Clinical Decision Making I: visual field interpretation.
Visual field assessment provides a measure of the neural pathway integrity from eye to visual cortex. Certain patterns of visual field defect are associated with damage to specific regions of this pathway. Inaccurate test results can compromise interpretation leading to potentially serious consequences for diagnosis and ultimately the management decisions for that patient.
Revision of the visual pathways
The anatomy of the sensory visual system is described here very briefly, and reference to a detailed text is strongly recommended. (1,2)
The optic nerve head (ONH) so readily discerned by ophthalmoscopy is considered the reference location to which features are related from an anatomical or structural perspective. However, from a functional perspective, when assessing the visual fields, its projected representative, the blind spot takes a minor role. Instead, the fovea and fixation with its significant representation at the cortical level becomes the key reference locus.
The inverted visual representation that is generated by the optical system focussing light entering the eye, is maintained throughout the visual system. Lesions temporal to the fovea give rise to nasal visual field defects whilst those superior to the fovea or involving superior-originating fibres at any point along the pathway produce inferior visual field loss.
The ganglion fibres originating from the innermost layer of the retina tend to group themselves by regions according to their origin relative to the fovea. The macula fibres nasal to the fovea (maculo-papilla bundle), follow a direct course across the retinal surface to turn down through the ONH at its temporal border. They form the core of the optic nerve with axons from the superior retina uppermost and those from the inferior half of the retina, beneath them. Those macula fibres temporal to the fovea arch around the maculo-papilla bundle to enter the supero-temporal and infero-temporal ONH boundaries. Fibres arising nasal to the optic disc travel radially directly to the nasal side of the ONH. The ONH forms the intraocular portion of the optic nerve. Beyond this region the 1.2 million afferent nerve fibres travel a further 25-30mm intraorbitally, passing via the optic foramen to the optic canal in the orbital wall to emerge into the intracranial section. The optic nerve travel for another approximately 10mm to reach the chiasm. (3)
The term, 'chiasm' is derived from the Greek letter chi that describes the shape of the neural tissue at the region where the optic nerves from each eye converge. It is about 4mm thick and on average 10-12mm wide by 8mm in length. At the chiasm approximately half of the nerve fibres from each eye decussate (cross-over) to the opposite side of the brain tissue en route to each occipital lobe. Axons from retinal ganglion cells nasal to the fovea, which carry information from the temporal visual field, cross the midline to join axons from the temporal retinal ganglion cells, that do not cross in the chiasm. Together these form the optic tracts. Once again the division of the fibres from each half of the retina is through the fovea as represented in the field of view by the point of fixation. The blind spot falls entirely within the temporal field.
The fibres leaving the optic chiasm course posterio-laterally to synapse in the lateral geniculate nucleus (LGN), where they retain a well-defined laminar organisation. The crossed fibres terminate in layers 1,4 and 6 whilst the uncrossed ipsilateral fibres synapse in layers 2, 3 and 5. The macula fibres occupy a proportionally large area within this structure. The LGN is quite small and it is unusual for a lesion to involve the nucleus alone without encroaching on the optic tract or radiations either side of it.
Upon leaving the LGN, the upper fibres of the optic radiations take a relatively direct course backwards, spreading in a broad fan through tile parietal lobe to terminate in the occipital visual cortex. The lower fibres initially loop forward towards the anterior pole of the temporal lobe to form Meyers Loop, before turning back to join the lower part of the optic radiations at the occipital pole.
Guidance in choosing an appropriate test strategy/program
To interpret visual field plots one needs knowledge of the visual pathways. An appreciation of the skill, or arguably the art, employed supervising a visual field test particularly under less than favourable conditions should also be expressed.
The human visual system is poor at estimating absolute magnitude of light intensity but remarkably good at perceiving contrast. This facility is evaluated when a visual field test is performed. By measuring the differential light sensitivity to a stimulus against a standardised, constantly illuminated background, one can obtain an estimate of the threshold for detection at a given retinal location.
The choice of visual field test depends on the degree of detail required and the patients' ability to cooperate. One of the most valuable techniques to master is confrontation testing, particularly in suspected neurological disease. Confrontation testing being both rapid and simple should always precede any more detailed attempts with more sophisticated automated static or manual kinetic perimetry. For those patients too poorly, whether mentally or physically, this test can be most informative. It can reveal the presence of a constricted field or altitudinal, quadrant or hemifield defect (see definitions later).
By employing simultaneous testing of opposite quadrants it is possible to detect asymmetric subtle relative visual field defects or 'extinction'. The latter phenomenon occurs when a target is missed in an affected hemifield only when both hemifield are tested simultaneously and is characteristic of parietal lobe lesions. Testing the macula area with an Amsler Chart is useful for rapidly screening the central 20[degrees] of the visual field, despite sensitivity being relatively low.
