Introduction

The accommodation reflex is the visual response for focusing on near objects. It also has the name of the accommodation-convergence reflex or the near reflex.[1][2] It is synkinesis which consists of the convergence of both eyes, contraction of the ciliary muscle resulting in a change of lens shape (accommodation), and pupillary constriction. Coordination of these three events changes the power of the eye, allowing the point of focus of the eye change from a distant object to a nearby object or vice versa.[3] Like the pupillary light reflex, the afferent limb of the reflex is through the optic nerve, and the efferent limb involves the Edinger Westphal nucleus and the oculomotor nerve. The supranuclear control over near reflex is different from that for light reflex. It includes cortical areas surrounding visual cortex and frontal eye fields. The midbrain center for near reflex is located more ventrally than that for the light reflex. 

Issues of Concern

Given the synkinesis required to coordinate near vision properly, any pathology that hinders convergence, ciliary contraction, or pupillary constriction can disrupt the 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.

Vision is not a prerequisite for accommodation reflex. In afferent pupillary defects as in optic nerve lesions, the pupil does not react to light reflex, but near reflex will be present. 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.[4] This action occurs because the midbrain center for near reflex is more ventral than the pretectal nucleus, which controls the light reflex. Examples of conditions causing light near dissociation are neurosyphilis, Adie pupil, dorsal midbrain syndrome caused by pinealoma, etc. Argyll-Robertson pupil, which is a known manifestation of neurosyphilis,[5] refers to a condition in which the pupil constricts during accommodation, but not in response to light stimulus. In Parinaud (dorsal midbrain) syndrome, there is upgaze palsy, accommodation paresis convergence retraction nystagmus, and light-near dissociation. The common causes are pinealoma, midbrain hemorrhage, or infarction.

Other pupillary defects that can disrupt accommodation include Gardener pupil,[6] where there is pharmacological mydriasis, Hutchinson pupil,[7] or Adie tonic pupil.[8] Adie pupil is caused by denervation of the postganglionic parasympathetic supply to the sphincter pupillae and the ciliary muscle.

In Horner syndrome, although there is miosis of the pupil, light reflex and near reflex will be normal. There are reports of some cases in which the accommodative amplitude has increased.[9] Accommodative amplitude refers to the change in the eye’s refractive power as the result of accommodation. Moreover, any disruption of the medial recti, either unilateral or bilateral, will alter accommodation as the medial rectus is the extraocular muscle most important to the convergence of the eyes.

As part of normal aging, there is a gradual loss of accommodation termed presbyopia, which refers to the hardening of the lens expected with age, with decreased ciliary muscular tension, that contributes to the loss of accommodation[10]. The near point of accommodation (NPA) is the nearest point on which the eyes can maintain a clear focus. Accommodation amplitude decreases with age, and the near point of accommodation recedes. For example, at the age of 20 years, the near point of accommodation is approximately 10 cm, and by the age of 50 years, it has receded to approximately 50 cm.[11][12]

Recently, dry eye has been linked to accommodative microfluctuations as well,[13] further emphasizing the vast pathologies that can impair the accommodation reflex. The effects of exercise have also been a topic of investigation as it can induce lag of the accommodation reflex.[14]

Cellular Level

On a cellular level, the accommodation reflex relies on neural signaling to conduct both afferent and efferent pathways. Impulses are carried along the fibers of the optic nerve, through projections of the cortex, and ultimately to the oculomotor and Edinger-Westphal nuclei. Moreover, the retinal neurons involved in the transmission of vision rely on phototransduction, which has a complex cellular mechanism.

Current understanding of accommodation has its basis in the capsular theory of accommodation or Helmholtz hypothesis. With accommodative effort, there is the contraction of the ciliary muscle, releasing the tension on zonules, that  “fatten” the lens, increasing the central thickness and optical power, aiding in near vision.[15] Schachar proposes that the mechanism of change in lens shape is by the equatorial zonules, whereas the anterior and posterior zonules function as passive components in determining the optical power of the lens.

Development

As with any other component of the eye, the important contributions of neural crest, homeobox genes, and growth factors are key to the development of the accommodation reflex. While neuroectoderm contributes to the retina and optic nerve required of accommodation, it is neural crest cells that compose connective tissue of the orbit and the ciliary ganglion. The lens itself is a derivative of surface ectoderm. Unlike the structures mentioned above, the extraocular muscles are derivatives of mesodermal tissue.

Organ Systems Involved

As already mentioned, the accommodation reflex involves several different components of the central and peripheral nervous system. Unlike the pupillary light reflex, this requires the participation of visual association cortex and the cerebellum in addition to the parasympathetic nervous system.[3][16]

The stimulus for accommodation reflex is either an 'out of focus' or blurred retinal image or conscious visual fixation on a near object. A The afferent limb of the reflex involves optic nerve, optic chiasm, optic tract, the lateral geniculate nucleus of the thalamus and the visual cortex including the primary visual and visual association areas in the occipital lobe.

