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TIA and CVA
- 1. TIA and CVA Robert K. O’Sullivan, PA-C, MPAS Clinical Medicine II May 20, 2011
- 2. Objectives Define Transient Ischemic Attack (TIA) Define Cerebral Vascular Accident (CVA) Identify the Anterior and Posterior Cerebral Vascular Supply Distinguish the Pathophysiological differences between Ischemic and Hemorrhagic strokes
- 3. Objectives (continued) Discuss the Epidemiology and Risk Factors for Ischemic & Hemorrhagic strokes For TIA & CVA’s, describe the significant historical and physical exam findings, appropriate diagnostic investigations, emergency treatment, rehab & prevention
- 4. (more) Objectives (we’re flyin’ now) As they relate to TIA’s/CVA, Discuss the significance of... Atherosclerosis Drug Abuse Venous Thrombosis Migraine Hematological disorders Cardiogenic Embolism Hypertension
- 5. Yet more Objectives (really???) Discuss Stroke Syndromes, including... Lucunar Infarctions Cerebral Infarctions Intracerebral Hemorrhage Subarachnoid Hemorrhage Intercranial Aneurism Arteriovenous Malformations Intracranial Venous thrombosis
- 6. Pre-Lecture Questions What artery is most commonly involved in a stroke? Define the abbreviation: FAST! What are the main categories of strokes? A 63 y.o. previously healthy man awakens at 6 am with weakness of the left arm and leg and difficulty walking. He arrives at the hospital at 7 am and a CT scan is immediately performed, the results of which are normal. What dose of t-PA should he receive?
- 7. Key Points for TIA/CVA TIA’s & CVA’s are emergencies Patients acutely suffering these disorders need IMMEDIATE MEDICAL ATTENTION Act FAST! (Face, Arm, Speech, Time) It is important for the PA to have a good understanding of neuroanatomy and brain function, because... There are significant risks associated with TIA/ CVA treatments (and patients must understand these risks) Prevention is the best therapy
- 8. Anatomy & Physiology Cerebral Review Arteries Coverings of the Brain Sensory Anatomy Functional Anatomy & Physiology
- 9. Cerebral Vasculature Review Fill in the blanks.... A= S= CC= V= IC= EC=
- 12. Internal Cerebral Arteries
- 13. Coverings of the Brain
- 14. Sensory Anatomy
- 17. Neurology Definitions Aphasia means... Aphagia example poor articulation inability to produce written or spoken language innate difficulty learning mathematics gross lack of coordination of muscle movements difficulty swallowing
- 18. Transient Ischemic Attacks Transient Ischemic Attack Video
- 19. Transient Ischemic Attacks Essential of Diagnosis Focal Neurological Deficit which completely resolves within 24 hours Often associated with risk factors for vascular diseases 40% of all people who have experienced a TIA will go on to have a stroke Nearly half within 2 days
- 20. Transient Ischemic Attack Etiology Cardiac sources Vessel wall embolus (most Atrial fibrillation common) Mitral valve stenosis Carotid artery most often the source Mitral valve prolapse Related to thrombus Calcified mitral annulus formation distal to stenosis Ventricular aneurysm Atrial or ventricular clot Valvular vegetation Atrial septal defect
- 21. Transient Ischemic Attack Etiology Less common etiologies (age <45 years) Other vascular sources Subclavian Steal Intracranial artery Syndrome thrombus (esp. African- Americans) Hyperviscosity (e.g. polycythemia vera) Aortic arch atherosclerotic plaque Hypercoagulable state Transient hypotension Carotid dissection with carotid stenosis >75% Vertebral artery dissection
- 22. Transient Ischemic Attack Signs and symptoms Carotid territory Abrupt onset without Weakness and warning heaviness of contralateral arm, leg, Symptoms vary markedly or face or combination between patients Numbness and paresthesias Bradykinesia, dysphasia, monocular vision loss on ipsilateral side +/- carotid bruit
- 23. Transient Ischemic Attack Signs and symptoms Weakness or sensory complaints on one, Vertebrobasilar TIAs both, or alternating sides of the body Vertigo Ataxia Diplopia Dysarthria Dimness or blurring of vision Perioral numbness or paresthesias
- 24. Transient Ischemic Attack (TIA) Risk of stroke increases with... Carotid TIAs > vertebrobasilar TIAs Age > 60 years Diabetes TIAs that last longer than 10 minutes Signs and symptoms of weakness, speech impairment, or gait disturbance
- 25. Transient Ischemic Attack Imaging CT of the head U/S of cerebral circulation Doppler U/S of carotid arteries Arteriography MR angiography less sensitive than conventional arteriography
