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PURPOSE: Because simple anisocoria is believed to decrease in bright light, the authors determined the prevalence of simple anisocoria under different lighting conditions. METHODS: The authors measured the pupil size of 104 healthy subjects with infrared videography at four clinically accessible light levels: darkness; darkness with a hand-held light shining from below; room light; and room light with the hand light shining from below. RESULTS: Of the 104 subjects, 40 (38%) were men and 64 (62%) were women. The ages ranged from 12 to 71 years (mean, 36.3 +/- 12.5 years). The mean decrease in pupillary diameter from darkness to the brightest condition was 1.89 mm. Based on the traditional definition of a pupillary diameter difference of 0.4 mm or greater, the prevalence of simple anisocoria decreased from 18% in darkness to 8% in room light with the hand-held light shining from below. The prevalence of anisocoria varied considerably when other definitions were used. Repeated measures analysis of variance showed that pupillary area difference decreased with brighter conditions (P = 0.026). However, the ratio of the pupillary areas did not change with brighter conditions (P = 0.666). CONCLUSIONS: The prevalence of simple anisocoria decreases with brighter conditions based on pupillary diameter difference. However, this decrease is not apparent when anisocoria is expressed as pupillary area ratio. Those clinicians who measure pupils will find that simple anisocoria decreases in bright light. However, with gross observation where perception of an anisocoria may be related more to the ratio of the pupillary areas, simple anisocoria may not seem to change much with brighter conditions.
OBJECTIVES: To determine whether an anisocoria can produce a relative afferent pupillary defect of clinical importance. MATERIAL AND METHODS: Anisocoria and relative afferent pupillary defect were measured with infrared videography in three clinical experiments: 1) every few minutes in eight normal subjects who remained in darkness as one pupil was dilating from mydriatic drops; 2) every 2 hours, for 8 hours in six normal subjects who remained in room light after one pupil was dilated with mydriatic drops; and 3) before and after dilation of one pupil in 24 patients with known afferent defects from optic nerve disease and who remained in room light. RESULTS: In the presence of an anisocoria, the relative afferent pupillary defect was almost always in the eye with the smaller pupil. The results of the three experiments were: 1) In darkness, the induced pupillary defect was found to be related to the ratio of the areas of the two pupils (R = 0.942), and 0.14 log unit of pupillary defect was produced in the eye with the smaller pupil for every millimeter of anisocoria. 2) In room light, the induced pupillary defect was in the eye with the smaller pupil but was less than in Experiment 1 and persisted throughout the 8 hours. This was presumably because the eye with the larger pupil had become more light adapted in the clinic light than the eye with the smaller pupil. 3) In room light, inducing an anisocoria in patients with preexisting afferent pupillary defect tended to shift the pupillary defect toward the eye with the smaller pupil (R = 0.68). CONCLUSIONS: Clinically, approximately 0.1 log unit of relative afferent pupillary defect is produced in the eye with the smaller pupil for every millimeter of anisocoria. Therefore, the anisocoria must be larger than 2 mm in diameter difference to induce a clinically significant relative afferent pupillary defect.
OBJECTIVE: To determine whether the time between onset of anisocoria and surgery for hematoma evacuation in the head-injured patient is a useful prognostic variable for outcome in the comatose patient with an acute epidural hematoma. DESIGN: Prospective. MATERIALS AND METHODS: Twenty-one patients with an acute traumatic epidural hematoma and an admission Glasgow Coma Scale score of less than 8 were analyzed. RESULTS: Anisocoria was present in 14 (67%) patients. Mortality rate was three times higher in this group than in the patients without anisocoria; however, this difference was not statistically significant (p = 0.21, Fisher's exact test). None of the patients with an anisocoria-craniotomy latency of 70 minutes or less died and all of these patients had a good or reasonable outcome. Analysis of the anisocoria-craniotomy latency in ten patients revealed that a lapse of more than 90 minutes was associated with a greater mortality compared with patients with a latency of less than 90 minutes (p = 0.0238, Fisher's exact test). CONCLUSIONS: In patients with an acute epidural hematoma, reducing the anisocoria-surgery interval below 90 minutes is significantly associated with a better outcome (p = 0.0238, Fisher's exact test).
