Stroke: Evaluation and Treatment

1. Stroke: Evaluation and Treatment John B. Terry, M.D. Medical Director, Neurocritical Care Via Christi Regional Medical Center I like this title. Neurologists intervening. Most will think of procedural intervention, but as I am about to show you it goes well beyond that.I like this title. Neurologists intervening. Most will think of procedural intervention, but as I am about to show you it goes well beyond that.

2. Stroke-in-Evolution Emergency Heterogenous group of etiologies Increasing number and complexity of treatment options Stroke in evolution is a term frequently used to describe patients with clinical worsening. I think it is a good description for current thought about stroke and its treatment. As we talk I want to cover 4 significant points.Stroke in evolution is a term frequently used to describe patients with clinical worsening. I think it is a good description for current thought about stroke and its treatment. As we talk I want to cover 4 significant points.

3. Stroke: Definition A syndrome characterized by acute onset of a neurologic deficit that persists for at least 24 hours, reflects focal involvement of the central nervous system, and is the result of a disturbance of the cerebral circulation. Acute onset Begins abruptly with stroke. Maximal deficit immediately with embolic stroke; maximal over minutes to hours with thrombotic stroke. If deficit evolves over days to weeks, then more likely tumor, inflammatory dis- order, or neurodegenerative disorder. Focal involvement Symptoms suggest where the lesion is, the exam accurately delineates the location, and x-ray confirms it. Cerebral circulation Vascular event suggested by acute onset and naure of symptoms and signs consistent with involvemnt of tissue in the territory of a particular blood vessel.Acute onset Begins abruptly with stroke. Maximal deficit immediately with embolic stroke; maximal over minutes to hours with thrombotic stroke. If deficit evolves over days to weeks, then more likely tumor, inflammatory dis- order, or neurodegenerative disorder. Focal involvement Symptoms suggest where the lesion is, the exam accurately delineates the location, and x-ray confirms it. Cerebral circulation Vascular event suggested by acute onset and naure of symptoms and signs consistent with involvemnt of tissue in the territory of a particular blood vessel.

4. Stroke: Definitions Transient Ischemic Attack (TIA) Reversible Ischemic Neurologic Deficit (RIND) Stroke in Evolution (Progressive Stroke) Completed Stroke TIA less than 24 hours RIND less than a few days Stroke in evolution Completed stroke deficits remain stableTIA less than 24 hours RIND less than a few days Stroke in evolution Completed stroke deficits remain stable

5. Stroke Epidemiology > 700,000 new or recurrent strokes occur per year Accounts for > 50% of all hospitalizations for acute neurologic disease ~ 4 million Americans are living with neurologic deficits due to stroke Leading cause of serious, long-term disability Risk and mortality increase with age Third leading cause of death in the U.S.; second leading cause worldwide Stroke is an improtant health problem Incidence is increasing with time It is a large problem in the US but even larger in the worldStroke is an improtant health problem Incidence is increasing with time It is a large problem in the US but even larger in the world

6. Stroke Subtypes Multple etiologies result in the sudden onset of a focal neurologic deficit. When patients present, it is not difficult to make the diagnosis of a hemorrhagic etiology. In ischemic stroke, however, almost half of the time the cause is undetermined.Multple etiologies result in the sudden onset of a focal neurologic deficit. When patients present, it is not difficult to make the diagnosis of a hemorrhagic etiology. In ischemic stroke, however, almost half of the time the cause is undetermined.

7. Stroke Risk Factors Tobacco use High blood pressure Previous TIA or Stroke Diabetes mellitus Atrial fibrillation Family history of stroke or heart attack hyperlipidemia

8. Stroke Risk Factors Cardiac structural conditions Cholesterol Serum homocysteine Sedentary lifestyle Gender Age heavy alcohol use oral contraceptives

10. Bar graph of probability of stroke during 10 years in men aged 70 years at two systolic blood pressure levles: impact of other risk factors. Hyp Rx, antihypertensive therapy; DM, diabetes mellitus; Cigs, cigarette smoking; CVD, previously diagnosed coronary heart dis, cardiac failure, or intermittent claudication; AF, atrial fibrillation; LVH-ECG, left ventricular hypertrophy by ECGBar graph of probability of stroke during 10 years in men aged 70 years at two systolic blood pressure levles: impact of other risk factors. Hyp Rx, antihypertensive therapy; DM, diabetes mellitus; Cigs, cigarette smoking; CVD, previously diagnosed coronary heart dis, cardiac failure, or intermittent claudication; AF, atrial fibrillation; LVH-ECG, left ventricular hypertrophy by ECG

11. Stroke: Symptoms & Signs Symptoms suggest the cause of the lesion and its location Signs accurately identify the location of the lesion (cortex, brainstem, or spinal cord; left or right side; anterior or posterior circulation) Neuroimaging confirms the location and excludes other disorders which might produce similar signs and symptoms.