- 26. Transient Ischemic Attack Labs and other studies EKG (why?) Chest x-ray CBC Consider Fasting blood glucose echocardiography or Holter monitor Serum cholesterol Homocysteine level Serologic tests for syphilis (bonus question: Organism that causes syphilis is...Treponema pallidum
- 27. Transient Ischemic Attacks Differential diagnosis Focal seizures Classic migraine Hypoglycemic episodes TIA mimick
- 28. Treatment of TIA’s Treatment is divided into two choices... Medical therapy aimed at preventing further attacks or strokes to include... Smoking cessation Treatment of underlying disease (HTN, DM, etc.) Carotid endarterectomy
- 30. Treatment of TIA Embolization from the heart Anticoagulation IV heparin until coumadin level is therapeutic Aspirin may be used for people who cannot tolerate coumadin Embolization from the cerebrovascular system Aspirin 325 mg daily Plavix (clopidogrel) 75 mg daily if intolerant of aspirin Coumadin for 3-6 months does not provide any benefits over aspirin
- 31. Quiz... Which thrombolytic agent is naturally occurring within the body (hint: secreted from MAST cells) A. Aspirin B. Heparin C. Warfarin D. Coumadin E. Clopidogrel
- 32. Cerebral Vascular Accidents (AKA: “the Stroke”)
- 33. Cerebrovascular Accident AKA stroke Essentials of diagnosis Sudden onset of characteristic neurologic deficit Often a history of HTN, DM, valvular heart disease or atherosclerosis Distinctive neurologic signs reflect the region of the brain involved
- 34. CVA; the “killer” stats Third leading cause of death in the US General decline in incidence over the past 30 years 87% are ischemic due to large artery atherosclerosis, cardioembiolism & other 13% due are hemorragic in intracerebral or subarachnoid locations
- 35. CVA Risk Factors include... HTN/Elevated BP Diabetes Mellitus Hyperlipidemia Cigarette smoking Cardiac disease AIDS Drug abuse/EtOH Family history of CVA Elevated blood homocysteine level
- 36. Cerebrovascular Accident Classification of Strokes True or False: Reliable distinction Infarcts between a Thrombotic intracerebral hemorrhage and Embolic ischemic stroke can only be done by neuroimagining Hemorrhages A reading...
- 37. Stroke Subtypes Lucunar Infarctions Cerebral Infarctions Intracerebral Hemorrhage Subarachnoid Hemorrhage Intercranial Aneurism Arteriovenous Malformations Intracranial Venous thrombosis
- 38. Lacunar Infarctions Small lesions (usually < 5 mm) Accounts for approx 25% of ischemic strokes Occurs in distribution of short penetrating arterioles in the basal ganglia, pons, cerebellum, anterior limb of the internal capsule, and less commonly deep cerebral white matter Associated with poorly controlled HTN or diabetes
- 39. Lacunar Infarctions Signs and symptoms Contralateral pure motor or pure sensory deficit Ipsilateral ataxia with crural paresis (weakness) Dysarthria with clumsiness of the hand Deficit may progress over 24-36 hours before stabilizing
- 40. Lacunar Infarction Imaging Sometimes seen on CT as small, punched-out, hypodense areas CT often normal Prognosis is usually good with partial or complete resolution in 4-6 weeks
- 41. Cerebral Infarction Thrombotic or embolic occlusion of a major vessel Cerebral ischemia leads to release of excitatory and other neuropeptides that increase Ca++ flux into neurons causing cell death and increasing the neurologic deficit Abrupt onset
- 42. Cerebral Infarction Obstruction of carotid Occlusion of anterior circulation cerebral artery Occlusion of ophthalmic Weakness and artery may cause sensory loss in the amaurosis fugax (can be contralateral leg seen with a TIA as well) May see contralateral grasp reflex, rigidity, abulia, or confusion Urinary incontinence Behavioral changes and memory disturbances
- 43. Cerebral Infarction Obstruction of carotid Global aphasia if circulation dominant hemisphere involved Occlusion of middle cerebral artery Drowsiness, stupor, and coma Contralateral hemiplegia, Dressing apraxia hemisensory loss, homonymous Constructional and hemianopsia spatial deficits Eyes deviate to side of the lesion
- 44. Cerebral Infarction Obstruction of Macular-sparing vertebrobasilar circulation homonymous hemianopia Occlusion of posterior cerebral artery Mild, usually temporary Thalamic syndrome: hemiparesis contralateral hemisensory Occlusion of vertebral disturbance artery followed by development of May be clinically spontaneous pain silent and hyperpathia (what is Hyperpathia?)
