Anisocoria represents one of the most intriguing and clinically vital physical findings in neurology and ophthalmology, serving as a direct window into the functional integrity of the autonomic nervous system. While a subtle disparity in pupil size can be a harmless physiologic quirk found in a substantial portion of the healthy population, its acute emergence may herald life-threatening intracranial emergencies, such as an expanding aneurysm or brain herniation. Differentiating between benign and pathological causes requires a systematic understanding of pupillary neuroanatomy, sympathetic and parasympathetic pathways, and pharmacological assessment techniques.
Anisocoria
1. Concise Definition
Anisocoria is defined as an inequality in the diameter of the pupils of the eyes, occurring as a result of an imbalance in the efferent autonomic pathways controlling pupillary dynamics, structural iris defects, or pharmacologic influences. In clinical practice, an asymmetry greater than 0.4 to 1.0 millimeter is conventionally recognized as clinically significant, depending on ambient lighting conditions and baseline individual variation.
Unlike afferent pupillary defects, which impair light perception and the symmetrical driving stimulus of the pupillary light reflex without altering resting symmetry, anisocoria is strictly an efferent phenomenon. It indicates a failure in either the sympathetic dilator pathway or the parasympathetic constrictor pathway servicing one eye relative to the other. Consequently, the condition requires a differential assessment based on whether the asymmetry is more pronounced in darkness (suggesting impaired dilation) or in bright illumination (indicating impaired constriction).
While physiological anisocoria represents a benign variation occurring in roughly 20 percent of the general population, pathological anisocoria can stem from traumatic brain injury, expanding intracranial aneurysms, ischemic stroke, demyelinating conditions, ocular trauma, or neoplasms. Discerning its underlying mechanism demands a structured clinical approach incorporating comparative ambient light testing, slit-lamp biomicroscopy, and pharmacological confirmation.
2. Etymology & Linguistic Origin
The term anisocoria derives directly from classical Greek roots. It is constructed from the negative or privative prefix an- (ἀν-, meaning “without” or “not”), the adjective ísos (ἴσος, meaning “equal”), the noun kórē (κόρη, historically meaning “maiden,” “girl,” or “doll,” which metaphorically evolved into “pupil” due to the tiny doll-like reflection of oneself visible in another person’s eye), and the abstract medical noun suffix -ia (-ία, denoting a pathological state or condition).
Historically, the use of kórē to represent the ocular aperture parallels the Latin term pupilla (little girl or doll), reflecting an ancient cross-cultural linguistic observation of corneal reflections. The compound clinical form entered the modern biomedical lexicon in the nineteenth century through German and French ophthalmological treatises, formalizing a physical sign that had previously been described through cumbersome descriptive phrases such as “pupillary inequality” or “inequality of the apertures.”
3. Pronunciation & Grammatical Form
Pronunciation: The standard English pronunciation is rendered phonetically as /ˌæn.aɪ.soʊˈkɔːr.i.ə/ or /ˌæn.ɪ.soʊˈkɔːr.i.ə/ (an-eye-so-KOR-ee-uh). In British English, it is frequently pronounced /ˌæn.ʌɪ.səʊˈkɔːr.ɪ.ə/.
Grammatical Form: Grammatically, anisocoria is an uncountable singular noun. The related adjectival form is anisocoric (/ˌæn.aɪ.soʊˈkɔːr.ɪk/), used to describe patients, eyes, or pupillary responses exhibiting unequal dimensions (e.g., “an anisocoric examination”). The antonymic baseline state is isocoria, denoting exact bilateral symmetry of the pupils.
4. Detailed Conceptual Explanation
Pupillary size is maintained by the finely tuned antagonism between two intraocular smooth muscles: the iris sphincter and the iris dilator. The circumferentially arranged sphincter muscle is innervated by the parasympathetic division of the autonomic nervous system via the oculomotor nerve (cranial nerve III), causing pupilloconstriction (miosis). Conversely, the radially oriented dilator muscle is mediated by the sympathetic nervous system originating in the posterolateral hypothalamus, which promotes pupillodilation (mydriasis). Anisocoria emerges whenever this autonomic balance is unilaterally or asymmetrically disrupted, or when mechanical damage impairs the structural movement of the iris stroma.
