Presented as DNB Resident at Sri Sankaradeva Nethralaya, Guwahati

1. OCULAR REFLEXES
PRESENTER- DR. TANVI GUPTA

2. OCULOCARDIAC REFLEX

3. Definition -decrease in heart rate by greater than 20%1/ greater than 10%2 following globe
pressure or traction of the extraocular muscles. The reflex most commonly results in sinus
bradycardia. However, it also has a reported association with reduced arterial pressure,
arrhythmia, asystole, and even cardiac arrest.
The incidence of the oculocardiac reflex is reported to be anywhere from 14% to 90% and
decreases with age, meaning pediatric patients are most at risk.
Pediatric patients are also more susceptible to the detrimental consequences of this reflex
secondary to having a greater dependency on heart rate to maintain cardiac output.
1. StatPearls [Internet]. Leah M. Dunville1; Jeremy Kramer2. Oculocardiac Reflex. Last Update: May 17, 2019
.
2.Apt. L; Isenberg, s. & Gaffney, W.L. : The oculocardiac reflex in strabismus surgery. Amer.J. Ophthalmol, 1973, 76. 533-35.

4. Risk Factors
The OCR has been associated with various triggering stimuli- this reflex has most notably been
depicted during ophthalmologic procedures, more specifically during strabismus surgery;
however, it also may be activated by facial trauma, regional anesthetic nerve blocks, and during
mechanical stimulation.
Most common - traction to the extraocular muscles (Medial Rectus most common)
Direct pressure to the globe
Ocular manipulation
Ocular pain
Retrobulbar blocks
Ocular hematomas
Facial or Orbital trauma
Fatigable reflex - meaning its intensity will decrease with multiple, repeated stimuli.

5. Activation of stretch receptors in ocular and peri-orbital tissues- > Short and
long ciliary nerves -> Ciliary Ganglion -> Ophthalmic division of Trigeminal
Nerve (V1) -> Gasserian Ganglion
CNS (processes the sensory information and there is internuclear
communication between the trigeminal sensory nucleus and the visceral
motor nucleus of the vagus nerve)
stimulation of efferent pathway
Impulses exit Brainstem -> reach myocardium (synapse at sino-atrial node
and activate of vagal motor response) leading to bradycardia

7. Complications
 Sinus bradycardia
 Arrhythmia
 Reduced arterial pressure
 Ventricular tachycardia
 Ventricular fibrillation
 Multifocal premature ventricular contractions
 Ventricular bigeminy
 Asystole
 Cardiac arrest
 Dizziness
 Light-headedness
 Nausea (PONV- post op nausea vomiting in children)
 Weakness

8. Definitive treatment - immediate cessation of the triggering stimulus.
When in the operating room, immediate removal of pressure to the globe or surrounding orbital tissues can
terminate the reflex. The next step of the procedure is to proceed with caution.
Unfortunately, in less controlled circumstances, such as trauma, cessation of the triggering stimulus can be more
challenging. In these instances, pharmacologic management may be required, and cardiac monitoring should be
initiated.
Pharmacologic management
Pretreatment with intravenous anticholinergics, such as atropine or glycopyrrolate, decreases the incidence of
OCR. Atropine works by blocking peripheral muscarinic receptors of the heart and causes increased firing at the
sinoatrial node as well as conduction through the AV node. This opposes the vagal response, or the efferent limb,
of the OCR.
Through its stimulation of sympathetic activity, ketamine may counteract vagal stimulation caused by OCR.
Blunting the afferent limb of the reflex arc can also decrease OCR occurrence. This can be done using a retro or
peribulbar block with xylocaine hydrochloride to block the ciliary ganglion. This in combination with another
agent shown to decreased OCR incidence, such as atropine, can provide further protection from OCR activation.

9. CORNEAL REFLEX

10. The tear production reflex utilizes the same pathways as the blink reflex. However it activates the lacrimal gland via
parasympathetic branches (green line).
Contact of cornea with
irritant or foreign substance
The corneal blink reflex is caused by a loop between the trigeminal sensory nerves and the facial motor (VII) nerve
innervation of the orbicularis oculi muscles.

11. The reflex activates when a sensory stimulus contacts either free nerve endings or
mechanoreceptors within the epithelium of the cornea.
Sensory information transmits through the ophthalmic division of the trigeminal nerve (V)
to synapse within the spinal trigeminal nucleus in the brainstem.
The contacted nerve within the spinal trigeminal nucleus then projects to the facial
nucleus and synapses with the facial nerve
The facial nerve exits the facial nucleus, wraps around the abducens nucleus, and exits the
skull at the stylomastoid foramen.
After exiting the skull, the facial nerve travels medially over the surface of the face to
activate the orbicularis oculi muscle. Contraction of this muscle causes a blink movement
(eye closure)

12. Unilateral trigeminal nerve dysfunction (i.e., in the ipsilateral brainstem, V1 or
V2 divisions) prevents both eyes from blinking after stimulation of the ipsilateral cornea
Unilateral facial nerve dysfunction prevents the ipsilateral eye from blinking when its
cornea is stimulated, although the contralateral eye blinks normally.
In patients with unilateral sensorineural hearing loss, it raises the possibility
of cerebellopontine angle tumors such as acoustic neuroma.
Nonetheless, the clinical utility of the asymmetrical corneal reflex is limited. The reflex is
inexplicably absent unilaterally in 8% of healthy elderly patients, and the sensitivity of
the absent reflex for acoustic neuroma is only 33%, the finding usually indicating the
tumor has already grown to a large size (>2 cm in diameter).

13. ACCOMODATION REFLEX

15. PUPILLARY REFLEX

16. The pupillary light reflex requires CN II, CN III, and central brain stem connections. Light
shined in one eye stimulates retinal photoreceptors, and subsequently retinal ganglion cells,
whose axons travel through the optic nerve, chiasm, and tract to terminate in
the pretectum (pretectal nucleus). The pretectal neurons project to a portion of the nucleus
of Edinger-Westphal on both sides. This preganglionic parasympathetic nucleus projects
to ciliary ganglion neurons, which in turn send postganglionic axons to innervate the
pupillary constrictor muscle. Thus, light shined in one eye normally results in the constriction
of both pupils (ipsilateral pupillary constriction—direct response; contralateral pupillary
constriction—consensual response).
Lesions of CN II produce an unresponsive pupillary light reflex on both sides (afferent
pupillary defect) from light shined in the eye on the side of the CN II lesion. With light shined
in the unaffected eye, both pupils constrict.
Lesions of CN III result in unresponsive ipsilateral pupillary constriction on the affected side
(the pupil is “fixed and dilated”) when light is shined in either eye (efferent pupillary defect).

18. THANK YOU