What instructions does the nurse give the patient before using the snellen visual acuity chart?

3.3.2 Advantages and disadvantages

Snellen charts have a major advantage at present in that they are widely available and Snellen notation of VA is universally understood. From a practical viewpoint, these charts can generally be produced in a smaller format as considerably fewer large letters are presented and this allows easier display on projector systems and the easy addition of other targets such as a duochrome and spotlight, etc. to wall charts. The charts provide a good target for refraction of patients with good VA as the number of lines between approximately 20/15 to 20/40 (6/5 to 6/12) is similar to logMAR charts and these lines typically have as many, if not more, letters than logMAR charts. Although the truncation of Snellen charts (to, say, 6/5 or 20/15 when some patients can see 6/3 or 20/10) can be a disadvantage, it can speed up the measurement and allows most patients to read your ‘bottom line’.

However, Snellen chart VAs are much less repeatable than VA measured using logMAR charts (Lovie-Kitchin 1988) and over three times less sensitive to inter-ocular differences in VA (McGraw et al. 2000) and thus much less sensitive to amblyopia and other uniocular VA loss. Its main disadvantages occur at large (>6/12) and small letter sizes (<6/6). The majority of Snellen charts have one 6/60 letter, two 6/36 and three 6/24 letters, whereas logMAR charts have five letters on each of these lines and additional lines of letters at 6/48 and 6/30. Many Snellen charts do not contain lines of small letters and are truncated to 6/4, 6/4.5, 6/5 or even 6/6. This takes the approach of measuring ‘distance vision adequacy’ (i.e. determining whether distance VA is adequate for a patient's daily needs, similar to the approach used for near VA) rather than distance VA (a threshold measurement). This makes the detection of slightly reduced VA due to eye disease or uncorrected refractive error in patients with good VA impossible. For example, if your chart is truncated to 6/5 or 20/15, you will not be able to detect a VA loss from 6/3 (or 6/4) to 6/5 or from 20/10 to 20/15.

Examination of acuity

This is best done using a Snellen's chart; alternatives include a near-vision chart. Refractive errors are best corrected using the patient's glasses but can be improved using a pin hole. The result of the Snellen's chart is expressed as two numbers: the distance from the chart (usually 6 m or 20 ft) and the distance at which the letter the patient could read should be read at. For example, 6/6 – letter read at the correct distance; 6/60 – the patient could read a letter at 6 m that could normally be read at 60 m. If the patient cannot read any letters, see if he or she can count fingers (abbreviated to CF), see hand movements (HM) or only has perception of light (PL).

Acuity can be affected by lesions anywhere in the visual pathway from ocular causes such as corneal lesions, cataracts and macular degeneration, through optic nerve disease and hemianopias involving the macula, to cortical blindness. Cortical blindness results from bilateral occipital lesions and is associated with normal pupillary responses and a normal eye examination.

Basics of the Bedside Eye Examination

When evaluating a headache patient, especially when there are any visual issues, it is important to do an adequate examination of the visual system.1

Optic Nerve: Cranial Nerve II

Begin with formal visual acuity testing using a Snellen chart or a “near card” in older children. Younger children are more difficult and many times only gross vision can be evaluated. Beyond 4 years of age, the E test is useful. The child is taught to recognize the E, and to discern the direction in which the three “arms” are pointing and point a finger accordingly.

Peripheral visual field testing is accomplished using a small (3-mm) white or red test object, a toy, or in a pinch, the examiner's fingers can be used. The test object is moved from the temporal to the nasal fields and then from the superior and inferior portions of the temporal and nasal fields while the child looks directly at the examiner's nose. Finger counting can be used if acuity is grossly distorted. In cases of extreme impairment, perception of a rapidly moving finger can be used.

The optic disc (i.e., optic nerve head) of the older child is sharply defined and often salmon-colored, which differs from the pale gray color of the disc in an infant. In the presence of a deep cup in the optic disc, the color may appear pale, but the pallor is localized to the center of the disc. The pallor of optic atrophy occurs centrally and peripherally, and is accompanied by a decreased number of arterioles in the disc margins. Most commonly, papilledema is associated with elevation of the optic disc, distended veins, and lack of venous pulsations. Hemorrhages may surround the disc. Before papilledema is obvious, there may be blurring of the nasal disc margins and hyperemia of the nerve head.

The presence or absence of the pupillary light reflex differentiates between peripheral and cortical blindness. Lesions of the anterior visual pathway (i.e., retina to lateral geniculate body) result in the interruption of the afferent limb of the pupillary light reflex, producing an absent or decreased reflex. Anterior visual pathway interruption can cause amblyopia in one eye. In this situation, the pupil fails to constrict when stimulated with direct light; however, the consensual pupillary response (i.e., response when the other eye is illuminated) is intact. The deficient pupillary reflex is revealed by alternately aiming a light source toward one eye and then the other. In the eye with decreased vision, consensual pupillary constriction is greater than the response to direct light stimulation (Marcus Gunn pupil); the pupil of the affected eye may dilate slightly during direct stimulation (Haymaker, 1969).

