CTA, MRA, DSA, and Venography

Vascular imaging covers CTA, MRA (TOF and contrast-enhanced), DSA (the gold standard), and venous studies (CTV, MRV). The right modality depends on what you’re looking for: acute LVO → CTA (fastest, widely available); aneurysm screening → MRA or CTA; vasculitis or dissection → vessel-wall MRI; CVT → CTV or MRV; AVM / dural fistula characterization → DSA.

CT Angiography (CTA)

Use

• Acute stroke: identify large-vessel occlusion (LVO), dissection, tandem lesions.
• SAH: aneurysm detection and characterization.
• Trauma: blunt cerebrovascular injury (BCVI).
• Acute ICH: spot sign (intra-hematoma contrast extravasation → expansion risk).
• Transient neurologic deficit: rule out high-grade stenosis or dissection.

What to Look For

• Large vessel occlusion (LVO): ICA terminus, MCA M1, M2 (proximal), basilar, vertebral. Asymmetric vessel cutoff or absent opacification distal to the clot.
• Tandem lesions: cervical ICA stenosis or occlusion + intracranial occlusion (worse outcomes; trickier to revascularize).
• Dissection: tapered narrowing or occlusion (“flame sign,” “string sign”), intimal flap, intramural hematoma (best on fat-sat T1 axial neck MRI), pseudoaneurysm.
• Aneurysm: focal saccular dilation; describe size, neck width, parent vessel, daughter sacs. AcomA is the commonest site. PcomA aneurysms cause CN III palsy.
• AVM nidus: tangle of dilated vessels with early venous drainage.
• Vasospasm: post-SAH (days 3–14); diffuse or focal narrowing.
• Atherosclerotic plaque: calcified vs non-calcified; ulceration; degree of stenosis (NASCET method for ICA).
• Spot sign (CTA performed during/after ICH): focal contrast extravasation within hematoma → expansion risk.

Pitfalls

• Pseudo-occlusion at the ICA terminus from contralateral collateral filling (rare).
• Calcified plaque overestimates stenosis (blooming).
• Catheter-related contrast bolus timing — early or late phase mimics occlusion or distal embolus.
• Contrast-induced nephropathy risk in renal insufficiency.

MR Angiography (MRA)

Time-of-Flight (TOF) MRA

• No contrast required — uses flow-related enhancement.
• Best for intracranial circle of Willis screening (3D TOF) and cervical vessels (2D TOF).
• Overestimates stenosis at sites of turbulent or slow flow (bifurcations, near plaque).
• Saturation effect: signal drops when flow direction is in-plane.
• Susceptibility artifact at skull base + dental hardware obscures arteries.

Contrast-Enhanced MRA (CE-MRA)

• Gadolinium bolus + fast acquisition.
• Less flow-sensitive — better for cervical and slow-flow lesions.
• Better for aneurysm size characterization than TOF.

What to Look For

• Vessel patency, stenosis, occlusion.
• Aneurysm — size, neck, parent vessel, multilobulated.
• AVM nidus + draining veins.
• Anatomic variants — fetal PCA, hypoplastic A1, accessory branches.
• Dissection — vessel narrowing, irregular contour; fat-sat T1 axial neck shows crescentic intramural hematoma directly.

Digital Subtraction Angiography (DSA)

Use

• Gold standard for cerebrovascular imaging.
• AVM and dural fistula characterization (feeder identification, venous drainage pattern, eloquent cortex involvement).
• Complex aneurysm planning (clipping vs coiling vs flow diversion).
• Supports the workup of suspected CNS vasculitis when non-invasive imaging is inconclusive — angiographic beading is sensitive but non-specific, so DSA does not by itself confirm vasculitis. Brain biopsy remains the gold standard for PACNS.
• Mechanical thrombectomy access + intervention.
• Endovascular treatment (coiling, stent-assisted coiling, flow diverter, embolization).

