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Clinical Presentation of Cerebrovascular Disease


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Clinical Presentation of Cerebrovascular Disease

  1. 1. Clinical Presentation ofClinical Presentation of CerebrovascularCerebrovascular DiseaseDisease David Griesemer, MDDavid Griesemer, MD Department of NeurosciencesDepartment of Neurosciences Medical University of South CarolinaMedical University of South Carolina
  2. 2. 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
  3. 3. The Patient PerspectiveThe Patient Perspective
  4. 4. 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
  5. 5. 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 elderlyStroke affects the elderly – Recovery happens for aRecovery 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 occursStroke recovery occurs throughout lifethroughout life
  6. 6. 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 speakingspeaking  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
  7. 7. 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)
  8. 8. The Three R’s for BrainThe Three R’s for Brain AttackAttack  ReduceReduce riskrisk  RecognizeRecognize symptomssymptoms  RespondRespond by calling 911by calling 911
  9. 9. TIA: The First ClueTIA: The First Clue
  10. 10. Transient IschemicTransient Ischemic AttackAttack  ““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 injury.injury.  Time criterion isTime criterion is arbitraryarbitrary..
  11. 11. 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 patientspatients  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..
  12. 12. 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)
  13. 13. AdvantagesAdvantages  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
  14. 14. TIATIA - Differential Diagnosis- Differential Diagnosis  Anxiety (panic attack)Anxiety (panic attack)  HyperventilationHyperventilation  Neuropathy (focal)Neuropathy (focal)  Neuropathy (ischemic)Neuropathy (ischemic)  VertigoVertigo  DisequilibriumDisequilibrium  MigraineMigraine  Orthostatic hypotensionOrthostatic hypotension  SyncopeSyncope  Arrhythmias (ischemia)Arrhythmias (ischemia)  SeizuresSeizures  Conversion disorderConversion disorder
  15. 15. 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
  16. 16. 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 eyeseyes  Stereotypic episodesStereotypic episodes oror positive family historypositive family history,, especially with familial hemiplegic migraineespecially with familial hemiplegic migraine
  17. 17. Stroke: The InitialStroke: The Initial SymptomsSymptoms
  18. 18. Clinical Presentations ofClinical Presentations of StrokeStroke  Focal ischemiaFocal ischemia (85%)(85%) – EmbolismEmbolism – ThrombosisThrombosis  HemorrhageHemorrhage (15%)(15%) – EpiduralEpidural – SubduralSubdural – IntraparenchymalIntraparenchymal
  19. 19. 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 recurrenceHigh recurrence riskrisk ThrombosisThrombosis  Preceded by TIAsPreceded by TIAs  Abrupt onsetAbrupt onset  Large vascular areaLarge vascular area  More complex symptomsMore complex symptoms  Acute CT normalAcute CT normal
  20. 20. Cerebral HemorrhageCerebral Hemorrhage Epidural hemorrhageEpidural hemorrhage  Smooth onsetSmooth onset  Arterial originArterial origin  Mass effect causesMass effect causes coma over hourscoma over hours  Similar (but slowerSimilar (but slower in evolution) toin evolution) to hemorrhage inhemorrhage in basal gangliabasal ganglia Subdural hemorrhageSubdural hemorrhage  Smooth onsetSmooth onset  Venous originVenous origin  May be recurrentMay be recurrent  Fluctuating, falselyFluctuating, falsely localizing signslocalizing signs
  21. 21. Remember Lacunar StrokesRemember Lacunar Strokes
  22. 22. 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 occlusionocclusion  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
  23. 23. Presentation of LacunarPresentation of Lacunar StrokeStroke  Risk factorsRisk factors – DiabetesDiabetes – HypertensionHypertension – PolycythemiaPolycythemia  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
  24. 24. Lacunar StrokeLacunar Stroke SyndromesSyndromes  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
  25. 25. Lacunar Stroke OutcomeLacunar Stroke Outcome  ManagementManagement – 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  PrognosisPrognosis – Good recovery of functionGood recovery of function – Other lacunes developOther lacunes develop
  26. 26. Prevention PearlsPrevention Pearls
  27. 27. ReducingReducing PrimaryPrimary Risk -Risk - 11  Obstructive sleep apneaObstructive sleep apnea  HomocysteineHomocysteine  folate, B6, B12folate, B6, B12  Hypertension – morning BP surgeHypertension – morning BP surge  SmokingSmoking  50% risk reduction in 1 yr50% risk reduction in 1 yr  HyperlipidemiaHyperlipidemia  statinsstatins  MigraineMigraine  triptanstriptans  Drugs – cocaine, ephedra, PPADrugs – cocaine, ephedra, PPA
  28. 28. ReducingReducing PrimaryPrimary Risk -Risk - 22  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
  29. 29. ReducingReducing SecondarySecondary RiskRisk 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)  anticoagulation?anticoagulation?
  30. 30. Reducing Risk inReducing 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 studiesTransfusion therapy for 2 abnormal studies  Congenital heart diseaseCongenital heart disease  Arterial dissections (trauma)Arterial dissections (trauma)  Prothrombotic disordersProthrombotic disorders  Mitochondria disorders (MELAS)Mitochondria disorders (MELAS)
  31. 31. Medical EvidenceMedical Evidence
  32. 32. 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.
  33. 33. 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%
  34. 34. 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
  35. 35. Diagnostic PitfallsDiagnostic Pitfalls
  36. 36. Practical GuidancePractical Guidance Goldszmidt and Caplan,Goldszmidt and Caplan, StrokeStroke EssentialsEssentials, Physicians’ Press, 2003, Physicians’ Press, 2003
  37. 37. 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 requiresrequires warfarinwarfarin..
  38. 38. 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.
  39. 39. 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 – SeizuresSeizures – Systemic infectionSystemic infection – Brain tumorBrain tumor – Toxic-metabolic encephalopathyToxic-metabolic encephalopathy
  40. 40. 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 awake.awake. Diffusion-weighted MRIDiffusion-weighted MRI may be helpful in determiningmay be helpful in determining benefit/risk of thrombolytic therapy.benefit/risk of thrombolytic therapy.
  41. 41. 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.
  42. 42. 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 the test of choice.
  43. 43. 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 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.
  44. 44. 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.
  45. 45. 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 extension.extension. Treat BP > 200/120Treat BP > 200/120 in absence of thrombolytics or >in absence of thrombolytics or > 180/115 with thrombolytics180/115 with thrombolytics
  46. 46. 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 a common cause of death at 1 – 4 weeks.