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Chance of takayasu in stroke
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Case Summary (from your notes)
The clinical notes on the continuation sheet document:
| Finding | Detail |
|---|---|
| General | Afebrile, no pallor, no edema |
| Carotid bruit | Present (+) |
| Bilateral plantars | Right - flexor; Right great toe extensor with rest in flexion |
| Left-sided pulse | Diminished / absent |
| Chest | B/L vesicular breath sounds present |
| Imaging | NCCT Brain + MRI Brain stroke protocol - done |
| Labs (18/7) | CRP - 11 µg (elevated), Na/K = 139/3, lipid profile pending |
| BP | "Phy initially high, now normal" |
| ABG | Normal |
| Plan | CT angiography to be completed (partially done) - Monday |
Is This Takayasu Arteritis? - High Clinical Suspicion
Short answer: Yes, this presentation has strong features pointing toward Takayasu Arteritis (TAK) as the underlying cause of stroke. Here is the breakdown:
Features in THIS patient that match TAK
| TAK Feature | This Patient |
|---|---|
| Carotid bruit | Present (+) - 20% of NIH TAK series had carotid bruit at presentation |
| Left-sided pulse diminished/absent | Present - reduced/absent pulse in 25% of TAK cases |
| Stroke in a young patient | Confirmed by MRI stroke protocol |
| Elevated CRP (inflammatory marker) | CRP 11 µg - active systemic inflammation |
| BP initially high | Hypertension is in 20% of presenting TAK cases |
| Bilateral extensor plantar (UMN signs) | Consistent with cerebral ischemia from carotid/vertebral stenosis |
| CT angiography planned | Appropriate next step for large vessel vasculitis |
Epidemiology of Stroke in TAK
- A meta-analysis found the pooled prevalence of stroke in TAK to be 8.9% (ischemic) - suggesting up to a tenfold increase in severe cardiovascular events compared to the general population (Firestein & Kelley's Textbook of Rheumatology).
- In a pediatric TAK cohort, stroke occurred in 6% of 101 patients with carotid artery involvement in 43% (Bradley & Daroff's Neurology in Clinical Practice).
- Stroke at onset of TAK is seen in <10% but is a recognized presenting feature (NIH series of 60 patients).
- A 2022 study in Stroke journal specifically examined cerebrovascular ischemic events in TAK patients (PMID: 35354303).
Mechanism of Stroke in TAK
Stroke in TAK occurs through two pathways:
- Hemodynamic/hypoperfusion - stenosis/occlusion of carotid and vertebral arteries reducing cerebral perfusion
- Thromboembolic - thrombosis over inflamed, stenotic large vessel walls with distal embolization
The carotid bruit + absent left radial/brachial pulse in this patient is the classic combination pointing to subclavian/carotid/aortic arch involvement - the hallmark of TAK.
ACR/EULAR Classification Criteria Points (TAK) - This Patient
| Criterion | Points | Present? |
|---|---|---|
| Vascular bruit | +2 | Yes (carotid bruit) |
| Reduced pulse in upper extremity | +2 | Yes (left pulse absent) |
| Carotid artery abnormality | +2 | Likely (bruit + stroke) |
| Arm/leg claudication | +2 | Possibly |
A score ≥5 is classified as TAK. This patient likely scores ≥6 on clinical grounds alone, pending imaging.
What CT Angiography Will Confirm
The planned CTA (wisely ordered) will show:
- Narrowing/occlusion of aorta, subclavian, carotid, or vertebral arteries
- "Macaroni sign" - smooth tapering/occlusion of major branches
- Skip lesions
- Wall thickening (better on MRA)
This will be diagnostic if consistent - clinching the TAK diagnosis.
Differential Diagnoses to Keep in Mind
- Giant Cell Arteritis (GCA) - but GCA typically >50 years old
- Fibromuscular dysplasia - no inflammation, no bruit usually
- Atherosclerotic large vessel disease - but CRP elevation and young age argue against
- Antiphospholipid syndrome - needs APS workup in parallel
Bottom Line
This is a classic TAK presentation. Young patient (implied by the clinical context), carotid bruit, absent left-sided pulse, stroke on MRI, and elevated CRP together make Takayasu Arteritis the leading diagnosis for this stroke. The chance is high - this is not incidental.
