There are reports of some cases in which the accommodative amplitude has increased. In Horner syndrome, although there is miosis of the pupil, light reflex and near reflex will be normal. Adie pupil is caused by denervation of the postganglionic parasympathetic supply to the sphincter pupillae and the ciliary muscle. Other pupillary defects that can disrupt accommodation include Gardener pupil, where there is pharmacological mydriasis, Hutchinson pupil, or Adie tonic pupil. The common causes are pinealoma, midbrain hemorrhage, or infarction. In Parinaud (dorsal midbrain) syndrome, there is upgaze palsy, accommodation paresis convergence retraction nystagmus, and light-near dissociation. Argyll-Robertson pupil, which is a known manifestation of neurosyphilis, refers to a condition in which the pupil constricts during accommodation, but not in response to light stimulus. Examples of conditions causing light near dissociation are neurosyphilis, Adie pupil, dorsal midbrain syndrome caused by pinealoma, etc. This action occurs because the midbrain center for near reflex is more ventral than the pretectal nucleus, which controls the light reflex. Interestingly, even though the same neural machinery is involved in both the accommodation reflex and the pupillary light reflex, certain conditions demonstrate a dissociation between the two pathways this is called light-near dissociation. In afferent pupillary defects as in optic nerve lesions, the pupil does not react to light reflex, but near reflex will be present. Vision is not a prerequisite for accommodation reflex.

Since parasympathetic fibers of the oculomotor nerve mediate ciliary contraction and pupillary constriction, parasympatholytics like atropine results in loss of accommodation and parasympathomimetics like pilocarpine induce accommodation. Given the synkinesis required to coordinate near vision properly, any pathology that hinders convergence, ciliary contraction, or pupillary constriction can disrupt the reflex.

Pupillary reaction test