General
- AKA diffuse axonal shearing
Definition
- Diffuse damage in the cerebral hemispheres, corpus callosum, brainstem and cerebellum
Location
- The parasagittal white matter,
- Large fiber bundles such as the
- Corpus callosum (92%),
- Internal capsule,
- Cerebellar peduncles (superior),
- Other sites where they are also known as
- Gliding (88%)
- Traumatic brain lesions consisting of tears and hemorrhages in the white matter of the dorsal paramedian portions of the cerebral hemispheres, mainly in the frontal lobe
- Thalamic (56%)
- Caudate (17%) contusions
Clinical presentation
- Often cited as the cause of prolonged loss of consciousness in patients rendered immediately comatose following head injury in the absence of a space occupying lesion on CT
- Concomitant subdural or epidural hematomas
Diagnosis
- Clinical
- Loss of consciousness (coma) lasts > 6 hours in absence of evidence of intracranial mass or ischemia.
- Pathology
- Definitive diagnosis
- Immunostaining for β- amyloid precursor protein (β- APP) at autopsy and identifying axonal retraction balls in the deep white matter.
Pathology
- Mech
- Rotational acceleration/deceleration head injury.
- Damage of axonal integrity
- Long- tract structures (axons and blood vessels) are especially at risk
- In its severe form, haemorrhagic foci occur in the
- Corpus callosum
- Dorsolateral rostral brainstem
- With microscopic evidence of diffuse injury to axons
- Axonal retraction balls
- Microglial stars
- Degeneration of white matter fibre tracts
- Minor degrees of axonal injury may provide the pathophysiologic basis for deficits experienced during and after mTBI/ concussion.
- Alternatively, functional and metabolic disturbances may be responsible with little structural axonal injury
- What are the biochemical changes in DAI?
- 1 hour: Neurofilament immunoreactivity
- 4–5 hours: Accumulation of amyloid precursor protein
- 6 hours: Ubiquitin (a marker of neural damage) is evident
- 12–24 hours: Axonal varicosities
- 1 day–2 months: Axonal swelling
- Microglial clusters around degenerating axons appear at 5 to 10 days
- 2 months–years: Wallerian degeneration and demyelination
DAI grading
Clinical
DAI grade | Description |
Mild | Coma > 6–24 hrs, followed by mild-to-moderate memory impairment, mild-to-moderate disabilities |
Moderate | Coma > 24 hrs, followed by confusion & long-lasting amnesia. Mild-to-severe memory, behavioral, and cognitive deficits |
Severe | Coma lasting months with flexor and extensor posturing. Cognitive, memory, speech, sensorimotor, and personality deficits. Dysautonomia may occur |
Histological/Radiological injury
DAI grade | Description |
Grade I | Axonal injury in the white matter of the cerebral hemisphere, corpus callosum, brainstem and, less commonly, cerebellum |
Grade II | Focal lesionᵃ in the corpus callosum in addition to above |
Grade III | Focal lesionᵃ in the dorsolateral quadrant(s) of the rostral brainstem in addition to above |
- ᵃFocal lesions often can only be perceived microscopically
Radiological MRI
DAI grade | Pathology |
I | Grey-white matter interface (commonly parasagittal white matter of frontal lobes, periventricular temporal lobes) |
II | Focal lesions in corpus callosum (commonly posterior body and splenium) in addition to Grade I lesions |
III | Brainstem (commonly rostral midbrain, cerebellar peduncles, medial lemnisci, and corticospinal tracts) in addition to Grade I and II lesions |
- GRE: T2-weighted gradient-recalled-echo (GRE) magnetic resonance (MR) technique
- SW: Susceptibility-weighted (SW) magnetic resonance (MR) technique.
- Grade I and II typically show marked improvement in GCS within 2 weeks
- Grade III requires ~2 months for recovery
- Suggestive of prolonged loss of consciousness or coma with DAI involving the brain stem
Made with Bullet