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| PG CORNER |
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| Year : 2019 | Volume
: 31
| Issue : 2 | Page : 167-171 |
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Pupil: Assessment and diagnosis
Rita Mary Tomy
Department of Ophthalmology, Oculoplastics and Neuroophthalmology Unit, Little Flower Hospital, Angamaly, Kerala, India
| Date of Web Publication | 27-Aug-2019 |
Correspondence Address:
Dr. Rita Mary Tomy
The Retreat, CN-203, Angamaly - 683 572, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/kjo.kjo_48_19
Pupil examinations are quick, noninvasive tests that give a clue to the health of our eyes and nervous system. Pupillary assessment is an important part of neurological assessment because changes in the size, equality, and reactivity of the pupils can provide vital diagnostic information. This article intends to throw light into the basic techniques of pupillary assessment and common conditions that should not be missed in your clinical evaluation.
Keywords: Anisocoria, Horner's, pupil, pupillary reflexes
How to cite this article:
Tomy RM. Pupil: Assessment and diagnosis. Kerala J Ophthalmol 2019;31:167-71 |
| Introduction | |  |
The pupil is an opening located at the center of the iris that allows light to enter the retina. The size of the pupil determines the amount of light that enters the eye. The pupil size is controlled by the dilator and sphincter muscles of the iris. Normally, there is one pupil that is almost central (slightly nasal), and the size varies from 2.5 to 4 mm depending on the illumination.
Functions of pupil
- It regulates the amount of light entering the eye
- It improves the visual acuity because it prevents the irregular refraction by the periphery of the cornea and lens
- It allows the passage of aqueous humor from the posterior chamber to the anterior chamber.
Anatomy
The iris contains two groups of smooth muscles [Figure 1]:
- A circular group called sphincter pupillae
- A radial group called dilator pupillae.
The pupillary reflexes
There are essentially three reflexes to test.[1]
- Light-reflex test
- Near-reflex test
- Swinging flashlight test – for afferent papillary defect.
Light-reflex test
- What it assesses – The integrity of the pupillary light reflex pathway
- How to perform – Dim the ambient light and ask the patient to fixate on a distant target. Shine on the right eye from the right side and on the left eye from the left side
- Normal response – A brisk, simultaneous, equal response of both pupils in response to light shone in one or the other eye.
Parasympathetic pathway is responsible [Figure 2].
- First order – Retina to pretectal nucleus in the brainstem (at the level of the superior colliculus)
- Second order – Pretectal nucleus to Edinger–Westphal nuclei (EWN, bilateral innervation)
- Third order – EWN to ciliary ganglion
- Fourth order – Ciliary ganglion to sphincter pupillae (via short ciliary nerves).
Consensual light reflex
The light reflex is mediated by the retinal photoreceptors and subserved by four neurons. The second internuncial connects each pretectal nucleus to both EWNs; thus, a unilocular light stimulus evoked a bilateral and symmetrical pupillary constriction.
Near-reflex test
- What it assesses – The miosis component of near fixation
- How to perform it – In a normally lit room, instruct the patient to look at a distant target. Bring an object into the near point and observe the pupillary reflex when their fixation shifts to the near target
- Normal response – Brisk constriction of pupils.
Accommodation is a component of near reflex [Figure 3].
The afferent stimulus is carried from retina via the optic nerve, tract, and radiation to the calcarine cortex of the occipital lobe. From here, fibers pass to the frontal lobe, and from here, the corticobulbar fibers go to the III cranial nerve (C.N.) nucleus (nucleus of the medial rectus and the EWN) which results in accommodation reflex.
Afferent pupillary defect
- Absolute afferent pupillary defect
An absolute afferent pupillary defect (amaurotic pupil) is caused by a complete optic nerve lesion and is characterized by the following:
- The involved eye is completely blind (i.e., no light perception)
- Both pupils are equal in size
- When the affected eye is stimulated by light, neither pupil reacts
- When the normal eye is stimulated, both pupils react normally
- The near reflex is normal in both eyes.
