszmidt and Caplan,Goldszmidt and Caplan, StrokeStroke
EssentialsEssentials, Physicians’ Press, 2003, Physicians’ Press, 2003
Pitfall #1Pitfall #1
Basing treatment on brain imaging aloneBasing treatment on brain imaging alone
without a vascular work-up.without a vascular work-up.
A left frontal stroke caused by tight carotidA left frontal stroke caused by tight carotid
stenosis requiresstenosis requires revascularizationrevascularization, but the, but the
same stroke caused by atrial fibrillationsame stroke caused by atrial fibrillation
Pitfall #2Pitfall #2
Basing work-up and treatment on theBasing work-up and treatment on the
temporal course of stroke.temporal course of stroke.
Intervention should focus on theIntervention should focus on the vascular lesion.vascular lesion.
In fact, the same vascular lesion could causeIn fact, the same vascular lesion could cause
TIA, evolving stroke, or completed stroke.TIA, evolving stroke, or completed stroke.
Pitfall #3Pitfall #3
Overlooking a mimic of TIA or stroke.Overlooking a mimic of TIA or stroke.
19% of patients diagnosed with stroke in ED19% of patients diagnosed with stroke in ED
have anhave an imitatorimitator of strokeof stroke
Common confoundersCommon confounders
– Systemic infectionSystemic infection
– Brain tumorBrain tumor
– Toxic-metabolic encephalopathyToxic-metabolic encephalopathy
Pitfall #4Pitfall #4
Mistaking the time of symptom onset forMistaking the time of symptom onset for
patients who wake up with stroke.patients who wake up with stroke.
Strokes are painless and do not wake people up.Strokes are painless and do not wake people up.
Because ofBecause of risk of late thrombolysisrisk of late thrombolysis, onset time, onset time
should be assumed to be when they were lastshould be assumed to be when they were last
Diffusion-weighted MRIDiffusion-weighted MRI may be helpful in determiningmay be helpful in determining
benefit/risk of thrombolytic therapy.benefit/risk of thrombolytic therapy.
Pitfall #5Pitfall #5
Failing to investigateFailing to investigate intracranialintracranial as wellas well
asas extracranialextracranial circulations.circulations.
Emboli or thrombi can come from anywhere in theEmboli or thrombi can come from anywhere in the
carotid or vertebrobasilar. Carotid duplex imagingcarotid or vertebrobasilar. Carotid duplex imaging
doesdoes notnot investigate the intracranial circulation.investigate the intracranial circulation.
Transcranial doppler or MRATranscranial doppler or MRA can non-invasivelycan non-invasively
detect intracranial lesions,l more common indetect intracranial lesions,l more common in
African-American and Asian patients.African-American and Asian patients.
Pitfall #6Pitfall #6
Failing to distinguish severe carotidFailing to distinguish severe carotid
stenosis from total occlusion.stenosis from total occlusion.
Severe stenosis may requireSevere stenosis may require urgent surgeryurgent surgery; total; total
occlusion usually requires medical therapy.occlusion usually requires medical therapy.
Neither carotid duplex imaging nor MRA canNeither carotid duplex imaging nor MRA can
fully distinguish between the two.fully distinguish between the two. ConventionalConventional
angiographyangiography is the test of choice.is the test of choice.
Pitfall #7Pitfall #7
Failing to check spinal fluid in patients withFailing to check spinal fluid in patients with
suspected subarachnoid hemorrhage.suspected subarachnoid hemorrhage.
CT has 90% sensitivity for subarachnoid blood onCT has 90% sensitivity for subarachnoid blood on
day of onset, but sensitivity decreases over time.day of onset, but sensitivity decreases over time.
Also, small hemorrhages can be missed.Also, small hemorrhages can be missed.
For patients with suspected SAH who have aFor patients with suspected SAH who have a
negative CT, lumbar puncture is needed.negative CT, lumbar puncture is needed.
Pitfall #8Pitfall #8
Considering only embolism in strokeConsidering only embolism in stroke
patients with atrial fibrillation.patients with atrial fibrillation.
More than 25% of ischemic strokes in patients with AFMore than 25% of ischemic strokes in patients with AF
havehave causes other than cardiogenic embolismcauses other than cardiogenic embolism (e.g.(e.g.
aortic arch atheroma and intrinsic vascular disease).aortic arch atheroma and intrinsic vascular disease).
Other interventions, such as carotid revascularization,Other interventions, such as carotid revascularization,
may be required.may be required.
Pitfall #9Pitfall #9
Overtreating hypertension in acute stroke.Overtreating hypertension in acute stroke.
BecauseBecause autoregulation is lostautoregulation is lost in ischemic brain,in ischemic brain,
aggressive lowering of BP may cause infarctaggressive lowering of BP may cause infarct
Treat BP > 200/120Treat BP > 200/120 in absence of thrombolytics or >in absence of thrombolytics or >
180/115 with thrombolytics180/115 with thrombolytics
Pitfall #10Pitfall #10
Failing to adequate evaluate the heart.Failing to adequate evaluate the heart.
Silent myocardial infarction and arrhythmias areSilent myocardial infarction and arrhythmias are
common complications of stroke.common complications of stroke.
MI occurs in 20%MI occurs in 20% of patients with acute stroke. Itof patients with acute stroke. It
is a common cause of death at 1 – 4 weeks.is a common cause of death at 1 – 4 weeks.
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