Diffuse axonal injury

Shearing injury of axons from rapid acceleration–deceleration / rotational head trauma → microscopic axonal damage ± tiny haemorrhages, often with CT that looks “too normal” for the level of coma.

Summary

Think: unconscious patient after high-energy trauma, minimal mass lesion, MRI shows multiple tiny lesions at grey–white junction, corpus callosum, brainstem.

Pathophysiology & terminology

Sudden rotational forces → stretch and shear axons → axonal swelling and disconnection (secondary Wallerian degeneration).
Usually associated with high-speed RTCs, falls from height, shaken-baby.
DAI = original histopathological term.
TAI often used as the imaging term (same concept for exams).

Typical locations

Cerebral hemispheric white matter
- Grey–white junction (especially frontal + temporal lobes)
- Centrum semiovale, corona radiata
Corpus callosum
- Classically splenium, also body
Dorsolateral upper brainstem
- Superior cerebellar peduncles, tegmentum, periaqueductal region

Shortcut (with caveats):

Grade 1 = hemispheres only
Grade 2 = + corpus callosum
Grade 3 = + brainstem

Imaging

CT

CT can be normal in many patients (especially non-haemorrhagic DAI).
When positive:
- Tiny punctate hyperdensities at grey–white junction and corpus callosum (haemorrhagic foci).
- No (or only mild) mass effect compared with clinical status.
Frequently coexists with other TBI findings (contusions, SDH, SAH).

Exam line: “Severe coma with essentially normal CT → suspect DAI → MRI.”

MRI (key sequences)

T2/FLAIR

Small hyperintense foci in the classic locations above.
May be subtle early; best seen after 24–48 h.

GRE / SWI (most sensitive for haemorrhagic DAI)

Multiple tiny blooming microhaemorrhages
Number and depth of lesions roughly correlate with severity and prognosis.

DWI

Restricted diffusion foci (non-haemorrhagic axonal injury).
Helpful when GRE/SWI is negative or lesions are very small.

Clinical / exam nuggets

Mechanism: high-speed deceleration, rotational injury, fall from height, shaken infant.
Presentation:
- Immediate loss of consciousness, often prolonged coma.
- Neurological status out of proportion to CT findings.
Prognosis worsens with:
- Increasing grade (especially brainstem involvement).
- Number and volume of microhaemorrhages.
DAI is a major cause of long-term cognitive and behavioural deficits after TBI.