Post-concussion syndrome (PCS) is a general term for a series of symptoms and signs that occur following traumatic brain injury (TBI). It develops when an external impact causes direct or indirect damage to the brain.
Epidemiologically, traumatic brain injury occurs in all age groups. In the United States, nonfatal traumatic brain injury results in approximately 235,000 hospitalizations and about 1.1 million emergency department visits annually (2018 estimate). Falls are the most common cause in children, while traffic accidents are most common in young adults. It is reported that 60–70% of patients with nonfatal traumatic brain injury complain of PCS-related visual symptoms.
Risk factors include age (75 years or older, under 4 years, 15–24 years), substance abuse, cognitive impairment/mental illness, low socioeconomic status, and participation in contact sports.
QWhat percentage of people experience visual symptoms after a concussion?
A
It is reported that 60–70% of patients with non-fatal traumatic brain injury complain of PCS-related visual symptoms. In adolescents seen at specialized clinics, oculomotor disorders have been reported in as many as 88% (Gowrisankaran 2021). Visual symptoms occur in both mild traumatic brain injury (concussion) and severe traumatic brain injury, but the type and severity vary depending on the extent of the injury.
When neck injury is also present, symptoms such as near vision difficulty due to accommodative dysfunction (2–3 months after injury), convergence insufficiency with mild myopia, dizziness and headache due to vertebrobasilar insufficiency, and eye strain may appear.
Optic atrophy: May occur secondary to papilledema due to increased intracranial pressure (postpapilledema optic atrophy).
Visual field defects: Homonymous hemianopsia and cortical visual loss. Occipital lobe lesions may present with homonymous hemianopsia without other neurological symptoms.
Oculomotor nerve palsy: Palsies of the oculomotor, trochlear, and abducens nerves. Trochlear nerve palsy is often bilateral in traumatic cases, with excyclotorsion of 10 degrees or more. Nystagmus may also occur.
Findings in Mild Traumatic Brain Injury (Concussion)
Saccadic dysfunction (SD): Decreased accuracy of eye movements. Since more than half of the brain’s pathways are involved in vision and eye movement control, abnormalities frequently appear even after mild trauma (Debacker 2018).
Other dysfunctions: These include a wide range of impairments such as color vision, stereopsis, pupillary function (miosis, delayed pupillary dilation), smooth pursuit eye movements, vestibulo-ocular reflex, and reading ability.
When cervical injury is also present, Horner syndrome (miosis, delayed pupillary dilation, mild ptosis, narrowing of the palpebral fissure) due to cervical sympathetic nerve damage may be observed.
QWhat is the most common visual impairment after concussion?
A
The most common visual impairments after mild traumatic brain injury (concussion) are convergence insufficiency (CI), accommodative insufficiency (AI), and saccadic dysfunction (SD). These cause reading difficulties and blurred vision. Details are explained along with rehabilitation methods in the “Standard Treatment” section.
The basic mechanism of traumatic brain injury is acceleration-deceleration injury. When an external force is applied to the skull, a rapid change in velocity occurs, causing the brain to move within the skull and collide with the cranial wall. The severity of injury ranges from mild (concussion) to severe (diffuse axonal injury).
The mechanism of traumatic optic neuropathy involves indirect force from a strong blow to the forehead (especially the brow area) acting on the optic canal, causing vasogenic edema within the optic nerve parenchyma. A characteristic feature is that it does not necessarily involve a fracture of the optic canal.
Neuroimaging may reveal extracranial lesions such as epidural hematoma or subarachnoid hemorrhage, or intraparenchymal hemorrhage, but in PCS, imaging findings are often normal.
Visual acuity test: Unilateral visual impairment suggests retinal to optic nerve disease. Lesions posterior to the optic chiasm cause bilateral visual impairment.
Color vision test: Optic nerve diseases tend to present with red-green color vision abnormalities. Color vision abnormalities are often observed even when visual acuity is preserved.
Visual field test: Central scotoma indicates papillomacular bundle damage, while homonymous hemianopia indicates lesions from the optic tract to the occipital lobe. The pattern of visual field defects can help estimate the lesion location.
Swinging flashlight test: Most important for diagnosing optic nerve disorders. Detects RAPD (Marcus-Gunn pupil). A weak light, such as from a penlight, provides higher detection sensitivity.
CT/MRI imaging is used to search for intracranial lesions. Fractures, hemorrhage, hematoma, and contusion after head trauma can be detected by CT. Occipital lobe lesions cause homonymous visual field defects and papilledema; if no other cranial nerve symptoms are present, chronic subdural hematoma should be suspected.
Differential diagnoses include myasthenia gravis (Tensilon test, diurnal variation), thyroid eye disease (extraocular muscle thickening), and Fisher syndrome (anti-GQ1b antibody), which need to be excluded.
Vision rehabilitation is the cornerstone of PCS treatment. It is performed through a combination of outpatient visits and home exercises, and is used together with other rehabilitation such as vestibular rehabilitation. Reports indicate that among CI cases who completed vision therapy, 85% were successful and 15% improved, while among AI cases, 33% were successful and 67% improved (Gallaway 2017). Comprehensive evaluation and management methods are summarized in the American Academy of Pediatrics clinical report (Master 2022).
Saccade and Pursuit Training
Hart Chart: Saccade training using a letter chart.
