Inflammatory Vasculopathies and Stroke
Inflammatory vasculopathies represent a heterogeneous group of disorders that cause stroke through vessel wall inflammation, thrombosis, or both. While rare compared to atherosclerotic disease, they disproportionately affect younger patients and require specific diagnostic and therapeutic approaches. This article reviews the clinical approach to suspected inflammatory stroke, primary CNS vasculitis, large vessel vasculitides, and inflammatory arteriopathies that mimic classic vasculitis.
🔹 Bottom Line: Inflammatory Stroke
- Suspect inflammatory etiology: Multifocal strokes, recurrent events despite optimal prevention, headache/encephalopathy, systemic symptoms, abnormal CSF, vessel wall enhancement, or young age without traditional risk factors
- Core workup: MRI with vessel wall imaging, CTA/MRA, lumbar puncture, ESR/CRP, autoimmune panel, infectious studies
- PACNS treatment: Glucocorticoids + cyclophosphamide induction → azathioprine/MMF/methotrexate maintenance; rituximab for refractory cases (French COVAC: 80% mRS 0-2 with combined therapy)
- GCA: Tocilizumab + steroid taper achieves 56% sustained remission vs 14% placebo (GiACTA); ~50% steroid-sparing effect
- Takayasu: TAKT trial showed trend toward benefit with tocilizumab (HR 0.41, p=0.06 ITT); used off-label for refractory disease
- Don’t miss mimics: RCVS (use RCVS2 score), Susac syndrome (corpus callosum “snowballs”), Sneddon syndrome (livedo + stroke)
Clinical Approach: When to Suspect Inflammatory Stroke
Inflammatory stroke should be considered when clinical and imaging features suggest a non-atherosclerotic mechanism, particularly in patients lacking traditional vascular risk factors. Early recognition is critical, as untreated vasculitis carries high morbidity and mortality.
🔴 Red Flags for Inflammatory Stroke
- Multifocal strokes in different vascular territories
- Recurrent stroke/TIA despite optimal secondary prevention
- Headaches, encephalopathy, or cognitive decline accompanying stroke
- Systemic symptoms: fever, weight loss, fatigue, rash, arthritis
- Abnormal CSF (elevated protein, pleocytosis)
- Vessel wall enhancement on MRI
- Young patient (<45 years) without traditional risk factors
- Unusual stroke locations (bilateral, posterior fossa, watershed)
Core Diagnostic Bundle
When inflammatory stroke is suspected, a systematic evaluation should include:
| Category | Tests | Rationale |
|---|---|---|
| Neuroimaging | MRI brain (DWI/FLAIR/SWI/T1 post-contrast) Vessel wall MRI CTA/MRA head and neck |
Identify infarct pattern, vessel wall enhancement (inflammation vs atherosclerosis), stenoses/aneurysms |
| CSF Analysis | Cell count, protein, glucose Oligoclonal bands Infectious studies (VZV PCR, VDRL, cryptococcal antigen) |
PACNS: elevated protein (80%), pleocytosis (50-80%); helps exclude infection |
| Inflammatory Markers | ESR, CRP | Elevated in systemic vasculitis; often normal in PACNS |
| Autoimmune Panel | ANA, ANCA (PR3/MPO), anti-dsDNA Complement (C3, C4) |
Screen for systemic autoimmune disease with CNS involvement |
| Infectious Workup | HIV, syphilis (RPR/TPPA), VZV IgG/IgM TB (QuantiFERON, chest imaging) |
Infectious vasculitis is a critical differential |
| Additional | Echocardiogram (TTE ± TEE) Hypercoagulable panel if indicated |
Exclude embolic source and prothrombotic states |
Mimics to Explicitly Exclude
Before diagnosing inflammatory vasculopathy, several important mimics must be ruled out:
| Mimic | Key Distinguishing Features |
|---|---|
| RCVS | Thunderclap headache, triggers (vasoactive drugs, postpartum), normal CSF, vasoconstriction resolves within 12 weeks, RCVS2 score ≥5 |
| Embolic shower | Cardiac source (endocarditis, myxoma), fat embolism (long bone fracture), air embolism, tumor embolism |
| Intracranial atherosclerosis (ICAD) | Risk factors present, eccentric plaque on vessel wall MRI, no enhancement (or eccentric enhancement) |
| Arterial dissection | Neck pain, trauma history, intramural hematoma on fat-sat MRI, “flame sign” on angiography |
| Moyamoya | Bilateral ICA/MCA stenosis with basal collaterals (“puff of smoke”), progressive course |
| Hypercoagulable states | Venous and arterial thromboses, pregnancy loss, livedo (consider APS if not covered separately) |
| Drug-induced vasospasm | Sympathomimetics (cocaine, amphetamines), triptans, cannabis, ergotamines |
Primary Angiitis of the Central Nervous System (PACNS)
PACNS is a rare vasculitis confined to the CNS, affecting small and medium-sized leptomeningeal and parenchymal vessels. Incidence is approximately 2.4 per million person-years with equal sex distribution and median age at diagnosis of 50 years. The diagnosis requires exclusion of systemic vasculitis and other CNS vasculopathy mimics.
