Abducens Nerve

Abducens Nerve

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Abducens nerve palsy can be caused by any structural pathology which leads to downwards pressure on the brainstem (e.g. space-occupying lesion). This can stretch the nerve from its origin at the junction of the pons and medulla.

Clinical features of abducens nerve palsy include diplopia, the affected eye resting in adduction (due to unopposed activity of the medial rectus), and inability to abduct the eye. The patient may attempt to compensate by rotating their head to allow the eye to look sideways.

At the tip of petrous temporal bone, the abducens nerve leaves Dorello's canal and enters the cavernous sinus (a dural venous sinus). It travels through the cavernous sinus and enters the bony orbit via the superior orbital fissure.

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 abducens nucleus is located in the pons, on the floor of the fourth ventricle, at the level of the facial colliculus. Axons from the facial nerve loop around the abducens nucleus, creating a slight bulge (the facial colliculus) that is visible on the dorsal surface of the floor of the fourth ventricle. The abducens nucleus is close to the midline, like the other motor nuclei that control eye movements (the oculomotor and trochlear nuclei).[citation needed]

Motor axons leaving the abducens nucleus run ventrally and caudally through the pons. They pass lateral to the corticospinal tract (which runs longitudinally through the pons at this level) before exiting the brainstem at the pontomedullary junction.[citation needed]

The abducens nerve emerges from the brainstem at the junction of the pons and the medulla,[1] superior to the medullary pyramid,[2] and medial to the facial nerve. It runs upwards and forwards from this position to reach the eye.

The nerve enters the subarachnoid space (more precisely, the pontine cistern[2]) when it emerges from the brainstem. It runs upward between the pons and the clivus, and then pierces the dura mater to run between the dura and the skull through Dorello's canal.[3][4] At the apex of the petrous part of the temporal bone, it makes a sharp turn forward to enter the cavernous sinus.[1] In the cavernous sinus, it runs anterior-ward alongside (inferolateral to) the internal carotid artery. It enters the orbit through (medial end of) the superior orbital fissure, passing through the common tendinous ring to reach and innervate the lateral rectus muscle of the eye.[2]

Damage to the peripheral part of the abducens nerve will cause double vision (diplopia), due to the unopposed muscle tone of the medial rectus muscle. The affected eye is pulled to look towards the midline. In order to see without double vision, patients will rotate their heads so that both eyes are toward the temple.[citation needed] Partial damage to the abducens nerve causes weak or incomplete abduction of the affected eye. The diplopia is worse on attempts at looking laterally.

The long course of the abducens nerve between the brainstem and the eye makes it vulnerable to injury at many levels. For example, fractures of the petrous temporal bone can selectively damage the nerve, as can aneurysms of the intracavernous carotid artery. Mass lesions that push the brainstem downward can damage the nerve by stretching it between the point where it emerges from the pons and the point where it hooks over the petrous temporal bone.

The central anatomy of the sixth nerve predicts (correctly) that infarcts affecting the dorsal pons at the level of the abducens nucleus can also affect the facial nerve, producing an ipsilateral facial palsy together with a lateral rectus palsy. The anatomy also predicts (correctly) that infarcts involving the ventral pons can affect the sixth nerve and the corticospinal tract simultaneously, producing a lateral rectus palsy associated with a contralateral hemiparesis. These rare syndromes are of interest primarily as useful summaries of the anatomy of the brainstem.

Indirect damage to the sixth nerve can be caused by any process (brain tumor, hydrocephalus, pseudotumor cerebri, hemorrhage, edema) that exerts downward pressure on the brainstem, causing the nerve to stretch along the clivus. This type of traction injury can affect either side first. A right-sided brain tumor can produce either a right-sided or a left-sided sixth nerve palsy as an initial sign. Thus a right-sided sixth nerve palsy does not necessarily imply a right-sided cause. Sixth nerve palsies are infamous as \"false localizing signs.\" Neurological signs are described as \"false localizing\" if they reflect dysfunction distant or remote from the expected anatomical location of pathology. Isolated sixth nerve palsies in children are assumed to be due to brain tumors until proven otherwise.

