Stroke Diagnosis and Prevention

• Cerebrovascular events (stroke) rank as the fifth leading cause of death in the U.S.

Stroke Classifications

• Ischemic strokes involve interruption/reduction of blood flow, leading to neuronal injury.
• Hemorrhagic strokes typically result from the rupture of weakened arteriosclerotic small arteries, often due to hypertension.

Risk Factors

• Modifiable risk factors include hypertension, diabetes, smoking, hyperlipidemia, obesity, poor diet, and physical inactivity.

Transient Ischemic Attack (TIA)

• TIA diagnosis relies on the quality of information available during assessment.
• TIAs involve brain dysfunction due to regional reduction in blood flow (ischemia).
• TIAs are difficult to diagnose, relying on reported history and physical exams.
• Stroke risk after TIA is up to 10%, but up to 80% of this risk is preventable with urgent assessment and treatment.
• TIA diagnosis includes clinical history, focal neurologic findings on examination, and brain imaging.
• Important symptoms include the time course of symptoms, distribution of deficits, and individual risk factors.

Incidence & Prevalence

• Annually, 795,000 people in the U.S. experience a stroke.
• Ischemic strokes account for 85% of reported strokes.
• Stroke deaths have decreased but remain the fifth leading cause in the U.S. and second globally.
• Decreased incidence is likely due to education and prevention medications.

Racial Disparities

• Black men and women are twice as likely to have a first stroke and are more likely to die from it.

Socioeconomic Impact

• Stroke is a leading cause of disability, with significant social and financial consequences.
• In 2018, stroke care costs were about $33.4 billion, and are projected to be $81.1 billion by 2035 for non-Hispanic White people, $32.2 billion for non-Hispanic Black people, and $16 billion for Hispanic people.
• Long-term care is often required, with 20% needing institutional care 3 months post-stroke.

Recovery

• 50% to 70% of stroke survivors regain functional independence, while 15% to 30% remain permanently disabled.

Ischemic Stroke Pathophysiology

• Thrombotic events: Atherosclerosis causes blockage of blood flow.
• Embolic events: A clot forms, travels, and blocks blood flow distally.
• Effects depend on occlusion location, collateral channels, ischemia degree/duration.
• Neurologic deficits relate to the location and size of infarction/ischemia.
• Tissue becomes pale; prolonged ischemia leads to sludging and endothelial damage and prevents reflow.
• Cellular breakdown and swelling lead to permanent tissue injury/infarction.
• Injured capillaries can lead to leakage and hemorrhagic infarction.

Hemorrhagic Stroke Pathophysiology

• 10%–15% of all strokes are hemorrhagic.
• Subtypes: subarachnoid, intracerebral, subdural, and epidural.
• Intracerebral hemorrhage (ICH) occurs from ruptured cerebral vessels, often due to high blood pressure.
  • Primary ICH (78%–88%): spontaneous rupture due to chronic hypertension or cerebral amyloid angiopathy.
  • Secondary ICH: bleeding from cerebrovascular abnormalities, tumors, or impaired coagulation.
• Subarachnoid hemorrhage (SAH) occurs in the subarachnoid space.
• Caused by aneurysm, arteriovenous malformation, or inherited bleeding disorder.
• Risk factors include smoking, hypertension, connective tissue disorders, known aneurysms, and polycystic kidney disease.
• ICH has a higher fatality risk compared to ischemic stroke.
• Hemorrhagic strokes damage brain cells, increase pressure on the brain, and cause blood vessel spasms.

Common Pathophysiology

• In both stroke types, the area dies within minutes due to lack of oxygen and failure of ATP metabolic pathway.
• In the penumbra, damage extends for 12 to 24 hours.
• Intracellular calcium release initiates apoptosis.