Signs

1

Visual acuity. Classically, patients read down the Snellen chart, missing the letters in their temporal field for each eye, although the visual loss tends to be asymmetric.

Color vision. Patients will miss reading the figure that falls in the temporal field if a two digit number is presented or will have temporal red desaturation when tested across the vertical midline.

Optic nerve appearance (Fig. 11.10). Patients with chiasmal syndromes may or may not have ophthalmoscopically apparent nerve fiber layer or optic atrophy.

Band or bow-tie atrophy. When optic atrophy is present, it occurs in a distinctive pattern called ‘band atrophy’, where the pallor extends horizontally in a band across the optic disc. This corresponds to degeneration of the peripheral retinal ganglion cells located nasal to the fovea that course directly into the nasal aspect of the disc and the nasal macula fibers (the papillomacular bundle), which course directly to the temporal disc. There is relative sparing of the superior and inferior portions of the disc, where the majority of spared temporal fibers which subserve the nasal visual field enter (Cushing 1930).

Papilledema. This is more frequently associated with suprachiasmal tumors which may occlude the third ventricle, but rarely with intrasellar lesions.

Decompensated phoria. This presents with a manifest comitant strabismus and is a result of loss of normal nasotemporal visual field overlap in patients with complete bitemporal visual field defects.

See-saw nystagmus. This is characterized by synchronous alternating elevation and intorsion of one eye and depression and extorsion of the other eye, and occurs in patients with tumors in the diencephalon or chiasmal lesions. It is thought to be caused by damage to the structures near the interstitial nucleus of Cajal.

Hypothalamic involvement:

Diabetes insipidus

Hypothalamic hypopituitarism

Growth retardation and delayed sexual development in pre-pubertal children.

Features of hydrocephalus from a tumor that has expanded postero-superiorly into the third ventricle and obstructed cerebrospinal fluid flow:

Impairment of upgaze

Pupillary light-near dissociation

Convergence retraction nystagmus

Papilledema.

Visual field loss. Two configurations of visual field loss are the ‘signatures’ of chiasmal involvement.

Bitemporal field defects (Fig. 11.11). The bitemporal hemianopia is seen in lesions that affect the central portion of the chiasm. The classic bitemporal hemianopia may involve only the superior visual fields if the lesion produces extrinsic compression initially from below such as occurs with a pituitary adenoma or any other infrachiasmal lesion (e.g., tuberculum sellae and medial sphenoidal ridge meningiomas). Gradually the defect descends into the lower temporal field and then into the lower nasal quadrant. In general, the upper nasal visual field is often preserved even in advanced chiasmal syndromes.

Conversely, superior chiasmatic compression may cause only an inferior hemianopic field loss. In most cases of bitemporal hemianopia, the visual acuity is normal. In addition, a suprachiasmal tumor is more likely to produce papilledema because such lesions can extend into and occlude the third ventricle.

Occasionally, a large posterior fossa tumor may cause chiasmal syndrome by compression of the third ventricle through increased intracranial pressure. Most of these cases are also associated with papilledema.

Iatrogenic causes of chiasmal syndrome occur most commonly after removal of a suprasellar meningioma, craniopharyngiomas or clipping of an aneurysm. A chiasmal syndrome can also occur from exuberant packing of the sphenoid sinus with fat following transsphenoidal resection of a pituitary adenoma resulting in inferior compression of the chiasm. The visual field defect usually improves immediately after emergency removal of the fat.

Radiation necrosis of the chiasm may also produce a chiasmal syndrome. This may begin months to several years after high dose radiation therapy.

Junctional scotoma or ‘anterior chiasmal syndrome’. A lesion that is located more anteriorly compressing the medial aspect of the junction between the chiasm and the optic nerve will affect the ipsilateral optic nerve fibers and the contralateral fibers of Willebrand knee (the crossing of the temporal retinal fibers). This results in an ipsilateral central scotoma and a contralateral superior temporal field cut, and is also called a junctional chiasmal syndrome. When a small lesion damages only the crossing fibers of the ipsilateral eye, the field defect is monocular and temporal with a midline hemianopic character that extends to the periphery of the visual field. If only the macular crossed fibers from one eye are damaged, the resultant field defect is still monocular and temporal but is scotomatous and located paracentrally.

