Relative Afferent Pupillary Defect
The relative afferent pupillary defect (RAPD) is a clinical manifestation of asymmetric afferent pupillomotor input.
When there is a significant unilateral or asymmetric afferent visual pathway disruption caused by optic nerve or widespread retinal disease, the pupils show a subnormal response to light stimulation of the eye with the greater field or (generally) acuity loss. The pupils have a more extensive constriction response with light stimulation of the normal or less involved eye. It is this combination of subnormal direct pupillary light response and a normal indirect (consensual) response when the opposite eye is illuminated that constitutes the RAPD.
TABLE 15-2 Characteristics of Pupils Encountered in Neuroophthalmology
Responses to Light and Near Stimuli
Room Condition in Which Anisocoria is Greater
Response to Mydriatics
Response to Miotics
Response to Pharmacologic Agents
Normal and rarely needed
Small, round, unilateral
Cocaine 4%, poor dilation
Paredrine 1%, no dilation if third-order neuron damage
Tonic pupil syndrome (Holmes-Adie syndrome)
Usually largera in bright light; sector pupil palsy, vermiform movement
Unilateral or, less often, bilateral
Absent to light, tonic to near; tonic redilation
Pilocarpine 0.1% or 0.125% constricts; mecholy 2.5% constricts
Argyll Robertson pupils
Small, irregular, bilateral
Poor to light, better to near
Mid-dilated; may be oval; bilateral
Poor to light, better to near (or fixed to both)
Pharmacologically dilated pupils
Very large,b round, unilateral
Pilocarpine 1% will not constrict
Oculomotor palsy (nonvascular)
Mid-dilated (6-7 mm), unilateral (rarely bilateral)
a Tonic pupil may appear smaller after prolonged near effort or in dim illumination; affected pupil is initially large but with passing time gradually becomes smaller.
b Atropinized pupils have diameters of 8 to 9 mm. No tonic, midbrain, or oculomotor palsy pupil even if this large.
c Pupils may be weakly reactive, depending on interim after instillation.
The RAPD can be demonstrated clinically by the alternate cover test, also known as the Marcus Gunn pupillary test, as described by Kestenbaum44
or by the swinging flashlight test of Levatin45
). The swinging flashlight test compares pupillary responses to brief bursts of light stimulation and is more sensitive than the Marcus Gunn test, which detects pupillary dilatation after prolonged light exposure.46
The swinging flashlight test is best performed in a dimly lit room, using a bright light, such as a muscle light
or penlight. During the test, the patient must look at a distant fixation target to avoid accommodative miosis.
FIG. 15.7 Swinging flashlight test for afferent pupil defect. The patient is a 72-year-old man with right visual loss due to ischemic optic neuropathy. A: Pupils are equal in dim light. B: Illumination of right eye results in modest bilateral constriction. C: When the light swings to the left, there is more extensive constriction in both pupils. D: When the light swings back to the right, both pupils dilate.
The test light is shone directly into the visual axis to first illuminate one pupil and then the other. The alternating or swinging light should pause 3 to 5 seconds in each eye, and this maneuver should be repeated several times. As a rule, the pupils are round and practically equal in diameter (see “Essential Anisocoria” section) and briskly and symmetrically reactive to light stimuli. After an initial, prompt pupil constriction, a slight “release” dilation generally occurs. For example, in the presence of a right afferent defect (see Fig. 15.7
), the following is observed with the swinging flashlight test: the pupillary diameters are equal and slightly larger bilaterally when the right eye is stimulated and bilaterally smaller when the normal left eye is illuminated. If only the illuminated pupil is observed—the other pupil being hidden in darkness— the following is seen: the normal left pupil constricts promptly on illumination; as the light is moved rapidly to the right, the right pupil is seen to dilate or “escape.” As the light moves again to the left, the left pupil again constricts briskly.
Afferent pupillary defects may be quantified conveniently by the use of neutral density filters placed before the normal eye. While performing the swinging light test, the neutral density filter is increased until the pupil responses are “balanced.” The neutral density value at which a positive (asymmetric) swinging light test is neutralized is read in log units.48
Previously used to assess the depth of amblyopia, the Sbisa bar (Bagolini filter bar) has also been found to be of comparable use in quantifying RAPD.49
Whether a dim, bright, or brilliant light is best-suited for pupil light-reaction testing is somewhat controversial,50
but an indirect ophthalmoscope light set at 6 V may be used as a handy “standardized” light source. Thompson and Jiang51
stress the importance of avoiding asymmetric retinal bleach, by maintaining a rhythmic “equal time” alternation of the light from one eye to the other and by not swinging the light too many times between the eyes. Finberg and Thompson48
and Thompson et al.52
provide detailed guidelines for proper performance of the pupillary examination and assessment of the RAPD.