Variations in anisocoria in light and dark conditions are used to help diagnose normal and pathologic conditions; however, there have been few observations of anisocoria in different lighting and accommodative conditions. The authors measured pupil size photographically in a group of normal subjects examined in six conditions that were controlled for illumination and accommodation. Greater variation and average extent of anisocoria were found in conditions that resulted in larger pupil size. A subset of subjects repeated several sessions. For this group, the average value of anisocoria and variability tended to be greater in dark conditions. These results show that the observation of anisocoria varies under different conditions, and they suggest careful consideration of conditions used clinically to assess pupil equality. Our analysis shows that for a given observation threshold, conditions that produce even modest changes in variability can cause dramatic changes in the probability of observing anisocoria.
Brain infarction caused by arterial occlusion of the internal carotid axis sometimes develops Horner syndrome. The purpose of this study is to clarify the characteristics and mechanism of "Horner type" anisocoria, which is one of the symptoms of Horner syndrome, in patients with brain infarction in regions supplied by the internal carotid artery (ICA). We studied 112 consecutive patients (71 males and 41 females, mean age of 60.8 +/- 12.3 years) with brain infarction with either ICA or the middle cerebral artery (MCA) occlusion, who were admitted to the National Cardiovascular Center within seven days after the onset of stroke. We examined differences in frequency of Horner type anisocoria and its duration after onset by the mechanism (embolic or thrombotic) and site (ICA proximal, ICA distal or MCA) of arterial occlusion. Horner type anisocoria was seen in 26 of 66 cases (39.4%) with embolic occlusion, which was more frequent than in those with thrombotic occlusion (8 of 46 cases, 17.4%) (p < 0.05). In the embolic occlusion group, Horner type anisocoria was seen in 17 of 32 cases (53.1%) with ICA occlusion, which was more frequent than in those with MCA occlusion (9 of 34 cases, 26.5%) (p < 0.05). Horner type anisocoria was more frequently seen in embolic (17 of 32 cases, 53.1%) than in thrombotic ICA occlusion (2 of 21 cases, 9.5%) (p < 0.01). The duration of Horner type anisocoria was shorter in patients with either distal ICA or MCA occlusion than in those with proximal ICA occlusion (p < 0.05). In patients with thrombotic occlusion, there was no distinct characteristics in between those ICA and MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: This study determines how pupil size, anisocoria, and ambient light influence miotic responses to dilute pilocarpine. The aim is to establish whether mechanical properties of the iris affect miotic behavior using a cholinergic agonist and, if so, to define a more specific clinical definition of supersensitivity testing for suspected tonic pupil disorders. METHODS: The right pupil of 42 normal subjects was first dilated with phenylephrine to create an experimental anisocoria. Then, pilocarpine 0.1% was placed in both eyes. Net constriction of the larger right pupil was determined by subtracting the amount of pilocarpine-induced constriction of the control left pupil from the amount of pilocarpine-induced constriction of the experimental right pupil. Pupil diameters were measured in room light and darkness. RESULTS: In only a few subjects, the larger right pupil became smaller than the left pupil after pilocarpine administration. Net constriction of the right pupil was greater when determined in room light than in darkness. The amount of net constriction of the right pupil showed good correlation with the degree of baseline anisocoria when evaluated in room light, but not so in darkness. CONCLUSION: Pupil size, degree of anisocoria, and light conditions influence the amount of pilocarpine-induced change in anisocoria. If a patient's larger pupil becomes the smaller pupil in darkness after dilute pilocarpine is applied to both eyes, then it is likely that such a response occurred independent of mechanical properties of the iris, and likely represents a supersensitive response. Ophthalmology.