The fundamental diagnostic heuristic for anisocoria rests on determining which pupil is abnormal: the smaller pupil or the larger pupil. This is resolved by evaluating pupillary inequality in both bright and dark lighting environments. Because darkness stimulates sympathetic mydriasis, anisocoria that increases in dim illumination signifies a failure of the smaller pupil to dilate appropriately. This points to a sympathetic paresis in the smaller eye, famously manifested in Horner’s syndrome. Conversely, bright light triggers parasympathetic miosis; an anisocoria that widens in bright light demonstrates a failure of the larger pupil to constrict, implicating parasympathetic denervation, mechanical sphincter damage, or pharmacological blockade in the larger eye.
Efferent parasympathetic pathway disruption typically arises along the course of cranial nerve III. Preganglionic parasympathetic fibers leave the Edinger-Westphal nucleus in the midbrain, travel along the superficial periphery of the oculomotor nerve, synapse in the ciliary ganglion within the posterior orbit, and finally innervate the iris sphincter via the short ciliary nerves. Compression along this route—most notoriously by an aneurysm of the posterior communicating artery, uncal herniation, or cavernous sinus pathology—leads to a non-reactive, dilated pupil (mydriasis). In contrast, postganglionic parasympathetic denervation within the orbit produces a distinctive state known as Adie syndrome (tonic pupil), marked by sector palsy and profound light-near dissociation.
The oculosympathetic pathway traverses an intricate three-neuron arc. The first-order (central) neuron descends from the hypothalamus through the brainstem to the ciliospinal center of Budge at levels C8–T2. The second-order (preganglionic) neuron exits the spinal cord, ascends the cervical sympathetic trunk over the lung apex, and synapses in the superior cervical ganglion near the carotid bifurcation. The third-order (postganglionic) neuron travels along the internal carotid artery through the cavernous sinus into the orbit to supply the iris dilator and Müller’s superior tarsal muscle. Lesions anywhere along this vulnerable anatomic trajectory induce oculosympathetic paralysis, manifesting as the classic triad of miosis, partial blepharoptosis, and variable facial anhidrosis.
5. Historical Development
Observations of unequal pupils date back to antiquity, with incidental mentions found in the writings of Galen and classical Greco-Roman physicians who observed pupillary changes following direct mechanical trauma to the globe. However, systematic scientific inquiry into pupillomotor function emerged only during the eighteenth and nineteenth centuries, driven by developments in experimental neurophysiology.
In 1727, the French anatomist François Pourfour du Petit experimentally demonstrated that the sympathetic system originated outside the brainstem by cutting the cervical sympathetic chain in dogs, observing pupillary constriction and conjunctival injection. More than a century later, in 1869, the Swiss ophthalmologist Johann Friedrich Horner synthesized clinical and physiological observations to describe the syndrome bearing his name, highlighting how disruption of the oculosympathetic chain causes miosis and ptosis. Simultaneously, British neurologist Jonathan Hutchinson noted the grave prognosis of a unilateral fixed, dilated pupil in victims of closed head trauma (the “Hutchinson pupil”), recognizing it as an outward indicator of rising intracranial pressure and temporal lobe herniation.
The twentieth century brought definitive systematization through the work of William John Adie, who in 1931 characterized the tonic pupil syndrome accompanied by diminished tendon reflexes. The mid-to-late twentieth century was dominated by the pioneering research of Irene Loewenfeld, whose monumental treatises on the pupil synthesized decades of clinical, pharmacological, and physiological literature. Loewenfeld documented normal variations in human pupillary size, establishing that minor, shifting asymmetries (physiologic anisocoria) were a regular facet of human biology rather than latent pathology.
6. Theoretical Foundations
The study of anisocoria is grounded in the theoretical framework of autonomic reciprocal innervation, formulated fundamentally by early physiologists such as John Newport Langley and Walter Cannon. The pupillary aperture represents a homeostatic effector system that constantly responds to internal neurological tone and external visual stimuli. The autonomic control of the pupil operates on principles of balanced antagonism: at any given moment, pupil caliber reflects the vector sum of sympathetic mydriatic force and parasympathetic miotic force.
