[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.

[3][4] At the apex of the petrous part of the temporal bone, it makes a sharp turn forward to enter the cavernous sinus.

[citation needed] Partial damage to the abducens nerve causes weak or incomplete abduction of the affected eye.

For example, fractures of the petrous temporal bone can selectively damage the nerve, as can aneurysms of the intracavernous carotid artery.

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.

Complete interruption of the peripheral sixth nerve causes diplopia (double vision), due to the unopposed action of the medial rectus muscle.

Other processes that can damage the sixth nerve include strokes (infarctions), demyelination, infections (e.g. meningitis), cavernous sinus diseases and various neuropathies.

Neurological signs are described as "false localizing" if they reflect dysfunction distant or remote from the expected anatomical location of pathology.

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.

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.