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Iritis

Home / Basic Ophthalmology Review / Anterior Chamber

Title: Iritis
Author: Kristen Russell, MS4, Texas Tech University
Summary

Iritis is inflammation of the colored portion of the eye (Figure 1). Because the iris is one component of the uvea, it is also categorized as anterior uveitis.  Iritis can be traumatic, infectious or autoimmune and can be localized to the eye or related to an underlying systemic disease.  It is categorized by its presentation and course—unilateral versus bilateral, acute versus chronic, infectious versus non-infectious and granulomatous versus non-granulomatous.

Figure 1: Iritis with posterior synechiae

Presentation

Iritis can be asymptomatic, but most patients present with eye pain, photophobia, decreased vision, small or poorly reactive pupils and eye redness. Iritis is more commonly unilateral in which case the vision remains relatively normal in the affected eye. The key to diagnosis is seeing individual white blood cells (referred to as “cell”) and inflammatory proteins (“flare”) floating in the anterior chamber of the eye using a slit lamp magnified 16 times or 16X setting. Over the course of several days, these inflammatory cells can deposit on the cornea forming keratic precipitates (KP’s). (Figure 2) The underlying inflammation can also cause the iris to adhere to the lens (posterior synechiae) or the cornea (peripheral anterior synechiae). Often the inflammation will decrease aqueous secretion and increase uveoscleral outflow resulting in lower intraocular pressure (IOP). However, if inflammatory cells block the trabecular meshwork, the IOP could increase. Iritis that is chronic or reoccurring, may cause depositions of calcium on the front of the eye, known as band keratopathy.

 

Figure 2: Keratic Precipitates

Differential
The differential for patients presenting with iritis-like symptoms (pain, photophobia, poorly reactive pupils and eye redness) is broad, including but not limited to keratitis, conjunctivitis, acute angle closure glaucoma, endophthalmitis, scleritis and episcleritis. A careful history and slit lamp examination can differentiate between these conditions.

Workup
When a patient presents with iritis confirmed on slit lamp, systemic disease must be considered. Some of the infectious causes include Lyme’s disease, syphilis, toxoplasmosis, tuberculosis and HIV.  Non-infectious or autoimmune causes include HLA-B27 related diseases (i.e. ankylosing spondylitis), juvenile idiopathic arthritis, Behcet’s disease, sarcoidosis and many more.  The non-infectious causes respond to steroids but sometimes require steroid-sparing agents like other rheumatologic disorders.  Before beginning these treatments, however, it is paramount to rule out the infectious causes.  Therefore, a uveitis workup might include the following studies:

Lyme’s Disease:         Anti-Borrelia burgdorferi antibodies
Syphilis:                      RPR, FT-ab
HLA-B27:                    HLA-B27 Genotype testing
Tuberculosis:              Quantiferon Gold, Chest x-ray
Sarcoidosis:                Chest x-ray, ACE
HIV:                             HIV-1, HIV-2 antibody screen
Behcet’s Disease:      HLA-B51
Juvenile Arthritis:        ANA

Treatment
Treatment of iritis involves trying to identify and treat an underlying cause (though many cases are idiopathic) while simultaneously decreasing the inflammation and minimize the discomfort and secondary damage to the eye from the inflammation. Once an underlying infectious cause has either been treated or ruled out, steroids are the primary therapy for decreasing inflammation—usually topical first but occasionally injectable or oral.  Prompt management of the inflammation is important in preventing long term sequelae. Cyclopelegic agents or dilating eye drops such as atropine are also helpful in preventing iris adhesions from forming and reducing the pain and photophobia.

References:
Gutteridge IF, Hall AJ. Acute anterior uveitis in primary care. Clinical and Experimental Optometry. 2007. 90(2):70-82.
Leitman, Mark W. Manual for eye examination and diagnosis. Hoboken, NJ: John Wiley & Sons Inc., 2017. Print.
Identifier: Moran_CORE_24085
Copyright statement: Copyright 2017. Please see terms of use page for more information.