Computerized infrared pupillography may allow the most reliable standardization of the swinging flashlight test.46
Personal computer-based infrared video pupillography has been developed for clinical use when detection and specific quantification is required. The proposed advantages to the swinging light test include the capacity to perform binocular tests, compensating for natural differences in midbrain decussation of the interneurons, asymmetric supranuclear influences on the EWN, and differences in efferent innervation of the pupils. Furthermore, the RAPD may be recorded at different light intensities independent of motion, pattern, and color, and free of observer bias.53
Pupillography also measures response latency and cycling time, which can be delayed in diseases of the afferent and efferent visual pathway and amblyopia.55
Quantification of RAPD may be used to gauge the degree to which the anterior visual pathway disruption
has occurred or as a prognostic indicator for final visual recovery. In a small series, Alford et al.56
found that patients with traumatic optic neuropathy and an initial RAPD of log 2.1 or greater showed minimal visual recovery even after megadose intravenous steroid therapy. Those with RAPD measurements less then log 2.1 recovered to visions of 20/30 or better. Younis and Eggenberger examined 72 patients with unilateral or asymmetric demyelinating optic neuropathy and found significant linear correlation between retinal nerve fiber thickness, measured with ocular coherence tomography (OCT) and RAPD, measured in log units. These findings indicate that the log unit value of RAPD may be used to predict the extent of retinal nerve fiber layer (RNFL) loss in this type of neuropathy.57
An afferent pupillary defect may be assessed even if one of the pupils is unreactive because of mydriatics, miotics, oculomotor palsy, trauma (Fig. 15.8
), or synechia formation. In such cases, when performing the swinging flashlight test, the direct and consensual responses of the single reactive pupil must be compared. The reactive pupil’s direct light response reflects the afferent function of the ipsilateral eye; its consensual response reflects the afferent function of the contralateral eye.
FIG. 15.8 Swinging flashlight test in two patients with mydriasis on side of orbital trauma. Pupils in bright (A) and dim (B) room lighting reveal normal responses on the uninjured side and minimal, if any, response on the affected side. As the flashlight is swung from right (C) to left (D) and again to right (E), one can observe the normally reactive pupil. The patient on the left has no afferent pupillary defect, whereas the patient on the right has a left RAPD.
Even severe unilateral visual loss due to retinal or optic nerve diseases associated with an afferent pupillary defect is not of itself a cause of anisocoria, despite past statements to the contrary (see Behr sign in the following text). If a patient with an RAPD also shows anisocoria, the pupillary inequality must be treated as a separate finding. The RAPD most typically provides objective evidence of optic nerve disease that is either unilateral or asymmetric, with more profound visual involvement on the side of the RAPD. In such cases, the RAPD is not specific and may
reflect optic neuropathy due to demyelination, ischemia, compression, or asymmetric glaucoma.
Because slightly more fibers cross than remain uncrossed at the level of the chiasm, RAPDs may also be seen with optic tract lesions, where greater visual field loss occurs in one eye. An obvious example would be an optic tract lesion with a complete homonymous hemianopia. In such a case, a RAPD would be expected in the eye with the temporal visual field loss (i.e., the eye contralateral to the side of the optic tract lesion).58
The same kind of RAPD can present without any associated visual field defect if there is a contralateral lesion affecting the pupillomotor fibers between the optic tract and pretectal region. The eye with the RAPD should have normal visual acuity, color vision, and visual field, and no other (occult) cause for the pupillary defect (i.e., no amblyopia, glaucoma, past optic neuritis). Ellis59
has reported an afferent pupillary defect contralateral to a pineal region tumor, suggesting that this was due to the involvement of afferent pupillary fibers between the optic tract and pretectal nucleus. Johnson and Bell60
have documented an RAPD in a pretectal lesion due to a pineal gland mixed-cell tumor and Kawasaki et al.61
have described four patients with dorsal midbrain lesions and normal visual fields who exhibited contralateral clinical and pupillographic RAPD. As with optic tract lesions, the midbrain RAPD is attributed to asymmetric nasal-temporal pupillomotor input. Unilateral disruption of homonymous paired fibers in the optic tract or midbrain result in a contralateral RAPD.61
Reported cases of isolated superior oblique palsy associated with RAPD and preserved vision similarly represent terminal retinotectal pupillomotor disruptions in the midbrain.62
Previous descriptions of an RAPD associated with anisocoria, with the larger pupil opposite the side of the optic tract lesion (Behr sign of optic tract disease), have not been supported by subsequent reports. Loewenfeld1
has argued that reports of this phenomenon resulted from observation errors or misinterpretation. Because all afferent optic fibers synapse in intercalated interneurons that project to either side of the EWN, pupillary innervation and, thus, responses are more or less symmetrical.1
Therefore, unless another cause for anisocoria exists, anisocoria does not usually result from lesions causing RAPD.
