Nerve Cupping

L. Jay Katz


BASICS


DESCRIPTION


• Optic nerve cupping can be physiological.


• Pathological optic nerve cupping is a manifestation of regional ganglion cell death and loss of ganglion cell axons from the optic nerve.


• The majority of eyes with pathologic enlargement of the optic cup have glaucoma (1).


• Distinguishing glaucomatous from nonglaucomatous disc cupping can be difficult—in a retrospective review of optic nerve head photographs, Trobe et al. reported that pallor of the neuroretinal rim is 94% specific in predicting nonglaucomatous cupping while focal or diffuse obliteration of the neuroretinal rim is 87% specific in predicting glaucomatous cupping (2).


EPIDEMIOLOGY


Incidence


• The incidence of pathological nonglaucomatous cupping is unknown.


• The observed 4-year incidence of open-angle glaucoma was 1.2% at ages 40–49 years, 1.5% at ages 50–59 years, 3.2% at ages 60–69 years, and 4.2% in persons aged 70 years or more according to the Barbados Incidence Study of Eye Diseases (1992–1997) (3).


Prevalence


• The prevalence of pathological nonglaucomatous cupping is unknown.


• Approximately 67 million people are affected with glaucoma worldwide, and approximately 2 million people in the U.S. have glaucoma (1 in 136 people) (1).


• In developed countries, probably only half of those with glaucoma have been diagnosed.


RISK FACTORS


• Larger optic discs tend to have larger physiologic cup/disc ratio (4)[A].


• Please refer to the “Differential Diagnosis” section of this chapter.


• Please refer to the “Risk Factors” section of the specific diagnosis responsible for the pathological optic disc cupping.


Genetics


There is some dependence of an individual’s physiologic cup/disc ratio on the cup/disc ratio of the parents—multifactorial inheritance is likely (5).


GENERAL PREVENTION


For glaucomatous optic disc cupping: lowering intraocular pressure (IOP)


PATHOPHYSIOLOGY


• Pathologic optic nerve head cupping is a manifestation of retinal ganglion cell death and loss of ganglion cell axons from the optic nerve.


• The primary site of glaucomatous optic nerve damage is thought to be the lamina cribrosa—deformations of the lamina, kinking of nerve fibers, misalignment of laminar pores, blockade of axonal transport; however, the relationship between these findings and glaucomatous damage have not been firmly established (1).


• Other contributing factors may act at the level of the ganglion cell body.


ETIOLOGY


• Elevated IOP


• Ischemia/hypoxia


• Trauma


• Excitotoxicity and aberrant immunity have also been hypothesized to be factors in optic nerve damage (1).


COMMONLY ASSOCIATED CONDITIONS


• Please refer to the “Differential Diagnosis” section of this chapter.


• Please refer to the “Commonly Associated Conditions” section of the specific diagnosis responsible for the pathological optic disc cupping.


DIAGNOSIS


HISTORY


• Presence, onset, and nature of visual disturbance


• Systemic vascular risk factors, such as migraine, Raynaud’s diabetes, and hypertension


• History of ocular trauma or surgeries


• Family history of glaucoma or other optic neuropathies


• Neurological disturbances such as headaches, dizziness, and weakness of extremities


PHYSICAL EXAM


• Check for an afferent pupillary defect.


• Slit lamp examination of the anterior segment to check for signs of secondary glaucoma, such as iris transillumination defects, pseudoexfoliation material, anterior chamber cell or flare, and signs of prior surgery or trauma


• Gonioscopy


• Direct and indirect stereoscopic slit lamp biomicrospy to evaluate the optic nerve head, paying particular attention to


– narrowing of the neuroretinal rim width (relatively narrow rim inferotemporally or superotemporally can indicate glaucomatous damage)


– asymmetry in disc cupping (≥0.2)


– optic disc hemorrhage


– optic nerve color


– beta zone parapapillary atrophy


– optic nerve edema


– loss of retinal nerve fiber layer (focal or diffuse)


• The normal optic disc neuroretinal rim is characteristically broadest inferiorly, followed by superior and nasal rims, and narrowest temporally (ISNT rule).


• An analysis of patients from the Ocular Hyperten-sive Treatment Study and the European Glaucoma Prevention Study showed that an ocular hypertensive patient’s risk of developing glaucoma increased almost 50% for every 0.1 difference between eyes in cup-to-disc ratio (6).


• Staging of the optic disc using Armaly’s cup-to-disc ratio is commonly used.


• Spaeth’s disc damage likelihood scale directs attention to the narrowest area on the optic disc rim (scale 1–10) (7).


DIAGNOSTIC TESTS & INTERPRETATION


Lab


Initial lab tests

• Lab tests as indicated for suspected cause of pathologic optic disc cupping.


• Please refer to the “Differential Diagnosis” section of this chapter.


Follow-up & special considerations

Follow-up as indicated for the suspected cause of pathologic optic disc cupping


Imaging


Initial approach

• Optic disc photographs should be obtained to evaluate and follow patients through their course of treatment.