Strabismus

Home / Basic Ophthalmology Review / Extraocular Muscles / Motility

Title: Strabismus

Author: Paul Chamberlain, 4th Year Medical Student, Baylor University

Strabismus is a misalignment of the two eyes. It has a broad differential that significant varies by age and varies in urgency.  First it is important to understand how to correctly describe strabismus and its nomenclature.  The deviated eye (in relationship to the other eye) can be elevated (hyper-), depressed (hypo-), pointed nasally (eso-) or pointed temporally (exo-). Next, the deviation may be occurring spontaneously (-tropia, called a “manifest” deviation) or only when fusion of the two eyes is broken during cover testing (-phoria).  Putting these first two elements together you can properly describe most strabismus—for example, a left hypertropia (the left eye is deviated upwards relative to the right eye). In general, phorias are not problematic and do not require treatment but can decompensate overtime into tropias. In further describing strabismus, it is important to delineate if the misalignment is constant or intermittent as well as comitant or incomitant.  An incomitant deviation is one that varies or changes based on the direction of gaze.  For instance, a left 6th nerve palsy is incomitant because it is worse in left gaze but better in right gaze.

As in many medical diagnoses, a careful history is paramount in narrowing a differential and understanding the urgency and nature of the strabismus.  Some critical questions include: When did you first notice this?  Has the amount of deviation worsened, improved, or stayed the same during that time?  Is it constant or intermittent?  Are you seeing double vision?  Are the images splayed horizontally, vertically, or diagonally?  A medical history also provides numerous clues to the etiology, such as assessing vascular risk factors, birth and pregnancy history, thyroid disease, prior eye disease or surgery, etc.

In eliciting and quantifying the deviation, it is important to perform a complete ophthalmic exam where possible: specifically visual acuity, motility, cycloplegic refraction (checking the patient’s prescription after dilating their eyes) and dilated retinal exam.  There are a few specific tests that help the examiner assess the eye alignment, such as the cover-uncover test. The examiner instructs the patient to look at a target, covers one eye for several seconds and then uncovers that eye, repeating this in the fellow eye. In a patient with a tropia, the misaligned eye will move to fixate on the target when the fixing eye is occluded. For instance, if a patient has a left esotropia (i.e. the left eye is deviated towards the nose) the examiner should see the left eye move laterally when the right eye is occluded. The second test is the alternate cover test which involves moving an occluder back and forth from eye to eye watching for eye movements in the uncovered eye.  Prisms can be used to quantify the amount of deviation, which are mainly used for surgical decision making.

There are several types of strabismus of which all physicians should have a fundamental knowledge. When the strabismus presents in the first year of life, specifically by 6 months of age, it is deemed congenital and warrants prompt referral to a pediatric ophthalmologist as failure to correct misalignment in a timely fashion may result in a permanent loss of binocular vision such as depth perception (stereopsis).  The optimal time to correct congenital misalignments is not universally agreed upon, but ranges from 6 months to 24 months.

Strabismus that presents in the toddler or young child is uniquely different that adult-onset strabismus in that children are still developing vision and have the potential to lose vision in a deviated eye due to amblyopia, or disuse of a deviated eye to avoid double vision (diplopia).  This is why children tend not to complain of diplopia with strabismus, they suppress the misaligned eye as an adaptive mechanism which is clever in the short term but can cause long term damage to visual development.

Sudden onset strabismus in a middle-aged individual has a broad differential, including a cranial nerve palsy (III, IV or VI) from a compressive lesion such as a mass or vascular anomaly.  Neuro-imaging of the brain and orbits is often warranted, with and without contrast.  The key to identifying cranial nerve palsies that affect eye alignment is looking for incomitance, or a deviation that varies depending on direction of gaze.  Patients who may not require neuro-imaging are those who are older than 50 with multiple vascular risk factors and have an isolated cranial nerve palsy.  In these cases the etiology is more likely ischemic and they tend to recover in variable degrees.  All of these cases warrant a consult or referral to ophthalmology, more specifically neuro-ophthalmology or pediatric ophthalmology.

If a patient or parent simply says they have a “lazy eye,” the interviewer should ask for an explanation of what this means to the patient as they may be referring to a number of things, most commonly ptosis, amblyopia or strabismus.

Treatment for strabismus includes watchful waiting, glasses with prism, eye patching or surgery. If there is an underlying medical problem causing the strabismus than this is typically addressed first. If left untreated in young children, strabismus may lead to amblyopia, loss of stereopsis, and negative psychosocial effects. Much of this is correctable if addressed promptly, but becomes irreversible within a matter of months to years, especially if not addressed by around age eight.