What to Look For

• Arterial phase: arterial anatomy, occlusion, stenosis, aneurysm, AVM feeders, vasospasm.
• Capillary phase: tissue perfusion, blush of meningioma / hypervascular tumor.
• Venous phase: venous drainage pattern, sinus patency, early venous filling (AVM marker), CVT.
• AVM grading (Spetzler-Martin): nidus size + eloquent location + deep venous drainage.
• Dural fistula classification (Cognard, Borden): based on cortical venous drainage (predicts hemorrhage risk).
• Vasculitis: “beading” — alternating focal stenosis and dilation in medium-sized vessels.

Risks

• Stroke ~0.5–1% (catheter-related embolus).
• Hematoma at access site.
• Contrast nephropathy.
• Pseudoaneurysm at access site.

Common Vascular Pathologies

Aneurysm

• Most are saccular (“berry”); fusiform aneurysms suggest atherosclerosis or vasculitis; mycotic from septic emboli.
• Common locations: AcomA (commonest), PcomA, MCA bifurcation, basilar tip, ICA terminus, PICA / vertebral.
• Multiplicity: ~15–20% of patients have multiple aneurysms.
• PHASES score: 5-year rupture risk for unruptured aneurysms (Population, Hypertension, Age, Size, Earlier SAH, Site).
• Size predicts risk: <7 mm anterior circulation rarely rupture; >7 mm + posterior circulation higher risk.
• Daughter sac / multilobulation: higher rupture risk.

Dissection

• Cervical ICA / VA dissection: young patients; spontaneous or post-traumatic (manipulation, sports, MVC).
• Imaging signs: intramural hematoma (crescent T1 bright on fat-sat axial neck MRI — the most reliable sign), tapered narrowing (“flame”), string sign, pseudoaneurysm, flap, “Y-shaped” double lumen.
• Horner syndrome in ipsilateral cervical ICA dissection (sympathetic chain).
• Treatment: anticoagulation vs antiplatelet (similar outcomes in CADISS); endovascular for failed medical therapy or expanding pseudoaneurysm.

Arteriovenous Malformation (AVM)

• High-flow direct artery-to-vein shunt through a tangled nidus.
• Imaging: tangle of dilated vessels + early venous drainage on CTA / DSA; T2 flow voids in cluster on MRI; SWI shows blooming around nidus.
• Spetzler-Martin grading (size + eloquent location + deep venous drainage) predicts surgical risk.
• Treatment: surgical resection (low grade), embolization, stereotactic radiosurgery, combination.

Dural Arteriovenous Fistula (dAVF)

• Abnormal connection between dural arteries and dural venous sinus (or cortical vein).
• Cognard / Borden classification: based on cortical venous drainage (cortical reflux predicts hemorrhage / venous infarction).
• Imaging: arterialized dural sinus signal on CTA/MRA; SWI shows engorged cortical veins; DSA is definitive (feeders, drainage, reflux).
• Causes: prior CVT, trauma, idiopathic. Treatment: endovascular embolization (commonly Onyx).

Cavernous Malformation (Cavernoma)

• Cluster of dilated capillary-like channels without intervening brain.
• Imaging: “popcorn” appearance on MRI — mixed-signal core (blood products of varying ages) + complete dark hemosiderin ring on T2/SWI.
• Not visible on DSA (“angiographically occult”).
• Multiplicity → familial form (KRIT1, CCM2, PDCD10). See Stroke / Vascular Genetics page.

Vasculitis

• Primary CNS vasculitis (PACNS): rare; typically middle-aged adults with progressive multifocal symptoms.
• Reversible cerebral vasoconstriction syndrome (RCVS): thunderclap headache + diffuse arterial beading (resolves over weeks); often vasoactive trigger.
• Imaging: DSA shows beading (alternating focal stenosis + dilation) in medium-sized vessels — sensitive but non-specific.
• Vessel-wall MRI: concentric wall enhancement supports vasculitis vs RCVS (atherosclerotic plaque is eccentric); plays an increasing role.
• RCVS vs PACNS: RCVS resolves over 1–3 months; PACNS does not. RCVS shows beading more diffusely.