Diagnostic Criteria
🔹 Calabrese-Mallek Criteria (1988)
- Criterion 1: Acquired neurologic or psychiatric deficit unexplained by other causes after thorough evaluation
- Criterion 2: Classic angiographic features (multifocal segmental stenoses/dilations) OR histopathologic evidence of CNS angiitis
- Criterion 3: No evidence of systemic vasculitis or any disorder that could mimic the angiographic or pathologic features
Birnbaum and Hellmann (2009) proposed a modification to improve specificity:
- “Definite” PACNS: Histopathologic confirmation of vasculitis on brain/leptomeningeal biopsy
- “Probable” PACNS: High-probability angiographic findings + abnormal MRI + CSF profile consistent with PACNS (without tissue confirmation)
Clinical Subtypes
PACNS presents heterogeneously, and recognition of clinical subtypes guides prognosis and treatment intensity:
| Subtype | Vessel Size | Features | Diagnosis |
|---|---|---|---|
| Small vessel PACNS | Arterioles, venules | Encephalopathy, cognitive decline, seizures more common; slower progression | Biopsy-positive, angiogram often negative |
| Medium/large vessel PACNS | Cortical arteries | Focal deficits, stroke-like presentation more common | Angiogram-positive, biopsy may be negative |
| Mass-lesion variant | Variable | Tumor-like presentation; biopsy essential to exclude malignancy | Biopsy required |
| Rapidly progressive PACNS | Multiple large vessels | Bilateral, fulminant course; poor response to therapy; high mortality | Usually angiogram-positive |
| Aβ-related angiitis (ABRA) | Small cortical vessels | Older patients; associated with cerebral amyloid angiopathy; responds to steroids | Biopsy shows amyloid + inflammation |
Treatment: Evidence from the French COVAC Cohort
No randomized controlled trials exist for PACNS. Treatment recommendations derive from the French COVAC multicenter cohort (de Boysson et al., Stroke 2018), which evaluated 112 patients with median follow-up of 53 months.
| Treatment Strategy | N | mRS 0-2 at Follow-up | Relapse Rate |
|---|---|---|---|
| Glucocorticoids alone | 23 | 43% | High |
| Glucocorticoids + cyclophosphamide (no maintenance) | 42 | 40% | High |
| Glucocorticoids + cyclophosphamide + maintenance IS | 47 | 80% | Lower |
The combined induction plus maintenance strategy showed significantly better outcomes (p=0.0004). Overall relapse rate was 46%, emphasizing the need for long-term immunosuppression.
🔹 PACNS Treatment Protocol
- Induction: High-dose glucocorticoids (methylprednisolone 1g IV × 3-5 days → prednisone 1 mg/kg/day) + cyclophosphamide (IV pulses 0.5-0.75 g/m² monthly × 6 or oral 2 mg/kg/day × 3-6 months)
- Maintenance: Azathioprine (2 mg/kg/day), mycophenolate mofetil (2-3 g/day), or methotrexate (15-25 mg/week) for ≥2 years
- Refractory disease: Rituximab 375 mg/m² weekly × 4 or 1000 mg × 2 doses; monitor CD19/CD20 for re-dosing (typically every 6 months)
- Steroid taper: Begin after 4-6 weeks of induction; taper over 6-12 months to lowest effective dose
Large Vessel Vasculitis
Giant Cell Arteritis (GCA)
GCA is the most common primary systemic vasculitis in adults over 50, with an incidence of 15-25 per 100,000 in populations of Northern European ancestry. While cranial involvement (temporal arteritis) is classic, large vessel GCA affecting the aorta and its branches is increasingly recognized and carries stroke risk through vertebral, carotid, or aortic arch involvement.