14. MCA distributes to the lateral surface of the hemisphere ACA distributes to the medial frontal and parietal lobes PCA distributes to the medial occipital and temporal lobes

17. Anterior Circulation Internal carotid artery and its branches anterior & middle cerebral arteries (ACA & MCA) anterior choroidal artery lenticulostriate branches of MCA Supplies much of cerebral hemispheres and adjacent subcortical white matter ACA medial frontal & parietal cortex, subjacent white mat., ant. corpus callosum MCA Ant. choroidal artery hippocampus, globus pallidus, lower internal capsule Lenticulostriate arteries caudate nucleus, putamen, upper internal capsule Symptoms: amaurosis fugax mono-, or hemiparesis hemisensory loss visual field deficit agnosia apraxia aphasiaACA medial frontal & parietal cortex, subjacent white mat., ant. corpus callosum MCA Ant. choroidal artery hippocampus, globus pallidus, lower internal capsule Lenticulostriate arteries caudate nucleus, putamen, upper internal capsule Symptoms: amaurosis fugax mono-, or hemiparesis hemisensory loss visual field deficit agnosia apraxia aphasia

18. Clinicoanatomical Correlates Anterior Cerebral Artery Parasagital cerebral cortex; motor & sensory cortex related to contralateral leg, bladder inhibitory & micturation center Paralysis and sensory loss contralateral leg; uninhibited bladder Uncommon; 85% of blood flow is to MCAUncommon; 85% of blood flow is to MCA

19. Clinicoanatomical Correlates Middle Cerebral Artery Superior div.: contralateral hemiparesis with relative sparing of the leg, contra- lateral hemisensory loss; Broca�s aphasia Inferior div.: homonymous hemianopsia, impaired cortical sensory function, ano- sognosia, apraxia, Wernicke�s aphasia

20. Clinicoanatomical Correlates Middle Cerebral Artery Superior div.: motor & sensory cortex for face, arm, hand; Broca�s area Inferior div.: visual radiations, macular vision; Wernicke�s area Lenticulostriate vessels: basal ganglia, genu & posterior limb internal capsule Most common site of strokeMost common site of stroke

21. Clinicoanatomical Correlates Middle Cerebral Artery Lenticulostriate vessels: dense hemi- paresis affecting arm/leg/face equally Bifurcation of MCA occlusion: combined superior and inferior division sx�s Stem of MCA: combined sup., inf., and lenticulostriate arteriesBifurcation of MCA occlusion: combined superior and inferior division sx�s Stem of MCA: combined sup., inf., and lenticulostriate arteries

22. Clinicoanatomical Correlates Internal Carotid Artery Signs and symptoms similar to MCA stroke Transient monocular blindness (amaurosis fugax)

23. Posterior Circulation Vertebral artery, basilar artery & their branches: posterior inferior cerebellar artery (PICA) posterior cerebral artery & its thalamoperforate and thalamogeniculate branches Symptoms coma, or LOC drop attacks vertigo ataxia hemianopsia dysarthria dysphagia diplopia cranial nerve signs hemiparesis hemisensory loss crossed motor and sensory findings cerebellar signsSymptoms coma, or LOC drop attacks vertigo ataxia hemianopsia dysarthria dysphagia diplopia cranial nerve signs hemiparesis hemisensory loss crossed motor and sensory findings cerebellar signs

24. Clinicoanatomical Correlates Posterior Cerebral Artery Occipital cerebral cortex, medial temporal lobes, thalamus, rostral midbrain Homonymous hemianopsia, cortical blindness, impaired recent memory, anomic aphasia, alexia without agraphia, visual agnosia (eg., prosopagnosia)

25. Clinicoanatomical Correlates Basilar Artery Occipital & medial temporal lobes, medial thalamus, posterior limb internal capsule, brainstem, cerebellum Bilateral neurologic signs, cranial nerve & cerebellar signs, diplopia, vertigo, crossed motor & sensory signs, hemi- or quadraplegia, ataxia, dysarthria, LOC PICA: Wallenberg�s Synd.; ipsilateral cerebellar ataxia, Horner�s, facial sensory loss, contralateral pain & temp, nystagmus, vertigo, N/V, dysphagia, dysarthria, hiccup AICA: lateral caudal pons; similar to PICA but with deafness & tinnitus, VII paralysis (no Horner�s, dysphagia, dysarthria) Sup. Cerebellar Art: similar to AICa Long penetrating paramedian vertebrobasilar branches Short basal vertebrobasialr branches PICA: Wallenberg�s Synd.; ipsilateral cerebellar ataxia, Horner�s, facial sensory loss, contralateral pain & temp, nystagmus, vertigo, N/V, dysphagia, dysarthria, hiccup AICA: lateral caudal pons; similar to PICA but with deafness & tinnitus, VII paralysis (no Horner�s, dysphagia, dysarthria) Sup. Cerebellar Art: similar to AICa Long penetrating paramedian vertebrobasilar branches Short basal vertebrobasialr branches

26. Clinicoanatomical Correlates Lacunar Stroke Atherosclerosis with fibrinoid necrosis & lipohyalinosis of small penetrating arteries (internal capsule, thalamus, pons) Occurs in setting of longstanding hypertension or diabetes mellitus Normal angiographyNormal angiography

27. Clinicoanatomical Correlates Lacunar Stroke Multiple syndromes including: Pure motor hemiparesis Pure hemisensory loss Ataxic hemiparesis Dysarthria-Clumsy Hand Syndrome Pure motor hemiparesis: pons or internal capsule Pure hemisensory loss: thalamus Ataxic hemiparesis: pons or internal capsule Dysarthria Clumsy Hand synd.: internal capsule or ponsPure motor hemiparesis: pons or internal capsule Pure hemisensory loss: thalamus Ataxic hemiparesis: pons or internal capsule Dysarthria Clumsy Hand synd.: internal capsule or pons

28. Stroke Management Algorithm

29. Pre-Hospital Care Recognition of symptoms: Weakness or numbness on one side of the body Speech difficulties Visual difficulties Balance problems Sudden severe headache Loss of consciousness Emergency requiring a prompt response Rapid Transport to hospital

30. After Arrival at Hospital Prompt examination CT scan Determination of etiology of symptoms Admission Pharmacologic treatment Diagnostic tests Physical therapy and swallowing evaluation Definitive stroke prevention and rehabilitation strategy

31. Stroke: Differential Diagnosis hypoglycemia tumor abcess syncope seizure trauma �classic� migraine multiple sclerosis Bell�s palsy conversion reaction Do not mistake hypoglycemia for a stroke as it may produce focal neurological deficits similar to a stroke.Do not mistake hypoglycemia for a stroke as it may produce focal neurological deficits similar to a stroke.

