Strokes in the Elderly

1. Strokes in the Elderly Edward Via Virginia College of Osteopathic Medicine Donald Noll DO FACOI Edited by Dr. Edward Warren Chair, Geriatrics Carolinas Campus May 2012

2. Learning objectives • Define stroke and list the types of stroke. • Evaluate patients for the signs and symptoms of different types of stroke. • List the differential diagnosis of stroke. • Order tests and evaluations rationally for stroke. • Treat and manage of stroke effectively.

3. General Considerations • Stroke is a neurologic deficit with a vascular etiology lasting over 24 hours. • Cerebral Vascular Accident is a synonym for stroke. • Stroke is third leading cause of death in the United States. • Cerebral ischemia is a reduction of blood flow and oxygen to the brain resulting in prompt neurologic deficits. If it persists, then infarctions of brain tissue occur with ischemic encephalopathy. • Transient ischemic attacks (TIA’s) are ischemia induced neurologic deficits persisting for < 24 hours. They generally resolve shortly.

4. Types of Stoke • Ischemic strokes occur from occluded arteries to part or all of the brain, resulting in brain infarction. • This is the most common type of stroke (80%) • It can be thrombotic where a clot forms in the artery • It can be embolic where clots break away upstream and lodge in the artery distally. • Hemorrhagic Strokes occur from bleeding inside or around the brain (20%) • Must be ruled out first, since treatment is vastly different. • Blood caused tissue swelling and edema, producing a “mass effect” in the brain.

5. Pathogenesis of Stroke • Atherosclerosis is the most common cause of stroke • Plaques cause strokes in three ways: • Thrombosis forms at the site of an atherosclerotic lesion, and the clot obstructs the artery there; • Ulceration or rupture of a plaque leads to formation of a clot with emboli to distal sites • Hemorrhage into a plaque obstructs the artery. • The clinical manifestations of a stroke depend on the rate of occlusion. If it occurs slowly, there may be time for collaterals to develop, and a stroke is avoided. • If the occlusion is abrupt, a stroke ensues. The degree of damage depends on the collaterals available to the territory of the brain that is supplied by the occluded vessel.

6. Hemorrhagic verses Ischemic • Early on, when acute therapy is potentially beneficial, it is impossible to predict whether a patient will recover spontaneously. • Hemorrhagic strokes are promptly diagnosed by seeing extravasated blood in the brain parenchyma, usually on a STAT CT scan. • Ischemic strokes can later bleed into the necrotic tissue, converting to hemorrhagic ones.

7. Lacunar Infarction • Small ischemic strokes, usually < 5 mm in size • Localized in the basal ganglia, pons, cerebellum, anterior limb of the internal capsule, and the deep cerebral white matter • Associated with poorly controlled HTN and DM • Cause pure contralateral motor or sensory loss, ipsilateral ataxia, dysarthria, or ataxia • Sometimes visible on CT scan as a punched out lesion, hypodense, but often unseen • Relatively good prognosis, partial or complete resolution common in 4 to 6 weeks

8. Emboli • Pieces of larger clots that break off from a mural thrombus in the heart or a more proximal artery and lodge downstream in the brain distally. • It is often impossible to distinguish thrombus from embolus by imaging methods, so the two processes are classified together.

9. Hemorrhagic stroke • Often severe at onset and may present with headache and rapidly evolving deficits • Ischemic strokes are normally painless and present as a fixed deficit or with a stuttering onset followed by rapid waxing and waning fluctuations

10. Subarachnoid Hemorrhage • It presents as a sudden and very severe headache (the worst headache of my life). Signs of meningeal irritation are usually present. Symptoms of mental confusion and obtundation are common. Focal deficits are frequently absent. • The CT scan is the best test to detect this promptly. Blood in the cerebrospinal fluid confirms subarachnoid hemorrhage, even if the CT scan is negative. • Treat with supportive care, slowly lower elevated blood pressure, but not below a diastolic level of 100mm Hg. Many patients are treated with phenytoin to prevent seizures prophylactically.

11. CEREBRAL VENOUS SINUS THROMBOSIS • Presents as headache, focal neurologic deficits, seizures, altered mental status, and papilledema. • Obstruction of the superior sagittal sinus is very serious andoften involves the veins draining the superior and medial surfaces of both cerebral convexities. • This results in bilateral weakness and sensory changes in the legs. • Seizures occur more often with venous than with arterial occlusion. • These venous occlusions occur most commonly in association with coagulopathies, often in the puerperal period, or in patients with disseminated cancer. The transverse sinus can be occluded as a consequence of inner ear infections, a condition called otitic hydrocephalus.

