Polytraumatized 17 year-old girl who came to the emergency room with low Glasgow Coma Scale score (7/15) and a previous blunt head trauma without apparent thoracoabdominal injuries.
1. CT EMERGENCY ROOM (Fig. 1)
-Multiple tiny hyperdense foci (microhaemorrhage) in the gray–white matter junction of the right frontal lobe and left parietal lobe, body and splenium of corpus callosum and right thalamus.
-Subtle intraventricular haemorrhage in the right occipital horn.
2- CT AFTER 2 DAYS (Fig. 2)
-More conspicuous intraventricular haemorrhage (Fig. 2a; yellow arrow).
-Persistent tiny hyperdense foci (microhaemorrhage) in the gray–white matter junction of the right frontal lobe and left parietal lobe, body and splenium of corpus callosum and new hyperdense foci in the right medial temporal lobe (Fig. 2a; red arrows).
-Increasing hypodensity and volume of the body/splenium of corpus callosum (Fig. 2b; red arrows).
3- MRI FINDINGS (Fig. 3; Fig. 4)
-Haemorrhagic lesions: Multiple supra and infratentorial susceptibility artefacts on SWI images (Fig. 3a; Fig. 4).
-Non-haemorrhagic lesions: Multiple hyperintense areas on FLAIR sequences (Fig. 3c)
-Prognosis: The region demonstrating restricted diffusion is assumed to have suffered irreversible injury. Note the presence of restricted diffusion within the corpus callosum (Fig. 3d).
1. BACKGROUND [1, 2]
Primary traumatic brain injury describes the lesion sustained to the brain parenchyma at the moment of trauma. Contusions are the most common intra-axial injuries. Other primary lesions are: focal brain injuries (lacerations), haemorrhage, diffuse axonal injury (DAI), or penetrating injuries/blast injuries.
Secondary TBI results from processes initiated by the trauma, as for example brain swelling, cerebral hypoxia, raised intracranial pressure, or hypothalamic–pituitary dysfunction among others.
We will focus on DAI, one of the most disabling conditions of primary traumatic brain. DAI occurs as a result of acceleration–deceleration/rotational force, and is typically located in the long white matter fibre tracts.
Cortex and white-matter have different densities and therefore rotate at different speeds during closed head injury, leading to misaligned axons or stretched axons (rarely sheared).
The stretching of axons causes depolarization, metabolic alterations, cellular swelling, cytotoxic oedema, and apoptosis.
2. CLINICAL PERSPECTIVE 
We should consider DAI when traumatic patients present with a loss of consciousness without or with minimal lesions on CT
3. IMAGING PERSPECTIVE [3, 4, 5]
DAI typically presents with haemorrhagic and non-haemorrhagic lesions.
- Often without relevant findings
- Tiny hyperdense foci (microhaemorrhage) in:
1. Gray matter–white matter, especially frontotemporal lobes.
2. Corpus callosum, especially splenium.
3. Brainstem, especially dorsolateral midbrain and upper pons.
4. Less common: Deep gray matter, basal ganglia and internal/external capsule, tegmentum, fornix, corona radiata and cerebellar peduncles
- Intraventricular haemorrhage correlates with DAI
- MRI is superior to CT in detecting haemorrhagic and non-haemorrhagic DAI lesions.
-Haemorrhagic lesions: SWI is the best tool to detect haemorrhagic DAIs.
-Non-haemorrhagic lesion: FLAIR is the best current tool to detect small and non-haemorrhagic parenchymal lesions, displayed as hyperintense lesions.
-Prognosis: The region demonstrating restricted diffusion (DWI) is assumed to have suffered irreversible injury. Schaefer et al. demonstrated that the volume of altered DWI shows a stronger correlation with clinical outcome and Glasgow coma scale than FLAIR. DTI (Diffusion tensor imaging) analyses water motion in order to evaluate the integrity of white matter tracts. Neuronal disruption can be implied by reductions in fractional anisotropy (FA).
Nuclear medicine findings
- PET may show hypometabolism in cingulate gyrus, lingual gyrus, and cuneus.
4. OUTCOME [4, 6]
Different degrees of DAI have been shown to be present in 80–90% of patients with traumatic brain injury. Prognosis greatly depends on its extension (Grade I to III).
Grading: Adams and Gennarelli staging
Stage 1 (mild): Frontal and temporal lobe grey-white matter interface lesions
Stage 2: Lesions in lobar white-matter and corpus callosum
Stage 3 (severe): Lesions of dorsolateral midbrain and upper pons
5. TAKE HOME MESSAGE
Most of the lesions are microscopic and non-haemorrhagic.
Differential Diagnosis List
Diffuse axonal injury grade III
Demyelinating disease (non-hemorrhagic lesions)
Cerebral amyloid angiopathy
Diffuse axonal injury grade III