A critical theoretical milestone is the distinction between afferent and efferent defects within reflex control loops. The pupillary light reflex consists of an afferent arm mediated by intrinsically photosensitive retinal ganglion cells and optic nerve fibers projecting to the pretectal nuclei, which distribute bilateral, symmetrical signals to both Edinger-Westphal nuclei via the posterior commissure. Because this input is distributed equally to both sides, an afferent defect (such as optic neuritis or retinal detachment) leads to a diminished bilaterally equal constriction response, known as a Relative Afferent Pupillary Defect (RAPD or Marcus Gunn pupil). It never causes anisocoria. Theoretical models dictate that anisocoria can only emerge when an efferent asymmetry occurs distal to the Edinger-Westphal nuclei or along the sympathetic outflows, confirming that pupil inequality is solely a dysfunction of motor output, not sensory reception.
Furthermore, autonomic denervation paradigms such as Cannon’s Law of Denervation Supersensitivity are essential for understanding chronic pupillary abnormalities. When a postganglionic parasympathetic or sympathetic neuron is severed, the denervated effector smooth muscle upregulates post-synaptic receptors. This principle underpins diagnostic pharmacological tests; for example, an Adie tonic pupil constricts vigorously in response to highly diluted cholinergic drops that would have no measurable impact on a healthy, innervated iris.
7. Key Components, Types & Dimensions
Anisocoria is classified into distinct etiologic and clinical subtypes based on ambient lighting responses, anatomic localization, and systemic presentation:
- Physiologic (Essential) Anisocoria: The most common form, characterized by a benign inequality (usually < 0.6 mm) that remains roughly proportional across both dim and bright lighting. The asymmetry may fluctuate, reverse sides, or temporarily disappear over hours or days, with intact light and near reflexes and without associated ptosis.
- Sympathetic Denervation (Horner’s Syndrome): Characterized by anisocoria that is greatest in the dark due to impaired dilation of the affected eye. It presents alongside mild ipsilateral ptosis (loss of Müller’s muscle tone), “upside-down ptosis” (elevation of the lower lid), and pupillary dilation lag during the first 5 seconds following lights-out.
- Parasympathetic Denervation (Cranial Nerve III Palsy): Defined by anisocoria that is greatest in bright light due to an underactive iris sphincter. When fully expressed, it is accompanied by complete ptosis, exotropia, and hypotropia (“down and out” ocular alignment), though isolated internal ophthalmoplegia can occur in compressive lesions.
- Adie’s Tonic Pupil: A postganglionic parasympathetic denervation of the iris sphincter and ciliary muscle, typically unilateral initially. It features a dilated pupil that shows poor or segmental reaction to light, delayed but sustained near constriction (light-near dissociation), and cholinergic denervation supersensitivity.
- Pharmacological Anisocoria: Caused by topical accidental contamination or deliberate administration of autonomic agents. Accidental contact with atropine, scopolamine patches, glycopyrronium, or sympathomimetic sprays causes profound, fixed mydriasis resistant to high-concentration miotics.
- Mechanical / Structural Anisocoria: Originates from physical damage to the iris stroma or sphincter muscle rather than autonomic dysfunction. Etiologies include blunt ocular trauma (sphincter tear), prior intraocular surgery, acute angle-closure glaucoma (ischemic iris paralysis), chronic uveitis with posterior synechiae, or intraocular tumors.
8. Examples & Illustrative Cases
The following case vignettes illustrate the presentation, clinical reasoning, and outcomes associated with different forms of anisocoria:
Case 1: Benign Physiologic Anisocoria
A 28-year-old software engineer presents with anxiety after noticing in a mirror that her right pupil is larger than her left. Examination reveals a 4.5 mm right pupil and a 3.8 mm left pupil in ambient room light (a 0.7 mm difference). In bright illumination, the pupils measure 2.5 mm and 2.0 mm (0.5 mm difference); in darkness, they measure 6.5 mm and 5.8 mm (0.7 mm difference). Both pupils react briskly and symmetrically to light and accommodation, with no ptosis, extraocular motility restrictions, or visual field deficits. Review of high-resolution digital photographs from five years earlier confirms identical pupillary asymmetry. The patient is diagnosed with physiologic anisocoria, and unnecessary neuroimaging is avoided.
Case 2: Emergent Compressive Third Nerve Palsy
A 54-year-old woman arrives at the emergency department reporting a severe, acute-onset right-sided fronto-orbital headache. Examination reveals a 6.0 mm non-reactive right pupil and a 3.0 mm briskly reactive left pupil in room light. The anisocoria markedly increases under bright light. The right eye demonstrates mild limitation of adduction, elevation, and depression, accompanied by a partial ptosis. Recognizing a pupil-involving third nerve palsy, the clinical team immediately orders urgent computed tomography angiography (CTA) of the head, which reveals an expanding 7 mm posterior communicating artery aneurysm compressing the right oculomotor nerve. She is promptly treated via endovascular coiling, preventing an aneurysmal subarachnoid hemorrhage.