Immediate management priorities:
- Await CTA - confirm large vessel stenosis pattern
- Start corticosteroids (prednisolone 1 mg/kg/day) once diagnosis confirmed
- Consider antiplatelet therapy (aspirin)
- Rule out APS, APLA, other vasculitides in parallel
- Immunosuppressant (methotrexate/azathioprine) if steroid-dependent
- Firestein & Kelley's Textbook of Rheumatology, pp. 5980-5990
- Bradley & Daroff's Neurology in Clinical Practice, pp. 1767-1771
What is macaroni sign
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Macaroni Sign in Takayasu Arteritis
The macaroni sign describes the appearance of smooth, homogeneous, circumferential thickening of the arterial wall seen primarily on carotid artery ultrasound in Takayasu arteritis.
Why "Macaroni"?
When you look at the cross-section of the carotid artery on ultrasound, the thickened vessel wall surrounds a small residual lumen - resembling a tube of macaroni pasta:
- Outer ring = thickened, edematous artery wall (inflammation of media + adventitia)
- Central hole = the small remaining vessel lumen
Here is the actual ultrasound appearance:
Both carotids in cross-section - note the circumferential hypoechoic wall thickening around the central lumen
Key Features
| Feature | Detail |
|---|---|
| Modality | Primarily B-mode / duplex carotid ultrasound |
| Appearance | Smooth, homogeneous, circumferential hypoechoic wall thickening |
| Intima-media thickness | ≥ 1 mm (diffuse, not focal/localized plaque) |
| Residual lumen | Small, central |
| Distribution | Long segment, bilateral common carotid arteries (non-patchy) |
| Specificity | Almost pathognomonic for Takayasu arteritis |
How It Differs from Atherosclerosis
| Macaroni Sign (TAK) | Atherosclerosis | |
|---|---|---|
| Wall thickening | Diffuse, circumferential, smooth | Focal, eccentric, irregular plaques |
| Echogenicity | Homogeneous, hypoechoic | Heterogeneous, calcified |
| Distribution | Long segment, bilateral | Patchy, focal |
| Age | Young women | Older patients |
| CRP | Elevated (active inflammation) | Usually normal |
On Other Modalities
- CTA / MRA: Smooth, long-segment narrowing of the aorta and its branches interspersed with normal segments; wall enhancement with contrast
- Echocardiography: Also described - thick vessel wall with small residual lumen (as noted in Fuster & Hurst's The Heart, 15th Ed.)
- PET scan: "Hot spots" at active Takayasu lesions - useful for disease activity
Clinical Relevance for Your Patient
Your patient has a carotid bruit on examination - this is the audible correlate of the structural change the macaroni sign represents. The CT angiography planned for Monday will show the full extent of luminal stenosis, and if carotid duplex ultrasound is added, the macaroni sign can provide additional early confirmation of active vasculitis even before significant luminal narrowing occurs.
- Fuster & Hurst's The Heart, 15th Edition, p. 4223
- Radiopaedia - Macaroni Sign
- PMC - Macaroni Sign in Takayasu Arteritis
Role of urine re me pcr in this pt
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Takayasu arteritis tuberculosis mycobacterium
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PMID: 31729680
Role of Urine MTB PCR (Remi PCR) in This Patient
Why is TB relevant here? Your patient has suspected Takayasu Arteritis - and the TB-TAK association is one of the most important and clinically actionable links in vasculitis medicine, especially in India.
The TAK-TB Connection
MTB has been incriminated but not fully proven as a causative or triggering pathogen in TAK pathogenesis (Henry's Clinical Diagnosis, laboratory textbook). The proposed mechanisms are:
- Molecular mimicry - Heat shock proteins (HSP65) of MTB share epitopes with aortic endothelial cells; immune response against MTB cross-reacts with vessel walls
- Bystander activation - Chronic mycobacterial antigen load drives a persistent granulomatous large-vessel inflammation
- Direct infection - MTB DNA has been found in aortic biopsy specimens in some studies (0-70% positivity range)
The key evidence:
- A 2020 systematic review (38 studies) found active TB prevalence of 6.3-20% in adult TAK patients, and latent TB in 20-82%
- A 2023 meta-analysis confirmed high pooled prevalence of TB infection in TAK
- India has one of the highest TAK incidences globally AND one of the highest TB burdens - the overlap here is not coincidental
Why Urine MTB PCR Specifically?
