Continuing Education Activity

Accommodative insufficiency is a condition characterized by a reduced ability to carry out near work. It occurs in as much as 10% of the population. It is the most common form of accommodative dysfunction in non-presbyopic disorders. This article describes the optics of the human eye and the principles of ametropia. The article also explains the concepts involved in a thorough differential diagnosis and managing patients with this condition. An interprofessional healthcare team approach is emphasized in helping patients with accommodative insufficiency.

Objectives:

• Describe accommodative insufficiency and explain methods of diagnosis.
• Review the risk factors for developing accommodative dysfunction.
• Explain the common physical exam findings associated with accommodative insufficiency.
• Outline the typical presentation and differential diagnosis of a patient with accommodative insufficiency.

Introduction

As an optical system, the eyes function in line with the basic principles of refraction.[1] Visual clarity depends on the ability to bring incident light rays to a point focus at the fovea centralis.[2] Schematically, the cornea and crystalline lens provide the requisite total dioptric power (about +60 diopters; the cornea makes up about + 40 to + 48 diopters).[3]

Accommodation is the adaptative faculty that enables clear vision with subjective variation in the linear distance of visual targets.[4] This is accomplished by the autonomic adjustment of crystalline lens dioptric powers to provide focus on the presented stimuli. The main stimulus is 'blur.'[5]

The focusing powers of the crystalline lens are directly proportional to the increase or decrease in lens convexity. At the near point of accommodation, the ciliary muscles contract and relax zonular tension, thus enabling increased convexity and focusing power. For the far point of accommodation, the ciliary muscles relax and exert greater tension on the zonules (of Zinn), thus reducing lenticular convexity. 

Under typical conditions, the healthy eye responds to near-point (linear) stimuli by activating the near triad, which includes accommodation, convergence, and miosis. These mechanisms are synergistically engaged to enable single, clear binocular vision.[6]

Inhibition in one of these reflexes can most likely lead to dysfunction of accommodative response. Concerning the near reflexes, accommodation and convergence are most closely intertwined. This interrelationship can be reported as the 'accommodative convergence to accommodation (AC/A)  ratio.[7] Depending on the underlying accommodative dysfunction, the ac/a ratio may be either low, normal, or high.[8]

The accommodative mechanisms can be subject to functional anomalies in maintaining visual clarity. Based on the Duke-Elder classification, these include:

• Accommodative insufficiency (AI)[9][10]
• Accommodative spasm[11]
• Accommodative inertia[12]
• Ill-sustained accommodation[13]
• Accommodative infacility[14]

AI is a functional vision anomaly characterized by the inability to sustain focus at near.[15] With this condition, the accommodative response is often suboptimal compared to expected normal ranges.[16]

Etiology

Depending upon the severity and type, errors of refraction are often characterized by intermittent or sustained periods of 'blur' resulting from a defocus of visual targets.[17] When significant (moderate to high) refractive errors are uncorrected or markedly under-corrected, an extra accommodative effort is involuntarily exerted in an attempt to clear the optical defocus.[18]

With repetitive exertion, fatigue of the ciliary muscles usually develops.[19] This, in turn, can cause an insufficient response from the accommodative faculty. Amongst the errors of refraction, hyperopic errors make up the most likely cause of AI, usually when the dioptric value of facultative hyperopia is significant (See hyperopia images).[20] At the far point of accommodation, the dioptric equivalent of accommodation is at its minimum. Individuals predisposed to near-functional visual limitations (of which hyperopes comprise a major group) are likely to present with symptoms of AI.[21]

This group of individuals at risk excludes presbyopes and those with organic causes, like autonomic degenerative diseases. These are related to other comorbid factors (such as age-related crystalline nuclear sclerosis and neurological involvement).[22]

Individuals with visual tasks that require prolonged and repetitive stimulation at the near point of accommodation can often develop symptoms of chronic fatigue consistent with AI.[11] These may include school-age children, office desk workers, high-precision artisans, etc.[23]

AI may also occur as a side effect of exposure to therapeutic doses of pharmacological agents, which include parasympatholytics (such as hyoscine and atropine) and sympathomimetic agents.[24]

Epidemiology

Accommodative dysfunction occurs in the majority of patients with binocular vision problems. Limited data are reported in the literature regarding the actual prevalence of accommodative dysfunction in the general population.[25] Several studies reviewing the prevalence of symptomatic accommodative dysfunction amongst non-presbyopic patients suggest AI is the most common finding.[26]

Most data account for the prevalence of accommodative dysfunction amongst school children ranging from 8 to 15 years of age.[27] Studies have shown that most children with CI also tend to have accommodative dysfunction.[28] Husainideen and Murali performed a meta-analysis of related literature and determined that accommodative dysfunction and asthenopia are the most commonly encountered signs in AI. Symptoms included floating words while reading, difficulty sustaining prolonged reading, and eyestrain, among others.[29][30] 

