Sequelae of diffuse axonal injury

In many cases, if a person's body suffers some kind of damage, there will be sequelae. For example, some people will suffer from many sequelae after cerebral hemorrhage. Symptoms like legs not being controlled by the brain, or hands not working properly. Once any part of the human body is damaged, it is impossible to restore it to its original intact state, and it can only be repaired through exercise as much as possible. Let’s take a look at the sequelae of diffuse axonal injury.

The clinical manifestation of the injured is impaired consciousness immediately after head trauma, often coma, and its duration varies depending on the degree of DAI injury. However, there are no symptoms and signs of focal damage commonly seen in cerebral contusion (laceration). However, if there is brain stem damage, changes in vital signs may occur, followed by manifestations of intracranial hypertension; in mild cases, after the temporary mental disorder subsides, there may be symptoms of autonomic nervous system disorders such as retrograde amnesia, dizziness, and headache, just like a concussion; in severe cases, there may be a persistent vegetative state, or even a continuous coma until death. If they survive, severely injured people may also suffer from dementia or other central nervous system dysfunctional disabilities.

Diagnostic points

① The head is in motion when injured, and external force can cause shear force on brain tissue; ② Coma or restlessness occurs immediately after injury, lasts for a long time, and recovery is slow. A few injured people may have an intermediate period of lucidity; ③ There are no clear localizing signs of focal damage to the nervous system; ④ CT scans have characteristic manifestations of DAI. A clear clinical diagnosis can only be made when the above four points are met at the same time.

Features of a head CT scan

① Diffuse bilateral leukoedema, brain swelling, and unclear gray-white matter boundaries; ② Narrowing or disappearance of the ventricles, cisterns, sulci, and subarachnoid spaces, with no midline shift; ③ Diffuse brain swelling with diffuse punctate and flaky hemorrhages in the white matter, but no hematoma and no space-occupying effect; ④ May be accompanied by a thin layer of hemorrhage under the dura mater.

Pathological changes

The basic pathological changes include diffuse axonal damage and focal damage to the corpus callosum and brainstem:

Diffuse axonal injury

Its location may be in the cerebral white matter, corpus callosum, brainstem, or cerebellar white matter. In the early stage, the long fiber axons become irregularly thickened, broken, or wavy, with normal fibers running parallel in between. The short fiber axons are irregularly curved and tortuous. The thickened axons may be 3 to 5 times longer than normal axons, and the broken ends may be conical or needle-shaped. As time goes by, the damaged axons become thicker and take on a sac-like, spherical, tadpole-like or beaded shape; some curl up into an arc or spiral shape. If the injured person survives, the broken end of the damaged axon will be spherical, which is called a retraction ball. Contractile bulbs can be connected to the axonal ends or exist in isolation. They are widely distributed in the white matter of the brain, brainstem, especially the basal ganglia and medial lemniscus. They are considered to be the characteristic lesions of DAI and the pathological morphological basis for the diagnosis of DAI. It is generally believed that contraction glomeruli begin to appear about 16 hours after axonal injury, and typical contraction glomeruli appear 72 hours after injury. There are reports that in patients who died several months to years after the injury, contractile glomeruli can still be found in the axons near the nuclear end of their brains. However, the best way to observe the contractile spheres is to use silver infiltration staining.