32. CT Scan

33. Immediate Treatment Options Thrombolysis (tPA) Aspirin Antiplatelet agents Fluids �Blood Thinner� (heparin) Future options

34. Barnett HJM, Buchan AM, JAMA, 283(23), June 21, 2000

35. Stroke: Treatment risk factor modification antiplatelet agents aspirin ticlopidine clopidogrel dipyridamole anticoagulants Heparin Coumadin LMWH carotid endarterectomy extracranial-intracranial bypass thrombolytics tissue plasminogen activator streptokinase glutamate antagonist

36. Neurovascular Evaluation Cardiogenic emboli Large arterial process embolic thrombotic Penetrating vessel process Hematologic process

37. Stroke: Evaluation History Onset and course Associated symptoms (seizure, headache) Predisposing risk factors Onset and course: stepwise w/ TIA�s suggests thrombotic abrupt w/ maximal deficit immediately suggest embolic Ass�d sx�s: seizure more common w/ embolus; rarely if ever w/ lacunar headache w/ 25% of patients w/ ischemic stroke (due to vaso- dilation of contralateral vessels) Predisposing risk factorsOnset and course: stepwise w/ TIA�s suggests thrombotic abrupt w/ maximal deficit immediately suggest embolic Ass�d sx�s: seizure more common w/ embolus; rarely if ever w/ lacunar headache w/ 25% of patients w/ ischemic stroke (due to vaso- dilation of contralateral vessels) Predisposing risk factors

38. Stroke: Evaluation Physical Examination Blood pressure (both arms) & pulse Ophthalmoscopic exam for retinal emboli Carotid or ocular bruits Cardiac murmur or dysrhythmia Temporal artery tenderness Neuro Exam (may be normal after TIA)

39. Stroke: Evaluation Routine laboratory tests CBC w/ diff Multichemistry profile including glucose Lipid profile Protime, PTT, ESR, VDRL Routine Urinalysis

40. Stroke: Evaluation Other Clinical Studies ECG & CXR CT or MRI Echocardiogram (transthoracic vs. TEE) Carotid & Transcranial Doppler Continuous ECG monitoring (eg., Holter) Cerebral arteriogram Lumbar Puncture EEG CT may be more advantageous than MRI. May show acute hemorrahage more easily than MRI, is easier to perform, less time required, requires less patient cooperation.CT may be more advantageous than MRI. May show acute hemorrahage more easily than MRI, is easier to perform, less time required, requires less patient cooperation.

41. Documentation of Cardiac Embolism Introduction of TEE Increased Proportion of Cardiogenic Embolism1 Additional Findings Aortic Arch Atheroma Patent Foramen Ovale Coronary Screening2 Stroke PreventionEchocardiographic Evaluation of Stroke

42. Stroke: Evaluation Special Laboratory Studies Serum viscosity antithrombin III, protein C & S lupus anticoagulant, anticardiolipins Homocysteine, Factor V mutation Sickle cell prep ANA Coagulation factor analysis

43. MRI Scan

44. Cerebrovascular Doppler

46. Neurovascular Evaluation

47. Stroke: Etiology (vascular) Atherosclerosis Fibromuscular dysplasia Carotid or vertebral artery dissection Lacunar stroke Drug abuse Venous sinus thrombosis �Complicated� migraine Atherosclerosios: esp�lly origin of CCA, bifurcation of ICA, w/i cavernous sinus, vertebral art. at origin & just above etrance to skull, basilar artery Pathogenesis: injury to vascular endothelial cells (LDL, biochemical, inflammatory, mechanical), w/ monocytes invade and accumulate lipids leading to fatty streak; stimulates proliferation & migration of intimal smooth muscle cells; fibrous plaque & further injury; platelet adhesion occludes vessel or causes platelet emboli. Fibromuscular dysplasia: segmental nonatheromatous condition of cerebral vessels; segmental thinning of media alternating w/ rings of fibrous & muscular hyperplasia. Extracranial>intracranial vessels; women>men. Rarely thrombose, usually thrombi embolize. Associated with saccular aneurysms of cerebral artery w/ increased risk of SAH. Dx: beaded appearance of artery on angiography. Tx: aspirin, or gradual intra- luminal dilation. Carotid or vertebral dissection: traumatic, Marfan�s, Ehlers Danlos. Occur spontaneously (usually young male); cystic medial necrosis. Pain in neck Tx: controversial, nothing? aspirin? anticoagulation? surgery? Drug abuse: cocaine, heroin, amphetamine, phenylpropanolamine. Moyamoya: �smoke...haze�; sickle cell, basilar meningitis, atherosclerosis Migraine: complicated migraine Venous or sinus thrombosis: ass�d w/ otitis, sinusitis, postpartum, dehydra- tion, coagulopathy Lacunar: occludes sm. penetrating art.; pons, int. cap., thalamus; fibrinoid necrosis, lipohyalinosis.Atherosclerosios: esp�lly origin of CCA, bifurcation of ICA, w/i cavernous sinus, vertebral art. at origin & just above etrance to skull, basilar artery Pathogenesis: injury to vascular endothelial cells (LDL, biochemical, inflammatory, mechanical), w/ monocytes invade and accumulate lipids leading to fatty streak; stimulates proliferation & migration of intimal smooth muscle cells; fibrous plaque & further injury; platelet adhesion occludes vessel or causes platelet emboli. Fibromuscular dysplasia: segmental nonatheromatous condition of cerebral vessels; segmental thinning of media alternating w/ rings of fibrous & muscular hyperplasia. Extracranial>intracranial vessels; women>men. Rarely thrombose, usually thrombi embolize. Associated with saccular aneurysms of cerebral artery w/ increased risk of SAH. Dx: beaded appearance of artery on angiography. Tx: aspirin, or gradual intra- luminal dilation. Carotid or vertebral dissection: traumatic, Marfan�s, Ehlers Danlos. Occur spontaneously (usually young male); cystic medial necrosis. Pain in neck Tx: controversial, nothing? aspirin? anticoagulation? surgery? Drug abuse: cocaine, heroin, amphetamine, phenylpropanolamine. Moyamoya: �smoke...haze�; sickle cell, basilar meningitis, atherosclerosis Migraine: complicated migraine Venous or sinus thrombosis: ass�d w/ otitis, sinusitis, postpartum, dehydra- tion, coagulopathy Lacunar: occludes sm. penetrating art.; pons, int. cap., thalamus; fibrinoid necrosis, lipohyalinosis.

