Stroke and Hemorrhage — Imaging Patterns

This page is the pattern-recognition reference for stroke and hemorrhage on imaging — acute ischemic stroke (CT + MRI), large vessel occlusion + extended-window thrombectomy criteria, ICH localization, SAH grading, CVT, dissection, hemorrhagic transformation, watershed patterns, and the common mimics.

Acute Ischemic Stroke — The Imaging Workflow

Step 1: NCT Head

• Rule out hemorrhage (absolute contraindication to tPA).
• Calculate ASPECTS for MCA strokes.
• Look for hyperdense vessel sign (MCA, basilar) — the earliest CT marker of acute LVO.
• Loss of insular ribbon + obscured lentiform + sulcal effacement = early ischemic change.

Step 2: CTA Head + Neck

• Identify LVO (ICA terminus, MCA M1, M2 proximal, basilar, vertebral).
• Identify tandem lesion (cervical ICA + intracranial occlusion).
• Identify dissection (tapered narrowing, intimal flap, “flame sign”).
• Identify collaterals (multiphase CTA scores collateral quality — predicts outcome).

Step 3: CTP or MRI/DWI (if 6–24 h from onset or unknown onset)

• CTP: core volume + penumbra mismatch (RAPID).
• MRI/DWI: DWI-positive core; FLAIR mismatch identifies treatable window.
• DAWN (6–24h): NIHSS ≥10 + core <31–51 mL.
• DEFUSE-3 (6–16h): core <70 mL + mismatch ratio ≥1.8 + mismatch volume ≥15 mL.

DWI Pattern of Acute Infarct

Watershed (Border-Zone) Patterns

• External (cortical) watershed: ACA-MCA (frontal vertex) and MCA-PCA (parieto-occipital) junction zones.
• Internal (deep) watershed: at the lateral ventricle border (centrum semiovale, corona radiata) — “string of beads” linear array of round/oval restricted foci.
• Suggests hemodynamic insufficiency: ICA stenosis, dissection, cardiac arrest, severe hypotension, cardiopulmonary bypass.

Acute MCA Stroke Signs Summary

1. Hyperdense MCA / dot sign (CT) — earliest, within minutes.
2. Insular ribbon loss + obscured lentiform (CT) — early.
3. Sulcal effacement (CT) — early.
4. DWI bright + ADC dark (MRI) — within minutes (universal).
5. FLAIR hyperintensity (MRI) — after ~4–6 hours.
6. Gyriform T1 / FLAIR enhancement — subacute (1–2 weeks).
7. T2 cystic encephalomalacia + volume loss — chronic.

Hemorrhagic Transformation

• Petechial → confluent hemorrhage within infarct territory.
• ECASS classification: HI-1, HI-2 (petechial); PH-1, PH-2 (parenchymal hematoma with mass effect).
• Higher risk: large core, advanced age, hypertension at presentation, longer time to revascularization, anticoagulation.
• SWI / GRE most sensitive for detection.

ICH — Hypertensive vs Amyloid vs Other

SAH — Patterns and Pitfalls

• CT sensitivity: ~98% within 6 hours; ~85% within 24 hours; drops to ~50% at 1 week.
• Hyperacute SAH on FLAIR: sulcal hyperintensity. False positives include hyperoxygenation, propofol, gadolinium leakage.
• Negative CT but high suspicion: LP for xanthochromia, or MRI FLAIR + SWI.

Distribution

• Anterior interhemispheric / suprasellar → AcomA aneurysm.
• Sylvian fissure → MCA bifurcation.
• Perimesencephalic / prepontine → non-aneurysmal venous (~50%); rule out basilar tip.
• Posterior fossa → vertebrobasilar, PICA.
• Diffuse → high-grade rupture.

Vasospasm

• Days 3–14 after SAH.
• Higher Fisher grade → higher risk.
• TCD, CTA, CTP for monitoring.
• Triple-H therapy (replaced by euvolemic hypertensive therapy in modern practice).

Cerebral Venous Sinus Thrombosis (CVT)

• Risk factors: pregnancy/postpartum, OCPs, hypercoagulability, dehydration, infection (mastoiditis, sinusitis), head/neck malignancy, JAK2 mutations, antiphospholipid syndrome.
• CT signs: hyperdense sinus (acute thrombus, ~70–90 HU); “cord sign” (linear hyperdensity in superficial cortical vein); “empty delta sign” (filling defect in superior sagittal sinus on post-contrast).
• MRI signs: loss of normal flow void in sinus + low T2 signal + blooming on SWI + filling defect on MRV.
• Parenchymal sequelae: venous infarcts ignore arterial territories; bilateral parasagittal (superior sagittal sinus); temporal lobe (transverse sinus); thalamic + basal ganglia (deep venous system / internal cerebral veins / vein of Galen) — bilateral edema/hemorrhage.
• Treatment: anticoagulation acutely (heparin then warfarin / DOAC); endovascular thrombectomy for severe deterioration.

