Vascular Neurology — Last Minute Review
Rapid Review
A last-minute review of high-yield vascular neurology facts for RITE and board exams. Dense tables, no prose — designed for rapid scanning in the final hours before your test.
IV tPA Criteria
Inclusion Criteria
| Criterion |
Detail |
| Time window | ≤4.5 hours from last known well (LKW) |
| Age | ≥18 years |
| Diagnosis | Measurable neurological deficit caused by ischemic stroke |
| CT head | No evidence of hemorrhage |
Absolute Exclusion Criteria
| Category |
Exclusions |
| Hemorrhage | Any ICH on CT; SAH suspicion |
| Coagulopathy | Platelets <100k; INR >1.7; aPTT >40s; PT >15s |
| Heparin | Heparin within 48h with elevated aPTT |
| DOACs | DOAC within 48h (unless normal drug-specific assay or anti-Xa) |
| Recent surgery | Major surgery or serious trauma within 14 days |
| GI/GU bleed | Within 21 days |
| Arterial puncture | Non-compressible site within 7 days |
| Prior stroke/head trauma | Within 3 months |
| BP | >185/110 despite treatment |
| Glucose | <50 mg/dL |
| Endocarditis | Infective endocarditis — risk of septic emboli hemorrhage |
| Aortic dissection | Known or suspected |
| Intracranial neoplasm | Intra-axial intracranial neoplasm |
Extended Window (3–4.5 h) — Additional Relative Exclusions (ECASS III)
| Relative Exclusion |
Note |
| Age >80 | AHA 2019: no longer an absolute exclusion |
| NIHSS >25 | Severe stroke — relative, not absolute |
| Oral anticoagulant use (regardless of INR) | Was exclusion in ECASS III; now relative per AHA 2019 |
| Diabetes + prior stroke | Combination was excluded in ECASS III; now relative |
Dosing & Administration
| Parameter |
Value |
| Dose | 0.9 mg/kg (max 90 mg) |
| 10% bolus | IV over 1 minute |
| Remaining 90% | IV infusion over 60 minutes |
| BP goal post-tPA | <180/105 for 24 hours |
| No antiplatelets/anticoagulants | For 24 hours post-tPA |
| Follow-up CT | At 24 hours (before starting antiplatelets) |
Only 2 tests required before giving tPA: NCCT head + blood glucose. Do NOT delay for other labs unless clinical suspicion of coagulopathy. Wake-up stroke with DWI-FLAIR mismatch can receive tPA (WAKE-UP trial). Tenecteplase (0.25 mg/kg, single bolus) is non-inferior and increasingly used off-label.
Mechanical Thrombectomy Criteria
Standard Window (0–6 hours)
| Criterion |
Requirement |
| LVO confirmed | ICA, M1, or proximal M2 occlusion on CTA/MRA |
| NIHSS | ≥6 |
| ASPECTS | ≥6 on NCCT |
| Pre-stroke mRS | 0–1 |
| Age | ≥18 |
Extended Window (6–24 hours)
| Trial |
Window |
Key Eligibility |
| DAWN | 6–24 h | Clinical-core mismatch (small infarct, large deficit); NIHSS ≥10; core <21–51 mL (age-dependent) |
| DEFUSE 3 | 6–16 h | Perfusion mismatch ratio ≥1.8; ischemic core <70 mL; mismatch volume ≥15 mL |
LVO Sites Amenable to Thrombectomy
| Vessel |
Evidence Level |
| ICA (intracranial) | Strong — included in all major RCTs |
| M1 (MCA) | Strong — most common target |
| Proximal M2 | Moderate — included in recent trials |
| Basilar artery | Moderate — ATTENTION & BAOCHE trials positive |
| Distal M2, A1, A2 | Insufficient — case-by-case basis |
TICI Reperfusion Grading
| Grade |
Definition |
| 0 | No perfusion |
| 1 | Penetration, no distal filling |
| 2a | <50% territory perfused |
| 2b | ≥50% territory perfused |
| 2c | Near-complete perfusion with slow flow |
| 3 | Complete perfusion |
Thrombectomy is NOT a substitute for tPA. If eligible for both, give tPA immediately and proceed to thrombectomy (bridging therapy). Target: TICI 2b–3. Successful reperfusion = TICI ≥2b. Basilar thrombectomy now supported up to 24 h (ATTENTION trial).