Identifier: Moran_CORE_24081


Amblyopia

Home / Basic Ophthalmology Review /Visual Acuity and Vision Loss

Home / Basic Ophthalmology Review / Refractive Errors

Title: Amblyopia—Pathophysiology 

 Author: Austin D. Bohner, MS4 University of Utah 

Date: 07/10/19 

Introduction/Definition: 

Brief description 

Amblyopia is caused by the dysfunction of the processing of visual information.1 This dysfunction results from the lack of visual stimulus on the retina and subsequent suppression of the development of cortical visual centers in the brain.2  

Epidemiology:  

Amblyopia is the most common cause of unilateral vision loss in the children with an estimated prevalence of 1-5%.3 

Reported categorical frequencies of amblyopia4 

  1. Strabismus – 50% 
  2. Refractive – 15 to 20% 
  3. Combined mechanism (strabismus and refractive) – 30% 
  4. Deprivation – Less than 5% 

 Pathophysiology: 

Overview— 

Amblyopia results from a disruption of development of the visual cortex early in life.1 After birth, a critical period of neuroplasticity in the development of the visual system occurs, during which, outside visual stimuli promote neuronal amplification and modification.2 At birth vison is roughly 20/400 and increases rapidly as cone density of the fovea increases nearly fivefold in the first few months and early years of life.5 An appropriately focused image on the retina is critical to create a normal visual stimulus for development. The developmentally sensitive period is thought to occur during the first few months of life until around the age of eight.6 Early visual disruption tends to result in more severe loss of vision/disruption to the development of the visual system.6 Treatments later in development have been less successful at restoring or improving vision, thus highlighting the need for early screening and intervention. The central suppression that leads to amblyopia is categorized into three causal processes: 

  1. Strabismus or ocular misalignment 
  2. Anisometropia or refractive error 
  3. Depravation or physical obstruction 

3 Major Classifications 

Strabismus, or eye misalignment, can cause amblyopia if this misalignment results in a loss of binocular vision (causing diplopia).The visual cortex is presented with two disparate images presented on the fovea and suppresses the neurological stimulus of one eye in order to prevent diplopia. This neuro-adaptation is a clever short-term solution to the diplopia but in the long-term can cause amblyopia. It is important to note that not all forms of strabismus result in amblyopia.  

Refractive amblyopia is caused by an uncorrected refractive error that causes image blur on the retina in one or both eyes.  The most common subtype of refractive amblyopia is unilateral and related to anisometropia, or a difference in the refractive error between the two eyes. In this subtype, one eye is able to see more clearly than the other eye.  The brain “ignores” neuronal information coming from the blurred eye, and preferentially focuses on the image from the clear eye.  This stimulates visual development of the good eye while neglecting development of the blurred eye, thus causing amblyopia.  

Bilateral refractive amblyopia, or ametropic/isometropia amblyopia, occurs in cases of bilateral severe uncorrected refractive error, and is less common.     

Deprivational amblyopia results for vison deprivation, because of a physical obstruction of the visual axis. Examples include congenital cataracts, ptosis, congenital corneal opacities, and vitreous hemorrhage. These physical obstructions block or severely distort the foveal image resulting in the most severe form of amblyopia. Deprivational amblyopia in infancy, if not corrected urgently, can result in permanent loss of visual development and vision.   

Keywords/Main Subjects: Amblyopia, Strabismus, Neuroplasticity 

Secondary CORE Category: Pediatric Ophthalmology and Strabismus 

Diagnosis: Amblyopia  

Faculty Approval by: Griffin Jardine, MD 

References: 

  1. Holmes, and Clarke. “Amblyopia.” The Lancet 367.9519 (2006): 1343-351. 
  1. Jefferis, Connor, and Clarke. “Amblyopia.” BMJ : British Medical Journal. 351.8033 (2015): H5811 
  1. Noorden, and Crawford. “The lateral geniculate nucleus in human strabismic amblyopia.” Investigative Ophthalmology & Visual Science. 33 (1992): 2729-2732 
  1. de Zárate, and Tejedor. Current concepts in the management of amblyopia. Clinical Ophthalmology. 1 (2007): 403 
  1. Hendrickson, Possin, Vajzovic, and Toth. Histologic development of the human fovea from midgestation to maturity. American Journal of Ophthalmology. 154 (2012): 767-778 
  1. Daw. Critical periods and amblyopia. Arch Ophthalmol 116 (1998): 502-505. 

