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Introduction to Cerebrovascular Diseases

Chapter 437 | Part 13: Neurologic Disorders · Part 13 – Neurologic Disorders · Chapter 437

Key Clinical Points

  1. Stroke is a clinical diagnosis defined as an abrupt onset of a neurologic deficit attributable to a vascular cause.
  2. Transient Ischemic Attack (TIA) requires resolution of all symptoms within 24 h without evidence of brain infarction on imaging.
  3. Ischemic stroke accounts for ~85% of cases; hemorrhagic stroke accounts for ~15%.
  4. The FAST acronym (Facial, Arm, Speech, Time) is the primary tool for public education on stroke recognition.
  5. Acute ischemic stroke management includes thrombolysis (rtPA) or mechanical thrombectomy if within the therapeutic window.
  6. Stroke is the second leading cause of death worldwide; it remains a major disabling condition in individuals aged 50+.
  7. Vascular territory identification (e.g., MCA, ACA, PCA) is critical for localizing stroke and determining etiology.
  8. Amaurosis fugax serves as a warning sign of internal carotid artery disease.
  9. Wallenberg's syndrome (lateral medullary) presents with ipsilateral Horner's syndrome, contralateral hemiparesis, and vertigo.
  10. Basilar artery occlusion can present with 'locked-in' syndrome or coma, requiring rapid identification for potential thrombectomy.

DEFINITION & OVERVIEW

• Stroke: Definition: An abrupt onset of a neurologic deficit attributable to a vascular cause. Diagnosis is clinical; imaging/labs support the diagnosis. • Cerebral Ischemia: Mechanism: Reduction in blood flow lasting > several seconds. Neurons lack glycogen → rapid energy failure → symptoms manifest within seconds. If flow is restored quickly, it results in a Transient Ischemic Attack (TIA). • Transient Ischemic Attack (TIA): Criteria: All neurologic signs and symptoms resolve within 24 h without evidence of brain infarction on imaging. • Stroke (Clinical Definition): Criteria: Neurologic signs/symptoms last for > 24 h OR brain infarction is demonstrated on imaging. • Hemorrhagic Stroke: Mechanism: Bleeding into or around the brain; causes mass effect, toxic effects of blood, or increased intracranial pressure. • Hypoxic-Ischemic Encephalopathy (HIE): Condition: Global hypoxia-ischemia (e.g., cardiac arrest) causing widespread brain injury and cognitive sequelae.

EPIDEMIOLOGY

• Global Impact: Mortality: Second leading cause of death worldwide; 7.1 million deaths in 2020. • U.S. Statistics: Prevalence: ~7 million Americans (age ≥ 20) have had a stroke; expected to rise by 3.4 million in the next decade (4% of the adult population). • Trends: Mortality: Increased from 6.2 million in 2010, but age-standardized death rate fell by 15% in the last decade due to better prevention/treatment. • Disability:* _Impact: Stroke is likely to remain the second most common disabling condition in individuals aged 50+ worldwide.

ETIOLOGY & PATHOPHYSIOLOGY

• Stroke Syndromes Classification: 1. Large-vessel stroke (Anterior circulation) 2. Large-vessel stroke (Posterior circulation) 3. Small-vessel disease (either vascular bed) • Anterior Circulation: Vessels: Internal carotid artery and its branches. Causes: Intrinsic disease (atherosclerosis, dissection) or embolic occlusion from proximal sources. • Ischemic Mechanisms: Proximal MCA: Often due to embolus (artery-to-artery, cardiac, or unknown source). Atherosclerosis: May cause distal emboli or low-flow TIAs; often prevented from being symptomatic by collateral formation via leptomeningeal vessels. • Hemorrhagic Mechanisms: Primary Causes: Aneurysmal subarachnoid hemorrhage (SAH) and hypertensive intracerebral hemorrhage.

CLINICAL FEATURES

• Urgency & Presentation: Time Sensitivity: Rapid evaluation is essential for thrombolysis or thrombectomy. Patient Behavior: Patients may not seek help due to anosognosia (lack of awareness) or lack of knowledge regarding treatment benefits; bystanders often call EMS. • Warning Signs (Call EMS immediately): Motor/Sensory: Loss of function on one side (present in ~85% of ischemic stroke patients). Vision/Speech: Change in vision, gait, or ability to speak/understand. Headache: Sudden, severe headache. • FAST Acronym: Components: Facial weakness, Arm weakness, Speech abnormality, Time. • Localization via History/Exam: Utility: Identec region of dysfunction → narrows possible causes (e.g., language loss + right homonymous hemianopia → search for left MCA emboli).

