The optic nerve is the visual signal pathway linking the brain and the eye, and damage to it can result in partial or even total loss of vision.
The most common type of traumatic optic neuropathy is optic nerve contusion, which is a serious ophthalmological emergency, causing vision loss in mild cases and blindness in severe cases.
Optic nerve contusion, or indirect injury to the optic nerve, is an impact injury to the optic nerve caused by an external force at a distance from the optic nerve transmitted through the bone or movement of the eye, and the injury can be without the manifestation of external or initial fundus injury, but with varying degrees of visual impairment.
First, the anatomical basis of optic nerve contusion
The optic nerve is a unique cerebral nerve containing approximately 1.2 million axons, divided into four segments: the intraspheric, intraorbital, intraductal, and intracranial segments.
The intracanalicular segment of the optic nerve is the most vulnerable site for indirect injury. The optic canal is located between the two bases of the pterygoid pterygoid and contains the optic nerve, meninges, ophthalmic artery, and sympathetic nerve fibers. The optic canal is a narrow bony lumen, and the optic nerve in the inner segment of the optic canal is held in place by the dura mater. At the optic foramen, the dura mater surrounding the optic nerve and the bony coating of the lumen fuse into a single layer and are firmly anchored to the surrounding periosteum and bone wall.
Special anatomy of the optic canal
The special anatomy of the optic nerve canal makes the inner segment of the optic nerve canal vulnerable to trauma: once the skull is struck by an external force, the external force is transmitted to the optic nerve canal through the bone wall, and the bone wall, periosteum, and dura mater are displaced, while the optic nerve is not displaced, resulting in relative shear force leading to optic nerve injury. The injured optic nerve then becomes edematous and can only “suffer” and be compressed in the limited space of the bony canal. At the same time, the tearing or pulling of the bony coat inside the bony canal can cause subdural hemorrhage of the optic nerve and compression of the optic nerve, resulting in “fascial gap syndrome” and physiological transection of the optic nerve.
Due to mechanical external shear injury, edema injury, physiological transection of the three forces together, the optic nerve appears temporary or even permanent damage.
Second, head trauma must be alert to the optic nerve contusion
Due to the specificity of the cranial orbital anatomy, facial and orbital fractures and closed head trauma can involve any part of the optic nerve, resulting in optic nerve contusion.
Optic nerve contusions are most often seen in traffic accidents, especially motorcycle or bicycle accidents without helmets, followed by falls from heights and violent blows. The injury area is mostly in the lateral region of the brow arch, i.e., the temporal frontal region (including the prefrontal and supraorbital crest temporal bone regions).
Common injury sites of optic nerve contusions
Since optic nerve contusion is often associated with severe cranial trauma, it is often easy to overlook, and the more timely the intervention time of optic nerve contusion, the better the treatment effect, preferably within 8 hours after the injury, therefore, once the head trauma occurs should be alert to optic nerve contusion.
Diagnosis and pupil examination of optic nerve contusion
Post-traumatic visual acuity loss, visual field defects and abnormal afferent pupillary reflex to light are the main clinical basis for diagnosing optic nerve contusion.
Pupillary examination is an objective test that not only effectively assesses the degree of visual impairment, but also evaluates false or exaggerated conditions. Performing a pupillary examination requires minimal patient cooperation, making it especially important for infants and children, the elderly, and seriously ill patients who have difficulty cooperating with other examinations.
The pupillary examination consists of.
1. the shape and size of the pupil.
2. the presence or absence of unequal pupil size
3. the presence or absence of relative pupillary afferent disorder (RAPD)
4. pupillary light reflex.
5. pupillary near reflex.
Pupillary examination is critical to the diagnosis of optic nerve contusion, therefore, every patient with trauma should have a pupillary examination, especially for relative pupillary afferent disorders.
Continuous interocular movement of the flashlight.
Illumination of the healthy eye (right eye) with bilateral pupillary narrowing.
Illumination of the affected eye (left eye) with dilated pupils in both eyes.
Relative pupillary afferent disorder in the affected eye (left eye).
IV. Treatment of optic nerve contusion
The treatment measures for optic nerve contusion mainly include glucocorticoid shock therapy, optic nerve canal decompression surgery, and neurotrophic therapy.
Currently, there are many controversies in the treatment of optic nerve contusion, therefore, the treatment of optic nerve contusion should be individualized according to the condition of each particular patient. All therapeutic measures, especially invasive ones, should be done with caution, making sure to fully consider the possible benefits and harms and to develop the most potentially beneficial treatment plan in the context of the individual patient’s condition.
First, in patients with multiple head injuries, an exhaustive ophthalmologic examination should be performed is to clarify the presence or absence of optic nerve contusions for early treatment.
High-dose glucocorticoid shock therapy should remain the current treatment option of choice for optic nerve contusion and is easily applied early and stopped by 3-5 days of ineffectiveness to avoid side effects.
For optic canal decompression, the indications should be strictly controlled, and only those patients who are determined to be likely to benefit by a rigorous clinical evaluation should be considered.
In addition, other adjuvant treatments, such as nerve growth factor, vasodilators (nimodipine), energy synergists, oxygen, vitamin B1, B12, and dehydrating agents, may be applied to restore visual function with certain effects.
V. Surgical indications for optic nerve canal decompression surgery
1.Late visual loss and no significant improvement by 12h of high-dose glucocorticoid treatment.
2.Persons with initial improvement after glucocorticoid treatment, followed by deterioration of visual acuity again.
3, CT fracture of the optic nerve canal and intra-optic nerve hemorrhage.
Progressive vision loss after injury or delayed visual impairment with residual vision a few hours or days after injury suggests that the optic nerve is compressed by edema or hemorrhage, which is a better indication for optic nerve canal decompression surgery, and early surgical intervention generally has a better prognosis.
Timing of optic nerve canal decompression surgery
The timing of optic canal decompression surgery has always been one of the concerns of clinicians.
By establishing animal models of optic nerve contusion and decompression at different times, domestic scholars have confirmed that decompression at 48h after trauma can better preserve and retinal morphology than decompression at 14d. Therefore, optic nerve contusion should be decompressed as early as possible to release the optic nerve compression.
However, optic nerve contusions are often associated with other serious life-threatening trauma, and clinicians often do not pay enough attention to optic nerve contusions, resulting in delayed treatment for most patients with optic nerve contusions.
The timing of surgery for optic canal decompression is currently controversial internationally. Although there are reports in the literature of improvement in vision after 2 weeks or even months of trauma treated with optic canal decompression, most scholars believe that the best time to operate is within 7 d of trauma.