RAPD most typically is an indicator of optic nerve disease. Retinopathy, maculopathy, or amblyopia can also lead to RAPD. However, even with very poor acuity and field depression, the latter diseases usually cause much less obvious RAPD than that found with optic neuropathy. An extensive retinal detachment, such as two detached quadrants, should cause an obvious RAPD, as do arterial occlusions. With unilateral or markedly asymmetric retinitis pigmentosa, one should see an RAPD; however, usually the disease process is quite symmetric, and thus an RAPD is typically not present.64
Furthermore, the preferential loss of photoreceptors in retinitis pigmentosa, as opposed to ip
RGC results in brisk symmetrical pupillary light reflexes and a normal circadian rhythm (see section on Pupil Light Reflex). RAPD in general is proportional to the extent of visual field loss, and the size of the visual field defect is more closely correlated with the extent of the RAPD than is visual acuity loss.65
As a rule, strictly macular disease leads to a much less profound afferent pupillary defect than the bulk of diseases affecting the optic nerve.67
Patients with central choroidopathy, for example, show either a small or no RAPD.68
Furthermore, the RAPD is much more likely to persist with resolved optic neuritis than resolved central serous choroidopathy.69
Patients have also been reported to have an RAPD70
with central retinal vein occlusion, the RAPD being more obvious (generally >1 log unit) in the ischemic than in the nonischemic variety, where most cases measure less than 0.3 log units. Thus, the RAPD may be helpful in distinguishing between ischemic and nonischemic central retinal vein occlusions.
RAPD may be observed in strabismic or refractive amblyopia71
but these are small, measuring 0.3 log units or less and do not correlate with visual acuity.71
If a very obvious RAPD is seen in cases of amblyopia, advanced cataracts, retinopathy, or maculopathy, additional tests are recommended to rule out the possibility of a superimposed occult optic neuropathy that would better explain the pupillary findings. Occasionally, a small RAPD of neutral density filter of 0.3 log unit or less is detected in patients with other ocular pathology. These findings may be assumed to be benign if there are no etiologic clues from the history or clinical examination.73
Asymmetric connections from the afferent visual pathways to the pretectal midbrain between the two eyes may partially explain the presence of RAPD in apparently normal patients. Wilhelm et al.75
obtained clinical and pupillographic measurements of 102 normal subjects and documented RAPD in 15% but none exceeded 0.39 log units. Followup with lack of progressive visual changes on subsequent examinations should provide further corroboration that small isolated RAPD are indeed “benign.” Interesting but rarely encountered in the usual clinical setting are RAPDs induced by contralateral monocular occlusion or resulting from dense contralateral cataracts.76
All pupils are not created equal. In fact, benign pupillary inequality exists in practically all individuals, but not
necessarily all of the time. Using photographic techniques, Lam et al.79
determined pupil size in 128 healthy individuals, measuring greatest pupil diameter twice each day for 5 consecutive days. Forty-one percent showed anisocoria of 0.4 mm or greater at one time or another and 80% showed anisocoria of 0.2 mm or greater at some time. A majority of the subjects, therefore, had anisocoria of some degree at one time or another (Fig. 15.9
). Anisocoria is as common in men as in women, in the morning as in the afternoon, in dark as in light irides, and in the young as in the aged (although Loewenfeld80
suggested that anisocoria is more common in the elderly). In a study of healthy neonates, anisocoria of 0.5 mm or more was found in about 20% of infants, but none had anisocoria greater than 1 mm.81
The physician can detect regularly a pupil difference of as little as 0.2 mm in diameter, given that clinical judgment of inequality is based more on impressions of pupil area than on measured diameter. Because the percentage difference in area is greater for smaller than for larger pupils, for any given diameter difference, anisocoria is detected more easily in smaller pupil pairs. The prevalence of anisocoria decreases in bright conditions when measured as a difference in pupil diameter but not when it is assessed as a ratio of pupil areas.82
Essential or “central” anisocoria should be identified easily because the pupillary light and near reactions are normal, eyelid positions are normal, and eye movements are full. The relative difference between pupil diameters is constant under various levels of illumination. With sympathetic disruption or Horner syndrome, the anisocoria is enhanced in dim lighting. Conversely, in parasympathetic disruption, the anisocoria is enhanced in bright illumination. Incidental ptosis due to traumatic or senile levator aponeurosis dehiscence and weakening, when ipsilateral to the smaller pupil of essential anisocoria, may be confused with a true Horner syndrome.83
When the distinction between true and pseudo-Horner syndrome is difficult by simple inspection alone, pharmacologic testing usually resolves the dilemma.