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Automated perimeters that include the Humphrey Visual field analysers and Henson perimeters are less operator dependent than for the manually operated Goldmann perimeter. The tested locations are standardised and provide a high level of quantitative data that allows statistical analysis and facilitates data storage and transfer of information. They can be tedious to perform irrespective of age, even with the benefit of the newer interactive algorithms. There are limited choices to test speeds and a degree of interpolation of the visual field is introduced in the post-test processing. Manual perimetry has been considered superior to automated perimetry for neurological fields, but recent studies have found the Swedish Interactive Thresholding Algorithms (SITA) to be comparable (4,5).
Static testing, whereby the stimuli are presented at specific locations and their brightness is varied are relatively sensitive to shallow depressions of the visual field where there are fiat almost equally sensitive areas. Kinetic testing is more useful in regions whose sensitivity sharply changes between adjacent areas. Goldmann perimetry employs primarily a kinetic technique to plot boundaries of isopters (points joined together by a drawn line with equal levels of estimated sensitivity) and scotomas (depressed areas of sensitivity) by moving a visual stimulus from a non-seeing to a seeing region. Additional static testing is then used to verify the regions within a given isopter and as catch trials to reveal false positive, negative and fixation losses.
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Supra-threshold testing until the newer thresholding algorithms were developed was considered the least time consuming. The stimuli brightness selected is chosen such that subtle shallow defects are unlikely to be revealed. By using multiple stimulus patterns the test duration can be further reduced. Threshold testing, on the other hand, uses single stimuli testing and an estimation of the threshold based on 'frequency-of-seeing' characteristics. Greater detail of defect depth and extent is possible when using a thresholding system.
The choice of programme for visual field assessment is dependent on the suspected lesion. Generally, central visual field programmes are considered adequate to reveal the majority of visual field defects that one is likely to encounter arising from intracranial lesions, including those at the optic chiasm or optic tract. There are however some exceptions that involve only the peripheral retinal fibres, the temporal crescent represented region of the occipital lobe or associated with a state-kinetic dissociation. Peripheral visual field programmes should be undertaken if doubt exists over the results of a central VE programme when neurological disease is suspected.
Should a group of 2 or 3 points (a 'cluster') at the edge of a 24[degrees] visual field examination be abnormal then one should consider repeat testing and include a peripheral plot. Similarly, if fixation and visual acuity are reasonable good, but visual field abnormalities are extensive and threaten the 5-10[degrees] region, then selecting a specific macula programme with greater sampling of locations close to fixation would reveal the risks to vision. The results are then interpreted both qualitatively for patterns of visual field abnormality and quantitatively in terms of depth or degree of damage.
Determination of test reliability
Sources of error can he broadly categorised into those arising during the test period and those introduced in the subsequent analysis and
By the subjective nature of a visual field test, the results can be profoundly affected should the test operator take insufficient care. It is they who generally provide initial instruction and a brief explanation of why the test is being performed and its relevance to the patients' management. Although the patient may claim to have done a similar test previously, one should repeat the instructions and consider running a demonstration programme to familiarise each person with the test. This allows for retinal adaptation and overcomes some of the apprehension that many experience when faced with the demands of formal perimetry.
Unless functional vision for driving or mobility purposes is being evaluated, the non-test eye should be appropriately occluded. Fixation should be directed to a single point to ensure steady fixation, with the patient alert and mentally competent.
The blind spot, temporal to fixation, represents the projection into visual space of the ONH, nasal to the fovea, where the ganglion cell axons exit at the hack of the eye. It produces a small, physiological, absolute scotoma. If fixation is not maintained the blind spot is less likely to be plottable and the credibility of the visual field test evidence derived from the rest of the procedure is brought into doubt.
A comfortable, correctly aligned setup for the patient should be established and maintained. Gentle encouragement at appropriate intervals may be required to optimise a relaxed yet attentive attitude. During the course of the test, the operator should seek to minimise fixation losses, by monitoring eye and head movements visually, alerting patients to poor stability and replotting the blind spot position if incorrectly identified by the suhroutines that most modern automated perimeters use. Brief rests can be incorporated within and between the test of each eye and the patient should be encouraged to blink naturally during the test sequence, without the perceived tear that stimuli may be missed to the detriment of their test result. The test may need to be restarted, repeated or even aborted if the operator judges the results being generated to be significantly unreliable.
The printout provides clues to the reliability of the test results. Comments made by the patient or by the operator documented at the time of the test are invaluable when considering the true value of the information generated. Patients may admit to having seen repeated stimuli to which they had not responded. They may have been distracted mentally by anxiety, their ill health, or extraneous noises. The test duration reported on the printout does not account exclusive for rest periods, that may, by necessity, have been frequent albeit brief.
Upon receiving the completed test results, several points need to be checked to establish their authenticity.
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The personal data (Figure 1, A) should be scanned to confirm the patient's full name, their date of birth (including correctly stated year), how recent the test. If the test duration stated was longer than expected for that test strategy, it is worth verifying that appropriate rest periods were given and the eye to which it relates.