- 45. Cerebral Infarction Obstruction of If hemiplegia is of vertebrobasilar circulation pontine origin, eyes are often deviated to Occlusion of both the paralyzed side vertebral arteries or basilar artery Coma with pinpoint pupils Flaccid quadriplegia and sensory loss Variable cranial nerve abnormalities
- 46. Cerebral Infarction Obstruction of vertebrobasilar circulation (cont’d) Occlusion of major cerebellar arteries Vertigo Nausea and vomiting Nystagmus Ipsilateral limb ataxia Contralateral spinothalamic sensory loss in the limbs
- 47. Cerebral Infarction Imaging CT of the head to exclude cerebral hemorrhage CT preferable to MRI in acute stages Carotid duplex studies MRI (diffusion- weighted more sensitive) and MR angiography
- 49. Labs for Cerebral Infarction Labs and other studies CBC Sed rate Blood glucose Serologic tests for syphilis Serum cholesterol Serum homocysteine EKG, Echo, Holter monitor Blood cultures
- 50. Treatment of Infarctions Ideally, in a stroke care unit Intravenous Thrombolytic Therapy rapid Tissue Plasminogen Activator (rTPA) Supportive Measures Anticoagulants if cardiac cause of emboli Warfarin Physical, occupational and speech therapy
- 51. r-TPA Therapy Effective in select patients with no CT evidence of hemorrhage Start as soon as possible, not more than 4.5 hrs after onset (some say only 3 hrs) Contra-indications include: Recent or increased risk for hemorrhage, (i.e. recent trauma, surgery), markedly high BP (>185/110), others...
- 52. Cerebral Infarction Prognosis Prognosis for cerebral infarction is better than for cerebral or subarachnoid hemorrhage Depends on time that elapses before arriving at the hospital – if patient has TPa they are 30% more likely to have no disability at 3 months Loss or consciousness implies a poorer prognosis
- 54. Intracerebral Hemorrhage Usually due to hypertension and presence of microaneurysms Most frequently in basal ganglia Less commonly in the pons, thalamus, cerebellum, and cerebral white matter Usually occur suddenly and without warning during activity
- 55. Intracerebral Hemorrhage May also occur with... EtOH Hematologic and Brain tumors bleeding disorders Leukemia Hemophilia DIC Anticoagulant therapy Liver disease Cerebral amyloid angiopathy
- 56. Intracerebral Hemorrhage Signs and symptoms Initial loss or impairment of consciousness Vomiting and headache Focal signs and symptoms Loss of gaze Cerebellar hemorrhage Nausea and vomiting, disequilibrium, headache Loss of consciousness that may lead to death within 48 hours
- 57. Intracerebral Hemorrhage Imaging CT scan without contrast (determines location and size of the bleed) Superior to MRI in first 48 hours Cerebral angiography if the patient’s condition allows
- 58. Intracerebral Hemorrhage Labs and other studies CBC Platelet count Liver function tests Renal function tests Bleeding times LP is contraindicated (may cause a herniation syndrome)
- 59. Intracerebral Hemorrhage Treatment Management is generally Treatment of underlying conservative and structural lesions supportive Trials of recombinant Ventricular drainage may activated factor VII be required given with a few hours have been tried (have Decompression of not shown improved superficial hematoma survival) Prompt surgical evacuation of cerebellar hemorrhage
- 61. Subarachnoid Hemorrhage Essentials of diagnosis General considerations Sudden, severe Causes 5 – 10% of headache “the worst strokes headache of my life” Signs of meningeal irritation Obtundation is common Focal deficits are frequently absent
- 62. Subarachnoid Hemorrhage Signs and symptoms Sudden onset of “worst headache of my life” Nausea and vomiting Loss or impairment of consciousness Altered mental status Nuchal rigidity and other signs of meningeal irritation Focal neurologic deficits may not be present
- 63. Subarachnoid Hemorrhage Imaging CT scan immediately If CT normal, a lumbar puncture should be done... 12 hours later Look for Xanthochromia (yellowish color to CSF from bilirubin) Once patient is stable, cerebral arteriography MR angiography is less useful
- 64. Brain-teaser Why is blood in CSF non-diagnostic in the case of a subarachnoid hemorrhage?