Anisocoria, or a difference in pupil size, is a common condition. Its aetiology ranges from benign to life-threatening conditions. The clinical evaluation of anisocoria is discussed, emphasising the pharmacological aids (e.g., cocaine 10% eye drops, hydroxyamphetamine eye drops, pilocarpine 0.1% eye drops, pilocarpine 1% eye drops, apraclonidine) used in differentiating the different causes of anisocoria (e.g., physiological anisocoria, Horner syndrome, Adie pupil, pharmacological anisocoria, third nerve palsy).
OBJECTIVE: Anisocoria after sinus surgery can be related to serious complications such as intraorbital hematoma or increased intracranial pressure secondary to an expanding hematoma. CASE REPORT: A 51-year-old man underwent endoscopic surgery of sinuses, and developed anisocoria; likely a result of the local spread of cocaine used to provide local anesthesia and vasoconstriction. The localized effect of this anesthetic agent produced a typical picture of nasociliary ganglion block that subsided in a few hours. In the results, the nasociliary nerve block was noticed on recovery from anesthesia with no other neurologic deficit. Ophthalmologic examination demonstrated a short-lasting anisocoria with loss of accommodation and sensory block over the tip of the nose. CONCLUSION: The central spread of the local anesthetics should be considered as a differential diagnosis of unexplained anisocoria, especially when it is associated with loss of corneal reflex.
A case of anisocoria associated with oral pharmacologic treatment of irritable bowel syndrome is reported. A 26-year-old woman developed sudden onset of anisocoria and compromised accommodation that lasted 2 days after the use of oral scopolamine methylbromide for treatment of irritable bowel syndrome. The anisocoria and compromised accommodation occurred after contamination of the ocular surface after administration of scopolamine methylbromide and resolved within 1 week without further contamination. Oral preparations used for the pharmacologic treatment of irritable bowel syndrome can cause anisocoria due to anticholinergic pharmacologic blockade of the iris sphincter muscle.
To compare the frequency of anisocoria in patients with chronic Chagas' disease a prospective double-blind study was done in 131 patients with positive serology for Chagas' disease and 138 negative, at Mambaí (GO-Brazil), which is an endemic area for Chagas' disease. To detect anisocoria, pupillometry was done with a millimetric ruler. Anisocoria was seen in 10(7.6%) patients with Chagas' disease and in 3(2.1%) normal subjects. The chi-square test showed statistical significance at level of 5%. Chagas' disease must be included among the causes of anisocoria.
We photographed the pupils of 128 normal subjects in dim light, morning and afternoon, for five consecutive days. Fifty-two of the subjects (41%) had an anisocoria of 0.4 mm or more at one time or another during these five days, but only four (3%) had unequal pupils of 0.4 mm or more in all ten photography sessions. At any given examination, a fairly constant 19% (24 of 128) of the subjects showed this amount of anisocoria. These numbers shifted dramatically when anisocoria was defined as a pupillary inequality of greater than, or less than, 0.4 mm. The prevalence of anisocoria did not vary with the time of day, from day to day, or from week to week, nor was it influenced by the sex, age, or iris color of the subject.
A four-year retrospective study among children who attend a Primary Care Pediatric Service has been made, in search of a connection between the infant anisocoria and the anisometropia and/or amblyopia detected on the screening of visual acuity at the age of three-four years. Four out of five children with anisocoria (that is, the 80%) later suffered anisometropia and/or amblyopia, and, reciprocally, four out of eight children with anisometropia and/or amblyopia (50%) have previously presented anisocoria. The existence of a clear association is shown between both pathologies, and consequently, children with anisocoria (after putting aside other possible reasons, oculars or neurologicals) should be promptly examined on refraction and visual acuity in order to diagnose anisometropia and to prevent development of amblyopia.
The incidence of anisocoria in the newborn period is not well described. Additionally, the normal range of infant pupil size is not well defined. Eight-eight healthy newborns were evaluated. Pupil size and color were obtained from photographs. The mean (+/- SD) pupil size was 3.8 +/- 0.8 mm. There was no statistical difference between right and left eyes. A statistically significant difference in pupil size was found between blue and brown eyes. The incidence of anisocoria was found to be 21%. No difference was greater than 1.0 mm. The incidence of anisocoria was no different on the basis of eye color.