Urine is a valid specimen for MTB molecular testing, especially in:
| Situation | Why urine MTB PCR matters |
|---|---|
| Extrapulmonary TB | Renal TB, disseminated/miliary TB often shed MTB in urine |
| Paucibacillary disease | Patient may not have obvious pulmonary TB but have disseminated/subclinical infection |
| Sputum-negative cases | Urine PCR can pick up TB that chest X-ray and sputum miss |
| Pre-immunosuppression workup | This is the most important reason in this patient |
The Critical Clinical Reason Here
This patient is about to receive corticosteroids ± immunosuppressants (the standard TAK treatment). If latent TB is undetected and reactivates after starting steroids/MTX/biologics, the consequences can be life-threatening.
The workup for TB before immunosuppression in a TAK patient should include:
| Test | Purpose |
|---|---|
| Urine MTB PCR (Remi) | Rule out active extrapulmonary / renal TB |
| Sputum MTB PCR / AFB | Pulmonary TB |
| HRCT chest | Miliary pattern, apical fibrosis, old TB |
| Mantoux / TST | Latent TB (PPD) - most studied method per systematic review |
| IGRA (T-SPOT / QuantiFERON) | Latent TB with better specificity than TST |
| Urine AFB smear/culture | Traditional renal TB detection |
The systematic review explicitly recommends: "greater care be taken with latent TB screening in patients who are TAK candidates for immunosuppressive therapy" (PMID 31729680).
Limitations of Urine MTB PCR Alone
- Urine PCR is most useful for renal/genitourinary TB - sensitivity is lower for ruling out pulmonary or latent TB
- A negative urine PCR does not exclude latent TB - IGRA or TST is the gold standard for latent TB
- Urine PCR positivity = active TB and would contraindicate/defer immunosuppression until TB treatment is completed
Bottom Line for This Patient
| Urine MTB PCR result | Action |
|---|---|
| Positive | Active extrapulmonary TB confirmed - start ATT (anti-TB therapy) first, defer steroids for 4-8 weeks |
| Negative | Still complete IGRA/TST + HRCT chest to rule out latent TB before immunosuppression |
The test is clinically justified and important - not just academically interesting. In India, where both TAK and TB are endemic, testing for TB before starting steroids is mandatory practice. Urine PCR is a reasonable non-invasive first step, but must be paired with IGRA and chest imaging for a complete pre-treatment TB screen.
On mri brain stroke protocol hyperdense area on T2 weighted imaging with neovascularsation seen in mca territory
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T2 hyperintense MCA territory neovascularization MRI Takayasu arteritis moyamoya pattern
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This is a rich and clinically important finding. Let me give you the full interpretation now.
MRI Brain: T2 Hyperintensity in MCA Territory + Neovascularization
What This Means - Step by Step
T2 hyperintensity in the MCA territory = ischemic injury to brain parenchyma (cytotoxic or vasogenic edema / infarct/gliosis in subacute-chronic stage)
Neovascularization (new vessel formation / collateral vessels seen on MRI) in the same territory = the brain has responded to chronic ischemia by growing compensatory collateral vessels
This combination - chronic ischemia + neovascularization in MCA territory in a patient with suspected Takayasu arteritis - defines a Moyamoya pattern/syndrome.
Moyamoya Syndrome Secondary to Takayasu Arteritis
This is the single most important interpretation of this MRI in your patient.
What Is Moyamoya?
| Moyamoya Disease | Moyamoya Syndrome (this patient) | |
|---|---|---|
| Definition | Idiopathic progressive stenosis/occlusion of distal ICA and proximal MCA/ACA with compensatory neovascularization | Same vascular/MRI pattern but caused by an underlying disease |
| Underlying cause | Unknown, genetic (RNF213 gene) | Takayasu arteritis, SLE, NF1, sickle cell, radiation |
| MRI appearance | Identical | Identical |
| Neovascular "puff of smoke" | Yes | Yes |
In TAK, progressive stenosis/occlusion of the carotid arteries (which you already have evidence of - carotid bruit, absent left pulse) extends intracranially to the MCA territory. The brain responds by growing a fragile network of collateral vessels - the "moyamoya vessels."