Significant alterations to pupil size can lead to diffuse visual field changes, so pupil diameter should have been recorded if the patient was known to be using miotic or mydriatic eyedrops. An alternative fixation target may have been chosen if severe foveal damage had obscured the view of the default fixation target. A refractive error correction should have been chosen appropriate to the test distance to compensate for significant ametropia, including astigmatism and presbyopia. The operator should always verify that the lenses chosen are single vision, full aperture, correctly powered and aligned, and do not 'steam-up' or get touched during the test. If contact lenses were worn for the test, one needs to ensure that suitable 'over' correction was chosen. Presbyopia corrective contact lens designs are becoming more common. Inappropriately corrected refractive error can produce an enlarged blind spot, diffuse field depression and a more negative Mean Deviation index.
Modern perimeters generally provide some form of reliability indices (Fig.1, B). These commonly include a measure of fixation losses, false positive and false negative responses. High fixation losses suggest poor eye or head fixation. Other causes include inadequate occlusion of non-tested eye, poor BS localisation, and poor response button control. Whether the index is a true representation of fixation stability can be corroborated by comments documented by the test operator from their direct visual observation at the time of the test. If an automated fixation monitor has been disabled, 'zero fixation losses' may not necessarily represent excellent fixation. False positive responses are generally associated with anticipation ('trigger happy') which can lead to a more positive Mean Deviation index and high Pattern Deviation values. False negative errors can be attributed to fatigue (health related or disturbed sleep patterns), but are also known to be present in patients with early onset of visual loss, developing a relative scotoma and demonstrating varying visual response, or who already have visual field defects that are progressing.
The time between testing for each eye should be noted. Adequate but not excessive rest should have been provided and the previously occluded eye given sufficient time to re-adapt to the background illumination. This can be particularly pertinent if delayed retinal adaptation is likely to be a factor for example, in those with rod/cone dystrophies.
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Goldmann visual field plots, similarly should include the patient name, date of birth, date of test, selected eye, refractive correction used and the stimuli characteristics employed. It is assumed that the instrument has been adequately maintained and is calibrated regularly. Generally the blind spot position/size and at least three isopters are presented, having been selected to demonstrate the location, depth and extent of any significant variation in the visual field. As with contour lines on an Ordinance Survev map, the closeness of the isopters to each other indicates the rate of change in sensitivity and the gradient of a boundary. It is good practice that each of the isopters is annotated, in addition to colour codes that indicate the stimuli characteristics from which they were derived. Subsequent evaluation of the raw threshold values (Fig. 1, D) in an automated perimetric printout, their associated age-corrected (Fig. 1, E), pattern corrected (Fig. 1, F) and probability-derived plots (Fig. 1, G) depends upon the overall impression of reliability that is given.
Grayscale plots (Fig. 1, C), despite their immediacy of visual field representation can be misleading. They have a limited palette of gray scale tone and regions between test locations undergo interpolation. The numeric grid provides an estimate of patient visual sensitivity in terms of decibel values at locations determined during the test sequence. The threshold values are a function of the instrument dynamic range of contrast between stimuli and the background illuminance. Small defects can be missed should they lie between the test locations.
The Total Deviation grid (Fig. 1, E) provides pointwise age-corrected numerical values of the estimated threshold. Comparisons across the horizontal and vertical meridia (:an alert one to potential abnormalities. The Pattern Deviation (Fig. 1, F) filters out the presumed diffuse sensitivity depression to highlight potential regions of focal depressed function. These are statistically analysed to generate the probability plots (Fig. 1, G) as to the likelihood of the estimated values indicative of normal function.
Identification of the likely location of a suspected visual pathway lesion
One of the primary tasks is to determine whether the lesion is intraocular (IO) or intracranial (IC) (6). The IO lesion needs ophthalmological investigation whereas the IC lesion needs neurological investigation. An inappropriate referral can cause delay in management by several weeks or even months. If a patient describes a visual loss as being 'missing' it suggests a 'Negative' scotoma that implies a neurological disease, whereas a smear, smudge, cloud or veil is classified as a 'Positive' scotoma and implies a retinal disease or media opacity.
Knowledge of the visual pathway anatomy is required to differentiate between specific VF patterns. One should always check the VF from the 'uninvolved' eye for subtle defects even when symptoms are unilateral (such as in the case of a temporal defect in junctional scotoma that could arise from a chiasmal compressive lesion). (See figures 2 and 3).
The key points to consider for each aspect, pertaining to the relevant ophthalmic and systemic factors, are a careful and thorough history, the reported symptoms and identified signs, and any visual field results.
The principal points of history taking in cases of impaired vision are, the type of involvement, whether unilateral or bilateral, the time course of vision dysfunction/disturbance and any associated symptoms.
The possible cause of" visual field loss implied by the speed of onset can only be inferred according to how soon the patient becomes aware of loss. In terms of the presumed time course in which the condition has developed, sudden onset (within minutes) usually indicates an ischaemic event (e.g. occlusion of retinal vessels from emboli), whilst rapid onset (over hours) is also characteristic of ischaemic event, but at the level of the optic nerve. Moderately rapid (days to weeks) is likely to be ischaemia-related, but cam also be linked to inflammation. Gradual progression over months are found in lesions of toxic origin, whilst slower progression of months to years is suggestive of 'compression'.
Associated symptoms can assist in localisation though not wholly specific. They can include ocular or orbital pain (as in retrobulbar ON), diplopia, hemiparesis, headaches, and in extreme cases variable levels of consciousness.