- Relative afferent pupillary defect
A relative pupillary defect (Marcus Gunn pupil) is caused by an incomplete optic nerve lesion or severe retinal disease. The pupils respond weakly to stimulation of the diseased eye and briskly to that of the normal eye.
Swinging flashlight test
- What it assesses – Relative afferent papillary defect
- How to perform it – In a dimly lit room, a light source is alternatively switched from one eye to the other and back, thus stimulating each eye in rapid succession
- Response – A right relative defect is characterized by the following
- When the normal left eye is stimulated, both pupils constrict
- When the light is swung to the diseased right eye, both pupils dilate instead of constricting
- When the normal left eye is again stimulated, both pupils constrict once more
- When the diseased right eye is stimulated, both pupils dilate.
Other pupillary reflexes
Ciliospinal reflex
The ciliospinal reflex (pupillary skin reflex) consists of dilation of the ipsilateral pupil (increases in size 1–2 mm from baseline) in response to pain applied to the neck, face, and upper trunk.
This reflex is absent in Horner's syndrome and lesions involving the cervical sympathetic fibers.
| Disorders of the Pupil | | |
[TAG:2]The Following are Common Disorders of the Pupil[1],[2].[/TAG:2]
Mydriasis
This results from paralysis of the parasympathetic fibers. Most commonly such lesions are due to vascular accidents in the midrain, tentorial herniation (due to cerebral space-occupying lesions), or aneurysms of the carotid artery. Other conditions commonly causing mydriasis are as follows:
- III C.N. palsy
- Adie's tonic pupil
- Posttraumatic iridoplegia
- Overdose – Glutethimide, amphetamine, cocaine
- Poisoning – Belladonna, Datura
- Drugs – Anticholinergics such as atropine, homatropine, and scopolamine; sympathomimetics such as epinephrine, norepinephrine, and phenylephrine.
Miosis
This indicates a lesion in the sympathetic pathway to the pupillary dilator.
Thus, the lesion may be in the hypothalamus, brainstem, lateral aspect (the spinal cord as far down as the upper thoracic segments), sympathetic chain, cervical sympathetic ganglion, precarotid plexus, and sympathetic fibers, which run to the orbit accompanying the ophthalmic division of the V C.N.
Miosis: Causes
- Horner's syndrome
- Argyll Robertson (AR) pupils
- Pontine tumors or hemorrhages
- Opiates
- Organophosphorus or alcohol poisoning
- Pilocarpine drops
- Old age
- Drugs – Cholinomimetics such as pilocarpine, methacholine, and muscarine; cholinesterase inhibitors such as physostigmine and neostigmine.
Light-near dissociation
The pupillary reaction to light is normally equal to or greater than the reaction to near. Light-near dissociation refers to a disparity between the light and near reactions. The most common form is a poor light response but a good-near response. The converse is rare.
Mechanism
The fibers mediating the pupillary light reflex enter the dorsal brainstem, but the near-response fibers ascend to the EWN from the ventral aspect. Pressure on the pupillary fibers in the region of the pretectum and posterior commissure impairs light reaction. However, fibers mediating the near response, the EWN, and efferent pupil fibers are spared.
AR pupil is the prototype.
AR pupils are small (miosis) and irregular in outline and have light-near dissociation. They react poorly to light but very well to near reflex. AR pupils are usually bilateral and symmetrical. Vision is not much affected. The lesion lies in the periaqueductal region, pretectal area, and rostral midbrain dorsal to the EWNs. It is found in neurosyphilis, tabes dorsalis, general paralysis of the insane (paralytic dementia), and aortic regurgitation.
Anisocoria
Anisocoria[2] is defined as a difference of 0.4 mm or more between the sizes of the pupils of the eyes. Physiological anisocoria is present in 20% [Figure 4].
Other causes are given in [Table 1].