FIG. 15.9 Prevalence of simple anisocoria. (From Thompson HS. The pupil. In: Lessell S, van Dalen JTW, eds. Current Neuroophthalmology. Chicago, IL: Year Book Medical Publishers; 1989:214.)
Some individuals with long-standing anisocoria may suddenly discover the condition while shaving or applying makeup or may have it called to their attention over the breakfast table. In such situations, inspection of previous photographs is an invaluable aid in determining the nature and duration of pupil anomalies. A hand magnifying glass, a trial frame lens, an indirect ophthalmoscope lens, or even the high magnification of the slit-lamp beam84
may prove useful for examining pupil details in snapshot or portrait-quality photographs (Fig. 15.10
FIG. 15.10 A: Anisocoria noted at age 14 months in otherwise healthy infant. B: Photograph at age 6 months confirms chronicity and benign nature of finding. There was no iris heterochromia.
The evaluation of anisocoria is facilitated by the presence of the following associated signs (see Table 15-2
): mild upper ptosis as well as lower lid elevation on the side of a relatively miotic pupil (Horner syndrome), a dilated pupil fixed to light but with very slow constriction on prolonged near fixation (tonic pupil), and small irregular pupils that react better to near than to light Argyll Robertson (AR) pupil. Table 15-3
outlines the conditions commonly associated with anisocoria and how alterations in illumination
affect the pupil size disparity. Generally, if anisocoria is greatest in the dark, the abnormal pupil is the miotic one. Conversely, if anisocoria is greatest in the light, the abnormal pupil is the mydriatic one. Because the etiology of anisocoria may range from abnormal iris structure to disruption of pupillomotor pathway and supranuclear integrity, it is imperative to take a comprehensive history and evaluate the patient for all levels of disruption.
TABLE 15-3 Causes of Anisocoria and Changes with Illumination
Anisocoria: Light = Dark
Anisocoria: Greater in Dark (Small Pupils)
Anisocoria: Greater in Light (Large Pupils)
Sphincter damage/traumatic mydriasis
Nonreactive unequal pupils (bilateral iritis, ischemia, atrophy)
Oculomotor nerve palsy
Old Adie pupil
Argyll Robertson pupil
Iritis (posterior synechiae)
The history should include onset and duration, association with pain, ocular redness, ptosis, and whether the patient has noticed visual disturbances such as diplopia, decreased accommodation, glare, and halos. An intercurrent or past history of head trauma, surgery, malignancy, diabetes mellitus, syphilis, and neurologic, autoimmune, and cardiovascular disease as well as a social history of smoking, narcotic drug abuse, or occupational exposure (such as, e.g., exposure of gardeners to insecticides or of hospital workers to atropine) will help to focus the clinical exam and investigations. Table 15-4
details the examination of a patient with anisocoria. Pupillography may be employed for accuracy and documentation and old photographs examined to determine the duration and progression of anisocoria. The clinical findings will determine the need, if any, for ancillary investigations such as complete blood count (CBC) and erythrocyte sedimentation rate (ESR), blood chemistry, HbA1c, Venereal Disease Research Laboratory (VDRL) and FTA-ABS, CXR, computed tomography (CT) scan, and MRI/MRA.
