Cranial nerves examination: Trochlear & abducens nerves
Ocular mobility is an important feature of the eyes that help individuals collect as much visual input as possible. Movement of the eyes is carried out by the six extraocular muscles. They allow the eyes to move in the two principal planes and also about the visual axis.
The nerve supply of these muscles is provided by three cranial nerves – namely the oculomotor (CN III), trochlear (CN IV), and abducens (CN VI)nerves. While the oculomotor nerve supplies most of the extraocular muscles, the trochlear and abducens nerves each supply their own muscle.
|Embryology||Basal plate; somatic efferent column|
|Type of Nerve||Pure motor (general somatic efferent)|
Trochlear CN IV – periaqueductal grey matter
Abducens CN VI – inferodorsal pons
Trochlear CN IV – Superior oblique muscle
Abducens CN VI – Lateral rectus muscle
|Trochlear CN IV Disorders||
Congenital trochlear CN IV palsy
Acquired trochlear CN IV palsy
|Abducens CN VI Disorders||Acquired abducens CN VI palsy|
The bulk of the article will address the clinical examination of the trochlear and abducens nerves. However, for a complete discussion, a review of the anatomy and a discussion of the pathological processes associated with these nerves will also be included.
- Review of trochlear and abducens nerve anatomy
- Clinical examination
- Clinical relations
Review of trochlear and abducens nerve anatomy
Both nerves are basal plate derivatives arising from the somatic efferent column at their respective locations. As such, they are purely motor nerves, which means they deliver general somatic efferent impulses to their respective target muscles.
The trochlear nerve (CN IV) is a paired cranial nerve that is responsible for innervating the superior oblique muscle. As a result, it causes the eyeball to move downward and inward. The nucleus of CN IV is located in the periaqueductal grey matter of the inferior part of the midbrain. The emerging fibers decussate beneath the superior medullary velum prior to emerging from the posterior surface of the brainstem. Another interesting point is that CN IV has the longest intracranial course of all the cranial nerves. These two facts are two prominent distinguishing features of this cranial nerve.
|Type||General somatic efferent nerve (motor)|
|Nucleus||Periaqueductal grey matter of the midbrain|
|Field of innervation||Superior oblique muscle|
After leaving the brainstem, CN IV enters the superior cistern. It turns laterally, then anteriorly as it wraps around the cerebral peduncles. It travels anterosuperiorly toward the middle cranial fossa, where it enters the lateral wall of the cavernous sinus. Within the sinus, CN IV is inferiorly related to the oculomotor nerve (CN III) and superiorly related to the ophthalmic division of the trigeminal nerve (CN V1). It emerges from the cavernous sinus through the superior orbital fissure. Subsequently, it passes lateral to the common tendinous ring (also called the common annular tendon and the annulus of Zinn) and continues superiorly, where it pierces and innervates the superior oblique muscle.
The abducens nerve (CN VI) is also a paired cranial nerve whose fibers innervate the lateral rectus muscle (another extraocular muscle). Therefore the abducens nerve function is to move the eyeball laterally on the horizontal plane. The nuclei can be found in the inferodorsal aspect of the pons, beneath the facial colliculus of the fourth ventricle.
|Type||General somatic efferent (motor)|
|Nucleus||Inferior and dorsal aspect of the pons|
|Field of innervation||Lateral rectus muscle|
The nucleus is partially encircled by the genu of the facial nerve (CN VII). The fibers arising from the nucleus of CN VI travel anteroinferiorly toward the pontomedullary junction. They leave the parenchyma of the brainstem at this point; medially related to the fibers of CN VII and vestibulocochlear nerve (CN VIII), superiorly related to the medullary pyramids, and inferiorly related to the basilar groove.
The nerve enters the pontine cistern and ascends the clivus. It then passes through Dorello’s canal, before entering the middle of the cavernous sinus. Within the cavernous sinus, CN VI travels alongside the horizontal segment of the cavernous part of the internal carotid artery. It also picks up some sympathetic fibers that were originally associated with the artery for a short part of its journey. The nerve then leaves the cavernous sinus via the superior orbital fissure and enters the common tendinous ring. It eventually innervates the lateral rectus muscle by piercing the medial surface of the organ.