Identifier: Moran_CORE_24066


Astigmatism

Home / Basic Ophthalmology Review / Refractive Errors

Title: Astigmatism

Author: Michael Murri, 4th Year Medical Student, Baylor College of Medicine

Astigmatism refers to a focusing power of the eye that is not symmetrical in all directions.1  There are many types of astigmatism.  One of the most common types is when the vertical and horizontal images of the eye are not focused together on the retina creating multiple points of focus (Figure 1A).  Different types of astigmatism can result in different types of horizontal, vertical, or otherwise irregularly blurred images on the retina (Figure 1B).2 Regular astigmatism refers to a consistent difference in two directions of the eye 90 degrees apart and can often be corrected through contact lenses or glasses.  Irregular astigmatism refers to complex patterns of irregularity and often requires refractive surgery such as LASIK or PRK or a gas permeable (or “hard”) contact lens to be corrected.

Figure 2: Representation of the refractive light path of horizontal and vertical light in one type of astigmatism known as mixed astigmatism (2A). Example of how the letter “H” might appear in different types of astigmatism (2B).

References:

  1. Kee C-S. Astigmatism and its role in emmetropization. Experimental Eye Research. 2013;114:89-95. doi:10.1016/j.exer.2013.04.020.
  2. Read SA, Vincent SJ, Collins MJ. The visual and functional impacts of astigmatism and its clinical management. Ophthalmic and Physiological Optics. 2014; 34(3):267-294. doi:10.1111/opo.12128.
  3. Mozayan E, Lee JK. Update on astigmatism management. Current Opinion in Ophthalmology. 2014; 25(4):286-290. doi:10.1097/icu.0000000000000068.

Identifier: Moran_CORE_24063


Alignment Assessment (Hirschberg)

Home / Basic Ophthalmology Review / Extraocular Motility

Title: Alignment Assessment (Hirschberg)

Author: Katherine Hu, 4th Year Medical Student, Saint Louis University

The Hirschberg test (also known as the corneal light reflex test) is a quick and simple way to check ocular alignment. This assessment is particularly useful for testing for strabismus (misalignment of the eyes) in newborns, young children, patients with poor vision, patients that are not able to fixate or track well – or in any situation where a full motility evaluation is not feasible.

To perform the assessment:

  1. Use a light source, such as a penlight or finhoff transilluminator.
  2. Instruct the patient to focus their gaze on your light source.
  3. From a distance of 2 feet, shine your light source equally into the patient’s eyes at midline.
  4. Observe the reflection of light off the cornea, which should appear as a pin-point white light near the center of the pupil in each eye.

Patient with normal alignment and corneal light reflex.

If there is normal alignment, the reflection will appear in the same position in each pupil. If there is misalignment of the eyes, the location of the corneal reflex will appear asymmetric and “off center” of the pupil in the deviating eye. The relative difference in the position of the reflex will be in the opposite direction as the eye deviation. For example, in an esotropia (where there is inward deviation of the eye), the light reflex will appear outwardly displaced from the center of the pupil; in a hypertropia (where there is an upward deviation of the eye) the light reflex will appear inferiorly displaced from the center of the pupil.

For every 1 millimeter of deviation from the center of the pupil, it will take approximately 15 diopters of prism to correct the misalignment.

This can be visually estimated with the Hirschberg test, or physically measured with the Krimsky test, where a prism is placed in front of the deviating eye until the corneal reflex is re-centered in the pupil.
Young children and patients of Asian descent can appear “cross-eyed” without a true misalignment. This pseudostrabismus is most commonly due to a flat nasal bridge with prominent epicanthal skin folds. These facial features can obscure the medial sclera and create an optical illusion of misalignment. In this case, the eyes may appear to be esotropic, but the corneal reflexes will appear symmetric and in the center of each pupil.

 

Additional patient examples (courtesy of Dr. Marielle Young):

Patient with normal alignment.

Patient with exotropia of the left eye.

Patient with hypertropia of the right eye.

Patient with esotropia of the left eye.