MRI Signs Explained in This Patient
1. T2 Hyperintensity in MCA Territory
- Represents subacute/chronic ischemic change - infarct or periinfarct gliosis
- In TAK-moyamoya: typically watershed/borderzone distribution (between ACA-MCA or MCA-PCA territories) due to chronic hypoperfusion rather than single embolic infarct
- Can also be territorial infarct if MCA itself is occluded
- On FLAIR this would appear as "ivy sign" - linear/curvilinear bright signal along sulcal surfaces from slow retrograde leptomeningeal flow
2. Neovascularization
This is the "puff of smoke" appearance on angiography/MRA:
- Fragile collateral vessels at the base of the brain (basal ganglia, thalamus)
- Seen as "flow voids" on T2 (dark dots/lines at basal ganglia = high-velocity flow through tiny collateral vessels)
- On MRA: plexiform network replacing the proximal MCA
- "Brush sign" on SWI: dilated deep medullary veins appearing as dark lines = oxygen-demand mismatch in hypoperfused territory
Differential Diagnosis of This MRI Pattern
| Diagnosis | For | Against |
|---|---|---|
| Moyamoya syndrome (TAK) | Carotid bruit, absent pulse, young patient, MCA territory, neovascularization | - |
| CNS vasculitis | T2 lesions, elevated CRP | Usually small vessel, multifocal lesions, not neovascularization |
| Tumefactive demyelination | T2 hyperintense mass-like lesion | No neovascularization, no TAK features |
| High-grade glioma | T2 hyperintensity + neovascularization | No stroke territory distribution, no carotid findings |
| RCVS | Young patient, stroke | No neovascularization, sausage-beading on angiography |
The key distinguishing feature here: neovascularization in MCA territory in the context of TAK = moyamoya syndrome until proven otherwise.
Why This Changes Management
| Implication | Detail |
|---|---|
| Confirms chronic large vessel occlusion | Not acute embolic stroke - this has been evolving |
| Revascularization may be needed | Surgical bypass (STA-MCA) or encephaloduroarteriosynangiosis (EDAS) in addition to immunosuppression |
| Anticoagulation risk | Moyamoya vessels are fragile - hemorrhagic transformation risk is high; anticoagulation is relatively contraindicated |
| Steroids address the inflammation | But will NOT reverse established moyamoya vessels - structural damage remains |
| Perfusion MRI needed | CBF/CBV maps to assess hemodynamic compromise - guides surgical decision |
What the CT Angiogram (Planned Monday) Will Show
This is now even more important given the MRI findings:
- Proximal MCA stenosis or occlusion (TAK extending intracranially)
- Basal collateral network = the moyamoya puff of smoke
- Carotid/subclavian stenosis (confirms TAK at the aortic arch level)
- Vessel wall thickening in the large vessels
Ideally, DSA (digital subtraction angiography) should follow if CTA shows this pattern - it is the gold standard for staging moyamoya (Suzuki stages I-VI) and planning revascularization surgery.
Summary
T2 hyperintensity + neovascularization in MCA territory in a young patient with TAK features = Moyamoya Syndrome secondary to Takayasu Arteritis - a chronic hypoperfusive process, not just an acute embolic stroke. This requires dual management: immunosuppression for the TAK + neurosurgical evaluation for revascularization.
This is a fascinating and clinically rich case - you are essentially seeing the full spectrum of TAK from the aortic arch (absent pulse, carotid bruit) all the way to its intracranial consequence (moyamoya pattern with MCA territory ischemia).
Bp is high 160/70 or higher, only amlodipine is given, should I give additional anti hypertensive
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BP Management in This Patient: Should You Add to Amlodipine?
The Core Dilemma
This patient has three competing issues that pull in opposite directions:
| Issue | Wants BP... |
|---|---|
| Active stroke / MCA ischemia + moyamoya | Higher - needs perfusion pressure |
| Takayasu with carotid/subclavian stenosis | Lower - to prevent further vascular injury |
| Renovascular HTN (renal artery stenosis from TAK) | May be RAAS-driven - ACE/ARB caution |
The Most Important Rule First
⚠️ DO NOT aggressively lower BP in acute/subacute ischemic stroke
In ischemic stroke with carotid stenosis and moyamoya pattern, the infarcted and penumbral tissue depends on collateral perfusion - which is pressure-dependent. The moyamoya vessels themselves are driven by systemic BP.