- 65. Subarachnoid Hemorrhage Treatment Conscious patients Confine to bed, avoid exertion or straining Treat symptoms (headache, constipation) Lower BP gradually keeping diastolic above 100 Phenytoin to prevent seizures
- 67. Intracranial Aneurysm Essentials of diagnosis Subarachnoid hemorrhage or focal deficit Abnormal imaging studies General considerations “Berry” aneurysms tend to occur at arterial bifurcations May be associated with PKD and coarctation of the aorta
- 68. Intracranial Aneurysm Risk factors Smoking Hypertension Hypercholesterolemia Signs and symptoms Most are asymptomatic May cause focal neurologic deficit from mass effect
- 69. Intracranial Aneurysm Imaging CT scan will show if a bleed has occurred Angiography Labs and other studies CSF may show blood EEG EKG
- 70. Intracranial Aneurysm Treatment Major aim of treatment is to prevent further hemorrhages Definitive treatment requires surgical clipping or coil embolization
- 71. Intracranial Aneurysm Treatment (continued)... Risk of further hemorrhage is greatest within first 6 months Calcium channel blockers to reduce vasospasm
- 72. Arteriovenous (AV) Malformations
- 73. Arteriovenous (AV) Malformations Essentials of diagnosis Sudden onset of subarachnoid and intracerebral hemorrhage Seizures or focal deficits General considerations Congenital lesions Vary in size May have associated obstructive hydrocephalus
- 74. Arteriovenous Malformations Signs and symptoms Infratentorial lesions Supratentorial lesions Often clinically silent Most AV May lead to malformations are progressive or supratentorial relapsing brainstem deficits S/S of hemorrhage, recurrent seizures or headaches Abnormal mental status Meningeal irritation Increased ICP
- 75. Arteriovenous (AV) Malformations Imaging CT scan if bleeding present Arteriography Labs and other studies EEG for patients presenting with seizures Treatment Surgical treatment to prevent further hemorrhages
- 76. Arteriovenous (AV) Treatment Malformations For patients with seizures and no bleeding, anticonvulsants are usually sufficient Definitive surgical treatment excision of AV malformation Embolization if not surgically accessible Injection of vascular occlusive polymer Gamma knife
- 78. Intracranial Venous Thrombosis Associated with... Intracranial or maxillofacial infections Hypercoagulable states Polycythemia Sickle cell disease Pregnancy
- 79. Intracranial Venous Thrombosis Signs and symptoms Imaging Headache CT scan, MRI, MR venography Focal or generalized convulsions Drowsiness, confusion Increased ICP Focal neurologic deficits
- 80. Intracranial Venous Thrombosis Treatment Anticonvulsants for seizures Dexamethasone to decrease ICP Anticoagulation with heparin followed by coumadin for 6 months Catheter-directed thrombolytic therapy with urokinase and thrombectomy
- 81. What we covered... TIA’s CVA’s to include... Anatomy, Physiology & Pathophysiology Definitions Classification of Strokes (Ischemic & Hemorrhage) Stroke Sub-types
- 82. Any Questions?