|Innervates||Superior oblique muscle|
|Anatomical terms of neuroanatomy|
The trochlear nerve ( // ), also known as the fourth cranial nerve, cranial nerve IV, or CN IV, is a cranial nerve that innervates just one muscle: the superior oblique muscle of the eye, which operates through the pulley-like trochlea. CN IV is a motor nerve only (a somatic efferent nerve), unlike most other CNs.
The trochlear nerve is unique among the cranial nerves in several respects:
Homologous trochlear nerves are found in all jawed vertebrates. The unique features of the trochlear nerve, including its dorsal exit from the brainstem and its contralateral innervation, are seen in the primitive brains of sharks.
The human trochlear nerve is derived from the basal plate of the embryonic midbrain. The words trochlea and trochlear ( // , // ) come from Ancient Greek τροχιλέα trokhiléa, “pulley; block-and-tackle equipment”.
The trochlear nerve emerges from the back (dorsal) brainstem,just below the inferior colliculus. It circles from behind around the brainstem and runs forward toward the eye in the subarachnoid space. It passes between the posterior cerebral artery and the superior cerebellar artery, and then pierces the dura just under free margin of the tentorium cerebelli, close to the crossing of the attached margin of the tentorium and within millimeters of the posterior clinoid process. It runs on the outer wall of the cavernous sinus. Finally, it enters the orbit through the superior orbital fissure and supplies the superior oblique muscle.
The nucleus of the trochlear nerve is located in the caudal mesencephalon beneath the cerebral aqueduct. It is immediately below the nucleus of the oculomotor nerve (III) in the rostral mesencephalon.
The trochlear nucleus is unique in that its axons run dorsally and cross the midline before emerging from the brainstem posteriorly. Thus a lesion of the trochlear nucleus affects the contralateral eye. Lesions of all other cranial nuclei affect the ipsilateral side.
The trochlear nerve provides motor supply to the superior oblique muscle of the eye,The trochlear nerve carries axons of type GSE, general somatic efferent, which innervate skeletal muscle of the superior oblique muscle.
The superior oblique muscle ends in a tendon that passes through a fibrous loop, the trochlea, located anteriorly on the medial aspect of the orbit. Trochlea means “pulley” in Latin; the fourth nerve is named after this structure.
In order to understand the actions of the superior oblique muscle, it is useful to imagine the eyeball as a sphere that is constrained—like the trackball of a computer mouse—in such a way that only certain rotational movements are possible. Allowable movements for the superior oblique are (1) rotation in a vertical plane—looking down and up (depression and elevation of the eyeball) and (2) rotation in the plane of the face (intorsion and extorsion of the eyeball).
The body of the superior oblique muscle is located behind the eyeball, but the tendon (which is redirected by the trochlea) approaches the eyeball from the front. The tendon attaches to the top (superior aspect) of the eyeball at an angle of 51 degrees with respect to the primary position of the eye (looking straight forward). The force of the tendon's pull therefore has two components: a forward component that tends to pull the eyeball downward (depression), and a medial component that tends to rotate the top of the eyeball toward the nose (intorsion).
The relative strength of these two forces depends on which way the eye is looking. When the eye is adducted (looking toward the nose), the force of depression increases. When the eye is abducted (looking away from the nose), the force of intorsion increases, while the force of depression decreases. When the eye is in the primary position (looking straight ahead), contraction of the superior oblique produces depression and intorsion in roughly equal amounts.
To summarize, the actions of the superior oblique muscle are (1) depression of the eyeball, especially when the eye is adducted; and (2) intorsion of the eyeball, especially when the eye is abducted. The clinical consequences of weakness in the superior oblique (caused, for example, by fourth nerve palsies) are discussed below.
This summary of the superior oblique muscle describes its most important functions. However, it is an oversimplification of the actual situation. For example, the tendon of the superior oblique inserts behind the equator of the eyeball in the frontal plane, so contraction of the muscle also tends to abduct the eyeball (turn it outward). In fact, each of the six extraocular muscles exerts rotational forces in all three planes (elevation-depression, adduction-abduction, intorsion-extorsion) to varying degrees, depending on which way the eye is looking. The relative forces change every time the eyeball moves—every time the direction of gaze changes. The central control of this process, which involves the continuous, precise adjustment of forces on twelve different tendons in order to point both eyes in exactly the same direction, is truly remarkable.
The recent discovery of soft tissue pulleys in the orbit—similar to the trochlea, but anatomically more subtle and previously missed—has completely changed and greatly simplified our understanding of the actions of the extraocular muscles. [ further explanation needed ]Perhaps the most important finding is that a two-dimensional representation of the visual field is sufficient for most purposes.
Injury to the trochlear nerve cause weakness of downward eye movement with consequent vertical diplopia (double vision). The affected eye drifts upward relative to the normal eye, due to the unopposed actions of the remaining extraocular muscles. The patient sees two visual fields (one from each eye), separated vertically. To compensate for this, patients learn to tilt the head forward (tuck the chin in) in order to bring the fields back together—to fuse the two images into a single visual field. This accounts for the “dejected” appearance of patients with “pathetic nerve” palsies.