Damage to the abducens nucleus does not produce an isolated sixth nerve palsy, but rather a horizontal gaze palsy that affects both eyes simultaneously. The abducens nucleus contains two types of cells: motor neurons that control the lateral rectus muscle on the same side, and interneurons that cross the midline and connect to the contralateral oculomotor nucleus (which controls the medial rectus muscle of the opposite eye). In normal vision, lateral movement of one eye (lateral rectus muscle) is precisely coupled to medial movement of the other eye (medial rectus muscle), so that both eyes remain fixed on the same object.

The control of conjugate gaze is mediated in the brainstem by the medial longitudinal fasciculus (MLF), a nerve tract that connects the three extraocular motor nuclei (abducens, trochlear and oculomotor) into a single functional unit. Lesions of the abducens nucleus and the MLF produce observable sixth nerve problems, most notably internuclear ophthalmoplegia (INO).

The sixth nerve is one of the final common pathways for numerous cortical systems that control eye movement in general. Cortical control of eye movement (saccades, smooth pursuit, accommodation) involves conjugate gaze, not unilateral eye movement.

\"Abducens\" is more common in recent literature, while \"abducent\" predominates in the older literature. The United States National Library of Medicine uses \"abducens nerve\" in its Medical Subject Heading (MeSH) vocabulary to index the vast MEDLINE and PubMed biomedical databases. The 39th edition of Gray's Anatomy (2005) also prefers \"abducens nerve.\"[1]

The abducens nerve controls the movement of a single muscle, the lateral rectus muscle of the eye. In most other mammals it also innervates the musculus retractor bulbi, which can retract the eye for protection. Homologous abducens nerves are found in all vertebrates except lampreys and hagfishes.

The abducens nerve, also known as cranial nerve VI, is responsible for ipsilateral eye abduction. Visualizing the anatomy of the nerve allows for better appreciation of the causes of abducens nerve palsy. This activity illustrates the anatomy of the abducens nerve, details diagnostic considerations, and reviews treatment options. This activity underscores the interprofessional team's role in the diagnosis and management of patients with this condition.

Objectives:Describe the observable ocular deficits typically present in abducens nerve palsy.Explain how the workup for abducens nerve palsy varies according to its presentation.Identify additional diagnoses that should be considered in patients with abducens nerve palsy. Explain how collaboration amongst interprofessional team members can help inform the diagnosis and management of abducens nerve palsy, leading to better patient outcomes.Access free multiple choice questions on this topic.

The sixth cranial nerve, the abducens nerve, is responsible for ipsilateral eye abduction. Dysfunction of the abducens nerve can occur at any point of its transit from the pons to the lateral rectus muscle, resulting in sixth nerve palsy. To understand the causes of abducens nerve palsy, one must have a good grasp of the anatomy of the nerve as it transverses the brain. The abducens nerve begins in the pons near the seventh cranial nerve before exiting the brainstem. At this point, it travels into the subarachnoid space and moves along the skull at the clivus. It then travels to the basal skull at the petrous apex of the temporal bone, where it enters the cavernous sinus. In the cavernous sinus, the internal carotid will be located medially as compared to the abducens nerve. The trigeminal nerve will be found just laterally in the cavernous sinus. The abducens nerve then enters the orbit via the superior orbital fissure and innervates the lateral rectus muscle, resulting in eye abduction.[1][2][3]

As discussed above, the determining etiology of abducens nerve palsy requires knowledge of the nerve path. Neoplasm and trauma may affect the abducens nerve at any point along its path and cause a resulting palsy. Other causes are best broken down by the location of the abducens nerve.[4][5][6]

Nuclear and fascicular causes include etiologies that affect the pons directly, including ischemic stroke and metabolic diseases such as Wernicke disease. Demyelinating lesions may also affect this portion of the nerve. These nuclear causes may be associated with facial nerve palsies, secondary to the proximity of the two cranial nerves in the pons. 781b155fdc