Pupil size should be measured, ideally with reference to a neurological observation chart or similar. The average size is mm Bersten et al, The pupils should be equal in size. Pupil shape should be ascertained. It should be round; abnormal shapes may indicate cerebral damage; oval shape could indicate intracranial hypertension Fairley, The pupils should be identical in shape.
Pupil reaction to light should be brisk and after removal of the light source, the pupil should return to its original size. There should also be a consensual reaction to the light source, that is the opposite pupil also constricts when the light source is applied to one eye Jevon, Pupil reaction should be documented as per local policy, for example B brisk , S sluggish or N no reaction. Both pupils should react equally to light. Unreactive pupils can be caused by an expanding mass, for example a blood clot exerting pressure on the third cranial nerve; a fixed and dilated pupil may be due to herniation of the medial temporal lobe.
This procedure should be undertaken only after approved training, supervised practice and competency assessment, and carried out in accordance with local policies and protocols. Sign in or Register a new account to join the discussion. The parasympathetic efferent pupillary pathway begins where the afferent pathway left off: the Edinger-Westphal nucleus. Sympathetic innervation to the eye involves a three-neuron chain. The sympathetic central first-order neuron begins in the dorsolateral hypothalamus and travels, uncrossed, through the brainstem to the ciliospinal center of Budge at the level of C8 to T2 in the cervical spinal cord.
The preganglionic second-order neuron then travels up the sympathetic chain, over the lung apex and through several ganglia to synapse at the superior cervical ganglion, located where the carotid bifurcates. When focus is changed from far to near, a triad of responses occurs: convergence, accommodation and pupillary constriction. The neural pathway for this triad of responses is not completely understood, but the pupillary response is dependent on a supranuclear frontal and occipital lobe influence connection between the pupillary sphincter, ciliary body muscles and medial recti neurons.
The afferent aspect of the pupillary near response follows the afferent visual pathway to higher cortical centers in the striate cortex; that information is relayed to the frontal eye fields then to the oculomotor and Edinger-Westphal nuclei.
This pathway bypasses the pretectal nuclei. Testing the near response is necessary only if the pupillary light reflex is abnormal; there is no pathologic situation where the near response will be abnormal with a normal pupillary light reflex. Having vision is not a requirement for an intact near response. A normal pupillary exam using a swinging flashlight will show equal constriction of both pupils, regardless of which eye the light is directed at, indicating an intact direct and consensual pupillary light reflex.
An afferent pupillary defect APD is observed when there is a reduced pupillary constriction of both eyes direct and consensual responses compared to the bilateral constriction response when the light is shone into the unaffected eye. An APD is always relative to the other eye i. With a swinging flashlight, a pupil with an APD will constrict less therefore appearing to partially dilate when the light is swung from the unaffected to the affected eye. Of note, a fixed pupil does not always exhibit an APD.
Neutral density filters of increasing density can be used over the unaffected eye until the pupillary responses are equal on the swinging flashlight test. This may be helpful to quantify the change in the relative depth of an APD; clinically, however, a subjective grading scale is usually used in lieu. The descriptions used in the grading scale indicate the reaction of the pupil with an APD when the light is swung from the unaffected to the affected pupil.
Also of note, anisocoria itself is not an indication of an APD; there most often is one without the other. Though they can coexist, generally an APD does not cause anisocoria. Anisocoria indicates a difference in pupil sizes of 0. Nonphysiologic anisocoria implies a diseased efferent pathway and can be caused by a plethora of conditions, which will be further discussed. Efferent parasympathetic pupillary defects will cause an abnormally dilated pupil and can occur due to disruption of the pupillary fibers anywhere along their path from the Edinger-Westphal nucleus to the iris sphincter.
This will manifest with anisocoria greater in the light than dark, due to poor constriction of the larger affected pupil. An abnormally dilated pupil could also be due to trauma, recent ocular surgery, angle closure or contact with pharmacologic agents.
Efferent sympathetic pupillary defects will cause an abnormally miotic pupil and can occur due to disruption of the pupillary fibers anywhere along their path from the hypothalamus to the iris dilator. This path is long and courses from the central head, down through the neck and back to the eye, so is susceptible to a variety of problems due to its long route.
Pupillary fiber disruption along this path will manifest with anisocoria greater in the dark than light, due to poor dilation of the smaller affected pupil.
An abnormally constricted pupil could also be due to uveitis or contact with pharmacologic agents. The accompanying table shows a list of some conditions that could cause efferent pupillary defects and thus anisocoria.
We will briefly review some of these conditions. The review will primarily discuss pupillary responses and testing in these conditions and will only briefly cover management of the specific conditions. CN III innervates the levator; medial, superior and inferior recti; the inferior oblique; and the iris sphincter. The palsy may be complete or partial, depending on the cause and location of CN III disruption, and may be pupil involving or sparing.
An involved pupil will be dilated and minimally reactive, but could be only partially involved and show a partially dilated and sluggishly responsive pupil. CN III palsy due to compression tumor, aneurysmal is likely to be pupil involving because the pupillary fibers are superficial in the cranial nerve, whereas ischemic CN III palsies typically are pupil sparing. Pupil involvement due to compression will result in lost direct, consensual and near responses in the affected eye.