2022 ACR/EULAR Classification Criteria
These criteria apply to patients with confirmed medium- or large-vessel vasculitis. Age ≥50 years at diagnosis is an absolute requirement. A cumulative score ≥6 points classifies GCA.
| Criterion | Points |
|---|---|
| Positive temporal artery biopsy OR halo sign on temporal artery ultrasound | +5 |
| ESR ≥50 mm/hr OR CRP ≥10 mg/L | +3 |
| Sudden visual loss | +3 |
| Morning stiffness in shoulders or neck | +2 |
| Jaw or tongue claudication | +2 |
| New temporal headache | +2 |
| Scalp tenderness | +2 |
| Temporal artery abnormality on examination (tenderness, decreased pulse) | +2 |
| Bilateral axillary artery involvement on imaging | +2 |
| FDG-PET activity throughout the aorta | +2 |
Validation showed sensitivity of 87% and specificity of 95% (AUC 0.91). These criteria perform better than the 1990 ACR criteria, particularly for large-vessel GCA phenotypes.
GiACTA Trial: Tocilizumab for GCA
The GiACTA trial (Stone et al., NEJM 2017) established tocilizumab as a steroid-sparing treatment for GCA. This phase 3 RCT randomized 251 patients with new-onset or relapsing GCA to four arms:
| Arm | Intervention | Sustained Remission at 52 Weeks |
|---|---|---|
| Tocilizumab weekly | TCZ 162 mg SC weekly + 26-week prednisone taper | 56% |
| Tocilizumab Q2W | TCZ 162 mg SC every 2 weeks + 26-week taper | 53% |
| Placebo + 26-week taper | Placebo + 26-week prednisone taper | 14% |
| Placebo + 52-week taper | Placebo + 52-week prednisone taper | 18% |
Both tocilizumab arms were superior to placebo (p<0.001). Median cumulative prednisone dose was 1,862 mg in tocilizumab arms versus 3,296-3,818 mg in placebo arms—approximately 50% steroid-sparing effect. Long-term extension data (GiACTA Part 2, Lancet Rheumatology 2021) showed ~48% of patients maintained drug-free remission after stopping tocilizumab, with weekly dosing superior to Q2W in relapsing disease.
🔹 Clinical Relevance: GCA and Stroke Prevention
- Stroke mechanisms in GCA: Vertebral/carotid involvement (particularly extracranial), aortic arch disease, rarely intracranial involvement
- Vision loss is the emergency: Anterior ischemic optic neuropathy (AION) requires immediate high-dose steroids; tocilizumab does not replace steroids acutely
- Treatment algorithm: New-onset or relapsing GCA → tocilizumab 162 mg SC weekly (or Q2W) + accelerated prednisone taper (26 weeks); weekly preferred for relapsing disease
- Duration: 1 year of tocilizumab may be sufficient; many maintain remission after discontinuation
- Monitoring caveat: Tocilizumab suppresses CRP/ESR; clinical monitoring essential during treatment
Takayasu Arteritis
Takayasu arteritis (TAK) is a large vessel vasculitis affecting the aorta and its major branches, predominantly in women under 40 years. Stroke mechanisms include subclavian steal, carotid stenosis, and cardiac embolism from aortic regurgitation. Incidence is 2-3 per million in Western populations but higher in Japan and Asia.
TAKT Trial: Tocilizumab for Takayasu Arteritis
The TAKT trial (Nakaoka et al., Ann Rheum Dis 2018) was the only phase 3 RCT of tocilizumab in TAK. This Japanese study randomized 36 patients with refractory, relapsing TAK to tocilizumab 162 mg SC weekly versus placebo, with glucocorticoid tapering.
| Outcome | Tocilizumab | Placebo | HR (95% CI) | P-value |
|---|---|---|---|---|
| Relapse-free at 24 weeks (ITT) | 51% | 23% | 0.41 (0.15-1.10) | 0.06 |
| Relapse-free at 24 weeks (per-protocol) | 52% | 17% | 0.34 (0.11-1.00) | 0.03 |
The primary endpoint was not met in the intention-to-treat analysis, though trends favored tocilizumab. The study was likely underpowered (N=36). Long-term extension (TAKT 96-week, Rheumatology 2020) showed 46% of patients reduced glucocorticoid dose to <0.1 mg/kg/day, and 86% of arteries remained stable or improved on imaging.
