Cranial nerve VI, also known as the abducens nerve, innervates the ipsilateral lateral rectus (LR), which functions to abduct the ipsilateral eye. The sixth cranial nerve has a long subarachnoid course. The sixth nerve nucleus is located in the pons, just ventral to the floor of the fourth ventricle and just lateral to the medial longitudinal fasciculus (MLF). About 40% of its neurons project into the ipsilateral MLF only to cross over to the contralateral side and ascend to innervate that contralateral medial rectus subnucleus to participate in contralateral eye adduction. [1, 2, 3]
Patients usually present with binocular horizontal diplopia (double vision producing a side-by-side image with both eyes open), worse in the distance, and esotropia in primary gaze. Patients also may present with a head-turn to maintain binocularity and binocular fusion and to minimize diplopia.
Congenital sixth nerve palsy (Duane syndrome) is a well-recognized entity in pediatric ophthalmology, but not common. Examination for a sixth nerve palsy involves documenting the presence or absence of papilledema, examining the ocular motility, evaluating the eyelids and pupils, and excluding involvement of other cranial nerves (eg, V, VII, VIII). Checking deep tendon reflexes (DTRs) and motor function to exclude corticospinal tract involvement may be important. MRI is indicated for any brainstem findings to exclude pontine glioma in children (most have papilledema and nystagmus without other cranial nerve involvement) and in adults who show no improvement.
In young adults, a lumbar puncture (LP) for cerebrospinal fluid (CSF) analysis is completed to exclude meningitis in patients who have no history of diabetes or hypertension and who have a head CT scan negative for other pathology. Elderly patients should have blood testing for an erythrocyte sedimentation rate (ESR) and/or a C-reactive protein to screen for giant cell arteritis (temporal arteritis). Poor or no resolution of sixth nerve palsy should prompt a full neurologic evaluation.
Only the ipsilateral lateral rectus that is solely innervated by the involved peripheral sixth cranial nerve is affected; therefore, only deviations in the horizontal plane are produced. In isolated cases of peripheral nerve lesions, no vertical or torsional deviations are present. Central nervous system lesions of the abducens nerve tract are localized easily secondary to the typical findings associated with each kind of lesion. Damage to the sixth nerve nucleus results in an ipsilateral gaze palsy. The lack of a contralateral adduction defect makes it easy to differentiate a nuclear lesion from a fascicular or nonnuclear lesion. 
Abducens palsy can be a false localizing sign with lesions that cause increased intracranial pressure and stretching of the sixth nerve as it ascends the clival area.
Abducens nerve palsy is frequently seen as a postviral syndrome in younger patients and as an ischemic mononeuropathy in the adult population.
Sixth nerve palsies fall into the following categories: 3%-30% trauma, 0%-6% aneurysm, 0%-36% ischemic, 8%-30% idiopathic, and 10%-30% demyelination/miscellaneous.
The sixth cranial nerve is the most commonly affected of the ocular motor nerves. In children, it is the second most common after the fourth nerve, with an incidence of 2.5 cases per 100,000 in the population.
A young patient should have an aggressive workup because of the greater likelihood of a neoplasm causing the palsy. Patients older than 55 years with isolated sixth nerve palsies may require a less aggressive initial workup if they have predisposing microvascular ischemic risk factors, but no history of cancer.
Cranial nerve VI palsy can occur in all age groups; however, the etiology varies depending on the age group.