Clinical Presentation & Physical Examination

• Cerebrovascular events (TIA, ischemic, hemorrhagic stroke) can have similar presentations, but time differentiates.
• Ischemic stroke usually presents as a single event evolving in hours, or "stuttering" progression over 72 hours.
• Symptoms vary based on vascular territory.
  • Carotid artery involvement: ipsilateral eye or contralateral body symptoms.
  • Visual disturbance (amaurosis fugax): transient, painless vision loss.
  • Hemispheric ischemia: contralateral face/limb weakness/numbness, language and cognitive difficulties.
  • Vertebrobasilar events: vertigo, nausea/vomiting, nystagmus, diplopia, dysconjugate gaze, cranial nerve deficits.
• SAH presents with abrupt severe headache ("worst headache of my life"), nausea/vomiting, meningeal irritation, neurologic dysfunction.
  • Loss of consciousness is common but short-lived.
  • Nearly 50% have atypical headaches days/weeks before the event, called sentinel headaches.
• Hypertensive ICH may lack warning signs.
  • It occurs typically when a patient is up and active.
• Neurologic signs vary with site/size of extravasation.
• Can lead to stupor/coma, hemiplegia, deteriorating to death in hours.
• Headache followed by unilateral facial sag, slurred speech, arm/leg weakness, eye deviation suggests intracerebral bleeding.
• Advanced cases include paralysis, aphasia, stupor, coma, irregular respiration, dilated/fixed pupils, and decerebrate rigidity.

Common Signs and Symptoms

• Common to both anterior and posterior circulation events: hemiparesis, hemisensory loss, visual field defects, ataxia, dysarthria, reflex asymmetry, and Babinski sign.
• Headache is more common and severe with hemorrhagic stroke.

Physical Examination

• Use risk stratification to guide urgency of workup and management.
  • ABCD2 score is valuable for this purpose.
• TIA patients sometimes need observation for 24 hours in a clinical decision unit.
• Neurologic examination findings correspond to the affected vascular territory.
• Initial focus on airway, breathing, and circulation (ABCs).
• Quick assessment of pupillary function, gaze deviation, blink to threat, motor tone, and purposeful movements helps identify neurologic syndrome.
• Vomiting, SBP >220 mm Hg, severe headache, coma, or symptom progression suggest ICH.
• The National Institutes of Health (NIH) Stroke Scale is the basic neurologic assessment for stroke patients.
• Quantifies deficits and provides a standardized scoring system.
• Should be done soon after arrival and accompany the patient throughout care.

Diagnostics

• Abrupt focal neurologic symptoms are presumed vascular until proven otherwise.
• Diagnostic studies determine stroke type, cause, complications, and confounding factors.

Essential Diagnostics

• Head CT scan is the most common initial imaging procedure.
• MRI is a reasonable choice if available.
• Consider time, cost, proximity to ED, patient tolerance, and availability when choosing.
• Atypical presentations may need contrast enhancement CT or MRI to exclude tumor.
• CT can miss small infarctions, especially soon after onset.
• CT is the gold standard for acute hemorrhage; gradient echo and T2 susceptibility-weighted MRI are as sensitive as CT for acute hemorrhage.
• Arteriography may be needed to determine underlying vascular disease and etiologies.
• Stroke centers aim to administer IV thrombolytics within 45 to 60 minutes of arrival at the ED.

Additional Diagnostics

• ECG, chest radiography, pulse oximetry or ABG assessment, CBC with platelets, PT, PTT, serum glucose, creatinine, BUN, and electrolytes.
• These tests shouldn't delay the CT scan.
• Cerebrospinal fluid examination is needed if CNS infection is suspected or if SAH is suggested but the head CT scan is normal.
• EEG is indicated for suspected seizures.
• Carotid ultrasonography (CUS) assesses carotid artery patency, especially when considering endarterectomy.
• CTA or MRA evaluates posterior circulation and intracranial arteries.
• Transesophageal echocardiography and Holter monitoring may be performed if the presentation is suggestive of cardioembolic or paradoxical events.
• Other possible tests: serum cholesterol, hemoglobin A1c, toxicology screening, ESR, fibrinogen, serum protein electrophoresis, antiphospholipid antibody level, serologic test for syphilis, protein C, protein S, antithrombin III, lupus anticoagulant, anticardiolipin antibody, β2 glycoprotein, and connective tissue disease screen.