Other visual field defects:

Bitemporal hemianopic scotoma

Lesions that damage the posterior aspect of the optic chiasm produce typically bitemporal hemianopic scotomas which are often taken for cecocentral scotomas attributed to toxic or hereditary processes rather than a tumor. However, bitemporal hemianopic scotomas will be associated with normal visual acuity and color vision, whereas toxic/nutritional processes are invariably associated with reduced visual acuity and dyschromatopsia

Homonymous hemianopic field defects. The homonymous hemianopic field defect is more likely with a pre-fixed chiasm or when the tumor involves the optic tract which is usually incongruous (Kearns & Rucker 1958)

Monocular visual field defect. If the posterior portion of the optic nerve is involved the visual field defect may be monocular with a central or cecocentral defect. Compression of the posterior optic nerve against the overlying anterior cerebral artery, the roof of the optic canal, or the falciform ligament may cause an inferior altitudinal defect.

Optical coherence tomography. Optical coherence tomography (OCT) is an imaging technique that has been developed to assess tissue thickness of the optic nerve head retinal nerve fiber layer (RNFL) thickness in vivo. It allows high resolution (approximately 10 µm) cross-sectional imaging of the eye. The peripapillary RNFL thickness can be evaluated and quantified using OCT. OCT RNFL has been shown to be able to predict visual recovery following surgery for pituitary tumors. Patients who have thin preoperative RNFL (<85 µm) have less recovery of visual acuity and visual field than patients who have thicker RNFL (Fig. 11.12) (Danesh-Meyer et al 2006, 2008b).

Extension into the cavernous sinus (see below):

Motility disturbance. Patients will have characteristics of IIIrd, IVth, or VI nerve palsy or a combination of these

Trigeminal sensory neuropathy. This is present when the ocular motor nerves are damaged in the cavernous sinus. There is no motor trigeminal nerve involvement

Horner's syndrome. If the oculosympathetic fibers are damaged, there will be a post-ganglionic Horner's, usually in combination with VIth involvement. When both the IIIrd and oculosympathetic fibers are damaged, the clinical picture will be one of a IIIrd nerve palsy with a small pupil that will be normally reactive if the paresis is pupil-sparing or poorly or non-reactive if the IIIrd nerve paresis has damaged the pupillomotor fibers.

Vision (cranial nerve II)

There are three aspects to optic nerve function:

1.

Visual acuity, which is usually assessed using a Snellen chart (Fig. 5.1).

Visual field testing to confrontation is a simple screen for homonymous hemianopia (an identical visual field defect due to cerebral hemisphere disease) and for sensory inattention (due to parietal lobe lesions). Sit opposite the patient and ask them to fixate on your nose. Get the patient to count fingers at the edge of each field in each eye in all four quadrants.

Fundoscopy takes practice; perform it only if competent with an ophthalmoscope.

Differential Diagnosis and Assessment

Standard visual acuity can be measured with a distance and near Snellen chart. Testing the effects of decreased contrast sensitivity, decreased illumination, and increased glare is not practical for the primary care provider, as the equipment necessary for such testing is specialized, and is not widely available to primary care providers.3,4 Rather, questioning older patients about their performance under these circumstances is easier. For contrast sensitivity, ask if a patient has much difficulty driving in the rain or seeing on a hazy day. For low illumination, ask if your patient has significantly greater difficulty seeing at dusk and at night. For glare, ask how debilitated your patient is by oncoming headlights, by walking from outside to inside on a sunny day, or by entering a tunnel from daylight.

Vision.

Vision is an important sensory component of intrinsic postural control as well as an important mechanism for avoiding balance challenges from environmental hazards. Significantly impaired visual acuity as well as impaired contrast sensitivity and depth perception have been associated with falls, as well as health conditions resulting in central or peripheral visual field cuts.59

OCULOMOTOR SYSTEM

Dynamic visual acuity

The patient's static visual acuity is determined with both eyes viewing using a standard eye chart, e.g., a Snellen chart. The procedure is then repeated, but under constant horizontal or vertical oscillation of the patient's head, typically with 2 Hz and 10° peak-to-peak amplitude. The head oscillation is passive and applied by the examiner standing behind the patient. The visual acuity with the head oscillating, i.e., dynamic visual acuity, is compared with the static visual acuity. The reduction of visual acuity due to the head oscillation should not exceed two lines on the chart of optotypes. Since the static visual acuity serves as reference, the test can be done with or without eye glasses.

The dynamic visual acuity test relies on an intact vestibulo-ocular reflex (Demer et al., 1994). Therefore, provided ocular motor function is normal, a reduced dynamic visual acuity is highly suggestive of a bilateral vestibular deficit. Effective catch-up saccades can improve dynamic visual acuity over time, despite an unchanged deficit of the vestibulo-ocular reflex. Thus, dynamic visual acuity may also serve as a bedside test to monitor the effects of vestibular rehabilitation.

Notice that, in contrast to the head impulse test, dynamic visual acuity does not allow a comparison of the vestibular function between the two sides. Such side-specific diagnostic information can only be obtained with computerized tests that measure visual acuity during head movement in different directions separately (Vital et al., 2010).