The ophthalmological or neuroophthahnological examination, is directed towards detecting, quantifying and localising the region of vision loss. Any visual field test should be interpreted in context with the other results arising from a full examination. This should include a measure of visual acuity, both best-corrected and pinhole vision at distance and near (line and single letter) and an evaluation of the pupillary responses. The aim is to detect a relative afferent pupillary defect (RAPD), which is characteristic of impaired optic nerve conduction. The presence of an RAPD is an extremely reliable and sensitive indicator of asymmetric optic nerve dysfunction. It is likely to accompany any substantial lesion that decreases ganglion cell output to the optic nerve, for example severe age-related macular degeneration, acute retrobulbar ON or retinal detachment. It is derived from a disparity between the direct and consensual light responses in an affected eye (not dealt with in this article). The pupil on the abnormal side appears to paradoxically dilate in response to a light stimulus. An RAPD becomes more apparent when the ambient lighting is dimmed. It can be detected in the presence of a total 3rd nerve palsy, as only one active pupil is necessary to detect an RAPD. Bilateral optic neuropathies (if equally impaired) may show no relative differences between the two pupil responses and an RAPD may not be detectable.
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Careful direct monocular and binocular slit lamp ophthamoscopy, preferably through dilated pupils, should establish whether a VFD arises wholly or partially from a retinal or anterior segment component. Optic atrophy, if present, indicates damage to the retinal ganglion cell, its cell body, or axon up to its synapse at the LGN. It can take 4-6 weeks from the time of damage until it becomes apparent. The resultant atrophy can be diffuse or segmental. Acute retrobulbar ON is not normally associated with a swollen optic disc. Atrophy, though not diagnostic in itself, demands immediate referral for thorough investigation as to its cause. A VA of 6/6 or better does not exclude the possibility of significant VF loss. Optic disc oedema results from impaired axoplasmic transport that includes raised intracranial pressure, ischaemia, or inflammation. It is characterised by an elevated ONH, indistinct disc borders, venous and capillary dilation and tortuosity, sometimes accompanied by peripapillary haemorhages and exudates. Bilateral optic disc swelling needs urgent referral to a neuroophthalmologist opinion as MRI scanning may need to be arranged, even in the absence of vision disturbance.
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Beware of the 'silent' neuroophthalmic patient presenting with blurred vision (with or without reports of loss of field). Confrontation field-testing and RAPD evaluation (before dilated fundoscopy) should always be performed, and if either are abnormal or the degree of vision loss is inconsistent with the ocular examination, formal perimetric testing is required.
The normal VF extends approximately 100 temporally, 60 nasally, 60 superiorly and 75 inferiorly from fixation in each eve;. Unilateral loss almost invariably indicates an intraorbital lesion or one anterior to the chiasm on the affected side. Bilateral loss, can be indicative of bilateral retinal or optic nerve origin, chiasmal or retrochiasmal location. There are several terms that are used to describe the type of defect that may be encountered with perimetry.
Scotomas represent a focal area of depressed sensitivity either relative (dependent on the perimeter used) or absolute (to any level of stimulus), surrounded by normal sensitivity. When the scotoma involves fixation, as often found with age-related maculopathy, it is termed 'central'. If it also involves the maculopapillae bundle as found in toxic optic neuropathies, or congenital optic disc pits associated with central serous detachments, a centrocaecal scotoma can develop. A paracentral scotoma adjacent to, bnt not involving, fixation is typical of early glaucoma. Arcuate patterns that can extend to the nasal boundary where a nasal step due to file asymmetry of sensitivity across the horizontal meridian, often arise from glaucomatons visual field progression are associated with damage to the retinal nerve fibre bundles at the optic disc poles. They can also be associated with ischaemic optic neuropathy or congenital disc drusen.
Congruency describes the similarity in the shape of visual field loss or conversely the visual field preservation between each eye. Generally, the greater the similarity or congruency, the more posteriorly located the lesion. Both anatomical and psychophysical variability, however, confounds its diagnostic value. The degree, of congruency is not only dependent on the visual field region involved but also the causative agent. An infarct to a cerebral vessel is generally associated with well defined boundaries, whilst the disorganised behaviour of tumour tissue can involve more diverse regions.
Altitudinal defects respect the horizontal meridian, involving either pair of superior or inferior quadrants (Figure 3 A). They are typical of ischaemic optic neuropathies or a hemiretinal vascular occlusion, though they can very rarely be due to bilateral symmetrical lesions of the visual cortex.
Hemianopia describes a defect involving the complete right or left half of the visual field. Quadrantanopic defects predominantly involve one of the four quadrants. 'Heteronymous' hemianopia refers to opposite halves for each eye as in bitemporal hemianopia. 'Homonymous' defects affect the same side for each eye, characteristic of retrochiasmal lesions. A complete homonymous hemianopia is nonlocalising. The entire hemifield being involved confounds attempts to differentiate between the likely retrochiasmal location that a visual pathway lesion has occupied. Homonymous visual field loss can be perceived by the patient as monocular loss to the eye of the affected hemifield until examined.