Aberrant regeneration may occur over several months and may lead to light-near dissociation, with the near response arising from misdirected innervation from the medial rectus. Pupil-involving cases require emergent evaluation because it is likely to be associated with an aneurysm see case report. Emergent imaging, preferably MRI and MRA, should be ordered to rule out aneurysm in acute pupil-involving presentations of CN III palsy and in patients with no vasculopathic risk factors, particularly young patients.
In pupil-sparing cases, where microvascular ischemia is the probable offender if the patient history includes vasculopathy e. Daily observation is recommended for the first 5 days to monitor for delayed pupil involvement, then every 4 to 6 weeks thereafter. Improved function is expected within about 3 months. Aberrant regeneration takes time, so is most often congenital or associated with a history of trauma or a slowly expanding aneurysm or mass, but is not associated with microvascular CN III palsy.
Pupil-sparing CN III palsies can also be related to giant cell arteritis, so in applicable patients, this must also be ruled out. Physiologic anisocoria. Notice approximately equal amounts of anisocoria in bright top and dim bottom lighting. When the light is moved back to the normal pupil again, that pupil will reconstrict again as there was no consensual reflex from the abnormal pupil. This clinical sign is known as a relative afferent pupillary defect RAPD. Even in the presence of bilateral optic nerve disease, an RAPD can still be detected as in most cases, the damage will not be equal: thus the optic nerve with the greater damage will manifest in a RAPD.
In exceptional cases, when the degree of damage to both optic nerves is very similar, both pupils will show sluggish reactions to light. Causes of RAPD include: optic nerve disorders optic nerve compression, optic neuritis , chiasm compression, retinal detachment, large unilateral macular lesion or advanced unilateral glaucoma.
Step 4 — Accommodation. Finally, accommodation can be tested by asking the patient to fixate on a distant point and then asking them to shift their focus quickly to a near object. Normally, the pupils constrict and the eyes converge while fixating on a near object. In exams, but certainly not in real life, pupils that constrict through accommodation but not through direct light stimulation, if due to neurosyphilis, are called Argyll Robertson pupils.
I guarantee you will never see a case of this in your entire career, but you will be punished by examiners for not knowing it. This is referred to as a light-near dissociation.
The pupil usually shows slow constriction on prolonged near effort and slow re-dilatation to distance. It is due to damage of the post-ganglionic fibres of the parasympathetic pathway. This condition usually affects females and can be caused by viral infection, diabetes or trauma but is often idiopathic.
If decreased tendon reflexes are present it is referred to as Holmes Adie syndrome. Diagnosis is confirmed by denervation hypersensitivity to weak cholinergic agents 0. This happens when the anterior chamber angle is closed mechanically by the crowding of the peripheral iris when the pupil is semi dilated.
This could be due to an intraocular tumour, formation of anterior synechiae or posterior synechiae following uveitis or rubeotic glaucoma caused by fibrovascular proliferation in the chamber angle secondary to retinal ischaemia diabetes and central retinal vein occlusion classically. This condition is an ocular emergency often suspected from the history alone but needs to be confirmed with slit-lamp examination.
A patient with this condition will need to be referred immediately to the ophthalmologist. Intraocular pressure lowering drugs, topical miotics and glaucoma drops are used to lower the eye pressure and these patients can be listed for an iridotomy or peripheral iridectomy.
A third nerve palsy can either be complete or partial. You can confirm that the lesion is in the efferent pathway by shining light into that eye and noting that the pupil does not constrict but the consensual light reflex in the contralateral pupil is intact.
Causes include microvascular infarction — occlusion of the vasa nervorum risks: hypertension diabetes, atherosclerosis , compressive lesion aneurysm, tumour or due to trauma. In a partial third nerve palsy, the symptoms are not so severe but could be a sign of an impending emergency. Rapidly increasing intracranial pressure resulting from an acute extradural or subdural haematoma, often compresses the third nerve against the crest of the petrous temporal bone.
The parasympathetic fibres are superficially placed and therefore the first to suffer, causing the pupil to dilate progressively on the affected side.
Pupillary dilatation is an urgent indication for surgical decompression of the brain and a computed tomography CT angiogram looking for intracranial aneurysms is almost always indicated.
This results in mild ptosis, a regular miotic pupil with pupil dilation lag, anhydrosis and pseudoenophthalmos due to the ptosis and smaller palpebral fissure — see Figure 4. Check the face for impaired sweating on the same side may be easier to ascertain this information from the history. Examine the colour of the iris. A deficient sympathetic stimulation in childhood results in impaired melanin deposition by the melanocytes in the superficial stroma of the iris.
Ten percent topical cocaine dilates a normal pupil, as it prevents the re-uptake of norepinephrine from the post-ganglionic synapse resulting in overstimulation at the synapse and pupil dilatation.
A post-cocaine anisocoria of greater than 0. A patient with a unilateral red, painful eye with impaired vision and a small irregular pupil is most likely suffering from anterior uveitis.
The diagnosis can be easily made on slit-lamp examination: an acute episode will show ciliary injection, endothelial dusting, aqueous cells, anterior vitreous cells and in severe cases hypopyon and posterior synechiae. Recurrent episodes of anterior uveitis will result in a painless irregular mitotic pupil which does not dilate in the dark.
On slit-lamp examination, pigment deposits on the lens, keratoprecipitates can be seen and in some cases iris nodules and atrophy will also be present.
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