You don’t need to understand spin physics to read brain MRI well, but you do need a working model of what makes each sequence bright vs dark. This page is the practical signal-intensity reference: T1, T2, FLAIR, DWI/ADC, SWI/GRE, post-contrast T1, and the common artifact patterns that fool readers.

T1-Weighted Imaging

What It Shows

• Anatomy. Best for gray-white differentiation in adults; visualizes atrophy patterns.
• Pre-contrast T1 = baseline; post-contrast T1 highlights BBB breakdown.

Bright on T1

• Fat — orbital fat, marrow, lipoma, dermoid.
• Subacute hemorrhage (methemoglobin) — extracellular methemoglobin, days to weeks after bleed.
• Melanin — primary melanoma, neurocutaneous melanosis.
• High-protein fluid — colloid cyst, Rathke cleft cyst, mucocele, abscess, hemorrhagic cyst.
• Mineralization — manganese (parenteral nutrition, liver disease → globus pallidus), calcium (variable), iron (variable).
• Contrast (post-contrast) — anywhere with BBB breakdown.
• Flow-related enhancement — vessels with slow flow.

Dark on T1

• CSF, water, cyst contents (unless high-protein).
• Edema, demyelination, chronic infarct (gliosis), encephalomalacia.
• Calcification, dense fibrosis.
• Acute hemorrhage (deoxyhemoglobin, hyperacute oxyhemoglobin briefly).

T2-Weighted Imaging

What It Shows

• Pathology screen. Water = bright.
• Most pathologies (edema, gliosis, inflammation, demyelination, tumor, infarct, cyst) appear bright on T2.

Bright on T2

• CSF, water, cyst, edema.
• Gliosis (chronic injury).
• Demyelination (MS plaques, leukodystrophy, ADEM, PML).
• Infarct (subacute and chronic).
• Tumor (most), edema surrounding tumor.
• Inflammation (encephalitis, abscess wall).
• Wallerian degeneration (chronic).

Dark on T2

• Iron — globus pallidus (normal aging), substantia nigra, red nucleus, dentate; NBIA, neuroferritinopathy.
• Calcium — variable (depends on crystal form; usually low T2).
• Acute / chronic blood products — deoxyhemoglobin (acute), hemosiderin (chronic).
• Dense fibrous tissue — meningioma, scar.
• Hypercellular tumor — lymphoma, medulloblastoma (high N:C ratio reduces water).
• Air, dental amalgam, metallic foreign body.
• Flow void — patent vessels (normal).

FLAIR (Fluid-Attenuated Inversion Recovery)

What It Shows

• T2-weighted physiology with CSF suppressed. Same lesions bright as T2, but CSF black instead of white.
• The workhorse for periventricular and cortical pathology — lesions next to CSF stand out.

Bright on FLAIR

• Same as T2 (edema, gliosis, demyelination, infarct, tumor) but with CSF dark.
• Cortical FLAIR hyperintensity — subacute infarct, encephalitis, status epilepticus, CJD (cortical ribbon).
• Sulcal FLAIR hyperintensity — leptomeningeal disease (carcinomatous, infectious), SAH (acute / hyperacute), hyperoxygenation artifact, IIH, propofol, gadolinium leakage.

Dark on FLAIR

• CSF (by design).
• Acute hemorrhage (depends on stage).

FLAIR Pitfalls

• CSF flow artifact in posterior fossa (4th ventricle) → false bright signal.
• Hyperoxygenation under anesthesia → diffuse sulcal FLAIR brightness.
• Propofol → FLAIR sulcal brightness from suppressed CSF flow.

Diffusion-Weighted Imaging (DWI) + ADC

What It Shows

• DWI measures restriction of free water motion.
• True restriction = bright on DWI AND dark on ADC.
• DWI alone is unreliable — always pair with ADC.

Causes of True Diffusion Restriction

• Cytotoxic edema — acute ischemic infarct (within minutes).
• Pus / abscess — viscous content restricts.
• Hypercellular tumor — lymphoma, medulloblastoma, high-grade glioma (focal areas).
• Prion disease — cortical ribbon + basal ganglia in CJD.
• Acute demyelination — center of MS / NMO plaque (transient).
• Encephalitis — herpes (medial temporal), autoimmune.
• Viscous fluid — epidermoid (classic), hematoma (acute, briefly).
• Hypoglycemia — cortical / hippocampal restriction.
• Wernicke encephalopathy — mammillary, periaqueductal, thalamic.
• Status epilepticus — peri-ictal cortical restriction.

T2 Shine-Through (The Trap)

• DWI is a heavily T2-weighted sequence at its base. Lesions that are bright on T2 (CSF, vasogenic edema, chronic infarct, MS plaque) can be bright on DWI without true restriction.
• Always confirm with ADC: true restriction = dark on ADC. T2 shine-through = bright or normal on ADC.

T2 Black-Out

• Lesions that are very dark on T2 (hemorrhage, calcium) can look “restricted” on DWI through black-out artifact. Cross-reference SWI / T2*.