48. Stroke: Etiology (vascular)-continued- Inflammatory disorders temporal arteritis systemic lupus erythematosus syphilitic arteritis AIDS granulomatous angiitis polyarteritis nodosa Herpes zoster Temporal arteritis: Giant cell arteritis; esp�lly elderly; visual loss, h.a., polymyalgia rheumatica, increased ESR, positive bx; Tx: steroids. SLE: microangiopathy, noninflammatory, w/ microinfarcts. Liebmann-Sacks endocarditis rarely embolizes Granulomatous angiitis: idiopathic inflam. d.o. affecting small art. & veins H.a., focal deficits, CSF pleocytosis, nl ESR, +angio or biopsy; Tx: prednisone w/ or w/o cytoxan Syphilitic arteritis: increased in male homosexuals; w/i 5 yrs after infection; medium vessels, lacunar infarcts, deep white matter Herpes Zoster: arteritis Polyarteritis nodosa: segmental vasculitis of small & medium sized art�s AIDS: increased risk of stroke (why?); toxic effects of HIV-1 on blood vessels? Immune complexes?Temporal arteritis: Giant cell arteritis; esp�lly elderly; visual loss, h.a., polymyalgia rheumatica, increased ESR, positive bx; Tx: steroids. SLE: microangiopathy, noninflammatory, w/ microinfarcts. Liebmann-Sacks endocarditis rarely embolizes Granulomatous angiitis: idiopathic inflam. d.o. affecting small art. & veins H.a., focal deficits, CSF pleocytosis, nl ESR, +angio or biopsy; Tx: prednisone w/ or w/o cytoxan Syphilitic arteritis: increased in male homosexuals; w/i 5 yrs after infection; medium vessels, lacunar infarcts, deep white matter Herpes Zoster: arteritis Polyarteritis nodosa: segmental vasculitis of small & medium sized art�s AIDS: increased risk of stroke (why?); toxic effects of HIV-1 on blood vessels? Immune complexes?

49. Stroke: Etiology (cardiac) mural thrombus rheumatic heart disease dysrhythmias (esp. atrial fibrillation) endocarditis bacterial marrantic mitral valve prolapse (?) paradoxical embolus patent foramen ovale atrial septal defect left atrial myxoma prosthetic heart valve Mural thrombus: after MI, cardiomyopathy Rheum. Hrt. Dis: esp�lly mitral stenosis w/ atrial fib. Dysrhythmias: a. fib.; sick sinus (bradytachy synd.) Endocarditis: bacterial (strept, staphy, & w/ drug users pseudomonas, candida, & aspergillosis); marrantic ass�d w/ cancer (adenoca lung and GI); Liebmann-Sacks endocarditis rarely embolizes MV prolapse: increased risk is small; massive stroke rare Paradoxical embolus Left atrial myxoma Prosthetic heart valve: anticoagulateMural thrombus: after MI, cardiomyopathy Rheum. Hrt. Dis: esp�lly mitral stenosis w/ atrial fib. Dysrhythmias: a. fib.; sick sinus (bradytachy synd.) Endocarditis: bacterial (strept, staphy, & w/ drug users pseudomonas, candida, & aspergillosis); marrantic ass�d w/ cancer (adenoca lung and GI); Liebmann-Sacks endocarditis rarely embolizes MV prolapse: increased risk is small; massive stroke rare Paradoxical embolus Left atrial myxoma Prosthetic heart valve: anticoagulate

50. Stroke: Etiology (hematologic) Thrombocytosis (platelets >1,000,000/uL) Polycythemia (hematocrit >50-60%) Leukocytosis (WBC>150,000/uL) Sickle Cell Disease Hypercoagulable states Polycythemia: treat with venasection Sickle cell dis. (HgbSS): large vessel occlusion esp�lly; occassionally small vessels. Decrease HgbSS to <20% if angio (contrast may cause sickling) Hypercoagulable states: hyperviscosity (paraproteinemia, macroglobulinemia) pregnancy estrogen therapy postpartum postop. cancer antiphospholipid antibody synd (Lupus anticoag., anticardiolipin antibody) heparin cofactor II deficiency protein C or S deficiency factor XII deficiency antithrombin III deficiencyPolycythemia: treat with venasection Sickle cell dis. (HgbSS): large vessel occlusion esp�lly; occassionally small vessels. Decrease HgbSS to <20% if angio (contrast may cause sickling) Hypercoagulable states: hyperviscosity (paraproteinemia, macroglobulinemia) pregnancy estrogen therapy postpartum postop. cancer antiphospholipid antibody synd (Lupus anticoag., anticardiolipin antibody) heparin cofactor II deficiency protein C or S deficiency factor XII deficiency antithrombin III deficiency