Initial Diagnostics List

• Stat CT scan of head (noncontrast) vs. stat CT brain perfusion vs stat MRI of brain.
• Electrocardiogram (ECG).
• Pulse oximetry.
• National Institutes of Health Stroke Scale.
• ABCD2 risk stratification for TIA.

Initial Laboratory Tests

• Complete blood count (CBC) and differential.
• Prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR).
• Metabolic profile.
• Toxic screen.
• Lumbar puncture (if severe headache and negative CT to rule out subarachnoid hemorrhage).

Additional Diagnostics List

• Tests to consider after emergency care, stabilization, and treatments.
• Imaging - Transesophageal echocardiography, chest X-ray studies.
• Laboratory - Lipid profile, Hemoglobin A1c, Erythrocyte sedimentation rate, Fibrinogen, Serum protein electrophoresis, Antiphospholipid antibody, Fluorescent treponemal antibody absorption test or rapid plasma reagina, Protein C, protein S, Antithrombin III, Lupus anticoagulant, Anticardiolipin antibody, β2 Glycoprotein, Connective tissue disease screening, Arterial blood gas.

Other Studies

• Consider the need for Carotid ultrasound, Electroencephalography, Arteriography, Holter, Zio patch, or event monitoring, Transesophageal echocardiogram (TEE), and Sleep study.

Differential Diagnosis

• Priority differentials include (1) stroke, (2) seizure, (3) subdural hematoma, (4) encephalitis, and (5) toxic or metabolic encephalopathies.
• Other diagnoses: migraine, brain tumor, syncope, demyelinating diseases, conversion disorders, and transient global amnesia.

Interprofessional Collaborative Management

• Time is critical; transport patients with stroke-like symptoms immediately for CT scan and to a center with tPA protocol.
• Transport patients with large vessel occlusion to a thrombectomy-capable center.
• Stroke units improve survival.
• Stroke centers use telemedicine to outlying hospitals.
• Consult neurosurgery or interventional radiology, based on injury type.
• After stabilization, use rehabilitation services, including physical therapy, occupational therapy, speech therapy, and vocational counseling.
• Counselors assist with patient and family issues.
• Palliative medicine clarifies treatment goals.
• Primary care focuses on primary or secondary intervention: blood pressure control, antithrombotic therapy, smoking cessation, diet/nutrition, physical activity, OSA assessment/treatment, and blood sugar/cholesterol management.
• Acute stroke: Early recognition and immediate 911 call.

Community Organization

• Integrated EMS and hospital systems are needed.
• National coalition establishes guidelines and protocols.
• Acute stroke-ready hospitals with trained personnel, standard protocols, telemedicine, clot-busting drugs, and rapid anticoagulation reversal.
• EMS agencies train in stroke recognition.
• Rapid transfer to tertiary facilities through interfacility agreement.

Stroke Symptoms

• Sudden numbness/weakness of face, arm, or leg, especially on one side.
• Sudden confusion or trouble speaking or understanding speech.
• Sudden trouble seeing in one or both eyes.
• Sudden trouble walking, dizziness, loss of balance or coordination.
• Sudden severe headache with no known cause.

Primary / Comprehensive Stroke Centers

• Primary stroke centers: accredited hospitals demonstrating consistent stroke response and measuring outcomes, specifically time from arrival to thrombolytics.
• Comprehensive stroke centers: neurosurgeons, neurologists, neurologic intensive care units, interventional radiologists, and extensive rehabilitation services.