NIHSS Key Components
| Item |
What It Tests |
Max Score |
| 1a | Level of consciousness (alertness) | 3 |
| 1b | LOC questions (month, age) | 2 |
| 1c | LOC commands (open/close eyes, grip/release) | 2 |
| 2 | Best gaze (horizontal eye movements) | 2 |
| 3 | Visual fields (confrontation) | 3 |
| 4 | Facial palsy | 3 |
| 5a/5b | Motor arm L/R (hold 90° sitting / 45° supine for 10 s) | 4 each |
| 6a/6b | Motor leg L/R (hold 30° supine for 5 s) | 4 each |
| 7 | Limb ataxia (finger-nose, heel-shin) | 2 |
| 8 | Sensory (pinprick) | 2 |
| 9 | Best language (aphasia) | 3 |
| 10 | Dysarthria | 2 |
| 11 | Extinction / inattention (neglect) | 2 |
Total: 0–42 | Minor ≤4 | Moderate 5–15 | Moderate-severe 16–20 | Severe ≥21
NIHSS is left-hemisphere/anterior biased. It heavily weights language (max 5 pts) and right-sided motor (scored equally). Posterior circulation strokes (vertigo, diplopia, ataxia, bilateral weakness) can score near zero despite devastating deficits. A “low NIHSS” does NOT rule out a dangerous stroke.
Stroke Syndromes by Territory
| Territory |
Vessel |
Classic Findings |
| ACA | A2 segment | Contralateral leg > arm weakness; abulia; urinary incontinence; alien hand (dominant); transcortical motor aphasia |
| MCA — superior division | M2 superior | Contralateral face/arm > leg weakness; Broca aphasia (dominant); contralateral gaze preference |
| MCA — inferior division | M2 inferior | Wernicke aphasia (dominant); hemineglect (non-dominant); superior quadrantanopia |
| MCA — complete | M1 | All of the above + global aphasia (dominant) or anosognosia (non-dominant); forced gaze deviation toward lesion |
| PCA | P2 segment | Contralateral homonymous hemianopia (with macular sparing); alexia without agraphia (dominant); visual agnosia; memory loss (hippocampus) |
| Basilar tip | Top of basilar | Bilateral PCA signs; “top of the basilar” syndrome; coma; peduncular hallucinosis |
| Basilar artery (pons) | Basilar trunk | Locked-in syndrome (ventral pons); quadriplegia + anarthria with preserved consciousness & vertical eye movements |
| PICA / lateral medulla | Vertebral / PICA | Wallenberg syndrome: ipsilateral Horner, facial pain/temp loss, ataxia, palatal weakness; contralateral body pain/temp loss; dysphagia; vertigo |
| AICA | AICA | Ipsilateral hearing loss + facial palsy + ataxia; lateral pontine syndrome |
| SCA | SCA | Ipsilateral ataxia, contralateral pain/temp loss; may have ipsilateral Horner |
| Anterior spinal artery | ASA | Medial medullary syndrome: contralateral hemiplegia (arm/leg), contralateral proprioception loss, ipsilateral tongue weakness |
| Anterior choroidal | AChA (from ICA) | Contralateral hemiplegia + hemianesthesia + homonymous hemianopia (triad) |
Wallenberg (lateral medullary) syndrome is the most tested posterior circulation stroke on boards. Remember: ipsilateral = face + Horner + ataxia; contralateral = body pain/temp. Dysphagia is common. It does NOT cause motor weakness (corticospinal tract spared). Nucleus ambiguus involvement → ipsilateral palatal/vocal cord paralysis.