🔹 Clinical Relevance: Takayasu Arteritis Management
- First-line therapy: High-dose glucocorticoids (prednisone 1 mg/kg/day); 50% achieve remission but relapse rates are high
- Refractory disease: Consider tocilizumab (off-label) or TNF inhibitors (infliximab); limited RCT evidence
- TAKT takeaway: Suggestive benefit with tocilizumab, significant steroid-sparing in extension; not FDA-approved for TAK but used off-label
- Surgical/endovascular intervention: Reserved for critical stenoses; avoid during active inflammation
- Monitoring: Clinical assessment, inflammatory markers, serial CTA/MRA or PET
Medium and Small Vessel Vasculitis
Systemic small and medium vessel vasculitides can involve the CNS, though isolated CNS involvement is rare. Key entities include:
| Vasculitis | Vessel Size | CNS Manifestations | Key Features |
|---|---|---|---|
| GPA (Wegener’s) | Small | Pachymeningitis, pituitary involvement, orbital pseudotumor, rare stroke | PR3-ANCA positive; upper/lower respiratory, renal involvement |
| MPA | Small | Peripheral neuropathy > CNS; mononeuritis multiplex | MPO-ANCA positive; pulmonary-renal syndrome |
| EGPA (Churg-Strauss) | Small | Peripheral neuropathy (70%); CNS rare | Asthma, eosinophilia, MPO-ANCA (40%) |
| Polyarteritis nodosa | Medium | Stroke, hemorrhage, aneurysms | ANCA-negative; HBV association; renal/mesenteric involvement |
| Behçet disease | Variable | Venous sinus thrombosis (most common), parenchymal neuro-Behçet, arterial aneurysms | Oral/genital ulcers, uveitis, pathergy; HLA-B51 |
Treatment typically follows protocols for the underlying systemic vasculitis. For ANCA-associated vasculitis, the RAVE trial demonstrated rituximab non-inferiority to cyclophosphamide for induction, with potential superiority in relapsing disease.
Inflammatory Arteriopathies That Aren’t Classic Vasculitis
Several conditions cause stroke through inflammatory or microangiopathic mechanisms but do not fit the classic vasculitis paradigm. Recognition is essential as treatment differs significantly.
Susac Syndrome
Susac syndrome is an autoimmune endotheliopathy affecting precapillary arterioles of the brain, retina, and cochlea. It predominantly affects young women (mean age 31, F:M ratio 3.5:1) and is often misdiagnosed as multiple sclerosis or ADEM.
| Clinical Triad | Features | Key Diagnostic Finding |
|---|---|---|
| Encephalopathy | Cognitive impairment, confusion, behavioral changes, headache, psychiatric symptoms | MRI: “Snowball” lesions in central corpus callosum (pathognomonic) |
| Branch retinal artery occlusions (BRAO) | Scotomata, visual disturbances; often peripheral and asymptomatic | Fluorescein angiography: BRAO, Gass plaques (yellow arterial wall plaques) |
| Sensorineural hearing loss | Low and mid-frequency loss; tinnitus; often sudden onset | Audiometry: Low/mid-frequency SNHL |
Critical point: The complete triad is present at onset in only 13% of cases. Components may appear sequentially over months to years, leading to diagnostic delay (mean 3 months when criteria met, up to 10 months with partial presentation).
🔹 Susac Syndrome: Diagnosis and Treatment
- Diagnostic workup: MRI brain (central callosal “snowball” lesions), fluorescein angiography (BRAO, arteriolar wall hyperfluorescence, Gass plaques), audiometry
- Differentiating from MS: Susac affects central corpus callosum fibers; MS typically affects callosal undersurface. OCT shows retinal infarcts in Susac vs optic nerve thinning in MS
- Treatment: Aggressive immunosuppression early prevents permanent deficits
- Acute: IV methylprednisolone + IVIG ± cyclophosphamide or rituximab
- Maintenance: MMF or azathioprine; very slow steroid taper over 2+ years
- Prognosis: Usually self-limiting (1-4 years) but may leave residual cognitive, visual, and hearing deficits. Cochlear implants for severe hearing loss
Sneddon Syndrome
Sneddon syndrome is a non-inflammatory thrombotic vasculopathy characterized by livedo racemosa and recurrent ischemic strokes or TIAs. It predominantly affects women aged 20-42 years, with estimated incidence of 4 per million annually.