- Autoregulation is lost in the ischemic zone
- Dropping BP sharply = cutting off the only blood supply reaching the penumbra through collaterals
- This is why 160/70 may actually be physiologically appropriate right now - the brain may need it
Standard AHA/ASA guidance for ischemic stroke without thrombolysis:
- Do NOT treat BP unless >220/120 mmHg
- Allow permissive hypertension up to 220/120 mmHg
- Only treat if hypertensive emergency features present (encephalopathy, aortic dissection, acute MI, renal failure)
Your patient at 160/70 = do NOT add antihypertensives urgently on that basis alone.
The TAK-Specific Complication: False BP Readings
This is critical and easily missed in TAK:
| Problem | Consequence |
|---|---|
| Subclavian stenosis (absent left pulse) | Left arm BP is falsely low |
| Bilateral subclavian stenosis | Both arm readings unreliable |
| Aortic involvement | Central aortic pressure may be higher than peripheral readings |
Always measure BP in both arms AND both legs in TAK:
- Use the higher reading as the true BP
- If bilateral subclavian stenosis: leg BP is the reference (normally 10-20 mmHg higher than arm)
- If left arm pulse is absent, the right arm reading is more reliable - but even that may be falsely low if right subclavian is involved
Your patient has absent left-sided pulse - the left arm BP is unreliable. If 160/70 is from the right arm, it may reflect central BP accurately. If you measured from the left arm, it may actually be much higher centrally.
Why Amlodipine Is a Good Choice Here
Amlodipine (CCB) is the preferred first-line agent in TAK hypertension because:
- No effect on renal perfusion pressure (safe if renal artery stenosis present)
- Vasodilatory - may improve peripheral perfusion in stenotic vessels
- No risk of acute GFR drop
- Safe with compromised cerebral autoregulation
When to Add a Second Agent - and Which One
| Situation | Add | Avoid |
|---|---|---|
| BP persistently >180/110 after acute stroke phase (>72h) | Consider adding | Don't add acutely |
| Renovascular HTN suspected (renal artery stenosis on CTA) | ARB/ACE-I - most effective for RAAS-driven HTN | ACE-I if bilateral renal artery stenosis |
| BP >180/110 AND no major carotid/MCA stenosis | Beta-blocker or ARB can be added | - |
| Bilateral subclavian stenosis | Measure leg BP before deciding anything | - |
Best second agent to consider (after acute phase):
- ARB (e.g., telmisartan/losartan) - especially if renovascular HTN; effective, renoprotective, well tolerated
- Monitor creatinine at 1 week after starting - a rise >20% = renal artery stenosis likely (Goodman & Gilman's Pharmacology)
- Avoid ACE-I if bilateral renal artery stenosis - causes acute GFR drop; bilateral stenosis is common in TAK
Practical Decision for Right Now
| Question | Answer |
|---|---|
| Is 160/70 dangerous enough to add a drug today? | No - in acute stroke, this is permissive HTN, tolerated |
| Should you optimize amlodipine dose first? | Yes - ensure it's at maximum dose (10 mg/day) before adding |
| Should you measure BP in both arms + legs? | Yes, urgently - determine the true BP given absent left pulse |
| When to add second drug? | After 72h post-stroke if BP remains >140-150 systolic, once collaterals are established and perfusion is stable |
| Best second drug? | ARB (e.g., telmisartan 40 mg) pending CTA result for renal arteries |
| What to absolutely avoid? | Rapid BP drop, IV antihypertensives, over-diuresis |
Summary
BP of 160/70 in an acute ischemic stroke with moyamoya collaterals and carotid stenosis = do not add antihypertensives urgently. Amlodipine is the right choice. Verify BP properly (right arm or leg) given absent left pulse. Revisit adding an ARB after 72 hours once the acute stroke phase has passed, titrate slowly, and monitor creatinine closely given likely renovascular involvement.
The elevated BP here may be protective, not harmful.
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