BACKGROUND: After unilateral photorefractive keratectomy (PRK) for myopia correction, relative mydriasis of the treated eye was noticed. The aim of this study was to determine the incidence and possible etiology of this anisocoria. PATIENTS AND METHODS: In a prospective clinical study we examined eight consecutive patients after PRK of a spherical equivalent of -1.0 to -8.5 D with a 6.5-7.0 mm optical zone (Schwind-Keratom) for up to 10 months. Measurements of the pharmacological uninfluenced pupillary diameter were carried out with a Goldmann perimeter under 31.5 asb and under four different room light and distance conditions. In five patients a hard contact lens of 0 D power was fitted to the treated eye, so that the laser-induced central corneal flattening was compensated for by the sublenticular tear film, and the pupillary diameter was measured again. The influence of pilocarpine 0.1% eye drops to the pupil was also examined. RESULTS: Postoperatively, the pupil of the PRK-treated eye measured up to 1.75 mm larger than that of the fellow eye in all patients. The amount of anisocoria showed a small negative correlation with the interval between the PRK procedure and the day of measurement. It did not correlate significantly with the amount of induced refractive change, applied energy, application of pilocarpine 0.1% eye drops or the contact lens fitting. CONCLUSION: After unilateral PRK, anisocoria can regularly be observed. At present its definite pathogenesis is unclear, although certain possible optical and neuronal mechanisms have been excluded. The most probable etiology is a mild lesion of the pupillary sphincter muscle because of its localization in the center of the laser shock wave distribution.
We report an unusual case of anisocoria in the dog provoked by Datura stramonium, and an experimental clinical assay to reproduce the anisocoria using simple contact with part of the plant in four healthy dogs. Any part of the D. stramonium plant produced anisocoria following simple contact with the eye.
A 27-year-old female rhesus macaque (Macaca mulatta) developed anisocoria. The left pupil was dilated and unresponsive to light. The macaque was euthanized because of unrelated reasons and the body was submitted for necropsy. On gross examination, a berry aneurysm of the right middle cerebral artery causing marked compression of the right optic tract was found. Arteriosclerotic changes were observed microscopically in the right middle cerebral and in the internal carotid arteries. The left iris was markedly degenerated, with atrophy of the constrictor muscle. Compression of the right optic tract may cause homonimus hemianopsia. A dilated and unresponsive left pupil indicated a lesion in the ipsilateral parasympathetic efferent pathway. In the absence of appreciable lesions of the left oculomotor nerve, the most likely cause of mydriasis was the iridic lesion. Intracranial aneurysms are common in humans (2 to 5%), but not in other species. Only about 10% of unruptured aneurysms are associated with neurologic deficits related to mechanical compression, such as visual deficits or anisocoria. Meticulous investigation of the ocular vascular and neural pathways led us to conclude that the anisocoria was unrelated to the aneurysm. To our knowledge, this report represents the first documented case of a naturally occurring intracranial aneurysm in nonhuman primates.
Fifty-three patients with cluster headache, mean age 42.6 years, were examined by means of pupillometry. Pharmacological stimulation was carried out by the instillation of eye drops; the sympathomimetic agents hydroxyamphetamine (a norepinephrine releaser) and phenylephrine (an agent acting directly on the postsynaptic receptors) were applied. Pupillary dilatation was measured at set time intervals, comparing the responses of the symptomatic and non-symptomatic sides. The material was divided into groups according to the degree of basal anisocoria. The subgroup with the most pronounced basal miosis of the symptomatic side demonstrated a uniform pattern of deficient symptomatic side dilatation after OH-amphetamine and supersensitivity to phenylephrine. The other groups demonstrated the same general pattern, but to a far lesser degree. In cluster headache, the extent of nonresponsiveness to OH-amphetamine and of phenylephrine supersensitivity on the symptomatic side thus, at least partly, seems to be a function of the degree of anisocoria. The response pattern in cluster headache seems to differ from that of 3rd neuron Horner's syndrome with an anisocoria of the same extent.