Traumatic Motor Neuropathies (Third, Fourth, Sixth)
Trauma to cranial nerve (CN) III (oculomotor nerve), CN IV (trochlear nerve) or CN VI (abducens nerve) can result in ocular motility dysfunction or pupillomotor dysfunction. These ocular motor cranial neuropathies can be isolated, meaning they affect only one nerve, or can be associated with other CN palsies, meaning multiple cranial neuropathies.
Population studies in Olmstead County have reported the incidences of each of these CN palsies. CN III palsy had an incidence of 4.0 per 100,000 persons per year, CN IV palsy had an incidence of 5.7 per 100,000 persons per year, and CN VI palsy had an incidence rate of 11.3 per 100,000 persons each year. These incidences may be reflected differently among different populations. CN III palsy is more common above the age of 60 years, and is rare in the pediatric population. CN IV and CN VI palsies are more common among men.
CN III originates in the ventral midbrain at the level of the superior colliculus. After exiting the midbrain medially to the cerebral peduncles, CN III splits into two branches in the superior orbital fissure: the superior division and the inferior division. The superior branch is responsible for the innervation of the superior rectus muscle and the levator palpebrae superioris muscle. The inferior branch of CN III innervates the inferior oblique, the inferior rectus, and the medial rectus. CN III has two main layers: the inner somatic layer and the outer parasympathetic layer. The inner somatic layer supplies input to the extraocular muscles, while the outer parasympathetic layers innervate the sphincter pupillae and ciliary muscles, responsible for the pupillary light reflex and accommodation. The parasympathetic innervation originates from the Edinger Westphal nucleus of the midbrain.
Cranial Nerve IV
CN IV originates from the nucleus within the dorsal midbrain at the level of the inferior colliculus. The fascicles first travel posteriorly and inferiorly around the cerebral aqueduct to decussate upon their exit of the dorsal midbrain. These two nerve fascicles then wrap around the brainstem, each maintaining their contralateral sides and extending around the lateral brainstem to continue anteriorly. CN IV enters the cavernous sinus where a few sympathetic fibers contribute to the nerve fascicle. It then pierces into the cavernous sinus dura and follows CN III to enter the orbits at the superior orbital fissure. The superior orbital fissure is a common pathway for all three ocular motor CNs, and as such, all three nerves are susceptible traumatic shearing forces at this location. CN IV is responsible for innervating the superior oblique muscle. CN IV has the longest intracranial length of any of the CNs, and is also the thinnest, increasing its vulnerability in the setting of trauma.
Cranial Nerve VI
CN IV nucleus is located at the level of the facial colliculus in the dorsal pons. Unlike the CN III and CN IV, it is exclusively somatic, with no contributions from the autonomic nervous system and with no sensory function. CN VI nucleus contains motorneurons for the ipsilateral lateral rectus muscle, as well as interneurons to relay signals to the contralateral medial rectus muscle. Approximately 40% of the fascicles course through the medial longitudinal fasciculus towards the contralateral medial rectus subnucleus. These fascicles then continue to innervate the medial rectus muscle. The remainders of the axons from the abducens nucleus exit at the pontomedullary junction of the brainstem and travel superiorly and anteriorly in the subarachnoid space close to the base of the skull and the anterior inferior cerebellar artery. As such, in the setting of traumatic basal skull fractures, CN VI is at risk of damage. It then travels towards the upper clivus anchored to a fibrous sheath called Dorello Canal. CN VI is vulnerable to stretching due to this configuration. CN VI then follows the CN III and CN IV into the cavernous sinus before entering the orbit through the superior orbital fissure to its final destination, the lateral rectus muscle. CN VI has the second-longest length of any CN.
CN III has two main layers: the inner somatic layer and the outer parasympathetic layer. The inner somatic layer innervates its respective extraocular muscles, while the outer parasympathetic layers innervate the sphincter pupillae and ciliary muscles responsible for the pupillary light reflex and accommodation. Similar to aneurysms, uncal herniation, or compressive tumors, trauma to CN III usually causes damage the outermost portion of the nerve first. On the other hand, non-compressive causes of CN III palsy, such as microvascular lesions to the vasa nervorum which supply the deeper somatic fibers, are usually related to diabetes mellitus and/or hypertension. These lesions are less likely to affect the parasympathetic fibers (sometimes referred to as pupil-sparing CN III palsies) but will instead result in oculomotor palsies involving the extraocular muscles and levator palpebrae superioris muscle. For more details on all types of lesions affecting CN III, please visit the oculomotor nerve palsy Eye Wiki article.
Lesions of CN III can occur at any point along its trajectory, but in the setting of trauma, CN III palsies occur mainly at the level of the basilar or intraorbital segments of the nerve. In the basilar region, both epidural or subdural hematomas secondary to head trauma can cause damage to the nerve due to mass effect when the hematomas cause intracranial hypertension and subsequent uncal herniation. Uncal herniation results in a tentorial pressure cone and compression of the oculomotor nerve as it passes over the tentorial edge. In the intraorbital region, trauma and tumors are the main causes of injury.
