Diplopia is typically experienced by adults with VI nerve palsies, but children with the condition may not experience diplopia due to suppression. The neuroplasticity present in childhood allows the child to switch off the information coming from one eye (in this case the esotropic eye), thus relieving any diplopic symptoms. Whilst this is a positive adaptation in the short term, in the long term it can lead to a lack of appropriate development of the visual cortex giving rise to permanent visual loss in the suppressed eye; a condition known as amblyopia or Lazy eye. Cause
Because the nerve emerges near the bottom of the brain, it is often the first nerve compressed when there is any rise in intracranial pressure. Different presentations of the condition, or associations with other conditions, can help to localize the site of the lesion along the VIth cranial nerve pathway. The most common causes of VIth nerve palsy in adults are:

More common: Vasculopathic (diabetes, hypertension, atherosclerosis), trauma, idiopathic. Less common: Increased intracranial pressure, giant cell arteritis, cavernous sinus mass (e.g. meningioma, Brain stem Glioblastoma aneurysm, metastasis), multiple sclerosis, sarcoidosis/vasculitis, postmyelography, lumbar puncture, stroke (usually not isolated), Chiari Malformation, hydrocephalus, intracranial hypertension, tuberculosis meningitis.In children, Harley reports typical causes as traumatic, neoplastic (most commonly brainstem glioma), as well as idiopathic. Sixth nerve palsy causes the eyes to deviate inward (see: Pathophysiology of strabismus). Vallee et al. report that benign and rapidly recovering isolated VIth nerve palsy can occur in childhood, sometimes precipitated by ear, nose and throat infections.
Pathophysiology
The pathophysiological mechanism of sixth nerve palsy with increased intracranial pressure has traditionally been said to be stretching of the nerve in its long intracranial course, or compression against the petrous ligament or the ridge of the petrous temporal bone. Collier, however, was "unable to accept this explanation", his view being that since the sixth nerve emerges straight forward from the brain stem, whereas other cranial nerves emerge obliquely or transversely, it is more liable to the mechanical effects of backward brain stem displacement by intracranial space occupying lesions. Brainstem
Isolated lesions of the VI nerve nucleus will not give rise to an isolated VIth nerve palsy because paramedian pontine reticular formation fibers pass through the nucleus to the opposite IIIrd nerve nucleus. Thus, a nuclear lesion will give rise to an ipsilateral gaze palsy. In addition, fibers of the seventh cranial nerve wrap around the VIth nerve nucleus, and, if this is also affected, a VIth nerve palsy with ipsilateral facial palsy will result. In Millard–Gubler syndrome, a unilateral softening of the brain tissue arising from obstruction of the blood vessels of the pons involving  sixth and seventh cranial nerves and the corticospinal tract, the VIth nerve palsy and ipsilateral facial paresis occur with a contralateral hemiparesis. Fovilles syndrome can also arise as a result of brainstem lesions which affect Vth, VIth and VIIth cranial nerves.