The efferent limb includes the Edinger Westphal nucleus and the oculomotor neurons. The Edinger Westphal nucleus in the midbrain is the parasympathetic preganglionic nucleus. It sends its axons through the oculomotor nerve to the ciliary ganglion and short ciliary nerve to control the pupil sphincter, ciliary muscles of the eye. The efferent fibers from the medial rectus subnucleus of the oculomotor complex innervate the medial rectus muscles, resulting in the convergence of the eyes.

Function

The function of the accommodation reflex is to coordinate visual attention to near objects. Proper convergence prevents diplopia. Constriction of the pupil increases the depth of field.

Mechanism

Light from the environment is brought to focus on the retina by the combined optical power of the cornea and the lens.

The mechanism of accommodation reflex involves three responses:

• The convergence of both eyes is such that the near object is in focus, which aids in image projection on the fovea. This action involves contraction of the medial rectus muscles of both eyes, with the relaxation of lateral recti resulting in the adduction of both the eyes.
• Constriction of the sphincter pupillae muscles, pupils constrict, which improves the depth of focus. The divergent rays from distant objects scatter off the periphery of the cornea, and hence they do not fall on the fovea.
• Contraction of bilateral ciliary muscles results in thickening of the lens, which shortens the focal length, which increases its refractive power (measured in diopters).

The afferent pathway begins with the transmission of the signal from the optic nerve to the primary visual cortex. This path involves phototransduction in the retina, thalamic interneurons in the lateral geniculate nucleus, and finally arrival at the visual cortex using optic radiations. From the visual cortex, the reflex initiates, and impulses get sent to the visual association cortex that in turn has projections to the superior colliculus and pretectal areas. From here, impulses swiftly relay to the oculomotor and Edinger-Westphal nuclei of cranial nerve III. The oculomotor nucleus stimulates contraction of the medial recti bilaterally, which results in convergence. Simultaneously the Edinger-Westphal nucleus coordinates parasympathetic pupillary constriction via the ciliary ganglion. The same general pathway is responsible for lens thickening, except that instead of arriving at the pupillary sphincter muscles, the short ciliary nerves from the ciliary ganglion terminate at the ciliary muscles and are responsible for muscle contraction. As the ciliary muscles contract, the suspensory zonules of the lens relax and release the tension of the lens. Thus, somewhat paradoxically, it is the contraction of the ciliary muscles that allows the lens to form a more spherical shape that facilitates accommodation.

Accommodative convergence is the convergence induced by accommodation as part of the near reflex. For each diopter of accommodation, there is an increase in convergence, the measurement of which is in prism diopters. The normal value is 3 to 5  prism diopters. Abnormalities of this ratio play an essential role in the etiology of strabismus and binocular vision problems. 

Related Testing

Examiners frequently check the accommodation reflex during a neurological exam by having the patient focus on a small target like the examiner's fingertip or a pen. The examiner asks the patient to focus on the target used for testing at a distance, and then gradually bring the finger within a few centimeters between the patient's eyes. Look for convergence of eyes and constriction of the pupils.

Clinical Significance

Dysfunction of the accommodation reflex can be physiological like in aging and presbyopia, pathological or pharmacological. Accommodation deficits can occur in neurological conditions like supranuclear lesions, encephalitis, pineal tumors, or in neuromuscular disorders like myasthenia gravis.[17] It can also occur in systemic conditions like in children after a viral illness, as well as a result of primary ocular conditions like glaucoma or cataract. It is best to consider the clinical context through a review of the three events that comprise the reflex.

Convergence

Damage to the medial rectus muscle itself can disrupt convergence. Moreover, a cortical or brainstem lesion can impair the neural machinery required to coordinate ocular convergence. Disorders of vergence can be due to organic causes or can be functional. It can be congenital, presenting with strabismus in childhood.

Near reflex insufficiency is a disorder of vergence; it can be mild paresis or complete paralysis. There is convergence or accommodation insufficiency. Mydriasis may present on attempted near fixation. For paresis, treatment involves reading glasses, or base in prisms.[18]

Convergence insufficiency can occur in individuals with the increased use of near work, like in school-age children. It can occur as idiopathic or following viral illness.[19][20] Spasm of the near reflex is a functional condition, associated with diplopia, blurred vision, and headaches. Near reflex triad occurs even when the patient is not focusing on a near object. It affects mostly females. Convergent squint (esotropia) with miosis and pseudo myopia is a presenting feature.[21]

Pupillary Constriction

Similarly, a disruption of the parasympathetic pathway can dysregulate the coordination of pupillary constriction.

Lens Accommodation

The most frequently encountered loss of accommodation is from presbyopia.[22] Symptoms include difficulty in near vision, blurred vision or double vision for near objects, and eye fatigue or headache. It is correctable with convex lenses for near vision. Moreover, any disruption to lens integrity or the ciliary body as in conditions like cataract or glaucoma can also cause accommodation reflex insufficiency.