Diffuse axonal injury (DAI) is a type of brain injury characterized by swelling and rupture of axons located primarily in the central regions of the brain, caused by shear stress during rotational forces to the head. It accounts for approximately 28% to 50% of severe traumatic brain injuries. DAI presents significant challenges in treatment and is associated with a poor prognosis.
Pathology
DAI commonly occurs in regions with dense axonal concentrations, including the corpus callosum, brainstem, gray-white matter junctions, cerebellum, internal capsule, and basal ganglia. Visible findings may include tissue clefts and vascular tearing with hemorrhagic foci in the affected regions, usually without significant cerebral contusion or intracranial hematomas. Microscopically, the presence of axonal retraction balls is a key hallmark for diagnosing DAI. Axonal retraction balls are the result of axoplasmic swelling at the ruptured ends of axons, forming small, spherical or ovoid structures with diameters of 5–20 μm. They typically appear approximately 12 hours after injury, increase in number within two weeks, and persist for around two months.
Based on pathological findings, DAI is classified into three grades:
- Grade I: Microscopic detection of axonal retraction balls in regions with dense axonal concentrations, primarily in the periventricular white matter of the corpus callosum.
- Grade II: Displays the features of Grade I, along with macroscopic evidence of corpus callosum tearing and hemorrhages.
- Grade III: Includes the characteristics of Grade II with additional tearing and hemorrhages in the dorsolateral upper brainstem.
Clinical Manifestations
Consciousness Impairment
Prolonged and severe disturbance of consciousness immediately following the injury is a hallmark clinical feature of DAI. Higher grades of injury are associated with more severe consciousness disturbances. Extremely severe cases may result in death within a few hours, and survivors are often left in a state of coma or prolonged unresponsive coma. Patients with DAI do not exhibit a lucid interval following the injury. Recovery of consciousness, if it occurs, is often correlated with the severity of primary and secondary brain injuries.
Pupillary and Ocular Movement Changes
Some patients may exhibit unilateral or bilateral pupillary dilation. Signs in cases of widespread injury may include conjugate eye deviation, downward gaze, or dissociation of ocular movements between the two eyes.
Diagnosis
Immediate post-injury consciousness impairment is a key indicator for DAI. Evidence of tearing and hemorrhage in midline brain structures via CT or MRI imaging supports the diagnosis. CT findings may reveal small hyperdense lesions in areas such as the corpus callosum, the upper brainstem, internal capsule, and white matter. These lesions are typically not surrounded by edema or other damage. Non-hemorrhagic tears of brain tissue are difficult to detect on CT, where MRI is more effective. In acute DAI, tissue tears with hemorrhages appear as high signal regions on T1-weighted MRI and non-hemorrhagic tears appear as low signal regions on T1 and high signal regions on T2-weighted MRI. Susceptibility-weighted imaging (SWI) shows higher sensitivity in detecting microlesions within the brain, which helps improve diagnostic accuracy when combined with clinical findings.
Current diagnostic criteria for DAI include:
- Prolonged post-injury coma lasting more than 6 hours.
- CT evidence of brain tissue tearing and hemorrhage or normal imaging despite clinical findings.
- Normal intracranial pressure despite poor clinical condition.
- Persistent post-injury consciousness disturbance without evident structural abnormalities on imaging.
- Diffuse cerebral atrophy during the later stages after trauma.
- Characteristic pathological changes in injured brain tissue.
Treatment
Although significant progress has been made in basic research on DAI, there have been no major breakthroughs in clinical treatment. Management primarily involves interventions such as airway management, hyperventilation with supplemental oxygen, hypothermia therapy, dehydration therapy, sedation, and analgesia. For patients whose conditions deteriorate during treatment, a repeat CT scan may be necessary to detect delayed intracranial hematomas or severe cerebral edema. Surgical interventions, such as hematoma evacuation or decompressive craniectomy, are required in these cases.