SWI / GRE / T2*

What They Show

• Susceptibility-sensitive sequences — detect anything that disrupts the local magnetic field.
• SWI is more sensitive than GRE; T2* is older and lower resolution.

Causes of SWI / GRE Blooming (Dark Signal)

• Blood products — hemosiderin (chronic), deoxyhemoglobin (acute), intracellular methemoglobin.
• Calcium — distinguishable from blood by phase imaging (calcium and blood have opposite phase shifts).
• Iron — globus pallidus, substantia nigra (normal); NBIA, neuroferritinopathy (pathological).
• Air — pneumocephalus, sinuses.
• Melanin — primary CNS melanoma.
• Metallic foreign body.

Practical Uses of SWI

• Microbleeds — CAA (lobar), hypertensive (basal ganglia / thalamus / pons / cerebellum), diffuse axonal injury, mitochondrial.
• Cavernous malformations — “popcorn” appearance, complete dark rim.
• Cerebral venous sinus thrombosis — low signal in sinus + blooming around occluded sinus.
• Hemorrhagic transformation of infarct.
• Substantia nigra dopaminergic loss — “loss of swallow-tail sign” in PD.
• Multiple sclerosis — central vein sign in plaques.

Post-Contrast T1

What It Shows

• Gadolinium shortens T1 → bright signal where it accumulates.
• Two reasons for enhancement: BBB breakdown (parenchymal lesions) OR vascular structures (vessels, sinuses, choroid plexus, pituitary stalk, area postrema — normally no BBB).

Enhancement Patterns

Normal Enhancement

• Pituitary gland + stalk (no BBB).
• Pineal gland.
• Choroid plexus.
• Area postrema, median eminence (circumventricular organs).
• Dural venous sinuses, intracranial arteries and veins.
• Cavernous sinuses + dura mater (thin linear enhancement is normal).

Gadolinium Cautions

• NSF (nephrogenic systemic fibrosis): risk with linear gadolinium contrast in severe renal failure (eGFR <30). Macrocyclic agents are much lower risk.
• Gadolinium deposition: visible T1 hyperintensity in dentate + globus pallidus with cumulative dosing (especially linear agents). Clinical significance debated.

Blood Products — Signal Evolution Over Time

Mnemonic for blood signal (“It Be Iddy Biddy Baby Doo Doo”): Intracellular Oxy → Intracellular Deoxy → Intracellular Met → Extracellular Met → Hemosiderin. T1: iso/dark → iso/dark → bright → bright → iso/dark. T2: bright → dark → dark → bright → dark.

Common Artifacts

CT Hounsfield Unit Reference

• Air: −1000
• Fat: −100 to −50
• Water / CSF: 0
• White matter: 22–32
• Gray matter: 30–40
• Acute blood: 50–80 (varies with hematocrit)
• Calcium / bone: 100–1000+
• Iodinated contrast: 100–300 (in vessels)

Pitfalls and Pearls

• Always pair DWI with ADC — never call restriction on DWI alone (T2 shine-through is the universal trap).
• FLAIR can lie in posterior fossa — CSF flow artifact mimics 4th ventricular pathology.
• Sulcal FLAIR bright signal in a healthy patient under anesthesia is usually hyperoxygenation, not pathology.
• Gadolinium can leak into CSF in renal failure → diffuse sulcal FLAIR bright signal mimics SAH.
• Blood signal evolution is reliable for dating — but motion artifacts and mixed-age products can fool you.
• Calcium vs blood on SWI: phase imaging distinguishes (opposite phase shifts) but is not always available — correlate with CT.
• Cortical T2 shine-through is rare — cortical DWI bright + ADC dark in the right context = stroke, CJD, encephalitis, status, or hypoglycemia.
• Open-ring enhancement distinguishes tumefactive demyelination from tumor / metastasis / abscess.
• Susceptibility artifact obliterates DWI in the inferior frontal + temporal poles (near sinuses) — be cautious calling restriction near skull base.
• “Brain on bone window” misses fractures just as “brain window on lung CT” misses lung pathology — always toggle windows.

References

1. Bradley WG. MR appearance of hemorrhage in the brain. Radiology. 1993;189(1):15-26.
2. Hagiwara A, Otsuka Y, Andica C, et al. Differentiation between multiple sclerosis and neuromyelitis optica spectrum disorders by 7-T magnetic resonance imaging. Mult Scler. 2020;26(3):288-298.
3. Schweitzer AD, Niogi SN, Whitlow CT, Tsiouris AJ. Traumatic brain injury: imaging patterns and complications. RadioGraphics. 2019;39(6):1571-1595.
4. Mittl RL Jr, Grossman RI, Hiehle JF, et al. Prevalence of MR evidence of diffuse axonal injury in patients with mild head injury and normal head CT findings. AJNR Am J Neuroradiol. 1994;15(8):1583-1589.