TABLE 15-4 Clinical Approach to the Patient with Anisocoria
VA (near and distant)
Patient to focus on distant object
Determine whether anisocoria is greater in bright light or in the dark
Evaluate pupillary response to near target to rule out light/near disparity
Check lid position for ptosis
Check for globe retraction and enophthalmos
EOM—look for limitations
Segmental paralysis of iris ± wriggling and undulating movements
Signs of iritis
Iris atrophy, holes, sphincter tears
Signs of ocular ischemia/iris neovascularization
Measure intraocular pressure (IOP)
Undilated funduscopy (defer dilation)
Determine whether the anisocoria is greater in dark or in bright light
Pharmacologic testing for suspected Adie or Horner syndrome
EOM, extraocular movements; IOP, intraocular pressure.
With exception of errors in testing techniques or poor patient cooperation, there is no pathologic situation in which pupillary light reflex is normal while the near response is defective. Therefore, if the pupils respond briskly to light, the near response need not be examined. Lack of direct and near responses, in the absence of ocular motility disturbances, should raise the question of bilateral pharmacologic pupillary dilation or local ocular disease, such as sphincter trauma or synechiae. Rarely such findings represent congenital mydriasis.85
Paradoxical pupillary responses (pupillary constriction induced by darkness) have
been reported in association with concomitant stationary night blindness and congenital achromatopsia and subsequently with other retinopathies and optic neuropathies.86
The distinctive clinical syndromes demonstrating pupillary light-near dissociation include the Holmes-Adie tonic pupil syndrome, Argyll Robertson syndrome, and Parinaud dorsal midbrain syndrome. The tonic pupil is characterized by light-near dissociation and supersensitivity to dilute parasympathomimetic agents. It is distinguished from the AR pupil by certain characteristic features, including a larger pupil (see “Tonic Pupil [Holmes-Adie] Syndrome” section). The dorsal midbrain syndrome produces light-near dissociation in association with moderate mydriasis and a constellation of signs, including vertical ocular motility deficits and accommodative defects (see “Dorsal Midbrain [Parinaud] Syndrome” section). Other causes of light-near dissociation include significant visual loss, diabetes mellitus, and aberrant oculomotor nerve regeneration.
Any eye with a severe visual deficit due to retinal or optic nerve disease, with significant field loss, has a diminished ipsilateral pupillary response to light (RAPD) but an intact near reflex. For example, an eye blind from glaucoma demonstrates a light-near dissociation. Patients with profound bilateral visual loss caused by anterior visual pathway disease have bilaterally poor pupillary light responses but intact accommodative responses. Therefore, patients with bilateral end-stage glaucoma, total retinal detachments, or blindness resulting from optic nerve/chiasmal injuries should not be misconstrued as having dorsal midbrain disease on the basis of mid-dilated pupils and light-near dissociation alone because these findings may result solely from bilateral blindness. On occasion, patients with long-standing type I diabetes demonstrate moderate symmetric mydriasis with light-near dissociation that is clearly disproportionate to any concurrent retinopathy. Indeed, some patients with type I and type II diabetes may exhibit findings consistent with tonic pupils resulting from widespread autonomic dysfunction87
or local nerve damage from diode laser photocoagulation.88
Diabetic patients may also have typical AR pupils, including miosis.89
When aberrant regeneration follows oculomotor nerve palsies, fibers originally associated especially with the medial rectus (although other oculomotor fibers are occasionally responsible) may anomalously innervate the pupillary sphincter as well. Frequently, aberrant-regeneration results from chronic oculomotor nerve compression, typically from meningiomas and aneurysms,91
as opposed to acute ischemic insults. In such cases, the light-paretic pupil can constrict when the medial rectus muscle acts, either in convergence or with conjugate lateral gaze. Therefore, a light-near dissociation (actually, a gaze-evoked) pupillary dissociation is observed. Unlike the AR pupil, the aberrant-regeneration pupil is large rather than miotic and is accompanied by other signs of third-nerve palsy, some paretic and some with “misdirection” features.92
Infrared videographic transillumination readily demonstrates denervated and aberrantly reinnervated sphincter segments.93
Pupillary changes seen on a slit-lamp examination may provide the early evidence of aberrant oculomotor regeneration; segmental pupillary sphincter contractions may be seen with attempted eye movements in the field of action of oculomotor innervated muscles.94
In more obvious cases, the pupillary constriction may be grossly visualized with attempted efforts by any of the muscles normally innervated by the oculomotor nerve.92
Ohno and Mukumo95
report anomalous pupillary innervation by the oculomotor nerve in 6 of 10 patients with aberrant oculomotor regeneration; pupillary constriction was seen most commonly with downgaze or adduction and less frequently with upgaze. In two patients, pupillary dilation was noted on abduction. Spiegel and Kardon96
evaluated 24 patients with aberrant oculomotor regeneration. Clinically, involvement of the eyelid and pupil was evident more commonly than that of ocular motility. Pupil signs of aberrant behavior, such as gaze-evoked anisocoria, were most noticeable in dim illumination.