Aberrant regeneration of CN III fibers, also referred to as oculomotor synkinesis, can occur when axons are transected after an acute traumatic or compressive incident. It is thought that regenerating axons are misdirected, resulting in irregular muscle activation. The incidence of aberrant regeneration in traumatic CN III palsy is approximately 15%.
CN IV palsies, when acquired in adulthood, are mostly due to trauma or microvascular disease. CN IV is the most vulnerable to trauma of all the CNs, due to its long course and thin, fragile configuration. Even mild injuries to the head may cause traumatic CN IV palsy, in contrast with CN III and CN VI nerve palsies that usually require a stronger force of impact. As a result, it is more common to see isolated CN IV palsies than isolated CN III or CN VI palsies in the setting of trauma. CN IV palsies with traumatic etiologies often present bilaterally due to the decussation of the nerve fascicles upon their exit in the dorsal midbrain.
Cranial Nerve VI
Basal skull fractures can result in unilateral or bilateral CN VI palsy, as the basilar part of CN VI passes close to the base of the skull. Changes in intracranial pressure (ICP) can also cause a CN VI palsy due to stretching of the nerve at the level of Dorello canal.
The general pathology related to traumatic CN palsies is not fully understood as there has been a poor correlation between trauma imaging results and specific cranial nerve palsies. For the ocular motor CNs, there are three main proposed locations of injury: at the level of the nuclei at the brainstem,  at the nerve’s exit of the brainstem,  and at the location in which the nerves pierce the dura.
The biggest risk factors for head injuries in older adults, which may cause ocular motor CN palsies, include polypharmacy (notably the use of antiarrhythmics) and environmental safety conditions (such as stair safety). Risk factors for neonates include instrumental techniques for delivery, such as forceps delivery. Children under the age of one are most at risk for severe head trauma. High-contact sports are also more associated with traumatic head injuries.
Various preventative strategies can be used to prevent head trauma in adults, such as implementing fall prevention strategies for older adults, wearing helmets when appropriate, and practicing vehicle safety (such as wearing a seat belt and never driving under the influence of drugs or alcohol). In the pediatric population, additional safety measures can be implemented to keep the home safe, such as installing stair safety gates in the home.
In cases of head trauma, it is important to assess the mechanism and severity of the injury, including loss of consciousness, vomiting or nausea, amnesia, and Glasgow coma scale score (please refer to the Canadian Head CT rules). Ophthalmic history and ocular symptoms can also provide important clues to help locate the injury: pain, blurry vision, diplopia, decreased visual field, swelling, tearing, and nystagmus. When patients with injury to CNs III, IV, and VI have diplopia, it is important to characterize the diplopia in terms of onset and duration, monocular or binocular, and vertical/horizontal/oblique displacement of the images.
- Visual acuity
- Pupil examination including evaluation for anisocoria and for a relative afferent pupillary defect (RAPD)
- Intraocular pressure (IOP)
- Visual fields
- Extraocular motility
- Strabismus testing: Options include cover and uncover test, prism alternating cover test, and Maddox rod testing; +/- double Maddox rod testing to evaluate for torsion
- Forced duction testing to distinguish restrictive vs paretic strabismus
- Margin to reflex distance of the palperbral margins (ptosis assessment)
- Hertel exophthalmometry (evaluation for proptosis or enophthalmos)
- Periorbital examination (edema, bone deformity, erythema, tenderness, wound entry or foreign body, eyelid laceration)
- Complete ocular examination with funduscopy to assess for: wound entry or foreign body, chemosis, subconjunctival hemorrhage, corneal abrasion, iritis, hyphema, depth of the anterior chamber, traumatic cataract, optic disc edema.
- Caveat: If there is concern for a third nerve palsy and/or if the patient's pupil status is being monitoring in a Neuro ICU setting, consider deferring dilation
- Resistance to orbital retropulsion
- Evaluation of corneal sensation (CN V function)
|CN III palsy||CN VI palsy||CN VI palsy|
Traumatic injuries can result in aberrant regeneration of CN III:
|Diagnosis can be made via the Parks-Bielschowsky three-step test. Please refer to Cranial Nerve 4 Palsy
CN III palsy:
- Binocular oblique diplopia (may not be noticed by patient if ptosis is complete)
CN IV palsy:
- Binocular vertical or oblique diplopia
- Patient may report difficulty with reading or difficulty with going down stairs
- Objects can seem tilted
CN VI palsy:
- Binocular horizontal diplopia worse when looking to the ipsilateral side involved and in distance vision
The choice of head computed tomography (CT) after trauma should be based on Canadian Head CT rules. Neuroimaging should be performed in case of involvement of more than one CN. If a cervical spine injury is suspected, perform a cervical spine CT. In case of a skull base fracture, perform a head CT.