• Other optic nerve head imaging devices are also currently being used for optic nerve head assessment in glaucoma:


– Scanning laser polarimetry


– Heidelberg retinal tomography


– Optical coherence topography


Follow-up & special considerations

• Follow-up as indicated for the suspected cause of pathologic optic disc cupping


• If glaucoma is suspected, optic disc imaging should be obtained regularly (e.g., annually, or more often if a change in optic disc appearance is suspected) to document and assess the optic nerve head for change.


Diagnostic Procedures/Other


• Visual fields should be obtained at baseline and at regular intervals (e.g., annually, or more often if a change is suspected).


• Diurnal IOP testing may be useful if large IOP fluctuations or periods of IOP spike are suspected.


• Consider neuroimaging for:


– Loss of central visual acuity or central visual field


– Acute onset or rapidly progressive visual loss


– Markedly asymmetric or strictly unilateral optic neuropathy


– Hemianopic visual field loss


– Neuroretinal rim pallor


Pathological Findings


Atrophy of the retinal ganglion cell layer can be noted.


DIFFERENTIAL DIAGNOSIS


• Glaucoma


• Tilted optic nerve insertion


• Coloboma


• Myopic disc


• Posterior staphyloma


• Optic pit


• Hereditary optic neuropathy


• Antecedent optic nerve infarction


• Trauma


• Demyelinating optic neuritis


• Intraorbital and intracranial mass lesions


• Carotic artery fusiform enlargement


• Ischemic optic neuropathy


TREATMENT


MEDICATION


First Line


Please refer to the “Treatment” section of the specific diagnosis responsible for pathological optic disc cupping.


Second Line


Please refer to the “Treatment” section of the specific diagnosis responsible for pathological optic disc cupping.


ADDITIONAL TREATMENT


General Measures


Please refer to the “Treatment” section of the specific diagnosis responsible for pathological optic disc cupping.


Issues for Referral


Referral to a neuro-ophthalmologist may be considered if there is suspicion that the cause of the patient’s optic neuropathy or visual field defect has a possible neurological etiology.


Additional Therapies


Please refer to the “Treatment” section of the specific diagnosis responsible for pathological optic disc cupping.


COMPLEMENTARY & ALTERNATIVE THERAPIES


Please refer to the “Treatment” section of the specific diagnosis responsible for pathological optic disc cupping.


SURGERY/OTHER PROCEDURES


Please refer to the “Surgery/Other Procedures” section of the specific diagnosis responsible for pathological optic disc cupping.


IN-PATIENT CONSIDERATIONS


Initial Stabilization

Please refer to the “Inpatient Considerations” section of the specific diagnosis responsible for pathological optic disc cupping.


Admission Criteria


Please refer to the “Inpatient Considerations” section of the specific diagnosis responsible for pathological optic disc cupping.


IV Fluids


Please refer to the “Inpatient Considerations” section of the specific diagnosis responsible for pathological optic disc cupping.


Nursing


Please refer to the “Inpatient Considerations” section of the specific diagnosis responsible for pathological optic disc cupping.


Discharge Criteria


Please refer to the “Inpatient Considerations” section of the specific diagnosis responsible for pathological optic disc cupping.


ONGOING CARE


FOLLOW-UP RECOMMENDATIONS


Please refer to the “Ongoing Care” section of the specific diagnosis responsible for pathological optic disc cupping.


Patient Monitoring


Please refer to the “Ongoing Care” section of the specific diagnosis responsible for pathological optic disc cupping.


DIET


Please refer to the “Ongoing Care” section of the specific diagnosis responsible for pathological optic disc cupping.


PATIENT EDUCATION


Please refer to the “Ongoing Care” section of the specific diagnosis responsible for pathological optic disc cupping.


PROGNOSIS


Please refer to the “Ongoing Care” section of the specific diagnosis responsible for pathological optic disc cupping.


COMPLICATIONS


Please refer to the “Ongoing Care” section of the specific diagnosis responsible for pathological optic disc cupping.



REFERENCES


1. Greenfield DS. Glaucomatous versus nonglaucomatous optic disc cupping: clinical differentiation. Semin Ophthalmol 1999;14(2):95–108.


2. Trobe JD, Glaser JS, Cassady J, et al. Nonglaucomatous excavation of the optic disc. Arch Ophthalmol 1980;98:1046–1050.


3. Wu SY, Nemesure B, Leske MC. Observed versus indirect estimates of incidence of open-angle glaucoma. Am J Epidemiol 2001;153(2):184–187.


4. Hoffmann EM, Zangwill LM, Crowston JG, et al. Optic disc size and glaucoma. Surv Ophthalmol 2007;52(1):32–49.


5. Armaly MF. Genetic determination of cup/disc ratio of the optic nerve. Arch Ophthal 1967;78:35–43.


6. The Ocular Hypertension Study Group and the European Glaucoma Prevention Study Group. The accuracy and clinical application of predictive models for primary open-angle glaucoma in ocular hypertensive individuals. Ophthalmol 2008; 115:2030–2036.


7. Bayer A, Harasymowycz P, Henderer JD, et al. Validity of a new disk grading scale for estimating glaucomatous damage: correlation with visual field damage. Am J Ophthalmol 2002;133(6):758–763.

Only gold members can continue reading. Log In or Register to continue

Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Nerve Cupping
Premium Wordpress Themes by UFO Themes