Vision is one of the most prized senses that most living organisms have. Visual disturbances may be caused by a problem along any part of the visual pathway. This could be ranging from a problem within the eye that disrupts the path of light (retinal detachment, cataracts, vitreous hemorrhages) or a problem in positioning the eyes to allow light to enter the eyeball (extraocular muscle weakness).
|Introduction & Informed Consent||
Outline the steps involved in the examination
Helps to build rapport and reduce patient anxiety
Check for strabismus
Evidence of nystagmus
|Assess Eye Movement||
Assess for diplopia in a neutral position and with movement
Burying the white
Assess brainstem function
Can be suppressed by voluntary cortical activity
|Cover-Uncover Test||Detects subtle strabismus|
A muscle palsy refers to weakness of a muscle. The words paresis or paretic are also sometimes used to describe a muscle that is weaker than normal. The trochlear (CN IV) and abducens (CN VI) nerves innervate the extraocular muscles that are responsible for positioning the eyeballs. The positioning ensures that the eyes can focus on a visual target. The examination techniques below can help to identify problems with either of these nerves that may result in visual disturbances.
Examination of CN IV and CN VI are rarely done in isolation. This is usually because the symptoms of CN IV or CN VI palsies can be caused by disorders of other extraocular muscles or their associated nerves. Therefore they are carried out as either part of a cranial nerve examination or specific examination of the eyes where other nerves are tested as well.
This discussion will focus on the steps involved in assessing the extraocular muscles, as the other elements of the examination (i.e. visual acuity, visual field testing, visual reflexes, and fundoscopy) are described with the respective cranial nerve examination. A proper introduction and informed consent are required before beginning the examination. Ask the patient to sit up if possible. The practitioner should then sit directly in front of the patient at a distance of roughly 1 yard (1 meter).
Inspection of the primary position
Start by observing the patient’s behavior. Patients with extraocular palsies often tilt their heads to refocus the target image and correct the diplopia (visualization of the same object in two spatially separate locations; which is just a fancy way to say double vision).
Look for evidence of nystagmus, which is an involuntary, rapid, repetitive movement of the eyes that affects visual acuity. In other words, the eyes will appear to be “dancing”. Nystagmus can occur in the horizontal, vertical, and oblique planes. In some cases, nystagmus is a physiological response to extremes of gaze. In other cases, it can be caused by internal ear, optic nerve (CN II), vestibulocochlear nerve (CN VIII), or cerebellar dysfunction. Vitamin deficiency, as well as drug toxicity, may also precipitate nystagmus. The most commonly used test to identify nystagmus is a part of the field sobriety test. Here, police officers ask the individual in question to follow an object with their eyes only. Rapid movement of the eyes suggests that nystagmus is present. However, this test has innate errors and is not commonly used in clinical practice. Alternately, the disorder can be detected on general observation or uncovered using an optokinetic drum or electrooculography. The depth of these tests is beyond the scope of this article.
Use an (also called a pen torch) to perform the corneal reflex (Hirschberg’s) test which will help to screen patients for strabismus (crossed eye). The light is shone into the patient’s eyes as they look straight ahead. The practitioner then makes note of the position of the reflection on the cornea. In the fixating eye (the one without extraocular muscle weakness) the reflection of the light is centered. However, the deviating eye (the one with the extraocular muscle weakness) the light is not centered on the cornea. Unfortunately, the test is not foolproof. One major confounding factor is the patient’s visual acuity is higher in the paretic eye than it is in the non-paretic eye. Consequently, they will fix on the visual stimulus with the eye with better acuity. This gives a false impression that the light source is centered in the deviating eye.
Assessment of ocular movements
The examiner sits in front of – or stands to the side of – the patient as they assess the ranges of motion each eye can execute. The practitioner starts by holding their index finger vertically at about 2 feet (roughly 60 cm) away from the patient’s face. Ask the patient how many fingers they see: if there is diplopia (double vision) at rest, the patient will report seeing items in duplicates.
