The Origin(s)

The GSE fibres arise from the abducens nucleus near the midline of pontine tegmentum.


The Course

  • Efferent fibres arch ventrally

  • Exit at the medullopontine junction near the ventral midline

  • Lie lateral to the basilar artery, between the anterior inferior cerebellar and labyrinthine arteries.

  • Pierces the dura mater to enter cavernous sinus

  • Courses within the cavernous sinus immediately below the internal carotid artery.

  • Enters orbit through the superior orbital fissure

  • Passes through the common tendinous ring, lateral to the optic nerve.


Functional Components
  • Predominantly somatic motor (GSE)

  • Few afferent fibres from the muscle spindle



  • Distributed to the lateral rectus .



Probable cause and sites of injury

  Pontine vascular lesions (see middle alternating hemiplegia)

•  Aneurysms of the basilar artery and its branches closely associated with the nerve

•  Meningeal tumors

  Cavernous venous sinus thrombosis

•  Fracture of base of the skull

•  Aneurysms of the cavernous portion of the internal carotid artery

  Increased intra-cranial pressure



Paralysis or weakening of extra-ocular muscles is called ophthalmoplegia. Ophthalmoplegias are caused by the damage of the nerves that supply the muscles. They are classified according to which nerve is affected.


1) Oculomotor paralysis or paresis occurs following damage to the oculomotor nerve. The following features characterize it:

•  External strabismus . The affected eye is turned down and out, owing to the unopposed action of the lateral rectus and superior oblique muscles.

•  Ptosis , drooping of the upper eyelid, occurs because of paralysis of the levator palpebrae superioris muscle.

•  Dilated pupil (mydriasis) with loss of the pupillary light reflex occurs due to interruption of the parasympathetic innervation of the pupillary constrictors and unopposed action of the sympathetic innervation of the pupillary dilators.

•  Loss of accommodation reflex , due to interruption of all the necessary efferent nerves.


2) Trochlear nerve paralysis or paresis occurs following damage to the trochlear nerve. There are two main features, related to each other.

•  External strabismus , with the eye rotating up and out, is due to paralysis of the superior oblique muscle, and unopposed action of the inferior oblique muscle. Usually the patient compensates by tilting the head (the chin points away from the side of the affected eye) to avoid

  Diplopia (double vision). On examination, the patient is unable to move the affected eye downward and outward.

3) Abducens nerve paralysis or paresis , occurs following damage to the abducens nerve and affects only the lateral rectus muscle. The major defect is internal strabismus, with the eye tending to deviate toward the nose because of the unopposed action of the medial rectus. The patient is unable to fully abduct the affected eye, and may tend to rotate the head towards the affected side to avoid diplopia. Some limited lateral movement of the eye is noted, because both the superior and inferior oblique muscles have a minor abductive component

Central Ophthalmoplegias

  • These are ophthalmoplegias due to damage to the brain stem structures that control eye movements.

  • Damage to some of the brain stem areas, nuclei gaze centres, and superior colliculus often affects both eyes because the structures are close to the midline.

  • Damage to the superior colliculus, among other symptoms, interferes with the vertical gaze centre. A loss of conjugate upward movement of the eyes takes place.

  • Damage to the PPRF may produce an associated loss of lateral conjugate gaze movements.

  • Similarly, damage to the MLF between the abducens nuclei in the pons and the trochlear and oculomotor nuclei in the midbrain alters the lateral gaze response, and leads to a complex nystagmus due to the interruption of many of the vestibulo-oculomotor fibres