12. Major Risk Factors for Stoke • hypertension • diabetes mellitus • hyperlipidemia • cigarette smoking • cardiac disease • AIDS • recreational drug use • heavy alcohol consumption • family `history of a stoke • personal history of stroke

13. SYMPTOMS OF STROKE • At first neurologic symptoms and signs fluctuate and then deteriorate rapidly. • Many patients delay seeking medical care due to denial hoping for improvement. Often, it is family and friends who bring stroke patient to the ER or doctor’s office. Prompt attention is crucial for intervention to work. • If the symptoms completely resolve in 1 or 2 hours, the patient had a TIA. This resolution is from dissolution of the embolus with restoration of normal regional blood flow and decreased vasospasm.

14. Vascular Territory & Stroke Syndromes The next 8 slides define the patterns of paralysis and neurologic dysfunction see in different parts of the brain and different parts of the cerebral vasculature are affected.

15. INTERNAL CAROTID ARTERY • The common carotid artery bifurcation is the most common site for atherosclerotic lesions of the cerebral vessels. • Occlusion of the internal carotid artery (ICA) is often clinically silent if the circle of Willis is complete • It is often impossible to distinguish ICA occlusion from similar damage to the middle cerebral artery (MCA) on clinical examination. Because the ophthalmic artery originates from the ICA, however, TIAs of the ICA may present as transient monocular blindness (called amaurosis fugax)

16. ANTERIOR CEREBRAL ARTERY • Isolated occlusion of the anterior cerebral artery (ACA) is only 2% of all cerebral infarcts. • The principal symptoms associated with occlusion of an ACA are upper motor neuron weakness and cortical sensory signs deficits (neglect) in the contralateral leg. • Other manifestations of ACA occlusion may include: • Urinary incontinence, • Generalized depression of psychomotor activity (abulia), • Aphasia with loss of verbal fluency, but preserved ability to repeat. • Bilateral occlusion may occur because the origins of the two ACAs are close together. They are occasionally from a common source • Bilateral damage usually causes a patient to be mute, with severe mood disturbances, and long-lasting incontinence from the damaged frontal lobes.

17. MIDDLE CEREBRAL ARTERY • Strokes involving the MCA are the most commontype of focal ischemic stroke, causing approximately two thirds of all infarcts. • Occlusion of the stem of the MCA causes massive, devastating infarction of the hemisphere. • Cerebral edema during the first 3 to 4 days may lead to increased intracranial pressure with brain herniation. • The classic picture of occlusion of the MCA is contralateral weakness and sensory loss in the face and arm (with relative sparing of the leg) and homonymous hemianopia on the side of the weakness. • Gaze deviates toward the side of the lesion. • Full recovery is unlikely. In right-handed people, occlusion of the left MCA produces global aphasiawhich is both receptive and expressive. • In the nondominant hemisphere, unilateral neglect, anosognosia (unawareness of the deficit), and spatial disorientation occur.

18. Embolus to the MCA • Often lodges in one of its two main divisions • Occlusion of the superior division can cause dense sensorimotor deficits in the contralateral face and arm without initial impairment of alertness • Occlusion of the inferior division in the dominant hemisphere characteristically produce receptive aphasia of Wernicke's type (severe loss of speech comprehension with preserved spoken and written language) • Damage to either hemisphere can cause contralateral loss of integrated sensation, such as perception of shapes (stereognosis)

19. POSTERIOR CEREBRAL ARTERY • Both posterior cerebral arteries (PCAs) arise from the basilar artery ¾ of the time. • One PCA can arise from the basilar artery, and the other from the ICA, or both from the ICA’s. Thus, the syndromes associated with occlusion of the PCA are variable. • Strokes of the perforating branches cause complete contralateral hemianesthesia with loss of all sensation and complete ipsilateral hemianopsia. • Macular (central) vision may be spared because of collateral blood supply from the MCA. Difficulty reading (dyslexia) and performing calculations (dyscalculia) may occur. Recovery is often good, but the initial numbness may be replaced by paresthesias or excruciating pain: Dejerine-Roussy syndrome from damage to the thalamus. • Involvement of the subthalamic nucleus may produce hemiballismus, with wild flinging movements of the limbs on one side of the body