A centrocaecal scotoma in one eye accompanied by a superior temporal quadrantanopia in the other eye, termed a 'junctional' scotoma, is suggestive of a prechiasmal lesion close to where the optic nerve meets the chiasm (Figure 3 C).
By far the most common cause of chiasmal disorders is compression by a tumour in the region of the pituitary gland, but rare non-compressive causes including infection, inflammation, and ischaemia and toxicity are encountered. About 10mm directly below the chiasm lies the sella turcica, a depression in the sphenoid bone that supports the pituitary gland. Significant enlargement, with suprasellar extension of pituitary tissue, is therefore necessary before it is likely to be associated with any field defects. Suprasellar masses infrequently cause raised intracranial pressure and optic atrophy occurs late in chiasmal lesions. The extent of the defect does not always correlate with the magnitude of the tumour since tile damage to the fibres can he both due to direct and indirect interference.
Chiasmal Lesions, whether arising from the pituitary gland itself or the surrounding tissue, are rarely accompanied by the classic, complete bitemporal field loss (Figure 3 D). They more commonly present with an optic neuropathy and a varied pattern of field defect, in one or both eyes, due to compression of more than one structure. They tend to fall into four basic groups; from above, from beneath, from the antero-lateral or postero-lateral direction depending on the direction the lesion impinges on the chiasm. Chiasmal lesions can produce an RAPD though they tend to be more subtle than those arising from a lesion of the optic nerve.
Anatomical variation in chiasm location and pathological variation in tumour growth pattern leads to diversity in the visual field defect presentation and confounds precise interpretation. Bitemporal hemianopias may be confined to the central visual fields particularly in lesions compressing the posterior portion of the chiasm. A bitemporal hemianopia which respects the vertical meridian that is predominantly superior strongly suggest compression from beneath, for example a pituitary adenoma whilst one biased infeiiii suggests a craniopharyngioma, exerting force from above. These latter, slow growing tumours, occur in all age groups, but particularly children.
Binasal visual field loss is much more likely to be caused by optic nerve damage, such as glaucoma since the temporal retinal fibres do not merge and are likely to only be simultaneously involved if there is bilateral eye lesions.
Retrochiasmal Lesions (affecting the optic tract, lateral geniculate body, optic radiation) cause a partial or complete homonymous hemianopia. Pure optic tract or LGN lesions are rare. They can be distinguished from lesions of the optic tract by the absence of an RAPD. The most common cause is cerehrovascular disease, and although brain tissue malignancy, inflammation, infection or arteriovenous maltormations are rare, neuroimaging is necessary to exclude these possibilities in all patients with homonymous visual field defects.
Three types of VED have been attributed to LGN lesions, and each can be accompanied by optic atrophy (8,9,10) . An incongruous homonymous hemianopia, a congruous sectoral hemianopia that crosses the horizontal meridian and sparing of this sector but damage to the upper and lower sections. The; latter two patterns result from occlusion of the lateral choroidal artery or ischaemia of the anterior choroidal artery, a branch of the internal carotid, respectively (Figure 3 F & E).
Partial homonymous hemianopias can be categorised in terms of their degree of congruity, whether predominantly in the superior or inferior field or whether accompanied by macular sparing. 'Macular sparing', whereby the hemifield defect includes preserved central 3-5 vision, suggests a posterior cerebral artery stroke with middle cerebral artery support, akin to the role of a cilio-retinal artery in maintaining vision in central retinal artery occlusion. It is diagnostic of an occipital lobe lesion, being rarely encountered with lesions anterior to the visual cortex (Figure 3 J). A homonymous hemianopia that does not spare the fovea, causing 'Macular splitting' has less localising value.
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A predominantly superior homonymous quadrantanopic field defect ('pie-in-the-sky') may be due to a temporal lobe lesion that impinges on the inferior bundle of nerve fibres that form the optic radiations (Figure 3 H). An inferior defect (pie-on-the-floor) can arise from a parietal lobe lesion interfering with the superior optic radiations (Figure 3 G). Parietal lesions typically present with additional neurological deficits that confound formal perimetry and may only be inferred from confrontation testing. Quadrant VFD that respects both the horizontal and vertical meridian is likely to be located along the calcarine fissure at the cortex.
Lesions that occur at the Occipital Primary Visual Cortex potentially retain good visual acuity, particularly with distance vision but may have more difficulty with near vision if the text is large or enlarged. Generally the lesion is not associated with optic atrophy unless associated with raised intracranial pressure. The pupil reactions are typically normal. The visual field defects are highly congruous. There may be additional neurological disturbances including hallucinations, alexia and loss of colour perception.
Rarely, if a lesion should damage the tip of one occipital lobe, the patient may complain of reading difficulties (despite no apparent macular abnormality) and Amsler grid testing or a central 10-2 threshold programme with Humphrey automated perimetry may reveal a small homonymous paracentral scotoma (Figure 3 1). The causes are primarily vascular, with occlusion along the posterior cerebral artery, or ischaemia caused by a cardiac embolus, vertebrobasilar occlusive disease, arteriovenous malformations or in some cases following cervical manipulations that injure the vertebral arteries. Other causes are primary and secondary tumours or trauma.
