Diffuse axonal injury is a variant of severe traumatic brain injury, the main substrate of which are diffuse breaks or tears of axons. Clinically, from the first minutes of injury, there is a coma with symptoms of a stem lesion, which can go into a vegetative state. The diagnosis is carried out according to the traumatic history, the features of the clinic and tomographic data. Coma treatment consists in ventilator and intensive therapy, after coming out of the coma, vascular, nootropic, metabolic drugs, physical therapy, psychostimulation, speech therapy correction are used.
ICD 10
S06.7 Intracranial trauma with prolonged comatose state
General information
Diffuse axonal injury as a separate type of severe TBI was described in 1956, the term was proposed in 1982. Diffuse axonal injury (DAI) is characterized by a prolonged comatose state that occurs from the moment of TBI. Its morphological substrate is caused by trauma diffusely distributed axon ruptures and small focal hemorrhages in cerebral structures. The most typical areas of damage are the brain stem, the white matter of the hemispheres, the corpus callosum and the periventricular areas. Diffuse axonal injury is prevalent mainly among young people and children. In childhood, it is accompanied by more severe neurological disorders and a deeper coma.
Some authors suggest the division of DAI by severity. A mild degree corresponds to the duration of a coma of 6-24 hours, a moderate one — a coma longer than a day, but without gross stem manifestations. Severe diffuse axonal injury is characterized by a prolonged coma with symptoms of decortication and decerebration. In any case, DAI is a serious condition with a high risk of transition to a vegetative state and death. In this regard, its effective treatment remains an urgent problem of practical traumatology and neurology.
Causes
Diffuse axonal injury occurs due to injuries caused by angular acceleration of the head. In this case, there may not be direct contact of the head with a solid object. Therefore, a number of patients with DAI have no skull fractures and other visual injuries. Observations have shown that acceleration in the sagittal plane causes mainly vascular damage with the formation of hemorrhages in the brain substance, and acceleration in the oblique and lateral planes causes injury to axons.
The causes of DAI are mainly car injuries, falls from a height (catatrauma) and barotrauma. It is with such injuries that angular acceleration of the head occurs. At the same time, the more mobile hemispheres of the brain are rotated, and the more fixed stem sections are twisted. In addition, mutual displacement of individual layers or parts of the brain is possible. Even a small displacement of cerebral structures can lead to partial or complete rupture of axons, as well as small vessels.
Morphologically, 3 signs are pathognomonic for DAI: a lesion in the corpus callosum, a lesion in the brain stem and diffuse axonal ruptures. The first 2 signs are macroscopic and initially look like a normal hemorrhage (hematoma) up to 5 mm in size. Sometimes they look like a tear in the fabric, the edges of which are soaked in blood. A few days after TBI, the lesions transform into areas pigmented in the color of rust, and then scars form in their place. Lesions in the corpus callosum may resolve with the formation of small cysts.
Detection of axonal lesions is possible only by special microscopic studies of brain tissues (by immunohistochemical method and by silver impregnation), which make it possible to see multiple axonal balls located at the sites of nerve fiber ruptures. Further changes are characterized by a macrophage reaction with the appearance of reactive microglyocytes and astrocytes. The absence of segmented elements sharply distinguishes the picture of DAI from the changes that occur with a brain injury. After 2-3 weeks, fragmentation and demyelination of damaged axons is observed. Moreover, the process of demyelination tends to spread along the pathways, and the longer the coma and vegetative state lasts, the more widespread it is.
Symptoms
A distinctive feature of DAI, in comparison with the clinic of other TBI, is a prolonged moderate or deep coma that occurs immediately after injury. In adults, the ratio of cases of moderate to deep coma is 63% to 37%, in children — 43% to 57%. The average duration of coma varies from 3 to 13 days.
Typical for coma in DAI are post-tonic reactions of a diffuse nature, provoked by various stimuli, periodic motor excitation against the background of adynamia. Stem symptoms are characteristic: a decrease or complete loss of photoreaction and corneal reflexes, anisocoria, a different arrangement of the pupils horizontally, a disorder of the respiratory rhythm and respiratory rate. In addition, the neurological status often reveals variable spontaneous nystagmus, rigidity of the occipital muscles and Kernig’s symptom, vegetative symptoms (hyperhidrosis, arterial hypertension, hypersalivation, etc.).
