Vascular distribution or wedge-shaped: Ischemia

Round “cystic” T2 hyperintense lesions: Abscess, septic emboli

Solid intermediate-low signal T2 round lesions: Solid cellular masses (e.g., lymphoma, metastases, meningioma)

Extra-axial cyst: Epidermoid (cholesteatoma in temporal bone)

Central pontine &/or deep nuclei: CPM/EPM, deep venous ischemia, PRES

Subacute & evolving strokes have less intense DWI brightness as cytotoxic changes fade over time & are replaced by progressively increasing vasogenic edema

Hypoperfusion infarcts usually have less intense DWI brightness

Inflammatory/infectious causes for diffusion restriction are characteristically less hyperintense than acute stroke

Abrupt clinical onset

Occur in a vascular distribution

Punctate white matter (WM) lesions often of small vessel origin

Venous ischemia may have increased or mixed DWI changes; often hemorrhagic

Restriction centrally in “cystic” or ring-enhancing lesions

T2 hypointense rim characteristic

DWI restriction may be seen in bacterial, granulomatous, or parasitic infections (e.g., neurocysticercosis)

Peripheral rim enhancement typical

Extra-axial fluid collections that restrict are usually pus-filled

Lobular extra-axial mass follows CSF intensity except on FLAIR & DWI

DWI (usually markedly bright) is more specific than FLAIR (may be bright or subtle “dirty CSF”); both show increased signal relative to CSF

Cholesteatoma of middle ear or petrous apex histologically same & DWI bright (thin slice DWI helpful)

DWI signal variable; bright or “black”

Conventional T1/T2 sequences & clinical history help to distinguish

GRE sequence may clarify (susceptibility reflects blood products in most stages of hemorrhage evolution except early hyperacute)

Classic locations: Gray-white junction, deep WM, corpus callosum, brainstem

Typically bright on DWI

Other useful sequences: FLAIR, GRE, SWI

Trauma history

DWI signal is variable: Increased, mixed, or decreased

Bright DWI signal is usually less intense than seen with acute ischemia & abscess

T2 hyperintense lesions

Mild restriction common due to cellularity

Enhancing extra-axial mass

Often DWI bright due high cellularity

Periventricular location & homogeneous enhancement typical

T2 hyperintensity in posterior circulation bilaterally in a hypertensive patient

Usually doesn’t restrict on DWI!!

Critical to assess ADC to separate the 2 components, both may be present

DWI restriction in basal ganglia (BG), thalami ± cortical ribbon (esp. insula)

DWI hyperintensity increases over time

Older patient with rapidly ↑ dementia

Demyelination rarely causes restriction

Most show increased diffusion on ADC

Callososeptal lesions characteristic

May restrict acutely

Classic locations (pons, BG) & clinical picture diagnostic