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Arguably, some of the most difficult cases to diagnose are those that produce a tunnel vision field defect (11) (Figure 3 B). One should differentiate between the 'true' funnel type of constricted visual field loss where the breadth of the defect changes with the distance at which the test is performed and the tunnel vision that remains the same angular subtense for different test distances, that is characteristic of a malingering cause. The more common causes are:
* End stage glaucoma that is associated with extensive optic disc cupping
* Retinitis Pigmentosa, accompanied bv retinal pigment clumping, disc pallor and attenuation of the retinal arteries
* Extensive panretinal photocoagulation in proliferative diabetic retinopathy
* Chronic Pailloedema with swollen or pale optic discs
* Chorioretinitis with widespread retinal pigment disturbance or functional loss
* Bilateral occipital lobe infarcts with macular sparing supported by the relevant history, neurological condition and neuroimaging
* Functional loss due to hysteria or malingering.
Selection of salient observations to support referral decision
Each referral should include the date, full name of referring optometrist, their practice address and contact telephone number and the patients' GP details in block capital letters. The full details of the patient, including their date of birth, NHS number (if known) and a contact telephone number should be provided.
The referral should be supported by a salient history, to include the prime complaint, its duration, whether constant, intermittent, progressive or stationary and the time of onset.
A list of current medication may also prove useful (if known). If additional neurological signs are observed, that could include any or all of the following; headaches, nausea/vomiting, loss or impaired consciousness, unsteady gait, speech or hearing impairment, hemiparesis: then they need stating.
Test results should included a measure of the current visual acuity and previous visual acuity (if known), indications as to the presence or absence of RAPD, and a summary of the ophthalmoscopic findings. If formal perimetry or merely confrontation has been undertaken, the type of visual field defect, its repeatability mid reliability should be shown. The reason for the referral, a provisional diagnosis and an indication of its urgency, should be clearly stated. (Figure 4).
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Recommendations for referral prioritisation
There is a wide range of causes of binocular visual field defects. Some are sight and life threatening and it is not easy to differentiate from those that are not, without further investigations, such as neuro-imaging. In general terms, all those suspected of having a neurological feature need urgent investigation. A young patient, particularly if symptomatic, needs a more urgent referral than an elderly asymptomatic patient. A suspected bitemporal hemianopia needs urgent same day referral as the sooner the cause is identified the greater the chance of any visual recovery.
It is not acceptable to send a patient to an acute referral centre without an arranged appointment. Should a patient present with a condition that warrants an emergency referral the centre to which the referral is directed should he informed and appropriate advice or guidance sought. Suspected serious, purely intraocular conditions require same day referral to an eye casualty unit, ophthalmic outpatient clinic or an Accident and Emergency Unit, dependent on the local services available. Suspected serious intracranial conditions with or without an intraocular component require referral to an Accident and Emergency Unit. This is for guidance only as there may be guidelines, in place, according to the local arrangements.
S.U.P.E.R Summary Points (adapted from Pane, Burdon and Miller (12))
Suspect the possibility of a serious intraorbital/cranial disease when a patient presents with a vision or eye complaint.
Understand and use the knowledge of the visual pathway to formulate a systematic series of questions and investigations.
Perform a thorough and careful examination including a full history, ocular examination, confrontation test, RAPD evaluation and formal perimetry.
Evaluate the visual field results for reliability and correlate with other evidence for unilaterality or bilaterality.
Refer to a neuro-ophthalmologist with appropriate urgency if the examination leads one to suspect a nonocular cause for a visual disturbance.
Module questions Please note, there is only one correct answer. Enter online or by form provided
An answer return form is included in this issue. It should be completed and returned to CET initiatives (c-8367) OT, Ten Alps plc, 9 Savoy Street, London WC2E 7HR by August 13 2008.
1. Which of these statements is true?
(a) Goldmann perimetry employs both a kinetic and static technique.
(b) In automated perimetry the background illumination is varied according to the testing programme.
(c) Kinetic perimetry is more reproducible than static perimetry.
(d) End stage glaucomatous visual field loss can only be monitored by Goldmann visual field testing
2. In non-arteritic anterior ischaemic optic neuropathy, which of these statements is true?
(a) It typically causes an inferior altitudinal field defect.
(b) Visual loss usually develops over 2-3 days.
(c) Visual acuity improves with time.
(d) It usually causes a centrocaecal type field defect.
3. Which of these statements is true? Acute retrobulbar ON is usually associated with:
(a) An altitudinal field defect.
(b) Normal pupil reactions.
(c) A swollen optic disc.
(d) Pain on eye movements.
4. Which of these statements about the LGN is true?
(a) The LGN is supplied by the anterior cerebral artery.
(b) The LGN receives input from both eyes.
(c) Pure optic tract or LGN lesions are relatively common.
(d) The most common cause of an LGN lesion is malignancy.
5. Which of these statements about an RAPD is false?
(a) It may be associated with normal visual acuity.
(b) It can be quantified using a neutral density filter.