Lacunar Syndromes
| Syndrome |
Location |
Presentation |
| Pure motor hemiparesis | Posterior limb of internal capsule OR basis pontis | Contralateral face, arm, leg weakness (equal); NO sensory/visual/cortical signs |
| Pure sensory stroke | VPL nucleus of thalamus | Contralateral numbness/paresthesias face, arm, leg; NO motor deficit |
| Ataxic hemiparesis | Posterior limb of internal capsule OR pons | Contralateral weakness + ipsilateral ataxia (out of proportion to weakness); cerebellar-type ataxia |
| Dysarthria–clumsy hand | Basis pontis OR anterior limb of internal capsule / genu | Dysarthria + ipsilateral hand clumsiness/weakness; facial weakness common |
| Mixed sensorimotor | Thalamus extending to posterior limb of internal capsule | Contralateral hemiparesis + hemisensory loss; thalamocapsular location |
Lacunar strokes are small (<1.5 cm), deep infarcts from lipohyalinosis of penetrating arteries. They do NOT cause cortical signs (no aphasia, no neglect, no hemianopia). If cortical signs are present, think embolic or large-artery disease, not lacunar. The most common lacunar syndrome is pure motor hemiparesis. Lacunar infarcts are often NIHSS-low and CT-negative early — MRI DWI is the gold standard.
ICH Management
Blood Pressure Targets
| Scenario |
SBP Target |
Evidence |
| SBP 150–220, no contraindication | <140 mmHg (acute lowering safe) | INTERACT2, ATACH-2 |
| SBP >220 | Aggressive reduction with IV infusion; consider <140 | AHA 2022 |
| Post-craniotomy | Individualized; typically <140–160 | Surgeon discretion |
Reversal Agents by Anticoagulant
| Anticoagulant |
Reversal Agent |
Key Notes |
| Warfarin | 4-factor PCC (preferred) + IV vitamin K 10 mg | Goal INR ≤1.3; FFP is second-line (volume overload, slower) |
| Dabigatran | Idarucizumab (Praxbind) 5 g IV | Specific reversal; instant onset; if unavailable, use aPCC (FEIBA) |
| Rivaroxaban / Apixaban / Edoxaban | Andexanet alfa (AndexXa) | Factor Xa inhibitor reversal; if unavailable, use 4-factor PCC |
| Heparin (UFH) | Protamine sulfate (1 mg per 100 units UFH) | Give within 2–3 h of last dose; max 50 mg |
| Enoxaparin (LMWH) | Protamine (partial reversal; ~60%) | 1 mg per 1 mg enoxaparin if within 8 h |
| tPA-related hemorrhage | Cryoprecipitate (goal fibrinogen >200) + tranexamic acid | Stop tPA infusion; check fibrinogen, platelets, PT/INR |
| Antiplatelet-related | Platelet transfusion (controversial) | PATCH trial showed no benefit; consider only pre-surgery |
ICH Score (Prognosis)
| Component |
Points |
| GCS 3–4 = 2 pts; GCS 5–12 = 1 pt; GCS 13–15 = 0 pts | 0–2 |
| ICH volume ≥30 mL = 1 pt | 0–1 |
| IVH present = 1 pt | 0–1 |
| Infratentorial origin = 1 pt | 0–1 |
| Age ≥80 = 1 pt | 0–1 |
Score range: 0–6 | Score 0 = 0% mortality | Score 5 = 100% mortality
The CTA “spot sign” (contrast extravasation) predicts hematoma expansion. ICH volume is estimated using ABC/2 method. For warfarin-ICH, 4-factor PCC is superior to FFP (faster, less volume). Never use the ICH score alone to make withdrawal-of-care decisions — it becomes a self-fulfilling prophecy.