Atherosclerosis

• Intracranial atherosclerotic disease (ICAD): more common in Asian, Black, Hispanic populations.
• Stenosis grading: WASID criteria (Warfarin-Aspirin Symptomatic Intracranial Disease).
• Vessel-wall MRI: eccentric plaque with surface enhancement supports symptomatic plaque vs vasculitis.

Venous Imaging (CTV / MRV)

Cerebral Venous Sinus Thrombosis (CVT)

• Risk factors: pregnancy/postpartum, oral contraceptives, prothrombotic states, dehydration, infection (mastoiditis, sinusitis).
• CT non-contrast: hyperdense sinus (acute thrombus, ~70–90 HU).
• CTV: filling defect in sinus.
• MRV (TOF or contrast-enhanced): filling defect / loss of flow signal. CE-MRV preferred (TOF has saturation artifacts at slow flow).
• SWI: low signal in sinus + blooming around occluded sinus + dilated/engorged cortical veins.
• Cortical vein thrombosis: linear dark signal on SWI in superficial cortex + adjacent cortical edema / hemorrhage.
• Parenchymal sequelae: venous infarcts that don’t respect arterial territories; often hemorrhagic; bilateral thalamic in deep venous system thrombosis (vein of Galen / internal cerebral veins).

IIH and Transverse Sinus Stenosis

• Bilateral transverse sinus stenosis on MRV often seen in IIH.
• Venous sinus stenting is now used in selected refractory IIH (with manometry gradient confirmation).

Vessel-Wall MRI (HR-VW-MRI)

• High-resolution intracranial vessel-wall imaging — distinguishes vasculitis (concentric, smooth wall enhancement) from atherosclerosis (eccentric plaque), RCVS (no wall enhancement), aneurysm wall inflammation (enhancing wall correlates with rupture risk).
• Increasingly used in diagnostic workup of unclear arteriopathy.

Pitfalls and Pearls

• TOF-MRA overestimates stenosis at turbulent flow sites — confirm with CE-MRA or CTA.
• Dissection requires fat-sat T1 axial neck MRI for the most sensitive sign (crescentic intramural hematoma).
• Cavernoma is angiographically occult — MRI / SWI is the diagnostic test.
• RCVS resolves; PACNS does not. Serial imaging matters.
• CVT is missed routinely on non-contrast CT — always look at the sinuses + venous structures in headache + altered mental status.
• Bilateral thalamic edema or hemorrhage = think deep venous thrombosis (internal cerebral veins / vein of Galen).
• “Empty delta sign” on post-contrast CT/MRI = filling defect in superior sagittal sinus (acute CVT).
• PHASES score helps decide observation vs treatment for unruptured aneurysm.
• Spot sign on CTA in ICH = high risk of expansion.
• Vessel-wall enhancement is increasingly clinically useful for distinguishing vasculitis, plaque inflammation, and unstable aneurysms.

References

1. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update. Stroke. 2019;50(12):e344-e418.
2. Kim BJ, Kim JS. Ischemic stroke subtype classification: an Asian viewpoint. J Stroke. 2014;16(1):8-17.
3. Calabrese LH, Dodick DW, Schwedt TJ, Singhal AB. Narrative review: reversible cerebral vasoconstriction syndromes. Ann Intern Med. 2007;146(1):34-44.
4. Saposnik G, Barinagarrementeria F, Brown RD Jr, et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(4):1158-1192.
5. Mandell DM, Mossa-Basha M, Qiao Y, et al. Intracranial vessel wall MRI: principles and expert consensus recommendations of the American Society of Neuroradiology. AJNR Am J Neuroradiol. 2017;38(2):218-229.