Tonic Pupil (Holmes-Adie) Syndrome
One of the commonest causes of isolated internal ophthalmoplegia is the tonic pupil. It typically presents with mydriasis, light-near dissociation, and denervation supersensitivity to dilute cholinergic agonists. First described in 1931, in two separate reports, it was recognized to occur with other neurologic anomalies and subsequently named Holmes-Adie syndrome
(after G.M. Holmes and W.J. Adie). Holmes-Adie syndrome has an annual incidence of 4.7 per 100,000.97
Pupillotonia is usually unilateral, but bilateral cases do occur in which the eyes are involved either simultaneously or sequentially (Fig. 15.11
). Unilateral cases become bilateral at a rate of 4% per year.98
Although all ages and both sexes are affected, there is an unexplained predilection for women in the third to fifth decades.
Typically, the involved pupil is larger than its fellow. Because both constriction and dilation are defective, however, the tonic pupil may appear smaller in dim illumination because the normal pupil is free to dilate widely. Thus, the diameter of the normal pupil may be smaller (in bright illumination) or larger (in dim illumination) than
the tonic pupil. With the passage of time, the anisocoria becomes less marked as the initially larger tonic pupil gradually becomes less dilated and eventually even miotic over the years93
FIG. 15.11 A: A 52-year-old woman with right tonic pupil (left); 1 year later, involvement of the left pupil developed as well (right). Pupils are shown in bright (A) and dim (B) room lighting after near-convergence attempt (C), and in dim room lighting after instillation of 0.125% pilocarpine in both eyes (D). Note that the right pupil is smaller 1 year later (A) (right) than when it was “fresh” (A) (left). With time, the right pupil has also become more responsive to near-accommodation effort (C) (left and right). Parasympathetic hypersensitivity is seen in the right pupil (D) (left) and 1 year later bilaterally (D) (right).
As a rule, the tonic pupil is grossly defective in its reaction to light stimulus but may show a minimal degree of contraction. On slit-lamp examination, however, irregular spontaneous low-amplitude movements may be observed. Segmental sector contractions may be seen in the portions of the sphincter that are still either not denervated or reinnervated. Also, areas of sector palsy of the iris sphincter are seen. The combination of segmental contractions and areas of sphincter palsy exhibit the characteristic wormlike vermiform movements. With prolonged accommodative effort, the pupil slowly constricts, usually not extensively. When near effort is relaxed, the dilation movement is also gradual, requiring minutes or hours for redilation. Therefore, with accommodative effort and before redilations are complete, the tonic pupil can be relatively miotic with respect to its normal opposite. These pupillary kinetics constitute the “tonic pupil,” and pharmacologic testing (Fig. 15.11
) is additive rather than diagnostic. Disruption of the final postganglionic nerve supply to the iris sphincter accounts for denervation supersensitivity, with pupillary constriction produced by dilute parasympathomimetic agents and is the basis for pharmacologic testing for the tonic pupil.
Supersensitivity to the parasympathomimetic drug methacholine 2.5%, with pupillary constriction, is a good but not foolproof test. Pilley and Thompson100
suggest the use of 0.125% pilocarpine as a substitute for methacholine. Actually, pilocarpine is, in some ways, the better drug because of its ready availability and stronger miotic action; supersensitivity is demonstrable in a greater proportion of patients with tonic pupils. Because it produces a more visible degree of anisocoria, a negative test is more valid with pilocarpine than with methacholine. Some authors have suggested the use of weaker solutions of pilocarpine, such as 0.0625% to 0.0313%.101
These lower concentrations insignificantly constrict normal pupils and more reliably distinguish normal pupils from tonic pupils with parasympathetic supersensitivity. Weak-concentration arecoline, a pilocarpine-like drug, has also been used; its advantage, if any, may be that it brings about maximal miosis more quickly.103
Pupillary parasympathetic supersensitivity may occur with ganglionic lesions as well as with preciliary and postciliary ganglionic lesions.36
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