51. Hypercoagulable States hyperviscosity syndrome pregnancy & postpartum estrogen therapy postoperative cancer antiphospholipid antibody syndrome protein C or S deficiency antithrombin III deficiency Factor V Leiden mutation

52. Prevention of Future Stroke Antiplatelet agents Coumadin Mechanical procedures (ie, Carotid Endarterectomy)

54. Secondary PreventionMedical Treatments

56. Stroke PreventionFatal or Nonfatal Stroke in CAPRIE

57. ESPS-2 Results: RRR for All Strokes

58. Stroke PreventionCardiogenic Brain Embolism

59. Stroke PreventionWarfarin on LV Dysfunction

63. Intracranial Hemorrhage The brain is a highly vascular organ It receives 20% of the cardiac output Prone to hemorrhage Fixed volume contraints of the skull result in unique consequences These consequences are the cause for concern and uneasiness of many physicians

64. Intracranial Hemorrhage Categorized based on location Intraparenchymal Subarachnoid Subdural Epidural Similar clinical presentations Easily diagnosed by CT scan Treatments differ

65. Intracranial Hemorrhage The brain is surrounded by multiple tissue layers Many areas of the brain are supplied by perforator arteries Berry aneurisms occur most frequently in the circle of Willis

66. Intracranial Hemorrhage Intraparenchymal Hemorrhage

67. Intracranial Hemorrhage Intraparenchymal Hemorrhage Charcot-Bouchard aneurism

68. Intracranial Hemorrhage Intraparenchymal Hemorrhage Charcot-Bouchard aneurism Hypertensive hemorrhage Spontaneous hemorrhage

69. Intracranial Hemorrhage Intraparenchymal Hemorrhage Charcot-Bouchard aneurism Hypertensive hemorrhage Spontaneous hemorrhage Occur in Basal ganglia, thalamus, pons, cerebellum

70. Intracranial Hemorrhage Intraparenchymal Hemorrhage Charcot-Bouchard aneurism Hypertensive hemorrhage Spontaneous hemorrhage Occur in Basal ganglia, thalamus, pons, cerebellum Controvery exists regarding best treatment

71. Intracranial Hemorrhage Subarachnoid Hemorrhage

72. Intracranial Hemorrhage Subarachnoid Hemorrhage Most blood is present in the basal cisterns

73. Intracranial Hemorrhage Subarachnoid Hemorrhage Most blood is present in the basal cisterns Results from rupture of a berry aneurism

74. Intracranial Hemorrhage Subarachnoid Hemorrhage Most blood is present in the basal cisterns Results from rupture of a berry aneurism Occur most commonly in the anterior circulation

75. Intracranial Hemorrhage Subarachnoid Hemorrhage Most blood is present in the basal cisterns Results from rupture of a berry aneurism Occur most commonly in the anterior circulation Has significant early and late complications

76. Intracranial Hemorrhage Subarachnoid Hemorrhage Most blood is present in the basal cisterns Results from rupture of a berry aneurism Occur most commonly in the anterior circulation Has significant early and late complications Treatment is prevention of complications

77. Intracranial Hemorrhage Subdural Hemorrhage

78. Intracranial Hemorrhage Subdural Hemorrhage Felt to be associated with venous bleeding

79. Intracranial Hemorrhage Subdural Hemorrhage Felt to be associated with venous bleeding May be associated with trauma

80. Intracranial Hemorrhage Subdural Hemorrhage Felt to be associated with venous bleeding May be associated with trauma Subjacent brain often traumatized

81. Intracranial Hemorrhage Subdural Hemorrhage Felt to be associated with venous bleeding May be associated with trauma Subjacent brain often traumatized Treatment is surgical drainage

82. Intracranial Hemorrhage Epidural Hemorrhage Arterial bleeding

83. Intracranial Hemorrhage Epidural Hemorrhage Arterial bleeding May be associated with a lucid period followed by rapid deterioration Often associated with trauma and skull fracture Treatment is surgical drainage

84. Intracranial Hemorrhage Future Challenges: To develop systems to provide rapid evaluation and treatment of these lesions To develop innovation in treatments Maximize potential for recovery

85. Case 1 52 y/o found confused in car by the side of the road on 3/14/01. Arrived in ER approximately 18:00 Intubated, sedated secondary to vomiting Right hemiparesis Bilateral upgoing toes Fluctuating level of consciousness

86. Case 1 Last seen normal at 17:15 CT scan showed no evidence of stroke or hemorrhage Received tPA at 19:58.

87. MRA 3/17/01

88. MRI 3/17/01

89. Discharge 3/27/01

90. Head CT 5/11/01

91. Clinic 5/10/01

92. Case 2 History 53 y/o female presenting with one week of headache and confusion and bilateral thalamic lesions. Exam Obtunded Reacted to pain with flexion

93. Initial MRI

94. Post Biopsy CT

95. MRV

99. Final CT

100. Again, these are special cases that do not represent the normal stroke patient but they illustrate the increasing complexity of the treatment of stroke and how it may be delivered in a Neurovascular center setting.Again, these are special cases that do not represent the normal stroke patient but they illustrate the increasing complexity of the treatment of stroke and how it may be delivered in a Neurovascular center setting.

102. Cerebrovascular Disorder . I like this title. Neurologists intervening. Most will think of procedural intervention, but as I am about to show you it goes well beyond that.I like this title. Neurologists intervening. Most will think of procedural intervention, but as I am about to show you it goes well beyond that.