Children with cerebral palsy are also reported to have lower accommodative amplitudes as compared to age-matched peers.[31] Reports of accommodative and vergence dysfunction amongst younger adults ranging from 18 to 35 years show that these are commonplace.[32] This may be due to the increasing amounts of tasks carried out with digital screens, computers, and cellular phones.[33]

History and Physical

An individual with AI tends to complain of blurry vision during near visual tasks, headaches, visual fatigue, and other asthenopic symptoms (such as eyestrain, diplopia, etc.).[15][34] Patients with this disorder can also experience a psychological ripple effect, manifesting as irritability, loss of concentration during near work, and even disinterest in academic activities (especially amongst school-age children).[35] Secondary convergence insufficiency (CI) in AI is possible, in which the symptoms tend predominantly to be due to AI.[36]

Young children may become symptomatic after an illness or fever.[37] For adults who experience vertigo, the presence of ataxia, facial asymmetry, palpebral ptosis, anisocoria, exophthalmos, excess fatigability, and strabismus should raise concerns about possible underlying severe diseases. A history of systemic vascular disease, especially diabetes mellitus, can be significant amongst adults, considering that these patients can develop autonomic denervation at the ciliary ganglion.

The clinician should consider other essential factors in the history of the patient, which include: substance abuse, trauma, infectious disease, anemia, demyelinating disease, myasthenia gravis (MG being the more localized finding), and Grave's orbitopathy.

Evaluation

For proper diagnosis of accommodative and vergence dysfunction, numerous tests and examinations should be performed to provide a proper diagnosis. Optimal correction of any existing refractive error is obligatory.[38] Measurements of accommodative function should be taken with the individual's optimal (near and distance) correction in place. Assessment of the accommodative parameters is essential to empirically determine if relevant parameters are within the expected spread of values from age and sex-matched individuals. Several tests are useful in the diagnosis of AI, including negative relative accommodation (NRA), near the point of convergence (NPC), and positive relative accommodation (PRA). Tests for accommodative facility, accommodative lead, and lag (using monocular estimation method retinoscopy) are also important in making a proper diagnosis.[39] 

The NPC, for example, is useful in detecting the presence of convergence insufficiency together with AI.[40] The presence of a manifest or latent deviation can be ascertained using a unilateral or alternate cover test (see strabismic image).[41] Deviations can then be measured using prism bars or loose prisms (See prism images).[42]

Parameters representing the ability to stimulate accommodative responses optimally to presented stimuli are often reduced for individuals with AI. These patients tend to show reduced amplitudes of accommodation (AoA) beyond the minimum expected finding based on Hofstetter's formulae (15-0.25×age) or Donders table of age-expected diopters of accommodation.[13] The A of A can be determined by applying either the push-up technique or minus lens-to-blur method.[43] The latter method usually produces lower values by about 2 diopters. 

Individuals who under-accommodate at near usually manifest a lag of accommodation, while patients who over-accommodate manifest an accommodative lead. Accommodative lag/lead can be determined either by the monocular estimated method (MEM) retinoscopy or by the fused cross-cylinder (FCC) test.[44]

The FCC test is the more subjective option and tends to be tedious and less accurate, especially for young children. MEM retinoscopy is performed with fixation directed to a near target. An attempt is then made to swiftly neutralize the movement of the reflex with spherical lenses of appropriate power. The expected finding is a lag between +0.25 DS and +0.75 DS. A lag greater than +1.00 DS indicates the presence of AI.

Accommodative facility testing is another method to assess the subject's ability to stimulate and relax accommodative responses at a normal rate. It also tests the accuracy of repetitive alterations in demand on the accommodative system. This is often determined using +/-2.00diopter flipper lenses.[45] This test can be conducted monocularly or binocularly. Normally, these lenses should be cleared monocularly to a minimum of 11 cycles per minute. Individuals with AI will fail the +/-2.00 diopter flipper test.

NRA/PRA values are indirect measurements of the fusional vergence abilities of the eye. The procedure for testing NRA involves adding plus lenses over the distance correction until the letters blur out. This same procedure is repeated for the PRA, with the only difference being that minus lenses are used in place of the plus lenses.[46]

Horizontal fusional vergence amplitudes (both near and far) are measured using base-in (BI) and base-out prisms (BO). BI prisms are used for negative fusional vergence (NFV), and BO prisms for positive fusional vergence (PFV) amplitudes. Blur, break, and recovery findings are then compared to Morgan's expected ranges. Individuals with symptomatic AI will demonstrate suboptimal fusional vergence in reserve to meet certain accommodative demands.