Thumb Rotations: Following the thumb while moving it at a constant speed.
Rotating pegboard: Gaze tracking training on a rotating board.
Sanet Vision Integrator: Visual integration training using electronic devices.
Vestibular Rehabilitation
Balance and head movement training: Perform balance training involving head movements.
Vestibulo-ocular reflex stimulation: Training to coordinate head movements and eye movements. Aimed at improving dizziness and balance disorders.
Symptomatic Treatment
Light-blocking lenses and tinted lenses: Prescribed for photophobia.
Prescription of reading glasses: Prescribed for near vision impairment after symptoms stabilize.
Vitamin preparations, etc.: Used as symptomatic treatment for cases with cervical spine injury.
Early diagnosis within 24 to 48 hours after injury significantly affects prognosis. Treatment includes steroid pulse therapy (prednisone equivalent 1,000 mg) for 2 to 3 days, or high-dose steroids (prednisolone equivalent 80 to 100 mg) combined with hyperosmotic agents (glycerol, D-mannitol 300 to 500 mL) for 3 to 7 days.
Cases where light perception loss does not recover quickly after injury are less responsive to treatment.
There is much controversy regarding the indications for optic canal decompression, and some believe that surgical efficacy is limited except in cases with marked deformity or bone fragment displacement of the optic canal.
Prism glasses prescription: Effective for mild strabismus (up to approximately 10 prism diopters).
Extraocular muscle surgery: Considered when prisms do not improve symptoms.
QWhat specific training does visual rehabilitation involve?
A
Saccade and pursuit training (Hart Chart, thumb rotation, rotary pegboard, Sanet Vision Integrator) is performed in combination at outpatient visits and at home. It is fundamentally combined with vestibular rehabilitation (balance and head movement exercises). For photophobia, tinted lenses are prescribed; for near vision impairment, reading glasses are prescribed after symptoms stabilize. Systematic reviews have reported improvements in fixation, saccades, convergence, and accommodation with computer-based training conducted 2–5 times per week for 3–10 weeks (Watabe 2019).
The basic mechanism of traumatic brain injury is acceleration-deceleration injury. External force to the skull causes a rapid change in velocity, moving the brain within the skull and colliding with the cranial wall. It forms a continuous spectrum from mild (concussion) to severe (diffuse axonal injury).
In traumatic optic neuropathy, a blow to the lateral brow transmits indirect force to the optic canal. Vasogenic edema within the optic nerve parenchyma (corresponding to cerebral white matter) is the main cause; direct damage to optic nerve fibers by hematoma or bone fragments is less common. Bilateral involvement suggests chiasmal injury.
The anatomical course of each nerve is directly linked to its vulnerability during trauma.
Trochlear nerve: It emerges from the dorsal midbrain, decussates immediately, and runs a long distance. When external force presses the dorsal midbrain against the tentorial edge, bilateral trochlear nerve palsy occurs. In trauma, bilateral involvement is common, and outward rotation deviation of 10 degrees or more is characteristic.
Abducens nerve: It emerges from the ventral pons, ascends along the clivus, and passes through the cavernous sinus and superior orbital fissure to reach the lateral rectus muscle. Due to its long intracranial course, it is easily damaged by trauma. It can be affected bilaterally during increased intracranial pressure.
In neck injury, Horner syndrome occurs due to damage to the cervical sympathetic nerve. Vertebrobasilar insufficiency causes dizziness and headache. Traumatic Horner syndrome is classified as a second-order neuron disorder (lower type palsy of cervical nerve root avulsion).
The visual pathway begins at the retinal ganglion cells and passes through the optic nerve (1 to 1.2 million nerve fibers), optic chiasm, optic tract, lateral geniculate body, and optic radiation to reach the primary visual cortex. Damage at different sites produces characteristic visual field defect patterns, allowing estimation of the lesion location from visual field findings. For occipital lobe lesions, CT/MRI evaluation is essential. If homonymous visual field defects or papilledema are present without other cranial nerve symptoms, chronic subdural hematoma should be suspected.
QWhy is the trochlear nerve easily damaged in head trauma?
A
The trochlear nerve has the anatomical feature of emerging from the dorsal midbrain, immediately decussating, and traveling a long intracranial course. Strong external force can press the dorsal midbrain against the tentorial edge, causing injury. Therefore, traumatic trochlear nerve palsy is often bilateral and characteristically shows more than 10 degrees of excyclotorsion.
Master CL, Scheiman M, Gallaway M, et al. Vision Diagnoses Are Common After Concussion in Adolescents. Clin Pediatr (Phila). 2016;55(3):260-267. PMID: 26156977
Gallaway M, Scheiman M, Mitchell GL. Vision Therapy for Post-Concussion Vision Disorders. Optom Vis Sci. 2017;94(1):68-73. PMID: 27505624
Watabe T, Suzuki H, Abe M, Sasaki S, Nagashima J, Kawate N. Systematic review of visual rehabilitation interventions for oculomotor deficits in patients with brain injury. Brain Inj. 2019;33(13-14):1592-1596. PMID: 31455098
Gowrisankaran S, Shah AS, Roberts TL, et al. Association between post-concussion symptoms and oculomotor deficits among adolescents. Brain Inj. 2021;35(10):1218-1227. PMID: 34383619
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