SAH Grading & Complications
Hunt-Hess Scale
| Grade |
Clinical Features |
Approximate Mortality |
| 1 | Asymptomatic or mild headache, slight nuchal rigidity | ~1% |
| 2 | Moderate-severe headache, nuchal rigidity, cranial nerve palsy only | ~5% |
| 3 | Drowsy, confused, or mild focal deficit | ~19% |
| 4 | Stupor, moderate-severe hemiparesis, early decerebrate posturing | ~42% |
| 5 | Deep coma, decerebrate posturing, moribund | ~77% |
Modified Fisher Grade (CT)
| Grade |
CT Findings |
Vasospasm Risk |
| 0 | No SAH or IVH | Low |
| 1 | Thin SAH, no IVH | Low |
| 2 | Thin SAH with IVH | Moderate |
| 3 | Thick SAH, no IVH | High |
| 4 | Thick SAH with IVH | Highest |
SAH Complications Timeline
| Complication |
Timing |
Key Points |
| Rebleeding | Day 0–1 (highest in first 6 h) | Secure aneurysm ASAP (clipping or coiling within 24 h); SBP <160 until secured |
| Acute hydrocephalus | Day 0–3 | Obstructive (IVH) or communicating; treat with EVD |
| Vasospasm / DCI | Day 3–14 (peak day 7–10) | Nimodipine 60 mg q4h × 21 days (improves outcomes, does NOT prevent vasospasm on angiogram); treat DCI with induced hypertension + IV fluids; intra-arterial verapamil/angioplasty for refractory |
| Delayed cerebral ischemia | Day 4–14 | New focal deficit or ↓GCS ≥2 pts not explained by other cause; TCD monitoring (MFV >120 = concern; >200 = severe spasm) |
| Hyponatremia | Day 2–14 | Cerebral salt wasting (volume depleted, high UNa) >> SIADH; treat CSW with isotonic/hypertonic saline; do NOT fluid restrict (worsens vasospasm) |
| Seizures | Acute (day 0–7) | Prophylactic AEDs controversial; avoid phenytoin (worse outcomes — Naidech 2005); levetiracetam preferred if used |
| Chronic hydrocephalus | Weeks to months | Communicating; may need VP shunt; triad: gait → dementia → incontinence |
| Cardiac complications | Day 0–7 | Neurogenic stunned myocardium; Takotsubo; troponin elevation; ECG changes (deep T inversions, QT prolongation) |
Nimodipine improves outcomes in SAH but does NOT reduce angiographic vasospasm — its benefit is likely neuroprotective. The most common cause of hyponatremia in SAH is cerebral salt wasting (NOT SIADH) — do NOT fluid restrict. CT sensitivity for SAH decreases with time: ~98% at 6 h, ~93% at 12 h, ~50% at 1 week — LP is required if CT negative and clinical suspicion remains.
Cerebral Venous Thrombosis (CVT)
Risk Factors
| Category |
Risk Factors |
| Prothrombotic | OCP / pregnancy / postpartum; Factor V Leiden; prothrombin G20210A; protein C/S deficiency; antithrombin III deficiency; antiphospholipid syndrome |
| Inflammatory | IBD; Behçet disease; SLE; vasculitis |
| Infectious | Mastoiditis / otitis (lateral sinus); sinusitis (cavernous sinus); meningitis |
| Hematologic | Polycythemia vera; essential thrombocythemia; PNH; sickle cell |
| Other | Dehydration; malignancy; head trauma; neurosurgery; lumbar puncture |
Clinical Presentation
| Feature |
Details |
| Headache | Most common symptom (~90%); progressive, may mimic IIH; worse with Valsalva |
| Seizures | ~40% of cases; more common than in arterial stroke |
| Focal deficits | Hemiparesis, aphasia; may fluctuate or be bilateral |
| Papilledema | From elevated ICP; bilateral, may have visual obscurations |
| Venous infarcts | Often hemorrhagic; do NOT follow arterial territories; bilateral, parasagittal |
| Cavernous sinus thrombosis | Proptosis, chemosis, CN III/IV/V1/V2/VI palsies; often septic (from sinusitis) |
Imaging & Diagnosis
| Test |
Key Findings |
| CT head | Hyperdense sinus sign (acute); cord sign; hemorrhagic venous infarct not in arterial territory |
| CT venography / MR venography | Gold standard — filling defect in dural sinus; “empty delta sign” on contrast CT |
| MRI | Absent flow void in sinus; variable signal depending on thrombus age |
| D-dimer | Sensitive but not specific; normal D-dimer has high NPV in low-risk cases |
Treatment
| Phase |
Treatment |
| Acute | Anticoagulation with heparin (UFH or LMWH) — even if hemorrhagic infarct present |
| Long-term | Warfarin (INR 2–3) for 3–12 months depending on cause; DOACs increasingly used |
| Provoked / transient RF | 3–6 months anticoagulation |
| Unprovoked or thrombophilia | 6–12 months; consider indefinite if recurrent or severe thrombophilia |
| Refractory / worsening | Endovascular thrombolysis or thrombectomy |
| Elevated ICP | Acetazolamide; serial LP; VP shunt if refractory |
Anticoagulate CVT even with hemorrhagic infarcts — the hemorrhage is caused by venous congestion, and anticoagulation prevents thrombus propagation. The classic board scenario: young woman on OCPs with headache + seizure + hemorrhagic infarct not in an arterial territory → think CVT, get MRV, start heparin.