Trochlear nerve palsy also affects torsion (rotation of the eyeball in the plane of the face). Torsion is a normal response to tilting the head sideways. The eyes automatically rotate in an equal and opposite direction, so that the orientation of the environment remains unchanged—vertical things remain vertical.
Weakness of intorsion results in torsional diplopia, in which two different visual fields, tilted with respect to each other, are seen at the same time. To compensate for this, patients with trochlear nerve palsies tilt their heads to the opposite side, in order to fuse the two images into a single visual field.
The characteristic appearance of patients with fourth nerve palsies (head tilted to one side, chin tucked in) suggests the diagnosis, but other causes must be ruled out. For example, torticollis can produce a similar appearance.
The clinical syndromes can originate from both peripheral and central lesions.
A peripheral lesion is damage to the bundle of nerves, in contrast to a central lesion, which is damage to the trochlear nucleus. Acute symptoms are probably a result of trauma or disease, while chronic symptoms probably are congenital.
The most common cause of acute fourth nerve palsy is head trauma.Even relatively minor trauma can transiently stretch the fourth nerve (by transiently displacing the brainstem relative to the posterior clinoid process). Patients with minor damage to the fourth nerve will complain of “blurry” vision. Patients with more extensive damage will notice frank diplopia and rotational (torsional) disturbances of the visual fields. The usual clinical course is complete recovery within weeks to months.
Isolated injury to the fourth nerve can be caused by any process that stretches or compresses the nerve. A generalized increase in intracranial pressure—hydrocephalus, pseudotumor cerebri, hemorrhage, edema—will affect the fourth nerve, but the abducens nerve (VI) is usually affected first (producing horizontal diplopia, not vertical diplopia). Infections (meningitis, herpes zoster), demyelination (multiple sclerosis), diabetic neuropathy and cavernous sinus disease can affect the fourth nerve, as can orbital tumors and Tolosa–Hunt syndrome. In general, these diseases affect other cranial nerves as well. Isolated damage to the fourth nerve is uncommon in these settings.
The most common cause of chronic fourth nerve palsy is a congenital defect, in which the development of the fourth nerve (or its nucleus) is abnormal or incomplete. Congenital defects may be noticed in childhood, but minor defects may not become evident until adult life, when compensatory mechanisms begin to fail. Congenital fourth nerve palsies are amenable to surgical treatment.
Central damage is damage to the trochlear nucleus. It affects the contralateral eye. The nuclei of other cranial nerves generally affect ipsilateral structures (for example, the optic nerves - cranial nerves II - innervate both eyes).
The trochlear nucleus and its axons within the brainstem can be damaged by infarctions, hemorrhage, arteriovenous malformations, tumors and demyelination. Collateral damage to other structures will usually dominate the clinical picture.
The fourth nerve is one of the final common pathways for cortical systems that control eye movement in general. Cortical control of eye movement (saccades, smooth pursuit, accommodation) involves conjugate gaze, not unilateral eye movement.
The trochlear nerve is tested by examining the action of its muscle, the superior oblique. When acting on its own this muscle depresses and abducts the eyeball. However, movements of the eye by the extraocular muscles are synergistic (working together). Therefore, the trochlear nerve is tested by asking the patient to look 'down and in' as the contribution of the superior oblique is greatest in this motion. Common activities requiring this type of convergent gaze are reading the newspaper and walking down stairs. Diplopia associated with these activities may be the initial symptom of a fourth nerve palsy.
Alfred Bielschowsky's head tilt test is a test for palsy of the superior oblique muscle caused by damage to cranial nerve IV (trochlear nerve).
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Cranial nerves are the nerves that emerge directly from the brain, of which there are conventionally considered twelve pairs. Cranial nerves relay information between the brain and parts of the body, primarily to and from regions of the head and neck, including the special senses of vision, taste, smell, and hearing.
The optic nerve, also known as the second cranial nerve, cranial nerve II, or simply CN II, is a paired cranial nerve that transmits visual information from the retina to the brain. In humans, the optic nerve is derived from optic stalks during the seventh week of development and is composed of retinal ganglion cell axons and glial cells; it extends from the optic disc to the optic chiasma and continues as the optic tract to the lateral geniculate nucleus, pretectal nuclei, and superior colliculus.
The abducens nerve or abducent nerve, also known as the sixth cranial nerve, cranial nerve VI, or simply CN VI, is a cranial nerve in humans and various other animals that controls the movement of the lateral rectus muscle, one of the extraocular muscles responsible for outward gaze. It is a somatic efferent nerve.
The oculomotor nerve, also known as the third cranial nerve, cranial nerve III, or simply CN III, is a cranial nerve that enters the orbit through the superior orbital fissure and innervates extraocular muscles that enable most movements of the eye and that raise the eyelid. The nerve also contains fibers that innervate the intrinsic eye muscles that enable pupillary constriction and accommodation. The oculomotor nerve is derived from the basal plate of the embryonic midbrain. Cranial nerves IV and VI also participate in control of eye movement.
The superior oblique muscle, or obliquus oculi superior, is a fusiform muscle originating in the upper, medial side of the orbit which abducts, depresses and internally rotates the eye. It is the only extraocular muscle innervated by the trochlear nerve.