 

References:

Bradford, Cynthia A. Basic Ophthalmology. San Francisco, CA: American Academy of Ophthalmology, 2004.

Copyright statement: Copyright Author Name, ©2016. Please see terms of use page for more information.

Disclosure (Financial or other): None

Identifier: Moran_CORE_24000


Intraocular Pressure

Home / Basic Ophthalmology Review / Intraocular Pressure

Title: Intraocular Pressure

Author: Gavin Gorrell, 4th Year Medical Student, University of New Mexico

What is it?

Just as the measurement of blood pressure and intracranial pressure have clinical significance, measurement of intraocular pressure (IOP) is useful in evaluating overall eye health and narrowing a differential diagnosis in presenting eye disease. The eye is filled with a clear jelly (vitreous humor) behind the lens and a continuously produced, nourishing fluid called aqueous humor that fills the space in front of the lens (the anterior chamber). Because the amount of vitreous humor is relatively static, IOP is primarily a function of aqueous humor production and drainage.

Aqueous humor is produced in the posterior chamber by the ciliary body, then it flows past the zonules supporting the lens, between the iris and lens, through the pupil into the anterior chamber, then through a trabecular meshwork into Schlemm’s canal into the episcleral veins (venous system underneath the scleral surface).

Normal IOP of 10-21mmHg is important in maintaining eye shape and perfusion of the cornea and lens (avascular structures which rely on aqueous humor for nutrients, oxygen and clearance of their metabolic waste).  Low IOP can cause vision impairment but almost exclusively occurs in post-surgical eyes. Elevated IOP is important to identify as it is the only modifiable risk factor for glaucoma. “Normal” IOP is a term that has fallen out of favor due to the fact that glaucoma can occur at almost any IOP—reaffirming the recommendation that all patients 40 and over have a thorough, dilated eye exam.

When to measure?

IOP is considered one of the “eye vital signs” and should be measured in every patient with an eye complaint or in whom the clinician suspects glaucoma.  The American Academy of Ophthalmology recommends all patients to have a baseline eye exam at age 40, during which exam IOP and other glaucoma risk factors are assessed.

When to postpone measurement?

Checking IOP should be avoided in cases of ocular trauma where there is a concern for ruptured globe or potential cornea perforation (thin cornea, recent corneal surgery, large corneal ulcer). In cases of hyphema or retrobular hemorrhage, the IOP is an important diagnostic clue but needs to be done with extra caution and should be deferred to an eye specialist.\

How is it measured?

Measurement of IOP is based off the Imbert-Fick principle which basically states the pressure inside a thin walled sphere can be determined by the force required to flatten part of the sphere; P =F/A, where P = pressure, F = force, A = Area.  A simple analogy is how hard your thumb must press on a basketball to make a dent when its deflated vs inflated.

There are several tools that can be used to measure IOP. The gold standard is the Goldmann applanation which requires a slit lamp and a cooperative, mobile patient.  When Goldmann applanation isn’t feasible, a quick and convenient way to check IOP is to use a portable hand-held device such as the Tono-Pen® or Icare tonometer.

 

References:

  1. “Icare Tonometer – Portable, Handheld IOP Measurement.” Icare Usa. Accessed June 25, 2017. http://icare-usa.com/.
  2. “IOP and Tonometry – EyeWiki.” Accessed June 25, 2017. http://eyewiki.aao.org/IOP_and_Tonometry.
  3. “Ocular Hypertension: Background, Pathophysiology, Epidemiology,” May 25, 2017. http://emedicine.medscape.com/article/1207470-overview#a2.
  4. “Tono-Pen AVIA® Applanation Tonometer.” Accessed June 25, 2017. http://www.reichert.com/product_details.cfm?pcId=474&skuId=2980&skuTk=1037022486#.WU_rM-vyuM8.