20. VERTEBRAL AND BASILAR ARTERIES • Occlusion of the blood supply to the brain stem causes a crossed syndrome with a contralateral weakness and selected contralateral and ipsilateral sensory symptoms below the level of the lesion, plus ipsilateral motor and sensory deficits localizing to the level of the lesion. • Weber's syndrome is a mesencephalic hematoma that produces an ipsilateral third cranial nerve palsy, resulting from damage to the oculomotor nucleus, plus contralateral weakness. • The vertebral arteries are the principal blood supply for the medulla. The posterior inferior cerebellar artery is usually a branch of the vertebral artery. The consequences of occlusion of a posterior inferior cerebellar artery vary. • Lateral medullary infarction with Wallenberg's syndrome is classically produced. In about 80% of cases, an occlusion of the vertebral artery causes lateral medullary syndrome, which consists of severe vertigo, nausea, vomiting, nystagmus, ipsilateral ataxia (of the cerebellar type), and ipsilateral Horner's syndrome (ptosis, myosis, and decreased sweating). • This syndrome also includes an ipsilateral loss of facial pain and temperature sensation and a contralateral loss of these in the trunk and limb.

21. Basilar Artery • Supplies most of the brain stem. • Its occlusion produces a variety of syndromes. • Obstruction of the trunk is often fatal. • Coma may occur, or patients may develop the locked-in syndrome, in which consciousness is preserved, but the victims are unable to move anything voluntarily except for their eyes or eyelids. • It is possible to communicate with these patients and demonstrate normal mental status by codes involving eye movements.

22. Brain Stem Strokes • Although small, ischemic strokes in the brain stem can produce major neurologic dysfunction • Tey may not be detected by CT • Brainstem hemorrhage also possible

23. HISTORY: Key things • As always, get the compete story of the HPI: onset, duration, symptoms, severity, modifying factors, etc. This is often neglected and is the most important evaluation to make the correct diagnosis. • Note if the onset on symptoms was less than three hours ago. If it was an ischemic stroke, and the patient is a candidate, thrombolytic therapy can be done. • Get a good past medical history, covering risk factors for stroke and any history of previous stroke.

24. History • TIA’s usually resolve quickly, certainly within the first hour or two • Rapid progression of deficits or the presence of headache occurs more often in patients with intracerebral hemorrhage • There is some diurnal variation in the onset of stroke, with a peak in the late morning.

25. PHYSICAL EXAMINATION • The neurologic exam is cost-effective and localizes the site of the lesion • The cardiovascular examination • arterial blood pressure (both arms); consider aortic dissection or subclavian steal • Extremely elevated blood pressure can lead to heart failure that may have to be managed urgently. • Overly aggressive reduction of BP may cause hypotension and enlarge the infarct. • The pulse may reveal arrhythmias, such as atrial fibrillation, that can cause cerebral embolism. • Cardiac murmurs may suggest valvular lesions that can cause cerebral embolism • Bruits of the carotid arteries can be produced by atherosclerotic disease of the arteries that is associated with embolic and thrombotic strokes. • Evidence of peripheral vascular disease may be a reflection of generalized atherosclerosis.

26. Neurologic Exam • If the patient's mental status is depressed, bilateral cerebral lesions or a brain stem lesion is suggested. • Multiple smaller strokes may lead to dementia. • Speech is commonly affected, with various aphasic patterns suggesting the site of the lesion. • The testing of strength, sensation, and deep tendon reflexes provides information about the patterns of the deficits and suggests the site of the vascular lesion. • Plantar stimulation (Babinski's sign), which is a classic finding in damage to long tracts, indicates upper motor neuron damage caused by strokes • During the early phases of a large stroke, reflexes may be depressed rather than hyperactive.

27. Differential Diagnosis • Seizure: Following a seizure, is a postictal period of mental fogginess during which temporary neurologic deficits may manifest. This is called Todd’s Paralysis. It is differentiated from a stroke by the history of seizures. • Tumor: Brain tumors may present as acute focal neurologic deficits. Tumors can cause cerebral bleeding, seizures, hydrocephalus, and a mass effect from cerebral edema. Imaging studies will usually identify a tumor. • Migraine Headaches: These can present with symptoms of cerebral ischemia and focal deficits at the onset. The pain classically occurs afterward, but some have no pain making diagnosis difficult. • Metabolic Encephalopathy: Neurologic damage from prior strokescan become “unmasked” during periods of metabolic encephalopathy from fever, infection, hypoglycemia, hypercalcemia, or hepatic encephalopathy. The deficits resolve when the condition is treated.

