Monday, 22 August 2011

Diffuse Axonal Injury MRI

A 30 yo male with RTA, brought unconscious. 
On admission CT brain nearly normal expect mild diffuse cerebral edema. So there is discrepancy between CT findings and pt's Glass Glow coma score. 

MRI is best in this case to rule out Diffuse Axonal Injury.

T2*GRE images show multiple punctate low signal intensities suggestive of petechial bleed with few foci of restricted diffusion involving cerebral white matter, corpus callosum and basal ganglia suggestive of typical diffuse axonal injury.

Diffuse Axonal Injury (DAI)

Unlike other brain trauma lesions like contusion that occurs due to direct impact on brain, DAI is the result of traumatic shearing / rotational forces that occur when the head is rapidly accelerated or decelerated, occurs commonly in Road traffic accidents.
Due to shearing injury there is acutual disruption of axons, which refers to damage inflicted as tissue slides over other tissue, parts of differing densities and distances from the axis of rotation slide over one another, stretching axons that traverse junctions between these areas of different density, especially at junctions between grey and white matter.

Imaging wise best diagnostic clue is multifocal punctate hemorrhages at corticomedullary junction, corpus callosum, deep gray matter & upper brainstem.

Often normal in ~ 50-80%.
May see small hypodense foci corresponds to edema and shearing injury or hyper dense foci of petechial hemorrhages.
Delayed scans often reveal the new lesions.

The investigation of choice.
Diffusion and T2 *GRE are the preferred sequences.
Multifocal hyperintense foci on T2 and FLAIR, ranging from punctate to 15 mm. Lesions hypo intense on T2*GRE secondary to susceptibility effect from blood products, may remain for several years. May show restricted diffusion on Dw images.

Most common location is gray/white matter interface (~67%), Corpus callosum (~20%) particularly its Splenium / under surface of posterior body, Brain stem particularly dorsolateral midbrain & upper pons. Less common locations are Caudate, thalamus, internal/external capsule, tegmentum, fornix, corona radiata, cerebellar peduncles.

DDs for multifocal hemorrhagic lesions
Amyloid angiopathy - elderly, normotensive, often demented
Hypertensive microhemorrhages – longstanding chronic HTN.

Adams & Gennarelli staging for DAI imaging 
Stage 1: Frontal & temporal lobe gray/white interface - mild head trauma
Stage 2: Lesions in lobar WM & corpus callosum – Moderate rotational force injury
Stage 3: Lesions of dorsolateral midbrain & upper pons – severe.

Natural History & Prognosis
> 90% remain in a persistent vegetative state.
Severe DAI rarely causes death.
Prognosis worsens as number of lesions increase.
Brainstem involvement is associated with worst prognosis.
10% of patients return to normal function, do so within the 1st year. May experience post-concussion syndrome, Persistent headache, cognitive decline, personality changes.

No real treatment for diffuse axonal injury
Supportive therapy.

Reference : Diagnostic Imaging Osborn

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