Emergency Department

• Assess ABCs (airway, breathing, and circulation) and vital signs.
• Secure airway, administer oxygen, attach cardiac monitor, pulse oximeter, and sphygmomanometer, establish IV access, perform physical exam, and obtain emergent, noncontrast head CT scan.
• 12-lead ECG, portable chest radiograph, and laboratory tests are indicated.
• Contact a neurosurgeon if hemorrhage has occurred.
• Ischemic stroke: consult a neurologist and administer thrombolytic therapy if the patient meets the criteria.
• Evaluate for revascularization with mechanical thrombectomy or carotid endarterectomy versus carotid stenting.
• IV thrombolysis with rtPA or tenecteplase (TNK) and endovascular thrombectomy with a retrievable stent improve neurologic outcome.
• Administer treatments quickly after stroke onset, combinations are safe in appropriate candidates.
• Studies haven't found endovascular therapy alone to be superior to endovascular therapy plus IV thrombolysis.
• Manage blood pressure carefully in both ischemic and hemorrhagic stroke.
• Elevated blood pressure is common during acute stroke events.
• Optimal SBP ranges between 121 and 200 mm Hg.
• Acute hypertensive response may represent a beneficial compensatory response to maintain cerebral perfusion.

Treatment Considerations

• Lowering blood pressure may exacerbate hypoperfusion in acute ischemic stroke.
• Base the decision to lower blood pressure on individual clinical judgment and rtPA candidacy unless SBP is 220 mm Hg or more.
• Blood pressure typically returns to baseline without additional treatment.
• With IV rtPA, the risk of symptomatic ICH is greater.
• Maintain SBPs between 141 and 150 mm Hg for best outcomes.
• For acute ICH, the American Stroke Association suggests lowering SBP to 140 mm Hg to prevent hematoma expansion.
• Labetalol and nicardipine are commonly used safe choices and if antihypertensive therapy is necessary, blood pressure reduction should be gradual and gentle.
• Monitor for neurologic fluctuations/deterioration.

Pharmacologic Management - Intravenous Thrombolytic Therapy

• In June 1996, the FDA approved IV thrombolysis for ischemic stroke if administered within 4.5 hours from symptom onset.
• Thrombolysis reduces neurologic disability despite increased bleeding complications.
• Time to treatment is the most important determinant (sooner = better outcome).
• Inclusion criteria: age ≥18 years, clinical diagnosis of ischemic stroke, and onset within 180 minutes of drug administration.
• Exclusion criteria focus on current bleeding or bleeding risk outweighing tPA benefits.
• Guidelines revised in 2018 confirm tPA administration up to 4.5 hours from symptom onset.
• Higher risk/lesser benefit patients receiving oral anticoagulation, with diabetes history and previous stroke older than 80 years, and NIH Stroke Scale score >25 need thorough assessment.
• Consider IV thrombolysis in patients with unknown onset or outside the 4.5-hour window and rapid advanced imaging to show diffusion-weighted imaging–fluid-attenuated inversion recovery (DWI-FLAIR) mismatch.
• IV thrombolysis limitations include short time window, contraindication list, and failure to recanalize proximal artery occlusions caused by large clots.

Antiplatelet Agents

• Benefit of antiplatelet agents in reducing stroke risk.
• Relative benefit is constant regardless of age, gender, blood pressure, and diabetes.
• Aspirin is the standard therapy for ischemic stroke prevention.
• Optimum aspirin dose ranges from 81 to 325 mg every day.
• More recent studies have established evidence to guide clinicians on dosing and longevity of antiplatelets.
• Warfarin (Coumadin) and direct oral anticoagulants (DOACs) (e.g., Eliquis, Xarelto) are indicated for stroke prevention in patients at risk.
• Thienopyridines (clopidogrel/Plavix, ticlopidine/Ticlid) are more effective than aspirin, but ticlopidine has potential side effects and needs hematologic monitoring.
• Dipyridamole (Persantine) with aspirin has similar recurrence rates to clopidogrel.
• Ticagrelor and cilostazol are other antiplatelet medications.
• Reverse anticoagulation when ICH patients are on anticoagulation agents.
• Vitamin K and three- or four-factor prothrombin complex concentrate (Kcentra) reverse warfarin effects.
• Platelets may aid clopidogrel/aspirin reversal, However, it is not well established but may be used in emergent neurosurgical cases.
• Protamine can be administered for heparin and low-molecular-weight heparin products.
• The FDA has approved antidotes for some DOACs, idarucizumab (Praxbind) but reversal agents might not exist for certain agents.