Secondary Stroke Prevention by Mechanism
| Mechanism |
Key Prevention Strategy |
Details |
| Large artery atherosclerosis (extracranial carotid) | CEA or CAS + antiplatelet + statin | CEA if symptomatic 50–99% stenosis (NASCET); CAS if high surgical risk; dual antiplatelet (ASA + clopidogrel) × 21 days if not revascularized, then mono; high-intensity statin (atorvastatin 80 mg) |
| Large artery atherosclerosis (intracranial) | Dual antiplatelet + statin + BP control | SAMMPRIS: aggressive medical therapy (DAPT 90 days + statin + BP/lifestyle) superior to stenting; NO intracranial stenting unless refractory |
| Cardioembolic (AF) | Anticoagulation (DOAC preferred) | DOACs > warfarin for non-valvular AF; start 4–14 days post-stroke (see timing table below); CHA₂DS₂-VASc to assess risk |
| Cardioembolic (mechanical valve) | Warfarin only | DOACs contraindicated in mechanical valves (RE-ALIGN trial); INR target 2.5–3.5 for mitral valves; 2.0–3.0 for aortic |
| Cardioembolic (PFO) | PFO closure (select patients) + antiplatelet | Consider closure if age <60 + cryptogenic stroke + high-risk features (large shunt, atrial septal aneurysm); RESPECT, CLOSE, DEFENSE-PFO trials |
| Small vessel (lacunar) | Single antiplatelet + BP control + statin | SPS3: DAPT increased bleeding without benefit in lacunar stroke; target SBP <130; no anticoagulation benefit |
| Cervical artery dissection | Antiplatelet or anticoagulation (equivalent) | CADISS trial: no difference between antiplatelet vs anticoagulation; typically treat 3–6 months, then reassess with imaging |
| Cryptogenic / ESUS | Antiplatelet + prolonged cardiac monitoring | NAVIGATE-ESUS & RE-SPECT ESUS: rivaroxaban and dabigatran NOT superior to aspirin for ESUS; prolonged monitoring may reveal AF |
DAPT (ASA + clopidogrel) for minor stroke (NIHSS ≤3) or high-risk TIA: start within 24 h, continue 21 days, then mono-antiplatelet (CHANCE / POINT trials). For intracranial stenosis, SAMMPRIS proved stenting is worse than aggressive medical therapy. For cryptogenic stroke, DO NOT empirically anticoagulate — look for AF first.
Anticoagulation Rules
CHA₂DS₂-VASc Score (AF Stroke Risk)
| Component |
Points |
| C — Congestive heart failure (EF ≤40%) | 1 |
| H — Hypertension | 1 |
| A₂ — Age ≥75 | 2 |
| D — Diabetes mellitus | 1 |
| S₂ — Stroke / TIA / thromboembolism | 2 |
| V — Vascular disease (MI, PAD, aortic plaque) | 1 |
| A — Age 65–74 | 1 |
| Sc — Sex category (female) | 1 |
Score ≥2 (men) or ≥3 (women) → anticoagulate | Score 1 (men) or 2 (women) → consider anticoagulation | Score 0 (men) or 1 (women) → no anticoagulation
Mechanical Valve Anticoagulation
| Valve Position |
INR Target |
Notes |
| Aortic (bileaflet / Medtronic Hall) | 2.0–3.0 | Lower risk position |
| Mitral | 2.5–3.5 | Higher thromboembolic risk |
| Both / older valve | 2.5–3.5 | Caged-ball valves = highest risk |
| DOACs | CONTRAINDICATED | RE-ALIGN trial: dabigatran caused increased thromboembolism + bleeding |
When to Start Anticoagulation After Acute Ischemic Stroke
| Stroke Severity |
Suggested Timing |
Rationale |
| TIA | Day 1 | No infarct; low hemorrhagic transformation (HT) risk |
| Minor stroke (NIHSS <8, small infarct) | Day 3–5 | Low HT risk |
| Moderate stroke (NIHSS 8–15) | Day 6–7 | Moderate HT risk; repeat imaging before starting |
| Severe stroke (NIHSS ≥16 or large infarct) | Day 12–14 | High HT risk; repeat CT to rule out HT before starting |
| Hemorrhagic transformation present | Delay further; reassess in 1–2 weeks | Individualized risk-benefit analysis |
Mnemonic: “1-3-6-12” rule — TIA = day 1, small = day 3, medium = day 6, large = day 12
DOACs are contraindicated in mechanical heart valves (RE-ALIGN) and moderate-to-severe mitral stenosis. For non-valvular AF, DOACs are first-line over warfarin. The “1-3-6-12” rule for anticoagulation timing is widely used but guidelines are evolving — the ELAN trial (2023) supported early DOAC initiation (within 48 h for mild-moderate stroke) without increased ICH risk.