The AC/A ratio is a key factor to consider in the proper diagnosis and management of accommodative and vergence dysfunction. The normal value is 4:1. Horizontal phoria findings at near can be used to determine the  AC/A ratio gradient. In determining the AC/A ratio gradient, +1.00D lenses are used to induce a prismatic effect (with the optimal near prescription in place) for esophoric findings, while -1.00D lenses are placed in the near prescription for exophoric findings. The difference between phorias with and without the gradient lens is then taken as a fractional value of the lens power used.

Treatment / Management

Treatment of AI should begin with proper refraction and correcting any underlying refractive error. It should be noted that low levels of ametropia may have an exacerbating effect on individuals with AI. Correction of these small refractive errors may substantially alleviate the symptoms of AI for the sufferer.[16] Plus, lenses are known to reduce the accommodative demand at near. Examination signs commonly found in AI patients point to the usefulness of added plus lenses in managing this condition.

Examples of these signs include low PRA and amplitude of accommodation values. Others are high retinoscopic values as measured with the MEM method and difficulty clearing the minus lenses during accommodative facility testing. This may be a problem for myopes as prescribing plus lenses can negate the refractive endpoint. Myopes, however, may benefit from bifocals or progressive lenses, especially if they are found to suffer AI or accommodative esophoria. Studies have shown that this may slow myopic progression.[47] 

In cases where the cause of AI is organic or due to a paralysis of the accommodative system, plus lenses can be recommended either permanently or temporarily as needed.[48] Because such causes are organic, they may present with different levels of accommodative dysfunction between the two eyes. It is, therefore, common to see such patients with varying amounts of "adds" between the two eyes. 

Vision therapy offers some promise in managing AI and is generally aimed at improving accommodative amplitude and positive fusional vergence in reserve.[16] Training regimens depend on the patient's age, personal motivation, and compliance.

Differential Diagnosis

The differential diagnosis of AI is key to the clinical decision-making processes regarding management and evaluation.[49] A key difference is that only AI presents with a reduced AoA. AI sufferers tend only to show difficulty in stimulating accommodation, while accommodative excess sufferers show difficulty in relaxing accommodation.[50] Patients with accommodative dysfunctions will find it difficult to stimulate and relax accommodation.[51] Local and/or systemic diseases may cause a phenomenon known as accommodative paralysis, marked by a sharp reduction in AoA. Drugs have also been shown to induce accommodative paralysis.

Pseudo-CI is a key differential diagnosis to actual CI. This is often considered an AI with a secondary CI finding. In true CI, the NPC is receded. However, measures of accommodation, such as the AoA, are within normal limits. In cases of CI, when an accommodative anomaly exists, there tends to be an accommodative excess. From a clinical perspective, repetition of the NPC with +0.75 or +1.00 lenses may improve performance in pseudo-CI cases. In contrast to just AI, high plus lenses tend to increase exophoria, thus making it more difficult for the patients to converge (while worsening symptoms). In such cases, tailored vision therapy can be of great value.

Certain ocular diseases like Adie's tonic pupil can present symptoms mimicking AI. Infective conditions that produce neuropathological sequelae like syphilis and meningitis may also affect accommodative ability by disrupting the parasympathetic pathway.[52] Several drugs can also affect the accommodative triad and cause an accommodative dysfunction.[53][54] A good case history is of great importance in the treatment of AI.

Prognosis

The prognosis of AI is directly related to the degree to which accompanying symptoms can be alleviated through oculovisual therapeutic management.

Complications

As with other vergence anomalies, AI can degenerate and become strabismic without proper management. AI can also present with poor academic performance in affected children.[25]

Deterrence and Patient Education

Successful outcomes of vision therapy are only achievable if the patient is compliant. Subjects with AI, particularly latent hyperopes, may become discouraged from wearing their spectacle routinely. Parents can show dissatisfaction and disagree with the recommendation of bifocal lenses for their children. Thorough approaches that encourage patient adherence and family support are crucial.[25]

Enhancing Healthcare Team Outcomes

Accommodative and vergence dysfunction can sometimes be indicative of a potentially debilitating disease.[55] Individuals with signs and symptoms of AI, especially those with a prior history of systemic vascular and autoimmune disease or patients with acute neurologic deficits, must be thoroughly assessed by clinicians.[56]

The patient may require interprofessional management, which includes neurological, hematological, pathological, and infectious disease evaluation and testing. Important signs and symptoms to consider, especially during triage, include persistent or intermittent diplopia. Cover testing and extraocular muscle (EOM) function assessment can provide better insight into underlying causes. Acute onsets of abnormalities of accommodation and vergence should seek urgent neuro-ophthalmic evaluation. [Level 1]

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Disclosure: Ehimare Enaholo declares no relevant financial relationships with ineligible companies.

Disclosure: Mutali Musa declares no relevant financial relationships with ineligible companies.

Disclosure: Marco Zeppieri declares no relevant financial relationships with ineligible companies.