Eye movement includes the voluntary or involuntary movement of the eyes, helping in acquiring, fixating and tracking visual stimuli. A special type of eye movement, rapid eye movement, occurs during REM sleep.
The lateral rectus muscle is a muscle on the lateral side of the eye in the orbit. It is one of six extraocular muscles that control the movements of the eye. The lateral rectus muscle is responsible for lateral movement of the eyeball, specifically abduction. Abduction describes the movement of the eye away from the midline, allowing the eyeball to move horizontally in the lateral direction, bringing the pupil away from the midline of the body.
The extraocular muscles, are the seven extrinsic muscles of the human eye. Six of the extraocular muscles, the four recti muscles, and the superior and inferior oblique muscles, control movement of the eye and the other muscle, the levator palpebrae superioris, controls eyelid elevation. The actions of the six muscles responsible for eye movement depend on the position of the eye at the time of muscle contraction.
Ophthalmoparesis refers to weakness (-paresis) or paralysis (-plegia) of one or more extraocular muscles which are responsible for eye movements. It is a physical finding in certain neurologic, ophthalmologic, and endocrine disease.
Sixth nerve palsy, or abducens nerve palsy, is a disorder associated with dysfunction of cranial nerve VI, which is responsible for causing contraction of the lateral rectus muscle to abduct the eye. The inability of an eye to turn outward, results in a convergent strabismus or esotropia of which the primary symptom is diplopia in which the two images appear side-by-side. Thus, the diplopia is horizontal and worse in the distance. Diplopia is also increased on looking to the affected side and is partly caused by overaction of the medial rectus on the unaffected side as it tries to provide the extra innervation to the affected lateral rectus. These two muscles are synergists or "yoke muscles" as both attempt to move the eye over to the left or right. The condition is commonly unilateral but can also occur bilaterally.
Congenital fourth nerve palsy is a condition present at birth characterized by a vertical misalignment of the eyes due to a weakness or paralysis of the superior oblique muscle.
Trochleitis is inflammation of the superior oblique tendon trochlea apparatus characterized by localized swelling, tenderness, and severe pain. This condition is an uncommon but treatable cause of periorbital pain. The trochlea is a ring-like apparatus of cartilage through which passes the tendon of the superior oblique muscle. It is located in the superior nasal orbit and functions as a pulley for the superior oblique muscle. Inflammation of the trochlear region leads to a painful syndrome with swelling and exquisite point tenderness in the upper medial rim of the orbit. A vicious cycle may ensue such that inflammation causes swelling and fraying of the tendon which then increases the friction of passing through the trochlea which in turn adds to the inflammation. Trochleitis has also been associated with triggering or worsening of migraine attacks in patients with pre-existing migraines.
Hypertropia is a condition of misalignment of the eyes (strabismus), whereby the visual axis of one eye is higher than the fellow fixating eye. Hypotropia is the similar condition, focus being on the eye with the visual axis lower than the fellow fixating eye. Dissociated vertical deviation is a special type of hypertropia leading to slow upward drift of one or rarely both eyes, usually when the patient is inattentive.
The trochlea of superior oblique is a pulley-like structure in the eye. The tendon of the superior oblique muscle passes through it. Situated on the superior nasal aspect of the frontal bone, it is the only cartilage found in the normal orbit. The word trochlea comes from the Greek word for pulley.
The Harada–Ito procedure is an eye muscle operation designed to improve the excyclotorsion experienced by some patients with cranial nerve IV palsy. In this procedure, the superior oblique tendon is split, and the anterior fibers – the fibers most responsible for incyclotorsion – are moved anteriorly and laterally. This selectively stretches and tightens these fibers, enhancing the incyclotorsion power of the superior oblique.
Fourth cranial nerve palsy or trochlear nerve palsy, is a condition affecting cranial nerve 4 (IV), the trochlear nerve, which is one of the cranial nerves. It causes weakness or paralysis of the superior oblique muscle that it innervates. This condition often causes vertical or near vertical double vision as the weakened muscle prevents the eyes from moving in the same direction together.
Oculomotor nerve palsy or oculomotor neuropathy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Damage to this nerve will result in an inability to move the eye normally. The nerve also supplies the upper eyelid muscle and is accompanied by parasympathetic fibers innervating the muscles responsible for pupil constriction. The limitations of eye movement resulting from the condition are generally so severe that patients are often unable to maintain normal eye alignment when gazing straight ahead, leading to strabismus and, as a consequence, double vision (diplopia).
Alternating hemiplegia is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Weber's syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. Some common symptoms of alternating hemiplegia are mental impairment, gait and balance difficulties, excessive sweating and changes in body temperature.
The Parks–Bielschowsky three-step test, also known as Park's three-step test or Bielschowsky head tilt test, is a method used to isolate the paretic extraocular muscle, particularly superior oblique muscle and trochlear nerve, in acquired vertical double vision. It was originally described by Marshall M. Parks.
In neuroanatomy, corticomesencephalic tract is a descending nerve tract that originates in the frontal eye field and terminate in the midbrain. Its fibers mediate conjugate eye movement.