Keep the index finger in a vertical position and proceed to trace the letter ‘H’. Ask the patient to follow the examining finger throughout its course with their eyes only–they should keep their head fixed. Use the free hand to stabilize the patient’s head if they are having difficulty keeping their head still while following the finger. Also, ask the patient to report whether or not they are experiencing diplopia at any point as they follow the index finger.
Diplopia can occur in the vertical or horizontal planes (indicating rectus muscle paresis), in the oblique plane (indicating oblique muscle paresis), or a combination of two or more planes. Observe the eyes at the extremes of horizontal gaze. Under normal circumstances, the sclera should not be visible on the side that the patient is looking. In other words, if the patient is looking to the right, then the sclera should not be visible on the right side of the eyeball. This phenomenon is referred to as “burying the white”. During downward gaze there is a tendency of the upper eyelids to droop, therefore use two fingers to elevate the upper eyelids while the patient is gazing downwards.
If the patient experiences diplopia, proceed to cover one eye then ask if the diplopia persists. If it does continue, then the patient is afflicted by monocular diplopia, which is related to an intrinsic issue such as astigmatism. However, if it resolves, then the patient is said to have binocular diplopia. With binocular diplopia, patients “see” an outer and an inner image. The outer image corresponds to the affected eye and is a false image, while the inner image is the true image. Therefore the clinician should verify which image disappears while covering the eye during this test. The examiner can determine the affected muscle(s) by noting the position in which diplopia is worst. For example, a patient with binocular diplopia affecting the left eye notes worsening of the diplopia while looking towards the left visual field is more likely to have a left lateral rectus paresis.
The oculocephalic test aids the clinician to tell whether or not a lesion has developed in the cortex or corticobulbar tract (a supranuclear lesion) or at the level of the cranial nerves (a nuclear or brainstem lesion). It is also called the doll’s-eye test owing to the fact that the normal response should be similar to the movement of a doll’s eyes when the toy is turned from side to side.
The test is performed by placing the patient in the supine position and holding the head with each of the examiner’s hands on the side of the patient’s head. Using the thumbs, hold the patient’s eyes open and ask them to maintain focus on the examiner’s eyes. As the patient’s head is rocked from one side to the other, the eyes should move in the opposite direction.
This response is seen in healthy, awake neonates within the first week of life because they are unable to inhibit the motion with voluntary eye movement. In the healthy, awake, older individual the response can be inhibited voluntarily with normal vision. The test also helps identify the presence of brainstem function in the comatose patient. The rationale is that since the patient is in a coma, the cortical function is impaired, therefore they are unable to voluntarily override the oculocephalic response. Consequently, their eyes will move opposite to the direction in which the head is turned. If the eyes fail to respond to the oculocephalic stimulus as described above, then it can be assumed that the neural pathways of the brainstem that is responsible for this activity are defective.
Strabismus, also referred to as a squint, lazy eye, or crossed-eyes refers to malalignment of the eyeballs. Patients with this disorder may have one eye that is able to focus on an object while the other diverges from the target image. The squint can occur superiorly (hypertropia), inferiorly (hypotropia), medially (esotropia), or laterally (exotropia). Both congenital and acquired disorders of the extraocular muscles may result in strabismus.
While some individuals have prominent crossed-eyes that can be seen initially, others are subtle. To test for this disorder, ask the patient to sit upright and cover one of their eyes. The patient should then look directly at the light from the penlight. Observe the eye and note if it moves (medially, laterally, superiorly, or inferiorly) to focus. If it does, then the patient has strabismus in that eye. Cover the opposite eye and repeat the test on the other side.
Disorders of the trochlear nerve (CN IV)
Since trochlear nerve function causes abduction, intorsion, and depression of the eyeball, disorders of this nerve would result in a combination of symptoms related to double vision. While there are cases of congenital trochlear nerve palsy, there is little information available about the etiology behind it. On the other hand, acquired trochlear nerve lesion is more likely to occur from head trauma. The injury may also be unilateral or bilateral; which would change how the patient presents.