103. Cerebrovascular Disorder References -Neurosonology by CH Tegeler et al Mosby 1995 -Principles of Neurology by RD Adams and M. Victor,5th edition ,1993 -AHA Guideline of management of unruptured intracranial aneurysm.Stroke 31:2742-2750.2000 -AHA Guideline :Surgery in intracerebral hemorrhage.Stroke .31:2511-2516,2000

104. Cerebrovascular Disorder References AHA Guideline:Theinopyridines VS ASA to prevent Stroke and Vascular disease.Stroke 31:31;1779-1784,2000 AHA Guideline: Atrial Fibrillation. Stroke 32:803-808,2001 AHA Guideline:Guideline for TIA management Stroke 30: 2502-2511,1999 AHA Guideline:Carotid Endarterectomy for asymptomatic stenosis:Stroke 29:554-562,1998

105. Cerebrovascular Disorder References AHA Guideline: Comparison of angioplasty VS endarterectomy for symptomatic carotid artery disease, Stroke 31;1439-1443,2000 AHA Guideline:Calcium antagonists, Stroke 32:570-576,2001- Meta analysis of 29 trials -Don�t help in acute stroke AHA Guideline: Intravenous Unfractionated Heparin is not helpful in acute stroke Stroke 32:579,2001

106. Cerebrovascular Disorder References CAST Study and IST study ( 40,000 patients) �ASA at the dose of160 mg and 300 mg as an acute treatment prevents early recurrence of stroke.The benefit is about 1%

107. Cerebrovascular Disorder Intracerebral Hemorrhage Cerebral Ischemia Stroke Classification Investigations Major Vascular anatomy Treatment

108. Cerebrovascular Disorder Intracerebral hemorrhage Epidural hematoma Subdural hematoma Subarachnoid hemorrhage Intraparenchymal hemorrhage Intraventricular hemorrhage

109. Cerebrovascular Disorder Epidural hematoma -Associated with head injury -Bleeding from arterial blood � middle meningeal artery -Bleeeding between the dura mater and skull -Lucid interval may be described -Radiographically- lens shape blood /skull x-rays �fracture across the middle meningeal artery groove -Treatment � surgical evacuation -Good prognosis if intervene early

110. Cerebrovascular Disorder Subdural hematoma Acute subdural hematoma Chronic subdural hematoma

111. Cerebrovascular Disorder Acute subdural hematoma -Almost always associated with head injury -Bleed between arachnoid and dura mater -Almost always associated parenchymal injury-hemorrhagic contusion -Prognosis is not so good because of associated with parenchymal injury -Radiographically showed blood covering along concavity of the brain

112. Cerebrovascular Disorder Chronic subdural hematoma -May or may not associated with head injury -Specific patient population-old age,alcoholic,demented and coagulopathic patient -Non specific symptoms- headache , partial or generalize seizure,mental status change,asymptomatic -Bleeding from the venous blood �bridging vein

113. Cerebrovascular Disorder Chronic subdural hematoma -Prognosis is not the best- probably due to underlying condition -Treatment � surgical ,if symptomatic

114. Cerebrovascular Disorder Subarachnoid hemorrhage a)Post traumatic subarachnoid hemorrhage b)Aneursysmal subarachnoid hemorrhage c)Subarachnoid hemorrhage from AVM � Need to know AHA guideline for incidental aneurysm�

115. Cerebrovascular Disorder Post traumatic subarachnoid hemorrhage a) History is very important-accident happen before headache b) Specific locations- frontal/temporal( due to the brain slide on the rough part of the skull) and occipital( due to contre coup) c) Occasionally associated with hemorrhagic contusion of of the temporal/frontal lobe d) No specific treatment e) If in doubt �get an angiogram to R/O aneurysm

116. Cerebrovascular Disorder Aneurysmal subarachnoid hemorrhage Hunt and Hess Scale Grade I-Asymptomatic or slight headache and stiff neck Grade II- Mod- severe headache and stiff neck without focal neurological finding Grade III- Drowsiness,Confusion, with mild neurological deficit Grade IV- Stupor/semicoma,decerebrate rigidity Grade V- Deep Coma and decerebrate rigidity

117. Cerebrovascular Disorder Aneurysmal subarachnoid hemorrhage -Need to know Hunt & Hess scale � clinical scale estimated the clinical outcome -Need to know Fisher�s scale � radiographic scale predict the risk of symptomatic vasospasm -Aneurysm usually arise around circle of Willis -Need 4 vessels cerebral angiogram with cross compression because of 20-25 % of patient with SAH has more than one aneurysm and need to evaluate the adequacy of collateral circulation if need to sacrifice the ICA

118. Cerebrovascular Disorder Aneurysmal subarachnoid hemorrhage Treatment of aneurysm is to exclude aneurysm from the circulation-clipping or coiling Pre- op � BP control,Pain control, laxative and Nimodipine Post �op- Watch for neurological changes- could be due to 1) Vasospasm 2) hydrocephalus 3) Other ongoing medical conditions and 4) less likely rebleeding

119. Cerebrovascular Disorder Aneurysmal subarachnoid hemorrhage Vasospasm- usually started around day #5 after hemorrhage -Monitor by TCD- high velocity of MCA and MCA/ICA ratio>3 -Treatment of vasospasm � HHH therapy-hypertensive,hemodiluation and hyperdynamic -If intractable �intraarterial papaverine or angioplasty or �Pentobarbital coma�

120. Cerebrovascular Disorder Aneurysmal subarachnoid hemorrhage -Radiographic and symptomatic vasospasm -Nimodipine study �The incidence of vasospasm are the same in both groups,but the clinical outcome in Nimodipine group is better. Believe that Nimodipine work at smaller vessels or the cellular level to prevent the ischemic cascade