Dissection

• Cervical ICA or VA: young, often spontaneous or post-trauma.
• Most reliable imaging sign: crescentic intramural hematoma on fat-sat T1 axial neck MRI (bright crescent in vessel wall).
• CTA / MRA: tapered narrowing (“flame sign”), string sign, pseudoaneurysm, intimal flap.
• Horner syndrome ipsilateral to cervical ICA dissection (sympathetic chain).
• Treatment: antiplatelet or anticoagulation (similar outcomes, CADISS trial); endovascular for medical failure.

Lacunar Infarcts

• <15 mm in penetrating artery territory (lenticulostriate, thalamoperforator, pontine, internal capsule).
• Most common syndromes:
  • Pure motor: posterior limb IC or pons.
  • Pure sensory: VPL thalamus.
  • Ataxic hemiparesis: pons or IC.
  • Dysarthria-clumsy hand: pons or genu IC.
  • Sensorimotor lacunar: thalamus + adjacent IC.
• Multiple lacunae + leukoaraiosis + microbleeds = small vessel disease (cerebral small vessel disease / SVD).

Mimics of Acute Stroke

• Tumor with hemorrhage or seizure: post-contrast enhancement + mass effect.
• Encephalitis (HSV): medial temporal DWI restriction + FLAIR + asymmetric — but slower clinical course.
• Status epilepticus: cortical DWI + FLAIR; often pulvinar T2 hyperintensity; correlates with EEG.
• Hypoglycemia: cortical, hippocampal, splenium DWI restriction.
• Wernicke encephalopathy: mammillary, periaqueductal, dorsomedial thalamus DWI/FLAIR.
• MELAS stroke-like episode: gyriform parieto-occipital cortical DWI + FLAIR — does not respect vascular territory.
• CJD: cortical ribbon + basal ganglia + pulvinar DWI restriction — sustained, evolving.
• MS (tumefactive plaque): open-ring enhancement + minimal mass effect.
• PRES: classically bilateral parieto-occipital cortical-subcortical T2/FLAIR — vasogenic, not cytotoxic. Atypical patterns can involve deep white matter, basal ganglia, thalami, cerebellum, and brainstem (“central PRES”).
• Migraine with aura: cortical DWI restriction possible but transient.

Pitfalls and Pearls

• Negative CT does not rule out hyperacute stroke — DWI is the standard for first hours.
• Calcified plaque vs hyperdense vessel: compare both sides; calcified is usually bilateral and longer.
• ASPECTS <6 reduces but does not eliminate thrombectomy benefit — newer evidence (SELECT2, RESCUE-Japan LIMIT) shows benefit in some large-core patients.
• “Spot sign” on CTA in ICH predicts expansion — reverse coagulopathy, close surgical follow-up.
• CVT is missed routinely on CT — always assess sinuses in headache + papilledema, postpartum, OCP use.
• Bilateral thalamic edema/hemorrhage → deep venous system thrombosis (vein of Galen / internal cerebral veins).
• Artery of Percheron variant: bilateral paramedian thalamic infarct ± rostral midbrain — embolic, dramatic encephalopathy.
• Hypertensive encephalopathy / PRES mimics stroke but is bilateral parieto-occipital and vasogenic (no DWI restriction).
• Hemorrhagic infarct vs primary ICH: gyriform CT hyperdensity = hemorrhagic infarct; rounded centered mass = primary ICH.
• Watershed pattern: specific for hemodynamic disease — look for proximal ICA stenosis / dissection / cardiac arrest.
• Don’t miss the basilar: hyperdense basilar is easily overlooked; check the prepontine region on every NCT.

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. Nogueira RG, Jadhav AP, Haussen DC, et al. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct (DAWN). N Engl J Med. 2018;378(1):11-21.
3. Albers GW, Marks MP, Kemp S, et al. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging (DEFUSE-3). N Engl J Med. 2018;378(8):708-718.
4. Thomalla G, Simonsen CZ, Boutitie F, et al. MRI-guided thrombolysis for stroke with unknown time of onset (WAKE-UP). N Engl J Med. 2018;379(7):611-622.
5. Saposnik G, Barinagarrementeria F, Brown RD Jr, et al. Diagnosis and management of cerebral venous thrombosis. Stroke. 2011;42(4):1158-1192.
6. Charidimou A, Boulouis G, Frosch MP, et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy: a multicentre, retrospective, MRI-neuropathology diagnostic accuracy study. Lancet Neurol. 2022;21(8):714-725.