Motor disorders are usually represented by a rough pyramidal-extrapyramidal tetrasyndrome. Most of the victims have arms with hanging hands brought to the body and bent at the elbows (so-called “kangaroo paws”). Tendon reflexes are initially elevated, then decrease or completely fall out. Often there are pathological stop signs. Disorders of muscle tone vary from generalized hypotension to gormetonia, tend to change, often have an asymmetric or dissociative character.
In surviving patients, the further course of DAI can go in 2 directions: coming out of a coma and going into a vegetative state. In the first case, eye opening begins to occur, accompanied by tracking and fixing the gaze. It can be either spontaneous or provoked by various stimuli (sound, pain). Gradually, consciousness is restored, the execution of simple instructions becomes possible, verbal contact expands. This process is accompanied by a slow regression of neurological manifestations.
Prolonged coma in most cases leads to a transition to a vegetative state, which can be persistent or transient in nature and last from 1-2 days to several months. The onset of a vegetative state is indicated by the opening of the eyes, not accompanied by fixation of the gaze and tracking. There are signs of separation of hemispheric and stem structures — variable, unusual, changing focal symptoms. With persistent vegetative states, neurotrophic disorders develop (including bedsores) and vegeto-visceral disorders (tachycardia, hyperthermia, facial hyperemia, tachypnea, etc.). A significant role in the occurrence of the latter is played by the damage of somatic organs that appears as a complication (multiple organ failure) and intercurrent infections (pneumonia, pyelonephritis, sepsis).
Diagnostics
The mechanism of the resulting TBI with angular acceleration of the head, the onset of coma immediately after the injury and the characteristic features of its clinic testify in favor of DAI. A distinctive feature is also the absence of stagnant changes in the optic nerve discs during ophthalmoscopy of patients with DAI, even in the case of prolonged coma. However, it is quite difficult for a neurologist and traumatologist to diagnose DAI clinically.
Reliably diagnose “Diffuse axonal damage” allows the presence of pathognomonic macroscopic signs on an MRI or CT scan of the brain. On CT and MRI of the brain in the acute period, cerebral edema is determined with a decrease in the ventricles and subarachnoid spaces; fluid accumulation is often visualized above the frontal lobes. More difficult is the diagnosis of mild and moderate degrees of DAI, in which macroscopic signs are usually absent, brain edema and hemorrhages are expressed slightly, and in some cases the tomographic picture does not differ significantly from the norm. In such a situation, they rely on typical tomographic dynamics — regression of hemorrhages and edema with a tendency to ventricular expansion, subsequent ventriculomegaly and an increase in diffuse atrophy of cerebral structures.
Treatment
Patients with DAI in a coma need long-term ventilation, parenteral nutrition and intensive therapy aimed at maintaining homeostasis and the main body systems, relieving brain edema, preventing infectious complications. In the case of an episode of severe motor arousal, sometimes it is necessary to resort to the therapeutic use of anesthesia. After coming out of a coma, it is advisable to start psychostimulotherapy early for the speedy regression of psychoemotional disorders, exercise therapy to restore motor activity and prevent joint contractures, speech therapy correction of speech disorders. In order to improve the functioning of the central nervous system, nootropic (nicergoline, piracetam, cortexin, gamma-aminobutyric acid) and vascular (vinpocetine, cinnarizine) drugs are prescribed. If indicated, the treatment regimen includes anticholinesterase (neostigmine, galantamine) agents and neurotransmitters (levadopa, piribedil).
Surgical treatment is not indicated. It is carried out only in the presence of concomitant intracranial injuries (subdural or intracerebral hematomas, foci of crushing, depressed fractures of the skull, etc.), dangerous for the development of compression of the brain.
Forecast
The outcome of DAI depends on its severity. Recently, a suggestion has been made about the possible regeneration of axons in children and young victims, in favor of which is evidenced by the partial recovery of neurological and mental functions occurring over time in DAI survivors. However, the longer the coma lasts and the more severe neurological symptoms it is accompanied by, the greater the likelihood of severe disability in case of survival of the victim. Diffuse axonal injury with a coma lasting no more than 7 days ends with a good recovery or moderate disability. DAI with a coma longer than 8 days, as a rule, leads to severe disability or transition to a vegetative state.
Residual residual phenomena after DAI are paresis and paralysis, mnestic disorders, mental disorders, speech disorders, bulbar syndrome, extrapyramidal disorders. In patients who have emerged from the vegetative state, extrapyramidal symptoms prevail: secondary parkinsonism and minor hyperkinesis, accompanied by severe mental disorders (dementia, affective disorders, amnestic confusion, spontaneity). Persistent vegetative state leads to death due to depletion of neurotransmitter reactions and the occurrence of somatic complications.