| Feature | Description |
|---|---|
| Livedo racemosa | Persistent, irregular, broken circular violaceous pattern; trunk and buttocks predominantly; does NOT resolve with warming (unlike livedo reticularis) |
| Cerebrovascular events | Recurrent TIAs and strokes (usually MCA/PCA territory); progressive cognitive decline; may lead to vascular dementia |
| Temporal relationship | Livedo precedes neurologic symptoms by ~10 years |
| Antiphospholipid antibodies | Present in ~60% (aPL-positive Sneddon); absence defines aPL-negative subtype |
Diagnosis: Deep skin biopsy from the center (not ring) of livedo lesions showing non-inflammatory thrombotic occlusion of small/medium dermal arteries. Sensitivity improves with multiple biopsies: 27% (1 biopsy), 53% (2 biopsies), 80% (3 biopsies). Brain MRI shows multifocal white matter infarcts.
🔹 Sneddon Syndrome: Management
- aPL-positive: Anticoagulation with warfarin (target INR 3-4 often recommended); similar to APS management
- aPL-negative: Less clear; antiplatelet therapy may be sufficient; some recommend warfarin
- Avoid: Estrogen-containing contraceptives, smoking
- Immunosuppression: Generally ineffective (non-inflammatory); anecdotal responses reported in aPL-positive cases
- Prognosis: Chronic, progressive; cognitive decline common even with treatment
Radiation-Induced Vasculopathy
Cranial and cervical radiation can cause delayed cerebrovascular complications through accelerated atherosclerosis, fibrous intimal thickening, and moyamoya-like vasculopathy. Risk increases with radiation dose >50 Gy and young age at treatment.
- Latency: Typically 5-20 years post-radiation; can be decades
- Patterns: Carotid stenosis (most common), intracranial stenosis, moyamoya-like collateralization
- Management: Standard stroke prevention; revascularization (bypass, stenting) for symptomatic stenosis; no role for immunosuppression
PACNS vs Systemic Vasculitis vs RCVS: Diagnostic Comparison
| Feature | PACNS | Systemic Vasculitis (CNS) | RCVS |
|---|---|---|---|
| Demographics | Any age; M=F | Varies by disease | Women 20-50 |
| Onset | Subacute/chronic (weeks-months) | Variable | Acute; thunderclap headache |
| Headache | Gradual, progressive | Variable | Thunderclap (peak <1 min) |
| Systemic symptoms | Absent | Present (fever, rash, arthritis, renal) | Absent |
| Triggers | None | None | Vasoactive drugs, postpartum, exertion, Valsalva |
| CSF | Abnormal (80%): elevated protein, pleocytosis | Variable | Usually normal (or minimal protein elevation) |
| ESR/CRP | Normal or mildly elevated | Elevated | Normal |
| Angiography | Multifocal stenoses/dilations; persists | Similar pattern | “String of beads”; resolves in ≤12 weeks |
| Vessel wall MRI | Concentric enhancement | Enhancement | Absent or faint, non-concentric enhancement |
| RCVS2 Score | <5 | Variable | ≥5 (high probability) |
| Brain biopsy | Diagnostic (granulomatous, lymphocytic, necrotizing) | May show vasculitis | Normal |
| Response to steroids | Yes | Yes | No benefit (may worsen) |
| Prognosis | Chronic; requires long-term IS | Depends on underlying disease | Self-limiting; resolves in weeks |
Treatment Principles and Safety Monitoring
Glucocorticoid Prophylaxis
Long-term steroid use requires vigilant prophylaxis against complications:
- PJP prophylaxis: TMP-SMX (single-strength daily or double-strength 3×/week) if prednisone ≥20 mg for >4 weeks AND additional immunosuppression
- Bone protection: Calcium (1000-1200 mg/day), vitamin D (800-2000 IU/day); bisphosphonate if high fracture risk (T-score <-1.5 or prior fragility fracture)
- GI prophylaxis: PPI if concurrent NSAID or anticoagulation; H2 blocker otherwise acceptable
- Glucose monitoring: Check fasting glucose at baseline and periodically; steroid-induced diabetes common
- Blood pressure: Monitor and treat hypertension
Cyclophosphamide Monitoring