Case 3: Incidental Oculosympathetic Paresis (Horner’s Syndrome)
A 62-year-old man with a 40-pack-year smoking history visits an optometrist for updated reading glasses. The clinician detects that in room light, the right pupil is 3.5 mm and the left pupil is 2.5 mm. In bright light, both pupils constrict to 2.0 mm (no anisocoria), but in complete darkness, the right pupil expands to 7.0 mm while the left expands to only 4.5 mm, revealing a prominent 2.5 mm anisocoria alongside a subtle 1 mm left upper eyelid ptosis. Pharmacological testing with topical apraclonidine 0.5% produces pupillary reversal—the left pupil dilates and the ptosis resolves, confirming a left-sided Horner’s syndrome. Subsequent magnetic resonance imaging (MRI) of the neck and chest identifies an apical lung lesion (Pancoast tumor) invading the left stellate ganglion.
9. Measurement & Assessment
The diagnostic evaluation of anisocoria relies on a systematic approach designed to differentiate harmless variations from impending neurological emergencies. The clinical protocol begins with high-precision measurements of pupil diameter in both bright light and darkness, accompanied by an assessment of dynamic pupillary kinetics.
The standard clinical assessment involves several structured steps:
- Ambient Light Differential: Measure pupil diameter using a handheld pupillometer, Rosenbaum pocket card, or slit-lamp graticule under uniform bright light, ambient room light, and after 5 to 10 seconds of complete darkness. A difference that increases in the dark implicates the smaller pupil; a difference increasing in light implicates the larger pupil.
- Slit-Lamp Biomicroscopy: Inspect the iris architecture under magnification to rule out structural tears, sphincter rupture from past trauma, transillumination defects, neovascularization, or mechanical tethering (posterior synechiae). In cases of Adie’s pupil, slit-lamp examination often reveals “vermiform” segmental contractions of the iris border.
- Automated Infrared Pupillometry: Modern critical care and neuro-ophthalmology clinics utilize quantitative infrared pupillometry. These devices measure baseline diameter, latency of constriction, constriction velocity, and percentage of constriction, providing objective, user-independent metrics such as the Neurological Pupil Index (NPI).
- Pharmacological Testing for Horner’s Syndrome: Instillation of apraclonidine (0.5% or 1.0%) has widely replaced cocaine drops. In Horner’s syndrome, denervation supersensitivity causes the affected pupil to dilate and the ptotic lid to elevate, reversing the anisocoria. Alternatively, cocaine 4% to 10% blocks norepinephrine reuptake; a normal pupil dilates, whereas a Horner pupil fails to dilate. Hydroxyamphetamine (1%) can subsequently differentiate preganglionic from postganglionic third-order lesions.
- Pharmacological Testing for Parasympathetic Deficits: Dilute pilocarpine (0.0625% to 0.125%) instillation does not alter a normal pupil but causes robust constriction of an Adie tonic pupil due to muscarinic supersensitivity. If the dilated pupil fails to respond to dilute pilocarpine, full-strength pilocarpine (1.0% to 2.0%) is applied. A mechanically or pharmacologically dilated pupil (e.g., atropine toxicity) will not constrict, whereas a third nerve palsy will rapidly constrict.
10. Applications & Practical Significance
Anisocoria serves as a sentinel physical marker across multiple clinical specialties. In emergency medicine and trauma surgery, continuous pupillary surveillance is central to the Glasgow Coma Scale and intracranial hypertension monitoring protocols. The development of a unilateral dilated, unreactive pupil (Hutchinson’s pupil) in an obtunded trauma patient indicates temporal lobe uncal herniation over the tentorial notch, which compresses the ipsilateral oculomotor nerve against the petroclinoid ligament. This heralds midbrain ischemia and demands immediate osmotic therapy (e.g., hypertonic saline, mannitol) or surgical decompression.
In neuro-ophthalmology and vascular neurology, acute anisocoria with a dilated pupil, with or without extraocular muscle palsy, is treated as an aneurysmal oculomotor palsy until proven otherwise. Aneurysms located at the junction of the internal carotid artery and posterior communicating artery run in close proximity to the pupillomotor fibers traversing the superior-medial sheath of cranial nerve III. Rapid detection through clinical pupillary examination followed by emergency CTA or MRA prevents aneurysm rupture, which carries a 50% mortality rate.