[INLINE:]
Oculosympathetic palsy (Horner's syndrome)
Anatomy
Sympathetic pathway
- First order – Posterior hypothalamus to ciliospinal center of budge (C8–T2) – uncrossed in the brainstem [Figure 5]
- Second order – Ciliospinal center of budge to superior cervical ganglion
- Third order – Superior cervical ganglion to dilator pupillae muscle (close to internal carotid artery and joins V1 intracranially) via nasociliary nerve and the long ciliary nerves.
Causes
Causes are listed in [Table 2]
Signs
- Partial ptosis
- Miosis
- Normal pupillary reactions to light and near
- Hypochromic heterochromia (may be seen if congenital)
- Slight elevation of inferior eyelid as a result of weakness of inferior tarsal muscle
- Reduced ipsilateral sweating, but only if lesion is below the superior cervical ganglion.
Confirmation of Horner's syndrome is with instillation of a drop of 4% cocaine. In physiological anisocoria, this results in dilatation, whereas it does not where there is a Horner's syndrome.
For further localization – 1% hydroxyamphetamine is added (48 h after cocaine test). Pupillary dilatation suggests a central or preganglionic Horner's syndrome, whereas if dilatation does not occur, the lesion is likely to be postganglionic.
Adie's tonic pupil
This describes a unilateral (80% of the cases) mydriatic pupil in otherwise healthy patients (typically young adults, especially women).
Cause
Denervation of the postganglionic supply to the sphincter pupillae and the ciliary muscle, which may follow a viral illness (e.g. herpes zoster).
Signs
- Large and regular pupil
- Sluggish reaction to light and is associated with vermiform movements of the pupillary border but normal-near reflex
- Re-dilatation after the near response is slow
- Consensual light reflex is absent or sluggish
- Over months to years, the pupil diminishes in size to eventually become miotic (little old Adie').
Associations
In some cases, there are diminished deep tendon reflexes (Holmes–Adie syndrome) with or without autonomic dysfunction.
Diagnosis
The diagnosis is confirmed by the pupil's hypersensitivity to weak miotic drops (0.05–0.125% pilocarpine), which causes the abnormal pupil to contract vigorously and the normal pupil minimally. It is a benign condition: with time, the accommodative response improves while the tonicity of the light response gets worse. There is no treatment and patient reassurance is important.
Hemianopic pupil (Wernicke's pupil)
It is seen in optic tract lesions with hemianopia. Stimulating the blind half of retina, pupil shows no reaction. Stimulating seeing half of retina, pupil shows reaction.
It is difficult to elicit – due to scattering and diffusion of light. Use a narrow streak of light.
Hutchinson's pupil
Hutchinson's pupil[3] is a clinical sign in which the pupil on the side of an intracranial mass lesion is dilated and unreactive to light, due to compression of the oculomotor nerve on that side.
Cause
Cause is concussion injury to brain and it is often associated with subdural hemorrhage and unconsciousness.
Mechanism
The parasympathetic fibers to the pupil are responsible for pupillary constriction. The fibers pass through the periphery of the oculomotor nerve and hence are the first to be affected in case of compression of the nerve.
Tectal (dorsal midbrain) pupil
- In dim light, there is bilateral mydriasis which may be asymmetrical
- In bright light, neither pupil constricts
- On accommodation, both pupils constrict normally
- After instillation of pilocarpine 0.1% to both eyes, neither pupil constricts.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Khurana A K. Comprehensive ophthalmology. 4 th ed. New Delhi: New Age International; 2007. p. 311.  |
| 2. | Miller N, Newman N, Walsh F, Hoyt W. Walsh and Hoyt's Clinical Neuro-Ophthalmology. 6 th ed., Vol. 1. Sec. 2. Philadelphia, PA: Lippincott Williams and Wilkins; 2005. p. 748. |
| 3. | Bowling B, Kanski J. Kanski's clinical ophthalmology. 8 th ed. Erscheinungsort nicht ermittelbar: Elsevier, 2016. p. 809 |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2]
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