Classic Board Traps
⚠️ Common Vascular Neurology Board Traps
| # |
Trap |
Correct Answer |
| 1 | Patient with posterior circulation stroke has low NIHSS — is it a minor stroke? | No. NIHSS underscores posterior circulation strokes. Low NIHSS does NOT mean low severity in basilar/PCA territory. |
| 2 | ICH on anticoagulation with hemorrhagic venous infarct — stop anticoagulation? | No — if it is CVT. Anticoagulate CVT even with hemorrhagic infarction. The hemorrhage is from venous congestion, not arterial rupture. |
| 3 | SAH patient with hyponatremia — fluid restrict for SIADH? | No. Most SAH hyponatremia is cerebral salt wasting (NOT SIADH). Fluid restriction worsens vasospasm. Treat with isotonic/hypertonic saline. |
| 4 | Young woman on OCP with thunderclap headache, normal CT — SAH ruled out? | No. CT sensitivity for SAH drops with time. Perform LP. Also consider CVT — get MRV. |
| 5 | Lacunar stroke patient — start dual antiplatelet long-term? | No. SPS3 trial showed DAPT increased bleeding without reducing recurrence in lacunar stroke. Use single antiplatelet. |
| 6 | Cryptogenic stroke — start empiric anticoagulation? | No. NAVIGATE-ESUS and RE-SPECT ESUS showed no benefit of DOACs over aspirin in ESUS. Do prolonged cardiac monitoring to find AF first. |
| 7 | Intracranial stenosis >70% — place a stent? | No. SAMMPRIS: stenting had higher stroke/death rate than aggressive medical therapy (DAPT + statin + BP control). |
| 8 | Mechanical valve patient — switch to DOAC? | Never. RE-ALIGN trial: dabigatran increased thromboembolism AND bleeding in mechanical valves. Warfarin is the only option. |
| 9 | tPA given → patient worsens with expanding ICH — what do you give? | Cryoprecipitate (goal fibrinogen >200 mg/dL) + tranexamic acid. Stop the infusion. Check fibrinogen, platelets, coags. |
| 10 | Nimodipine prevents angiographic vasospasm in SAH? | No. Nimodipine improves outcomes (reduces DCI and death) but does NOT reduce angiographic vasospasm. Its mechanism is likely neuroprotective. |
| 11 | Wallenberg syndrome causes contralateral weakness? | No. Lateral medullary (Wallenberg) syndrome does NOT cause motor weakness — the corticospinal tract is in the medial medulla and is spared. It causes ipsilateral face + contralateral body pain/temperature loss. |
| 12 | Wake-up stroke — cannot give tPA? | Not true. WAKE-UP trial: DWI-FLAIR mismatch identifies patients who may benefit from tPA even with unknown onset time. |
| 13 | Carotid dissection — must anticoagulate? | Either is fine. CADISS trial showed no difference between antiplatelet and anticoagulation for cervical artery dissection. Both are acceptable. |
| 14 | PFO found after stroke — always close it? | No. PFO closure only in select patients: age <60, cryptogenic stroke, high-risk PFO features (large shunt, atrial septal aneurysm). Not all PFOs are pathologic. |