DIFFERENTIAL DIAGNOSIS

• Seizure: Distinction: Absence of convulsive activity at onset usually excludes seizure; however, complex partial seizures without tonic-clonic activity can mimic stroke. • Migraine: Mimicry: Can occur even without prior history (acephalgic migraine). Key Features: Sensory disturbance is prominent; deficits migrate slowly over minutes (not seconds); diagnosis confirmed if symptoms cross vascular boundaries or present with scintillating scotomata. • Metabolic Encephalopathy: Distinction: Typically produces fluctuating mental status changes without focal neurologic findings. • Tumors: Presentation: May cause acute symptoms due to hemorrhage, seizure, or hydrocephalus.

INVESTIGATIONS & DIAGNOSIS

  1. Initial Imaging (CT): Purpose: Standard modality to detect presence/absence of intracranial hemorrhage.
  2. Advanced Imaging:
  3. MRA/CTA: Rapidly detect basilar thrombosis (especially in cases of suspected seizure and cranial nerve deficits).
  4. MRI (DWI/ADC): Superior for identifying early ischemic infarction, especially in the posterior fossa; DWI/ADC can identify ischemia within minutes to hours.
  5. CT Perfusion (CTP): Identifies 'mismatch' between core infarct (CBF < 30%) and penumbra (Tmax > 6.0s) to determine candidacy for reperfusion therapy (e.g., mismatch ratio of 1.4).
  6. Clinical Correlation: Localization: Identifying the specific artery (MCA, ACA, PCA) based on clinical deficits allows narrowing of potential causes.

MANAGEMENT & TREATMENT

  1. Initial Stabilization: Actions: ABCs, glucose management.
  2. Acute Ischemic Stroke Management:
  3. Reperfusion: rtPA or endovascular mechanical thrombectomy (if within the therapeutic window).
  4. Secondary Prevention:
  5. Anticoagulation for atrial fibrillation.
  6. CEA or stent for carotid artery disease.
  7. Hemorrhagic Stroke Management:
  8. Blood pressure management; treat specific cause.
  9. Supportive Care:
  10. Deep venous thrombosis prophylaxis.
  11. Physical, occupational, and speech therapy.

PROGNOSIS & COMPLICATIONS

• Mortality: Trend: Death rate fell by 15% in the last decade due to better prevention/treatment. • Disability: Impact: Stroke remains a leading cause of long-term disability in patients aged 50+ worldwide.

SPECIAL CONSIDERATIONS

• Epilepsy in the Elderly: Distribution: Bimodal (very young and elderly). Causes: Stroke, neoplasm, dementia. _Management:* Selection of antiseizure medication requires consideration of comorbidities, side effects, mood/cognition impact, and drug-drug interactions.

FLOWCHARTS & ALGORITHMS

  1. Medical Management of Stroke and TIA (Figure 2): Initial Assessment (ABCs, glucose) → Obtain brain imaging → [Decision: Ischemic stroke/TIA (85%) OR Hemorrhage (15%)]
  2. Ischemic Path:
  3. Consider thrombolysis/thrombectomy → Establish cause → [Identify Etiology: Atrial fibrillation (17%), Carotid artery disease (4%), Other (14%)] → [Interventions: Consider oral anticoagulation, Consider CEA or stent, Deep venous thrombosis prophylaxis].
  4. Hemorrhage Path:
  5. Consider BP lowering → [Identify Etiology: Hypertensive ICH (7%), Other (3%)] → Treat specific cause.

KEY PEARLS & CLINICAL TRAPS

• Amaurosis Fugax: Significance: A critical warning sign of internal carotid artery disease. • Basilar Artery Occlusion: Clinical Presentation: May present with 'locked-in' syndrome or coma; requires rapid identification for potential thrombectomy. • Anosognosia: Trap: Patients may not seek help because they lack awareness that something is wrong. • Migraine Mimicry: Distinction: Look for slow migration of symptoms (minutes) and presence of scintillating scotomata to differentiate from stroke.