121. Cerebrovascular Disorder Unruptured aneurysm �seen incidentally What to do ?/ What to do ? Data from ISUIA( international study for unruptured intracranial aneurysm) Rate of rupture chiefly depends on size( <10mm �0.005% / year,>10mm � 1% /year,>25 mm- 6% for the first year) Locations- Posterior circulation have greater rate of rupture MRA is useful as a screening test up to 93% sensitivity compared with cerebral angiogram

122. Cerebrovascular Disorder Unruptured aneurysm �seen incidentally What to do ?/ What to do ? Cerebral angiogram come with neurological morbidity ~ 0.5% Special group of patient warrant screening- Coarctation of Aorta,Polycystic Kidney,Type IV Ehlers-Danlos syndrome and familial intracranial aneurysm syndrome Symptomatic unruptured aneurysm ( eg 3rd palsy) have more risk than truly unruptured aneurysm

123. Cerebrovascular Disorder Unruptured/ Ruptured aneurysm What to do ?/ What to do ?- AHA recommendation -Treatment of small incidental intracavernous aneurysm is not generally indicated.Large ones should be individualized -Symptomatic intradural aneurysm should be considered for treatment with urgency All remaining aneursym of patient with prior SAH should be considered for treatment Treatment of small incidental aneurysm without prior SAH are not advised

124. Cerebrovascular Disorder Unruptured/ Ruptured aneurysm What to do ?/ What to do ?- AHA recommendation -Treatment is recommend for > 10 mm in size Need to consider the patient age and coexisting medical problems as well as life span rate of rupture per year and calculate the necessity of treatment

125. Cerebrovascular Disorder Intracerebral hemorrhage -Hypertensive Hemorrhage- 4 common locations 1)Basal ganglion � Caudate/Putaminal � be careful A-com aneurysm pointing backward 2) Thalamus 3) Pontine and 4) Cerebellar Hemorrhage Need to know Charcot � Bouchard aneurysm- in the matching section

126. Cerebrovascular Disorder Intracerebral hemorrhage -Non hypertensive �Peripheral located a) Age ? �old � consider amyloid angiopathy /Congophillic angiopathy- presented with recurrent lobar hemorrhage and dementia.The most common location of hemorrhage is parietal lobe. Finding under polarized microscope- Birefringent crystral

127. Cerebrovascular Disorder Intracerebral hemorrhage -Non hypertensive �Peripheral located Age ? �old � another consideration is bleeding in metastatic tumor Metastatic tumor likely to go to brain early-Thyroid ,Lungs ,Breast,Renal cell carcinoma ,testicular,Choriocarcinoma ,melanoma and Colon plus GBM( which is primary brain tumor)� these types of tumor can manifest by bleeding in the brain

128. Cerebrovascular Disorder Intracerebral hemorrhage To remember - Paired organ mets to the brain early Use ovary( which is paired organ link to Choriocarcionoma) If one wants to remember � paired organ + Colon+ Melanoma+ GBM

129. Cerebrovascular Disorder -Intracerebral hemorrhage �non hypertensive/non- lobar,doesn�t look like tumor and patient is not old 1)Vasculitis � underlying connective tissue disease 2)Venous sinus thrombosis- post partum /severe dehydration 3)Drug abuse-Needle track-Cocaine or Heroin 4)Endocarditis �Mycotic aneurysm �Fever and cardiac murmer 5)Teenager- Diet Pill-Amphetamine/Phenyl Propranolamine

130. Cerebrovascular Disorder Isolated intraventricular hemorrhage-not common -Vascular anomaly- AVM or aneurysm -Hypertensive hemorrhage that rupture in ventricular system with minimal blood in the parenchyma -Coagulopathy

131. Cerebrovascular Disorder Evaluation of Ischemic stroke -Need to know the etiology of stroke -The treatment plan tailor according to etiology and need to be addressed accordingly -Need to evaluate the whole vascular system, if possible

132. Cerebrovascular Disorder Evaluation of Ischemic stroke Carotid ultrasound and TCD MRI and MRA �both intracranially and extracranially Transesophageal Echocardiogram CT angiogram

133. Cerebrovascular Disorder Evaluation of Ischemic stroke Carotid Ultrasound Screening test �usually give the range of stenosis,use velocity as to predict stenosis B-Mode is use to identify anatomy and plaque characteristic Color doppler �help locate the location to sample the velocity d) Use to follow the carotid non- invasively

134. Cerebrovascular Disorder Evaluation of Ischemic stroke Carotid Ultrasound Pitfall Accelerating flow without stenosis-Anemia,hyperthyroidism,Aortic insufficiency ,old patient with tortuousity Difficult or impossible to differentiate between preocclusion and occlusion-unless Power Doppler is used.

135. Cerebrovascular Disorder Evaluation of Ischemic stroke Trancranial Doppler Use Continuous wave doppler to evaluate the velocity of the 1st order of intracranial vessels 10-15 % of the studies are technically limited due to skull thickness and displacement from normal location Other use including monitoring vasospasm and evaluate the need to do blood exchange in sickle cell disease

136. Cerebrovascular Disorder Evaluation of Ischemic stroke Trancranial Doppler �Viewing Vessels� according to the window Transtemporal � distal ICA, MCA-M1 portion, ACA and PCA- P1 portion Transorbital- distal ICA,Carotid siphon,Opthalmic artery Foramen Magnum- vertebral arteries and basilar artery

137. Cerebrovascular Disorder Evaluation of Ischemic stroke 2-D echocardiogram -Limited sensitivity -Can�t evaluate aortic arch ,which is one of the independent risk factor - Inadequate sensitivity as a complete evaluation