(c) Optic nerve disorders can be differentiated from retinal disorders purely based on its findings.
(d) It can be detected in the presence of a total 3rd nerve palsy.
6. Which of these statements about chiasmal lesions is true?
(a) Bitemporal hemianopias always involve the peripheral visual fields.
(b) Optic atrophy is an early sign of chiasmal involvement.
(c) Suprasellar masses are often associated with papilloedema.
(d) In a child, an inferior bitemporal hemianopia suggests craniopharyngioma.
7. Which of these statements about post-chiasmal lesions is true?
(a) Pupil reactions are normal in lesions of the LGN.
(b) A macula splitting homonymous hemianopia indicates an occipital lobe lesion.
(c) A contralateral, homonymous, inferior quadrantanopia arises from damage to the inferior fibres of the optic radiations.
(d) Lesions of the anterior optic radiations are more congruous than those involving the posterior radiations.
8. At what level of the visual pathway does the lesion that gives rise to the pair of visual field plots illustrated in Figure 5a and b most likely lie?
(a) Retina or Optic nerve
(b) Chiasm or Optic Tract
(c) LGN or Optic radiations
(d) Visual Cortex
9. At what level of the visual pathway does the lesion that gives rise to this pair of visual field plots illustrated in Figure 6a and b most likely lie?
(a) Retina or Optic nerve
(b) Chiasm or Optic Tract
(c) LGN or Optic radiations
(d) Visual Cortex
10. At what level of the visual pathway does the lesion that gives rise to this pair of visual field plots illustrated in Figure 7a and b most likely lie?
(a) Retina or Optic nerve
(b) Chiasm or Optic Tract
(c) LGN or Optic radiations
(d) Visual Cortex
11. At what level of the visual pathway does the lesion that gives rise to this pair of visual field plots illustrated in Figure 8a and b most likely lie?
(a) Retina or Optic nerve
(b) Chiasm or Optic Tract
(c) LGN or Optic radiations
(d) Visual Cortex
12. What do the visual field plots illustrated in Figure 9a and b demonstrate?
(b) Preservation of foveal function
CET Answer Special
A round-up of the latest answers to our previous CET series
C-7636 January 25 Dispensing I: Simple dispensing
1. Correct answer is C. Being a negative lens the thinnest part of the lenses are at the Optical Centres
2. Correct answer is A. The base up prism induced by looking off centre lo mm through the distance lens is partially or fully offset by the base up prism induced by viewing through the segment 8 mm below its dividing line
3. Correct answer is D. When used for reading the reduced spectacle magnification can cause the wearer to feel they are not as "strong" as their old spectacles
4. Correct answer is D. The OC must be repositioned by mm for every 2[degrees] change in pantoscopic angle
5. Correct answer is B. A regular bridge, with its "no pads" format, should be made to follow the contours of the shape of the nose, and hug them closely
6. Correct answer is C. With the optical centre of the segment placed on the dividing line this is the first part of the reading portion the patient's line of gaze meets as it enters the segment
7. Correct answer is B. The pantoscopic angle and the angle of side, although not the same are dependant on one another; adjust one and the other one changes
8. Correct answer is A. The lack of enough decentration will induce unwanted base out prism which will neutralise the prescribed prism
9. Correct answer is B. All the other Best Form designs change the form of the spherical surfaces the lens to achieve their objective
10. Correct answer is C. The off axis blur will only be solved by a lens with a higher Abbe number, whereas the peripheral blur and co[our fringing can be explained and tolerated (on most occasions)
11. Correct answer is C. The freeform design does not have a preset inset, unlike the other, older designs
12. Correct answer is B. If the optician's eye level is higher than that of the subject, then the line of vision will displace the segment top position upwards in the spectacle plane
C-8180 February 22 Dispensing II: Complex lens dispensing
1. Correct answer is B. +8.25/+2.25 x 90
2. Correct answer is D. To reduce the centre thickness of the lens
3. Correct answer is D. To control spectacle magnification
4. Correct answer is A. Decentre 2 mm in.
5. Correct answer is C. Fitting the spectacle frame with as large a vertex distance as possible
6. Correct answer is C. The density of a material is given by mass/volume
7. Correct answer is C. Zeiss Lantal
8. Correct answer is B. A 44-year-old medium to high myope might enjoy more comfortable near vision in spherical as opposed to aspheric lenses
9. Correct answer is B. If a high-powered plus lens with a spherical back vertex power is manufactured with a convex prolate ellipsoidal surface, both aberrational oblique astigmatism and distortion will be reduced
10. Correct answer is B. NVEE is of significance with medium/strong plus spectacle lenses and is more significant when an aspheric lens is used
