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Cerebrovascular Diseases

Cerebrovascular Diseases

Cerebrovascular Diseases

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Cerebral Circulation & Stroke Basics - Vascular Roadmap

  • Key Arteries:
    • Anterior Circulation: Internal Carotid Artery (ICA) → Anterior Cerebral Artery (ACA) & Middle Cerebral Artery (MCA).
    • Posterior Circulation: Vertebral Arteries → Basilar Artery → Posterior Cerebral Artery (PCA).
  • Circle of Willis: Anastomotic arterial ring at brain base; connects anterior & posterior systems. Anatomy of Circle of Willis and major cerebral arteries
  • Stroke: Acute neurological deficit of vascular origin.
    • Ischemic: Due to ↓ blood flow (e.g., thrombosis, embolism).
    • Hemorrhagic: Due to bleeding.
  • Transient Ischemic Attack (TIA): Brief episode of neurological dysfunction; no acute infarction; typically < 1 hour.

⭐ Most common artery involved in ischemic stroke is the Middle Cerebral Artery (MCA).

Ischemic Stroke - Clot Chaos

  • Patho: Arterial occlusion → focal brain ischemia; central core (irreversible infarct) vs. surrounding penumbra (salvageable tissue).

  • Etiology: Thrombotic (atherosclerosis), Embolic (e.g., AFib, valvular), Lacunar (small vessel, chronic HTN, DM).

  • Sx: Sudden focal deficit. 📌 FAST (Face, Arm, Speech, Time). Common syndromes: MCA, ACA, PCA, Vertebrobasilar.

  • Dx: NCCT (r/o bleed); MRI (DWI confirms); CTA/MRA (vascular occlusion).

  • Acute Management Algorithm:

    ⭐ The therapeutic window for IV thrombolysis (tPA) in acute ischemic stroke is typically <4.5 hours from symptom onset.

  • Key Meds: IV Alteplase. Aspirin 160-325mg (if no tPA, or 24h post-tPA). Statins. Ischemic stroke progression with and without treatment

Hemorrhagic Stroke - Bleed Breakdown

  • Intracerebral Hemorrhage (ICH): Bleeding within brain parenchyma.
    • Causes: Hypertension (commonest), AVMs, amyloid angiopathy.
    • Sites: Basal ganglia, thalamus, pons, cerebellum.
    • Management: BP control (SBP <140 mmHg), reverse anticoagulation, surgery if indicated.
  • Subarachnoid Hemorrhage (SAH): Bleeding into subarachnoid space.
    • Causes: Ruptured berry aneurysm (85%), AVM.
    • Presentation: Sudden "thunderclap" headache.
    • Dx: CT head; LP (xanthochromia if CT neg).
    • Management: Nimodipine, secure aneurysm (coiling/clipping).

Intracranial Hemorrhage Types Diagram

⭐ Subarachnoid Hemorrhage (SAH) classically presents with a sudden, severe "thunderclap" headache, often described as the "worst headache of my life".

TIA, Mimics & Diagnostics - Fleeting Shadows & Clear Views

  • Transient Ischemic Attack (TIA): Focal neurological deficit, symptoms resolve typically <1 hour, no acute infarction on imaging.
  • Key Mimics: Seizure, migraine aura, hypoglycemia, syncope, labyrinthitis.
  • Diagnostics:
    • Initial: Non-Contrast CT (NCCT) head to exclude hemorrhage.
    • MRI Brain (especially DWI) confirms ischemia.

    ⭐ Diffusion-Weighted Imaging (DWI) on MRI is the most sensitive modality for detecting acute cerebral ischemia within minutes of onset.

    • Vascular imaging (Carotid Doppler, CTA/MRA); Cardiac workup (ECG, Echo).
  • Risk Stratification: 📌 ABCD2 Score:
    • Age (≥60 years = 1 pt)
    • Blood Pressure (≥140/90 mmHg = 1 pt)
    • Clinical Features (Unilateral Weakness = 2 pts; Speech disturbance without weakness = 1 pt)
    • Duration of symptoms (≥60 min = 2 pts; 10-59 min = 1 pt)
    • Diabetes Mellitus (1 pt)
    • Interpretation: Score 0-3 (low risk); 4-5 (moderate risk, consider hospitalization); ≥6 (high risk, urgent hospitalization). MRI Brain: FLAIR, DWI, and ADC in Acute Stroke

Brainstem Stroke Syndromes - Crossed Signs & Cranial Nerves

Brainstem strokes often present with characteristic crossed syndromes - ipsilateral cranial nerve deficits with contralateral motor/sensory deficits due to the compact anatomy of the brainstem.

Foville Syndrome & Millard-Gubler Syndrome

Both syndromes result from pontine lesions affecting the facial nerve nucleus/fascicle and corticospinal tract, but differ in their specific anatomical involvement:

FeatureFoville SyndromeMillard-Gubler Syndrome
Anatomical LocationDorsal pons (tegmentum)Ventral pons (base)
Cranial Nerves AffectedCN VI (abducens) + CN VII (facial)CN VII (facial) only
Ipsilateral Signs• Facial paralysis (CN VII)
• Lateral gaze palsy (CN VI)
• Possible hearing loss
• Facial paralysis (CN VII)
Contralateral Signs• Hemiparesis
• Hemisensory loss
• Hemiparesis
Key Distinguishing FeatureLateral gaze palsy (cannot look toward lesion side)No gaze palsy
Vascular TerritoryParamedian pontine branchesParamedian pontine branches
Clinical Mnemonic"Foville = Facial + gaze Failure""Millard = just Motor + facial"
  • Weber Syndrome (Midbrain): Ipsilateral CN III palsy + contralateral hemiparesis
  • Benedikt Syndrome (Midbrain): Ipsilateral CN III palsy + contralateral tremor/ataxia
  • Wallenberg Syndrome (Lateral medulla): Ipsilateral facial sensory loss + contralateral body sensory loss + ataxia

Key Clinical Pearl: In brainstem strokes, the presence or absence of gaze palsy is crucial for differentiating Foville syndrome (gaze palsy present) from Millard-Gubler syndrome (gaze palsy absent).

Stroke Sequelae & Prevention - Road to Recovery

  • Common Sequelae: Motor deficits (hemiparesis), sensory loss, aphasia, cognitive impairment, depression, spasticity, dysphagia.
  • Secondary Prevention:
    • Antiplatelets (e.g., aspirin, clopidogrel).
    • Statins (target LDL < 70 mg/dL).
    • Strict BP control (target < 130/80 mmHg).
    • Diabetes management (HbA1c < 7%).
    • Lifestyle changes: diet, exercise, smoking cessation.

    ⭐ For patients with ischemic stroke or TIA and atrial fibrillation, long-term anticoagulation (e.g., with DOACs or warfarin) is crucial for secondary prevention.

  • Rehabilitation: Multidisciplinary approach including physiotherapy, occupational therapy, and speech therapy.

High‑Yield Points - ⚡ Biggest Takeaways

  • MCA stroke is most common: contralateral weakness/sensory loss, aphasia (dominant), neglect (non-dominant).
  • Lacunar infarcts: small, deep; pure motor/sensory deficits; linked to hypertension.
  • SAH: "worst headache of life"; berry aneurysm rupture; xanthochromia in CSF.
  • Ischemic stroke: IV thrombolysis (alteplase) within 4.5 hrs; thrombectomy up to 24 hrs for large vessel occlusion.
  • TIA: transient deficit <1 hr, no infarct; high stroke risk (use ABCD2 score).
  • Key modifiable risk factors: Hypertension, diabetes, atrial fibrillation, smoking.

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