Surgical and Interventional Treatment

• Mechanical Thrombectomy: Endovascular recanalization treatment helps to remove blood clots.
• Improved devices, techniques, imaging, and patient flow have been improving the approach.
• Patients were initially treated up to 6 hours from symptom onset, but advances have been made up to 24 hours post-symptom onset.
• The optimal radiologic method to select candidates for endovascular therapy is CTA angiography or CT/MRI perfusion.

Surgery

• Neurosurgical consultation is needed for SAH, ICH, and increased intracranial pressure.
• Carotid endarterectomy benefits patients with symptomatic carotid stenosis.
• For optimal effect and minimizing future ischemic episodes, surgery should be performed as soon as possible and within the first two weeks following a stroke or TIA.
• SAH can be treated by interventional radiology by inserting a coil into the aneurysm.

Pregnancy Considerations

• Stroke during pregnancy is a major tragedy, fortunately rare.
• Incidence is reported at around 4.8 per 100,000 in Canada and as high as 46.2 per 100,000 pregnancies among Chinese women in Taiwan.
• Risk factors include hypertensive disorders, prothrombotic state, migraine history, and gestational diabetes.
• Health care providers can best address this topic through pregnancy preparation counseling, especially the need for prenatal care, risk identification, and management.
• Extreme weight change, proteinuria, or elevated blood pressure in the gravid patient require early intervention.

Geriatric Patients

• Stroke disproportionately affects older persons.
• Therapeutic interventions like surgery and thrombolysis can be contraindicated.
• Comprehensive assessment determines appropriate care.
• Age directly predicts mortality and morbidity.
• In older adults, death rates within the first year can be as high as 35% for White women older than 65 years.
• A surrogate decision maker must be identified and their role defined through advance directives.
• Patients should state on record about the use of feeding tubes or IV hydration and what aspects bring meaning to their lives.
• Palliative care consultation addresses comfort, end-of-life decisions, community resources, family engagement, and education.

Complications

• Early complications: cerebral edema, increased intracranial pressure, infections, seizures, hypertension, hypotension, cardiac arrhythmias, myocardial ischemia and infarction, deep venous thrombosis, pulmonary embolism, dysphagia, dysarthria, pressure sores, depression, and extension or progression of the stroke.
• Later complications: permanent residual problems with mobility, activities of daily living, communication, nutrition, swallowing, behavior, continence, sexual function, limb contractures, and dementia.

Hospital Admission

• Manage treatment to prevent complications.
• Complications include pneumonia, seizures, myocardial infarction, deep venous thrombosis, pressure injuries, hyperglycemia, hypoglycemia, depression, limb contractures, and constipation.
• Specific therapies directed toward their prevention will dramatically reduce the stroke patient’s morbidity and mortality.
• Physical, occupational, and speech therapy should be initiated asap.

Patient Education

• Risk factor reduction and stroke symptom recognition and emergency treatment.
• Educate about hypertension and the importance of medical therapy and lifestyle changes.
• Other modifiable factors need patient education and treatment, namely cigarette smoking, obesity, diabetes, sedentary lifestyle, and hypercholesterolemia.
• Atrial fibrillation results in a 5 times greater risk of stroke; treatment with anticoagulation is essential.
• For patients with high bleeding risk, left atrial appendage (LAA) closure should be considered with interdisciplinary discussion including neurology and interventional cardiology.
• Interdisciplinary collaboration between cardiology and neurology can include consideration for patent foramen ovale closure.
• Public must be educated about stroke signs and symptoms, using FAST (face, arm, speech, time).
• Factors associated with delay in treatment include lack of recognition of stroke signs, calls made to the health care provider, living alone, onset while asleep, onset at home rather than at work, posterior circulation symptoms, and milder severity of stroke.

Rehabilitation Services

• Survivors have physical and psychological impairments.
• Family will be stressed by the recovery process and need support.
• Rehabilitation services should begin within 48 hours of stabilization.
• Adaptive training is needed for the patient, family, and caregivers.

This quiz covers the diagnosis, risk factors, and prevention strategies related to stroke and transient ischemic attacks (TIAs). It includes questions on modifiable risk factors, racial disparities, and the importance of timely assessment and treatment.