28. LABORATORY EXAMINATION CBC • Polycythemia leads to hyerviscosityresulting in stroke • Thrombocytosis leading to hypercoagulable states • High WBC from bacterial endocarditis showering the brain with septic emboli • Severe anemia with poor oxygen carrying capacity Erythrocyte Sedimentation Rate • Elevated in patients with hypercoagulable states • Markedly elevated in patients with polymyalgia rheumatica and associated giant cell arteritis Blood glucose level • Hyperglycemia and hypoglycemia can produce focal and global neurologic deficits • Diabetes increases the risk of a stroke

29. LABORATORY EXAMINATION PT and INR • Determines whether warfarin patients have been taking their medications or are excessively anticoagulated. EKG • Atrial fibrillation which causes embolic strokes • Acute myocardial infarctions • Echocardiogram to detect valvular lesions and vegetations if clinically indicated. Spinal tap • Detects subarachnoid hemorrhage and helps provide its age • Neurosyphilis is diagnosed with a positive CSF VDRL. • Meningitis

30. Imaging • A STAT CT scan of the head without contrast is obtained first to rule out hemorrhage. • CT scanning is superior to an MRI scan for detecting intracranial hemorrhage in the first 48 hours of a bleed and it is quicker to do. • The initial CT scan may not detect cerebral ischemia or differentiate a tumor from cerebral ischemia, which is why a 2nd CT or MRI scan is ordered after 24 - 48 hours to reveal the ischemic stroke region. • Cerebral angiography or MRI angiography are ordered to determine the source of bleeding, identify aneurysms, and AV malformations in hemorrhagic strokes.

31. CT scan imaging studies

32. Ischemic Infarction • Subtle infarct has only scattered red cells • Noted to the right: recent ischemic infarct due to thrombosis of the left middle cerebral artery (less than 12 hours) 

33. Hemorrhagic Conversion • Varies from patchy petechial bleeding to confluent hemorrhage • In general do not fully anti-coagulate a brain infarct

34. MRI • More sensitive than CT for detecting early ischemia, but not blood • MRI cannot be used in patients who have ferromagnetic materials within their bodies

35. MRI Image An infarction, visible on an MRI, indicates a patient has had a small subcortical stroke. Multiple infarctions indicate the patient has had numerous subcortical strokes that could lead to severe disability and cognitive decline (dementia) in this patient.

36. CEREBRAL ANGIOGRAPHY • Reserved for patients who are suspected to have a surgically correctable lesion • Arterial vessels are displayed initially, and delayed images can outline the venous system This is a brain magnetic resonance angiogram (MRA). The image is a "scout" image of the Circle of Willis at the base of the brain. The yellow arrows point to 6 different brain aneurysms. 

37. Ischemic Stroke: treatment • Anticoagulate with heparin to limit the size of the stroke. • Cerebral edema is managed with prednisone or dexamethasone. • Treatment is mainly supportive. Correct dehydration. • Blood pressure should be lowered with caution, since cerebral autoregulation of blood flow is disturbed and lowering it too rapidly can extend the stoke. Lower blood pressure cautiously to asystolic 170 - 200 & diastolic of 100 for the first two weeks following an ischemic stroke. • Anti-coagulation for patient with an embolic source is crucial. Titrate warfarin to an INR of 2.0 to 3.0

38. Ischemic Stroke: Treatment • Physical therapy, occupational therapy and speech therapy to restore function. • Prognosis for an ischemic stroke is better than that for a cerebral bleed or subarachnoid hemorrhage. • The larger the infarction the worse the prognosis. • One stroke increases the chances of suffering another stroke. • Lowering serum cholesterol and other risk factors, lowers the risk of future ischemic strokes. • Anti-platelet therapy reduces the risk of a future ischemic stroke by about 30%. • In one two year comparison study, warfarin was not shown to be proven to be superior to aspirinin ischemic stroke.

39. Thrombolytic Therapy • Thrombolytic therapy is for acute management of ischemic stroke if given within 3 hours of onset. • Intravenous: • tissue plasminogen activator (tPA), • streptokinase, or • intra-arterial recombinant prourokinase (rpro-UK). • Thrombolytic therapy can improve the chances for a full or nearly full clinical recover by about 30%. • Most ER’s have protocols written up to follow.

40. TPA FOR ACUTE ISCHEMIC STROKE

41. Acute Stroke Thrombolysis In this angiogram, an artery in the brain (left middle cerebral) is blocked. When clot dissolving medicine is injected directly into the artery, combined with mechanical clot disruption, blood flow is restored.

42. Prevention of Stroke • Hypertension is the most important risk factor for ischemic and hemorrhagic stroke • Approximately 10% of men and 7% of women older than age 65 have asymptomatic carotid stenosis over 50% occluded. Epidemiologic studies suggest that the rate of stroke ipsilateral to such stenosis is about 1 to 2% annually. • Ipsilateral carotid endarterectomy was shown to benefit patients who had 60% or greater diameter reduction of the artery without ulceration, provided that the perioperative complication rate was less than 3%.