CN III palsy: Orbital CT (coronal views) to rule out orbital fracture. CT head to evaluate for hemorrhage.
CN IV palsy: Head CT should be obtained for initial evaluation. Some studies report midbrain or cisternal concussion. Brain magnetic resonance imaging (MRI) may be useful if the CT scan is normal. Some studies report lesions in the dorsal midbrain that were not visualized in the CT scans.
*CN IV palsy can be associated with low-intermediate head injury. In most cases, neuroimaging is unremarkable.
Other imaging modalities may be indicated to rule out associated injuries, such as orbital fracture (orbital CT and midface CT) and intraorbital foreign body (CT, MRI [no MRI if metallic foreign body suspected] or B-scan). In the case of a CN III or VI palsy with unremarkable CT head and/or in the setting of minimal trauma, strongly consider MRI (and noninvasive angiography in the setting of CN III palsy) for evaluation for alternative etiologies.
Accompanying traumatic injuries
Orbital fracture: Orbital fracture is most commonly associated with a CN III palsy, but can also be seen with CN IV or VI palsies. The fracture can compress or dissect the orbital portion of the CN. The orbital floor is the most common site, the second most common being the medial wall .
Symptoms: binocular diplopia, pain on eye movement (e.g., pain in upward gaze if fracture of the orbital floor), oculo-cardiac reflex (nausea, vomiting, bradycardia) indicating muscle entrapment.
Signs: edema and tenderness, enophthalmos, subcutaneous emphysema, hypoesthesia in the territory of the involved nerve (e.g., infraorbital or supraorbital nerve), positive forced-duction test, increased IOP more than 4mm Hg in the direction of limited movement
In the case of an orbital floor fracture and involvement of infraorbital nerve, patients may complain of hypoesthesia of the cheek and upper lip. If the supraorbital nerve is involved in the case of an orbital roof fracture, the patient may complain of hypoesthesia of the forehead and ptosis. In a zygomatic fracture, patients can report trismus, malar flattening and deformity.
*For patients with orbital fracture not complaining of any visual symptoms, ophthalmic evaluation may be done within 48h.
See https://eyewiki.org/White-Eyed_Blow_Out_Fracture for more information.
*Always have a high index of suspicion of foreign body in all trauma (especially children)
See https://eyewiki.aao.org/Orbital_Foreign_Body for more information.
An extraocular muscle rupture is uncommon and can be seen in penetrating trauma or blow-out fracture. The rupture can be surgically repaired, but if the eye does not regain its motility, nerve damage should be considered as the etiology of diplopia.
Uncal herniation: Uncal or transtentorial herniation can result in a CN III palsy by directly compressing the nerve between the temporal lobe and the tentorium. It can cause contralateral or/and ipsilateral CN III palsy (in case of Kernohan’s notch). Patients with uncal herniation could present with Cushing triad (bradycardia, abnormal breathing pattern, widened pulse pressure), altered mental status and other signs and symptoms of intracranial hypertension, contralateral homonymous hemianopia and absence of blinking reflex and contralateral hemiparesis (“false localizing signs”).
For an in-depth review of the uncal herniation, please visit: http://www.ncbi.nlm.nih.gov/books/NBK537108/.
Cervical spine fracture: Some traumatic injuries of the cervical spine can cause CN VI palsy by several mechanisms, i.e., whiplash injury, hangman’s fracture, and halo traction. Several case reports describe traumatic CN VI traction after a C2 distraction and a C1 ligamentous injury.
Patients can suffer from whiplash trauma and complain of tenderness to palpation, motor and sensory deficits (paraplegia, quadriplegia), restriction of neck motility. According to the localization of the fracture, phrenic nerve palsy (above C5) and Horner syndrome (C8 to T1 injury) can also be observed. For an in-depth review of the cervical spine fracture, please visit: http://www.ncbi.nlm.nih.gov/books/NBK448129/
Basilar skull fracture can cause CN VI palsy. Signs of skull base fracture included racoon eyes sign, Battle sign, CSF leak (rhinorrhea, otorrhea) and hemotympanum. For an in-depth review of the basilar skull fracture, please visit: http://www.ncbi.nlm.nih.gov/books/NBK470175/
Orbital floor fracture with muscle entrapment: ocular motor CN palsy can be distinguished from muscle entrapment in orbital fracture with the forced-duction test (negative for a palsy, positive for entrapment). Note that the force generation testing is abnormal in an ocular motor CN palsy.
Orbital edema and hemorrhage: Post-traumatic orbital edema and hemorrhage can cause limitation in movement of the extraocular muscles. However this should resolve within 7 to 10 days. Retrobulbar hemorrhage can also cause limited EOM.