Lesions of CN IV seldom occur in isolation. It usually develops as part of another disorder such as a stroke affecting the nucleus or supranuclear aspect of the nerve. For causes of traumatic isolated trochlear nerve palsy, the offending force must be great enough to cause a loss of consciousness. Otherwise, one should have a high degree of suspicion for a non-benign lesion if a low impact force causes loss of nerve function. Demyelinating disorders (loss of myelin sheeth) such as multiple sclerosis, a mass effect from tumors, or accidental injury during medical procedures are also well-documented causes of CN IV palsies.
Patients with chronic CN IV palsy may have an underlying abnormality of the attachment of the muscle, or a dysgenetic (defective development) CN IV nucleus. In either case, the patient compensates for the defective superior oblique muscle by performing a head tilt to the side that is opposite the lesion.
The length of CN IV makes it vulnerable to coup and contrecoup forces that will compress CN IV against the tentorium cerebelli dural fold. Coup and contrecoup injuries are a type of head injury that describes the parts of the brain that are injured with respect to the point of contact. Coup describes the part of the brain that is on the same side as the object of impact, while contrecoup refers to the side of the brain on the opposite side of the point of injury. For example, if the individual strikes the forehead on an object, then the anterior pole of the brain (frontal lobe) will undergo a coup injury, while the posterior pole of the brain (the occipital lobe) can undergo a contrecoup injury.
However, a noxious insult is possible at any point along the course of the nerve. If the insult occurs at the level of the nucleus or within the brainstem, then the contralateral eye would be affected. If the injury occurs after decussation of the nerve, then the affected eye would be ipsilateral to the lesion.
Unlike patients with a chronic CN IV palsy, those who were acutely injured experience torsional, oblique, or vertical diplopia. This phenomenon arises because the eyes are no longer evenly fixed on the object so there is an illusion that there is more than one item. The presentation of vertical or torsional diplopia is related to the fact that the superior oblique muscle is no longer functional. As a result, whenever there is an attempt to move the eye downward or inward, the patient experiences diplopia. Myasthenia Gravis, oculomotor nerve (CN III) lesion, giant cell arteritis, or thyroid ophthalmopathy can also result in a similar presentation to that seen with CN IV palsies.
While there are surgical procedures in which the length of the muscle is altered in order to reposition the eye, medical treatment options to treat the underlying cause should be considered first. The surgical option may offer some relief for patients with worsening diplopia.
Disorders of the abducens nerve (CN VI)
As is the case with trochlear nerve (CN IV), the abducens nerve (CN VI) is also vulnerable to traumatic injury because of its extensive intracranial course. Patients who are unfortunate enough to suffer from an abducens nerve palsy will be unable to abduct the eye that is ipsilateral to the CN VI nucleus (and lesion). The patient will appear esotropic at rest (affected eye pulled nasally) and will complain about binocular horizontal diplopia (double vision) that is made worse by looking at objects far away.
The patient is esotropic because the action of the medial rectus muscle is unopposed. The lesion affects the horizontal gaze because the lateral rectus muscle abducts the eye on the horizontal plane. Finally, eyes usually undergo divergence in order to focus on a distant object, and convergence to focus on a nearby object. Since divergence would be facilitated by the lateral recti muscles, the patient experiences worsening diplopia under these circumstances. Unlike with CN IV, CN VI patients will not experience torsional or vertical nystagmus.
Papilledema is a sign of raised intracranial pressure–a condition that can cause compression of CN VI. A full neurological examination may also be warranted as this disorder can arise from supranuclear areas (corticobulbar tract).
Giant cell arteritis, myasthenia gravis, and thyroid ophthalmopathy are all conditions that may present like CN VI palsy. Patients who are victims of polytrauma may also suffer from a blow out fracture of the medial orbital wall. The medial rectus muscle can become entrapped, making it difficult for the lateral rectus to pull the eyeball in the opposite direction. The workup for these patients should include investigations to rule out other likely causes – erythrocyte sedimentation rate (ESR) and capsular reactive protein (C-reactive protein or CRP) to rule out an inflammatory process. Both medical and surgical options are available for treating a blow out fracture of the medial orbital wall.
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