Identifier: Moran_CORE_23991


Perform the Pupillary Exam

Home / Basic Ophthalmology Review / Pupillary Exam

Title: Pupillary Exam

Author: Marshall Huang, 4th Year Medical Student, University of Pittsburgh

Performing the Pupillary Exam

The pupillary exam is considered one of the “vital signs” of ophthalmology. It is important to assess the pupils of all patients because any abnormalities can be a sign of a serious neurological disease.  A complete pupillary exam includes assessing the direct and consensual response to light, as well as the near response. Any asymmetry should prompt further evaluation.  Here are the basic steps of performing the pupillary exam:

  1. Have patient fixate on a distant target and turn the room lights down
  2. Measure the pupillary diameters of each eye separately in both light and dark
    1. This is the best way to detect anisocoria (unequal pupil diameters). Anisocoria can be physiologic or normal if the difference in diameter is the same in light and dark.
  3. Shine a light in one eye and measure the constriction in the illuminated eye (direct) and the constriction of the other eye (consensual)
    1. Both pupils should constrict simultaneously and equally
  4. Perform the swinging light test (see RAPD for more details)
  5. In moderate light, have the patient shift their gaze from a distant target to a near object
    1. Both pupils should constrict simultaneously and equally (see light/near dissociation for more information)

See Also in the CORE:

The Neuro-ophthalmology Exam: Pupils; Color; Eye Movements; Prism

Identifier: Moran_CORE_23989


4th Nerve Palsy

Home / Basic Ophthalmology Review / Extraocular Muscles / Motility

Title: 4th Nerve Palsy

Authors: Alex Wright, 4th Year Medical Student, University of Utah School of Medicine; Tanner Ferguson, 4th year medical student, University of South Dakota Sanford School of Medicine

The 4th cranial nerve (CN), or trochlear nerve, is a motor nerve solely responsible for innervating the superior oblique muscle. The superior oblique muscle has unique rotational actions for the eye that are dependent upon the position of the eye. This summary will provide a brief review of the function of the superior oblique muscle and the clinical significance of a 4th nerve palsy.1

The superior oblique’s unique insertion on the eye permits a “pulley” type action on the eye. In the eye’s primary position (fixating straight ahead), the primary action of the muscle is intorsion (rotation of 12 o’clock position of limbus towards nose). It also provides depression (particularly in adduction) and abduction.1

When a trochlear nerve palsy occurs, the clinical signs can differ depending on acute versus chronic. The most common cause of a 4th nerve palsy is trauma, followed by congenital and ischemic causes.2 Traumatic 4th nerve palsies may occur with a relatively mild blow to the head not associated with loss of consciousness or skull fracture.  This is due to the long course that the 4th CN takes as it exits the pons posteriorly.  If a patient has vasculopathic risk factors and has accompanying pain with the symptoms, ischemia is more likely. When it occurs in an acute setting, patients often complain of a binocular, vertical diplopia that is worse with downward or side gaze. Patients may also complain of difficulty reading or with near vision.  Congenital cases typically present with a longstanding compensatory head tilt and occasionally have facial asymmetry from the head tilt (see image 1).

Clinical diagnosis of vertical diplopia can be localized with the Parks-Bielschowsky Three Step Test. Step one involves identifying which eye is higher in primary gaze (hypertropia). Step two is for establishing if the hypertropia is worse in right or left gaze and step three in right or left head tilt.  For example, a right 4th CN palsy will present with a right hypertropia, worse in left gaze and right head tilt.  A left 4th nerve palsy will present with a left hypertropia, worse in right gaze and left head tilt.  Because the eye alignment is worse when tilting towards the lesion, many patients will demonstrate a compensatory head tilt away from the lesion.3 If you note a compensatory head tilt in a patient and suspect a CN IV palsy, it may be helpful to look at older photos to assess how long the patient’s head tilt has been present.

If a patient presents with a sudden onset of a CN IV palsy without a history of trauma and no cardiovascular risk factors, the patient may necessitate neuroimaging to further evaluate, particularly if other neurological signs/symptoms are present.4 The palsy can be caused by increased intracranial pressure or a cerebellar tumor. It is therefore important to look for papilledema and evaluate for signs of cerebellar disease in conjunction with neuroimaging.

References: 

  1. Prasad S, Volpe NJ. Paralytic Strabismus: Third, Fourth, and Sixth Nerve Palsy. Neurologic Clinics. 2010;28(3):803-833. doi:10.1016/j.ncl.2010.04.001.
  2. Keane JR. Fourth nerve palsy Historical review and study of 215 inpatients. Neurology. 1993;43(12):2439-2439. doi:10.1212/WNL.43.12.2439.
  3. Prasad S, Volpe NJ, Tamhankar MA. Clinical reasoning: a 36-year-old man with vertical diplopia. Neurology. 2009;72(19):e93-e99. doi:10.1212/WNL.0b013e3181a55ee3.
  4. Tamhankar MA, Biousse V, Ying G-S, et al. Isolated third, fourth, and sixth cranial nerve palsies from presumed microvascular versus other causes: a prospective study. Ophthalmology. 2013;120(11):2264-2269. doi:10.1016/j.ophtha.2013.04.009.