In general outpatient medicine and pediatrics, the discovery of anisocoria warrants careful consideration. In infants and children, an acute or newly recognized Horner’s syndrome requires an immediate search for an underlying neuroblastoma along the sympathetic chain. In adults, recognizing physiologic anisocoria avoids costly, high-anxiety diagnostic workups, allowing clinicians to reassure patients based on past portraiture, photographic records, and symmetric light kinetics.
11. Research & Empirical Evidence
Epidemiological and physiological studies over several decades have characterized the prevalence and behavioral dynamics of pupillary asymmetry. In a seminal investigation, Lam, Thompson, and Corbett (1987) evaluated 128 healthy subjects over time and revealed that 19% exhibited clinical anisocoria (> 0.4 mm) at any single examination, with the asymmetry fluctuating dynamically across evaluations. Their findings established that physiologic anisocoria is not a fixed anatomical flaw, but an expression of asymmetrical autonomic tone that can change from hour to hour.
Clinical trials validating apraclonidine as an alternative to cocaine for the diagnosis of Horner’s syndrome have reshaped modern neuro-ophthalmology protocols. Research published by Koc et al. (2005) demonstrated that apraclonidine achieves an exceptionally high diagnostic sensitivity (over 93%) and specificity for identifying oculosympathetic denervation via α1-receptor supersensitivity, providing an accessible in-clinic alternative to controlled cocaine drops.
In neurocritical care, the emergence of automated infrared pupillometry has transformed patient assessment. Empirical work by Chen et al. (2011) and subsequent multi-center trials have demonstrated that automated pupillometry identifies subclinical changes in pupillary constriction velocity hours before manual penlight exams detect visible anisocoria. This allows for earlier interventions in patients developing secondary brain injury from cerebral edema, midline shift, or intracranial mass lesions.
12. Cultural & Cross-Cultural Considerations
Anisocoria occupies an interesting space in modern culture and medical anthropology. Perhaps the most famous cultural reference is the rock musician David Bowie, whose permanent, pronounced pupillary asymmetry was widely assumed by the public to be heterochromia or congenital anisocoria. In reality, Bowie sustained traumatic blunt eye injury during an adolescent altercation, resulting in a paralyzed iris sphincter (traumatic mydriasis). This gave the visual impression of two different colored eyes due to the permanent dilation of one pupil, popularizing the visual aesthetic of pupillary asymmetry in modern media.
From a cross-cultural clinical perspective, the diagnostic accessibility of anisocoria reveals health disparities between resource-rich and resource-limited settings. In high-income countries, patients with new-onset anisocoria are routinely evaluated with high-resolution neuroimaging (CTA/MRI) and specialized pharmacological agents like apraclonidine. In developing nations and rural clinical centers, such confirmatory tools are often unavailable. Clinicians in these settings rely heavily on refined penlight examination skills, past family photographs, and manual pharmacological testing with readily available ophthalmic agents.
13. Criticisms, Debates & Limitations
Despite centuries of documentation, clinical debates persist regarding the diagnosis and management of pupillary asymmetry. One ongoing challenge involves the strict demarcation between “physiologic” and “pathologic” cut-offs. While many textbooks use a 0.4 mm or 1.0 mm difference as a standard guideline, real-world variations are continuous. Healthy individuals can periodically demonstrate an asymmetry exceeding 1.0 mm, while subtle, early Horner’s syndrome may initially produce an inequality of less than 0.5 mm, creating diagnostic ambiguity in border zones.
Pharmacological testing with apraclonidine has also introduced controversy, particularly in pediatric populations. While safe in adults, apraclonidine can cause central nervous system depression, severe bradycardia, and hypotension in neonates and young infants due to systemic absorption across an immature blood-brain barrier. Neurologists caution against its use in patients under one year of age, favoring traditional, albeit hard-to-acquire, cocaine solutions or proceeding directly to non-pharmacologic imaging protocols.