11. Correct answer is B. +6.00/+3.00 x 180
12. Correct answer is B. Oval with the long axis horizontal
C-8737 March 21 Dispensing III: The low vision patient
1. Correct answer is B. Hyperocular
2. Correct answer is A. 1 in 100
3. Correct answer is C. They are only available up to a maximum of 10x magnification
4. Correct answer is D. Increasing the dioptric power
5. Correct answer is B. 10:1
6. Correct answer is D. 9x
7. Correct answer is C. Transverse magnification
8. Correct answer is D. 'All of the above'
9. Correct answer is A. Negative objective lens and positive eyepiece lens
10. Correct answer is C. 31%
11. Correct answer is A. Electronic Vision Enhancement System
12. Correct answer is B. 6x
C-8954 May 16 Dispensing V: Dispensing for sport
1. Correct answer is C. 68%
2. Correct answer is A. Aiming
3. Correct answer is C. Analytical testing
4. Correct answer is D. The Bassin Anticipation Timing Test is a measure for dynamic fixation
5. Correct answer is B. Worsen sporting performance
6. Correct answer is C. Protection from trauma
7. Correct answer is C. Small eye size
8. Correct answer is C. Sport
9. Correct answer is C. Tennis
10. Correct answer is B. Contact lenses reduce peripheral awareness
11. Correct answer is A. Anticipation / depth perception
12. Correct answer is D.
C-8899 April 18 Dispensing IV: Occupational dispensing
1. Correct answer is B. The employer
2. Correct answer is B. The Health & Safety Executive
3. Correct answer is C. The wrong protector for the task being provided
4. Correct answer is C. Specific for one employee alone undertaking a limited range of tasks
5. Correct answer is D. Around 50% compared with penetrating injuries
6. Correct answer is A. Around 20% of all occupational eye injuries
7. Correct answer is B. Comments on the maintenance of eye protectors
8. Correct answer is D. The employer
9. Correct answer is A. Employers
10. Correct answer is A. The lenses and housings
11. Correct answer is A. Compulsory on all protectors
12. Correct answer is C. N
C-9098 June 13 Dispensing VI: Spectacle lens design
1. Correct answer is C. Inset near zone
2. Correct answer is A. Is more impact resistant.
3. Correct answer is C. 75
4. Correct answer is A. Can cut any mathematically defined surface
5. Correct answer is B. Go darkest in cold weather
6. Correct answer is D. Were originally developed for aphakic prescriptions
7. Correct answer is B. Require both surfaces to be aspheric to optimise both meridians
8. Correct answer is A. Have a narrower distance stable area than longer corridor designs
9. Correct answer is C. Do not indicate whether a lens can be successfully worn
10. Correct answer is B. May be compensated at near by the supplier to allow for position of wear
11. Correct answer is D. Would change density in a fraction of a second
12. Correct answer is B. Can be supplied as low vision aids
Thanks for invaluable assistance with this article to Mike Burden, Neuroophthalmologist at Selly Oak Hospital, Birmingham and Dr Leon Davies, Aston University, Birmingham.
(1.) Harrington DO, Drake MV (1990) The Visual Fields. Text and Atlas of Clinical Perimetry. The C.V Mosby Company, St. Louis, USA
(2.) Rowe F (2006) Visual Fields via the Visual Pathway. Blackwell Publishing Ltd.
(3.) Kanski J (2003) Clinical ophlhahnology: A Systematic Approach, 5th edition. London, Butterworth-Heinemann.
(4.) Szamdry G, Biousse V, Newman NJ (2202) Can Swedish Interactive Thresholding Algorithm Fast preimetry be used as an alternative to Goldmann perimetry in neuro-ophthalmic practice? Archives of ophthalmology 120: 1162-1173
(5.) Wall M, Punke SG, Stickney TL, Brito CF, Witbrow KR, Kardon RH (2001) SITA Standard in optic neuropathies and hemianopias: A comparison with Full Threshold testing. Investigative Ophthalmology & Visual Science 42: 528-537
(6.) Farris B K (1991) The Basics of Neuro-Ophthalmology. Mosby Year Book
(7.) Douglas RA (1999) Automated Static Perimetiy (second edition) Mosby International Limited.
(8.) Rosen ES, Eustace R Thompson HS, Cumming HJK (1998) NeuroOpthamology. Mosby International Limited.
(9.) Martin TJ, Corbet JJ (2000) Neuro-ophthahnology: The Requisites in Ophthalmology Mosby. international Limited.
(10.) Walsh T J (1997) Neuro-Ophthahnology Clinical Signs and Symptoms. 4th Edition. Williams and Wilkins.
(11.) Kline LB, Arnold AC, Eggenberger E, Forozan R, Golnik KC, Rizzo III JR Shaw HE (2007) Basic & Clinical Science Course: Neuro-Ophthalmology Section 5 2007-2008. American Academy of Ophthalmology.
(12.) Pane A, Burden M A and Miller N R (2006) The NeuroOphthalmology Survival Guide. Mosby Elsevier Limited. http://www.academy.org.uk/tutorials/pathway.htm
Shirley Ann Hancock PhD, BSc (Hons), MCOptom
Shirley Ann Hancock PhD, BSc (Hens), MCOptom, is a Principal Optometrist based at the Heart of England NHS Foundation Trust, Birmingham Heartlands Hospital with special interests in ophthalmic imaging and perimetry.
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|Title Annotation:||COURSE CODE: C-8367: 2 CET POINTS|
|Author:||Hancock, Shirley Ann|
|Date:||Jul 11, 2008|
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