Although there are no clear guidelines for the management of traumatic ocular motor CN palsies according to current evidence, a few concepts remain constant regardless of which nerve is affected. First, any identified underlying cause should be addressed. In case of trauma, that means treating any intracranial condition such as a subdural hematoma or intracranial hypertension as a priority. Once an intracranial lesion has been excluded, the mainstay of traumatic motor neuropathy management is observation +/- monocular occlusion for comfort and safety initially, with follow-up thereafter.
Spontaneous resolution rates are variable among studies. For example, Park UC et al. defined the meaning of a complete recovery, partial recovery, and persistence in a retrospective study on the natural history of acquired CN III, CN IV and CN VI palsy. They reported partial recovery rate of nearly 100% at 6-months. In comparison, Park H et al. reported a 47.5% spontaneous recovery of traumatic unilateral CN IV palsy.
Regardless of these variations, certain characteristics at presentation seem to influence the prognosis of recovery. The angle of deviation at initial presentation is a significant prognostic factor for recovery, with the smallest angles of deviation having the best prognosis. Coello AF et al. reported that a CN III palsy after a mild head trauma had a good chance to recover if no lesion was identified from the initial CT scan. For traumatic unilateral CN IV palsy, Park H et al. reported that the angle of deviation and fundus torsion are better predictive factors for spontaneous resolution than the factors related to trauma type, presence of intracranial lesion, loss of consciousness, or Glasgow Coma Scale score.
Monocular occlusion with a patch, Bangerter occlusion foil, or gift wrapping tape may be considered in all patients with symptomatic double vision. Fresnel prisms can be a temporary option during the period of potential progressive resolution. This option is especially useful when the angle of deviation is small. Correction of a less than 10 prism diopter (PD) is generally successful, though some patients may tolerate larger amount of prismatic correction with a Fresnel.
Follow-up treatment with occlusion and prisms should continue at regular intervals until the ocular motor CN palsy resolves or stabilizes. Maximal spontaneous improvement is typically achieved within 6-9 months after the traumatic event, regardless of the ocular motor CN involved.
Once the deviation has become stable after adequate follow-up time, long-term management can be considered for residual symptomatic double vision. Prism and/or botulinum toxin injection can be offered as alternatives to surgery. Prismatic correction can be incorporated into spectacles.
Botulinum toxin injection is a treatment option to manage diplopia. By blocking the release of acetylcholine at the motor endplates of neuromuscular junctions, botulinum toxin prevents muscle contraction, thus causing a temporary paralysis of the extraocular muscle injected. This allows the opposing muscles to align the eye by taking on a greater force movement. This intervention is rarely curative, but it can temporarily alleviate diplopia and compensatory anomalous head posture in some cases. In the case of CN VI palsy, the injection is made into the ipsilateral medial rectus muscle under topical anesthesia and possibly with electromyographic guidance. Preventing contracture of the medial rectus in the affected eye might be another advantage of botulinum toxin injection. It can also be used to diminish the angle of deviation and ease correction with prisms. However, a Cochrane review rated the effectiveness of botulinum toxin injection as low, Injection of botulinum toxin into the inferior oblique muscle to treat an acute traumatic CN IV palsy and into the lateral rectus muscle to treat an acute traumatic CN III palsy have also been described. Although the results from the clinical trials of small samples have shown potential benefits of these procedures, their clinical use seems to be limited due to their possible complications.  Once the injection is done, the effect will gradually increase until it reaches its maximum 1–2 weeks after the procedure. The effect is temporary and is expected to dissipate within 3 months. The injections will therefore have to be repeated every 3-4 months indefinitely or until the next step of management (e.g., surgery).
Strabismus surgery aims to relieve diplopia by restoring binocularity and alleviating normal head positioning, if present. CN III palsy is difficult to treat surgically due to the involvement of several extraocular muscles. Several techniques have been described. The presence of ptosis can also be addressed surgically at this stage of management. Surgery is frequently required for traumatic CN IV palsy. The surgical indications include deviation greater than 10 PD and unsuccessful prism treatment. Different surgical options are possible: strengthening of the superior oblique muscle (tuck procedure), myectomy or recession of ipsilateral inferior oblique muscle, and/or recession of the contralateral inferior rectus muscle. The magnitude of the deviation will guide the choice of procedure. Excyclotorsion may also need to be corrected, mostly with bilateral CN IV palsy. For CN VI palsy, surgical intervention also depends on the severity of the palsy. In case of partial paralysis, a lateral rectus resection and medial rectus recession in one eye or bilateral medial rectus recessions can be considered. A combination of weakening of the ipsilateral medial rectus and transposition of the superior and inferior recti above and below the affected lateral rectus muscle can be used to treat a complete CN IV palsy.
For more information on strabismus surgery, please refer to these EyeWiki articles:
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