- CBC: Every 1-2 weeks during induction; hold if WBC <3,500 or ANC <1,500
- Bladder protection: Aggressive hydration; mesna with IV cyclophosphamide; avoid overnight bladder retention
- Fertility: Counsel on gonadal toxicity; consider sperm banking or oocyte cryopreservation before treatment
- Cumulative dose: Lifetime limit ~25g to minimize malignancy risk (bladder cancer, lymphoma)
- Infection surveillance: Monitor for opportunistic infections; low threshold for empiric treatment
Relapse Monitoring
- Clinical assessment: Regular neurologic examination; ask about new headaches, cognitive changes, focal symptoms
- Imaging: Serial MRI every 3-6 months during active treatment, then annually; vessel wall imaging if available
- CSF: Consider repeat LP if clinical concern for relapse
- Lab monitoring: ESR/CRP helpful in systemic vasculitis; less reliable in PACNS or when on tocilizumab (suppresses acute phase reactants)
Antithrombotic Therapy: Entity-Specific Approach
🔴 Antithrombotic Cautions in Inflammatory Vasculopathy
- Active CNS vasculitis: Anticoagulation generally NOT indicated unless specific indication (AF, DVT/PE); may increase hemorrhagic risk
- Post-stroke: Standard secondary prevention (antiplatelet) once acute inflammation controlled and hemorrhage excluded
- Sneddon syndrome: Anticoagulation with warfarin (aPL-positive) or antiplatelet (aPL-negative)
- Behçet with CVT: Anticoagulation is standard; duration debated (often long-term)
- GCA: Low-dose aspirin often recommended for cardiovascular protection; no proven benefit for stroke prevention specifically
- Avoid blanket statements: Individualize based on etiology, stroke mechanism, and bleeding risk
Anti-Inflammatory Strategies: Current Evidence
The concept of targeting residual inflammatory risk for stroke prevention has generated interest, particularly with colchicine. However, stroke-specific trials have been disappointing:
| Trial | Year | Population | Intervention | Result |
|---|---|---|---|---|
| CHANCE-3 | 2023 | Minor stroke/TIA with CRP ≥2 mg/L (N=8,369) | Colchicine 0.5 mg daily × 90 days vs placebo | Neutral: Stroke 6.3% vs 6.5% (p=NS) |
| CONVINCE | 2024 | Non-cardioembolic stroke/TIA (N=3,154) | Colchicine 0.5 mg daily vs usual care | Neutral: MACE 9.8% vs 11.7% (HR 0.84, p=0.12) |
| CLEAR Colchicine | 2024 | Post-MI (N=7,062) | Colchicine 0.5 mg daily vs placebo | Neutral: Primary composite 9.1% vs 9.3% (p=0.93) |
A meta-analysis pooling CONVINCE with coronary trials (COLCOT, LoDoCo2) showed a 27% reduction in ischemic stroke (RR 0.73, p<0.004), but stroke-dedicated trials have not confirmed benefit. Colchicine is not currently recommended for routine stroke secondary prevention.
Trial Comparison Table
| Trial | Year | Population | N | Intervention | Primary Outcome | Key Result |
|---|---|---|---|---|---|---|
| GiACTA | 2017 | GCA (new/relapsing) | 251 | Tocilizumab 162 mg SC weekly or Q2W + 26-wk taper vs placebo | Sustained remission at 52 wks | 56% vs 14% (p<0.001); 50% steroid-sparing |
| GiACTA Long-term | 2021 | GCA (extension) | 215 | Open-label tocilizumab | Drug-free remission | ~48% maintained remission after stopping TCZ |
| TAKT | 2018 | Takayasu (refractory) | 36 | Tocilizumab 162 mg SC weekly vs placebo | Time to relapse | HR 0.41 (p=0.06 ITT); 0.34 (p=0.03 PP) |
| TAKT Longterm | 2020 | Takayasu (extension) | 36 | Open-label tocilizumab × 96 wks | Steroid-sparing, imaging | 46% reduced to <0.1 mg/kg/day; 86% stable/improved imaging |
| French COVAC | 2018 | PACNS | 112 | GC alone vs GC+CYC vs GC+CYC+maintenance | mRS 0-2 | 43% vs 40% vs 80% (p=0.0004) |
| CHANCE-3 | 2023 | Minor stroke/TIA, CRP ≥2 | 8,369 | Colchicine 0.5 mg daily × 90 days | Stroke at 90 days | 6.3% vs 6.5% (NS) |
| CONVINCE | 2024 | Non-CE stroke/TIA | 3,154 | Colchicine 0.5 mg daily | MACE | 9.8% vs 11.7% (HR 0.84, p=0.12) |
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