Clinical Presentation of Cerebrovascular Disease David Griesemer, MD Department of Neurosciences Medical University of South Carolina.
Download ReportTranscript Clinical Presentation of Cerebrovascular Disease David Griesemer, MD Department of Neurosciences Medical University of South Carolina.
Clinical Presentation of Cerebrovascular Disease David Griesemer, MD Department of Neurosciences Medical University of South Carolina Presentation Outline Stroke from the patient’s perspective Definition of transient ischemic attacks “Classic” presentations of stroke types Focus on lacunar strokes Prevention pearls Diagnostic pitfalls The Patient Perspective Stroke Statistics 15% of adults > age 50 cannot name a single symptom of stroke 13 hours after onset of symptoms is the median time to presentation 58% of stroke patients don’t present during the first 24 hours after onset 52% of stroke patients in the ED are unaware that they are experiencing a stroke Stroke Knowledge MYTHS – – – – – Can’t prevent stroke Can’t treat stroke Stroke affects the heart Stroke affects the elderly Recovery happens for a few months after stroke FACTS – – – – – Stroke is preventable Stroke is treatable Stroke is a brain attack Stroke affects anyone Stroke recovery occurs throughout life Stroke Symptoms Sudden numbness or weakness of face, arm or leg, especially on one side of the body Sudden confusion, trouble understanding or speaking Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance or coordination Sudden severe headache with no known cause Other Symptoms Sudden nausea, fever and vomiting, distinguished from a viral illness by rapid onset (minutes or hours vs. days) Brief loss of consciousness or period of decreased consciousness (fainting, confusion, convulsions or coma) The Three R’s for Brain Attack Reduce risk Recognize symptoms Respond by calling 911 TIA: The First Clue Transient Ischemic Attack “Sudden, focal neurologic deficit lasting less than 24 hours, confined to an area of the brain or eye perfused by a specific artery.” Based on assumption that TIAs do not cause infarction or other permanent brain injury. Time criterion is arbitrary. Problems with TIA Definition Most TIAs last seconds to 10 minutes, with symptoms lasting greater than 1 hour in only 25% of patients Less than 15% of patients with symptoms lasting > 1 hour resolve within 24 hours Following TIAs, evidence of infarction is found in 20% by CT imaging and almost 50% with MRI The “24-hour” rule leads to complacency and delay. Tissue Definition of TIA “A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.” Parallel to distinction between angina and myocardial infarction (i.e. depends on the absence of tissue injury rather than the resolution of symptoms) Advantages Acknowledges that transient neurologic symptoms may cause permanent brain injury Supports rapid intervention to diagnose and treat acute brain ischemia More accurately reflects the presence or absence of brain infarction Avoids assigning an arbitrary time criterion to define TIA TIA - Differential Diagnosis Anxiety (panic attack) Hyperventilation Neuropathy (focal) Neuropathy (ischemic) Vertigo Disequilibrium Migraine Orthostatic hypotension Syncope Arrhythmias (ischemia) Seizures Conversion disorder TIA v. Dizziness Isolated symptom unlikely to be ischemic (true also for blurred vision or diplopia) Evidence of brainstem dysfunction – Ataxia or nystagmus – Cranial nerve abnormality – Contralateral corticospinal tract abnormality TIA v. Migraine Onset in middle age Aura without headache Dysfunction in periaqueductal gray region of brainstem, not vascular Progressive visual scintillation affecting both eyes Stereotypic episodes or positive family history, especially with familial hemiplegic migraine Stroke: The Initial Symptoms Clinical Presentations of Stroke Focal ischemia (85%) – Embolism – Thrombosis Hemorrhage (15%) – Epidural – Subdural – Intraparenchymal Cerebral Ischemia Embolism Abrupt onset Small vascular area Focal deficit Thrombosis Preceded by TIAs Abrupt onset Large vascular area More complex symptoms Acute CT normal – Pure aphasia – Pure hemianopia Acute CT normal High recurrence risk Cerebral Hemorrhage Epidural hemorrhage Smooth onset Arterial origin Mass effect causes coma over hours Similar (but slower in evolution) to hemorrhage in basal ganglia Subdural hemorrhage Smooth onset Venous origin May be recurrent Fluctuating, falsely localizing signs Remember Lacunar Strokes Lacunar Strokes 15 – 20% of ischemic strokes – Small penetrating branches of circle of Willis, MCA, or vertebrobasilar artery – Atherothrombotic or lipohyalinotic occlusion Infarct of deep brain structures – Basal ganglia, cerebral white matter, thalamus, pons, and cerebellum – From 3 mm to 2 cm Presentation of Lacunar Stroke Risk factors – Diabetes – Hypertension – Polycythemia Variable course progressing over days – Fluctuating; progressing in steps; or remitting – Preceded by TIAs in 25% – Without headache or vomiting Lacunar Stroke Syndromes Well-defined syndromes – Pure motor hemiparesis (with dysarthria) – Pure sensory stroke (loss or paresthesias) – Dysarthria-clumsy hand (with contralateral face and tongue weakness) – Ataxia-hemiparesis (contralateral face and leg weakness) – Isolated motor-sensory stroke Lacunar Stroke Outcome Management – Long-term blood pressure control – Empiric anti-platelet therapy – Omega-3 oil 1 gm TID to improve viscosity Prognosis – Good recovery of function – Other lacunes develop Prevention Pearls Reducing Primary Risk - 1 Obstructive sleep apnea Homocysteine folate, B6, B12 Hypertension – morning BP surge Smoking 50% risk reduction in 1 yr Hyperlipidemia statins Migraine triptans Drugs – cocaine, ephedra, PPA Reducing Primary Risk - 2 Asymptomatic carotid stenosis – Endarterectomy for > 60% stenosis – Risk reduction for 3% to 1% per year – Benefit related to surgical risk Nonvalvular atrial fibrillation – Aspirin for patients < 65 years, healthy – Warfarin for patients > 65 years or having other stroke risk factors Reducing Secondary Risk Reducing risk of recurrence TIA with ipsilateral carotid stenosis endarterectomy for > 70% stenosis Cardiogenic embolism warfarin Lacunar infarcts aspirin, dipyridamole Cryptogenic infarcts (40% embolic) anticoagulation? Reducing Risk in Children Sickle cell disease – Screen with transcranial doppler q 6 mo – Transfusion therapy for 2 abnormal studies Congenital heart disease Arterial dissections (trauma) Prothrombotic disorders Mitochondria disorders (MELAS) Medical Evidence www.jr2.ox.ac.uk/bandolier/knowledge.html Decreasing Salt Intake Reducing salt intake by 3 g per day lowers blood pressure; the effect is doubled with a 6 gm/day reduction and tripled with a 9 gm/d reduction. Reduction in stroke risk parallels reduction in salt intake. Using Statins Pooled results after 5 years Pravastatin or Simvastatin 40 mg/day Changes in cholesterol levels – Total cholesterol decreased 20% – LDL cholesterol decreased 28% – HDL cholesterol increased 5% – Triglycerides decreased 13% Using Statins Reducing LDL cholesterol by 1 mmol/L – 22% stroke reduction in patients with known vascular disease – 6% stroke reduction in patients without known vascular disease – 28% reduction in thromboembolic stroke Diagnostic Pitfalls Practical Guidance Goldszmidt and Caplan, Stroke Essentials, Physicians’ Press, 2003 www.physicianspress.com Pitfall #1 Basing treatment on brain imaging alone without a vascular work-up. A left frontal stroke caused by tight carotid stenosis requires revascularization, but the same stroke caused by atrial fibrillation requires warfarin. Pitfall #2 Basing work-up and treatment on the temporal course of stroke. Intervention should focus on the vascular lesion. In fact, the same vascular lesion could cause TIA, evolving stroke, or completed stroke. Pitfall #3 Overlooking a mimic of TIA or stroke. 19% of patients diagnosed with stroke in ED have an imitator of stroke Common confounders – – – – Seizures Systemic infection Brain tumor Toxic-metabolic encephalopathy Pitfall #4 Mistaking the time of symptom onset for patients who wake up with stroke. Strokes are painless and do not wake people up. Because of risk of late thrombolysis, onset time should be assumed to be when they were last awake. Diffusion-weighted MRI may be helpful in determining benefit/risk of thrombolytic therapy. Pitfall #5 Failing to investigate intracranial as well as extracranial circulations. Emboli or thrombi can come from anywhere in the carotid or vertebrobasilar. Carotid duplex imaging does not investigate the intracranial circulation. Transcranial doppler or MRA can non-invasively detect intracranial lesions,l more common in African-American and Asian patients. Pitfall #6 Failing to distinguish severe carotid stenosis from total occlusion. Severe stenosis may require urgent surgery; total occlusion usually requires medical therapy. Neither carotid duplex imaging nor MRA can fully distinguish between the two. Conventional angiography is the test of choice. Pitfall #7 Failing to check spinal fluid in patients with suspected subarachnoid hemorrhage. CT has 90% sensitivity for subarachnoid blood on day of onset, but sensitivity decreases over time. Also, small hemorrhages can be missed. For patients with suspected SAH who have a negative CT, lumbar puncture is needed. Pitfall #8 Considering only embolism in stroke patients with atrial fibrillation. More than 25% of ischemic strokes in patients with AF have causes other than cardiogenic embolism (e.g. aortic arch atheroma and intrinsic vascular disease). Other interventions, such as carotid revascularization, may be required. Pitfall #9 Overtreating hypertension in acute stroke. Because autoregulation is lost in ischemic brain, aggressive lowering of BP may cause infarct extension. Treat BP > 200/120 in absence of thrombolytics or > 180/115 with thrombolytics Pitfall #10 Failing to adequate evaluate the heart. Silent myocardial infarction and arrhythmias are common complications of stroke. MI occurs in 20% of patients with acute stroke. It is a common cause of death at 1 – 4 weeks.