Another common source of diagnostic confusion is the presence of an isolated internal ophthalmoplegia—a single dilated pupil without extraocular motility deficits. While microvascular ischemia (e.g., from diabetes or hypertension) regularly causes pupil-sparing third nerve palsies, clinicians debate the extent to which an isolated pupil can represent an emerging aneurysm. Although isolated internal ophthalmoplegia is almost always caused by an Adie’s tonic pupil or pharmacologic blockade, conservative neurosurgical guidelines still recommend neuroimaging when acute pain is present, generating debates over resource utilization.
14. Related Terms & Distinctions
Understanding anisocoria requires distinguishing it from other neuro-ophthalmological and pupillary terms:
- Relative Afferent Pupillary Defect (RAPD / Marcus Gunn Pupil): An afferent defect of the optic pathway. Crucially, a patient with an RAPD has completely equal pupil sizes (isocoria) in any fixed ambient light. The abnormality is revealed only dynamically during the “swinging-flashlight test,” when both pupils paradoxically dilate when the light swings from the healthy eye to the diseased eye.
- Mydriasis: The physiological or pathological enlargement (dilation) of the pupil. Mydriasis can be bilateral (e.g., in response to darkness, fright, or sympathomimetic drugs) or unilateral. Unilateral mydriasis causes anisocoria that worsens in light.
- Miosis: The constriction of the pupil. Like mydriasis, miosis can be bilateral (e.g., in sleep, bright light, or opiate toxicity) or unilateral. Unilateral miosis produces anisocoria that worsens in darkness.
- Corectopia: The eccentric displacement or malposition of the pupil away from its normal central location on the iris, which can occur alongside or independently of anisocoria due to trauma, congenital dysgenesis, or anterior segment dysgenesis.
- Dyscoria: An abnormal, irregular, or non-circular shape of the pupil. While frequently observed in eyes with traumatic or mechanical anisocoria (e.g., post-surgical iris tears), dyscoria refers specifically to geometric distortion rather than size inequality.
- Hippus: A physiologic, rhythmic, unprompted oscillation of pupil diameter occurring under continuous lighting conditions. Although hippus can occasionally appear asymmetrical, it represents a normal phenomenon and does not denote unilateral autonomic paralysis.
15. Summary / Key Takeaways
Anisocoria is a cardinal clinical sign reflecting unequal pupil sizes that stems fundamentally from efferent autonomic dysfunction or mechanical iris pathology. The cornerstone of clinical evaluation rests on comparing pupillary asymmetry between bright light and dark environments: an asymmetry that increases in the dark indicates failure of sympathetic dilation in the smaller pupil (suggestive of Horner’s syndrome), whereas an asymmetry that widens in bright light points toward parasympathetic underactivity or structural damage in the larger pupil (raising concern for oculomotor nerve palsy or an Adie’s tonic pupil).
While physiological anisocoria remains a common, benign finding with preserved light reactivity and long-term stability, acute-onset pupillary disparity warrants systematic investigation. Armed with an understanding of autonomic neuroanatomy, careful slit-lamp evaluation, targeted pharmacological testing, and modern quantitative pupillometry, clinicians can confidently differentiate benign variations from high-stakes neurovascular emergencies.
References
- Adie, W. J. (1932). Tonic pupils and absent tendon reflexes: A benign disorder sui generis; its complete and incomplete forms. Brain, 55(1), 98–113. https://doi.org/10.1093/brain/55.1.98
- Chen, J. W., Gombart, Z. J., Rogers, S., Gardiner, S. K., Cecil, S., & Bullock, R. M. (2011). Pupillary reactivity as an early indicator of increased intracranial pressure: The introduction of the Neurological Pupil Index. Surgical Neurology International, 2, 82. https://doi.org/10.4103/2152-7806.82248
- Horner, F. (1869). Über eine Form von Ptosis. Klinische Monatsblätter für Augenheilkunde, 7, 193–198.
- Koc, F., Kavuncu, S., Kansu, T., Acaroglu, G., & Firat, E. (2005). The sensitivity and specificity of 0.5% apraclonidine in the diagnosis of oculosympathetic paresis. Journal of Neuro-Ophthalmology, 25(2), 101–104. https://doi.org/10.1097/01.wno.0000165108.97036.bf
- Lam, B. L., Thompson, H. S., & Corbett, J. J. (1987). The prevalence of simple anisocoria. American Journal of Ophthalmology, 104(1), 69–73. https://doi.org/10.1016/0002-9394(87)90296-0
- Loewenfeld, I. E. (1999). The Pupil: Anatomy, Physiology, and Clinical Applications. Butterworth-Heinemann.