Identifier: Moran_CORE_23987


Presbyopia

Home / Basic Ophthalmology Review / Refractive Errors

Title: Presbyopia

Author: Tanner Ferguson, 4th year medical student, University of South Dakota Sanford School of Medicine

Presbyopia is the age-related stiffness of our lens that reduces our ability to accommodate, or focus on near objects1,2. Normally, people are born with a clear and flexible lens.  It is helpful to think of the lens as the “reading” lens with two functions: vision clarity and near vision (accommodation). These both may be compromised as we age (cataracts and presbyopia, respectively).

When the eye accommodates, the pliable, crystalline lens becomes more rounded to increase its refractive power for closer viewing.  An object at distance has light rays that are nearly parallel and do not require as much refraction to focus the rays on the retina. Light rays from a near object diverge and require a more converging (convex) lens to shorten the focal length and bring a near object into focus1,2. The figures below illustrate normal accommodation and presbyopia.

As we age, our ability to focus on near images is diminished due to reduced lens flexibility1. This typically starts around age 40 but worsens over the next 10-20 years and varies patient to patient.  Individuals often first complain of difficulty reading after a long day of “near work” (e.g. working on the computer) or indicating they require increased lighting to read. They may also have discovered the first line treatment, which is using “cheaters” or reading glasses available over-the-counter that assist with focusing on near objects.

Images:

   

References

  1. Glasser A, Campbell MC. Presbyopia and the optical changes in the human crystalline lens with age. Vision Res. 1998;38(2):209-229.
  2. Atchison D. Accommodation and presbyopia. Ophthalmic and Physiological Optics. 1995;15(4):255-272. doi:10.1016/0275-5408(95)00020-E.

Identifier: Moran_CORE_23980


Myopia vs. Hyperopia

Home / Basic Ophthalmology Review / Refractive Errors

Title: Myopia vs. Hyperopia

Author: Michael Murri, 4th Year Medical Student, Baylor College of Medicine

When light is perfectly focused onto the retina, it is called emmetropia (Figure 1A).  Hyperopia, or farsightedness, occurs when there is not enough focusing power in the lens and cornea, and the image is focused behind the retina (Figure 1B).  This often occurs in eyes that are “short” or those with a flatter cornea and can be corrected with a “positive power” convex lens to give the eye more focus.1  Hyperopia is present in most newborns, which decreases over time as the eye develops.2

Myopia, or nearsightedness, is when the focusing power of the eye is too powerful, causing the image to be focused in front of the retina (Figure 1C). This is common in “long” eyes or those with a steeper cornea and is corrected with a “minus power” concave lens to decrease the focusing power of the eye.1 In myopia, near vision is often clear due to the fact that light rays are still diverging, or travelling outward, at a close distance instead of being virtually parallel (Figure 1D). Myopia has been associated with higher economic classes, with recent studies suggesting that increased time spent outdoors may reduce myopia in children.3,4

Figure 1: Refractive path of light in the human eye in emmetropia (1A), hyperopia (1B), myopia (1C), and near-vision myopia (1D)

References:

  1. Stambolian D. Genetic susceptibility and mechanisms for refractive error. Clinical Genetics. 2013; 84(2):102-108. doi:10.1111/cge.12180.
  2. Ozdemir O, Tunay ZO, Acar DE, Acar U. Refractive errors and refractive development in premature infants. French Journal of Ophthalmology. 2015; 38(10):934-940. doi:10.1016/j.jfo.2015.07.006.
  3. French AN, Ashby RS, Morgan IG, Rose KA. Time outdoors and the prevention of myopia. Experimental Eye Research. 2013; 114:58-68. doi:10.1016/j.exer.2013.04.018.
  4. Foster PJ, Jiang Y. Epidemiology of myopia. Eye. 2014; 28(2):202-208. doi:10.1038/eye.2013.280.

Identifier: Moran_CORE_23973