138. Cerebrovascular Disorder Evaluation of Ischemic stroke Tranesophageal echocardiogram -Much superior sensitivity -Taking advantage of the anatomy of the esophagus lies just behind the left side of the heart and much closer in location,therefore increase ultrasound resolution -Capable to evaluate aortic arch plaque and LAA -Not invasive/or expensive as we thought -2 cases of endocarditis being missed by 2-D echocardiogram -Role of TEE of �asymptomatic� CAD

139. Cerebrovascular Disorder Evaluation of Ischemic stroke MRI -Evaluated infarcted area esp brain stem . -Evaluated brain parenchyma at risk -DWI showed the acute infarction earlier than T2 and FLAIR -R/O any �surprised� lesion

140. Cerebrovascular Disorder Evaluation of Ischemic stroke MRA -Need to evaluate both extracranial and intracranial vessels -Intracranial stenosis is another new entity of risk factor Limitationn of MR Severe claustophobic Metallic fragment in head and neck area Recent stenting � either heart or head Pacemaker and AICD

141. Cerebrovascular Disorder Evaluation of Ischemic stroke CT angiography Recent new technology Use Iodine dye Small slice of the of each portion of the vessels

143. Cerebrovascular Disorder Evaluation of Ischemic stroke CT angiography Limitation Uncooperative patient Dye allergy Time consuming of radiologist Renal dysfunction

144. Cerebrovascular Disorder Evaluation of Ischemic stroke Cerebral angiogram -Gold standard test -Able to evaluate both intracranial and extracranialvessels -Give the anatomical data -Associated with small risk-stroke,groin hematoma etc -Can discover ostial vertebral artery stenosis- potential risk of stroke

145. Cerebrovascular Disorder Evaluation of Ischemic stroke Newly identified / less common risk factors of stroke -Lupus anticoagulant? Anticardiolipin antibody syndrome -Protein C/S deficiency -Factor V Leiden Mutation- Activated protein C resistance -Heterozygote form of Hyperhomocysteine- methionine loading test -Vasculitis process- either primary or secondary angiitis

146. Cerebrovascular Disorder Treatment of stroke Acute treatment a) Thrombolysis- t �PA intravenously 2 landmark studies- NINNDS and ECASS Intraarterial � with various medications /time windows- have not been demonstrate successful( doesn�t mean they don�t work) Total more than 17 studies- 2 intraarterial and 15 intravenous consisted total of 5144 Patients

147. Cerebrovascular Disorder Treatment of stroke Acute treatment Neuroprotective agents- attack various locations of of ischemic cascades-free radical scarvenger, glutamate antagonist esp NMDA receptor ,Na and Ca channel blockers,ICAM - Up to 47 studies showed no benefit-doesn�t mean they don�t work though

148. Cerebrovascular Disorder Treatment of stroke Primary stroke prevention- the only well known data is AF SPAF I-compared placebo and anticoagulation( either ASA or coumadin) The study terminated prior to complete enrollment because of the placebo group got to end point sooner The data suggest that patient with AF required some type of anticoagulation This study also identified 3 more risk factors associated with AF including diastolic hypertension,poor LV function and remote history of thromboembolism( more than 3 months)

149. Cerebrovascular Disorder Treatment of stroke- Primary stroke prevention in AF SPAF II- compared the efficacy of ASA and coumadin at different age group( less than and more than 75 YO) This study showed coumadin is slightly more effective than ASA in younger age group- but this group of patient has low risk any way In older age group, coumadin is much more effective than ASA in term of preventing ischemic stroke but after adding the risk of ICH make the beneficial effect marginal.

150. Cerebrovascular Disorder Treatment of stroke- Primary stroke prevention in AF SPAF III- comparing the efficacy of fixed dose coumadin plus ASA to against adjusted dose of coumadin to keep INR in the good range The study was terminated early by safety committee because the fixed dose of coumadin plus ASA group reach the primary end point more often and faster.

151. Cerebrovascular Disorder Treatment of stroke- Secondary stroke prevention in AF The study that worth mentioned is EAFT-European atrial fibrillation trial The randomization was pretty much similar to SPAF study but the mean age is older and INR level was higher. The result of the study is the similar to SPAF suggest that coumadin is better than ASA The risk of intracerebral bleeding in coumadin group is higher and almost eliminate the beneficial effect of prevention from coumadin

152. Cerebrovascular Disorder Treatment of stroke- Meta-analysis of antiplatelet drug trialist comparing various doses of ASA and various different entering criteria and end-points The meta-analysis showed that ASA reduce the risk of recurrent stroke approximately 25% comparing with placebo

153. Cerebrovascular Disorder Carotid stenosis �2 Major worth mentioned studies NASCET � North American symptomatic carotid endartectomy trial- Secondary prevention ACAS � Asymptomatic Carotid Artery Study-Primary prevention

154. Cerebrovascular Disorder NASCET study -Symptomatic patient- either TIA or non- disabling stroke -Comparing best medical treatment and CEA+ best medical treatment -Relatively low risk patient -Strict angiographic criteria-not ultrasound nor MRA -No tandem lesion/R/O cardioembolic source -Best surgeons in the world with very low morbidity and mortality

155. Cerebrovascular Disorder NASCET study Less than 50% stenosis � Best medical treatment More than 70 % stenosis � Surgery with best medical treatment is better In between, medical and surgical treatment + medical treatment are equally good. Subgroup analysis � Women do poorer than men, left carotid do poorer than right carotid Overall the absolute risk reduction is around 25% over 24 months period

156. NASCETIpsilateral Stroke (18 Months)

157. Cerebrovascular Disorder ACAS study -Asymptomatic carotid stenosis -Very low risk patient -Over all risk of ipsilateral stroke in the 60% stenosis around 11% over 60 months -Overall the surgical risk around 5% on the day of surgery